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Sample records for attenuates vascular calcification

  1. Insulin attenuates vascular smooth muscle calcification but increases vascular smooth muscle cell phosphate transport.

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    Wang, Cecilia C Low; Sorribas, Victor; Sharma, Girish; Levi, Moshe; Draznin, Boris

    2007-11-01

    Medial artery vascular smooth muscle cell (VSMC) calcification increases the risk of cardiovascular mortality in type 2 diabetes. However, the influence of insulin on VSMC calcification is unclear. We explored the effects of insulin on rat VSMC calcification in vitro and found that in a dose-dependent fashion, insulin attenuates VSMC calcification induced by high phosphate conditions as quantified by the o-cresolphthalein calcium (OCPC) method. In an in vitro model of insulin resistance in which cells are exposed to elevated insulin concentrations and the PI 3-kinase pathway is selectively inhibited, increased VSMC calcification was observed, suggesting that the PI 3-kinase pathway is involved in this attenuating effect of insulin. We postulated that insulin may also have an effect on phosphate or calcium transport in VSMC. We found that insulin increases phosphate transport at 3 and 24 h. This effect was mediated by increased Vmax for phosphate transport but not Km. Because type III sodium-phosphate co-transporters Pit-1 and Pit-2 are found in VSMC, we examined their expression by Western blot and real-time RT-PCR. Insulin stimulates Pit-1 mRNA modestly (*p<0.01 versus control), an effect inhibited by PD98059 but not by wortmannin. Pit-1 protein expression is induced by insulin, an effect also inhibited by PD98059 (*p<0.001 versus insulin alone). Our results suggest a role for insulin in attenuating VSMC calcification which may be disrupted in selective insulin signaling impairment seen in insulin resistance. This effect of insulin contrasts with its effect to induce phosphate transport in VSMC.

  2. Quercetin Attenuates Vascular Calcification through Suppressed Oxidative Stress in Adenine-Induced Chronic Renal Failure Rats

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    Xue-ying Chang

    2017-01-01

    Full Text Available Background. This study investigated whether quercetin could alleviate vascular calcification in experimental chronic renal failure rats induced by adenine. Methods. 32 adult male Wistar rats were randomly divided into 4 groups fed normal diet, normal diet with quercetin supplementation (25 mg/kg·BW/d, 0.75% adenine diet, or adenine diet with quercetin supplementation. All rats were sacrificed after 6 weeks of intervention. Serum renal functions biomarkers and oxidative stress biomarkers were measured and status of vascular calcification in aorta was assessed. Furthermore, the induced nitric oxide synthase (iNOS/p38 mitogen activated protein kinase (p38MAPK pathway was determined to explore the potential mechanism. Results. Adenine successfully induced renal failure and vascular calcification in rat model. Quercetin supplementation reversed unfavorable changes of phosphorous, uric acid (UA and creatinine levels, malonaldehyde (MDA content, and superoxide dismutase (SOD activity in serum and the increases of calcium and alkaline phosphatase (ALP activity in the aorta (P<0.05 and attenuated calcification and calcium accumulation in the medial layer of vasculature in histopathology. Western blot analysis showed that iNOS/p38MAPK pathway was normalized by the quercetin supplementation. Conclusions. Quercetin exerted a protective effect on vascular calcification in adenine-induced chronic renal failure rats, possibly through the modulation of oxidative stress and iNOs/p38MAPK pathway.

  3. Vascular calcification: Inducers and inhibitors

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    Lee, Donghyun, E-mail: dhlee@cau.ac.kr [Department of Biomedical Engineering, Division of Integrative Engineering, Chung-Ang University, 221 Heukseok-Dong, Dongjak-Gu, Seoul 156-756 (Korea, Republic of)

    2011-09-15

    Highlights: {center_dot} Types of vascular calcification processes. {center_dot} Inducers of vascular calcification. {center_dot} Inhibitors of vascular calcifications. {center_dot} Clinical utility for vascular calcification therapy. {center_dot} Implications for the development of new tissue engineering strategies. - Abstract: Unlike the traditional beliefs, there are mounting evidences suggesting that ectopic mineral depositions, including vascular calcification are mostly active processes, many times resembling that of the bone mineralization. Numbers of agents are involved in the differentiation of certain subpopulation of smooth muscle cells (SMCs) into the osteoblast-like entity, and the activation and initiation of extracellular matrix ossification process. On the other hand, there are factors as well, that prevent such differentiation and ectopic calcium phosphate formation. In normal physiological environments, activities of such procalcific and anticalcific regulatory factors are in harmony, prohibiting abnormal calcification from occurring. However, in certain pathophysiological conditions, such as atherosclerosis, chronic kidney disease (CKD), and diabetes, such balances are altered, resulting in abnormal ectopic mineral deposition. Understanding the factors that regulate the formation and inhibition of ectopic mineral formation would be beneficial in the development of tissue engineering strategies for prevention and/or treatment of such soft-tissue calcification. Current review focuses on the factors that seem to be clinically relevant and/or could be useful in developing future tissue regeneration strategies. Clinical utilities and implications of such factors are also discussed.

  4. Prevention of vascular calcification with bisphosphonates without affecting bone mineralization: a new challenge?

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    Neven, Ellen G; De Broe, Marc E; D'Haese, Patrick C

    2009-03-01

    Arterial calcification has been found to coexist with bone loss. Bisphosphonates, used as standard therapy for osteoporosis, inhibit experimentally induced vascular calcification, offering perspectives for the treatment of vascular calcification in renal failure patients. However, Lomashvili et al. report that the doses of etidronate and pamidronate that are effective in attenuating aortic calcification also decrease bone formation and mineralization in uremic rats, limiting their therapeutic use as anticalcifying agents.

  5. Vascular Adventitia Calcification and Its Underlying Mechanism.

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    Na Li

    Full Text Available Previous research on vascular calcification has mainly focused on the vascular intima and media. However, we show here that vascular calcification may also occur in the adventitia. The purpose of this work is to help elucidate the pathogenic mechanisms underlying vascular calcification. The calcified lesions were examined by Von Kossa staining in ApoE-/- mice which were fed high fat diets (HFD for 48 weeks and human subjects aged 60 years and older that had died of coronary heart disease, heart failure or acute renal failure. Explant cultured fibroblasts and smooth muscle cells (SMCswere obtained from rat adventitia and media, respectively. After calcification induction, cells were collected for Alizarin Red S staining. Calcified lesions were observed in the aorta adventitia and coronary artery adventitia of ApoE-/-mice, as well as in the aorta adventitia of human subjects examined. Explant culture of fibroblasts, the primary cell type comprising the adventitia, was successfully induced for calcification after incubation with TGF-β1 (20 ng/ml + mineralization media for 4 days, and the phenotype conversion vascular adventitia fibroblasts into myofibroblasts was identified. Culture of SMCs, which comprise only a small percentage of all cells in the adventitia, in calcifying medium for 14 days resulted in significant calcification.Vascular calcification can occur in the adventitia. Adventitia calcification may arise from the fibroblasts which were transformed into myofibroblasts or smooth muscle cells.

  6. Proatherogenic pathways leading to vascular calcification

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    Mazzini, Michael J. [Department of Cardiology, Boston University Medical Center, Boston, MA (United States); Schulze, P. Christian [Department of Medicine, Boston University Medical Center, Boston, MA (United States)]. E-mail: christian.schulze@bmc.org

    2006-03-15

    Cardiovascular disease is the leading cause of morbidity and mortality in the western world and atherosclerosis is the major common underlying disease. The pathogenesis of atherosclerosis involves local vascular injury, inflammation and oxidative stress as well as vascular calcification. Vascular calcification has long been regarded as a degenerative process leading to mineral deposition in the vascular wall characteristic for late stages of atherosclerosis. However, recent studies identified vascular calcification in early stages of atherosclerosis and its occurrence has been linked to clinical events in patients with cardiovascular disease. Its degree correlates with local vascular inflammation and with the overall impact and the progression of atherosclerosis. Over the last decade, diverse and highly regulated molecular signaling cascades controlling vascular calcification have been described. Local and circulating molecules such as osteopontin, osteoprogerin, leptin and matrix Gla protein were identified as critical regulators of vascular calcification. We here review the current knowledge on molecular pathways of vascular calcification and their relevance for the progression of cardiovascular disease.

  7. Mechanisms of vascular calcification and associated diseases.

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    Marulanda, Juliana; Alqarni, Saleh; Murshed, Monzur

    2014-01-01

    Mineralization of bone and tooth extracellular matrix (ECM) is a physiologic process, while soft tissue mineralization, also known as ectopic mineralization (calcification), is a pathologic condition. Vascular calcification is common in aging and also in a number of genetic and metabolic disorders. The calcific deposits in arteries complicate the prognosis and increase the morbidity in diseases such as atherosclerosis, diabetes and chronic kidney disease (CKD). To completely understand the pathophysiology of these lifethreatening diseases, it is critical to elucidate the molecular mechanisms underlying vascular calcification. Unveiling these mechanisms will eventually identify new therapeutic targets and also improve the management of the associated complications. In the current review, we discussed the common determinants of ECM mineralization, the mechanism of vascular calcification associated with several human diseases and outlined the most common therapeutic approaches to prevent its progression.

  8. [Vascular Calcification - Pathological Mechanism and Clinical Application - . Role of vascular smooth muscle cells in vascular calcification].

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    Kurabayashi, Masahiko

    2015-05-01

    Vascular calcification is commonly seen with aging, chronic kidney disese (CKD), diabetes, and atherosclerosis, and is closely associated with cardiovascular morbidity and mortality. Vascular calcification has long been regarded as the final stage of degeneration and necrosis of arterial wall and a passive, unregulated process. However, it is now known to be an active and tightly regulated process involved with phenotypic transition of vascular smooth muscle cells (VSMC) that resembles bone mineralization. Briefly, calcium deposits of atherosclerotic plaque consist of hydroxyapatite and may appear identical to fully formed lamellar bone. By using a genetic fate mapping strategy, VSMC of the vascular media give rise to the majority of the osteochondrogenic precursor- and chondrocyte-like cells observed in the calcified arterial media of MGP (- / -) mice. Osteogenic differentiation of VSMC is characterized by the expression of bone-related molecules including bone morphogenetic protein (BMP) -2, Msx2 and osteopontin, which are produced by osteoblasts and chondrocytes. Our recent findings are that (i) Runx2 and Notch1 induce osteogenic differentiation, and (ii) advanced glycation end-product (AGE) /receptor for AGE (RAGE) and palmitic acid promote osteogenic differentiation of VSMC. To understand of the molecular mechanisms of vascular calcification is now under intensive research area.

  9. Magnesium Attenuates Phosphate-Induced Deregulation of a MicroRNA Signature and Prevents Modulation of Smad1 and Osterix during the Course of Vascular Calcification

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    Loïc Louvet

    2016-01-01

    Full Text Available Vascular calcification (VC is prevalent in patients suffering from chronic kidney disease (CKD. High phosphate levels promote VC by inducing abnormalities in mineral and bone metabolism. Previously, we demonstrated that magnesium (Mg2+ prevents inorganic phosphate- (Pi- induced VC in human aortic vascular smooth muscle cells (HAVSMC. As microRNAs (miR modulate gene expression, we investigated the role of miR-29b, -30b, -125b, -133a, -143, and -204 in the protective effect of Mg2+ on VC. HAVSMC were cultured in the presence of 3 mM Pi with or without 2 mM Mg2+ chloride. Total RNA was extracted after 4 h, 24 h, day 3, day 7, and day 10. miR-30b, -133a, and -143 were downregulated during the time course of Pi-induced VC, whereas the addition of Mg2+ restored (miR-30b or improved (miR-133a, miR-143 their expression. The expression of specific targets Smad1 and Osterix was significantly increased in the presence of Pi and restored by coincubation with Mg2+. As miR-30b, miR-133a, and miR-143 are negatively regulated by Pi and restored by Mg2+ with a congruent modulation of their known targets Runx2, Smad1, and Osterix, our results provide a potential mechanistic explanation of the observed upregulation of these master switches of osteogenesis during the course of VC.

  10. Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification

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    Cai-Mei Zheng

    2011-01-01

    Full Text Available Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

  11. Associations between Thyroid Hormones, Calcification Inhibitor Levels and Vascular Calcification in End-Stage Renal Disease.

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    Christiaan Lucas Meuwese

    Full Text Available Vascular calcification is a common, serious and elusive complication of end-stage renal disease (ESRD. As a pro-calcifying risk factor, non-thyroidal illness may promote vascular calcification through a systemic lowering of vascular calcification inhibitors such as matrix-gla protein (MGP and Klotho.In 97 ESRD patients eligible for living donor kidney transplantation, blood levels of thyroid hormones (fT3, fT4 and TSH, total uncarboxylated MGP (t-ucMGP, desphospho-uncarboxylated MGP (dp-ucMGP, descarboxyprothrombin (PIVKA-II, and soluble Klotho (sKlotho were measured. The degree of coronary calcification and arterial stiffness were assessed by means of cardiac CT-scans and applanation tonometry, respectively.fT3 levels were inversely associated with coronary artery calcification (CAC scores and measures of arterial stiffness, and positively with dp-ucMGP and sKlotho concentrations. Subfractions of MGP, PIVKA-II and sKlotho did not associate with CAC scores and arterial stiffness. fT4 and TSH levels were both inversely associated with CAC scores, but not with arterial stiffness.The positive associations between fT3 and dp-ucMGP and sKlotho suggest that synthesis of MGP and Klotho is influenced by thyroid hormones, and supports a link between non-thyroidal illness and alterations in calcification inhibitor levels. However, the absence of an association between serum calcification inhibitor levels and coronary calcification/arterial stiffness and the fact that MGP and Klotho undergo post-translational modifications underscore the complexity of this association. Further studies, measuring total levels of MGP and membrane bound Klotho, should examine this proposed pathway in further detail.

  12. A preliminary study of periodontitis and vascular calcification compound model

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    MENGYun; DENGJing; PanKe-qing

    2015-01-01

    Objective This experiment is desired to establish a compound model of chronic periodontitis and vascular calcification,so as to study the relation of periodontal and vascular calcification.Methods Forty male Wistar rats were randomly divided into:control group(group C),periodontitis group(group CP),vascular calcification group(group VDN),compound group (group CP+VDN).Every groups accepted the corresponding manages to establish the animal model.Eight weeks later,al the rats were sacrificed and the fol owing items were observed:inflam-matory factor in serum were tested,Hematoxylin-eosin staining(HE)staining of vascular tissue were taken to test.Results Through detection of periodontal tissue,serum and vascular tissue,an-imal models were successful.Histopathologic observation revealed:obvious inflammation of periodontal tissue was obversed in group CP and CP+VDN.The red Mineralized nodules deposition in group VDN and CP+VDN were higher than in group C and CP(P<0.05)by HE staining,and that in group CP+VDN was significantly higher than in group VDN(P<0.05);Animals in group CP+VDN showed higher level of IL-1 in serum than that in group CP,VDN and C.Conclusion This study has demonstrated that periodontitis have some promoting ef ect on vascular cal-cification.

  13. Inflammatory, metabolic, and genetic mechanisms of vascular calcification.

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    Demer, Linda L; Tintut, Yin

    2014-04-01

    This review centers on updating the active research area of vascular calcification. This pathology underlies substantial cardiovascular morbidity and mortality, through adverse mechanical effects on vascular compliance, vasomotion, and, most likely, plaque stability. Biomineralization is a complex, regulated process occurring widely throughout nature. Decades ago, its presence in the vasculature was considered a mere curiosity and an unregulated, dystrophic process that does not involve biological mechanisms. Although it remains controversial whether the process has any adaptive value or past evolutionary advantage, substantial advances have been made in understanding the biological mechanisms driving the process. Different types of calcific vasculopathy, such as inflammatory versus metabolic, have parallel mechanisms in skeletal bone calcification, such as intramembranous and endochondral ossification. Recent work has identified important regulatory roles for inflammation, oxidized lipids, elastin, alkaline phosphatase, osteoprogenitor cells, matrix γ-carboxyglutamic acid protein, transglutaminase, osteoclastic regulatory factors, phosphate regulatory hormones and receptors, apoptosis, prelamin A, autophagy, and microvesicles or microparticles similar to the matrix vesicles of skeletal bone. Recent work has uncovered fascinating interactions between matrix γ-carboxyglutamic acid protein, vitamin K, warfarin, and transport proteins. And, lastly, recent breakthroughs in inherited forms of calcific vasculopathy have identified the genes responsible as well as an unexpected overlap of phenotypes. Until recently, vascular calcification was considered a purely degenerative, unregulated process. Since then, investigative groups around the world have identified a wide range of causative mechanisms and regulatory pathways, and some of the recent developments are highlighted in this review.

  14. [Vascular calcifications, the hidden side effects of vitamin K antagonists].

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    Bennis, Youssef; Vengadessane, Subashini; Bodeau, Sandra; Gras, Valérie; Bricca, Giampiero; Kamel, Saïd; Liabeuf, Sophie

    2016-09-01

    Despite the availability of new oral anticoagulants, vitamin K antagonists (VKA, such as fluindione, acenocoumarol or warfarin) remain currently the goal standard medicines for oral prevention or treatment of thromboembolic disorders. They inhibit the cycle of the vitamin K and its participation in the enzymatic gamma-carboxylation of many proteins. The VKA prevent the activation of the vitamin K-dependent blood clotting factors limiting thus the initiation of the coagulation cascade. But other proteins are vitamin K-dependent and also remain inactive in the presence of VKA. This is the case of matrix Gla-protein (MGP), a protein that plays a major inhibitory role in the development of vascular calcifications. Several experimental and epidemiological results suggest that the use of the VKA could promote the development of vascular calcifications increasing thus the cardiovascular risk. This risk seems to be higher in patients with chronic kidney disease or mellitus diabetes who are more likely to develop vascular calcifications, and may be due to a decrease of the MGP activity. This review aims at summarizing the data currently available making vascular calcifications the probably underestimated side effects of VKA.

  15. The role of vascular peroxidase 1 in ox-LDL-induced vascular smooth muscle cell calcification.

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    Tang, Yixin; Xu, Qian; Peng, Haiyang; Liu, Zhaoya; Yang, Tianlun; Yu, Zaixin; Cheng, Guangjie; Li, Xiaohui; Zhang, Guogang; Shi, Ruizheng

    2015-12-01

    Reactive oxygen species (ROS)-induced osteogenic differentiation of vascular smooth muscle cells (VSMCs) is associated with the pathogenesis of vascular calcification. Vascular peroxidase 1 (VPO1), a peroxidase in the cardiovascular system, utilizes the hydrogen peroxide (H2O2) produced by co-expressed NADPH oxidases to produce hypochlorous acid (HOCl) and catalyze peroxidative reactions. The aim of this study was to determine whether VPO1 plays a role in the osteogenic differentiation of VSMCs in the setting of the vascular calcification induced by oxidized low-density lipoprotein (ox-LDL). In cultured primary rat VSMCs, we observed that the expression of VPO1 was significantly increased in combination with increases in calcification, as demonstrated via increased mineralization, as well as increased alkaline phosphatase (ALP) activity and up-regulated runt-related transcription factor 2 (Runx2) expression in ox-LDL-treated cells. Ox-LDL-induced VSMC calcification and Runx2 expression were both inhibited by knockdown of VPO1 using a small interfering RNA or by an NADPH oxidase inhibitor. Moreover, the knockdown of VPO1 in VSMCs suppressed the production of HOCl and the phosphorylation of AKT, ERK and P38 MAPK. Furthermore, HOCl treatment facilitated the phosphorylation of AKT, ERK1/2 and P38 MAPK and the expression of Runx2, whereas LY294002 (a specific inhibitor of PI3K), U0126 (a specific inhibitor of ERK1/2) and SB203580 (a specific inhibitor of P38 MAPK) significantly attenuated the HOCl-induced up-regulation of Runx2. Collectively, these results demonstrated that VPO1 promotes ox-LDL-induced VSMC calcification via the VPO1/HOCl/PI3K/AKT, ERK1/2, and P38 MAPK/Runx2 signaling pathways. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  16. The role of cellular senescence during vascular calcification: a key paradigm in aging research.

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    Mackenzie, N C W; MacRae, V E

    2011-07-01

    Vascular calcification has severe clinical consequences and is considered an accurate predictor of future adverse cardiovascular events. Vascular calcification refers to the deposition of calcium phosphate mineral, most often hydroxyapatite, in arteries. Extensive calcification of the vascular system is a key characteristic of aging. In this article, we outline the mechanisms governing vascular calcification and highlight its association with cellular senescence. This review discusses the molecular mechanisms of cellular senescence and its affect on calcification of vascular cells, the relevance of phosphate regulation and the function of FGF23 and Klotho proteins. The association of vascular calcification and cellular senescence with the rare human aging disorder Hutchison-Gilford Progeria Syndrome (HGPS) is highlighted and the mouse models used to try to determine the underlying pathways are discussed. By understanding the pathways involved in these processes novel drug targets may be elucidated in an effort to reduce the effects of cellular aging as a risk factor in cardiovascular disease.

  17. Arterial ageing: from endothelial dysfunction to vascular calcification.

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    Tesauro, M; Mauriello, A; Rovella, V; Annicchiarico-Petruzzelli, M; Cardillo, C; Melino, G; Di Daniele, N

    2017-05-01

    Complex structural and functional changes occur in the arterial system with advancing age. The aged artery is characterized by changes in microRNA expression patterns, autophagy, smooth muscle cell migration and proliferation, and arterial calcification with progressively increased mechanical vessel rigidity and stiffness. With age the vascular smooth muscle cells modify their phenotype from contractile to 'synthetic' determining the development of intimal thickening as early as the second decade of life as an adaptive response to forces acting on the arterial wall. The increased permeability observed in intimal thickening could represent the substrate on which low-level atherosclerotic stimuli can promote the development of advanced atherosclerotic lesions. In elderly patients the atherosclerotic plaques tend to be larger with increased vascular stenosis. In these plaques there is a progressive accumulation of both lipids and collagen and a decrease of inflammation. Similarly the plaques from elderly patients show more calcification as compared with those from younger patients. The coronary artery calcium score is a well-established marker of adverse cardiovascular outcomes. The presence of diffuse calcification in a severely stenotic segment probably induces changes in mechanical properties and shear stress of the arterial wall favouring the rupture of a vulnerable lesion in a less stenotic adjacent segment. Oxidative stress and inflammation appear to be the two primary pathological mechanisms of ageing-related endothelial dysfunction even in the absence of clinical disease. Arterial ageing is no longer considered an inexorable process. Only a better understanding of the link between ageing and vascular dysfunction can lead to significant advances in both preventative and therapeutic treatments with the aim that in the future vascular ageing may be halted or even reversed. © 2017 The Association for the Publication of the Journal of Internal Medicine.

  18. Association of conjunctival and corneal calcification with vascular calcification among hepatitis-C-seropositive hemodialysis patients

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    Khaled AbouSeif

    2016-01-01

    Full Text Available Disorders associated with the hepatitis C virus (HCV have been reported including cardiovascular, metabolic, and central nervous system diseases. Since chronic HCV infections may be curable, their identification as causal contributors to cardiovascular risk could offer new perspectives in the prevention of cardiovascular disease. The aim of this study is to investigate the association between HCV and aortic arch calcification (AAC and corneal and conjunctival calcification (CCC in maintenance hemodialysis (MHD patients; further, we assessed the correlation of CCC with vascular calcification. A total of 100 patients undergoing hemodialysis (HD in our hospital were included in this study. Patients underwent a complete ocular examination including intraocular pressure, and CCC was looked for by slit lamp and fundoscopy. CCC was graded according to modified Porter and Crombie classification system described by Tokuyama et al. Helical computerized tomographic chest examination was used to evaluate the grading of AAC. Demographic, hematological, biochemical, and dialysis-related data were obtained. There was significant difference between seropositive (n = 51 and seronegative patients (n = 49 regarding grading of AAC and CCC (P <0.001. Significant positive correlation was found between grading of CCC, AAC, age (P <0.001, duration on HD (P <0.001, HCV-antibody positivity (P <0.001, serum calcium level (P <0.001, serum phosphorus level (P <0.001, calcium × phosphorus product (P <0.001, and i-parathormone level (P < 0.001. In addition, CCC grading positively correlated with AAC. Our results suggest that patients undergoing HD infected with the HCV have high degree of CCC, AAC, and mineral metabolism disorder. The strong correlation between CCC and AAC indicates that CCC evaluation is an easy, fast, non-invasive method, and might be used as an indirect indicator to detect vascular calcification in patients undergoing MHD.

  19. ADVANCE: Study to Evaluate Cinacalcet Plus Low Dose Vitamin D on Vascular Calcification in Subjects With Chronic Kidney Disease Receiving Hemodialysis

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    2014-07-14

    Chronic Kidney Disease; End Stage Renal Disease; Coronary Artery Calcification; Vascular Calcification; Calcification; Cardiovascular Disease; Chronic Renal Failure; Hyperparathyroidism; Kidney Disease; Nephrology; Secondary Hyperparathyroidism

  20. Activating transcription factor 4 is involved in endoplasmic reticulum stress-mediated apoptosis contributing to vascular calcification.

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    Duan, Xiao-Hui; Chang, Jin-Rui; Zhang, Jing; Zhang, Bao-Hong; Li, Yu-Lin; Teng, Xu; Zhu, Yi; Du, Jie; Tang, Chao-Shu; Qi, Yong-Fen

    2013-09-01

    Our previous work reported that endoplasmic reticulum stress (ERS)-mediated apoptosis was activated during vascular calcification (VC). Activating transcription factor 4 (ATF4) is a critical transcription factor in osteoblastogenesis and ERS-induced apoptosis. However, whether ATF4 is involved in ERS-mediated apoptosis contributing to VC remains unclear. In the present study, in vivo VC was induced in rats by administering vitamin D3 plus nicotine. Vascular smooth muscle cell (VSMC) calcification in vitro was induced by incubation in calcifying media containing β-glycerophosphate and CaCl2. ERS inhibitors taurine or 4-phenylbutyric acid attenuated ERS and VSMC apoptosis in calcified rat arteries, reduced calcification and retarded the VSMC contractile phenotype transforming into an osteoblast-like phenotype in vivo. Inhibition of ERS retarded the VSMC phenotypic transition into an osteoblast-like cell phenotype and reduced VSMC calcification and apoptosis in vitro. Interestingly, ATF4 was activated in calcified aortas and calcified VSMCs in vitro. ATF4 knockdown attenuated ERS-induced apoptosis in calcified VSMCs. ATF4 deficiency blocked VSMC calcification and negatively regulated the osteoblast phenotypic transition of VSMCs in vitro. Our results demonstrate that ATF4 was involved at least in part in the process of ERS-mediated apoptosis contributing to VC.

  1. Vitamin K Status and Vascular Calcification: Evidence from Observational and Clinical Studies12

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    Shea, M. Kyla; Holden, Rachel M.

    2012-01-01

    Vascular calcification occurs when calcium accumulates in the intima (associated with atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts cardiovascular disease (CVD) and mortality. A preventive role for vitamin K in vascular calcification has been proposed based on its role in activating matrix Gla protein (MGP), a ...

  2. Does treatment with statins have the potential of enhancing Vascular calcification?

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    ZHANG Ming; LI Xu-ping; QIAO Yan; NIE Shao-ping; MA Chang-sheng

    2008-01-01

    @@ Vascular calcification is commonly found in atherosclerosis and recognized as a marker of atherosclerotic plaque burden.Many evdiences have demonstrated that vascular calcification is an active process and can be seen in all stages of development and intimately associated with atherosclerosis.

  3. Dietary vitamin K and therapeutic warfarin alter susceptibility to vascular calcification in experimental chronic kidney disease

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    The leading cause of death in patients with chronic kidney disease (CKD) is cardiovascular disease (CVD), with vascular calcification (VC) being a key modifier of disease progression. A local regulator of vascular calcification is vitamin K. This gamma-glutamyl carboxylase substrate is an essential ...

  4. Vascular calcification is associated with cortical bone loss in chronic renal failure rats with and without ovariectomy: the calcification paradox.

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    De Schutter, Tineke M; Neven, Ellen; Persy, Veerle P; Behets, Geert J; Postnov, Andrei A; De Clerck, Nora M; D'Haese, Patrick C

    2011-01-01

    Increased bone loss has been associated with the development of vascular calcification in patients with chronic renal failure (CRF). In this study, the effect of impaired bone metabolism on aortic calcifications was investigated in uremic rats with or without ovariectomy. CRF was induced by administration of a 0.75% adenine/2.5% protein diet for 4 weeks. In one group, osteoporosis was induced by ovariectomy (CRF-OVX), while the other group underwent a sham-operation instead (CRF). A third group consisted of ovariectomized rats with normal renal function (OVX). At regular time intervals throughout the study, bone status and aortic calcifications were evaluated by in vivo micro-CT. At sacrifice after 6 weeks of CRF, bone histomorphometry was performed and vascular calcification was assessed by bulk calcium analysis and Von Kossa staining. Renal function was significantly impaired in the CRF-OVX and CRF groups. Trabecular bone loss was seen in all groups. In the CRF-OVX and CRF groups, trabecular bone density was restored after adenine withdrawal, which coincided with cortical bone loss and the development of medial calcifications in the aorta. No significant differences with regard to the degree of aortic calcifications were seen between the two CRF groups. Neither cortical bone loss nor calcifications were seen in the OVX group. Cortical bone loss significantly correlated with the severity of vascular calcification in the CRF-OVX and CRF groups, but no associations with trabecular bone changes were found. Cortical rather than trabecular bone loss is associated with the process of calcification in rats with adenine- induced CRF. Copyright © 2011 S. Karger AG, Basel.

  5. Resveratrol Ameliorated Vascular Calcification by Regulating Sirt-1 and Nrf2.

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    Zhang, P; Li, Y; Du, Y; Li, G; Wang, L; Zhou, F

    2016-12-01

    Pathologic vascular calcification is a significant reason for mortality and morbidity in patients who suffer from end-stage renal disease (ESRD). Resveratrol, a scavenger for many free radicals, is a crucial compound for biomedicine. However, the role and mechanism of resveratrol in vascular calcification is still unknown. In this study, to mimic vascular calcification in ESRD, we used β-glyceophosphate to stimulate the rat vascular smooth muscle cells (RASMCs). We investigate the therapeutic role of resveratrol pretreatment in vascular calcification. In the current in vitro study, we observe the effects of resveratrol on improving intracellular calcium deposition and protecting against mitochondria dysfunction in calcific RASMCs. Resveratrol decreased the mRNA level of fibroblast growth factor-23, then increased the mRNA level of klotho and the nuclear transcription factor NF-E2-related factor 2 (nuclear factor-erythroid 2-related factor 2 [Nrf2]) in RASMCs after calcification. Further, resveratrol activated the expression of sirtuin-1 and Nrf2, and inhibited the expression of osteopontin, runt-related transcription factor 2, and heme oxygenase-1. Our study shows that resveratrol could ameliorate oxidative injury of RASMCs by preventing vascular calcification-induced calcium deposition and mitochondria dysfunction through involving sirtuin-1 and Nrf2. These results might indicate a novel role for resveratrol in resistance to oxidative stress for ESRD patients suffering from vascular calcification.

  6. Comparison of the x-ray attenuation properties of breast calcifications, aluminium, hydroxyapatite and calcium oxalate.

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    Warren, L M; Mackenzie, A; Dance, D R; Young, K C

    2013-04-07

    Aluminium is often used as a substitute material for calcifications in phantom measurements in mammography. Additionally, calcium oxalate, hydroxyapatite and aluminium are used in simulation studies. This assumes that these materials have similar attenuation properties to calcification, and this assumption is examined in this work. Sliced mastectomy samples containing calcification were imaged at ×5 magnification using a digital specimen cabinet. Images of the individual calcifications were extracted, and the diameter and contrast of each calculated. The thicknesses of aluminium required to achieve the same contrast as each calcification when imaged under the same conditions were calculated using measurements of the contrast of aluminium foils. As hydroxyapatite and calcium oxalate are also used to simulate calcifications, the equivalent aluminium thicknesses of these materials were also calculated using tabulated attenuation coefficients. On average the equivalent aluminium thickness was 0.85 times the calcification diameter. For calcium oxalate and hydroxyapatite, the equivalent aluminium thicknesses were 1.01 and 2.19 times the thickness of these materials respectively. Aluminium and calcium oxalate are suitable substitute materials for calcifications. Hydroxyapatite is much more attenuating than the calcifications and aluminium. Using solid hydroxyapatite as a substitute for calcification of the same size would lead to excessive contrast in the mammographic image.

  7. Losartan Inhibits Vascular Calcification by Suppressing the BMP2 and Runx2 Expression in Rats In Vivo.

    Science.gov (United States)

    Li, Mincai; Wu, Panfeng; Shao, Juan; Ke, Zhiqiang; Li, Dan; Wu, Jiliang

    2016-04-01

    The blockade of renin-angiotensin II system has been shown to reduce morbidity and mortality in hypertension, atherosclerosis, diabetes and chronic kidney disease. Since vascular calcification (VC) is commonly found in these diseases, the aim of this study was to examine whether or not losartan, a widely used angiotensin II receptor blockers, inhibits VC in rats in vivo. A rat model of VC was generated by treating rats with a combination of warfarin and vitamin K1. Two weeks after the treatments, the rats were treated with vehicle or without losartan (100 ng/kg/day) for 2 weeks. At the end of the experiments, aortic arteries were isolated for the examination of calcification morphology, mRNA and protein expression of BMP2 and Runx2, and osteoblast differentiation. Warfarin and vitamin K instigated vascular remodeling with calcified plaques in the aortic arteries in rats. Losartan significantly attenuated warfarin- and vitamin K-induced vascular injury and calcification. Consistently, losartan suppressed the levels of mRNA and protein expression of BMP2 and Runx2, two key factors for VC. Further, vascular calcified lesion areas expressed angiotensin II 1 receptor (AT1R). Finally, losartan treatment significantly inhibited apoptosis in vascular smooth muscle cell (VSMC) in rat arteries. We conclude that losartan suppresses VC by lowering the expression of AT1R, Runx2 and BMP2, and by inhibiting the apoptosis of VSMC in rat aortic arteries.

  8. Microvesicles from the plasma of elderly subjects and from senescent endothelial cells promote vascular calcification

    Science.gov (United States)

    Bodega, Guillermo; Noci, María Victoria; Troyano, Nuria; Bohórquez, Lourdes; Luna, Carlos; Luque, Rafael; Carmona, Andrés; Carracedo, Julia; Ramírez, Rafael

    2017-01-01

    Vascular calcification is commonly seen in elderly people, though it can also appear in middle-aged subjects affected by premature vascular aging. The aim of this work is to test the involvement of microvesicles (MVs) produced by senescent endothelial cells (EC) and from plasma of elderly people in vascular calcification. The present work shows that MVs produced by senescent cultured ECs, plus those found in the plasma of elderly subjects, promote calcification in vascular smooth muscle cells. Only MVs from senescent ECs, and from elderly subjects' plasma, induced calcification. This ability correlated with these types of MVs' carriage of: a) increased quantities of annexins (which might act as nucleation sites for calcification), b) increased quantities of bone-morphogenic protein, and c) larger Ca contents. The MVs of senescent, cultured ECs, and those present in the plasma of elderly subjects, promote vascular calcification. The present results provide mechanistic insights into the observed increase in vascular calcification-related diseases in the elderly, and in younger patients with premature vascular aging, paving the way towards novel therapeutic strategies. PMID:28278131

  9. Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease.

    Science.gov (United States)

    Zelt, Jason G E; McCabe, Kristin M; Svajger, Bruno; Barron, Henry; Laverty, Kim; Holden, Rachel M; Adams, Michael A

    2015-12-01

    Chronic kidney disease (CKD) patients are commonly treated with vitamin D analogs, such as calcitriol. Recent epidemiologic evidence revealed a significant interaction between vitamin D and magnesium, since an inverse relationship between vitamin D levels and mortality mainly occurs in patients with a high magnesium intake. The aim of the study was to assess the mechanisms involved by determining whether magnesium alone or combined with calcitriol treatments differentially impacts vascular calcification (VC) in male Sprague-Dawley rats with adenine-induced CKD. Treatment with moderate doses of calcitriol (80 μg/kg) suppressed parathyroid hormone to near or slightly below control levels. Given alone, this dose of calcitriol increased the prevalence of VC; however, when magnesium was given in combination, the severity of calcification was attenuated in the abdominal aorta (51% reduction), iliac (44%), and carotid arteries (46%) compared with CKD controls. The decreases in vascular calcium content were associated with a 20-50% increase in vascular magnesium. Calcitriol treatment alone significantly decreased TRPM7 protein (↓ to ∼11%), whereas the combination treatment increased both mRNA (1.7×) and protein (6.8×) expression compared with calcitriol alone. In summary, calcitriol increased VC in certain conditions, but magnesium prevented the reduction in TRPM7 and reduced the severity of VC, thereby increasing the bioavailable magnesium in the vascular microenvironment. These findings suggest that modifying the adverse effect profile of calcitriol with magnesium may be a plausible approach to benefiting the increasing number of CKD patients being prescribed calcitriol.

  10. Vitamin K status and vascular calcification: evidence from observational and clinical studies.

    Science.gov (United States)

    Shea, M Kyla; Holden, Rachel M

    2012-03-01

    Vascular calcification occurs when calcium accumulates in the intima (associated with atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts cardiovascular disease (CVD) and mortality. A preventive role for vitamin K in vascular calcification has been proposed based on its role in activating matrix Gla protein (MGP), a calcification inhibitor that is expressed in vascular tissue. Although animal and in vitro data support this role of vitamin K, overall data from human studies are inconsistent. The majority of population-based studies have relied on vitamin K intake to measure status. Phylloquinone is the primary dietary form of vitamin K and available supplementation trials, albeit limited, suggest phylloquinone supplementation is relevant to CAC. Yet observational studies have found higher dietary menaquinone, but not phylloquinone, to be associated with less calcification. Vascular calcification is highly prevalent in certain patient populations, especially in those with chronic kidney disease (CKD), and it is plausible vitamin K may contribute to reducing vascular calcification in patients at higher risk. Subclinical vitamin K deficiency has been reported in CKD patients, but studies linking vitamin K status to calcification outcomes in CKD are needed to clarify whether or not improving vitamin K status is associated with improved vascular health in CKD. This review summarizes the available evidence of vitamin K and vascular calcification in population-based studies and clinic-based studies, with a specific focus on CKD patients.

  11. The Role of AGE/RAGE Signaling in Diabetes-Mediated Vascular Calcification

    Directory of Open Access Journals (Sweden)

    Amber M. Kay

    2016-01-01

    Full Text Available AGE/RAGE signaling has been a well-studied cascade in many different disease states, particularly diabetes. Due to the complex nature of the receptor and multiple intersecting pathways, the AGE/RAGE signaling mechanism is still not well understood. The purpose of this review is to highlight key areas of AGE/RAGE mediated vascular calcification as a complication of diabetes. AGE/RAGE signaling heavily influences both cellular and systemic responses to increase bone matrix proteins through PKC, p38 MAPK, fetuin-A, TGF-β, NFκB, and ERK1/2 signaling pathways in both hyperglycemic and calcification conditions. AGE/RAGE signaling has been shown to increase oxidative stress to promote diabetes-mediated vascular calcification through activation of Nox-1 and decreased expression of SOD-1. AGE/RAGE signaling in diabetes-mediated vascular calcification was also attributed to increased oxidative stress resulting in the phenotypic switch of VSMCs to osteoblast-like cells in AGEs-induced calcification. Researchers found that pharmacological agents and certain antioxidants decreased the level of calcium deposition in AGEs-induced diabetes-mediated vascular calcification. By understanding the role the AGE/RAGE signaling cascade plays diabetes-mediated vascular calcification will allow for pharmacological intervention to decrease the severity of this diabetic complication.

  12. Isolated intrasplenic vascular calcifications in a child with type 1 diabetes mellitus---A case report.

    Science.gov (United States)

    Patil, Parag V; Patil, Manojkumar G; Patil, Abhijit M

    2017-09-01

    We report a case of vascular calcifications in the spleen of a 7-year-old girl who was diagnosed with type 1 diabetes mellitus (DM). The possible etiology for vascular calcifications might be medial sclerosis associated with DM. To the best of our knowledge, this finding has not yet been reported in the literature. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound 45:438-440, 2017. © 2016 Wiley Periodicals, Inc.

  13. Osteopontin protects against high phosphate-induced nephrocalcinosis and vascular calcification.

    Science.gov (United States)

    Paloian, Neil J; Leaf, Elizabeth M; Giachelli, Cecilia M

    2016-05-01

    Pathologic calcification is a significant cause of increased morbidity and mortality in patients with chronic kidney disease. The precise mechanisms of ectopic calcification are not fully elucidated, but it is known to be caused by an imbalance of procalcific and anticalcific factors. In the chronic kidney disease population, an elevated phosphate burden is both highly prevalent and a known risk factor for ectopic calcification. Here we tested whether osteopontin, an inhibitor of calcification, protects against high phosphate load-induced nephrocalcinosis and vascular calcification. Osteopontin knockout mice were placed on a high phosphate diet for 11 weeks. Osteopontin deficiency together with phosphate overload caused uremia, nephrocalcinosis characterized by substantial renal tubular and interstitial calcium deposition, and marked vascular calcification when compared with control mice. Although the osteopontin-deficient mice did not exhibit hypercalcemia or hyperphosphatemia, they did show abnormalities in the mineral metabolism hormone fibroblast growth factor-23. Thus, endogenous osteopontin plays a critical role in the prevention of phosphate-induced nephrocalcinosis and vascular calcification in response to high phosphate load. A better understanding of osteopontin's role in phosphate-induced calcification will hopefully lead to better biomarkers and therapies for this disease, especially in patients with chronic kidney disease and other at-risk populations.

  14. [Vascular Calcification - Pathological Mechanism and Clinical Application - . Vascular calcification in chronic kidney disease-mineral and bone disorder (CKD-MBD)].

    Science.gov (United States)

    Omata, Momoyo; Fukagawa, Masafumi; Kakuta, Takatoshi

    2015-05-01

    Chronic kidney disease-mineral and bone disorder (CKD-MBD), is sequential pathophysiology that starts in the very early stages of CKD. Three major aspects of CKD-MBD are laboratory abnormalities, bone abnormalities and vascular calcification. In dialysis patients, the prevalence of death due to cardiovascular disease accounts for more than 40% of all-cause mortality. Therefore, arteriosclerosis with vascular calcification may be an important pathophysiological mechanism in the development of cardiovascular disease. Vascular calcification is known to be an important risk factor influencing mortality in CKD patients. A number of studies have suggested a close association between serum FGF23 concentration and the risks of mortality, cardiovascular disease vascular calcification as well as CKD progression. Renal insufficiency leads to decline in klotho level and impaired phosphate excretion. However serum phosphate levels are maintained in the normal range by up regulation of FGF23 and PTH in early CKD stage. Early treatment intervention is necessary to improve the prognosis of the CKD patient.

  15. MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23

    Directory of Open Access Journals (Sweden)

    Shouhua Zheng

    2016-12-01

    Full Text Available Objective(s: Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much attention. Materials and Methods: In the current study, we built a vascular calcification rat model using vitamin D3 plus nicotine and analyzed miRNA expression profile by miRNA chip assay. Potential target of one selected miRNA with sharpest variation in expression were predicted by both PicTar and TargetScan. The impact of the selected miRNA on the expression of the potential target on both mRNA and protein levels were measured by RT-PCR and Western blot, respectively. Results: Our results identified 16 dysregulated miRNAs, among which miR-297a showed the sharpest variation. Further analysis focusing on miR-297a revealed that fibroblast growth factor 23 (FGF23 was a potential target of miR297a. Measurement of FGF23 and its regulator Klotho on both mRNA and protein levels demonstrated that FGF23 was significantly increased while Klotho was decreased in rats with vascular calcification. Conclusion: Our results indicated that FGF23 was target of miR-297a and decreased miR-297a in vascular calcification lead to the increase of FGF23, which together with Klotho might enhance vascular calcification. The findings of this study could provide valuable information for the understanding of mechanisms underlying miR-dependent vascular calcification as well as potential treatment target for the disease.

  16. Haemodialysis session: the perfect storm for vascular calcification.

    Science.gov (United States)

    Seras, Miguel; Martín de Francisco, Ángel Luis; Piñera, Celestino; Gundin, Simón; García-Unzueta, Marta; Kislikova, Maria; Albines, Zoila; Serrano, Mara; Arias, Manuel

    2015-01-01

    Vascular calcification (VC) associated to chronic kidney disease (CKD) is a complex phenomenon closely related to mineral bone metabolism disorders. Many are the factors implicated, as the drugs used in the treatment of CKD. Some in vitro studies suggest that electrolyte and acid-base disorders induced by hemodialysis (HD) may play a key role in VC. We analyzed electrolyte and acid-base disorders that occur during an HD session in 26 patients randomly assigned to 1,25 mM or 1,5 mM calcium bath. There is a calcium load in all the patients, independently of calcium bath concentration or basal serum calcium levels. At the end of the session, 100% of the patients dialyzed with 1,5 mM calcium bath have calcium serum levels > 1,3 mM. However, this only occurs in 15% of the patients dialysed with 1,25 mM calcium bath. During this calcium load, phosphorus levels persist uncontrolled. Besides, there is a progressive alkalinization in all the patients. In the end of the session 50% have serum bicarbonate > 30 mM and 23% pH > 7,5. During HD sessions occur electrolyte and acid-base disorders that induce VC: Calcium load and alkalization in presence of elevated phosphorus levels. It is necessary to perform studies with kinetic models of calcium load and alkalinization different from the actual ones. Copyright © 2015 The Authors. Published by Elsevier España, S.L.U. All rights reserved.

  17. Acid-Base Balance in Uremic Rats with Vascular Calcification

    Directory of Open Access Journals (Sweden)

    Alan Peralta-Ramírez

    2014-07-01

    Full Text Available Background/Aims: Vascular calcification (VC, a major complication in humans and animals with chronic kidney disease (CKD, is influenced by changes in acid-base balance. The purpose of this study was to describe the acid-base balance in uremic rats with VC and to correlate the parameters that define acid-base equilibrium with VC. Methods: Twenty-two rats with CKD induced by 5/6 nephrectomy (5/6 Nx and 10 nonuremic control rats were studied. Results: The 5/6 Nx rats showed extensive VC as evidenced by a high aortic calcium (9.2 ± 1.7 mg/g of tissue and phosphorus (20.6 ± 4.9 mg/g of tissue content. Uremic rats had an increased pH level (7.57 ± 0.03 as a consequence of both respiratory (PaCO2 = 28.4 ± 2.1 mm Hg and, to a lesser degree, metabolic (base excess = 4.1 ± 1 mmol/l derangements. A high positive correlation between both anion gap (AG and strong ion difference (SID with aortic calcium (AG: r = 0.604, p = 0.02; SID: r = 0.647, p = 0.01 and with aortic phosphorus (AG: r = 0.684, p = 0.007; SID: r = 0.785, p = 0.01 was detected. Conclusions: In an experimental model of uremic rats, VC showed high positive correlation with AG and SID.

  18. Calcifications

    Energy Technology Data Exchange (ETDEWEB)

    Reichelt, S.; Erlemann, R.

    1989-02-01

    Juvenile dermatomyositis is a rare disease in early to mid-childhood. We describe the case of a young girl who was found to have prominent soft-tissue calcifications on the preoperative chest study. The clinical and radiological symptoms of dermatomyositis are demonstrated and the differential diagnosis of this kind of calcification is discussed.

  19. Lipids in biocalcification: contrasts and similarities between intimal and medial vascular calcification and bone by NMR.

    Science.gov (United States)

    Reid, David G; Shanahan, Catherine M; Duer, Melinda J; Arroyo, Luis G; Schoppet, Michael; Brooks, Roger A; Murray, Rachel C

    2012-08-01

    Pathomechanisms underlying vascular calcification biogenesis are still incompletely understood. Biomineral from human atherosclerotic intimal plaques; human, equine, and bovine medial vascular calcifications; and human and equine bone was released from collagenous organic matrix by sodium hydroxide/sodium hypochlorite digestion. Solid-state (13)C NMR of intimal plaque mineral shows signals from cholesterol/cholesteryl esters and fatty acids. In contrast, in mineral from pure medial calcifications and bone mineral, fatty acid signals predominate. Refluxing (chloroform/methanol) intimal plaque calcifications removes the cholesterylic but not the fatty acyl signals. The lipid composition of this refluxed mineral now closely resembles that of the medial and bone mineral, which is unchanged by reflux. Thus, intimal and medial vascular calcifications and bone mineral have in common a pool of occluded mineral-entrained fatty acyl-rich lipids. This population of fatty acid may contain methyl-branched fatty acids, possibly representing lipoprotein particle remnants. Cell signaling and mechanistic parallels between physiological (orthotopic) and pathological (ectopic) calcification are also reflected thus in the NMR spectroscopic fingerprints of mineral-associated and mineral-entrained lipids. Additionally the atherosclerotic plaque mineral alone shows a significant independent pool of cholesterylic lipids. Colocalization of mineral and lipid may be coincidental, but it could also reflect an essential mechanistic component of biomineralization.

  20. Osteocalcin, Vascular Calcification, and Atherosclerosis: A Systematic Review and Meta-analysis

    Directory of Open Access Journals (Sweden)

    Sophie A. Millar

    2017-07-01

    Full Text Available BackgroundOsteocalcin (OC is an intriguing hormone, concomitantly being the most abundant non-collagenous peptide found in the mineralized matrix of bone, and expanding the endocrine function of the skeleton with far-reaching extra-osseous effects. A new line of enquiry between OC and vascular calcification has emerged in response to observations that the mechanism of vascular calcification resembles that of bone mineralisation. To date, studies have reported mixed results. This systematic review and meta-analysis aimed to identify any association between OC and vascular calcification and atherosclerosis.Methods and resultsDatabases were searched for original, peer reviewed human studies. A total of 1,453 articles were retrieved, of which 46 met the eligibility criteria. Overall 26 positive, 17 negative, and 29 neutral relationships were reported for assessments between OC (either concentration in blood, presence of OC-positive cells, or histological staining for OC and extent of calcification or atherosclerosis. Studies that measured OC-positive cells or histological staining for OC reported positive relationships (11 studies. A higher percentage of Asian studies found a negative relationship (36% in contrast to European studies (6%. Studies examining carboxylated and undercarboxylated forms of OC in the blood failed to report consistent results. The meta-analysis found no significant difference between OC concentration in the blood between patients with “atherosclerosis” and control (p = 0.13, n = 1,197.ConclusionNo definitive association was determined between OC and vascular calcification or atherosclerosis; however, the presence of OC-positive cells and histological staining had a consistent positive correlation with calcification or atherosclerosis. The review highlighted several themes, which may influence OC within differing populations leading to inconclusive results. Large, longitudinal studies are required to further

  1. Sortilin mediates vascular calcification via its recruitment into extracellular vesicles

    DEFF Research Database (Denmark)

    Goettsch, Claudia; Hutscheson, JD; Aikawa, M

    2016-01-01

    obscure. Here, we have demonstrated that sortilin is a key regulator of smooth muscle cell (SMC) calcification via its recruitment to extracellular vesicles. Sortilin localized to calcifying vessels in human and mouse atheromata and participated in formation of microcalcifications in SMC culture. Sortilin...

  2. Pathology of Human Coronary and Carotid Artery Atherosclerosis and Vascular Calcification in Diabetes Mellitus.

    Science.gov (United States)

    Yahagi, Kazuyuki; Kolodgie, Frank D; Lutter, Christoph; Mori, Hiroyoshi; Romero, Maria E; Finn, Aloke V; Virmani, Renu

    2017-02-01

    The continuing increase in the prevalence of diabetes mellitus in the general population is predicted to result in a higher incidence of cardiovascular disease. Although the mechanisms of diabetes mellitus-associated progression of atherosclerosis are not fully understood, at clinical and pathological levels, there is an appreciation of increased disease burden and higher levels of arterial calcification in these subjects. Plaques within the coronary arteries of patients with diabetes mellitus generally exhibit larger necrotic cores and significantly greater inflammation consisting mainly of macrophages and T lymphocytes relative to patients without diabetes mellitus. Moreover, there is a higher incidence of healed plaque ruptures and positive remodeling in hearts from subjects with type 1 diabetes mellitus and type 2 diabetes mellitus, suggesting a more active atherogenic process. Lesion calcification in the coronary, carotid, and other arterial beds is also more extensive. Although the role of coronary artery calcification in identifying cardiovascular disease and predicting its outcome is undeniable, our understanding of how key hormonal and physiological alterations associated with diabetes mellitus such as insulin resistance and hyperglycemia influence the process of vascular calcification continues to grow. Important drivers of atherosclerotic calcification in diabetes mellitus include oxidative stress, endothelial dysfunction, alterations in mineral metabolism, increased inflammatory cytokine production, and release of osteoprogenitor cells from the marrow into the circulation. Our review will focus on the pathophysiology of type 1 diabetes mellitus- and type 2 diabetes mellitus-associated vascular disease with particular focus on coronary and carotid atherosclerotic calcification.

  3. [Ectopic calcification].

    Science.gov (United States)

    Fukumoto, Seiji

    2014-02-01

    Calcium deposition can be observed in many tissues in addition to bones and teeth which physiologically calcify. This unphysiological calcification can damage several organs. It has been shown that vascular calcification which is a risk factor for cardiovascular events develops through similar mechanisms to physiological calcification. Further studies to clarify detailed mechanisms of calcification are necessary to develop measures that inhibit unphysiological ectopic calcification without affecting physiological calcification in bones and teeth.

  4. T3 inhibits the calcification of vascular smooth muscle cells and the potential mechanism.

    Science.gov (United States)

    Chang, Xiaodan; Zhang, Baohong; Lihua, Li; Feng, Zhichun

    2016-01-01

    This study aimed to investigate the potential molecular mechanism underlying the T3 induced vascular calcification and phenotype transformation of vascular smooth muscle cells (VSMCs). Rat thoracic aortic smooth muscle cells (A7r5) were cultured in vitro and randomly assigned into normal control group, calcification group, T3 group and inhibitor group. When compared with normal control group, the osteocalcin content, ALP activity, Osterix and Runx2 mRNA expression and OPN protein expression increased significantly (P<0.01), and the protein expression of SMα and SM22α reduced dramatically in A7r5 cells of calcification group (P<0.01). After T3 treatment, the osteocalcin content and ALP activity reduced markedly, mRNA expression of Osterix and Runx2 and OPN protein expression reduced significantly. However, MMI (inhibitor of T3) was able to block the above effects of T3. When compared with calcification group, Osterix and Runx2 mRNA expression and OPN protein expression increased markedly (P<0.01). In addition, the protein expression of ERK1/2, p-ERK, Akt and p-Akt increased significantly in calcification group. In the presence of integrin αvβ3/ERK blocker (PD98059) and/or PI3K/Akt antagonist (LY294002), T3 was still able to inhibit the calcification, and this effect was similar to that after treatment with inhibitors alone. Moreover, LY294002 had a better inhibitory effect as compared to PD98059. T3 may act on PI3K/Akt signaling pathway to inhibit the phenotype transformation of VSMC, which then suppresses the calcium/phosphate induced calcification of rat VSMCs. Thus, T3 is an endogenous molecule that can protect the blood vessels against calcification.

  5. Correlation of serum 25-hydroxyvitamin D level with vascular calcification in hemodialysis patients

    Science.gov (United States)

    Wang, Fang; Wu, Shukun; Ruan, Yizhe; Wang, Li

    2015-01-01

    Objective: The aim of this study was to analyze the correlation of serum 25-hydroxyvitamin D level with vascular calcification in patients treated with hemodialysis. Methods: As a cross-sectional study, 126 patients receiving maintenance hemodialysis (MHD) in our hospital were enrolled in this study. According to the serum 25-hydroxyvitamin D level, the patients were divided into 25-hydroxyvitamin D deficiency group (30 ηg/ml or less than 30 ηg/ml) and 25-hydroxyvitamin D normal level group (>30 ηg/ml). All of the subjects underwent lateral lumbar, pelvis and hands X-ray examination to score the degree of calcification (Kauppila score). Results: Among the 126 patients treated with MHD, there were 110 patients with 25-hydroxyvitamin D deficiency and 16 patients with normal 25-hydroxyvitamin D level. There was no significant difference found in gender, age, age of dialysis, active vitamin D treatment, blood calcium, blood phosphorus, blood parathyroid hormone (PTH) and other related indicators between the two groups. The incidence of vascular calcification in patients with 25-hydroxyvitamin D deficiency was significantly higher than that in patients with normal 25-hydroxyvitamin D level (P = 0.001). Serum 25-hydroxyvitamin D level had a negative correlation with the calcification score (r = 0.193, P = 0.193). Logistic regression showed that 25-hydroxyvitamin D was not a risk factor for vascular calcification in MHD patients. Serum 25-hydroxyvitamin D level is generally low in patients with MHD. Conclusions: Patients with 25-hydroxyvitamin D deficiency have a higher incidence of vascular calcification with a markedly negative correlation. Thus, for the patients treated with MHD, vitamin D deficiency should be actively treated. PMID:26629071

  6. Vascular calcification and chronic kidney disease; the role of vitamin K

    Science.gov (United States)

    Risk factors for vascular calcification such as dialysis vintage, higher mean phosphorus concentrations and higher prescribed daily doses of vitamin D and calcium-containing phosphorus binders are unique to the dialysis population. Therefore, consideration of risk factors beyond those within the tr...

  7. Safety of Tourniquet Use in Total Knee Arthroplasty in Patients With Radiographic Evidence of Vascular Calcifications.

    Science.gov (United States)

    Koehler, Steven M; Fields, Adam; Noori, Naudereh; Weiser, Mitchell; Moucha, Calin S; Bronson, Michael J

    2015-09-01

    Tourniquets are often used in total knee arthroplasty (TKA) to improve visualization of structures, shorten operative time, reduce intraoperative bleeding, and improve cementing technique. Despite these advantages, controversy remains regarding the safety of tourniquet use. Tourniquets have been associated with nerve palsies, vascular injury, and muscle damage. Some have hypothesized they may also cause deep vein thrombosis. Last, increased incidence of postoperative wound complications has been reported with use of tourniquets. We conducted a retrospective cohort study to determine whether tourniquet use in TKA in patients with preexisting radiographic evidence of vascular disease increases the risk for wound complications or venous thromboembolism (VTE). Patients (N = 373) were placed in 2 groups: One had no preoperative radiographic evidence of knee arterial calcification (n = 285), and the other had arterial calcifications (n = 88). Overall, arterial calcification did not increase the risk for wound complication or VTE (P > .05). Furthermore, location of arterial calcification did not affect risk for wound complication or VTE. There were no arterial injuries. Diabetes, hypertension, prior VTE, coronary artery disease, and male sex were linked to higher wound complication rates (P < .05). Patients who have preoperative radiographic evidence of arterial calcification can safely undergo tourniquet-assisted TKA.

  8. Lanthanum prevents high phosphate-induced vascular calcification by preserving vascular smooth muscle lineage markers.

    Science.gov (United States)

    Ciceri, Paola; Elli, Francesca; Brenna, Irene; Volpi, Elisa; Romagnoli, Solange; Tosi, Delfina; Braidotti, Paola; Brancaccio, Diego; Cozzolino, Mario

    2013-06-01

    Vascular calcification (VC) represents a major cardiovascular risk factor in chronic kidney disease patients. High phosphate (Pi) levels are strongly associated with VC in this population. Therefore, Pi binders are commonly used to control high Pi levels. The aim of this work was to study the mechanism of action of lanthanum chloride (LaCl3) on the progression of Pi-induced VC through its direct effect on vascular smooth muscle cells (VSMCs) in vitro. High Pi induced VSCM Ca deposition. We evaluated the action of LaCl3, compared to gadolinium chloride (GdCl3), and found different effects on the modulation of VSMC lineage markers, such as α-actin and SM22α. In fact, only LaCl3 preserved the expression of both VSMC lineage markers compared to high Pi-treated cells. Interestingly, both LaCl3 and GdCl3 reduced the high Pi-induced elevations of bone morphogenic protein 2 mRNA expression, with no reduction of the high core binding factor-alpha 1 mRNA levels observed in calcified VSMCs. Furthermore, we also found that only LaCl3 completely prevented the matrix GLA protein mRNA levels and osteonectin protein expression elevations induced by high Pi compared to GdCl3. Finally, LaCl3, in contrast to GdCl3, prevented the high Pi-induced downregulation of Axl, a membrane tyrosine kinase receptor involved in apoptosis. Thus, our results suggest that LaCl3 prevents VC by preserving VSMC lineage markers and by decreasing high Pi-induced osteoblastic differentiation.

  9. Lanthanum acetate inhibits vascular calcification induced by vitamin D3 plus nicotine in rats.

    Science.gov (United States)

    Zhou, Ye-Bo; Jin, Shao-Ju; Cai, Yan; Teng, Xu; Chen, Li; Tang, Chao-Shu; Qi, Yong-Fen

    2009-08-01

    Lanthanum, a rare earth element, has been used to decrease serum phosphorus level in patients with chronic renal disease and hyperphosphatemia. We aimed to observe the effect and mechanism of two doses of lanthanum acetate (375 and 750 mg/kg/day) on vascular calcification induced by vitamin D3 plus nicotine treatment in rats for 4 weeks. As compared with control rats, rats with calcification showed widespread calcified nodules and irregular elastic fibers in calcified aorta on von Kossa calcium staining and increased aortic calcium and phosphorus contents, alkaline phosphatase (ALP) activity and bone-related protein expressions for osteopontin (OPN) and type III sodium dependent phosphate cotransporter Pit-1 (Pit-1). After treatment with either dose of lanthanum acetate, the calcified nodules and degree of irregular elastic fibers decreased in aortas. Lanthanum acetate at 750 mg/kg/day was more effective than 375 mg/kg/day in lessening vascular calcification by significantly reducing plasma phosphorus level, calcium x phosphorus product and ALP activity, by 30.3%, 28.6%, and 68.6%, respectively; reducing aortic phosphorus and calcium contents and ALP activity, by 48%, 53.1%, and 63.5% (all P nicotine alone. Lanthanum acetate could effectively inhibit the pathogenesis of vascular calcification.

  10. Vascular calcifications on hand radiographs in rheumatoid arthritis and associations with autoantibodies, cardiovascular risk factors and mortality

    Science.gov (United States)

    Solow, E. Blair; Yu, Fang; Thiele, Geoffrey M.; Sokolove, Jeremy; Robinson, William H.; Pruhs, Zachary M.; Michaud, Kaleb D.; Erickson, Alan R.; Sayles, Harlan; Kerr, Gail S.; Gaffo, Angelo L.; Caplan, Liron; Davis, Lisa A.; Cannon, Grant W.; Reimold, Andreas M.; Baker, Joshua; Schwab, Pascale; Anderson, Daniel R.

    2015-01-01

    Objective. To examine whether vascular calcifications on hand films in RA might aid in determining mortality risk. Methods. Hand radiographs from 906 RA patients were scored as positive or negative for vascular calcifications. Patient characteristics associated with vascular calcifications were assessed using multivariable logistic regression, and associations with mortality were examined using Cox proportional hazards regression. Cytokines and multiplex ACPA were measured in both groups. Results. A total of 99 patients (11%) demonstrated radiographic vascular calcifications. Factors independently associated with vascular calcifications included diabetes [odds ratio (OR) 2.85; 95% CI 1.43, 5.66], cardiovascular disease at enrolment (OR 2.48; 95% CI 1.01, 6.09), prednisone use (OR 1.90; 95% CI 1.25, 2.91), current smoking (OR 0.06; 95% CI 0.01, 0.23) and former smoking (OR 0.36; 95% CI 0.27, 0.48) vs never smoking. In cytokine and ACPA subtype analysis, IL-4 and anti-citrullinated apolipoprotein E were significantly increased in patients with vascular calcifications in fully adjusted multivariable models. After multivariable adjustment, vascular calcifications were associated with an increase in all-cause mortality (hazard ratio 1.41; 95% CI 1.12, 1.78; P = 0.004). Conclusion. Vascular calcifications on hand radiographs were independently associated with increased all-cause mortality in RA. Mechanisms underpinning the associations of IL-4 and select ACPA with vascular calcifications and their utility as biomarkers predictive of cardiovascular disease risk in RA merit further study. PMID:25854268

  11. Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin

    DEFF Research Database (Denmark)

    Olesen, Ping; Knudsen, Kirsten Quyen Nguyen; Wogensen, Lise

    2007-01-01

    Arterial medial calcifications occur often in diabetic individuals as part of the diabetic macroangiopathy. The pathogenesis is unknown, but the presence of calcifications predicts risk of cardiovascular events. We examined the effects of insulin on calcifying smooth muscle cells in vitro...... and measured the expression of the bone-related molecule osteoprotegerin (OPG). Human vascular smooth muscle cells (VSMCs) were grown from aorta from kidney donors. Induction of calcification was performed with beta-glycerophosphate. The influence of insulin (200 microU/ml or 1,000 microU/ml) on calcification...... calcification in human smooth muscle cells from a series of donors after variable time in culture. Decreased OPG amounts were observed from the cells during the accelerated calcification phase. High dose of insulin (1,000 microU/ml) accelerated the calcification, whereas lower concentrations (200 microU/ml) did...

  12. Gallic acid inhibits vascular calcification through the blockade of BMP2-Smad1/5/8 signaling pathway.

    Science.gov (United States)

    Kee, Hae Jin; Cho, Soo-Na; Kim, Gwi Ran; Choi, Sin Young; Ryu, Yuhee; Kim, In Kyeom; Hong, Young Joon; Park, Hyung Wook; Ahn, Youngkeun; Cho, Jeong Gwan; Park, Jong Chun; Jeong, Myung Ho

    2014-11-01

    Vascular calcification is associated with increased risk of morbidity and mortality in patients with cardiovascular diseases, chronic kidney diseases, and diabetes. Gallic acid, a natural compound found in gallnut and green tea, is known to be antifungal, antioxidant, and anticancer. Here we investigated the effect of gallic acid on vascular smooth muscle cell (VSMC) calcification and the underlying mechanism. Gallic acid inhibited inorganic phosphate-induced osteoblast differentiation markers as well as calcification phenotypes (as determined by calcium deposition, Alizarin Red, and Von Kossa staining). Knockdown of BMP2 or Noggin blocked phosphate-induced calcification. Gallic acid suppressed phosphorylation of Smad1/5/8 protein induced by inorganic phosphate. Taken together, we suggest that gallic acid acts as a novel therapeutic agent of vascular calcification by mediating BMP2-Smad1/5/8 signaling pathway.

  13. Advanced Glycation End-Products Induce Apoptosis of Vascular Smooth Muscle Cells: A Mechanism for Vascular Calcification

    Directory of Open Access Journals (Sweden)

    Sayo Koike

    2016-09-01

    Full Text Available Vascular calcification, especially medial artery calcification, is associated with cardiovascular death in patients with diabetes mellitus and chronic kidney disease (CKD. To determine the underlying mechanism of vascular calcification, we have demonstrated in our previous report that advanced glycation end-products (AGEs stimulated calcium deposition in vascular smooth muscle cells (VSMCs through excessive oxidative stress and phenotypic transition into osteoblastic cells. Since AGEs can induce apoptosis, in this study we investigated its role on VSMC apoptosis, focusing mainly on the underlying mechanisms. A rat VSMC line (A7r5 was cultured, and treated with glycolaldehyde-derived AGE-bovine serum albumin (AGE3-BSA. Apoptotic cells were identified by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL staining. To quantify apoptosis, an enzyme-linked immunosorbent assay (ELISA for histone-complexed DNA fragments was employed. Real-time PCR was performed to determine the mRNA levels. Treatment of A7r5 cells with AGE3-BSA from 100 µg/mL concentration markedly increased apoptosis, which was suppressed by Nox inhibitors. AGE3-BSA significantly increased the mRNA expression of NAD(PH oxidase components including Nox4 and p22phox, and these findings were confirmed by protein levels using immunofluorescence. Dihydroethidisum assay showed that compared with cBSA, AGE3-BSA increased reactive oxygen species level in A7r5 cells. Furthermore, AGE3-induced apoptosis was significantly inhibited by siRNA-mediated knockdown of Nox4 or p22phox. Double knockdown of Nox4 and p22phox showed a similar inhibitory effect on apoptosis as single gene silencing. Thus, our results demonstrated that NAD(PH oxidase-derived oxidative stress are involved in AGEs-induced apoptosis of VSMCs. These findings might be important to understand the pathogenesis of vascular calcification in diabetes and CKD.

  14. Vascular calcification is not associated with increased ambulatory central aortic systolic pressure in prevalent dialysis patients

    Science.gov (United States)

    Freercks, Robert J; Swanepoel, Charles R; Turest-Swartz, Kristy L; Rayner, Brian L; Carrara, Henri RO; Moosa, Sulaiman EI; Lachman, Anthony S

    2014-01-01

    Summary Introduction Central aortic systolic pressure (CASP) strongly predicts cardiovascular outcomes. We undertook to measure ambulatory CASP in 74 prevalent dialysis patients using the BPro (HealthStats, Singapore) device. We also determined whether coronary or abdominal aortic calcification was associated with changes in CASP and whether interdialytic CASP predicted ambulatory measurement. Methods All patients underwent computed tomography for coronary calcium score, lateral abdominal radiography for aortic calcium score, echocardiography for left ventricular mass index and ambulatory blood pressure measurement using BPro calibrated to brachial blood pressure. HealthStats was able to convert standard BPro SOFT® data into ambulatory CASP. Results Ambulatory CASP was not different in those without and with coronary (137.6 vs 141.8 mmHg, respectively, p = 0.6) or aortic (136.6 vs 145.6 mmHg, respectively, p = 0.2) calcification. Furthermore, when expressed as a percentage of brachial systolic blood pressure to control for peripheral blood pressure, any difference in CASP was abolished: CASP: brachial systolic blood pressure ratio = 0.9 across all categories regardless of the presence of coronary or aortic calcification (p = 0.2 and 0.4, respectively). Supporting this finding, left ventricular mass index was also not different in those with or without vascular calcification (p = 0.7 and 0.8 for coronary and aortic calcification). Inter-dialytic office blood pressure and CASP correlated excellently with ambulatory measurements (r = 0.9 for both). Conclusion Vascular calcification was not associated with changes in ambulatory central aortic systolic pressure in this cohort of prevalent dialysis patients. Inter-dialytic blood pressure and CASP correlated very well with ambulatory measurement. PMID:24626513

  15. NT-proBNP and potential vascular calcification in Black and Caucasian African men

    DEFF Research Database (Denmark)

    Kruger, Ruan; Schutte, Rudolph; Huisman, Hugo W;

    2012-01-01

    The N-terminal prohormone B-type natriuretic peptide (NT-proBNP) is a reliable marker of cardiac strain. In hypertensive heart disease, NT-proBNP levels increase and may lose its protective function. Simultaneously, the vasculature is also subject to hemodynamic stress, resulting in vascular matrix...... remodeling and stiffening which contribute to further cardiac alterations. Alkaline phosphatase (ALP) is a marker of osteoblast activity and is involved in vascular calcification. We explored the link between NT-proBNP and ALP in Black and Caucasian African men....

  16. The vascular phenotype in pseudoxanthoma elasticum and related disorders: Contribution of a genetic disease to the understanding of vascular calcification.

    Directory of Open Access Journals (Sweden)

    Georges eLeftheriotis

    2013-02-01

    Full Text Available Vascular calcification is a complex and dynamic process occurring in various physiological conditions such as aging and exercise or in acquired metabolic disorders like diabetes or chronic renal insufficiency. Arterial calcifications are also observed in several genetic diseases revealing the important role of unbalanced or defective anti- or pro-calcifying factors. Pseudoxanthoma elasticum (PXE is an inherited disease (OMIM 264800 characterized by elastic fiber fragmentation and calcification in various soft conjunctive tissues including the skin, eyes and arterial media. The PXE disease results from mutations in the ABCC6 gene, encoding an ATP-binding cassette transporter primarily expressed in the liver, kidneys suggesting that it is a prototypic metabolic soft-tissue calcifying disease of genetic origin. The clinical expression of the PXE arterial disease is characterized by an increased risk for coronary (myocardial infarction, cerebral (aneurysm and stroke and lower limb peripheral artery disease. However, the structural and functional changes in the arterial wall induced by PXE are still unexplained. The use of a recombinant mouse model inactivated for the Abcc6 gene is an important tool for the understanding of the PXE pathophysiology although the vascular impact in this model remains limited to date. Overlapping of the PXE phenotype with other inherited calcifying diseases could bring important informations to our comprehension of the PXE disease.

  17. Reduction of advanced-glycation end products levels and inhibition of RAGE signaling decreases rat vascular calcification induced by diabetes.

    Directory of Open Access Journals (Sweden)

    Mathieu R Brodeur

    Full Text Available Advanced-glycation end products (AGEs were recently implicated in vascular calcification, through a process mediated by RAGE (receptor for AGEs. Although a correlation between AGEs levels and vascular calcification was established, there is no evidence that reducing in vivo AGEs deposition or inhibiting AGEs-RAGE signaling pathways can decrease medial calcification. We evaluated the impact of inhibiting AGEs formation by pyridoxamine or elimination of AGEs by alagebrium on diabetic medial calcification. We also evaluated if the inhibition of AGEs-RAGE signaling pathways can prevent calcification. Rats were fed a high fat diet during 2 months before receiving a low dose of streptozotocin. Then, calcification was induced with warfarin. Pyridoxamine was administered at the beginning of warfarin treatment while alagebrium was administered 3 weeks after the beginning of warfarin treatment. Results demonstrate that AGEs inhibitors prevent the time-dependent accumulation of AGEs in femoral arteries of diabetic rats. This effect was accompanied by a reduced diabetes-accelerated calcification. Ex vivo experiments showed that N-methylpyridinium, an agonist of RAGE, induced calcification of diabetic femoral arteries, a process inhibited by antioxidants and different inhibitors of signaling pathways associated to RAGE activation. The physiological importance of oxidative stress was demonstrated by the reduction of femoral artery calcification in diabetic rats treated with apocynin, an inhibitor of reactive oxygen species production. We demonstrated that AGE inhibitors prevent or limit medial calcification. We also showed that diabetes-accelerated calcification is prevented by antioxidants. Thus, inhibiting the association of AGE-RAGE or the downstream signaling reduced medial calcification in diabetes.

  18. Vitamin D Affects Survival Independently of Vascular Calcification in Chronic Kidney Disease

    Science.gov (United States)

    Barreto, Daniela Veit; Barreto, Fellype Carvalho; Liabeuf, Sophie; Temmar, Mohammed; Boitte, Francis; Choukroun, Gabriel; Fournier, Albert; Massy, Ziad A.

    2009-01-01

    Background and objectives: Cardiovascular disease is the main cause of mortality in chronic kidney disease (CKD) patients. Vitamin D might have beneficial effects on vascular health. The aim of this study was to determine the prevalence of vitamin D deficiency (25-hydroxyvitamin D [25D] ≤ 15 ng/ml) and insufficiency (25D levels between 16 and 30 ng/ml) in a cohort of patients at different CKD stages and the relationships between vitamin D serum levels, vascular calcification and stiffness, and the mortality risk. Design, setting, participants & measurements: One hundred forty CKD patients (85 men, mean age 67 ± 12 yr; CKD stages 2 [8%], 3 [26%], 4 [26%], 5 [7%], and 5D [(33%]) were allocated for a prospective study. Serum levels of 25D and 1,25-dihydroxyvitamin D, aortic calcification score, and pulse wave velocity (PWV) were evaluated. Results: There was a high prevalence of vitamin D deficiency (42%) and insufficiency (34%). Patients with 25D ≤ 16.7 ng/ml (median) had a significantly lower survival rate than patients with 25D >16.7 ng/ml (mean follow-up, 605 ± 217 d; range, 10 to 889; P = 0.05). Multivariate adjustments (included age, gender, diabetes, arterial pressure, CKD stage, phosphate, albumin, hemoglobin, aortic calcification score and PWV) confirmed 25D level as an independent predictor of all-cause mortality. Conclusions: Vitamin D deficiency and insufficiency were highly prevalent in this CKD cohort. Low 25D levels affected mortality independently of vascular calcification and stiffness, suggesting that 25D may influence survival in CKD patients via additional pathways that need to be further explored. PMID:19443628

  19. The Association between Fibroblast Growth Factor-23 and Vascular Calcification Is Mitigated by Inflammation Markers

    Directory of Open Access Journals (Sweden)

    Mohamed M. NasrAllah

    2013-11-01

    Full Text Available Background: Fibroblast growth factor-23 (FGF-23 has been linked to vascular calcification, ventricular hypertrophy and mortality in chronic kidney disease (CKD, although these links may not be direct and independent. Similar grave outcomes are associated with inflammation and oxidative stress in CKD. Recently, accumulating evidence has linked components of phosphate homeostasis to inflammation and oxidative stress. The interaction between the triad of inflammation, FGF-23 and cardiovascular outcomes is underinvestigated. Methods: We studied 65 patients with stage 5 CKD on hemodialysis. Serum levels of FGF-23, high-sensitivity C-reactive protein (hsCRP, endogenous soluble receptor of advanced glycation end products (esRAGE, advanced oxidation protein products (AOPP, parathormone, lipids, calcium and phosphorous were measured. The aortic calcification index (ACI was determined using non-contrast CT scans of the abdominal aorta. Results: FGF-23 was elevated (mean: 4,681 pg/ml, SD: 3,906 and correlated with hsCRP, esRAGE, AOPP, dialysis vintage and phosphorus in univariate analysis. In multiple regression analysis, hsCRP, AOPP and phosphorus but not esRAGE were all significantly correlated to FGF-23 (R2 = 0.7, p 2 = 0.65, p Conclusion: FGF-23 is strongly correlated to various markers of inflammation and oxidative stress in hemodialysis patients. The association between FGF-23 and vascular calcification was mitigated when corrected for inflammation markers.

  20. A new in vitro model to delay high phosphate-induced vascular calcification progression.

    Science.gov (United States)

    Ciceri, Paola; Elli, Francesca; Cappelletti, Laura; Tosi, Delfina; Braidotti, Paola; Bulfamante, Gaetano; Cozzolino, Mario

    2015-12-01

    An increasing amount of patients affected by advanced chronic kidney disease suffer from vascular calcification (VC) that associates with cardiovascular morbidity and mortality. In this study, we created a new experimental in vitro model, trying to better elucidate high phosphate (Pi)-induced VC pathogenic mechanisms. Rat aortic vascular smooth muscle cells (VSMCs) were challenged for 7-10 days with high Pi with a repeated and short suspensions of high Pi treatment (intermittent suspension, IS) that was able to induce a significant inhibition of high Pi calcification, maximal at 5 h. Interestingly, the delay in calcification is a consequence of either the absence of free Pi or calcium-phosphate crystals being comparable to the total effect obtained during the 5 h-IS. The protective effect of IS was mediated by the reduction of apoptosis as demonstrated by the action of 20 μmol/L Z-VAD-FMK and by the preservation of the pro-survival receptor Axl expression. Furthermore, autophagy, during IS, was potentiated by increasing the autophagic flux, evaluated by LC3IIB western, while treating VSMCs with 1 mmol/L valproic acid did not affect VC. Finally, IS prevented VSMC osteoblastic differentiation by preserving smooth muscle lineage markers expression. Our data support the hypothesis that to delay significantly VC is necessary and sufficient the IS of high Pi challenge. The IS was able to prevent significantly apoptosis, to induce a potentiation in autophagy, and to prevent osteoblastic differentiation by preserving SM lineage markers.

  1. Cinacalcet reduces vascular and soft tissue calcification in secondary hyperparathyroidism (SHPT) in hemodialysis patients.

    Science.gov (United States)

    Aladrén Regidor, M J

    2009-02-01

    Management of secondary hyperparathyroidism (SHPT) in chronic kidney disease patients on hemodialysis (HD) can be challenging. Conventional treatments can lead to hypercalcemia and hyperphosphatemia, both of which are associated with vascular and soft tissue calcification and increased risk of cardiovascular disease. We report the effect of treatment with the Type II calcimimetic cinacalcet on vascular calcification in a HD patient with SHPT. A 40-year-old male with a 24-year history of kidney failure secondary to mesangial proliferative glomerulonephritis, commenced HD in October 2004 following chronic graft dysfunction. The patient was admitted to hospital with renal insufficiency and metabolic abnormalities. An anatomopathological study showed calcium (Ca) deposits in the alveolar septa, bronchial wall and pulmonary arterioles. Parathyroid methoxy isobutyl isonitrile (MIBI) scintigraphy revealed multiglandular parathyroid disease and an ectopic gland behind the sternal notch. Serum intact parathyroid hormone (iPTH) was repeatedly found to be > or = 2,500 pg/ml, and was accompanied by significant abnormalities in phosphorus (P) and Ca metabolism which were difficult to control. The patient was initially treated with sevelamer, low dose calcium carbonate, a low P and reduced protein diet and high doses of intravenous erythropoietin. In addition, he received HD with a high efficiency membrane for 4.5 hours, 4-times weekly. Treatment with cinacalcet was initiated at 30 mg/day and adjusted to achieve National Kidney Foundation Kidney Disease Outcomes Quality Initiative targets for iPTH, P, Ca and Ca-P product. One year following cinacalcet treatment, a chest x-ray showed a moderate reduction in Ca deposits, a bone X-ray showed a significant reduction in vascular calcifications, and parathyroid MIBI scintigraphy showed a disappearance of ectopic focus and minimal remains of glands. Significant reductions in calcemia were controlled by concomitant modifications to oral

  2. Critical Parameters of the In Vitro Method of Vascular Smooth Muscle Cell Calcification.

    Directory of Open Access Journals (Sweden)

    Luis Hortells

    Full Text Available Vascular calcification (VC is primarily studied using cultures of vascular smooth muscle cells. However, the use of very different protocols and extreme conditions can provide findings unrelated to VC. In this work we aimed to determine the critical experimental parameters that affect calcification in vitro and to determine the relevance to calcification in vivo.Rat VSMC calcification in vitro was studied using different concentrations of fetal calf serum, calcium, and phosphate, in different types of culture media, and using various volumes and rates of change. The bicarbonate content of the media critically affected pH and resulted in supersaturation, depending on the concentration of Ca2+ and Pi. Such supersaturation is a consequence of the high dependence of bicarbonate buffers on CO2 vapor pressure and bicarbonate concentration at pHs above 7.40. Such buffer systems cause considerable pH variations as a result of minor experimental changes. The variations are more critical for DMEM and are negligible when the bicarbonate concentration is reduced to ¼. Particle nucleation and growth were observed by dynamic light scattering and electron microscopy. Using 2mM Pi, particles of ~200nm were observed at 24 hours in MEM and at 1 hour in DMEM. These nuclei grew over time, were deposited in the cells, and caused osteogene expression or cell death, depending on the precipitation rate. TEM observations showed that the initial precipitate was amorphous calcium phosphate (ACP, which converts into hydroxyapatite over time. In blood, the scenario is different, because supersaturation is avoided by a tightly controlled pH of 7.4, which prevents the formation of PO43--containing ACP.The precipitation of ACP in vitro is unrelated to VC in vivo. The model needs to be refined through controlled pH and the use of additional procalcifying agents other than Pi in order to reproduce calcium phosphate deposition in vivo.

  3. Pharmacological inhibition of PHOSPHO1 suppresses vascular smooth muscle cell calcification.

    Science.gov (United States)

    Kiffer-Moreira, Tina; Yadav, Manisha C; Zhu, Dongxing; Narisawa, Sonoko; Sheen, Campbell; Stec, Boguslaw; Cosford, Nicholas D; Dahl, Russell; Farquharson, Colin; Hoylaerts, Marc F; Macrae, Vicky E; Millán, José Luis

    2013-01-01

    Medial vascular calcification (MVC) is common in patients with chronic kidney disease, obesity, and aging. MVC is an actively regulated process that resembles skeletal mineralization, resulting from chondro-osteogenic transformation of vascular smooth muscle cells (VSMCs). Here, we used mineralizing murine VSMCs to study the expression of PHOSPHO1, a phosphatase that participates in the first step of matrix vesicles-mediated initiation of mineralization during endochondral ossification. Wild-type (WT) VSMCs cultured under calcifying conditions exhibited increased Phospho1 gene expression and Phospho1(-/-) VSMCs failed to mineralize in vitro. Using natural PHOSPHO1 substrates, potent and specific inhibitors of PHOSPHO1 were identified via high-throughput screening and mechanistic analysis and two of these inhibitors, designated MLS-0390838 and MLS-0263839, were selected for further analysis. Their effectiveness in preventing VSMC calcification by targeting PHOSPHO1 function was assessed, alone and in combination with a potent tissue-nonspecific alkaline phosphatase (TNAP) inhibitor MLS-0038949. PHOSPHO1 inhibition by MLS-0263839 in mineralizing WT cells (cultured with added inorganic phosphate) reduced calcification in culture to 41.8% ± 2.0% of control. Combined inhibition of PHOSPHO1 by MLS-0263839 and TNAP by MLS-0038949 significantly reduced calcification to 20.9% ± 0.74% of control. Furthermore, the dual inhibition strategy affected the expression of several mineralization-related enzymes while increasing expression of the smooth muscle cell marker Acta2. We conclude that PHOSPHO1 plays a critical role in VSMC mineralization and that "phosphatase inhibition" may be a useful therapeutic strategy to reduce MVC.

  4. Vitamin E protection of obesity-enhanced vascular calcification in uremic rats.

    Science.gov (United States)

    Peralta-Ramírez, A; Montes de Oca, A; Raya, A I; Pineda, C; López, I; Guerrero, F; Diez, E; Muñoz-Castañeda, J R; Martinez, J; Almaden, Y; Rodríguez, M; Aguilera-Tejero, E

    2014-02-15

    This study aimed to determine the extent of extraskeletal calcification in uremic Zucker rats, by comparing obese and lean phenotypes, and to evaluate the influence of vitamin E (VitE) on the development of calcifications in both uremic rats and human vascular smooth muscle cells (HVSMCs) cultured in vitro. Zucker rats of lean and obese phenotypes with normal renal function [control (C); C-lean and C-obese groups] and with uremia [5/6 nephrectomy (Nx); Nx-lean and Nx-obese groups] and uremic rats treated with VitE (Nx-lean + VitE and Nx-obese + VitE groups) were studied. Uremic groups were subjected to Nx, fed a 0.9% phosphorus diet, and treated with calcitriol (80 ng/kg ip). The aortic calcium concentration was significantly higher (P Nx-obese rats (10.0 ± 2.1 mg/g tissue) than in Nx-lean rats (3.6 ± 1.3 mg/g tissue). A decrease in plasma glutathione peroxidase activity was observed in Nx-obese rats compared with Nx-lean rats (217.2 ± 18.2 vs. 382.3 ± 15.5 nmol·min(-1)·ml(-1), P Nx-lean, Nx-obese, Nx-lean + VitE, and Nx-obese + VitE rats were also evidenced in other soft tissues. In HVSMCs incubated with high phosphate, VitE also prevented oxidative stress and reduced calcium content, bone alkaline phosphatase, and gene expression of core-binding factor-α1. In conclusion, uremic obese rats develop more severe calcifications than uremic lean rats and VitE reduces oxidative stress and vascular calcifications in both rats and cultures of HVSMCs.

  5. 血管钙化的分子机理与临床展望%Molecular Mechanism and clinical perspective of vascular calcification

    Institute of Scientific and Technical Information of China (English)

    Masahiko Kurabayashi

    2010-01-01

    @@ Cardiovascular disease is a major consideration in the patients with diabetes and chronic kidney disease (CKD).Vascular calcification is an important problem among these patients,and contributes to the increased risk of cardiovascular events by a variety of mechanism,including an increase in arterial stiffness by medial calcification or an increase in plaque vulnerability by a specific type of atherosclerotic calcification.

  6. Lipids in biocalcification: contrasts and similarities between intimal and medial vascular calcification and bone by NMR[S

    Science.gov (United States)

    Reid, David G.; Shanahan, Catherine M.; Duer, Melinda J.; Arroyo, Luis G.; Schoppet, Michael; Brooks, Roger A.; Murray, Rachel C.

    2012-01-01

    Pathomechanisms underlying vascular calcification biogenesis are still incompletely understood. Biomineral from human atherosclerotic intimal plaques; human, equine, and bovine medial vascular calcifications; and human and equine bone was released from collagenous organic matrix by sodium hydroxide/sodium hypochlorite digestion. Solid-state 13C NMR of intimal plaque mineral shows signals from cholesterol/cholesteryl esters and fatty acids. In contrast, in mineral from pure medial calcifications and bone mineral, fatty acid signals predominate. Refluxing (chloroform/methanol) intimal plaque calcifications removes the cholesterylic but not the fatty acyl signals. The lipid composition of this refluxed mineral now closely resembles that of the medial and bone mineral, which is unchanged by reflux. Thus, intimal and medial vascular calcifications and bone mineral have in common a pool of occluded mineral-entrained fatty acyl-rich lipids. This population of fatty acid may contain methyl-branched fatty acids, possibly representing lipoprotein particle remnants. Cell signaling and mechanistic parallels between physiological (orthotopic) and pathological (ectopic) calcification are also reflected thus in the NMR spectroscopic fingerprints of mineral-associated and mineral-entrained lipids. Additionally the atherosclerotic plaque mineral alone shows a significant independent pool of cholesterylic lipids. Colocalization of mineral and lipid may be coincidental, but it could also reflect an essential mechanistic component of biomineralization. PMID:22651923

  7. Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

    Institute of Scientific and Technical Information of China (English)

    Sheng-ying WU; Chun-shui PAN; Bin GENG; Jing ZHAO; Fang YU; Yong-zheng PANG; Chao-shu TANG; Yong-fen QI

    2006-01-01

    Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in vivo.Methods:A rat vascular calcitication model was established by administration of vitamin D3 plus nicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was determined by using semi-quantitative reverse-transcription polymerase chain reaction.The calcium content,45Ca2+ accumulation and alkaline phosphatase(ALP)activity were measured.H2S production and CSE activity were measured.Results:von Kossa staining produced strong positive black/brown staining in areas among the elastic fibers of the medial layer in the calcified aorta.The calcium content,45Ca2+ accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with controls.The expression of the OPN gene was upregulated(P<0.01).Expression of the CSE gene was downregulated.However,calcium content.45Ca2+ uptake and ALP activity in the VDN plus NaHS group was lower than that in the VDN group.The content of calcium and 45Ca2+ accumulation and activity of ALP in the aorta were 34.8%,40.75%and 63.5%lower in the low-dosage NaHS group than in the VDN group,respectively(P<0.01),and the calcium content and deposition of 45Ca2+ and activity of ALP was 83.9%,37.8%and 46.2% lower in the aorta in the high-dosage NaHS group than in the VDN group,respectively(P<0.01).The expression of the OPN gene was downregulated.Conclusion:The production of H2S,and CSE activity were decreased and CSE gene expression was downregulated in rats with vascular catcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

  8. Autophagy inhibits PDGF-BB-induced calcification in vascular smooth muscle cells

    Institute of Scientific and Technical Information of China (English)

    PEI Qian-qian; MEI Han; ZHANG Xu-hui; DONG Li-hua

    2016-01-01

    AIM:To investigate the relationship between autophagy and calcification in vascular smooth muscle cells ( VSMCs) after platelet-derived growth factor (PDGF)-BB stimulation.METHODS:Cultured VSMCs were stimulated with PDGF-BB for different time, the expression of vascular calcification-related proteins and autophagy-related proteins were detected by Western blot .The interaction be-tween Beclin1 and PI3KC3 was detected by co-immunoprecipitation.RESULTS: The expression of BMP2 and ALP showed a trend from decline to rise.ALP slumped at 12 h, and BMP2 slumped at 6 h.Moreover, the expression of Beclin-1 showed a trend from rise to decline, and peaked at 12 h.The conversion of LC3-ⅠtoⅡincreased in a time-dependent manner , and peaked at 24 h.The ex-pression of BMP2 and ALP was increased in VSMCs incubated with PDGF-BB and autophagy inhibitor 3-MA, compared with PDGF-BB-stimulated VSMCs.Furthermore, the interaction between Beclin1 and PI3KC3 was enhanced at 6 h after PDGF-BB stimulated, peaked at 12 h, and kept in high level at 24 h.Moreover, the phosphorylation level of Beclin 1 was enhanced by PDGF-BB stimulation, and peaked at 6 h.CONCLUSION:Our findings demonstrate that PDGF-BB-induced autophagy inhibits VSMC calcification by en-hancing Beclin1 phosphorylation and interaction between Beclin 1 and PI3KC3.

  9. Delayed sodium (18)F-fluoride PET/CT imaging does not improve quantification of vascular calcification metabolism

    DEFF Research Database (Denmark)

    Blomberg, Björn Alexander; Thomassen, Anders; Takx, Richard A P

    2014-01-01

    This study aimed to determine if delayed sodium (18)F-fluoride (Na(18)F) PET/CT imaging improves quantification of vascular calcification metabolism. Blood-pool activity can disturb the arterial Na(18)F signal. With time, blood-pool activity declines. Therefore, delayed imaging can potentially im...

  10. 糖尿病相关血管钙化%Diabetes-related vascular calcification

    Institute of Scientific and Technical Information of China (English)

    王晓来

    2015-01-01

    多项研究显示糖尿病患者的冠状动脉钙化(CAC)积分升高,CAC进展迅速.糖尿病相关血管钙化与高血糖、维生素D缺乏、胰岛素抵抗、肥胖、贲门上部脂肪、肾脏疾病等多种危险因素相关.心血管疾病(CVD)是导致成人糖尿病患者死亡的主要原因.CAC是斑块负担较好标志,其与糖尿病患者的CVD风险增加显著相关.在糖尿病人群中,CAC的发生及程度可以预测未来心血管事件.%Several studies have shown that in patients with diabetes if the coronary artery calcification (CAC) score increases, the CAC will progress rapidly.Diabetes-related vascular calcification is associated with hyperglycemia, vitamin D deficiency, insulin resistance, obesity, epicardial fat, renal disease and other risk factors.Cardiovascular disease (CVD) is the leading cause of death in adults with diabetes.CAC is a useful marker of plaque burden.It is significantly correlated with the increase of CVD risk in diabetic patients.In diabetic population, the occurrence and level of CAC can be used to predict cardiovascular events in the future.

  11. Involvement of parathyroid hormone-related protein in vascular calcification of chronic haemodialysis patients.

    Science.gov (United States)

    Liu, Fang; Fu, Ping; Fan, Wenxing; Gou, Rong; Huang, Youqun; Qiu, Hongyu; Zhong, Hui; Huang, Songmin

    2012-08-01

    To investigate the role of parathyroid hormone-related protein (PTHrP) in vascular calcification of patients with chronic hemodialysis. The inferior epigastric arteries were obtained from 23 patients on chronic haemodialysis and 16 patients with renal carcinoma as control. Haematoxylin-eosin staining, elastic fibre staining, Alizarin Red calcium staining and immunohistochemical staining of PTHrP, bone morphogenetic protein-2 (BMP-2), Cbfa1/Runx2 were performed. Real-time polymerase chain reaction (PCR) was used to examine mRNA expressions of PTHrP, BMP-2 and Cbfa1/Runx2. Western blot and real-time PCR were used to detect the effects of PTHrP-siRNA and rh-PTHrP-1-34 on the expressions of PTHrP, BMP-2 and Cbfa1/Runx2 in human aortic smooth muscle cells (HASMC). Alkaline phosphatase (ALP) activities and intracellular calcium content in HASMCs were assessed after treatment with 10 mmol/L β-glycerol phosphoric acid for 48 h. Vascular calcification was confirmed in 78.2% of patients on chronic haemodialysis, and the expressions of PTHrP, BMP-2 and Cbfa1 in the arteries were significantly upregulated. PTHrP-siRNA could downregulate the expression of PTHrP by 60%, BMP-2 by 25% and Cbfa1 by 25% at 24 h (P PTHrP-1-34 could upregulate the expressions of BMP-2 and Cbfa1 by 1.37-fold and 1.46-fold, respectively, at 24 h in a time-independent manner (P PTHrP-siRNA. Moreover, it could promote intracellular calcium deposition and increase ALP activities, which were partially blocked by PTHrP-siRNA (P PTHrP might contribute by activating BMP-2/ Cbfa1 signalling pathway. © 2012 The Authors. Nephrology © 2012 Asian Pacific Society of Nephrology.

  12. Androgen receptor-dependent transactivation of growth arrest-specific gene 6 mediates inhibitory effects of testosterone on vascular calcification.

    Science.gov (United States)

    Son, Bo-Kyung; Akishita, Masahiro; Iijima, Katsuya; Ogawa, Sumito; Maemura, Koji; Yu, Jing; Takeyama, Kenichi; Kato, Shigeaki; Eto, Masato; Ouchi, Yasuyoshi

    2010-03-05

    Recent epidemiological studies have found that androgen deficiency is associated with a higher incidence of cardiovascular disease in men. However, little is known about the mechanism underlying the cardioprotective effects of androgens. Here we show the inhibitory effects of testosterone on vascular calcification and a critical role of androgen receptor (AR)-dependent transactivation of growth arrest-specific gene 6 (Gas6), a key regulator of inorganic phosphate (P(i))-induced calcification of vascular smooth muscle cells (VSMC). Testosterone and nonaromatizable androgen dihydrotestosterone inhibited P(i)-induced calcification of human aortic VSMC in a concentration-dependent manner. Androgen inhibited P(i)-induced VSMC apoptosis, an essential process for VSMC calcification. The effects on VSMC calcification were mediated by restoration of P(i)-induced down-regulation of Gas6 expression and a subsequent reduction of Akt phosphorylation. These effects of androgen were blocked by an AR antagonist, flutamide, but not by an estrogen receptor antagonist, ICI 182,780. We then explored the mechanistic role of the AR in Gas6 expression and found an abundant expression of AR predominantly in the nucleus of VSMC and two consensus ARE sequences in the Gas6 promoter region. Dihydrotestosterone stimulated Gas6 promoter activity, and this effect was abrogated by flutamide and by AR siRNA. Site-specific mutation revealed that the proximal ARE was essential for androgen-dependent transactivation of Gas6. Furthermore, chromatin immunoprecipitation assays demonstrated ligand-dependent binding of the AR to the proximal ARE of Gas6. These results indicate that AR signaling directly regulates Gas6 transcription, which leads to inhibition of vascular calcification, and provides a mechanistic insight into the cardioprotective action of androgens.

  13. Vascular calcification of the lower extremities demonstrated by Tc-99m MDP bone scintigraphy in a patient with diabetes mellitus

    Energy Technology Data Exchange (ETDEWEB)

    Lim, Seok Tae; Sohn, Myung Hee [Chonbuk National University Medical School, Chonju, l (Korea, Republic of)

    2001-06-01

    The femoral vessels are sometimes visualized on bone scintigraphy. This is almost always caused by calcification of the femoral artery associated with atherosclerotic changes of the arterial wall. Vascular calcification is frequently seen in the elderly and in diabetics. A 78 year old woman was admitted for non-insulin dependent diabetes mellitus. In this patient with diabetes mellitus, tibial arteries as well as femoral arteries were visualized onTc-99m MDP bone scintigraphy in contrast with visualization of femoral artery alone observed in the elderly.

  14. Vascular ossification – calcification in metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, and calciphylaxis – calcific uremic arteriolopathy: the emerging role of sodium thiosulfate

    Directory of Open Access Journals (Sweden)

    Sowers James R

    2005-03-01

    Full Text Available Abstract Background Vascular calcification is associated with metabolic syndrome, diabetes, hypertension, atherosclerosis, chronic kidney disease, and end stage renal disease. Each of the above contributes to an accelerated and premature demise primarily due to cardiovascular disease. The above conditions are associated with multiple metabolic toxicities resulting in an increase in reactive oxygen species to the arterial vessel wall, which results in a response to injury wound healing (remodeling. The endothelium seems to be at the very center of these disease processes, acting as the first line of defense against these multiple metabolic toxicities and the first to encounter their damaging effects to the arterial vessel wall. Results The pathobiomolecular mechanisms of vascular calcification are presented in order to provide the clinician – researcher a database of knowledge to assist in the clinical management of these high-risk patients and examine newer therapies. Calciphylaxis is associated with medial arteriolar vascular calcification and results in ischemic subcutaneous necrosis with vulnerable skin ulcerations and high mortality. Recently, this clinical syndrome (once thought to be rare is presenting with increasing frequency. Consequently, newer therapeutic modalities need to be explored. Intravenous sodium thiosulfate is currently used as an antidote for the treatment of cyanide poisioning and prevention of toxicities of cisplatin cancer therapies. It is used as a food and medicinal preservative and topically used as an antifungal medication. Conclusion A discussion of sodium thiosulfate's dual role as a potent antioxidant and chelator of calcium is presented in order to better understand its role as an emerging novel therapy for the clinical syndrome of calciphylaxis and its complications.

  15. Vascular Calcification in Uremia: New-Age Concepts about an Old-Age Problem.

    Science.gov (United States)

    Smith, Edward R

    2016-01-01

    A hallmark of aging, and major contributor to the increased prevalence of cardiovascular disease in patients with chronic kidney disease (CKD), is the progressive structural and functional deterioration of the arteries and concomitant accrual of mineral. Vascular calcification (VC) was long viewed as a degenerative age-related pathology that resulted from the passive deposition of mineral in the extracellular matrix; however, since the discovery of "bone-related" protein expression in calcified atherosclerotic plaques over 20 years ago, a plethora of studies have evoked the now widely accepted view that VC is a highly regulated and principally cell-mediated phenomenon that recapitulates many features of physiologic ossification. Central to this theory are changes in vascular smooth muscle cell (VSMC) phenotype and viability, thought to be driven by chronic exposure to a number of dystrophic stimuli characteristics of the uremic state. Here, dedifferentiated synthetic VSMCs are seen to spawn calcifying matrix vesicles that actively seed mineralization of the arterial matrix. This review provides an overview of the major epidemiological, histological, and molecular aspects of VC in the context of CKD, and a counterpoint to the prevailing paradigm that emphasizes the primacy of VSMC-mediated mechanisms. Particular focus is given to the import of protein and small molecule inhibitors in regulating physiologic and pathological mineralization and the emerging role of mineral nanoparticles and their interplay with proinflammatory processes.

  16. Effects of unfractionated heparin on renal osteodystrophy and vascular calcification in chronic kidney disease rats.

    Science.gov (United States)

    Meng, Yan; Zhang, Hao; Li, Yingbin; Li, Qingnan; Zuo, Li

    2014-01-01

    Unfractionated heparin (UFH) is the most widely used anticoagulant in hemodialysis for chronic kidney disease (CKD) patients. Many studies have verified that UFH can induce bone loss in subjects with normal bone, but few have focused on its effect on renal osteodystrophy. We therefore investigated this issue in adenine-induced CKD rats. As CKD also impairs mineral metabolism systemically, we also studied the impacts of UFH on serum markers of CKD-mineral and bone disorder (CKD-MBD) and vascular calcification. We administered low and high doses of UFH (1U/g and 2U/g body weight, respectively) to CKD rats and compared them with CKD controls. At sacrifice, the serum markers of CKD-MBD did not significantly differ among the two UFH CKD groups and the CKD control group. The mean bone mineral densities (BMDs) of the total femur and a region of interest (ROI) constituted of trabecular and cortical bone were lower in the high-dose UFH (H-UFH) CKD group than in the CKD control group (P<0.05 and P<0.01, respectively). The BMD of the femoral ROI constituted of cortical bone did not differ between the H-UFH CKD group and the CKD control group. Histomorphometrical changes in the CKD rats indicated secondary hyperparathyroidism, and the femoral trabecular bone volume, but not cortical bone volume, significantly decreased with increasing UFH dose. The same decreasing trend was found in osteoblast parameters, and an increasing trend was found in osteoclast parameters; however, most differences were not significant. Moreover, no distinct statistical differences were found in the comparison of vascular calcium or phosphorus content among the CKD control group and the two UFH CKD groups. Therefore, we concluded that UFH could induce bone loss in CKD rats with secondary hyperparathyroidism, mainly by reducing the trabecular volume and had little effect on cortical bone volume. The underlying mechanism might involve inhibition of osteoblast activity and promotion of osteoclast activity

  17. Usefulness of abdominal aortic calcification for screening of peripheral vascular disease

    Energy Technology Data Exchange (ETDEWEB)

    Park, Chul Hi; Kim, Jeong Ho; Choi, Soo Jin; Kim, Hyung Sik [Gachon University Gil Medical Center, Incheon (Korea, Republic of); Jin, Wook; Yang, Dal Mo [East-West Neo Medical Center, Seoul (Korea, Republic of)

    2006-12-15

    We wanted to evaluate the value of abdominal aortic calcification (AAC), as detected on CT, as a predictor of atherosclerotic stenotic disease of the lower extremity arteries. One hundred three patients who had CT angiography performed for the evaluation of peripheral vascular disease were enrolled in this retrospective study. The volume (mm{sup 3}) of the AAC was measured on CT. Each lower extremity was divided into 8 segments. The extent of stenosis of the lower extremity artery was manifested as the sum of the stenosis scores for 16 segments (total stenosis score: TSS). The significant stenosis scores (SSS-50 and SSS-75) were defined as the sum of scores for the lower extremity artery segments that had significant stenosis of more than 50% and 75%, respectively. AAC was correlated to the TSS, SSS-50 and SSS-75 with using Spearman's correlation coefficient. The diagnostic performance of AAC for stenosis of a lower extremity artery of more than 50% and 75%, respectively, was evaluated by using the receiver operating characteristic (ROC) curve. The Spearman's correlation coefficients were 0.728 (AAC vs. TSS), 0.662 (AAC vs. SSS-50), and 0.602 (AAC vs. SSS-75), respectively. For significant stenosis more than 50% and 75%, the areas under the ROC curve were 0.898 and 0.866, respectively. The cutoff value, sensitivity, specificity, positive predictive value, negative predictive value and accuracy were 1030 mm{sup 3}, 87%, 88%, 89%. 86% and 87% for stenosis more than 50% and 1030 mm{sup 3}, 87%, 80%, 79%, 88% and 84% for stenosis more than 75%, respectively. Abdominal aortic calcification detected on CT may be a useful predictor of atherosclerotic stenotic disease of lower extremity arteries.

  18. Indoxyl Sulfate Enhance the Hypermethylation of Klotho and Promote the Process of Vascular Calcification in Chronic Kidney Disease

    Science.gov (United States)

    Chen, Jing; Zhang, Xiaoyan; Zhang, Han; Liu, Tongqiang; Zhang, Hui; Teng, Jie; Ji, Jun; Ding, Xiaoqiang

    2016-01-01

    Chronic kidney disease (CKD) is a state of Klotho deficiency. The Klotho expression may be suppressed due to DNA hypermethylation in cancer cells so we have investigated the effects and possible mechanisms by which Klotho expression is regulated in human aortic smooth muscle cells (HASMCs). The vascular Klotho hypermethylation in radial arteries of patients with end-stage renal disease was described. Cultured HASMCs and 5/6-nephrectomized Sprague Dawley (SD) rats treated with indoxyl sulfate (IS) were used as in vitro and in vivo models, respectively. IS increased CpG hypermethylation of the Klotho gene and decreased Klotho expression in HASMCs, and potentiated HASMCs calcification. The expression of DNA methyltransferase (DNMT) 1 and 3a in HASMCs treated with IS was significantly increased and specific inhibition of DNA methyltransferase 1 by 5-aza-2'-deoxycytidine(5Aza-2dc) caused demethylation of the Klotho gene and increased Klotho expression. In rats, injection of IS potentiated vascular calcification, increased CpG hypermethylation of the Klotho gene and decreased Klotho expression in the aortic medial layer and all of these changes could be reverted by 5Aza-2dc treatment. Transcriptional suppression of vascular Klotho gene expression by IS and epigenetic modification of Klotho by IS may be an important pathological mechanism of vascular calcification in CKD. PMID:27766038

  19. Extracellular Matrix Proteins, Alkaline Phosphatase and Pyrophosphate as Molecular Determinants of Bone, Tooth, Kidney and Vascular Calcification

    Science.gov (United States)

    McKee, Marc D.

    2008-09-01

    Progress in biomineralization research in recent years has identified, characterized and described functions for key noncollagenous extracellular matrix proteins regulating crystal growth in the skeleton and dentition. Some of these same proteins expressed in soft tissues undergoing pathologic calcification also inhibit ectopic crystal growth. In addition to extracellular matrix proteins regulating matrix mineralization, the enzyme tissue-nonspecific alkaline phosphatase—which is highly expressed by cells in mineralized tissues—cleaves pyrophosphate, an anionic small-molecule inhibitor of mineralization. Together with the required mineral ion availability necessary for crystal growth, these molecular determinants appear to function in limiting the spread of pathologic calcification seen in soft tissues such as blood vessels and kidneys. Osteopontin, in particular, is a potent calcification inhibitor that accumulates in mineralized tissues and in calcified deposits during vascular calcification and nephrolithiasis/urolithiasis. Additional research is required to establish the exact temporal sequence in which the molecular determinants of pathologic calcification appear relative to mineral crystal growth in different tissues, and to establish their relationship (if any) to the activation of osteogenic differentiation programs.

  20. No influence of OPG and its ligands, RANKL and TRAIL, on proliferation and regulation of the calcification process in primary human vascular smooth muscle cells

    DEFF Research Database (Denmark)

    Olesen, Malene; Skov, Vibe; Mechta, Mie;

    2012-01-01

    The aim of this study was to examine the effects of the OPG-RANKL-TRAIL system on proliferation, regulation of calcification-associated genes and calcification of human vascular smooth muscle cells (HVSMCs). Small interfering (si)RNA-mediated knockdown of OPG was followed by treatment of HVSMCs...... with recombinant RANKL or TRAIL. Regulation of a calcification-associated gene set was assayed by pathway analysis of microarray results. The lack of OPG in HVSMCs or treatment with RANKL or TRAIL did not affect proliferation of HVSMCs. In addition, OPG, RANKL or TRAIL did not modify the regulation...... of a calcification-associated gene set. Finally, in the long term calcification assay, we found that cells isolated from seven different human donors showed a great variability in the response to RANKL and insulin. However, overall RANKL and/or insulin did not affect the development of calcification of HVSMCs...

  1. The relationship between neutrophil-to-lymphocyte ratio and vascular calcification in end-stage renal disease patients.

    Science.gov (United States)

    Turkmen, Kultigin; Ozcicek, Fatih; Ozcicek, Adalet; Akbas, Emin Murat; Erdur, Fatih Mehmet; Tonbul, Halil Zeki

    2014-01-01

    Chronic inflammation was found to be correlated with coronary (CAC) and thoracic peri-aortic calcification (TAC) in end-stage renal disease (ESRD) patients. Neutrophil-to-lymphocyte ratio (NLR) was introduced as a potential marker to determine inflammation in cardiac and noncardiac disorders. Data regarding NLR and its association with TAC and CAC are lacking. We aimed to determine the relationship between NLR and vascular calcification in ESRD patients. This was a cross-sectional study involving 56 ESRD patients (22 females, 34 males; mean age, 49.9 ± 14.2 years) receiving peritoneal dialysis or hemodialysis for ≥6 months in the Dialysis Unit of Necmettin Erbakan University. TAC and CAC scores were measured by using an electrocardiogram-gated 64-multidetector computed tomography. NLR was calculated as the ratio of the neutrophils and lymphocytes. There was a statistically significant correlation between NLR, TACS and CACS in ESRD patients (r = 0.43, P = 0.001 and r = 0.30, P = 0.02, respectively). The stepwise linear regression analysis revealed that age, as well as NLR were independent predictors of TACS. However, increased age was the only independent predictor of CACS according to linear regression analysis. Simple calculation of NLR can predict vascular calcification in ESRD patients.

  2. Associations between oxidized LDL to LDL ratio, HDL and vascular calcification in the feet of hemodialysis patients.

    Science.gov (United States)

    An, Won Suk; Kim, Seong-Eun; Kim, Ki-Hyun; Bae, Hae-Rahn; Rha, Seo-Hee

    2009-01-01

    Cardiovascular mortality is associated with vascular calcification (VC) in hemodialysis (HD) patients. The present study was designed to find factors related with medial artery calcification on the plain radiography of feet by comparing C-reactive protein (CRP), plasminogen activator inhibitor type 1 (PAI-1) and lipid profile including oxidized low density lipoprotein (ox-LDL) and to elucidate associations among these factors in HD patients. Forty-eight HD patients were recruited for this study. VC in the feet was detected in 18 patients (37.5%) among total patients and 12 patients (85.7%) among diabetic patients. Diabetes, cardiovascular disease (CVD), pulse pressure, ox-LDL/LDL were higher and high density lipoprotein (HDL) was lower in patients with VC than in patients without VC. Negative associations were found between HDL and CRP, PAI-1. PAI-1 had positive association with ox-LDL/LDL. History of CVD was the only determinant of vascular calcification on the plain radiography of feet. Ox-LDL/LDL, HDL, CRP, and PAI-1 were closely related with one another in HD patients. History of CVD is the most important factor associated with the presence of VC and low HDL and relatively high oxidized LDL/LDL ratio may affect VC formation on the plain radiography in the feet of HD patients.

  3. Genistein Attenuates Vascular Endothelial Impairment in Ovariectomized Hyperhomocysteinemic Rats

    Directory of Open Access Journals (Sweden)

    Panpan Zhen

    2012-01-01

    Full Text Available Hyperhomocysteinemia (HHcy is a well-known independent risk factor for vascular diseases in the general population. This study was to explore the effect of genistein (GST, a natural bioactive compound derived from legumes, on HHcy-induced vascular endothelial impairment in ovariectomized rats in vivo. Thirty-two adult female Wistar rats were assigned randomly into four groups (n=8: (a Con: control; (b Met: 2.5% methionine diet; (c OVX + Met: ovariectomy + 2.5% methionine diet; (d OVX + Met + GST: ovariectomy + 2.5% methionine diet + supplementation with genistein. After 12 wk of different treatment, the rats' blood, toracic aortas and liver samples were collected for analysis. Results showed that high-methionine diet induced both elevation of plasma Hcy and endothelial dysfunction, and ovariectomy deteriorated these injuries. Significant improvement of both functional and morphological changes of vascular endothelium was observed in OVX + Met + GST group; meanwhile the plasma Hcy levels decreased remarkably. There were significant elevations of plasma ET-1 and liver MDA levels in ovariectomized HHcy rats, and supplementation with genistein could attenuate these changes. These results implied that genistein could lower the elevated Hcy levels, and prevent the development of endothelial impairment in ovariectomized HHcy rats. This finding may shed a novel light on the anti-atherogenic activities of genistein in HHcy patients.

  4. Metformin inhibits vascular calcification in female rat aortic smooth muscle cells via the AMPK-eNOS-NO pathway.

    Science.gov (United States)

    Cao, Xiaorui; Li, Huan; Tao, Huiren; Wu, Ning; Yu, Lifeng; Zhang, Dawei; Lu, Xiaozhao; Zhu, Jinyu; Lu, Zifan; Zhu, Qingsheng

    2013-10-01

    Metformin exhibits diverse protective effects against diabetic complications, such as bone loss. Here, we investigated the effect of metformin on vascular calcification, another type 2 diabetes complication. In female rat aortic smooth muscle cells (RASMCs), we observed that metformin significantly alleviated β-glycerophosphate-induced Ca deposition and alkaline phosphatase activity, corresponding with reduced expression of some specific genes in osteoblast-like cells, including Runx2 and bone morphogenetic protein-2, and positive effects on α-actin expression, a specific marker of smooth muscle cells. Mechanistic analysis showed that phosphorylation levels of both AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) were increased with NO overproduction. After inhibition of either AMPK or eNOS with the pharmacologic inhibitors, compound C or Nω-Nitro-L-arginine methyl ester, NO production was lowered and metformin-meditated vascular protection against β-glycerophosphate-induced Ca deposition was removed. Our results support that metformin prevents vascular calcification via AMPK-eNOS-NO pathway.

  5. Atorvastatin Protects Vascular Smooth Muscle Cells From TGF-β1-Stimulated Calcification by Inducing Autophagy via Suppression of the β-Catenin Pathway

    Directory of Open Access Journals (Sweden)

    Demin Liu

    2014-01-01

    Full Text Available Background: Arterial calcification is a major event in the progression of atherosclerosis. It is reported that statins exhibit various protective effects against vascular smooth muscle cell (VSMC inflammation and proliferation in cardiovascular remodeling. Although statins counteract atherosclerosis, the molecular mechanisms of statins on the calcium release from VSMCs have not been clearly elucidated. Methods: Calcium content of VSMCs was measured using enzyme-linked immunosorbent assay (ELISA. The expression of proteins involved in cellular transdifferentiation was analyzed by western blot. Cell autophagy was measured by fluorescence microscopic analysis for acridine orange staining and transmission electron microscopy analysis. The autophagic inhibitors (3-MA, chloroquine, NH4Cl and bafilomycin A1 and β-catenin inhibitor JW74 were used to assess the effects of atorvastatin on autophagy and the involvement of β-catenin on cell calcification respectively. Furthermore, cell transfection was performed to overexpress β-catenin. Results: In VSMCs, atorvastatin significantly suppressed transforming growth factor-β1 (TGF-β1-stimulated calcification, accompanied by the induction of autophagy. Downregulation of autophagy with autophagic inhibitors significantly suppressed the inhibitory effect of atorvastatin on cell calcification. Moreover, the beneficial effect of atorvastatin on calcification and autophagy was reversed by β-catenin overexpression. Conversely, JW74 supplement enhanced this effect. Conclusion: These data demonstrated that atorvastatin protect VSMC from TGF-β1-stimulated calcification by inducing autophagy through suppression of the β-catenin pathway, identifying autophagy induction might be a therapeutic strategy for use in vascular calcification.

  6. Porphyromonas gingivalis-derived outer membrane vesicles promote calcification of vascular smooth muscle cells through ERK1/2-RUNX2.

    Science.gov (United States)

    Yang, Wen Wei; Guo, Bin; Jia, Wen Yuan; Jia, Yue

    2016-12-01

    The outer membrane vesicle (OMV) derived from Porphyromonas gingivalis plays an essential role in causing inflammation which, in turn, plays an important part in the pathogenesis of cardiovascular diseases such as atherosclerosis and thromboembolism. However, the contribution of oral bacteria to vascular calcification is yet to be determined. Here, we evaluated the effect of OMV on vascular smooth muscle cell (VSMC) calcification both in vitro and ex vivo. We established a reproducible P. gingivalis OMV-induced differentiation and calcification model of VSMCs in vitro. The results indicate that OMV promotes VSMC calcification in a concentration-dependent manner, modulating the expression of bone markers and SMC markers both on genes and proteins that are important for osteoblastic differentiation and mineralization of VSMCs. We also showed that the key osteogenic transcription factor, runt-related transcription factor 2 (Runx2), which is affected by upstream extracellular-regulated kinase (ERK) signaling, is a key regulator of OMV-induced VSMC differentiation and calcification. Taken together, our research demonstrates that Runx2 is a crucial component of OMV-induced calcification of VSMCs, and ERK signaling plays a vital role in mediating Runx2 up-regulation and VSMC calcification.

  7. [Vascular Calcification - Pathological Mechanism and Clinical Application - . Regulation of mineral metabolism and mineralization by FGF23].

    Science.gov (United States)

    Fukumoto, Seiji

    2015-05-01

    Fibroblast growth factor 23 (FGF23) decreases serum phosphate by inhibiting proximal tubular phosphate reabsorption and intestinal phosphate absorption through the reduction of serum 1,25-dihydroxyvitamin D [1,25 (OH) (2)D] levels. Excessive actions of FGF23 cause hypophosphatemic diseases with impaired mineralization of bone. On the other hand, impaired actions of FGF23 result in hyperphosphatemic familial tumoral calcinosis characterized by hyperphosphatemia and high 1,25 (OH) (2)D levels. Ectopic calcification around large joints and in blood vessels can be observed in patients with this disease. Therefore, FGF23 plays essential roles in the regulation of bone mineralization and prevention of ectopic calcification.

  8. Dietary magnesium, not calcium, prevents vascular calcification in a mouse model for pseudoxanthoma elasticum

    NARCIS (Netherlands)

    Gorgels, T.G.M.F.; Waarsing, J.H.; de Wolf, A.; ten Brink, J.B.; Loves, W.J.P.; Bergen, A.A.B.

    2010-01-01

    Pseudoxanthoma elasticum (PXE) is a heritable disorder characterized by ectopic calcification of connective tissue in skin, Bruch's membrane of the eye, and walls of blood vessels. PXE is caused by mutations in the ABCC6 gene, but the exact etiology is still unknown. While observations on patients s

  9. Dietary magnesium, not calcium, prevents vascular calcification in a mouse model for pseudoxanthoma elasticum

    NARCIS (Netherlands)

    T.G.M.F. Gorgels (Theo); J.H. Waarsing (Jan); A. de Wolf (Anneke); J.B. ten Brink (Jacoline); W.J.P. Loves (Willem); A.A.B. Bergen (Arthur)

    2010-01-01

    textabstractPseudoxanthoma elasticum (PXE) is a heritable disorder characterized by ectopic calcification of connective tissue in skin, Bruch's membrane of the eye, and walls of blood vessels. PXE is caused by mutations in the ABCC6 gene, but the exact etiology is still unknown. While observations o

  10. Vascular Calcification and Stone Disease: A New Look towards the Mechanism

    Directory of Open Access Journals (Sweden)

    Allen J. Yiu

    2015-06-01

    Full Text Available Calcium phosphate (CaP crystals are formed in pathological calcification as well as during stone formation. Although there are several theories as to how these crystals can develop through the combined interactions of biochemical and biophysical factors, the exact mechanism of such mineralization is largely unknown. Based on the published scientific literature, we found that common factors can link the initial stages of stone formation and calcification in anatomically distal tissues and organs. For example, changes to the spatiotemporal conditions of the fluid flow in tubular structures may provide initial condition(s for CaP crystal generation needed for stone formation. Additionally, recent evidence has provided a meaningful association between the active participation of proteins and transcription factors found in the bone forming (ossification mechanism that are also involved in the early stages of kidney stone formation and arterial calcification. Our review will focus on three topics of discussion (physiological influences—calcium and phosphate concentration—and similarities to ossification, or bone formation that may elucidate some commonality in the mechanisms of stone formation and calcification, and pave the way towards opening new avenues for further research.

  11. Menaquinone-7 Supplementation to Reduce Vascular Calcification in Patients with Coronary Artery Disease: Rationale and Study Protocol (VitaK-CAC Trial).

    Science.gov (United States)

    Vossen, Liv M; Schurgers, Leon J; van Varik, Bernard J; Kietselaer, Bas L J H; Vermeer, Cees; Meeder, Johannes G; Rahel, Braim M; van Cauteren, Yvonne J M; Hoffland, Ge A; Rennenberg, Roger J M W; Reesink, Koen D; de Leeuw, Peter W; Kroon, Abraham A

    2015-10-28

    Coronary artery calcification (CAC) develops early in the pathogenesis of atherosclerosis and is a strong and independent predictor of cardiovascular disease (CVD). Arterial calcification is caused by an imbalance in calcification regulatory mechanisms. An important inhibitor of calcification is vitamin K-dependent matrix Gla protein (MGP). Both preclinical and clinical studies have shown that inhibition of the vitamin K-cycle by vitamin K antagonists (VKA) results in elevated uncarboxylated MGP (ucMGP) and subsequently in extensive arterial calcification. This led us to hypothesize that vitamin K supplementation may slow down the progression of calcification. To test this, we designed the VitaK-CAC trial which analyses effects of menaquinone-7 (MK-7) supplementation on progression of CAC. The trial is a double-blind, randomized, placebo-controlled trial including patients with coronary artery disease (CAD). Patients with a baseline Agatston CAC-score between 50 and 400 will be randomized to an intervention-group (360 microgram MK-7) or a placebo group. Treatment duration will be 24 months. The primary endpoint is the difference in CAC-score progression between both groups. Secondary endpoints include changes in arterial structure and function, and associations with biomarkers. We hypothesize that treatment with MK-7 will slow down or arrest the progression of CAC and that this trial may lead to a treatment option for vascular calcification and subsequent CVD.

  12. Effects of Sucroferric Oxyhydroxide Compared to Lanthanum Carbonate and Sevelamer Carbonate on Phosphate Homeostasis and Vascular Calcifications in a Rat Model of Chronic Kidney Failure.

    Science.gov (United States)

    Phan, Olivier; Maillard, Marc; Malluche, Hartmut H; Stehle, Jean-Christophe; Funk, Felix; Burnier, Michel

    2015-01-01

    Elevated serum phosphorus, calcium, and fibroblast growth factor 23 (FGF23) levels are associated with cardiovascular disease in chronic renal disease. This study evaluated the effects of sucroferric oxyhydroxide (PA21), a new iron-based phosphate binder, versus lanthanum carbonate (La) and sevelamer carbonate (Se), on serum FGF23, phosphorus, calcium, and intact parathyroid hormone (iPTH) concentrations, and the development of vascular calcification in adenine-induced chronic renal failure (CRF) rats. After induction of CRF, renal function was significantly impaired in all groups: uremic rats developed severe hyperphosphatemia, and serum iPTH increased significantly. All uremic rats (except controls) then received phosphate binders for 4 weeks. Hyperphosphatemia and increased serum iPTH were controlled to a similar extent in all phosphate binder-treatment groups. Only sucroferric oxyhydroxide was associated with significantly decreased FGF23. Vascular calcifications of the thoracic aorta were decreased by all three phosphate binders. Calcifications were better prevented at the superior part of the thoracic and abdominal aorta in the PA21 treated rats. In adenine-induced CRF rats, sucroferric oxyhydroxide was as effective as La and Se in controlling hyperphosphatemia, secondary hyperparathyroidism, and vascular calcifications. The role of FGF23 in calcification remains to be confirmed.

  13. Dietary magnesium, not calcium, prevents vascular calcification in a mouse model for pseudoxanthoma elasticum

    OpenAIRE

    Gorgels, Theo; Waarsing, Jan; Wolf, Anneke; Brink, Jacoline; Loves, Willem; Bergen, Arthur

    2010-01-01

    textabstractPseudoxanthoma elasticum (PXE) is a heritable disorder characterized by ectopic calcification of connective tissue in skin, Bruch's membrane of the eye, and walls of blood vessels. PXE is caused by mutations in the ABCC6 gene, but the exact etiology is still unknown. While observations on patients suggest that high calcium intake worsens the clinical symptoms, the patient organization PXE International has published the dietary advice to increase calcium intake in combination with...

  14. The effect of magnesium supplementation on vascular calcification in chronic kidney disease-a randomised clinical trial (MAGiCAL-CKD)

    DEFF Research Database (Denmark)

    Bressendorff, Iain; Hansen, Ditte; Schou, Morten

    2017-01-01

    INTRODUCTION: Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular disease and mortality, which is thought to be caused by increased propensity towards vascular calcification (VC). Magnesium (Mg) inhibits phosphate-induced VC in vitro and in animal models and serum ...

  15. Phosphocalcic Markers and Calcification Propensity for Assessment of Interstitial Fibrosis and Vascular Lesions in Kidney Allograft Recipients

    Science.gov (United States)

    Berchtold, Lena; Ponte, Belen; Moll, Solange; Hadaya, Karine; Seyde, Olivia; Bachtler, Matthias; Vallée, Jean-Paul; Martin, Pierre-Yves; Pasch, Andreas; de Seigneux, Sophie

    2016-01-01

    Renal interstitial fibrosis and arterial lesions predict loss of function in chronic kidney disease. Noninvasive estimation of interstitial fibrosis and vascular lesions is currently not available. The aim of the study was to determine whether phosphocalcic markers are associated with, and can predict, renal chronic histological changes. We included 129 kidney allograft recipients with an available transplant biopsy in a retrospective study. We analyzed the associations and predictive values of phosphocalcic markers and serum calcification propensity (T50) for chronic histological changes (interstitial fibrosis and vascular lesions). PTH, T50 and vitamin D levels were independently associated to interstitial fibrosis. PTH elevation was associated with increasing interstitial fibrosis severity (r = 0.29, p = 0.001), while T50 and vitamin D were protective (r = -0.20, p = 0.025 and r = -0.23, p = 0.009 respectively). On the contrary, fibroblast growth factor 23 (FGF23) and Klotho correlated only modestly with interstitial fibrosis (p = 0.045) whereas calcium and phosphate did not. PTH, vitamin D and T50 were predictors of extensive fibrosis (AUC: 0.73, 0.72 and 0.68 respectively), but did not add to renal function prediction. PTH, FGF23 and T50 were modestly predictive of low fibrosis (AUC: 0.63, 0.63 and 0.61) but did not add to renal function prediction. T50 decreased with increasing arterial lesions (r = -0.21, p = 0.038). The discriminative performance of T50 in predicting significant vascular lesions was modest (AUC 0.61). In summary, we demonstrated that PTH, vitamin D and T50 are associated to interstitial fibrosis and vascular lesions in kidney allograft recipients independently of renal function. Despite these associations, mineral metabolism indices do not show superiority or additive value to fibrosis prediction by eGFR and proteinuria in kidney allograft recipients, except for vascular lesions where T50 could be of relevance. PMID:28036331

  16. Relationship between cardio-ankle vascular index (CAVI) and coronary artery calcification (CAC) in patients with type 2 diabetes mellitus.

    Science.gov (United States)

    Mineoka, Yusuke; Fukui, Michiaki; Tanaka, Muhei; Tomiyasu, Ki-ichiro; Akabame, Satoshi; Nakano, Koji; Yamazaki, Masahiro; Hasegawa, Goji; Oda, Yohei; Nakamura, Naoto

    2012-03-01

    Early detection of atherosclerosis is important for patients with type 2 diabetes mellitus because cardiovascular disease (CVD) is a main cause of death in these people. In this study, we investigated the relationship between an arterial stiffness parameter called cardio-ankle vascular index (CAVI) and coronary artery calcification (CAC). We performed a cross-sectional study in 371 type 2 diabetic patients with clinical suspicion of coronary heart disease (CHD). We evaluated the relationships between CAVI and CAC score determined by multislice computed tomography as well as major cardiovascular risk factors, including age, body mass index, hemoglobinA1c and the Framingham CHD risk score. CAVI was correlated with age (r = 0.301, p CAC + 1) (r = 0.303, p CAC >0, CAC >100, CAC >400, or CAC >1000. CAVI is positively correlated with CAC, and is considered to be a useful method to detect CAC.

  17. Phosphate-induced rat vascular smooth muscle cell calcification and the implication of zinc deficiency in a7r5 cell viability.

    Science.gov (United States)

    Shin, Mee-Young; Kwun, In-Sook

    2013-06-01

    The calcification of vascular smooth muscle cells (VSMCs) is considered one of the major contributors for vascular disease. Phosphate is known as the inducer for VSMC calcification. In this study, we assessed whether phosphate affected cell viability and fetuin-A, a calcification inhibitor protein, both which are related to VSMC calcification. Also, VSMC viability by zinc level was assessed. The results showed that phosphate increased Ca and P deposition in VSMCs (A7r5 cell line, rat aorta origin). This phosphate-induced Ca and P deposition was consistent with the decreased A7r5 cell viability (Pviability. As phosphate increased, the protein expression of fetuin-A protein was up-regulated. A7r5 cell viability decreased as the addition of cellular zinc level was decreased (Pviability and it would be the future study to clarify how zinc does act for VSMC cell viability. The results suggest that the decreased VSMC viability by high P or low Zn in VSMCs may be the risk factor for vascular disease.

  18. The combination of lanthanum chloride and the calcimimetic calindol delays the progression of vascular smooth muscle cells calcification

    Energy Technology Data Exchange (ETDEWEB)

    Ciceri, Paola; Volpi, Elisa; Brenna, Irene; Elli, Francesca [Renal Division and Laboratory of Experimental Nephrology, Dipartimento di Medicina e Chirurgia, Universita di Milano, Milan (Italy); Borghi, Elisa [Dipartimento di Salute Pubblica, Microbiologia e Virologia, Universita di Milano, Milan (Italy); Brancaccio, Diego [Renal Division and Laboratory of Experimental Nephrology, Dipartimento di Medicina e Chirurgia, Universita di Milano, Milan (Italy); Cozzolino, Mario, E-mail: mario.cozzolino@unimi.it [Renal Division and Laboratory of Experimental Nephrology, Dipartimento di Medicina e Chirurgia, Universita di Milano, Milan (Italy)

    2012-02-24

    Highlights: Black-Right-Pointing-Pointer Lanthanum reduces the progression of high phosphate-induced calcium deposition. Black-Right-Pointing-Pointer Calcium receptor agonists and the calcimimetic calindol reduce calcium deposition. Black-Right-Pointing-Pointer Lanthanum and calindol cooperate on reducing calcium deposition. Black-Right-Pointing-Pointer Lanthanum and calindol may interact with the same receptor. -- Abstract: Phosphate (Pi)-binders are commonly used in dialysis patients to control high Pi levels, that associated with vascular calcification (VC). The aim of this study was to investigate the effects of lanthanum chloride (LaCl{sub 3}) on the progression of high Pi-induced VC, in rat vascular smooth muscle cells (VSMCs). Pi-induced Ca deposition was inhibited by LaCl{sub 3}, with a maximal effect at 100 {mu}M (59.0 {+-} 2.5% inhibition). Furthermore, we studied the effects on VC of calcium sensing receptor (CaSR) agonists. Gadolinium chloride, neomycin, spermine, and the calcimimetic calindol significantly inhibited Pi-induced VC (55.9 {+-} 2.2%, 37.3 {+-} 4.7%, 30.2 {+-} 5.7%, and 63.8 {+-} 5.7%, respectively). To investigate the hypothesis that LaCl{sub 3} reduces the progression of VC by interacting with the CaSR, we performed a concentration-response curve of LaCl{sub 3} in presence of a sub-effective concentration of calindol (10 nM). Interestingly, this curve was shifted to the left (IC{sub 50} 9.6 {+-} 2.6 {mu}M), compared to the curve in the presence of LaCl{sub 3} alone (IC{sub 50} 19.0 {+-} 4.8 {mu}M). In conclusion, we demonstrated that lanthanum chloride effectively reduces the progression of high phosphate-induced vascular calcification. In addition, LaCl{sub 3} cooperates with the calcimimetic calindol in decreasing Ca deposition in this in vitro model. These results suggest the potential role of lanthanum in the treatment of VC induced by high Pi.

  19. The angiotensin II type 1 receptor blocker losartan attenuates bioprosthetic valve leaflet calcification in a rabbit intravascular implant model.

    Science.gov (United States)

    Shin, Hong Ju; Kim, Dae-Hyun; Park, Han Ki; Park, Young Hwan

    2016-12-01

    There is evidence that angiotensin II type I receptor blocker (ARB) could reduce structural valve deterioration. However, the anticalcification effect on the bioprosthetic heart valve (BHV) has not been investigated. Thus, we investigated the effects of losartan (an ARB) on calcification of implanted bovine pericardial tissue in a rabbit intravascular implant model. A total of 16 male New Zealand White rabbits (20 weeks old, 2.98-3.34 kg) were used in this study. Commercially available BHV leaflet of bovine pericardium was trimmed to the shape of a 3-mm triangle and implanted to both external jugular veins of the rabbit. The ARB group (n = 8) was given 25 mg/kg of powdered losartan daily until 6 weeks after surgery by direct administration in the buccal pouch of the animals. The control group (n = 8) was given 5 ml of normal saline by the same method. After 6 weeks, quantitative calcium determination, histological evaluation and western blot analysis of interleukin-6 (IL-6), osteopontin and bone morphogenetic protein 2 (BMP-2) were performed to investigate the mechanisms of the anticalcification effect of losartan. No deaths or complications such as infection or haematoma were recorded during the experiment. All animals were euthanized on the planned date. The calcium measurement level in the ARB group (2.28 ± 0.65 mg/g) was significantly lower than that in the control group (3.68 ± 1.00 mg/g) (P = 0.0092). Immunohistochemistry analyses revealed that BMP-2-positive reactions were significantly attenuated in the ARB group. Western blot analysis showed that losartan suppressed the expression of IL-6, osteopontin and BMP-2. Our results indicate that losartan significantly attenuates postimplant degenerative calcification of a bovine pericardial bioprosthesis in a rabbit intravascular implant model. Further studies are required to assess the effects of ARBs on BHV tissue in orthotopic implantations using a large animal model. © The Author 2016. Published by Oxford

  20. Ablation of adenosine monophosphate-activated protein kinaseα1 in vascular smooth muscle cells promotes diet-induced atherosclerotic calcification in vivo

    Institute of Scientific and Technical Information of China (English)

    CAI Zhe-jun; DING Ye; ZHANG Miao; LU Qiu-lun; WU Sheng-nan; ZHU Huai-ping; SONG Ping; ZOU Ming-hui

    2016-01-01

    AIM:Atherosclerotic calcification is highly linked with plaque instability and cardiovascular events .Adenosine monophosphate-activated protein kinase ( AMPK) has been involved in the pathogenesis of various cardiovascular disease .The contributions of AMPKαsubunits to the development of atherosclerotic calcification in vivo remained unknown .We hypothesized that AMPKαsubunits may play a role in the development of atherosclerotic calcification .METHODS: Atherosclerotic calcification was generated by 24-week fed of western diet in ApoE-/-background mice .Calcification was evaluated in aortic roots and innominate arteries of ApoE-/-mice or in mice with dual deficiencies of ApoE and AMPKαsubunits globally ( AMPKα1 and AMPKα2 ) , or vascular smooth muscle cell ( VSMC)-specific or macrophage-specific knockout of AMPKα1 with atherosclerotic calcification pone diet . The mechanism of AMPKα1 in regulating Runx2 was further explored in human aortic VSMC .RESULTS: Ablation of AMPKα1 but not AMPKα2 in ApoE-/-background promoted atherosclerotic calcification with increased Runt -related transcription factor ( Runx2 ) expression in VSMC compared with ApoE-/-mice.Conversely, chronic administration of metformin, which activated AMPK, markedly reduced ath-erosclerotic calcification and Runx2 expression in ApoE-/-mice but had less effects in ApoE-/-/AMPKα1 -/-mice.Furthermore, VSMC-but not macrophage-specific deficiency of AMPKα1 in ApoE-/-background promoted atherosclerotic calcification in vivo com-pared with the controls .AMPKα1 silencing in human aortic VSMC prevented Runx 2 from proteasome degradation to trigger osteoblastic differentiation of VSMC .Conversely , activation of AMPK led to Runx 2 instability by inducing its small ubiquitin-like modifier modifi-cation (SUMOylation).Protein inhibitor of activated STAT-1 (PIAS1), the SUMO E3-ligase of Runx2, was directly phosphorylated by AMPKα1 at serine 510, to enhance its SUMO E3-ligase activity.Ablation of PIAS1

  1. The Wnt5a/Ror2 pathway is associated with determination of the differentiation fate of bone marrow mesenchymal stem cells in vascular calcification.

    Science.gov (United States)

    Xin, Huaping; Xin, Fang; Zhou, Shaoqiong; Guan, Siming

    2013-03-01

    Accumulating evidence have demonstrated that mesenchymal stem cells (MSCs) are involved in the initiation and progression of various vascular diseases. Canonical Wnt signaling controls the fate of MSCs, and plays an important role in vascular calcification. However, vascular calcification can be inhibited by the non-canonical Wnt signaling pathway Wnt5a/Ror2. This study aimed to investigate whether the Wnt5a/Ror2 pathway is associated with determination of the differentiation fate of MSCs in vascular calcification. Direct co-cultures were established by seeding smooth muscle cells (SMCs) or calcified SMCs and MSCs together at ratios of SMCs or calcified SMCs 15x104; SMCs or calcified SMCs 5x104: MSCs 10x104, SMCs or calcified SMCs 10x104: MSCs 5x104. Osteosynthesis-inducing medium (OS) was added to the culture medium in the groups of MSCs with non-calcified SMCs. Cells were cultured for nine days. Osteoblastic differentiation was evaluated by cell morphology and the activity of alkaline phosphatase (ALP) in cell lysates and ALP staining. Furthermore, we investigated the inhibition of Wnt signaling, and observed that the members of the non-canonical signaling pathway Wnt5a/Ror2 were expressed in each group. Additionally, MSCs cultured in culture media with OS did not differentiate into an osteoblast phenotype when in direct contact with non-calcified SMCs, irrespective of the number of MSCs. However, an osteoblast phenotype was observed when MSCs were cultured in media without OS differentiation towards direct contact with calcified SMCs, and the levels of osteoblastic markers had a direct correlation with the number of MSCs. Of note, the Wnt5a protein was associated with the levels of calcification, thus, although rarely detected in non-calcification, Ror2 mRNA in the non-calcified groups was significantly higher compared to that in the calcified groups. Therefore, the Wnt5a/Ror2 pathway is associated with determination of the differentiation fate of bone marrow

  2. Dietary vitamin D inadequacy accelerates calcification and osteoblast-like cell formation in the vascular system of LDL receptor knockout and wild-type mice.

    Science.gov (United States)

    Schmidt, Nadine; Brandsch, Corinna; Schutkowski, Alexandra; Hirche, Frank; Stangl, Gabriele I

    2014-05-01

    Vitamin D insufficiency is highly associated with cardiovascular morbidity and mortality. We have demonstrated enhanced vascular calcification in LDL receptor knockout (LDLR(-/-)) mice fed a diet low in vitamin D. This study aimed to investigate the impact of a diet low in vitamin D on vascular calcification in wild-type (WT) mice lacking atherosclerotic plaques and the effects of a persistent and discontinuous vitamin D insufficiency on atherosclerotic plaque composition in LDLR(-/-) mice. The study was performed with 4-wk-old male WT and LDLR(-/-) mice that were fed a normal calcium/phosphate Western diet (210 g/kg fat, 1.5 g/kg cholesterol) containing either adequate (+D; 1000 IU/kg) or low (-D; 50 IU/kg) amounts of vitamin D-3 for 16 wk. Four groups of LDLR(-/-) mice received 1 of the 2 diets for additional 16 wk (total 32 wk) and were compared with mice fed the diets for only 16 wk. WT and LDLR(-/-) mice that were fed the -D diet for 16 wk tended to develop more calcified spots in the aortic valve than mice fed the +D diet (+50% and +56%, respectively; P < 0.10). In LDLR(-/-) mice, the extent of calcification increased from week 16 to week 32 and was higher in the -D than in the +D group (P < 0.05). The calcification, owing to the -D diet, was accompanied by highly expressed osteoblast differentiation factors, indicating a transdifferentiation of vascular cells to osteoblast-like cells. Feeding the +D diet subsequent to the -D diet reduced the vascular calcification (P < 0.05). LDLR(-/-) mice fed the -D diet for 32 wk had higher plaque lipid depositions (+48%, P < 0.05) and a higher expression of cluster of differentiation 68 (+31%, P < 0.05) and tumor necrosis factor α (+134%, P < 0.001) than the +D group. Collectively, the findings imply low vitamin D status as a causal factor for vascular calcification and atherosclerosis.

  3. Relationship between arterial vascular calcifications seen on screening mammograms and biochemical markers of endothelial injury

    Energy Technology Data Exchange (ETDEWEB)

    Pidal, Diego [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain)], E-mail: dpidal@hotmail.com; Sanchez Vidal, M Teresa [Servicio de Medicina Interna, Hospital de Jove (Spain)], E-mail: medicinainterna@hospitaldejove.com; Rodriguez, Juan Carlos [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain); Servicio de Cirugia General, Hospital de Jove (Spain); Instituto Universitario de Oncologia del Principado de Asturias, Oviedo (Spain)], E-mail: investigacion@hospitaldejove.com; Corte, M Daniela [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain); Instituto Universitario de Oncologia del Principado de Asturias, Oviedo (Spain)], E-mail: mdanielac@hotmail.com; Pravia, Paz [Servicio de Radiodiagnostico, Hospital de Jove (Spain)], E-mail: radiologia@hospitaldejove.com; Guinea, Oscar [Servicio de Radiodiagnostico, Hospital de Jove (Spain)], E-mail: oscarfguinea@seram.org; Pidal, Ivan [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain)], E-mail: ivanpida@hotmail.com; Bongera, Miguel [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain)], E-mail: mbchoppy@hotmail.com; Escribano, Damaso [Servicio de Medicina Interna, Hospital de Jove (Spain)], E-mail: medicinainterna@hospitaldejove.com; Gonzalez, Luis O. [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain)], E-mail: lovidiog@telefonica.net; Diez, M Cruz [Servicio de Cirugia General, Hospital de Jove (Spain)], E-mail: cirugiageneral@hospitaldejove.com; Venta, Rafael [Servicio de Analisis Clinicos, Hospital de San Agustin, Aviles (Spain); Departamento de Bioquimica y Biologia Molecular, Universidad de Oviedo (Spain)], E-mail: rafael.venta@sespa.princast.es; Vizoso, Francisco J. [Unidad de Investigacion del, Hospital de Jove, Gijon (Spain); Servicio de Cirugia General, Hospital de Jove (Spain); Instituto Universitario de Oncologia del Principado de Asturias, Oviedo (Spain)], E-mail: fjvizoso@telefonica.net

    2009-01-15

    To assess whether breast arterial calcifications (BAC) are associated with altered serum markers of cardiovascular risk, mammograms and records from 1759 women (age range: 45-65 years) screened for breast cancer were revised. One hundred and forty seven (8.36%) women showed BAC. A total of 136 women with BAC and controls (mean age: 57 and 55 years, respectively) accepted entering the study. There were no significant differences in serum levels of urea, glucose, uric acid, creatinine, total cholesterol, HDL-C, LDL-C, folic acid, vitamin B{sub 12}, TSH or cysteine, between both groups of patients. However, women with BAC showed higher serum levels of triglycerides (p = 0.006), homocysteine (p = 0.002) and hs-CRP (p = 0.003) than women without BAC. Likewise, we found a significantly higher percentage of cases with an elevated LDL-C/HDL-C ratio (coronary risk index >2) amongst women with BAC than in women without BAC (56.7 and 38.2%, respectively; p = 0.04). Our results indicate that the finding of BAC identify women showing altered serum markers of cardiovascular risk.

  4. Relationship between arterial vascular calcifications seen on screening mammograms and biochemical markers of endothelial injury.

    Science.gov (United States)

    Pidal, Diego; Sánchez Vidal, M Teresa; Rodríguez, Juan Carlos; Corte, M Daniela; Pravia, Paz; Guinea, Oscar; Pidal, Iván; Bongera, Miguel; Escribano, Dámaso; González, Luis O; Díez, M Cruz; Venta, Rafael; Vizoso, Francisco J

    2009-01-01

    To assess whether breast arterial calcifications (BAC) are associated with altered serum markers of cardiovascular risk, mammograms and records from 1759 women (age range: 45-65 years) screened for breast cancer were revised. One hundred and forty seven (8.36%) women showed BAC. A total of 136 women with BAC and controls (mean age: 57 and 55 years, respectively) accepted entering the study. There were no significant differences in serum levels of urea, glucose, uric acid, creatinine, total cholesterol, HDL-C, LDL-C, folic acid, vitamin B(12), TSH or cysteine, between both groups of patients. However, women with BAC showed higher serum levels of triglycerides (p=0.006), homocysteine (p=0.002) and hs-CRP (p=0.003) than women without BAC. Likewise, we found a significantly higher percentage of cases with an elevated LDL-C/HDL-C ratio (coronary risk index >2) amongst women with BAC than in women without BAC (56.7 and 38.2%, respectively; p=0.04). Our results indicate that the finding of BAC identify women showing altered serum markers of cardiovascular risk.

  5. Erythropoietin Attenuates Pulmonary Vascular Remodeling in Experimental Pulmonary Arterial Hypertension through Interplay between Endothelial Progenitor Cells and Heme Oxygenase

    NARCIS (Netherlands)

    van Loon, Rosa Laura E; Bartelds, Beatrijs; Wagener, Frank A D T G; Affara, Nada; Mohaupt, Saffloer; Wijnberg, Hans; Pennings, Sebastiaan W C; Takens, Janny; Berger, Rolf M F

    2015-01-01

    BACKGROUND: Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease with a high mortality, characterized by typical angio-proliferative lesions. Erythropoietin (EPO) attenuates pulmonary vascular remodeling in PAH. We postulated that EPO acts through mobilization of endothelial progeni

  6. Inhibition of Receptor Activator of NF-κB Ligand by Denosumab Attenuates Vascular Calcium Deposition in Mice

    Science.gov (United States)

    Helas, Susann; Goettsch, Claudia; Schoppet, Michael; Zeitz, Ute; Hempel, Ute; Morawietz, Henning; Kostenuik, Paul J.; Erben, Reinhold G.; Hofbauer, Lorenz C.

    2009-01-01

    Osteoporosis and vascular calcification frequently coincide. A potential mediator of bone metabolism and vascular homeostasis is the triad cytokine system, which consists of receptor activator of nuclear factor-κB (RANK) ligand (RANKL), its receptor RANK, and the decoy receptor osteoprotegerin. Unopposed RANKL activity in osteoprotegerin-deficient mice resulted in osteoporosis and vascular calcification. We therefore analyzed the effects of RANKL inhibition by denosumab, a human monoclonal antibody against RANKL, on vascular calcium deposition following glucocorticoid exposure. Prednisolone pellets were implanted into human RANKL knock-in (huRANKL-KI) mice, which unlike wild-type mice are responsive to denosumab. No histomorphological abnormalities or differences in aortic wall thickness were detected between wild-type and huRANKL-KI mice, regardless of treatment with prednisolone, denosumab, or both. However, concurrent treatment with denosumab reduced aortic calcium deposition of prednisolone-treated huRANKL-KI mice by up to 50%, based on calcium measurement. Of note, aortic calcium deposition in huRANKL-KI mice was correlated negatively with bone mineral density at the lumbar spine (P = 0.04) and positively with urinary excretion of deoxypyridinoline, a marker of bone resorption (P = 0.01). In summary, RANKL inhibition by denosumab reduced vascular calcium deposition in glucocorticoid-induced osteoporosis in mice, which is further evidence for the link between the bone and vascular systems. Therefore, the prevention of bone loss by denosumab might also be associated with reduced vascular calcification in certain conditions. PMID:19590040

  7. Inhibition of receptor activator of NF-kappaB ligand by denosumab attenuates vascular calcium deposition in mice.

    Science.gov (United States)

    Helas, Susann; Goettsch, Claudia; Schoppet, Michael; Zeitz, Ute; Hempel, Ute; Morawietz, Henning; Kostenuik, Paul J; Erben, Reinhold G; Hofbauer, Lorenz C

    2009-08-01

    Osteoporosis and vascular calcification frequently coincide. A potential mediator of bone metabolism and vascular homeostasis is the triad cytokine system, which consists of receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL), its receptor RANK, and the decoy receptor osteoprotegerin. Unopposed RANKL activity in osteoprotegerin-deficient mice resulted in osteoporosis and vascular calcification. We therefore analyzed the effects of RANKL inhibition by denosumab, a human monoclonal antibody against RANKL, on vascular calcium deposition following glucocorticoid exposure. Prednisolone pellets were implanted into human RANKL knock-in (huRANKL-KI) mice, which unlike wild-type mice are responsive to denosumab. No histomorphological abnormalities or differences in aortic wall thickness were detected between wild-type and huRANKL-KI mice, regardless of treatment with prednisolone, denosumab, or both. However, concurrent treatment with denosumab reduced aortic calcium deposition of prednisolone-treated huRANKL-KI mice by up to 50%, based on calcium measurement. Of note, aortic calcium deposition in huRANKL-KI mice was correlated negatively with bone mineral density at the lumbar spine (P = 0.04) and positively with urinary excretion of deoxypyridinoline, a marker of bone resorption (P = 0.01). In summary, RANKL inhibition by denosumab reduced vascular calcium deposition in glucocorticoid-induced osteoporosis in mice, which is further evidence for the link between the bone and vascular systems. Therefore, the prevention of bone loss by denosumab might also be associated with reduced vascular calcification in certain conditions.

  8. Correlation between Circulating Levels of Pro-Inflammatory Cytokines TNF-alpha and Vascular Calcification Inhibitor Matrix Gla Protein in Obese Men

    Directory of Open Access Journals (Sweden)

    Trilis Yulianti

    2010-12-01

    Full Text Available BACKGROUND: Adult obesity is rapidly increasing in the world including Indonesia. Tumor necrosis factor α (TNF-α was chronically elevated in obese adipose tissue. TNF-α, a pleiotropic cytokine and also a regulator of bone formation, may might represent an important link between obesity and vascular calcification. Elegant genetic studies in mice and human have highlighted the important roles for Matrix Gla Protein (MGP as an inhibitor of vascular calcification. The aim of this study was to examine the correlation between circulating levels of pro-inflammatory cytokines TNF-α and vascular calcification inhibitor MGP in obese men. METHODS: This was an observational cross-sectional study including 40 central obese men (waist circumference ≥90 cm aged 31-60 years old. Serum MGP and serum TNF-α concentrations were quantified by ELISA principle. Fasting plasma glucose was assessed using hexokinase methods, triglyceride by GPO-PAP methods, and creatinine by Jaffe methods. All assays were performed according to the manufacture instruction. Statistical analysis was performed with SPSS for windows ver 16. Univariate analysis were performed to analyze mean, maximum, minimum value and SD. Pearson correlation statistic were performed to determine the correlation between variables. Significance value were define as alpha level=0.05 based on two-tailed tests. RESULTS: The cross-sectional study (n=40 showed that the advancing age was correlated with plasma TNF-α concentration (r = 0.348; p = 0.028. The mean concentration of TNF-α and MGP were 8.323 and 8.368, respectively. We found a significant negative correlation between TNF-α with MGP (r=-0.425; p=0.006 and a significant correlation between TNF-α and triglyceride (r=0.375; p=0.017. CONCLUSIONS: Circulating level of TNF-α was inversely correlated with MGP concentration in obese men. This finding suggested that high level TNF-α leads to low MGP concentration obese men, hence, limits inhibitory

  9. Relationship of vascular calcification and cardiovascular disease in maintenance hemodialysis patients%维持性血液透析患者血管钙化情况及其与心血管疾病的关系

    Institute of Scientific and Technical Information of China (English)

    王英; 贾艳丽; 刘惠兰

    2009-01-01

    目的 调查维持性血液透析(MHD)患者血管钙化的发生情况.方法应用X线摄片方法调查MHD患者胸主动脉及四肢血管发生的钙化情况,初步分析血管钙化与心血管疾病的关系.结果 69例患者中38例有至少一处血管钙化,占55%(38/69).23例有四肢血管钙化的患者中,大部分(14/23)为内膜、中膜钙化同时存在.有血管钙化患者与无血管钙化患者相比,年龄更大,既往有缺血性心脏病的患者更多(P<0.05).随访1年,有16例患者在此期间发生心衰.有血管钙化患者发生心衰的人数明显多于无血管钙化患者(P<0.01).结论血管钙化可能与MHD患者心血管疾病有关.%Objective To observe the occurrence of vascular calcification in maintenance hemedialysis (MHD) patients. Method Sixty-nine MHD patients were enrolled in this study. Vascular calcification was evaluated by plain X-my films of chest, upper and lower extremites. Analyzed the relationship of vascular calcification and cardiovascular disease. Results Vascular calcification on X-ray films presented in 38 cases (55%). Of the 23 cases with calcification on arteries of extremites, 14 cases were found to have both intimal calcification and medial calcification. Patients with vascular calcification were older. Ischemic heart disease and cardiac failure appeared more frequently in the patients with vascular calcification. Conclusions Both intimal calcification and medial calcification are frequently found in the MHD patients. Vascular calcification is probablly associated with cardiovascular disease in MHD patients.

  10. Restoration of bone mineralization by cinacalcet is associated with a significant reduction in calcitriol-induced vascular calcification in uremic rats.

    Science.gov (United States)

    De Schutter, Tineke M; Behets, Geert J; Jung, Susanne; Neven, Ellen; D'Haese, Patrick C; Querfeld, Uwe

    2012-11-01

    The present study investigated to what extent normalization of bone turnover goes along with a reduction of high-dose calcitriol-induced vascular calcifications in uremic rats. Five groups of male Sprague-Dawley rats were studied: sham-operated controls (n = 7), subtotally nephrectomized (SNX) uremic (CRF) animals (n = 12), CRF + calcitriol (vitD) (0.25 μg/kg/day) (n = 12), CRF + vitD + cinacalcet (CIN) (10 mg/kg/day) (n = 12), and CRF + vitD + parathyroidectomy (PTX) (n = 12). Treatment started 2 weeks after SNX and continued for the next 14 weeks. High-dose calcitriol treatment in hyperparathyroid rats went along with the development of distinct vascular calcification, which was significantly reduced by >50 %, in both CIN-treated and PTX animals. Compared to control animals and those of the CRF group, calcitriol treatment either in combination with CIN or PTX or not was associated with a significant increase in bone area comprising ±50 % of the total tissue area. However, whereas excessive woven bone accompanied by a dramatically increased osteoid width/area was seen in the CRF + vitD group, CIN treatment and PTX resulted in significantly reduced serum PTH level, which was accompanied by a distinct reduction of both the bone formation rate and the amount of osteoid. These data indicate that less efficient calcium and phosphorus incorporation in bone inherent to the severe hyperparathyroidism in vitamin D-treated uremic rats goes along with excessive vascular calcification, a process which is partially reversed by CIN treatment in combination with a more efficacious bone mineralization, thus restricting the availability of calcium and phosphate for being deposited in the vessel wall.

  11. Inhibition of Phosphate-Induced Vascular Smooth Muscle Cell Osteo-/Chondrogenic Signaling and Calcification by Bafilomycin A1 and Methylamine

    Directory of Open Access Journals (Sweden)

    Ioana Alesutan

    2015-09-01

    Full Text Available Background/Aims: Excessive phosphate concentrations trigger vascular calcification, an active process promoted by osteoinduction of vascular smooth muscle cells (VSMCs with increased expression and activity of transcription factor RUNX2 (Core-binding factor α1, CBFA1, alkaline phosphatase (ALPL, TGFß1, transcription factor NFAT5, and NFAT5-sensitive transcription factor SOX9. The osteoinductive signaling and vascular calcification of hyperphosphatemic klotho-hypomorphic mice could be reversed by treatment with NH4Cl, effects involving decrease of TGFß1 and inhibition of NFAT5-dependent osteoinductive signaling. Known effects of NH4Cl include alkalinization of acidic cellular compartments. The present study explored whether osteo-/chondrogenic signaling could be influenced by alkalinization of acidic cellular compartments following inhibition of the vacuolar H+ ATPase with bafilomycin A1 or following dissipation of the pH gradient across the membranes of acidic cellular compartments with methylamine. Methods: Primary human aortic smooth muscle cells (HAoSMCs were treated with high phosphate to trigger osteo-/chondrogenic signaling and calcification in the absence or presence of bafilomycin A1 or methylamine. Calcium content was determined using a QuantiChrom Calcium assay, ALP activity by a colorimetric assay and transcript levels by quantitative RT-PCR. Results: High phosphate increased significantly the calcium deposition, CBFA1 and ALPL mRNA expression as well as alkaline phosphatase activity in HAoSMCs, all effects ameliorated by both, bafilomycin A1 and methylamine. High phosphate further significantly up-regulated the mRNA levels of TGFB1, NFAT5 and SOX9, effects significantly blunted by additional treatment with bafilomycin A1 or methylamine. Treatment of HAoSMCs with human TGFß1 protein or high phosphate up-regulated NFAT5, SOX9, CBFA1 and ALPL mRNA expression to similarly high levels which could not be further increased by combined

  12. Adventitial gene transfer of catalase attenuates angiotensin II-induced vascular remodeling.

    Science.gov (United States)

    Liu, Cun-Fei; Zhang, Jia; Shen, Kai; Gao, Ping-Jin; Wang, Hai-Ya; Jin, Xin; Meng, Chao; Fang, Ning-Yuan

    2015-04-01

    Vascular adventitia and adventitia‑derived reactive oxygen species (ROS) contribute to vascular remodeling following vascular injury. A previous ex vivo study in adventitial fibroblasts showed that catalase, one of most important anti‑oxide enzymes, was downregulated by angiotensin II (AngII). The aim of the present study was to investigate whether adventitial gene transfer of catalase affects AngII‑induced vascular remodeling in vivo. Adenoviruses co‑expressing catalase and enhanced green fluorescent protein (eGFP) or expressing eGFP only were applied to the adventitial surface of common carotid arteries of Sprague‑Dawley rats. Alzet minipumps administering AngII (0.75 mg/kg/day) were then implanted subcutaneously for 14 days. Systolic blood pressure and biological parameters of vascular remodeling were measured in each group. Adventitial fibroblasts were cultured and p38 mitogen‑activated protein kinase (MAPK) phosphorylation was measured using western blot analysis. The results showed that adventitial gene transfer of catalase had no effect on AngII‑induced systolic blood pressure elevation. However, catalase adenovirus transfection significantly inhibited AngII‑induced media hypertrophy compared with that of the control virus (Pcatalase transfection significantly attenuated AngII‑induced ROS generation, macrophage infiltration, collagen deposition and adventitial α‑smooth muscle actin expression. Furthermore, catalase transfection significantly inhibited the AngII‑induced increase in p38MAPK phosphorylation. In conclusion, the results of the present study demonstrated that adventitial gene transfer of catalase significantly attenuated AngII‑induced vascular remodeling in rats via inhibition of adventitial p38MAPK phosphorylation.

  13. Fenofibrate attenuates nicotine-induced vascular endothelial dysfunction in the rat.

    Science.gov (United States)

    Chakkarwar, Vishal Arvind

    2011-01-01

    The study has been designed to investigate the effect of fenofibrate on nicotine-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg/kg/day, i.p., 4 weeks) was administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy of thoracic aorta. The expression of mRNA for p22phox and eNOS was assessed by using reverse transcriptase-polymerase chain reaction. Serum thiobarbituric acid reactive substances concentration (TBARS) and aortic superoxide anion concentration were estimated to assess oxidative stress. Moreover, the serum lipid profile was assessed by estimating serum cholesterol, triglycerides and high density lipoprotein. The administration of nicotine induces VED by increased oxidative stress, altered lipid profile and impaired the integrity of vascular endothelium as assessed in terms of decrease in expression of mRNA for endothelial nitric oxide synthase (eNOS), impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine produced oxidative stress, assessed in terms of increase in serum TBARS and aortic superoxide anion generation and increase in expression of mRNA for p22phox. Nicotine altered the lipid profile by increasing the serum cholesterol, triglycerides and decreasing the high density lipoprotein. However, treatment with fenofibrate (32 mg/kg, p.o.) markedly prevented nicotine-induced VED by decreasing oxidative stress and improving integrity of vascular endothelium, normalising the altered lipid profile, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic

  14. Recombinant Bcl-xL attenuates vascular hyperpermeability in a rat model of hemorrhagic shock

    Science.gov (United States)

    Tharakan, B; McNeal, SI; Hunter, FA; Sawant, DA; Smythe, WR; Childs, EW

    2015-01-01

    Following hemorrhagic shock (HS), vascular hyperpermeability, that is, the leakage of fluid, nutrients and proteins into the extravascular space occurs primarily due to the disruption of the endothelial cell–cell adherens junctional complex. Studies from our laboratory demonstrate that activation of the mitochondria-mediated ‘intrinsic’ apoptotic signaling cascade has a significant role in modulating HS-induced hyperpermeability. Here we report the novel use of recombinant Bcl-xL, an anti-apoptotic protein, to control HS-induced vascular hyperpermeability. Our results corroborate involvement of vascular hyperpermeability and apoptotic signaling. HS (the mean arterial pressure (MAP) was reduced to 40 mm Hg for 60 min followed by resuscitation to 90 mm Hg for 60 min) in rats resulted in vascular hyperpermeability as determined by intravital microscopy. Treatment of Bcl-xL (2.5 µg/ml of rat blood in non-lipid cationic polymer, i.v.) before, during and even after HS attenuated or reversed HS-induced vascular hyperpermeability significantly (P<0.05). Conversely, treatment using Bcl-xL inhibitors, 2-methoxy antimycin (2-OMeAA) and ABT 737, significantly increased vascular hyperpermeability compared with sham (P<0.05). Bcl-xL treatment also decreased the amount of fluid volume required to maintain a MAP of 90 mm Hg during resuscitation (P<0.05). HS resulted in an increased mitochondrial reactive oxygen species formation, reduction of ΔΨm, mitochondrial release of cytochrome c and significant activation of caspase-3 (P<0.05). All of these effects were significantly inhibited by Bcl-xL pre-treatment (P<0.05). Our results show that recombinant Bcl-xL is effective against HS-induced vascular hyperpermeability that appears to be mediated through the preservation of ΔΨm and subsequent prevention of caspase-3 activation. PMID:27042339

  15. Effects of the Use of Non-Calcium Phosphate Binders in the Control and Outcome of Vascular Calcifications: A Review of Clinical Trials on CKD Patients

    Directory of Open Access Journals (Sweden)

    Piergiorgio Bolasco

    2011-01-01

    Full Text Available Vascular calcifications produce a high impact on morbidity and mortality rates in patients affected by chronic kidney disease and mineral bone disorder (CKD-MBD. Effects are manifested from the more advanced stages of CKD (stages 3-4, particularly in patients undergoing dialysis (CKD5D. In recent years, a large number of therapeutic options have been successfully used in the treatment of secondary hyperparathyroidism (SHPT, despite eliciting less marked effects on nonbone calcifications associated with CKD-MBD. In addition to the use of Vitamin D and analogues, more recently treatment with calcimimetic drugs has also been undertaken. The present paper aims to analyze comparative and efficacy studies undertaken to assess particularly the impact on morbidity and mortality rates of non-calcium phosphate binders. Moreover, the mechanism of action underlying the depositing of calcium and phosphate along blood vessel walls, irrespective of the specific contribution provided in reducing the typical phosphate levels observed in CKD largely at more advanced stages of the disease, will be investigated. The aim of this paper therefore is to evaluate which phosphate binders are characterised by the above action and the mechanisms through which these are manifested.

  16. Testosterone replacement attenuates intimal hyperplasia development in an androgen deficient model of vascular injury.

    Science.gov (United States)

    Freeman, Brian M; Univers, Junior; Fisher, Richard K; Kirkpatrick, Stacy S; Klein, Frederick A; Freeman, Michael B; Mountain, Deidra J H; Grandas, Oscar H

    2017-01-01

    not correlate with any change in proliferative markers. F:G actin staining revealed that DHT-induced cytoskeletal organization in a dose-dependent manner. AD increased IH development in response to vascular injury, whereas physiological TST replacement attenuated this effect. AD-induced IH occurs independent of matrix remodeling mechanisms known to be heavily involved in vascular dysfunction, and AD alone does not affect the UTS and/or UTSR mechanism. Exogenous TST and/or DHT increases UTSR pathway signaling in vitro and in vivo. This modulation correlates to a shift in cytoskeletal organization and may exacerbate vasoconstrictive pathogenesis. While physiological TST replacement attenuates AD-modulated IH development, its UTS-mediated effect on vasotone may prove deleterious to overall vascular function. Copyright © 2016 Elsevier Inc. All rights reserved.

  17. Research Progress of MicroRNAs in Vascular Calcification Mechanisms in Chronic Kidney Disease%微RNA与慢性肾脏病血管钙化机制的研究进展

    Institute of Scientific and Technical Information of China (English)

    邢莹(综述); 郝丽荣(审校)

    2016-01-01

    慢性肾脏病( CKD)及终末期肾脏疾病患者有较高的心血管疾病发病率,主要原因是血管钙化。与骨形成有很多相似之处,血管钙化是一个主动的可调节进程。最近关于血管钙化的研究发现,微RNA( miRNA)与启动和促进 CKD患者血管钙化的机制有关。 miRNA 在调节细胞表型、钙磷平衡及基质小囊泡中起重要作用,并影响CKD患者的血管钙化。这种 miRNA 在血管钙化方面的重要作用对未来CKD和终末期肾脏疾病患者血管钙化进行生物标记及治疗方法的探索有重要意义。%Patients with chronic kidney disease( CKD) and end stage renal disease have significant car-diovascular morbidity and mortality due to vascular calcification.Vascular calcification is an active,highly regulated process that has many similarities with bone formation .Recent discoveries revealed that microRNA ( miRNA) is involved in the initiation and progression of vascular calcification in CKD .miRNA regulates vas-cular calcification through controlling cell phenotype ,calcium and phosphorous homeostasis and matrix vesi-cles.The important role of miRNA in vascular calcification is of great significance for the development of bio-markers and therapeutic options for patients with CKD and end stage renal disease .

  18. Hepatocellular calcification

    DEFF Research Database (Denmark)

    Ladefoged, Claus; Frifelt, J J

    1987-01-01

    Autopsy of a twenty year old girl dying from complications of renal and cardiac failure demonstrated severe hepatocellular calcification, a rare finding. The pathogenesis is thought to be a combination of dystrophic calcification caused by severe centrilobular necrosis and metastatic calcification...

  19. Benfotiamine attenuates nicotine and uric acid-induced vascular endothelial dysfunction in the rat.

    Science.gov (United States)

    Balakumar, Pitchai; Sharma, Ramica; Singh, Manjeet

    2008-01-01

    The study has been designed to investigate the effect of benfotiamine, a thiamine derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg(-1)day(-1), i.p., 4 weeks) and uric acid (150 mg kg(-1)day(-1), i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg(-1)day(-1), p.o.) or atorvastatin (30 mg kg(-1)day(-1) p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.

  20. Vascular Effects of Advanced Glycation End-Products: Content of Immunohistochemically Detected AGEs in Radial Artery Samples as a Predictor for Arterial Calcification and Cardiovascular Risk in Asymptomatic Patients with Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Katarzyna Janda

    2015-01-01

    Full Text Available Objectives. Our aim was to determine whether vascular deposition of advanced glycation end-products (AGEs is associated with arterial calcification and cardiovascular mortality in chronic kidney disease (CKD patients and to assess the relationships between vascular content of AGEs and selected clinical and biochemical parameters. Materials and Methods. The study comprised 54 CKD patients (33 hemodialyzed, 21 predialyzed. Examined parameters included BMI, incidence of diabetes, plasma fasting glucose, AGEs, soluble receptor for AGEs and 2,2-diphenyl-1-picrylhydrazyl (DPPH scavenging, serum C-reactive protein (hsCRP, plasminogen activator inhibitor-1 (PAI-1, and fetuin-A. Fragments of radial artery obtained during creation of hemodialysis access were stained for calcifications using alizarin red. AGEs deposits were identified immunohistochemically and their relative content was quantified. Results. Vascular content of AGEs was positively correlated with BMI, hsCRP, fetuin-A, PAI-1, and DPPH scavenging in simple regression; only fetuin-A was an independent predictor in multiple regression. There was a significant positive trend in the intensity of AGEs immunostaining among patients with grades 1, 2, and 3 calcifications. AGEs immunostaining intensity predicted 3-year cardiovascular mortality irrespective of patient’s age. Conclusions. The present study demonstrates an involvement of AGEs in the development of medial arterial calcification and the impact of arterial AGE deposition on cardiovascular mortality in CKD patients.

  1. Eccentric-exercise induced inflammation attenuates the vascular responses to mental stress.

    Science.gov (United States)

    Paine, Nicola J; Ring, Christopher; Aldred, Sarah; Bosch, Jos A; Wadley, Alex J; Veldhuijzen van Zanten, Jet J C S

    2013-05-01

    Mental stress has been identified as a trigger of myocardial infarction (MI), with inflammation and vascular responses to mental stress independently implicated as contributing factors. This study examined whether inflammation moderates the vascular responses to mental stress. Eighteen healthy male participants completed a stress task under two counter balanced conditions. In the exercise condition, a morning bout of eccentric exercise (12×5 repetitions of unilateral eccentric knee extension at 120% intensity of concentric one repetition maximum) was used to increase levels of inflammatory-responsive cytokines during an afternoon stress session scheduled 6h later. In the control condition, participants sat and relaxed for 45min, 6h prior to the afternoon stress session. Forearm blood flow, calf blood flow (measured in the leg which completed the exercise task), blood pressure, heart rate and cardiac output were assessed at rest and in response to mental stress. As expected, interleukin-6 was higher (p=.02) 6h post exercise, i.e., at the start of the stress session, as compared to the no-exercise control condition. Mental stress increased forearm blood flow, calf blood flow, blood pressure, heart rate, and cardiac output in both conditions (p'sexercise condition compared to the control condition (peccentric exercise attenuated the vascular responses to mental stress locally at the site of eccentric exercise-induced inflammation. The observed impairment in vascular responses to stress associated with increased levels of inflammation suggests a mechanism through which inflammation might increase the risk for MI. Copyright © 2010 Elsevier Inc. All rights reserved.

  2. Selective V1a agonism attenuates vascular dysfunction and fluid accumulation in ovine severe sepsis

    Science.gov (United States)

    Yamamoto, Yusuke; Sousse, Linda; Bartha, Eva; Jonkam, Collette; Hasselbach, Anthony K.; Traber, Lillian D.; Cox, Robert A.; Westphal, Martin; Enkhbaatar, Perenlei; Traber, Daniel L.

    2012-01-01

    Vasopressin analogs are used as a supplement to norepinephrine in septic shock. The isolated effects of vasopressin agonists on sepsis-induced vascular dysfunction, however, remain controversial. Because V2-receptor stimulation induces vasodilation and procoagulant effects, a higher V1a- versus V2-receptor selectivity might be advantageous. We therefore hypothesized that a sole, titrated infusion of the selective V1a-agonist Phe2-Orn8-Vasotocin (POV) is more effective than the mixed V1a-/V2-agonist AVP for the treatment of vascular and cardiopulmonary dysfunction in methicillin resistant staphylococcus aureus pneumonia-induced, ovine sepsis. After the onset of hemodynamic instability, awake, chronically instrumented, mechanically ventilated, and fluid resuscitated sheep were randomly assigned to receive continuous infusions of either POV, AVP, or saline solution (control; each n = 6). AVP and POV were titrated to maintain mean arterial pressure above baseline − 10 mmHg. When compared with that of control animals, AVP and POV reduced neutrophil migration (myeloperoxidase activity, alveolar neutrophils) and plasma levels of nitric oxide, resulting in higher mean arterial pressures and a reduced vascular leakage (net fluid balance, chest and abdominal fluid, pulmonary bloodless wet-to-dry-weight ratio, alveolar and septal edema). Notably, POV stabilized hemodynamics at lower doses than AVP. In addition, POV, but not AVP, reduced myocardial and pulmonary tissue concentrations of 3-nitrotyrosine, VEGF, and angiopoietin-2, thereby leading to an abolishment of cumulative fluid accumulation (POV, 9 ± 15 ml/kg vs. AVP, 110 ± 13 ml/kg vs. control, 213 ± 16 ml/kg; P < 0.001 each) and an attenuated cardiopulmonary dysfunction (left ventricular stroke work index, PaO2-to-FiO2 ratio) versus control animals. Highly selective V1a-agonism appears to be superior to unselective vasopressin analogs for the treatment of sepsis-induced vascular dysfunction. PMID:22961865

  3. Selective V(1a) agonism attenuates vascular dysfunction and fluid accumulation in ovine severe sepsis.

    Science.gov (United States)

    Rehberg, Sebastian; Yamamoto, Yusuke; Sousse, Linda; Bartha, Eva; Jonkam, Collette; Hasselbach, Anthony K; Traber, Lillian D; Cox, Robert A; Westphal, Martin; Enkhbaatar, Perenlei; Traber, Daniel L

    2012-11-15

    Vasopressin analogs are used as a supplement to norepinephrine in septic shock. The isolated effects of vasopressin agonists on sepsis-induced vascular dysfunction, however, remain controversial. Because V(2)-receptor stimulation induces vasodilation and procoagulant effects, a higher V(1a)- versus V(2)-receptor selectivity might be advantageous. We therefore hypothesized that a sole, titrated infusion of the selective V(1a)-agonist Phe(2)-Orn(8)-Vasotocin (POV) is more effective than the mixed V(1a)-/V(2)-agonist AVP for the treatment of vascular and cardiopulmonary dysfunction in methicillin resistant staphylococcus aureus pneumonia-induced, ovine sepsis. After the onset of hemodynamic instability, awake, chronically instrumented, mechanically ventilated, and fluid resuscitated sheep were randomly assigned to receive continuous infusions of either POV, AVP, or saline solution (control; each n = 6). AVP and POV were titrated to maintain mean arterial pressure above baseline - 10 mmHg. When compared with that of control animals, AVP and POV reduced neutrophil migration (myeloperoxidase activity, alveolar neutrophils) and plasma levels of nitric oxide, resulting in higher mean arterial pressures and a reduced vascular leakage (net fluid balance, chest and abdominal fluid, pulmonary bloodless wet-to-dry-weight ratio, alveolar and septal edema). Notably, POV stabilized hemodynamics at lower doses than AVP. In addition, POV, but not AVP, reduced myocardial and pulmonary tissue concentrations of 3-nitrotyrosine, VEGF, and angiopoietin-2, thereby leading to an abolishment of cumulative fluid accumulation (POV, 9 ± 15 ml/kg vs. AVP, 110 ± 13 ml/kg vs. control, 213 ± 16 ml/kg; P < 0.001 each) and an attenuated cardiopulmonary dysfunction (left ventricular stroke work index, PaO(2)-to-FiO(2) ratio) versus control animals. Highly selective V(1a)-agonism appears to be superior to unselective vasopressin analogs for the treatment of sepsis-induced vascular dysfunction.

  4. Cardiac Calcification

    Directory of Open Access Journals (Sweden)

    Morteza Joorabian

    2011-05-01

    Full Text Available There is a spectrum of different types of cardiac"ncalcifications with the importance and significance"nof each type of cardiac calcification, especially"ncoronary artery calcification. Radiologic detection of"ncalcifications within the heart is quite common. The"namount of coronary artery calcification correlates"nwith the severity of coronary artery disease (CAD."nCalcification of the aortic or mitral valve may indicate"nhemodynamically significant valvular stenosis."nMyocardial calcification is a sign of prior infarction,"nwhile pericardial calcification is strongly associated"nwith constrictive pericarditis. A spectrum of different"ntypes of cardiac calcifications (linear, annular,"ncurvilinear,... could be seen in chest radiography and"nother imaging modalities. So a carful inspection for"ndetection and reorganization of these calcifications"nshould be necessary. Numerous modalities exist for"nidentifying coronary calcification, including plain"nradiography, fluoroscopy, intravascular ultrasound,"nMRI, echocardiography, and conventional, helical and"nelectron-beam CT (EBCT. Coronary calcifications"ndetected on EBCT or helical CT can be quantifie,"nand a total calcification score (Cardiac Calcification"nScoring may be calculated. In an asymptomatic"npopulation and/or patients with concomitant risk"nfactors like diabetes mellitus, determination of the"npresence of coronary calcifications identifies the"npatients at risk for future myocardial infarction and"ncoronary artery disease. In patients without coronary"ncalcifications, future cardiovascular events could"nbe excluded. Therefore, detecting and recognizing"ncalcification related to the heart on chest radiography"nand other imaging modalities such as fluoroscopy, CT"nand echocardiography may have important clinical"nimplications.

  5. Nitrate decreases xanthine oxidoreductase-mediated nitrite reductase activity and attenuates vascular and blood pressure responses to nitrite

    Directory of Open Access Journals (Sweden)

    Célio Damacena-Angelis

    2017-08-01

    Full Text Available Nitrite and nitrate restore deficient endogenous nitric oxide (NO production as they are converted back to NO, and therefore complement the classic enzymatic NO synthesis. Circulating nitrate and nitrite must cross membrane barriers to produce their effects and increased nitrate concentrations may attenuate the nitrite influx into cells, decreasing NO generation from nitrite. Moreover, xanthine oxidoreductase (XOR mediates NO formation from nitrite and nitrate. However, no study has examined whether nitrate attenuates XOR-mediated NO generation from nitrite. We hypothesized that nitrate attenuates the vascular and blood pressure responses to nitrite either by interfering with nitrite influx into vascular tissue, or by competing with nitrite for XOR, thus inhibiting XOR-mediated NO generation. We used two independent vascular function assays in rats (aortic ring preparations and isolated mesenteric arterial bed perfusion to examine the effects of sodium nitrate on the concentration-dependent responses to sodium nitrite. Both assays showed that nitrate attenuated the vascular responses to nitrite. Conversely, the aortic responses to the NO donor DETANONOate were not affected by sodium nitrate. Further confirming these results, we found that nitrate attenuated the acute blood pressure lowering effects of increasing doses of nitrite infused intravenously in freely moving rats. The possibility that nitrate could compete with nitrite and decrease nitrite influx into cells was tested by measuring the accumulation of nitrogen-15-labeled nitrite (15N-nitrite by aortic rings using ultra-performance liquid chromatography tandem mass-spectrometry (UPLC-MS/MS. Nitrate exerted no effect on aortic accumulation of 15N-nitrite. Next, we used chemiluminescence-based NO detection to examine whether nitrate attenuates XOR-mediated nitrite reductase activity. Nitrate significantly shifted the Michaelis Menten saturation curve to the right, with a 3-fold increase in

  6. Knockdown of connexin 43 attenuates balloon injury-induced vascular restenosis through the inhibition of the proliferation and migration of vascular smooth muscle cells.

    Science.gov (United States)

    Han, Xiao-Jian; He, Dan; Xu, Liang-Jing; Chen, Min; Wang, Yi-Qi; Feng, Jiu-Geng; Wei, Min-Jun; Hong, Tao; Jiang, Li-Ping

    2015-11-01

    Coronary artery disease (CAD) or atherosclerotic heart disease is one of the most common types of cardiovascular disease. Although percutaneous coronary intervention [PCI or percutaneous transluminal coronary angioplasty (PTCA)] is a mature, well-established technique used to treat atherosclerotic heart disease, its long‑term therapeutic effects are compromised by a high incidence of vascular restenosis (RS) following angioplasty. In our previous study, we found that the principal gap junction protein, connexin 43 (Cx43), in vascular smooth muscle cells (VSMCs) was involved in the development of vascular RS following angioplasty-induced balloon injury. However, the exact role action of Cx43 in vascular RS remains unclear. In the present study, we aimed to further examine whether the knockdown of Cx43 attenuates the development of vascular RS through the inhibition of the proliferation and migration of VSMCs. We found that the use of a lentiviral vector expressing shRNA targeting Cx43 (Cx43‑RNAi-LV) efficiently silenced the mRNA and protein expression of Cx43 in cultured VSMCs. In addition, MTT and Transwell assays were used to examined the proliferation and migration of the VSMCs, respectively. The results revealed that the knockdown of Cx43 by Cx43-RNAi-LV at a multiplicity of infection (MOI) of 100 significantly inhibited the proliferation and migration of the VSMCs in vitro. Notably, the knockdown of Cx43 also effectively attenuated the development of vascular RS and intimal hyperplasia following balloon injury in vivo. Taken together, our data suggest that Cx43 is involved in the development of vascular RS and intimal hyperplasia through the regulation of the proliferation and migration of VSMCs. Thus, the present study provides new insight into the pathogenesis of vascular RS, and suggests that further comfirms that Cx43 may well be a novel potential pharmacological target for preventing vascular RS following PCI.

  7. Antagonism of Stem Cell Factor/c-kit Signaling Attenuates Neonatal Chronic Hypoxia-Induced Pulmonary Vascular Remodeling

    Science.gov (United States)

    Young, Karen C; Torres, Eneida; Hehre, Dorothy; Wu, Shu; Suguihara, Cleide; Hare, Joshua M.

    2015-01-01

    Background Accumulating evidence suggests that c-kit positive cells are present in the remodeled pulmonary vasculature bed of patients with pulmonary hypertension (PH). Whether stem cell factor (SCF)/ c-kit regulated pathways potentiate pulmonary vascular remodeling is unknown. Here, we tested the hypothesis that attenuated c-kit signaling would decrease chronic hypoxia-induced pulmonary vascular remodeling by decreasing pulmonary vascular cell mitogenesis. Methods Neonatal FVB/NJ mice treated with non-immune IgG (PL), or c-kit neutralizing antibody (ACK2) as well as c-kit mutant mice (WBB6F1- Kit W− v/ +) and their congenic controls, were exposed to normoxia (FiO2=0.21) or hypoxia (FiO2=0.12) for two weeks. Following this exposure, right ventricular systolic pressure (RVSP), right ventricular hypertrophy (RVH), pulmonary vascular cell proliferation and remodeling were evaluated. Results As compared to chronically hypoxic controls, c-kit mutant mice had decreased RVSP, RVH, pulmonary vascular remodeling and proliferation. Consistent with these findings, administration of ACK2 to neonatal mice with chronic hypoxia-induced PH decreased RVSP, RVH, pulmonary vascular cell proliferation and remodeling. This attenuation in PH was accompanied by decreased extracellular signal-regulated protein kinase (ERK) 1/2 activation. Conclusion SCF/c-kit signaling may potentiate chronic hypoxia-induced vascular remodeling by modulating ERK activation. Inhibition of c-kit activity may be a potential strategy to alleviate PH. PMID:26705118

  8. Captopril attenuates hypertension and renal injury induced by the vascular endothelial growth factor inhibitor sorafenib

    Science.gov (United States)

    Nagasawa, Tasuku; Khan, Abdul Hye; Imig, John D

    2013-01-01

    SUMMARY Vascular endothelial growth factor inhibitors (VEGFi) are known to cause hypertension and renal injury that severely limits their use as an anticancer therapy. We hypothesized that the angiotensin-converting enzyme inhibitor captopril not only prevents hypertension, but also decreases renal injury caused by the VEGFi sorafenib.Rats were administered sorafenib (20 mg/kg per day) alone or in combination with captopril (40 mg/kg per day) for 4 weeks. Sorafenib administration increased blood pressure, which plateaued by day 10.Concurrent treatment with captopril for 4 weeks resulted in a 30 mmHg decrease in blood pressure compared with sorafenib alone (155 ± 5 vs 182 ± 6 mmHg, respectively; P captopril treatment reduced albuminuria by 50% compared with sorafenib alone (20 ± 8 vs 42 ± 9 mg/day, respectively; P captopril-treated rats administered sorafenib. Renal autoregulatory efficiency was determined by evaluating the afferent arteriolar constrictor response to ATP. Sorafenib administration attenuated the vasoconstriction to ATP, whereas concurrent captopril treatment improved ATP reactivity.In conclusion, captopril attenuated hypertension and renal injury and improved renal autoregulatory capacity in rats administered sorafenib. These findings indicate that captopril treatment, in addition to alleviating the detrimental side-effect of hypertension, decreases the renal injury associated with anticancer VEGFi therapies such as sorafenib. PMID:22443474

  9. Dimethylfumarate attenuates restenosis after acute vascular injury by cell-specific and Nrf2-dependent mechanisms

    Directory of Open Access Journals (Sweden)

    Chang Joo Oh

    2014-01-01

    Full Text Available Excessive proliferation of vascular smooth muscle cells (VSMCs and incomplete re-endothelialization is a major clinical problem limiting the long-term efficacy of percutaneous coronary angioplasty. We tested if dimethylfumarate (DMF, an anti-psoriasis drug, could inhibit abnormal vascular remodeling via NF−E2-related factor 2 (Nrf2-NAD(PH quinone oxidoreductase 1 (NQO1 activity. DMF significantly attenuated neointimal hyperplasia induced by balloon injury in rat carotid arteries via suppression of the G1 to S phase transition resulting from induction of p21 protein in VSMCs. Initially, DMF increased p21 protein stability through an enhancement in Nrf2 activity without an increase in p21 mRNA. Later on, DMF stimulated p21 mRNA expression through a process dependent on p53 activity. However, heme oxygenase-1 (HO-1 or NQO1 activity, well-known target genes induced by Nrf2, were dispensable for the DMF induction of p21 protein and the effect on the VSMC proliferation. Likewise, DMF protected endothelial cells from TNF-α-induced apoptosis and the dysfunction characterized by decreased eNOS expression. With knock-down of Nrf2 or NQO1, DMF failed to prevent TNF-α-induced cell apoptosis and decreased eNOS expression. Also, CD31 expression, an endothelial specific marker, was restored in vivo by DMF. In conclusion, DMF prevented abnormal proliferation in VSMCs by G1 cell cycle arrest via p21 upregulation driven by Nrf2 and p53 activity, and had a beneficial effect on TNF-α-induced apoptosis and dysfunction in endothelial cells through Nrf2–NQO1 activity suggesting that DMF might be a therapeutic drug for patients with vascular disease.

  10. [Arterial calcification and risk of cardiovascular events in diabetes mellitus].

    Science.gov (United States)

    Iwai, Kunimitu; Morimoto, Shigeto

    2010-11-01

    The cohort studies reported the subclinical vascular calcification including atheroslerosis starts during prediabetic state characterized by impaired fasting glucose. In the cardiovascular systems of diabetes mellitus there is an original mechanism to induce the medial calcification other than intimal calcification observed in the classical atherosclerosis. This is characterized as the ectipic osteogenesis induced by paracrine signals from inflammatory lesions in the adventitia. On the other hand, many internal systems have been discovered to inhibit vascular calcification.

  11. Application of plain radiography for diagnosis of vascular calcification in maintenance hemodialysis patients%X线平片在诊断血液透析患者血管钙化中的应用

    Institute of Scientific and Technical Information of China (English)

    甘良英; 王梅; 于小勇; 蔡美顺

    2009-01-01

    目的 评价X线平片检测维持性血液透析(MHD)患者动脉钙化的敏感性和特异性.方法 54例MHD患者行腹部-股骨上1/3多层螺旋CT(MSCT)平扫及侧位腹平片、骨盆片X线榆测.以腰椎(L)2~3间隙为界将腹主动脉分为上段、下段.MSCT结果据钙化严重程度分为0~5级.两位放射科医师分别盲法阅片诊断.以MSCT结果为金标准,X线平片结果作为诊断性指标,评价X线平片诊断腹主动脉和髂、股动脉钙化的敏感性和特异性.结果 MSCT结果显示,腹主动脉钙化发生率为86.1%,髂、股动脉钙化发生率为74.5%,二者差异有统计学意义(X2=5.695,P=0.017);腹主动脉2级以上钙化的发生率为60.2%,髂、股动脉为42.6%,腹主动脉钙化的严重程度显著高于髂、股动脉(X2=8.922,P=0.003).X线平片结果表明,腹主动脉钙化发生率为51.9%,髂、股动脉钙化发生率为18.5%.X线平片诊断腹主动脉和髂、股动脉钙化的特异性均为100%,敏感性随MSCT动脉钙化程度的加重而增高.据MSCT钙化评分的不同,其诊断腹主动脉和髂、股动脉钙化的敏感性分别如下:≥1级:60.2%和24.8%;≥2级:76.9%和43.5%;≥3级:100%和74.4%.结论 X线平片诊断中、重度动脉钙化敏感性高,诊断腹主动脉钙化的敏感度高于髂、股动脉,可用于MHD患者中、重度动脉钙化的检测.%Objective To evaluate the sensitivity and specificity of plain radiography in the diagnosis of vascular calcification in maintenance hemodialysis (MHD) patients. Methods Multi-slice computed tomography (MSCT) was used as the reference standard in the assessment of vascular calcification in MHD patients. A total of 54 MHD patients, 26 male and 28 female, mean age (60.4±13.3) years, underwent both MSCT and plain radiography of lateral abdomen and pelvis to evaluate abdominal aortic calcification, bilateral iliac and femoral artery calcification. Abdominal aorta was divided into upper and lower segment by L2-L3

  12. Vascular smooth muscle cell differentiation to an osteogenic phenotype involves matrix metalloproteinase-2 modulation by homocysteine.

    Science.gov (United States)

    Liu, Tingjiao; Lin, Jinghan; Ju, Ting; Chu, Lei; Zhang, Liming

    2015-08-01

    Arterial calcification is common in vascular diseases and involves conversion of vascular smooth muscle cells (VSMCs) to an osteoblast phenotype. Clinical studies suggest that the development of atherosclerosis can be promoted by homocysteine (HCY), but the mechanisms remain unclear. Here, we determined whether increases in HCY levels lead to an increase in VSMC calcification and differentiation, and examined the role of an extracellular matrix remodeler, matrix metalloproteinase-2 (MMP-2). Rat VSMCs were exposed to calcification medium in the absence or presence of HCY (10, 100 or 200 μmol/L) or an MMP-2 inhibitor (10(-6) or 10(-5) mol/L). MTT assays were performed to determine the cytotoxicity of the MMP-2 inhibitor in calcification medium containing 200 μmol/L HCY. Calcification was assessed by measurements of calcium deposition and alkaline phosphatase (ALP) activity as well as von Kossa staining. Expression of osteocalcin, bone morphogenetic protein (BMP)-2, and osteopontin, and MMP-2 was determined by immunoblotting. Calcification medium induced osteogenic differentiation of VSMCs. HCY promoted calcification, increased osteocalcin and BMP-2 expression, and decreased expression of osteopontin. MMP-2 expression was increased by HCY in a dose-dependent manner in VSMCs exposed to both control and calcification medium. The MMP-2 inhibitor decreased the calcium content and ALP activity, and attenuated the osteoblastic phenotype of VSMCs. Vascular calcification and osteogenic differentiation of VSMCs were positively regulated by HCY through increased/restored MMP-2 expression, increased expression of calcification proteins, and decreased anti-calcification protein levels. In summary, MMP-2 inhibition may be a protective strategy against VSMC calcification.

  13. Nicorandil attenuates monocrotaline-induced vascular endothelial damage and pulmonary arterial hypertension.

    Directory of Open Access Journals (Sweden)

    Makoto Sahara

    pathways in HUVECs, accompanied with the upregulation of both eNOS and Bcl-2 expression. CONCLUSIONS: Nicorandil attenuated MCT-induced vascular endothelial damage and PAH through production of eNOS and anti-apoptotic factors, suggesting that nicorandil might have a promising therapeutic potential for PAH.

  14. Magnolol inhibits migration of vascular smooth muscle cells via cytoskeletal remodeling pathway to attenuate neointima formation

    Energy Technology Data Exchange (ETDEWEB)

    Karki, Rajendra [Division of Pharmacology and Toxicology, School of Pharmacy, University of Missouri-Kansas City (United States); Department of Oriental Medicine Resources, Mokpo National University (Korea, Republic of); Kim, Seong-Bin [Jeollanamdo Development Institute for Korean Traditional Medicine, Jangheung gun, Jeollanamdo (Korea, Republic of); Kim, Dong-Wook, E-mail: dbkim@mokpo.ac.kr [Department of Oriental Medicine Resources, Mokpo National University (Korea, Republic of)

    2013-12-10

    Background: Increased proliferation and migration of vascular smooth muscle cells (VSMCs) contribute importantly to the formation of both atherosclerotic and restenotic lesions. The objective of this study was to investigate the effect of magnolol on VSMC migration. Methods: The proteolytic activity of matrix metalloproteinases (MMPs) in tumor necrosis factor alpha (TNF-α) stimulated VSMCs was performed by gelatin zymography. VSMC migration was assessed by wound healing and Boyden chamber methods. Collagen induced VSMC adhesion was determined by spectrofluorimeter and stress fibers formation was evaluated by fluorescence microscope. The expression of signaling molecules involved in stress fibers formation was determined by western blot. The phosphorylation of myosin light chain (MLC20) was determined by urea-glycerol polyacrylamide gel electrophoresis. Immunohistochemistry was performed to determine the expression of β1-integrin and collagen type I in the injured carotid arteries of rats on day 35 after vascular injury. Results: VSMC migration was strongly inhibited by magnolol without affecting MMPs expression. Also, magnolol inhibited β1-integrin expression, FAK phosphorylation and RhoA and Cdc42 activation to inhibit the collagen induced stress fibers formation. Moreover, magnolol inhibited the phosphorylation of MLC20. Our in vivo results showed that magnolol inhibited β1-integrin expression, collagen type I deposition and FAK phosphorylation in injured carotid arteries without affecting MMP-2 activity. Conclusions: Magnolol inhibited VSMC migration via inhibition of cytoskeletal remodeling pathway to attenuate neointima formation. General significance: This study provides a rationale for further evaluation of magnolol for the management of atherosclerosis and restenosis. - Highlights: • Magnolol strongly inhibited migration of VSMCs. • Magnolol inhibited stress fibers formation. • MLC20 phosphorylation was also inhibited by magnolol. • Anti

  15. Small interference RNA targeting vascular endothelial growth factor gene effectively attenuates retinal neovascularization in mice model

    Institute of Scientific and Technical Information of China (English)

    KONG Yi-chun; SUN Bei; ZHAO Kan-xing; HAN Mei; WANG Yu-chuan

    2013-01-01

    Background The mechanism of retinal neovascularization is not understood completely.Many growth factors are involved in the process of retinal neovascularization,such as vascular endothelial growth factor (VEGF) and pigment epithelium-deprived factor (PEDF),which are the representatives of angiogenic and antiangiogenic molecules respectively.Oxygen induced retinopathy (OIR) is a useful model to investigate retinal neovascularization.The present study was conducted to investigate the feasibility of small interference RNA (siRNA) targeting VEGF gene in attenuating oxygen induced retinopathy (OIR) by regulating VEGF to PEDF ratio (VEGF/PEDF).Methods In vitro,cultured EOMA cells were transfected with VEGF-siRNA (psi-HITM/EGFPNEGF siRNA) and LipofectamineTM 2000 for 24,48,and 72 hours,respectively.Expression of VEGF mRNA was evaluated by real time polymerase chain reaction (PCR) and the level of VEGF protein was analyzed by Western blotting.In vivo,OIR model mice were established,the mice (C57BL/6J) received an intra-vitreal injection of 1 μl of mixture of psi-HITM/EGFPNEGF siRNA and Lipofectamine 2000.Expressions of retinal VEGF and PEDF protein were measured by Western blotting,retinal neovascularization was observed by fluorescein angiography,and quantified.Results In vitro psi-HITM/EGFP/VEGF siRNA treatment significantly reduced VEGF mRNA and protein expression.In vivo,with decreased VEGF and VEGF-PEDF ratio,significant attenuation of neovascular tufts,avascular regions,tortuous,and dilated blood vessels were observed in the interfered animals.Conclusions VEGF plays an important role in OIR,and the transfection of VEGF-siRNA can effectively downregulate VEGF expression in vivo,accompanied by the downregulation of VEGF-PEDF ratio,and simultaneous attenuation of retinal neovascularization was also observed.These findings suggest that VEGF/PEDF may serve as a potential target in the treatment of retinal neovascularization and RNA interference targeting VEGF expression

  16. Panax notoginseng Saponins Attenuate Phenotype Switching of Vascular Smooth Muscle Cells Induced by Notch3 Silencing

    Science.gov (United States)

    Liu, Nan; Shan, Dazhi; Li, Ying; Chen, Hui; Gao, Yonghong; Huang, Yonghua

    2015-01-01

    Panax notoginseng saponins (PNS) could maintain vascular smooth muscle cells (VSMCs) in stable phenotypes so as to keep blood vessel elasticity as well as prevent failing in endovascular treatment with stent. Downregulation of Notch3 expression in VSMCs could influence the phenotype of VSMCs under pathologic status. However, whether PNS is able to attenuate the Notch3 silencing induced phenotype switching of VSMCs remains poorly understood. Primary human VSMCs were transfected with a plasmid containing a small interfering RNA (siRNA) against Notch3 and then exposed to different doses of PNS. The control groups included cells not receiving any treatment and cells transfected with a control siRNA. Phenotypic switching was evaluated by observing cell morphology with confocal microscopy, as well as examining α-SM-actin, SM22α, and OPN using Western blot. Downregulated Notch3 with a siRNA induced apparent phenotype switching, as reflected by morphologic changes, decreased expression of α-SM-actin and SM22α and increased expression of OPN. These changes were inhibited by PNS in a dose-dependent manner. The phenotype switching of VSMCs induced by Notch3 knockdown could be inhibited by PNS in a dose-dependent manner. Our study provided new evidence for searching effective drug for amending stability of atherosclerotic disease. PMID:26539217

  17. Panax notoginseng Saponins Attenuate Phenotype Switching of Vascular Smooth Muscle Cells Induced by Notch3 Silencing

    Directory of Open Access Journals (Sweden)

    Nan Liu

    2015-01-01

    Full Text Available Panax notoginseng saponins (PNS could maintain vascular smooth muscle cells (VSMCs in stable phenotypes so as to keep blood vessel elasticity as well as prevent failing in endovascular treatment with stent. Downregulation of Notch3 expression in VSMCs could influence the phenotype of VSMCs under pathologic status. However, whether PNS is able to attenuate the Notch3 silencing induced phenotype switching of VSMCs remains poorly understood. Primary human VSMCs were transfected with a plasmid containing a small interfering RNA (siRNA against Notch3 and then exposed to different doses of PNS. The control groups included cells not receiving any treatment and cells transfected with a control siRNA. Phenotypic switching was evaluated by observing cell morphology with confocal microscopy, as well as examining α-SM-actin, SM22α, and OPN using Western blot. Downregulated Notch3 with a siRNA induced apparent phenotype switching, as reflected by morphologic changes, decreased expression of α-SM-actin and SM22α and increased expression of OPN. These changes were inhibited by PNS in a dose-dependent manner. The phenotype switching of VSMCs induced by Notch3 knockdown could be inhibited by PNS in a dose-dependent manner. Our study provided new evidence for searching effective drug for amending stability of atherosclerotic disease.

  18. Garlic and Onion Attenuates Vascular Inflammation and Oxidative Stress in Fructose-Fed Rats

    Science.gov (United States)

    Vazquez-Prieto, Marcela Alejandra; Rodriguez Lanzi, Cecilia; Lembo, Carina; Galmarini, Claudio Rómulo; Miatello, Roberto Miguel

    2011-01-01

    This study evaluates the antioxidant and the anti-inflammatory properties of garlic (G) and onion (O) in fructose-fed rats (FFR). Thirty-day-old male Wistar rats were assigned to control (C), F (10% fructose in drinking water), F+T (tempol 1 mM as control antioxidant), F+G, and F+O. Aqueous G and O extracts were administered orally in doses of 150 and 400 mg/kg/d respectively, and along with tempol, were given during the last 8 weeks of a 14-week period. At the end of the study, FFR had developed insulin resistance, aortic NADPH oxidase activity, increased SBP, plasma TBARS and vascular cell adhesion molecule-1 (VCAM-1) expression in mesenteric arteries, and a decrease in heart endothelial nitric oxide synthase (eNOS). Garlic and onion administration to F rats reduced oxidative stress, increased eNOS activity, and also attenuated VCAM-1 expression. These results provide new evidence showing the anti-inflammatory and antioxidant effect of these vegetables. PMID:21876795

  19. Garlic and Onion Attenuates Vascular Inflammation and Oxidative Stress in Fructose-Fed Rats

    Directory of Open Access Journals (Sweden)

    Marcela Alejandra Vazquez-Prieto

    2011-01-01

    Full Text Available This study evaluates the antioxidant and the anti-inflammatory properties of garlic (G and onion (O in fructose-fed rats (FFR. Thirty-day-old male Wistar rats were assigned to control (C, F (10% fructose in drinking water, F+T (tempol 1 mM as control antioxidant, F+G, and F+O. Aqueous G and O extracts were administered orally in doses of 150 and 400 mg/kg/d respectively, and along with tempol, were given during the last 8 weeks of a 14-week period. At the end of the study, FFR had developed insulin resistance, aortic NADPH oxidase activity, increased SBP, plasma TBARS and vascular cell adhesion molecule-1 (VCAM-1 expression in mesenteric arteries, and a decrease in heart endothelial nitric oxide synthase (eNOS. Garlic and onion administration to F rats reduced oxidative stress, increased eNOS activity, and also attenuated VCAM-1 expression. These results provide new evidence showing the anti-inflammatory and antioxidant effect of these vegetables.

  20. Vitamin K intake and calcifications in breast arteries

    NARCIS (Netherlands)

    Maas, Angela H. E. M.; van der Schouw, Yvonne T.; Beijerinck, David; Deurenberg, Jan J. M.; Mali, Willem P. Th. M.; Grobbee, Diederick E.; van der Graaf, Yolanda

    2007-01-01

    Objectives: Vitamin K is an important co-factor in the production of proteins that inhibit vascular calcification. A low dietary Vitamin K intake has been associated with aortic and coronary calcifications and an elevated cardiovascular risk. Calcifications in the arteries of the breasts have also b

  1. Vitamin K intake and calcifications in breast arteries

    NARCIS (Netherlands)

    Maas, Angela H. E. M.; van der Schouw, Yvonne T.; Beijerinck, David; Deurenberg, Jan J. M.; Mali, Willem P. Th. M.; Grobbee, Diederick E.; van der Graaf, Yolanda

    2007-01-01

    Objectives: Vitamin K is an important co-factor in the production of proteins that inhibit vascular calcification. A low dietary Vitamin K intake has been associated with aortic and coronary calcifications and an elevated cardiovascular risk. Calcifications in the arteries of the breasts have also b

  2. Eccentric-exercise induced inflammation attenuates the vascular responses to mental stress

    NARCIS (Netherlands)

    Paine, N.J.; Ring, C.; Aldred, S.; Bosch, J.A.; Wadley, A.J.; Veldhuijzen van Zanten, J.J.C.S.

    2013-01-01

    Mental stress has been identified as a trigger of myocardial infarction (MI), with inflammation and vascular responses to mental stress independently implicated as contributing factors. This study examined whether inflammation moderates the vascular responses to mental stress. Eighteen healthy male

  3. Eccentric-exercise induced inflammation attenuates the vascular responses to mental stress

    NARCIS (Netherlands)

    Paine, N.J.; Ring, C.; Aldred, S.; Bosch, J.A.; Wadley, A.J.; Veldhuijzen van Zanten, J.J.C.S.

    2013-01-01

    Mental stress has been identified as a trigger of myocardial infarction (MI), with inflammation and vascular responses to mental stress independently implicated as contributing factors. This study examined whether inflammation moderates the vascular responses to mental stress. Eighteen healthy male

  4. Vaccine-induced inflammation attenuates the vascular responses to mental stress

    NARCIS (Netherlands)

    N.J. Paine; C. Ring; J.A. Bosch; M.T. Drayson; S. Aldred; J.J.C.S. Veldhuijzen van Zanten

    2014-01-01

    Inflammation is associated with poorer vascular function, with evidence to suggest that inflammation can also impair the vascular responses to mental stress. This study examined the effects of vaccine-induced inflammation on vascular responses to mental stress in healthy participants. Eighteen male

  5. Repeated sauna therapy attenuates ventricular remodeling after myocardial infarction in rats by increasing coronary vascularity of noninfarcted myocardium.

    Science.gov (United States)

    Sobajima, Mitsuo; Nozawa, Takashi; Shida, Takuya; Ohori, Takashi; Suzuki, Takayuki; Matsuki, Akira; Inoue, Hiroshi

    2011-08-01

    Repeated sauna therapy (ST) increases endothelial nitric oxide synthase (eNOS) activity and improves cardiac function in heart failure as well as peripheral blood flow in ischemic limbs. The present study investigates whether ST can increase coronary vascularity and thus attenuate cardiac remodeling after myocardial infarction (MI). We induced MI by ligating the left coronary artery of Wistar rats. The rats were placed in a far-infrared dry sauna at 41°C for 15 min and then at 34°C for 20 min once daily for 4 wk. Cardiac hemodynamic, histopathological, and gene analyses were performed. Despite the similar sizes of MI between the ST and non-ST groups (51.4 ± 0.3 vs. 51.1 ± 0.2%), ST reduced left ventricular (LV) end-diastolic (9.7 ± 0.4 vs. 10.7 ± 0.5 mm, P myocardial atrial natriuretic peptide mRNA levels. Vascular density was reduced in the noninfarcted myocardium of non-ST rats, and the density of cells positive for CD31 and for α-smooth muscle actin was decreased. These decreases were attenuated in ST rats compared with non-ST rats and associated with increases in myocardial eNOS and vascular endothelial growth factor mRNA levels. In conclusion, ST attenuates cardiac remodeling after MI, at least in part, through improving coronary vascularity in the noninfarcted myocardium. Repeated ST might serve as a novel noninvasive therapy for patients with MI.

  6. Erythropoietin attenuates pulmonary vascular remodeling in experimental pulmonary arterial hypertension through interplay between endothelial progenitor cells and heme-oxygenase

    Directory of Open Access Journals (Sweden)

    Rosa L.E. Loon

    2015-08-01

    Full Text Available BackgroundPulmonary arterial hypertension (PAH is a pulmonary vascular disease with a high mortality, characterized by typical angio-proliferative lesions. Erythropoietin (EPO attenuates pulmonary vascular remodeling in PAH. We postulated that EPO acts through mobilization of endothelial progenitor cells (EPCs and activation of the cytoprotective enzyme heme oxygenase-1 (HO1.MethodsRats with flow-associated PAH, resembling pediatric PAH, were treated with HO-1 inducer EPO in the presence or absence of the selective HO-activity-inhibitor tin-mesoporphyrin (SnMP. HO-activity, circulating EPCs and pulmonary vascular lesions were assessed after 3 weeks.ResultsIn PAH-rats, circulating EPCs were decreased and HO-activity was increased compared to control. EPO-treatment restored circulating EPCs and improved pulmonary vascular remodeling, as shown by a reduced wall thickness and occlusion rate of the intra-acinar vessels. Inhibition of HO-activity with SnMP aggravated PAH. Moreover, SnMP treatment abrogated EPO-induced amelioration of pulmonary vascular remodeling, while surprisingly further increasing circulating EPCs as compared with EPO alone.ConclusionsIn experimental PAH, EPO treatment restored the number of circulating EPC’s to control level, improved pulmonary vascular remodeling, and showed important interplay with HO-activity. Inhibition of increased HO-activity in PAH-rats exacerbated progression of pulmonary vascular remodeling, despite the presence of restored numbers of circulating EPC’s. We suggest that both EPO-induced HO1 and EPCs are promising targets to ameliorate the pulmonary vasculature in PAH.

  7. Cigarette Smoking-Induced Cardiac Hypertrophy, Vascular Inflammation and Injury are Attenuated by Antioxidant Supplementation in An Animal Model

    Directory of Open Access Journals (Sweden)

    Moustafa Al Hariri

    2016-11-01

    hypertrophy in cigarette smoke exposed animals.Conclusion Findings from this work showed that cigarette smoking exposure is associated with significant cardiovascular pathology such as cardiac hypertrophy, inflammation, pro-fibrotic and atherogenic markers and aortic calcification in an animal model as assessed 1 month post exposure. Antioxidant supplementation prevented cardiac hypertrophy and attenuated indicators of atherosclerosis markers associated with cigarette smoke exposure.Key words: Cigarette smoking, pomegranate Juice, inflammation, hypertrophy, calcification, reactive oxygen species, cardiovascular diseases.

  8. Morphological Atherosclerosis Calcification Distribution (MACD) Index is a Strong Predictor of Cardio-Vascular Death and Include Predictive Power of BMD

    DEFF Research Database (Denmark)

    Christiansen, Claus; Karsdal, Morten; Ganz, Melanie;

    followed for 8.3±0.3 years and CVD deaths were recorded. BMD and several aortic calcification markers were computed: number, morphology, distribution, from outlines of the calcified plaques in lumbar X-rays. These markers were compared to BMD, SCORE card, Framingham score, and the Aortic Calcification...... Severity score - AC24. AC24 adjusted by age, waist circumference, and triglyceride levels (ATW) predicted mortality in postmenopausal women (CVD p=0.03, All-cause p=0.006). The SCORE card and the Framingham score resulted in mortality odds ratios (MOR) of 5.0 and 5.2 - defining high risk as =6 and =18......, respectively. BMD and BMD adjusted for ATW was lower in the group of deceased than in survivors (pscores based on the calcification geometry provided highly significant predictions. The number of calcified deposits...

  9. Morphological Atherosclerosis Calcification Distribution (MACD) Index is a Strong Predictor of Cardio-Vascular Death and Include Predictive Power of BMD

    DEFF Research Database (Denmark)

    Christiansen, Claus; Karsdal, Morten; Ganz, Melanie

    Aortic calcification is a major risk factor for cardiovascular disease (CVD) related deaths. We investigated the relation between mortality and aspects of number, size, morphology and distribution of calcified plaques in the lumbar aorta and BMD of postmenopausal women. 308 women aged 48 to 76 were...

  10. Association of ectopic fat with abdominal aorto-illiac and coronary artery calcification in african ancestry men.

    Science.gov (United States)

    Kuipers, Allison L; Zmuda, Joseph M; Carr, J Jeffrey; Terry, James G; Nair, Sangeeta; Cvejkus, Ryan; Bunker, Clareann H; Patrick, Alan L; Wassel, Christina L; Miljkovic, Iva

    2017-08-01

    There is strong evidence that fat accumulating in non-adipose sites, "ectopic fat", is associated with cardiovascular disease (CVD), including vascular calcification. Most previous studies of this association have assessed only a single ectopic fat depot. Therefore, our aim was to assess the association of total, regional, and ectopic fat with abdominal aorto-illiac calcification (AAC) and coronary artery calcification (CAC) in 798 African ancestry men. Participants (mean age 62) were from the Tobago Bone Health Study cohort. Adiposity was assessed via clinical examination, dual x-ray absorptiometry, and computed tomography (CT). Ectopic fat depots included: abdominal visceral adipose tissue (VAT), liver attenuation, and calf intermuscular adipose tissue (IMAT). Vascular calcification was assessed by CT and quantified as present versus absent. Associations were tested using multiple logistic regression adjusted for traditional cardiovascular risk factors. Models of ectopic fat were additionally adjusted for total body fat and standing height. All adiposity measures, except VAT, were associated with AAC. Lower liver attenuation or greater calf IMAT was associated with 1.2-1.3-fold increased odds of AAC (p ectopic fat measure was associated with CAC. Greater adiposity in the skeletal muscle and liver, but not in the visceral compartment, was associated with increased odds of AAC in African ancestry men. These results highlight the potential importance of both quantity and location of adiposity accumulation throughout the body. Copyright © 2017 Elsevier B.V. All rights reserved.

  11. Serum Osteoprotegerin level and the extent of cardiovascular calcification in haemodialysis patients

    Directory of Open Access Journals (Sweden)

    Waleed Ammar

    2014-03-01

    Conclusion: There is strong positive relationship between osteoprotegerin and both vascular and valvular calcification in hemodialysis patients. This positive correlation may open the gate for routine estimation of this agent as a surrogate marker of cardiovascular calcification in hemodialysis patients.

  12. Curcumin Attenuates Rapamycin-induced Cell Injury of Vascular Endothelial Cells.

    Science.gov (United States)

    Guo, Ning; Chen, Fangyuan; Zhou, Juan; Fang, Yuan; Li, Hongbing; Luo, Yongbai; Zhang, Yong

    2015-10-01

    Although drug-eluting stents (DES) effectively improve the clinical efficacy of percutaneous coronary intervention, a high risk of late stent thrombosis and in-stent restenosis also exists after DES implantation. Anti-smooth muscle proliferation drugs, such as rapamycin, coating stents, not only inhibit the growth of vascular smooth muscle cells but also inhibit vascular endothelial cells and delay the reendothelialization. Therefore, the development of an ideal agent that protects vascular endothelial cells from rapamycin-eluting stents is of great importance for the next generation of DES. In this study, we demonstrated that rapamycin significantly inhibited the growth of rat aortic endothelial cells in both dose- and time-dependent manner in vitro. Cell apoptosis was increased and migration was decreased by rapamycin treatments in rat aortic endothelial cells in vitro. Surprisingly, treatment with curcumin, an active ingredient of turmeric, significantly reversed these detrimental effects of rapamycin. Moreover, curcumin increased the expression of vascular nitric oxide synthases (eNOS), which was decreased by rapamycin. Furthermore, caveolin-1, the inhibitor of eNOS, was decreased by curcumin. Knockdown of eNOS by small interfering RNA significantly abrogated the protective effects of curcumin. Taken together, our results suggest that curcumin antagonizes the detrimental effect of rapamycin on aortic endothelial cells in vitro through upregulating eNOS. Therefore, curcumin is a promising combined agent for the rescue of DES-induced reendothelialization delay.

  13. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis

    DEFF Research Database (Denmark)

    Ma, Liqun; Zhong, Jian; Zhao, Zhigang

    2011-01-01

    Activation of transient receptor potential vanilloid type-1 (TRPV1) channels may affect lipid storage and the cellular inflammatory response. Now, we tested the hypothesis that activation of TRPV1 channels attenuates atherosclerosis in apolipoprotein E knockout mice (ApoE(-/-)) but not ApoE...

  14. Adipocyte induced arterial calcification is prevented with sodium thiosulfate

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Neal X., E-mail: xuechen@iupui.edu [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); O’Neill, Kalisha; Akl, Nader Kassis [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); Moe, Sharon M. [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); Roudebush VA Medical Center, Indianapolis, IN (United States)

    2014-06-20

    Highlights: • High phosphorus can induce calcification of adipocytes, even when fully differentiated. • Adipocytes can induce vascular calcification in an autocrine manner. • Sodium thiosulfate inhibits adipocyte calcification. - Abstract: Background: Calcification can occur in fat in multiple clinical conditions including in the dermis, breasts and in the abdomen in calciphylaxis. All of these are more common in patients with advanced kidney disease. Clinically, hyperphosphatemia and obesity are risk factors. Thus we tested the hypothesis that adipocytes can calcify in the presence of elevated phosphorus and/or that adipocytes exposed to phosphorus can induce vascular smooth muscle cell (VSMC) calcification. Methods: 3T3-L1 preadipocytes were induced into mature adipocytes and then treated with media containing high phosphorus. Calcification was assessed biochemically and PCR performed to determine the expression of genes for osteoblast and adipocyte differentiation. Adipocytes were also co-cultured with bovine VSMC to determine paracrine effects, and the efficacy of sodium thiosulfate was determined. Results: The results demonstrated that high phosphorus induced the calcification of differentiated adipocytes with increased expression of osteopontin, the osteoblast transcription factor Runx2 and decreased expression of adipocyte transcription factors peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding protein α (CEBPα), indicating that high phosphorus led to a phenotypic switch of adipocytes to an osteoblast like phenotype. Sodium thiosulfate, dose dependently decreased adipocyte calcification and inhibited adipocyte induced increase of VSMC calcification. Co-culture studies demonstrated that adipocytes facilitated VSMC calcification partially mediated by changes of secretion of leptin and vascular endothelial growth factor (VEGF) from adipocytes. Conclusion: High phosphorus induced calcification of mature adipocytes, and

  15. Azelnidipine inhibits Msx2-dependent osteogenic differentiation and matrix mineralization of vascular smooth muscle cells.

    Science.gov (United States)

    Shimizu, Takehisa; Tanaka, Toru; Iso, Tatsuya; Kawai-Kowase, Keiko; Kurabayashi, Masahiko

    2012-01-01

    Vascular calcification is an active and regulated process that is similar to bone formation. While calcium channel blockers (CCBs) have been shown to improve outcomes in atherosclerotic vascular disease, it remains unknown whether CCBs have an effect on the process of vascular calcification. Here we investigated whether CCBs inhibit osteogenic differentiation and matrix mineralization of vascular smooth muscle cells induced by Msx2, a key factor of vascular calcification. Human aortic smooth muscle cells (HASMCs) were transduced with adenovirus expressing MSX2 and were treated with 3 distinct CCBs. Azelnidipine, a dihydropyridine subclass of CCBs, significantly decreased alkaline phosphatase (ALP) activity of Msx2-overexpressed HASMCs, whereas verapamil and diltiazem had no effect. Furthermore, azelnidipine, but not verapamil and diltiazem, significantly decreased matrix mineralization of Msx2-overexpressing HASMCs. Azelnidipine significantly attenuated the induction of ALP gene expression by Msx2, a key transcription factor in osteogenesis, while it did not reduce enzymatic activity of ALP. Furthermore, azelnidipine inhibited the ability of Msx2 to activate the ALP gene, but had no effect on Notch-induced Msx2 expression. Given that L-type calcium channels are equally blocked by these CCBs, our results suggest that azelnidipine inhibits the Msx2-dependent process of vascular calcification by mechanisms other than inhibition of calcium channel activity.

  16. Renal Denervation Attenuates Multi-Organ Fibrosis and Improves Vascular Remodeling in Rats with Transverse Aortic Constriction Induced Cardiomyopathy

    Directory of Open Access Journals (Sweden)

    Kai Wang

    2016-11-01

    Full Text Available Background/Aims: To investigate the effects of renal denervation (RDN on multi-organ fibrosis and vascular remodeling in cardiomyopathy. Methods: Thirty-six male Sprague-Dawley rats underwent transverse aortic constriction (TAC. Five weeks later, 28 surviving TAC rats were randomly assigned to three groups: (1 RDN, (2 Sham, (3 Carvedilol. Six male Sham TAC rats served as the Control. Ten weeks after TAC, samples were collected. Results: TAC rats showed an increased diastolic interventricular septal thickness at week 5. At 10 weeks, Masson staining showed that left ventricular and renal glomerular fibrosis were significantly reduced in RDN compared with Sham group. In comparison to Sham group, hepatic perivascular fibrosis was attenuated in both RDN and Carvedilol group, so were the media thickness and the media/lumen of aorta. The plasma levels of B-type natriuretic peptide (BNP, Cystatin C (Cys-C, Alanine Transaminase, angiotensin II (Ang II, transforming growth factor beta 1 (TGF-β1, and malondialdehyde increased, and total superoxide dismutase (T-SOD decreased in Sham but not in RDN group, compared with Control group. Both RDN and Carvedilol reduced the Cys-C and TGF-β1 levels, and restored T-SOD concentration, compared with Sham group. While only RDN lowered the plasma levels of BNP and Ang II. No significant effects of RDN on blood pressure (BP and heart rate (HR were oberved. Conclusions: RDN can attenuate multi-organ fibrosis and improve vascular remodeling independent of BP and HR change in TAC-induced cardiomyopathy. These effects of RDN may be associated with the direct inhibition of renin-angiotensin-aldosterone system and oxidative stress.

  17. The sesame lignan sesamin attenuates vascular dysfunction in streptozotocin diabetic rats: involvement of nitric oxide and oxidative stress.

    Science.gov (United States)

    Baluchnejadmojarad, Tourandokht; Roghani, Mehrdad; Jalali Nadoushan, Mohammad-Reza; Vaez Mahdavi, Mohammad-Reza; Kalalian-Moghaddam, Hamid; Roghani-Dehkordi, Farshad; Dariani, Sharareh; Raoufi, Safoura

    2013-01-05

    The effect of chronic administration of sesamin was studied on aortic reactivity of streptozotocin diabetic rats. Male diabetic rats received sesamin for 7 weeks after diabetes induction. Contractile responses to KCl and phenylephrine and relaxation response to acetylcholine were obtained from aortic rings. Maximum contractile response of endothelium-intact rings to phenylephrine was significantly lower in sesamin-treated diabetic rats relative to untreated diabetics and endothelium removal abolished this difference. Meanwhile, endothelium-dependent relaxation to acetylcholine was significantly higher in sesamin-treated diabetic rats as compared to diabetic ones and pretreatment of rings with nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester significantly attenuated the observed response. Two-month diabetes also resulted in an elevation of malondialdehyde and decreased superoxide dismutase activity and sesamin treatment significantly improved these changes. Therefore, chronic treatment of diabetic rats with sesamin could prevent some abnormal changes in vascular reactivity in diabetic rats through nitric oxide and via attenuation of oxidative stress and tissue integrity of endothelium is necessary for its beneficial effect.

  18. Vascular angiotensin II type 2 receptor attenuates atherosclerosis via a kinin/NO-dependent mechanism.

    Science.gov (United States)

    Takata, Hiroki; Yamada, Hiroyuki; Kawahito, Hiroyuki; Kishida, Sou; Irie, Daisuke; Kato, Taku; Wakana, Noriyuki; Miyagawa, Sonoko; Fukui, Kensuke; Matsubara, Hiroaki

    2015-06-01

    The angiotensin II (Ang II) type 1 receptor exerts pro-atherogenic action by augmenting oxidative stress, whereas the Ang II type 2 receptor (AT2)-mediated effect on atherosclerosis remains controversial. AT2 transgenic (AT2-Tg) mice, which overexpress AT2 in their vascular smooth muscle cells, were crossed with apoE-deficient (apoE(-/-)) mice to generate AT2 transgenic apoE(-/-) mice (AT2-Tg/apoE(-/-)). A subpressor dose of Ang II infusion exaggerated atherosclerosis development in apoE(-/-) mice, which was markedly suppressed in AT2-Tg/apoE(-/-) mice. Inhibitors of nitric oxide (NO) synthase (L-NAME) or bradykinin type 2 receptor completely abolished AT2-mediated anti-atherogenic actions. The vascular cell adhesion molecule-1 expression levels and degree of monocyte/macrophage accumulation in the intima were also considerably reduced in AT2-Tg/apoE(-/-) mice; these phenomena were completely reversed by L-NAME treatment. Ang II infusion significantly enhanced the accumulation of dihydroethidium-positive mononuclear cells in the intima and mRNA expression levels of Nox2, a phagocytic cell-type NADPH oxidase subunit in apoE(-/-) mice, which was completely inhibited in AT2-Tg/apoE(-/-) mice. Vascular AT2 stimulation exerts anti-atherogenic actions in an endothelial kinin/NO-dependent manner, and its anti-oxidative effect is likely to be exerted by inhibiting the accumulation of superoxide-producing mononuclear leukocytes. © The Author(s) 2013.

  19. Vitamin K antagonism aggravates chronic kidney disease-induced neointimal hyperplasia and calcification in arterialized veins: role of vitamin K treatment?

    Science.gov (United States)

    Zaragatski, Emma; Grommes, Jochen; Schurgers, Leon J; Langer, Stephan; Kennes, Lieven; Tamm, Miriam; Koeppel, Thomas A; Kranz, Jennifer; Hackhofer, Tina; Arakelyan, Karen; Jacobs, Michael J; Kokozidou, Maria

    2016-03-01

    Arteriovenous fistula (AVF) is the common vascular access type for a hemodialysis patient. Its failure is due to neointimal hyperplasia. Vitamin K antagonists are given to lower thrombosis tendency, but have side effects that enhance arterial calcifications. Here, we investigated the effects of vitamin K antagonists and vitamin K2 (K2) treatment on neointimal hyperplasia development and calcification in rats and in arterialized human veins. AVF was generated in female rats while chronic kidney disease (CKD) was induced using an adenine-enriched diet. Arterialization, CKD, and vitamin K antagonists all significantly enhanced venous neointimal hyperplasia. K2 treatment, additional to vitamin K antagonists, significantly reduced neointimal hyperplasia in arterialized veins in healthy rats but not in rats with CKD. Arterialization, CKD, and vitamin K antagonism all significantly increased, whereas K2 supplementation attenuated calcification in healthy rats and rats with CKD. K2 significantly enhanced matrix Gla protein carboxylation in control rats and rats with CKD. Arterialized human vein samples contained inactive matrix Gla protein at calcification and neointimal hyperplasia sites, indicating local vitamin K deficiency. Thus, vitamin K antagonists have detrimental effects on AVF remodeling, whereas K2 reduced neointimal hyperplasia and calcification indicating vasoprotective effects. Hence, K2 administration may be useful to prevent neointimal hyperplasia and calcification in arterialized veins

  20. Inhibitors of soluble epoxide hydrolase attenuate vascular smooth muscle cell proliferation

    Science.gov (United States)

    Davis, Benjamin B.; Thompson, David A.; Howard, Laura L.; Morisseau, Christophe; Hammock, Bruce D.; Weiss, Robert H.

    2002-02-01

    Atherosclerosis, in its myriad incarnations the foremost killer disease in the industrialized world, is characterized by aberrant proliferation of vascular smooth muscle (VSM) cells in part as a result of the recruitment of inflammatory cells to the blood vessel wall. The epoxyeicosatrienoic acids are synthesized from arachidonic acid in a reaction catalyzed by the cytochrome P450 system and are vasoactive substances. Metabolism of these compounds by epoxide hydrolases results in the formation of compounds that affect the vasculature in a pleiotropic manner. As an outgrowth of our observations that urea inhibitors of the soluble epoxide hydrolase (sEH) reduce blood pressure in spontaneously hypertensive rats as well as the findings of other investigators that these compounds possess antiinflammatory actions, we have examined the effect of sEH inhibitors on VSM cell proliferation. We now show that the sEH inhibitor 1-cyclohexyl-3-dodecyl urea (CDU) inhibits human VSM cell proliferation in a dose-dependent manner and is associated with a decrease in the level of cyclin D1. In addition, cis-epoxyeicosatrienoic acid mimics the growth-suppressive activity of CDU; there is no evidence of cellular toxicity or apoptosis in CDU-treated cells when incubated with 20 μM CDU for up to 48 h. These results, in light of the antiinflammatory and antihypertensive properties of these compounds that have been demonstrated already, suggest that the urea class of sEH inhibitors may be useful for therapy for diseases such as hypertension and atherosclerosis characterized by exuberant VSM cell proliferation and vascular inflammation.

  1. Matrix Gla Protein polymorphisms are associated with coronary artery calcification

    Science.gov (United States)

    Matrix Gla Protein (MGP) is a key regulator of vascular calcification. Genetic variation at the MGP locus could modulate the development of coronary artery calcification (CAC). We examined the cross-sectional association between MGP SNPs [rs1800802 (T-138C), rs1800801 (G-7A),and rs4236 (Ala102Thr)...

  2. 血清可溶性CD40L和C反应蛋白在慢性血透患者外周血管钙化的作用%Role of soluble CD40L and C-reactive protein in peripheral vascular calcification in patients undergoing of chronic hemodialysis

    Institute of Scientific and Technical Information of China (English)

    伍强; 孙艳; 杨铁城; 张海燕

    2010-01-01

    Objective To investigate the role of soluble CD40 ligand (sCD40L) and C-reactive protein (CRP) in peripheral vascular calcification in hemodialytic patients.Methods 40 hemodialytic patients with uremia underwent arteriovenous fistula reconstruction.The stumps of radial artery were removed for assessing vascular calcification.The patients were grouped according to the presence or absence of calcification and its degree.Serum levels of sCD40L and CRP were detected.The differences in levels of sCD40L and CRP were compared between calcification group and non-calcification group and between calcification groups at different degrees calcification.Results Radial artery calcification was detectable in 23 of the patients with calcium staining,9 of whom had severe calcification and the rest 14 had mild to moderate calcification.Levels of sCD40L and CRP were significantly higher in calcification group than in non-calcification group (P<0.01); they were also higher in severe calcification group than in mild to moderate calcification group (P<0.05).Levels of sCD40L were positively correlated with those of CRP.%目的 探讨血清可溶性白细胞分化抗原40配体(sCD40L)和C反应蛋白(CRP)在尿毒症血液透析患者外周血管钙化中的作用.方法 尿毒症血液透析患者40例因动静脉内瘘失功行内瘘重建术,术中取桡动脉残端行钙化染色观察血管钙化情况,依据血管钙化有无及程度分组,同时检测血清sCD40L和CRP水平,比较钙化组与非钙化组,不同程度钙化组间血清sCD40L和CRP水平的差异.结果 40例患者桡动脉钙化染色检出血管钙化23例,其中重度钙化9例,轻中度钙化14例,钙化组血清sCD40L和CRP水平高于非钙化组,有统计学差异(P<0.01).重度钙化组sCD40L和CRP水平高于轻中度钙化组.有统计学差异(P<0.05).血清sCD40L和CRP含量呈正相关.结论 sCD40L和炎症反应可能参与了尿毒症血液透析患者外周血管钙化的发生.

  3. MEK1/2 inhibition attenuates vascular ETA and ETB receptor alterations after cerebral ischaemia

    DEFF Research Database (Denmark)

    Henriksson, Marie; Stenman, Emelie; Vikman, Petter;

    2007-01-01

    Cerebral ischaemia is associated with elevated levels of endothelin B (ETB) receptors in the ipsilateral middle cerebral artery (MCA). This up-regulation of ET receptors occurs via de novo transcription involving mitogen-activated protein kinases (MAPK). The aim of this study was to examine the e......, neurological symptoms, and ET receptor alteration. The vascular effects of U0126 provide new perspective on possible mechanisms of actions of MAPK inhibition in cerebral ischaemia.......Cerebral ischaemia is associated with elevated levels of endothelin B (ETB) receptors in the ipsilateral middle cerebral artery (MCA). This up-regulation of ET receptors occurs via de novo transcription involving mitogen-activated protein kinases (MAPK). The aim of this study was to examine...... the effect of inhibition of the MAP kinase/ERK kinase (MEK)1/2 on ET receptor alteration, brain damage, and neurology in experimental cerebral ischaemia. Transient middle cerebral artery occlusion (MCAO) was induced in male Wistar rats by the intraluminal filament technique. The animals received 100 mg...

  4. Elevation of iron storage in humans attenuates the pulmonary vascular response to hypoxia.

    Science.gov (United States)

    Bart, Nicole K; Curtis, M Kate; Cheng, Hung-Yuan; Hungerford, Sara L; McLaren, Ross; Petousi, Nayia; Dorrington, Keith L; Robbins, Peter A

    2016-08-01

    Sustained hypoxia over several hours induces a progressive rise in pulmonary artery systolic pressure (PASP). Administration of intravenous iron immediately prior to the hypoxia exposure abrogates this effect, suggesting that manipulation of iron stores may modify hypoxia-induced pulmonary hypertension. Iron (ferric carboxymaltose) administered intravenously has a plasma half-life of 7-12 h. Thus any therapeutic use of intravenous iron would require its effect on PASP to persist long after the iron-sugar complex has been cleared from the blood. To examine this, we studied PASP during sustained (6 h) hypoxia on 4 separate days (days 0, 1, 8, and 43) in 22 participants. On day 0, the rise in PASP with hypoxia was well matched between the iron and saline groups. On day 1, each participant received either 1 g of ferric carboxymaltose or saline in a double-blind manner. After administration of intravenous iron, the rise in PASP with hypoxia was attenuated by ∼50%, and this response remained suppressed on both days 8 and 43 (P iron, values for ferritin concentration, transferrin saturation, and hepcidin concentration rose significantly (P iron stores persists long after the artificial iron-sugar complex has been eliminated from the blood. The persistence of this effect suggests that intravenous iron may be of benefit in some forms of pulmonary hypertension.

  5. Attenuation of endothelin-1-induced calcium response by tyrosine kinase inhibitors in vascular smooth muscle cells.

    Science.gov (United States)

    Liu, C Y; Sturek, M

    1996-06-01

    Although tyrosine kinases play an important role in cell growth and have been implicated in regulation of smooth muscle contraction, their role in agonist-induced myoplasmic Ca2+ responses is unclear. We examined effects of the tyrosine kinase inhibitors genistein and methyl 2,5-dihydroxycinnamate (MDHC) on the endothelin-1 (ET-1)-induced Ca2+ response and determined underlying mechanisms for the effects. Freshly isolated smooth muscle cells from porcine coronary arteries were loaded with fura 2 ester, and myoplasmic free Ca2+ (Ca2+ (m)) concentration was estimated with fura 2 microfluorometry. Both genistein and MDHC inhibited the initial transient Cam2+ response to ET by 54 and 81%, respectively (P latent period from ET-1 application to the beginning of the Cam2+ response being increased from 1.08 +/- 0.17 to 2.65 +/- 0.52 min (P < 0.05). In the absence of extracellular Ca2+, genistein inhibited the ET-1-induced Cam2+ response by 93% (P < 0.05). The Cam2+ responses to caffeine (5 mM) or inositol trisphosphate (IP3) applied intracellularly via a patch-clamp pipette were not affected by genistein. Both genistein and MDHC also abolished the sustained Cam2+ response to ET-1. However, the Cam2+ response to depolarization by 80 mM K+ was not inhibited by MDHC and only inhibited 22% by genistein (P < 0.05). These results indicate that 1) activation of tyrosine kinases is an important regulatory mechanism for the ET-1-induced Cam2+ response in vascular smooth muscle and 2) tyrosine kinases mediate ET-1-induced Ca2+ release with no direct effect on IP3-mediated Ca2+ release. Thus ET-1-mediated signaling upstream of IP3 interaction with the Ca2+ stores is regulated by tyrosine kinases.

  6. 碳酸镧对透析患者血管钙化的影响及其可能机制%Effect and Possible Mechanism of Lanthanum Carbonate on Vascular Calcification in Dialysis Patients

    Institute of Scientific and Technical Information of China (English)

    杨璞; 杨京新; 谢础能

    2015-01-01

    目的:探讨碳酸镧对透析患者血管钙化的影响及可能作用机制。方法:选择本院2013年1月-2014年8月收治的30例规律透析患者(透析至少3个月)为研究对象,给予所有患者为期12周的碳酸镧治疗,比较治疗前后该组患者iPTH(血清全段甲状旁腺素)、FGF23(成纤维细胞生长因子23)、25(OH) D(血清25羟维生素D)等指标水平。另外停用碳酸镧后继续服用1个月的碳酸钙,比较两组上述指标水平。结果:碳酸镧治疗前后血磷水平比较,差异有统计学意义(P<0.05)。碳酸镧治疗后、碳酸钙用药1个月后患者血磷、FGF23比较,差异有统计学意义(P<0.05)。另外,碳酸镧治疗期间不良反应发生率20.00%。结论:碳酸镧在治疗透析患者高磷血症、防止血管钙化中有重要作用,且碳酸镧可能是通过降低FGF23及血磷水平达到预防血管钙化的目的。%Objective:To investigate the effect and possible mechanism of lanthanum carbonate on vascular calcification in dialysis patients. Method:30 regular hemodialysis patients(dialysis for at least 3 months)admitted to our hospital from January 2013 to August 2014 as the research objects,and were given the lanthanum carbonate treatment for 12 weeks,to compare iPTH(serum intact parathyroid hormone),FGF23(fibroblast growth factor 23),25(OH) D(serum 25 hydroxy vitamin D)and other indicators level before and after treatment of patients. In addition,to take calcium carbonate for 1 month after disable lanthanum carbonate,and compare the index level of the two groups. Result:The serum phosphate before and after lanthanum carbonate treatment between the two groups,the difference was statistically significant(P<0.05). In addition,lanthanum carbonate,calcium carbonate treatment for 1 month after the patients blood phosphorus,the differences were significant(P<0.05). In addition,the incidence of adverse reactions was 20.00%during the

  7. Application of dual-energy X-ray in vascular calcification in patients with chronic kidney disease%双能X线在慢性肾脏病患者血管钙化中的应用

    Institute of Scientific and Technical Information of China (English)

    吴晓婵; 罗福漳; 洪国保

    2015-01-01

    目的:探讨双能X线骨密度检测在慢性肾脏病(CKD)患者血管钙化诊断中的应用价值。方法选取2013年1月~2014年12月本院接诊的42例CKD 3~5期患者作为研究对象,所有患者均行双能X线检查。以多层螺旋CT诊断为金标准,评价双能X线检测在CKD 3~5期患者血管钙化诊断中的敏感度和特异性。结果多层螺旋 CT在 CKD 3期、CKD 4期、CKD 5期的检出率分别为33.3%、52.2%、100.0%,双能X线的检出率分别为22.2%、43.5%、90.0%,且多层螺旋CT的总检出率为59.5%,与双能X线检测的50.0%比较,差异无统计学意义(P跃0.05)。以多层螺旋CT检测为金标准,双能X线检测的特异性为100.0%,敏感度为84.0%。结论双能X线可应用于检测CKD 3~5期患者的血管钙化,具有较好的临床价值。%Objective To exolore the application value of dual-energy X-ray in the detection of vascular calcification in chronic kidney disease (CKD) patients. Methods 42 cases of CKD 3-5 stages from January 2013 to December 2014 in our hospital were selected as the research objects.All patients were given dual-energy X-ray examination.The sensi-tivity and specificity of dual-energy X-ray examination in the diagnosis of vascular calcification in patients with CKD 3-5 stages were evaluated by using the gold standard of the diagnosis of multi-slice spiral CT. Results The detection rate in CKD 3-5 stages by multi-slice spiral CT was 33.3%,52.2%,100.0% respectively,while the detection rate in CKD 3-5 stages by dual-energy X-ray was 22.2%,43.5%,90.0% respectively.The total detection rate of multi-slice spiral CT was 59.5%,the otal detection rate of multi-slice spiral CT was 50.0%,there was no significant difference (P>0.05).The specificity of dual energy X-ray detection was 84%,and the sensitivity was 100%,with the detection of multi slice spiral CT as gold standard. Conclusion Dual-energy X-ray can be used in the detection of vascular calcification in chronic

  8. Influence of teriparatide on the vascular calcification in aged ovariec-tomized rats%特立帕肽对老年去卵巢大鼠血管钙化的影响

    Institute of Scientific and Technical Information of China (English)

    陈斌花; 袁; 陈秋霞; 姜醒华

    2015-01-01

    目的:观察特立帕肽对老年去卵巢大鼠血管钙化的影响,并探讨其发挥作用的分子机制。方法用30只10个月龄SD大鼠,随机分为3组院假手术组、去卵巢组及特立帕肽治疗组。特立帕肽治疗组给予20μg/kg特立帕肽皮下注射,隔天1次,持续12周。术前及给药期间收集大鼠血清,给药结束后观察子宫的组织学变化。酶联免疫吸附法(ELISA)检测血中未羧化基质羧基谷氨酸蛋白(uc-MGP)的量及雌激素的变化;原子分光光度计测量血管总钙含量;Von Kossa染色观察动脉钙化;免疫组化法观察血管uc-MGP的表达;荧光实时定量PCR扩增MGP mRNA,观察其在胸主动脉的表达水平。结果血清中uc-MGP含量去卵巢组最高,特立帕肽治疗组其次,假手术组最低(P<0.05)。去卵巢组及特立帕肽治疗组雌激素水平明显下降(P<0.05)。去卵巢组血管总钙含量明显高于假手术组(P<0.01),特立帕肽治疗组明显低于去卵巢组(P<0.01)。血管未羧化MGP表达出现在血管钙化周围区域,钙化严重组表达较多。特立帕肽治疗组阳性较少表达。去卵巢组表达量最低,假手术组MGP mRNA表达量最高,特立帕肽治疗组表达量介于两者之间,差异有统计学意义(P<0.01)。结论特立帕肽对绝经后血管钙化有改善作用,可能是通过调节MGP的基因表达及活性发挥作用。%Objective To explore the effect and mechanism of teriparatide on the vascular calcification in aged ovariec-tomized rats. Methods Thirty ten months female SD rats were allocated into three groups randoml:sham operation group,ovariectomized group and teriparatide treatment group.Subcutaneous injection with teriparatide (20 μg/kg,every other day)after two weeks of ovariectomy for 12 weeks was used in teriparatide treatment group.All rats were kept serum before ovariectomy and during the administration period.After administration,HE stain of the uterus.The content of MGP in serum

  9. Vascular endothelial growth factor attenuates hepatic sinusoidal capillarization in thioacetamide-induced cirrhotic rats

    Institute of Scientific and Technical Information of China (English)

    Hao Xu; Bao-Min Shi; Xiao-Fei Lu; Feng Liang; Xing Jin; Tai-Huang Wu; Jian Xu

    2008-01-01

    AIM: To investigate the effect of vascular endothelial growth factor (VEGF) transfection on hepatic sinusoidal capillarization.MEthODS: Enhanced green fluorescent protein (EGFP)/VEGF transfection was confirmed by immunofluorescencemicroscopy and immunohistoche-mistry both in primaryhepatocytes and in normal liven Cirrhotic rats weregenerated by thioacetamide (TAA) administration andthen divided into a treatment group, which receivedinjections of 400 μg of plasmid DNA encoding an EGFP-VEGF fusion protein, and a blank group, which receivedan equal amount of normal saline through the portalvein. The portal vein pressure was measured in the normal and cirrhotic state, in treated and blank groups.The average number of fenestrae per hepatic sinusoidwas determined using transmission electron microscopy(TEM), while the relative abundance of VEGF transcriptswas examined by Gene array.RESULTS: Green fluorescent protein was observed in the cytoplasms of liver cells under immunofluorescence microscopy 24 h after transfection with EGFP/VEGFplasmid in vitro. Staining with polyclonal antibodies against VEGF illustrated that hepatocytes expressed immunodetectable VEGF both in vitro and in vitro. There were significant differences in the number of fenestrae and portal vein pressures between normal and cirrhotic rats (7.40±1.71 vs 2.30± 2.26 and 9.32± 0.85 cmH2Ovs 27.92± 0.90 cmH2O1, P < 0.02), between cirrhotic and treated rats (2.30 + 1.16 cmH2O vs 4.60± 1.65 and 17.92± 0.90 cmH2O vs 15.52±0.93 cmH20, P < 0.05)and between the treatment group and the blank group (4.60±1.65 cmH20 vs 2.10 ± 1.10 cmH20 and 25.52 +0.93 cmH20 vs 17.26 ± 1.80 cmH20, P < 0.05). Gene-array analysis revealed that the relative abundance oftranscripts of VEGF family members decreased in the cirrhotic state and increased after transfection. CONCLUSION: Injection of a plasmid encoding VEGFthrough the portal vein is an effective method toinduce the formation of fenestrae and decrease portalvein

  10. Lentivirus-mediated RNAi knockdown of the gap junction protein, Cx43, attenuates the development of vascular restenosis following balloon injury.

    Science.gov (United States)

    Han, Xiao-Jian; Chen, Min; Hong, Tao; Zhu, Ling-Yu; He, Dan; Feng, Jiu-Geng; Jiang, Li-Ping

    2015-04-01

    Percutaneous coronary intervention [PCI or percutaneous transluminal coronary angioplasty (PTCA)] has been developed into a mature interventional treatment for atherosclerotic cardiovascular disease. However, the long-term therapeutic effect is compromised by the high incidence of vascular restenosis following angioplasty, and the underlying mechanisms of vascular restenosis have not yet been fully elucidated. In the present study, we investigated the role of the gap junction (GJ) protein, connexin 43 (Cx43), in the development of vascular restenosis. To establish vascular restenosis, rat carotid arteries were subjected to balloon angioplasty injury. At 0, 7, 14 and 2 days following balloon injury, the arteries were removed, and the intimal/medial area of the vessels was measured to evaluate the degree of restenosis. We found that the intimal area gradually increased following balloon injury. Intimal hyperplasia and restenosis were particularly evident at 14 and 28 days after injury. In addition, the mRNA and protein expression of Cx43 was temporarily decreased at 7 days, and subsequently increased at 14 and 28 days following balloon injury, as shown by RT-PCR and western blot analysis. To determine the involvement of Cx43 in vascular restenosis, the lentivirus vector expressing shRNA targeting Cx43, Cx43-RNAi-LV, was used to silence Cx43 in the rat carotid arteries. The knockdown of Cx43 effectively attenuated the development of intimal hyperplasia and vascular restenosis following balloon injury. Thus, our data indicate the vital role of the GJ protein, Cx43, in the development of vascular restenosis, and provide new insight into the pathogenesis of vascular restenosis. Cx43 may prove to be a novel potential pharmacological target for the prevention of vascular restenosis following PCI.

  11. Silence of STIM1 attenua=tes the proliferation and migration of EPCs after vascular injury and its mechanism

    Institute of Scientific and Technical Information of China (English)

    Xin-Peng Cong; Wen-Hui Wang; Xi Zhu; Can Jin; Liang Liu; Xin-Min Li

    2014-01-01

    Objective:To investigate the effect of stromal interaction molecule1(STIM1) knockdown on the proliferation and migration of endothelial progenitor cells(EPCs) after vascular injury and its mechanism.Methods:The rat bone marrow derivedEPCs were divided into three groups: adenovirus negative control(groupNSC), ratSTIM1 adenovirus vector transfection group (group si/rSTIM1) and rat &human recombinantSTIM1adenovirus transfection group(group si/rSTIM1+hSTIM1).TheSTIM1 expressions in each group were detected by reverse transcription PCR after transfection; the cell proliferation was tested by [3H] thymidine incorporation assay(3H-TdR);Cell cycle was analyzed by flow cytometry; the cells’ migration activity was detected by Boyden assay;Calcium ion concentration was detected by using laser confocal method.Results:48 h later after transfection, the expression level ofSTIM1 in si/rSTIM1 cells was significantly lower than that inNSC group(0.21±0.12vs1.01±0.01,P<0.05);EPCs that stayed inG1 phase in si/rSTIM1 group [(93.31±0.24)%] were significantly more than that inNSC group [(78.03±0.34)%, P<0.05];EPCs’ migration activity in si/rSTIM1 group(10.03±0.33) was significantly lower than that inNSC group:(32.11±0.54,P<0.05);EPCs calcium ion concentration changes inEPCs in si/rSTIM1 group(38.03±0.13) was significantly lower than that inNSC group(98.11±0.34,P<0.05).While there was no significant difference between si/rSTIM1+hSTIM1 group andNSC group on the four indexes above.Conclusions:Silence ofSTIM1 attenuatesEPCs proliferation and migration after vascular injury, by mediating the calcium ion concentration inEPCs.

  12. High-Dose Menaquinone-7 Supplementation Reduces Cardiovascular Calcification in a Murine Model of Extraosseous Calcification

    Directory of Open Access Journals (Sweden)

    Daniel Scheiber

    2015-08-01

    Full Text Available Cardiovascular calcification is prevalent in the aging population and in patients with chronic kidney disease (CKD and diabetes mellitus, giving rise to substantial morbidity and mortality. Vitamin K-dependent matrix Gla-protein (MGP is an important inhibitor of calcification. The aim of this study was to evaluate the impact of high-dose menaquinone-7 (MK-7 supplementation (100 µg/g diet on the development of extraosseous calcification in a murine model. Calcification was induced by 5/6 nephrectomy combined with high phosphate diet in rats. Sham operated animals served as controls. Animals received high or low MK-7 diets for 12 weeks. We assessed vital parameters, serum chemistry, creatinine clearance, and cardiac function. CKD provoked increased aortic (1.3 fold; p < 0.05 and myocardial (2.4 fold; p < 0.05 calcification in line with increased alkaline phosphatase levels (2.2 fold; p < 0.01. MK-7 supplementation inhibited cardiovascular calcification and decreased aortic alkaline phosphatase tissue concentrations. Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA expression (10-fold; p < 0.05. CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation. Our results show that high-dose MK-7 supplementation inhibits the development of cardiovascular calcification. The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures.

  13. Cardiovascular calcifications in chronic kidney disease: Potential therapeutic implications.

    Science.gov (United States)

    Bover, Jordi; Ureña-Torres, Pablo; Górriz, José Luis; Lloret, María Jesús; da Silva, Iara; Ruiz-García, César; Chang, Pamela; Rodríguez, Mariano; Ballarín, José

    Cardiovascular (CV) calcification is a highly prevalent condition at all stages of chronic kidney disease (CKD) and is directly associated with increased CV and global morbidity and mortality. In the first part of this review, we have shown that CV calcifications represent an important part of the CKD-MBD complex and are a superior predictor of clinical outcomes in our patients. However, it is also necessary to demonstrate that CV calcification is a modifiable risk factor including the possibility of decreasing (or at least not aggravating) its progression with iatrogenic manoeuvres. Although, strictly speaking, only circumstantial evidence is available, it is known that certain drugs may modify the progression of CV calcifications, even though a direct causal link with improved survival has not been demonstrated. For example, non-calcium-based phosphate binders demonstrated the ability to attenuate the progression of CV calcification compared with the liberal use of calcium-based phosphate binders in several randomised clinical trials. Moreover, although only in experimental conditions, selective activators of the vitamin D receptor seem to have a wider therapeutic margin against CV calcification. Finally, calcimimetics seem to attenuate the progression of CV calcification in dialysis patients. While new therapeutic strategies are being developed (i.e. vitamin K, SNF472, etc.), we suggest that the evaluation of CV calcifications could be a diagnostic tool used by nephrologists to personalise their therapeutic decisions.

  14. Inhibitory role of Notch1 in calcific aortic valve disease.

    Directory of Open Access Journals (Sweden)

    Asha Acharya

    Full Text Available Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs. We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of Sox9 expression has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism.

  15. Breast Arterial Calcifications and Heart Disease Risk in women

    NARCIS (Netherlands)

    Maas, A.H.E.M.

    2006-01-01

    Imaging of vascular calcification is increasingly used for cardiovascular screening purposes in asymptomatic patients. Coronary and aortic calcium deposits in the vascular wall have been shown to be related to atherosclerotic plaque burden. New imaging techniques with electron beam computed tomograp

  16. Effects of advanced glycation end-products on the expression of parathyroid hormone related peptide and vascular calcification on vascular smooth muscle cells%糖基化终产物对人血管平滑肌细胞表达及分泌甲状旁腺激素相关肽和血管钙化的影响

    Institute of Scientific and Technical Information of China (English)

    张琴; 刘乃丰

    2014-01-01

    Objective:To investigate the effects of advanced glycation end-products(AGEs) on expression and secretion of parathyroid hormone related peptide(PTHrP)in vitro cultured human vascular smooth muscle cells (HVSMCs), and explore the related mechanism of PTHrP influencing vascular smooth muscle cells calcification . Methods:HVSMCs were treated with AGE-BSA of indicated concentration or non-glycated BSA for same periods . The calcium contents and activity of alkaline phosphatase of cells were analyzed by microplate reader ;PTHrP levels in the supernatant were detected by the enzyme-linked immunosorbent method .Real-time fluorescent quantitative reverse transcription polymerase chain reaction ( RT-PCR) was performed to detect the expressive of PTHrP , core- binding factor α1(cbfα1) in human and bone morphogenetic protein-2(BMP-2) in vascular smooth muscle cells . Results:AGE-BSA increased calcium deposition and activity of alkaline phosphatase in HVSMCs in dose-independent manners( P<0.05) , but reduced the secretion of PTHrP.Futhermore, the elevated AGE-BSA treatment on HVSMCs significantly enhanced the expression of cbfα1, BMP-2 and PTHrP, compared with the controls( P <0.05 ) .Conclusion: The expression and secretion of PTHrP on human vascular smooth muscle cells can be effected by AGEs , and PTHrP may induce deposition of calcium on vascular smooth muscle cells, thereby contributing to the vascular calcification .However, the related mechanism will be further explored .%目的:观察糖基化终末产物(AGEs)对人血管平滑肌细胞表达及分泌甲状旁腺激素相关肽(PTHrP)功能的影响,探讨PTHrP影响血管平滑肌细胞钙化发生的相关机制。方法:不同浓度的AGE-BSA分别与人血管平滑肌细胞孵育相同时间后,检测各组细胞钙含量及碱性磷酸酶( ALP)活性判断钙化程度;酶联免疫吸附法检测各组细胞PTHrP的分泌量;实时荧光定量逆转录聚合酶链反应检

  17. Hydrogen sulfide releasing aspirin, ACS14, attenuates high glucose-induced increased methylglyoxal and oxidative stress in cultured vascular smooth muscle cells.

    Science.gov (United States)

    Huang, Qian; Sparatore, Anna; Del Soldato, Piero; Wu, Lingyun; Desai, Kaushik

    2014-01-01

    Hydrogen sulfide is a gasotransmitter with vasodilatory and anti-inflammatory properties. Aspirin is an irreversible cyclooxygenase inhibitor anti-inflammatory drug. ACS14 is a novel synthetic hydrogen sulfide releasing aspirin which inhibits cyclooxygenase and has antioxidant effects. Methylglyoxal is a chemically active metabolite of glucose and fructose, and a major precursor of advanced glycation end products formation. Methylglyoxal is harmful when produced in excess. Plasma methylglyoxal levels are significantly elevated in diabetic patients. Our aim was to investigate the effects of ACS14 on methylglyoxal levels in cultured rat aortic vascular smooth muscle cells. We used cultured rat aortic vascular smooth muscle cells for the study. Methylglyoxal was measured by HPLC after derivatization, and nitrite+nitrate with an assay kit. Western blotting was used to determine NADPH oxidase 4 (NOX4) and inducible nitric oxide synthase (iNOS) protein expression. Dicholorofluorescein assay was used to measure oxidative stress. ACS14 significantly attenuated elevation of intracellular methylglyoxal levels caused by incubating cultured vascular smooth muscle cells with methylglyoxal (30 µM) and high glucose (25 mM). ACS14, but not aspirin, caused a significant attenuation of increase in nitrite+nitrate levels caused by methylglyoxal or high glucose. ACS14, aspirin, and sodium hydrogen sulfide (NaHS, a hydrogen sulfide donor), all attenuated the increase in oxidative stress caused by methylglyoxal and high glucose in cultured cells. ACS14 prevented the increase in NOX4 expression caused by incubating the cultured VSMCs with MG (30 µM). ACS14, aspirin and NaHS attenuated the increase in iNOS expression caused by high glucose (25 mM). In conclusion, ACS14 has the novel ability to attenuate an increase in methylglyoxal levels which in turn can reduce oxidative stress, decrease the formation of advanced glycation end products and prevent many of the known deleterious effects

  18. Hydrogen sulfide releasing aspirin, ACS14, attenuates high glucose-induced increased methylglyoxal and oxidative stress in cultured vascular smooth muscle cells.

    Directory of Open Access Journals (Sweden)

    Qian Huang

    Full Text Available Hydrogen sulfide is a gasotransmitter with vasodilatory and anti-inflammatory properties. Aspirin is an irreversible cyclooxygenase inhibitor anti-inflammatory drug. ACS14 is a novel synthetic hydrogen sulfide releasing aspirin which inhibits cyclooxygenase and has antioxidant effects. Methylglyoxal is a chemically active metabolite of glucose and fructose, and a major precursor of advanced glycation end products formation. Methylglyoxal is harmful when produced in excess. Plasma methylglyoxal levels are significantly elevated in diabetic patients. Our aim was to investigate the effects of ACS14 on methylglyoxal levels in cultured rat aortic vascular smooth muscle cells. We used cultured rat aortic vascular smooth muscle cells for the study. Methylglyoxal was measured by HPLC after derivatization, and nitrite+nitrate with an assay kit. Western blotting was used to determine NADPH oxidase 4 (NOX4 and inducible nitric oxide synthase (iNOS protein expression. Dicholorofluorescein assay was used to measure oxidative stress. ACS14 significantly attenuated elevation of intracellular methylglyoxal levels caused by incubating cultured vascular smooth muscle cells with methylglyoxal (30 µM and high glucose (25 mM. ACS14, but not aspirin, caused a significant attenuation of increase in nitrite+nitrate levels caused by methylglyoxal or high glucose. ACS14, aspirin, and sodium hydrogen sulfide (NaHS, a hydrogen sulfide donor, all attenuated the increase in oxidative stress caused by methylglyoxal and high glucose in cultured cells. ACS14 prevented the increase in NOX4 expression caused by incubating the cultured VSMCs with MG (30 µM. ACS14, aspirin and NaHS attenuated the increase in iNOS expression caused by high glucose (25 mM. In conclusion, ACS14 has the novel ability to attenuate an increase in methylglyoxal levels which in turn can reduce oxidative stress, decrease the formation of advanced glycation end products and prevent many of the known

  19. Sonographic Findings of Calcific Tendinitis around the Hip

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Hyun Seok; Lee, Young Hwan; Sung, Nak Kwan; Jung, Kyung Jae; Park, Young Chan; Kim, Ho Kyun [Catholic University of Daegu, College of Medicine, Daegu (Korea, Republic of); Kim, Mi Jeong; Lee, Sung Moon; Cho, Kil Ho [Keimyung University, College of Medicine, Daegu (Korea, Republic of); Suh, Kyung Jin [Dankook University, College of Medicine, Cheonan (Korea, Republic of)

    2005-09-15

    To evaluate the sonographic findings of calcific tendinitis around the hip. Ten patients (7 women and 3 men: mean age, 42 years: age range, 34-52 years) with a diagnosis of calcific tendinitis around the hip were evaluated. All the patients underwent radiography and sonography (color Doppler sonography in 6 patients). The sonographic findings were analyzed to determine the level of tendon thickening compared with the contralateral side as well as the shape and posterior acoustic shadowing of the calcification, and vascularity on color Doppler sonography. In all cases, sonography showed a thickening of the tendon compared with the contralateral normal tendon as well as hyperechoic calcific shadows within the thickened tendon. Intratendinous calcifications were mainly observed as a homogeneous ovoid hyperechoic shadow with or without acoustic shadowing. Color Doppler sonography showed increased vascularity within or around the thickened tendon in four of the six patients. Sonography is effective in detecting a thickening of the tendon as well as intratendinous calcification, and can be used to diagnose calcific tendinitis around the hip

  20. Tumour Calcification and Calciphylaxis in End-Stage Renal Disease

    Directory of Open Access Journals (Sweden)

    Jia Di

    2014-01-01

    Full Text Available Although soft tissue and vascular calcifications are common in CKD and progress as an independent risk factor of all-cause mortality, tumour calcification and calciphylaxis are uncommon in patients with end-stage renal disease (ESRD. Here, we discuss a rare case of a patient with tumour calcification complicated with calciphylaxis developed septic shock from infection. Our patient is a 57-year-old man in his late stage of renal disease who presented with a huge mass at the right hip and necrotic cutaneous ulcers on the lower legs followed by local and systemic infection and death due to septic shock.

  1. Association of mitral annulus calcification, aortic valve calcification with carotid intima media thickness

    Directory of Open Access Journals (Sweden)

    Scuteri Angelo

    2004-10-01

    Full Text Available Abstract Background Mitral annular calcification (MAC and aortic annular calcification (AVC may represent a manifestation of generalized atherosclerosis in the elederly. Alterations in vascular structure, as indexed by the intima media thickness (IMT, are also recognized as independent predictors of adverse cardiovascular outcomes. Aim To examine the relationship between the degree of calcification at mitral and/or aortic valve annulus and large artery structure (thickness. Methods We evaluated 102 consecutive patients who underwent transthoracic echocardiography and carotid artery echoDoppler for various indications; variables measured were: systemic blood pressure (BP, pulse pressure (PP=SBP-DBP, body mass index (BMI, fasting glucose, total, HDL, LDL chlolesterol, triglycerides, cIMT. The patients were divided according to a grading of valvular/annular lesions independent scores based on acoustic densitometry: 1 = annular/valvular sclerosis/calcification absence; 2 = annular/valvular sclerosis; 3 = annular calcification; 4 = annular-valvular calcification; 5 = valvular calcification with no recognition of the leaflets. Results Patient score was the highest observed for either valvular/annulus. Mean cIMT increased linearly with increasing valvular calcification score, ranging from 3.9 ± 0.48 mm in controls to 12.9 ± 1.8 mm in those subjects scored 5 (p 0.0001. Conclusion MAC and AVC score can identify subgroups of patients with different cIMT values which indicate different incidence and prevalence of systemic artery diseases. This data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease.

  2. Growth Pattern of Atherosclerotic Calcifications

    DEFF Research Database (Denmark)

    Larsen, Lene Lillemark; Ganz, Melanie; Dam, Erik

    2008-01-01

    of the calcifications are matched longitudinally using thin plate spline registration and area overlap calculations. The growth of the calcifications is measured by the distribution of the geometry statistics of the calcifications. The method was evaluated on 135 subjects with a total number of 611 calcifications. Our...

  3. Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk : results of the CAMONA study

    NARCIS (Netherlands)

    Blomberg, Bjorn A.; de Jong, Pim A.; Thomassen, Anders; Lam, Marnix G E; Vach, Werner; Olsen, Michael H.; Mali, Willem P T M; Narula, Jagat; Alavi, Abass; Høilund-Carlsen, Poul F.

    2017-01-01

    Purpose: Arterial inflammation and vascular calcification are regarded as early prognostic markers of cardiovascular disease (CVD). In this study we investigated the relationship between CVD risk and arterial inflammation (18F-FDG PET/CT imaging), vascular calcification metabolism (Na18F PET/CT imag

  4. Calcific Uremic Arteriolopathy: Pathophysiology, Reactive Oxygen Species and Therapeutic Approaches

    Directory of Open Access Journals (Sweden)

    Kurt M. Sowers

    2010-01-01

    Full Text Available Calcific uremic arteriolopathy (CUA/calciphylaxis is an important cause of morbidity and mortality in patients with chronic kidney disease requiring renal replacement. Once thought to be rare, it is being increasingly recognized and reported on a global scale. The uremic milieu predisposes to multiple metabolic toxicities including increased levels of reactive oxygen species and inflammation. Increased oxidative stress and inflammation promote this arteriolopathy by adversely affecting endothelial function resulting in a prothrombotic milieu and significant remodeling effects on vascular smooth muscle cells. These arteriolar pathological effects include intimal hyperplasia, inflammation, endovascular fibrosis and vascular smooth muscle cell apoptosis and differentiation into bone forming osteoblast-like cells resulting in medial calcification. Systemic factors promoting this vascular condition include elevated calcium, parathyroid hormone and hyperphosphatemia with consequent increases in the calcium × phosphate product. The uremic milieu contributes to a marked increased in upstream reactive oxygen species—oxidative stress and subsequent downstream increased inflammation, in part, via activation of the nuclear transcription factor NFκB and associated downstream cytokine pathways. Consitutive anti-calcification proteins such as Fetuin-A and matrix GLA proteins and their signaling pathways may be decreased, which further contributes to medial vascular calcification. The resulting clinical entity is painful, debilitating and contributes to the excess morbidity and mortality associated with chronic kidney disease and end stage renal disease. These same histopathologic conditions also occur in patients without uremia and therefore, the term calcific obliterative arteriolopathy could be utilized in these conditions.

  5. Spironolactone treatment attenuates vascular dysfunction in type 2 diabetic mice by decreasing oxidative stress and restoring NO/GC signaling

    Directory of Open Access Journals (Sweden)

    Marcondes Alves Barbosa Da Silva

    2015-10-01

    Full Text Available Type 2 diabetes (DM2 increases the risk of cardiovascular disease. Aldosterone, which has pro-oxidative and pro-inflammatory effects in the cardiovascular system, is positively regulated in DM2. We assessed whether blockade of mineralocorticoid receptors (MR with spironolactone decreases ROS-associated vascular dysfunction and improves vascular NO signaling in diabetes. Leptin receptor knockout [LepRdb/LepRdb (db/db] mice, a model of DM2, and their counterpart controls [LepRdb/LepR+, (db/+ mice] received spironolactone (50 mg/kg body weight/day or vehicle (ethanol 1% via oral per gavage for 6 weeks. Spironolactone treatment abolished the endothelial dysfunction and increased endothelial nitric oxide synthase (eNOS phosphorylation (Ser1177, determined by acetylcholine-induced relaxation and Western Blot analysis, respectively. MR antagonist therapy also abrogated augmented ROS-generation in aorta from diabetic mice, determined by lucigenin luminescence assay. Spironolactone treatment increased superoxide dismutase-1 (SOD1 and catalase expression, improved sodium nitroprusside (SNP and BAY 41-2272-induced relaxation, as well as increased soluble guanylyl cyclase (sGC subunit β protein expression in arteries from db/db mice. Our results demonstrate that spironolactone decreases diabetes-associated vascular oxidative stress and prevents vascular dysfunction through processes involving increased expression of antioxidant enzymes and sGC. These findings further elucidate redox-sensitive mechanisms whereby spironolactone protects against vascular injury in diabetes.

  6. Hu'rthle Cell Thyroid Adenoma with an Eggshell Calcification: A Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Dong Gil; Lee, Sang Kwon; Choe, Mi Sun; Chang, Hyuk Won; Rho, Byung Hak [Dongsan Medical Center, Keimyung University School of Medicine, Daegu (Korea, Republic of)

    2009-09-15

    We report here a case of Hu'rthle cell adenoma with eggshell calcification that presented as a thyroid incidentaloma on ultrasonography (US) in a 58-year-old woman. The mass was hypoechoic with continuous eggshell calcification and intranodular vascularity as seen on gray-scale and power Doppler (PD) US. Hu 'rthle cell adenoma should be considered in the differential diagnosis of a thyroid nodule with eggshell calcification

  7. 维生素K2对老年去卵巢大鼠血管钙化的影响%Effect of Vitamin K2 on the Vascular Calcification of Old Ovariectomized Rats

    Institute of Scientific and Technical Information of China (English)

    陈雪英; 杨雅; 游志刚; 丁颖; 吴韦; 姜醒华

    2012-01-01

    Aim To explore the effect of Vitamin K2 on vascular calcifiction in old ovariectomized rats model. Methods Thirty-six ten months female SD rats were allocated into three groups randomly; sham operation group, ovariec-tomized (OVX) group and OVX + Vitamin K2 (OVX + VK2) group. Rats in OVX + VK2 group were administered orally with Vitamin K2 (30 mg( kg ? d) , 5 times a week) after three weeks of ovariectomy for 12 weeks. The urine and serum of all rats were kept every three weeks. All rats were sacrificed after 18 weeks, uterus and arteries were observed by his-tochemical method. The contents of MGP in serum and urine were determined by enzyme-linked immunosorbent assay (ELJSA). Relative quantification of MGP mRNA expression in arterial was detected by Fluorescent real-time quantitative reverse-transcription polymerase chain reaction. Expression of ucMGP was detected by immunochistochemistry. Aterial calcification was evaluated by Von Kossa staining. The content of arterial calcium was measured. Results After 18 weeks of ovariectomized, the pathological section of uterus and aortic had differernt variation in different groups. The con-tent of estrogen in serum had no difference before ovariectomized. Before sacrifice, the content of estrogen of sham group had no change, the other groups reduced (P < 0. 05). The content of MGP in serum and urine had no difference before ovariectomized, the content of MGP in serum and urine decreased in OVX group, the content of MGP in serum and urine decreased and then increased in OVX + VK2 group. Relative quantification of MGP mRNA expression of aterial in OVX + VK2 group was significantly lower than sham group ( P < 0.01) , and was higher than that in OVX group (P < 0.01).The size of ucMGP localized in OVX + VK2 group was less than that in OVX group. The contents of arterial calcium in OVX + VK2 group were higher than that in sham group ( P < 0. 05) and lower than that in OVX group (P < 0. 01). Conclusions Vitamin K2 can improve

  8. Adiponectin attenuates angiotensin II-induced vascular smooth muscle cell remodeling through nitric oxide and the RhoA/ROCK pathway.

    Directory of Open Access Journals (Sweden)

    Wared eNour-Eldine

    2016-04-01

    Full Text Available INTRODUCTION: Adiponectin (APN, an adipocytokine, exerts protective effects on cardiac remodeling, while angiotensin II (Ang II induces hypertension and vascular remodeling. The potential protective role of APN on the vasculature during hypertension has not been fully elucidated yet. Here, we evaluate the molecular mechanisms of the protective role of APN in the physiological response of the vascular wall to Ang II.METHODS AND RESULTS: Rat aortic tissues were used to investigate the effect of APN on Ang II-induced vascular remodeling and hypertrophy. We investigated whether nitric oxide (NO, the RhoA/ROCK pathway, actin cytoskeleton remodeling, and reactive oxygen species (ROS mediate the anti-hypertrophic effect of APN. Ang II-induced protein synthesis was attenuated by pre-treatment with APN, NO donor (SNAP, or cGMP. The hypertrophic response to Ang II was associated with a significant increase in RhoA activation and vascular force production, which were prevented by APN and SNAP. NO was also associated with inhibition of Ang II-induced phosphorylation of cofilin. In addition, immunohistochemistry revealed that 24 hr Ang II treatment increased the F- to G-actin ratio, an effect that was inhibited by SNAP. Ang II-induced ROS formation and upregulation of p22phox mRNA expression were inhibited by APN and NO. Both compounds failed to inhibit Nox1 and p47phox expression. CONCLUSIONS: Our results suggest that the anti-hypertrophic effects of APN are due, in part, to NO-dependent inhibition of the RhoA/ROCK pathway and ROS formation.

  9. Quantitative assessment of abdominal aortic calcification and associations with lumbar intervertebral disc height loss: the Framingham Study.

    Science.gov (United States)

    Suri, Pradeep; Hunter, David J; Rainville, James; Guermazi, Ali; Katz, Jeffrey N

    2012-04-01

    Vascular disease has been proposed as a risk factor for disc height loss (DHL). To examine the relationship between quantitative measures of abdominal aortic calcifications (AACs) as a marker of vascular disease, and DHL, on computed tomography (CT). Cross-sectional study in a community-based population. Four hundred thirty-five participants from the Framingham Heart Study. Quantitative AAC scores assessed by CT were grouped as tertiles of "no" (reference), "low," and "high" calcification. Disc height loss was evaluated on CT reformations using a four-grade scale. For analytic purposes, DHL was dichotomized as moderate DHL of at least one level at L2-S1 versus less than moderate or no DHL. We examined the association of AAC and DHL using logistic regression before and after adjusting for cardiovascular risk factors and before and after adjusting for age, sex, and body mass index (BMI). In crude analyses, low AAC (odds ratio [OR], 2.05 [1.27-3.30]; p=.003) and high AAC (OR, 2.24 [1.38-3.62]; p=.001) were strongly associated with DHL, when compared with the reference group of no AAC. Diabetes, hypercholesterolemia, hypertension, and smoking were not associated with DHL and did not attenuate the observed relationship between AAC and DHL. Adjustment for age, sex, and BMI markedly attenuated the associations between DHL and low AAC (OR, 1.20 [0.69-2.09]; p=.51) and high AAC (OR, 0.74 [0.36-1.53]; p=.42). Abdominal aortic calcification was associated with DHL in this community-based population. This relationship was independent of cardiovascular risk factors. However, the association of AAC with DHL was explained by the effects of age, sex, and BMI. Published by Elsevier Inc.

  10. cAMP attenuates the enhanced expression of Gi proteins and hyperproliferation of vascular smooth muscle cells from SHR: role of ROS and ROS-mediated signaling.

    Science.gov (United States)

    Gusan, Svetlana; Anand-Srivastava, Madhu B

    2013-06-15

    We previously showed that angiotensin II (ANG II)-induced overexpression of inhibitory G proteins (Gi) was attenuated by dibutyryl-cAMP (db-cAMP) in A10 vascular smooth muscle cells (VSMC). Since enhanced levels of endogenous ANG II contributed to the overexpression of Gi protein and hyperproliferation of VSMC from spontaneously hypertensive rats (SHR), the present study was therefore undertaken to examine if cAMP could also attenuate the overexpression of Gi proteins and hyperproliferation of VSMC from SHR and to explore the underlying molecular mechanisms responsible for this response. The enhanced expression of Giα proteins in VSMC from SHR and Nω-nitro-L-arginine methyl ester hypertensive rats was decreased by db-cAMP. In addition, enhanced inhibition of adenylyl cyclase by inhibitory hormones and forskolin-stimulated adenylyl cyclase activity by low concentration of GTPγS in VSMC from SHR was also restored to Wistar-Kyoto (WKY) levels by db-cAMP. Furthermore, db-cAMP also attenuated the hyperproliferation and the increased production of superoxide anion, NAD(P)H oxidase activity, overexpression of Nox1/Nox2/Nox4 and p47phox proteins, increased phosphorylation of PDGF-receptor (R), EGF-R, c-Src, and ERK1/2 to control levels. In addition, the protein kinase A (PKA) inhibitor reversed the effects of db-cAMP on the expression of Nox4 and Giα proteins and hyperproliferation of VSMC from SHR to WKY levels, while stimulation of the exchange protein directly activated by cAMP did not have any effect on these parameters. These results suggest that cAMP via PKA pathway attenuates the overexpression of Gi proteins and hyperproliferation of VSMC from SHR through the inhibition of ROS and ROS-mediated transactivation of EGF-R/PDGF-R and MAPK signaling pathways.

  11. Expression prolife of mitogen-activated protein kinase pathway genes in vascular calcification associated with osteogenic differentiation of smooth muscle cells%平滑肌细胞成骨分化致血管钙化中MAPK信号通路基因的表达谱变化*☆

    Institute of Scientific and Technical Information of China (English)

    金波; 尹恒冲; 汪凌清; 包丽雯; 李延林; 朱军; 施海明

    2013-01-01

      背景:血管钙化是一种细胞介导的主动的、可调控的复杂生物学过程,血管平滑肌细胞转分化为成骨样细胞发挥着重要作用,其确切机制尚不清楚。目的:探讨尿毒症背景下动脉粥样硬化血管钙化的病理生理机制。方法:采用5/6肾切除法建立尿毒症背景下 ApoE-/-小鼠动脉血管钙化模型,苏木精-伊红染色和 Von Kossa染色观察主动脉组织形态学特点,明确造模成功。应用小鼠全基因组Agilent芯片筛查MAPK 信号通路的差异表达基因,实时定量PCR分析验证部分与MAPK信号通路相关的差异表达基因,并结合通路分析来探索MAPK信号通路与血管钙化的内在联系。结果与结论:造模12周后,尿毒症ApoE-/-小鼠主动脉组织形态学特点证实动脉粥样硬化钙化斑块形成。Agilent基因芯片检测结果显示,MAPK信号通路中存在14个差异表达基因,RT-PCR验证结果与芯片检测结果相符合。经KEGG通路分析,ERK1/2信号通路可能在血管钙化的病理生理过程中扮演着重要的角色。说明5/6肾切除ApoE-/-小鼠主动脉钙化斑块形成与MAPK 信号通路激活密切相关,该信号通路可能在平滑肌细胞转分化过程中起着至关重要作用。%BACKGROUND: Vascular calcification is recognized as an active and regulated biological process involving osteoblast-like cell transdifferentiation of vascular smooth muscle cells. However, the precise mechanism of vascular calcification is stil unclear. OBJECTIVE: To explore the pathophysiological mechanism of atherosclerotic calcification in uremic mice. METHODS: The animal model of atherosclerotic calcification in Apolipoprotein E knock-out mice was established with 5/6 nephrectomy. Histomorphological changes of aorta sections of mice were evaluted by hematoxylin-eosin staining and Von Kossa staining to confirm atherosclerotic calcification. The differential y expressed genes in mitogen

  12. Intracranial calcifications. A pictorial review.

    Science.gov (United States)

    Grech, R; Grech, S; Mizzi, A

    2012-09-01

    Brain calcifications are a common radiographic finding. The pathogenesis is diverse and ranges from benign physiological calcifications to a variety of pathological disorders. Whereas certain calcifications are considered an incidental finding, their presence can sometimes be crucial in making a specific diagnosis. Several pathological conditions affecting the brain parenchyma are associated with calcifications and their recognition and location might help in narrowing the differential. Knowledge of physiological calcifications is essential to avoid misinterpretation. This review illustrates a broad spectrum of CNS disorders associated with calcifications, and tries to highlight the salient radiological findings.

  13. Inducers and inhibitors of biomineralization: lessons from pathological calcification.

    Science.gov (United States)

    Giachelli, C M

    2005-11-01

    Ectopic calcification is a common response to soft tissue injury and systemic mineral imbalance and can lead to devastating clinical consequences when present in joints, heart valves and blood vessels. We have hypothesized that mineralization of matrices in any tissue is normally controlled by a balance between procalcific and anticalcific regulatory proteins such that abnormal deposition of apatite is avoided. Alterations in this balance induced by injury, disease or genetic deficiency are postulated to induce ectopic mineral deposition. Over the past several years, we have developed in vitro and in vivo models of ectopic calcification to investigate potential inducers and inhibitors of this process. Osteopontin, a secreted phosphoprotein, has emerged as a major inhibitor of ectopic mineralization. Osteopontin is a potent inhibitor of vascular cell calcification in vitro and mice lacking osteopontin are highly susceptible to ectopic calcification. Furthermore, osteopontin treatment of biomaterials protected against ectopic mineralization. Our studies indicate that in addition to inhibiting apatite crystal initiation and growth, osteopontin stimulates resorption of ectopic calcification via peripheral macrophages and giant cells. In contrast, inorganic phosphate has emerged as a major inducer of mineralization in these systems. Elevated inorganic phosphate (Pi) was shown to induce smooth muscle cell matrix calcification with morphological properties similar to those observed in calcified human valves and atherosclerotic plaques. Furthermore, mineralization induced by inorganic phosphate was dependent on the activity of the sodium-dependent phosphate cotransporter, Pit-1. These studies implicate controlled, transcellular transport of Pi as a major requirement for matrix calcification.

  14. Heme oxygenase-1 alleviates cigarette smoke-induced restenosis after vascular angioplasty by attenuating inflammation in rat model.

    Science.gov (United States)

    Ni, Leng; Wang, Zhanqi; Yang, Genhuan; Li, Tianjia; Liu, Xinnong; Liu, Changwei

    2016-03-14

    Cigarette smoke is not only a profound independent risk factor of atherosclerosis, but also aggravates restenosis after vascular angioplasty. Heme oxygenase-1 (HO-1) is an endogenous antioxidant and cytoprotective enzyme. In this study, we investigated whether HO-1 upregulating by hemin, a potent HO-1 inducer, can protect against cigarette smoke-induced restenosis in rat's carotid arteries after balloon injury. Results showed that cigarette smoke exposure aggravated stenosis of the lumen, promoted infiltration of inflammatory cells, and induced expression of inflammatory cytokines and adhesion molecules after balloon-induced carotid artery injury. HO-1 upregulating by hemin treatment reduced these effects of cigarette smoke, whereas the beneficial effects were abolished in the presence of Zincprotoporphyrin IX, an HO-1 inhibitor. To conclude, hemin has potential therapeutic applications in the restenosis prevention after the smokers' vascular angioplasty. Copyright © 2016. Published by Elsevier Ireland Ltd.

  15. Ectopic calcification in lambs from feeding the plant Cestrum diurnum.

    Science.gov (United States)

    Simpson, C F; Bruss, M L

    1979-01-01

    Hypercalcemia and ectopic calcification were induced in 5 lambs by supplementing the diet with the dried leaves of the plant Cestrum diurnum, for 8 to 9 weeks. Lambs developed mineralization of blood vessels, heart, kidneys, and lungs. These tissues were examined by light and electron microscopy. In the vascular tissue there was calcification of elastic fibers in the hyperplastic intima and the media, along with mineralization of mitochondria of aortic smooth muscle cells. Myocardial cells and their mitochondria were mineralized. In the kidney, there was calcification of the epithelium of the distal convoluted tubules and collecting tubules, Bowman's capsule, and the mesangial cells of the glomeruli. In the lung, there was mineralization of the alveolar septal walls and the bronchi and bronchioles. Feeding of the calcinogenic plant to lambs caused extensive soft tissue calcification. Results of the study indicated that degeneration was the early soft tissue lesion in this plant toxicity.

  16. Implications of Klotho in vascular health and disease

    Institute of Scientific and Technical Information of China (English)

    Ernesto; Martín-Nú?ez; Javier; Donate-Correa; Mercedes; Muros-de-Fuentes; Carmen; Mora-Fernández; Juan; F; Navarro-González

    2014-01-01

    Cardiovascular disease(CVD) is a prevalent condition in general population and the first cause of death overall. Klotho, a pleiotropic protein related to longevity that acts as a co-receptor of the fibroblast growth factor 23, has been proposed as a key regulator of the development of CVD. In the few clinical studies made, it has been observed a relationship between low levels of soluble Klotho and the occurrence and severity of CVD, as well as a reduction of cardiovascular risk when they are high. Also, different polymorphisms of human Klotho gene have been related to the incidence of cardiovascular events. Moreover, several experimental studies indicate that this protein acts in the maintenance of vascular homeostasis. Klotho improves endothelial dysfunction through promotion of NO production and mediates antiinflammatory and anti-aging effects such as suppression of adhesion molecules expression, attenuation of nuclear factor-kappa B or inhibition of Wnt signaling. Furthermore,this protein is related to the attenuation of vascular calcification as well as prevention of cardiac hypertrophy. The expression of this protein in the vascular wall implies a new scenario for the treatment of vascular disorders. The purpose of this review is to provide an overview of the relationship between the Klotho protein and CVD, in addition to its role in the maintenance of functional vascular integrity.

  17. Calcific tendonitis : a model.

    Science.gov (United States)

    Gohr, Claudia M; Fahey, Mark; Rosenthal, Ann K

    2007-01-01

    Calcific tendonitis is a common clinical condition associated with high rates of tendon rupture, prolonged symptoms, and poor response to therapy. Little is known about the pathogenesis of calcifications in tendons and consequently few effective therapies are available. We hypothesized that tendon calcification, like pathologic calcification in other sites, was generated by extracellular organelles known as matrix vesicles and that isolated matrix vesicles would constitute the basis for a useful model of this process. Tendon matrix vesicles were isolated from adult porcine patellar tendons using enzymatic digestion and differential centrifugation. Vesicle morphology was examined with electron microscopy. Levels of calcium, phosphate, pyrophosphate, ATP, and mineralization-associated enzymes were measured and compared with articular cartilage vesicles from porcine articular cartilage. Vesicles were embedded in agarose gels with or without type I collagen or dermatan sulfate and incubated in calcifying salt solution trace labeled with (45)calcium. (45)Calcium in the vesicle fraction was measured after 5-7 days. The type of mineral formed was determined by micro-x-ray diffraction. Matrix vesicles isolated from adult porcine tendon were similar morphologically to those obtained from articular cartilage. They contained mineralization-related enzymes and formed hydroxyapatite mineral in vitro. Mineralization was suppressed by levamisole and modulated by extracellular matrix components. Matrix vesicles isolated from tendons mineralize in vitro. This model may aid in the study of the pathogenesis of calcific tendonitis as well as serve as a means to identify effective therapies for this common disorder.

  18. The vascular secret of Klotho

    DEFF Research Database (Denmark)

    Lewin, Ewa; Olgaard, Klaus

    2015-01-01

    Klotho is an evolutionarily highly conserved protein related to longevity. Increasing evidence of a vascular protecting effect of the Klotho protein has emerged and might be important for future treatments of uremic vascular calcification. It is still disputed whether Klotho is locally expressed ...

  19. Acute Prevertebral Calcific Tendinitis.

    Science.gov (United States)

    Tamm, Alexander; Jeffery, Caroline C; Ansari, Khalid; Naik, Sandeep

    2015-11-01

    We present a case of neck pain in a middle-aged woman, initially attributed to a retropharyngeal infection and treated with urgent intubation. With the help of computed tomography, the diagnosis was later revised to acute prevertebral calcific tendinitis, a self-limiting condition caused by abnormal calcium hydroxyapatite deposition in the longus colli muscles. It is critical to differentiate between these two disease entities due to dramatic differences in management. A discussion of acute prevertebral calcific tendinitis and its imaging findings is provided below.

  20. [Multidetector row CT in assessment of coronary artery calcification on hemodialisis].

    Science.gov (United States)

    Caro, P; Delgado, R; Dapena, F; Núñez, A

    2007-01-01

    Vascular calcification is a strong predictor of cardiovascular and all-cause mortality. Coronary artery calcification is more frequent, more extensive and progresses more rapidly in CKD than in general population. They are also considered a marker of coronary heart disease, with high prevalence and functional significance. It suggests that detection and surveillance may be worthwhile in general clinical practice. New non-invasive image techniques, like Multi-detector row CT, a type of spiral scanner, assess density and volume of calcification at multiple sites and allow quantitative scoring of vascular calcification using calcium scores analogous to those from electron-beam CT. We have assessed and quantified coronary artery calcification with 16 multidetector row CT in 44 patients on hemodialysis and their relationship with several cardiovascular risk factors. Coronary artery calcification prevalence was of 84 % with mean calcium score of 1580 +/- 2010 ( r 0-9844) with calcium score > 400 in 66% of patients. It was usually multiple, affecting more than two vessels in more than 50%. In all but one patient, left anterior descending artery was involved with higher calcium score level at right coronary artery. Advanced age, male, diabetes, smoking, more morbidity, cerebrovascular disease previous, and calcium-binders phosphate and analogous vitamin D treatment would seem to be associated with coronary artery calcification. Coronary artery calcification is very frequent and extensive, usually multiple and associated to modifiable risk factors in hemodialysis patients. Multi-detector-row CT seems an effective, suitable, readily applicable method to assess and quantify coronary artery calcification.

  1. Attenuated NOx responses and myocardial ischemia, a possible risk for structural vascular disease in African men: the SABPA study.

    Science.gov (United States)

    Uys, A S; Malan, L; van Rooyen, J M; Steyn, H S; Reimann, M; Ziemssen, T

    2014-07-01

    Chronically elevated blood pressure has been associated with impaired NO-mediated vasodilation and structural vascular disease risk. This study aimed to determine whether significant associations exist regarding NO metabolite (NOx) responses, cardiovascular function and structural vascular disease in a cohort of African and Caucasian men. The study included 81 African and 94 Caucasian male teachers stratified via median splits into low and high NOx ethnic groups. Ambulatory blood pressure, electrocardiogram monitoring and ultrasound carotid intima-media thickness (CIMT) images were obtained. Cardiovascular measurements and fasting blood for NOx responses were measured during rest and on challenging the cardiovascular system with the Stroop colour-word conflict test. African men displayed significantly higher resting NOx as well as higher number of 24 h silent ischemic events than their Caucasian counterparts. Low NOx African men displayed enhanced α-adrenergic and ECG ST segment depression acute mental stress responses as well as 24 h silent ischemic events associated with CIMT (adjusted R(2) = 0.47; β = 0.25; confidence interval (CI) = 0.13, 0.41). African men demonstrated a vulnerable cardiovascular profile. Novel findings revealed α-adrenergic-driven blood pressure responses and less NO bioavailability during acute stress. The association between myocardial ischemia and CIMT in this group emphasized their risk for future coronary artery disease and cerebrovascular events.

  2. Tetrahydrocurcumin in combination with deferiprone attenuates hypertension, vascular dysfunction, baroreflex dysfunction, and oxidative stress in iron-overloaded mice.

    Science.gov (United States)

    Sangartit, Weerapon; Pakdeechote, Poungrat; Kukongviriyapan, Veerapol; Donpunha, Wanida; Shibahara, Shigeki; Kukongviriyapan, Upa

    2016-12-01

    Excessive iron can generate reactive oxygen species (ROS), leading to oxidative stress that is closely associated with cardiovascular dysfunction. Iron overload was induced in male ICR mice by injection of iron sucrose (10mg/kg/day) for eight weeks. Iron overload was evidenced by increased serum iron indices. The mice developed increased blood pressure, impaired vascular function and blunted response of the autonomic nervous system. These effects were accompanied by increased malondialdehyde levels in various tissues, increased nitric oxide metabolites in plasma and urine, and decreased blood glutathione. Tetrahydrocurcumin (THU, 50mg/kg/day), deferiprone (or L1, 50mg/kg/day) or both was orally administered throughout the period of iron sucrose injection. The treatments significantly alleviated the deleterious cardiovascular effects of iron overload, and were associated with modulation of nitric oxide levels. An imbalance between endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) expression in response to iron overload was normalized by THU, L1 or the combination treatment. Moreover, the treatment decreased the upregulated expression levels of gp91(phox), p47(phox) and HO-1. The combination of THU and L1 exerted a greater effect than THU or L1 monotherapy. These results suggest beneficial effects of THU and L1 on iron-induced oxidative stress, hypertension, and vascular dysfunction.

  3. Neural stimulation does not mediate attenuated vascular response in ACL-deficient knees: potential role of local inflammatory mediators.

    Science.gov (United States)

    Miller, Daniel; Salo, Paul; Hart, David A; Leonard, Catherine; Mammoto, Takeo; Bray, Robert C

    2010-01-01

    Chronic inflammation associated with osteoarthritis (OA) alters normal responses and modifies the functionality of the articular vasculature. Altered responsiveness of the vasculature may be due to excessive neural activity associated with chronic pain and inflammation, or from the production of inflammatory mediators which induce vasodilation. Using laser speckle perfusion imaging (LSPI), blood flow to the medial collateral ligament (MCL) of adult rabbits was measured in denervated ACL transected knees (n = 6) and compared to unoperated control (n = 6) and 6-week anterial cruciate ligament (ACL)-transected knees (n = 6). Phenylephrine and neuropeptide Y were applied to the MCL vasculature in topical boluses of 100 microL (dose range 10(-14) to 10(-8) mol and 10(-14) to 10(-9) mol, respectively). Denervation diminished vasoconstrictive responsiveness to phenylephrine compared to both control and ACL-transected knees. Denervation minimally enhanced vascular responses to neuropeptide Y (NPY) compared to ACL deficiency alone, which nevertheless remained significantly diminished from control responses. To evaluate the potential role of inflammatory dilators in the diminished contractile responses, phenylephrine was coadministered with histamine, substance P, and prostaglandin E(2). High-dose histamine, and low-dose substance P and PGE(2) were able to inhibit contractile responses in the MCL of control knees. Excessive neural input does not mediate diminished vasoconstrictive responses in the ACL transected knee; inflammatory mediators may play a role in the deficient vascular responsiveness of the ACL transected knee.

  4. Intracranial Convexity Lipoma with Massive Calcification: Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Eung Tae; Park, Dong Woo; Ryu, Jeong Ah; Park, Choong Ki; Lee, Young Jun; Lee, Seung Ro [Dept. of Radiology, Hanyang University College of Medicine, Seoul (Korea, Republic of)

    2011-12-15

    Intracranial lipoma is a rare entity, accounting for less than 0.5% of intracranial tumors, which usually develops in the callosal cisterns. We report a case of lipoma with an unusual location; in the high parietal convexity combined with massive calcification, and no underlying vascular malformation or congenital anomaly.

  5. The realm of vitamin K dependent proteins: shifting from coagulation toward calcification.

    Science.gov (United States)

    Willems, Brecht A G; Vermeer, Cees; Reutelingsperger, Chris P M; Schurgers, Leon J

    2014-08-01

    In the past few decades vitamin K has emerged from a single-function "haemostasis vitamin" to a "multi-function vitamin." The use of vitamin K antagonists (VKA) inevitably showed that the inhibition was not restricted to vitamin K dependent coagulation factors but also synthesis of functional extrahepatic vitamin K dependent proteins (VKDPs), thereby eliciting undesired side effects. Vascular calcification is one of the recently revealed detrimental effects of VKA. The discovery that VKDPs are involved in vascular calcification has propelled our mechanistic understanding of this process and has opened novel avenues for diagnosis and treatment. This review addresses mechanisms of VKDPs and their significance for physiological and pathological calcification.

  6. Sensitivity of Different Evaluation Methods for Peripheral Vascular Calcifi-cation in Patients with Uremia and Receiving Hemodialysis%不同方法评价尿毒症血液透析患者外周血管钙化探究

    Institute of Scientific and Technical Information of China (English)

    李根; 王晶

    2015-01-01

    目的:比较各类尿毒症血液透析患者外周血管钙化评价方法的敏感性和差异性。方法随机选择该院于2013年1月-2014年7月该院收治的30例尿毒症且长期血液透析患者作为研究对象,30例患者因动静脉内瘘失功,在该院行内瘘重建术。术前该组患者均行彩色多普勒超声、X线检查,获得桡动脉血管钙化结果。比较两种检查方法的敏感性。结果术前多普勒超声检查动脉血管钙化检出率为16.7%;X线摄片检查,检出率为33.3%。两种评估方法(两类影像学检测方法),差异有统计学意义(P<0.05)。影像学方法中,X线摄片检查的检出率最高。结论长期接受血液透析的尿毒症患者多存在外周血管钙化,提示临床治疗中应注意外周血管钙化的诊断;X线摄片检查是影像学检测中较为敏感性的评估方法,应作为首选评估方法。%Objective To compare the sensitivity of different evaluation methods for peripheral vascular calcification in patients with uremia and receiving hemodialysis. Methods 30 patients with uremia who were admitted to our hospital from January 2013 July 2014 July and receiving long-term hemodialysis patients were selected as research subjects. All of them received fistula re-construction for arteriovenous internal fistula dysfunction. Before operation, color Doppler ultrasound and X-ray examination were performed on all patients to obtain the radial artery calcification results. Sensitivity of two methods of inspection was compared. Results The preoperative Doppler ultrasonography arterial calcification detection rate was 16.7%;X-ray examination, the detection rate was 33.3%. Two assessment methods (detection method for two kinds of imaging), the significant difference of P< 0.05 was considered statistically significant. Imaging method, X-ray examination of the highest detection rate. Conclusion Long term accep-tance of uremic patients with hemodialysis exists

  7. Pineal calcification among black patients.

    Science.gov (United States)

    Fan, K J

    1983-08-01

    A postmortem histopathological study was done in 233 pineal glands of black patients. Among them, 70 percent showed microscopic evidence of calcification in the pineal parenchyma. The frequency of calcification increased with age. However, the severity of calcification reached the peak in the 60 to 69 year old age group and then gradually declined. As compared to males, females had slightly higher frequency and reached the peak of severity in younger age groups. When pineal calcification was compared among patients with various malignancies, a higher frequency and more severe calcification were observed in patients with carcinoma of the prostate and the pancreas. A lower frequency and less severe calcification were observed in patients with carcinoma of the breast and the cervix. The results of this study emphasize the important role of sex hormone in genesis of pineal calcification.

  8. Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells.

    Directory of Open Access Journals (Sweden)

    Li-Long Pan

    Full Text Available BACKGROUND: Hydrogen sulfide (H(2S, the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2S donor on tumor necrosis factor (TNF-α-induced human umbilical vein endothelial cells (HUVEC dysfunction. METHODOLOGY AND PRINCIPAL FINDINGS: Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1, mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1, was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS. SIGNIFICANCE: H(2S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1.

  9. DHEA attenuates PDGF-induced phenotypic proliferation of vascular smooth muscle A7r5 cells through redox regulation

    Energy Technology Data Exchange (ETDEWEB)

    Urata, Yoshishige; Goto, Shinji; Kawakatsu, Miho [Department of Biochemistry and Molecular Biology in Disease, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Medical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523 (Japan); Yodoi, Junji [Department of Biological Responses, Institute for Viral Research, Graduate School of Medicine, Kyoto University, 53 Shogain, Kawahara-cho, Sakyo-ku, Kyoto 606-8397 (Japan); Eto, Masato [Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 (Japan); Akishita, Masahiro, E-mail: akishita-tky@umin.ac.jp [Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 (Japan); Kondo, Takahito [Department of Biochemistry and Molecular Biology in Disease, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Medical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523 (Japan)

    2010-05-28

    It is known that dehydroepiandrosterone (DHEA) inhibits a phenotypic switch in vascular smooth muscle cells (VSMC) induced by platelet-derived growth factor (PDGF)-BB. However, the mechanism behind the effect of DHEA on VSMC is not clear. Previously we reported that low molecular weight-protein tyrosine phosphatase (LMW-PTP) dephosphorylates PDGF receptor (PDGFR)-{beta} via a redox-dependent mechanism involving glutathione (GSH)/glutaredoxin (GRX)1. Here we demonstrate that the redox regulation of PDGFR-{beta} is involved in the effect of DHEA on VSMC. DHEA suppressed the PDGF-BB-dependent phosphorylation of PDGFR-{beta}. As expected, DHEA increased the levels of GSH and GRX1, and the GSH/GRX1 system maintained the redox state of LMW-PTP. Down-regulation of the expression of LMW-PTP using siRNA restored the suppression of PDGFR-{beta}-phosphorylation by DHEA. A promoter analysis of GRX1 and {gamma}-glutamylcysteine synthetase ({gamma}-GCS), a rate-limiting enzyme of GSH synthesis, showed that DHEA up-regulated the transcriptional activity at the peroxisome proliferator-activated receptor (PPAR) response element, suggesting PPAR{alpha} plays a role in the induction of GRX1 and {gamma}-GCS expression by DHEA. In conclusion, the redox regulation of PDGFR-{beta} is involved in the suppressive effect of DHEA on VSMC proliferation through the up-regulation of GSH/GRX system.

  10. Pulmonary metastatic calcification: a case report

    Energy Technology Data Exchange (ETDEWEB)

    Bozi, Lilian Christine Franchiotti [Radiology, Hospital Universitario Antonio Pedro (HUAP), Niteroi, RJ (Brazil); Melo, Alessandro Severo Alves de; Marchiori, Edson, E-mail: edmarchiori@gmail.com [Department of Radiology, School of Medicine, Universidade Federal Fluminense (UFF), Niteroi, RJ (Brazil)

    2012-09-15

    The present report describes the case of a 48-year-old female patient suffering from chronic renal failure on dialysis for 13 years. She presented with hemoptysis, fever, productive cough and dyspnoea. Chest radiography showed predominance of ill-defined opacities in the middle and lower lung fields, bilaterally. Chest computed tomography showed ground glass opacities associated with poorly defined centrilobular nodules with ground-glass attenuation. The patient was submitted to bronchoalveolar lavage that was negative for mycobacteria and fungi. On the basis of such findings, open lung biopsy was performed, which revealed metastatic pulmonary calcification. (author)

  11. Protein kinase C inhibition attenuates vascular ETB receptor upregulation and decreases brain damage after cerebral ischemia in rat

    Directory of Open Access Journals (Sweden)

    Vikman Petter

    2007-01-01

    Full Text Available Abstract Background Protein kinase C (PKC is known to be involved in the pathophysiology of experimental cerebral ischemia. We have previously shown that after transient middle cerebral artery occlusion, there is an upregulation of endothelin receptors in the ipsilateral middle cerebral artery. The present study aimed to examine the effect of the PKC inhibitor Ro-32-0432 on endothelin receptor upregulation, infarct volume and neurology outcome after middle cerebral artery occlusion in rat. Results At 24 hours after transient middle cerebral artery occlusion (MCAO, the contractile endothelin B receptor mediated response and the endothelin B receptor protein expression were upregulated in the ipsilateral but not the contralateral middle cerebral artery. In Ro-32-0432 treated rats, the upregulated endothelin receptor response was attenuated. Furthermore, Ro-32-0432 treatment decreased the ischemic brain damage significantly and improved neurological scores. Immunohistochemistry showed fainter staining of endothelin B receptor protein in the smooth muscle cells of the ipsilateral middle cerebral artery of Ro-32-0432 treated rats compared to control. Conclusion The results suggest that treatment with Ro-32-0432 in ischemic stroke decreases the ischemic infarction area, neurological symptoms and associated endothelin B receptor upregulation. This provides a new perspective on possible mechanisms of actions of PKC inhibition in cerebral ischemia.

  12. 血液透析患者血清软骨寡聚基质蛋白浓度与血管钙化及心血管事件关系的探讨%The correlation of plasma cartilage oligomeric matrix protein with vascular calcification and cardiovascular events in hemodialysis patients

    Institute of Scientific and Technical Information of China (English)

    赵伟; 戈艳蕾; 王田力; 孔炜; 王悦

    2011-01-01

    目的 探讨血液透析患者血清软骨寡聚基质蛋白(cartilage oligomeric matrix protein,COMP)浓度与血管钙化及心血管事件的关系.方法 比较血液透析患者与正常对照组血清COMP浓度的差异,且根据患者血清COMP水平,将北京大学第三医院血液净化中心54例维持性血液透析患者分成高、低浓度2组,胸片法评估2组间基线血管钙化情况,并随访20个月,观察2组间心血管事件的发生情况.结果 低浓度组和高浓度组的基线血管钙化发生率分别是64.5%(20/31)和91.3%(21/23),差异有统计学意义(x2=5.184,P=0.023),相应的随访过程中心血管事件的发生率分别是10.4%(3/29)和40.9%(9/22),差异有统计学意义(x2=6.495,P=0.011).回归分析提示高浓度血清COMP是维持性血液透析患者发生严重心血管事件的预测因素之一.结论 血液透析患者血清COMP浓度可能是血管钙化及心血管事件的危险因素.%Objective To investigate the correlation of plasma cartilage oligomeric matrix protein (COMP)with vascular calcification and cardiovascular events in hemodialysis patients. Methods Plasma COMP levels in hemodialysis patients and normal controls were determined and analyzed. Fifty-four hemodialysis patients were divided into two groups based on plasma COMP level, and they were followed up for 20 months. Vascular calcification of thoracic aorta was evaluated by chest X-ray examination at the beginning. Cardiovascular events were analyzed at the end of the follow-up period. Results At the beginning of the follow-up period, vascular calcification was detected in 20/31 and 21/23 patients in the low COMP group and the high COMP group, respectively (64.5% vs. 91.3%, P =0.023). During the follow-up period, cardiovascular events were found in 3/29 and 9/22 patients in the low COMP group and the high COMP group, respectively (10.4% vs. 40.9%, p=0.011). Regression analysis showed that higher plasma COMP level was one of risk

  13. Rectus Femoris Tendon Calcification

    Science.gov (United States)

    Zini, Raul; Panascì, Manlio; Papalia, Rocco; Franceschi, Francesco; Vasta, Sebastiano; Denaro, Vincenzo

    2014-01-01

    Background: Since it was developed, hip arthroscopy has become the favored treatment for femoroacetabular impingement. Due to recent considerable improvements, the indications for this technique have been widely extended. Injuries of the rectus femoris tendon origin, after an acute phase, could result in a chronic tendinopathy with calcium hydroxyapatite crystal deposition, leading to pain and loss of function. Traditionally, this condition is addressed by local injection of anesthetic and corticosteroids or, when conservative measures fail, by open excision of the calcific lesion by an anterior approach. Purpose: To assess whether arthroscopic excision of calcification of the proximal rectus is a safe and effective treatment. Study Design: Case series; Level of evidence, 4. Methods: Outcomes were studied from 6 top amateur athletes (age range, 30-43 years; mean, 32.6 years) affected by calcification of the proximal rectus who underwent arthroscopic excision of the calcification. Patients were preoperatively assessed radiographically, and diagnosis was confirmed by a 3-dimensional computed tomography scan. To evaluate the outcome, standardized hip rating scores were used pre- and postoperatively (at 6 and 12 months): the Hip disability and Osteoarthritis Outcome Score, Oxford Hip Score, and Modified Harris Hip Score. Moreover, visual analog scales (VAS) for pain, sport activity level (SAL), and activities of daily living (ADL) were also used. Results: One year after surgery, all patients reported satisfactory outcomes, with 3 of 6 rating their return-to-sport level as high as preinjury level, and the remaining 3 with a percentage higher than 80%. Five patients ranked their ability to carry on daily activities at 100%. Statistical analysis showed significant improvement of the Oxford Hip Score, the Modified Harris Hip Score, and all 3 VAS subscales (pain, SAL, and ADL) from pre- to latest postoperative assessment (P < .05). Conclusion: Arthroscopic excision of

  14. Transduction of interleukin-10 through renal artery attenuates vascular neointimal proliferation and infiltration of immune cells in rat renal allograft.

    Science.gov (United States)

    Xie, Jingxin; Li, Xueyi; Meng, Dan; Liang, Qiujuan; Wang, Xinhong; Wang, Li; Wang, Rui; Xiang, Meng; Chen, Sifeng

    2016-08-01

    Renal transplantation is the treatment of choice for end-stage renal failure. Although acute rejection is not a major issue anymore, chronic rejection, especially vascular rejection, is still a major factor that might lead to allograft dysfunction on the long term. The role of the local immune-regulating cytokine interleukin-10 (IL-10) in chronic renal allograft is unclear. Many clinical observations showed that local IL-10 level was negatively related to kidney allograft function. It is unknown this negative relationship was the result of immunostimulatory property or insufficient immunosuppression property of local IL-10. We performed ex vivo transduction before transplantation through artery of the renal allograft using adeno-associated viral vectors carrying IL-10 gene. Twelve weeks after transplantation, we found intrarenal IL-10 gene transduction significantly inhibited arterial neointimal proliferation, the number of occluded intrarenal artery, interstitial fibrosis, peritubular capillary congestion and glomerular inflammation in renal allografts compared to control allografts receiving PBS or vectors carrying YFP. IL-10 transduction increased serum IL-10 level at 4 weeks but not at 8 and 12 weeks. Renal IL-10 level increased while serum creatinine decreased significantly in IL-10 group at 12 weeks compared to PBS or YFP controls. Immunohistochemical staining showed unchanged total T cells (CD3) and B cells (CD45R/B220), decreased cytotoxic T cells (CD8), macrophages (CD68) and increased CD4+ and FoxP3+ cells in IL-10 group. In summary, intrarenal IL-10 inhibited the allograft rejection while modulated immune response.

  15. MORPHOLOGICAL QUANTIFICATION OF AORTIC CALCIFICATION FROM LOW MAGNIFICATION IMAGES

    Directory of Open Access Journals (Sweden)

    Jesús Angulo

    2011-05-01

    Full Text Available Atherosclerotic and medial vascular calcifications are frequent in chronic renal failure patiens and predict their increased cardiovascular mortality. Experimental models for mice have been recently developed in order to study these disorders. The aim of this paper is to present the morphological image processing algorithms developed for the semi-automated measurement of calcification from sections of aorta stained using von Kossa's silver nitrate procedure and acquired at low magnification power (x 2.5 on colour images. The approach is separated into two sequential phases. First, the segmentation is aimed to extract the calcification structures and on the other hand to demarcate the region of the atherosclerotic lesion within the tissue. The segmentation yields the image data which is the input to the second phase, the quantification. Calcified structures are measured inside and outside the lesion using a granulometric curve which allows the calculation of statistical parameters of size. The same operator computes the shape of the lesion. The relative proportion of the area of calcification is also calculated respectively for the atherosclerotic lesion area and the area outside such lesions. In conclusion, the here developed method allows quantification of vascular calcified deposits in mouse aorta. This method will be useful for the quantitative assessment of pathological vascular changes in animals and man.

  16. Bilateral acute corneal calcification.

    Science.gov (United States)

    Freddo, T F; Leibowitz, H M

    1985-04-01

    A 38-year-old man with brittle, juvenile onset diabetes mellitus and bilateral severe dry eyes with recurrent corneal ulcers developed atypical band-shaped calcifications of both corneas during a 24-hour period. Serum calcium, phosphate, and carbon dioxide levels all were within normal limits. The patient was mildly uremic but was not in renal failure. When EDTA chelation failed to clear the deposits, partial keratectomies were performed in both eyes and the specimens were examined by light and electron microscopy, including energy dispersive x-ray analysis. Microscopic studies revealed an atypical calcific keratopathy which involved neither Bowman's layer nor the most superficial stromal lamellae. The deposits were confined to deeper lamellae in the anterior stroma and by electron microscopy were composed of extracellular crystalline aggregates. Energy dispersive x-ray analysis of these aggregates confirmed the presence of calcium and phosphate. Corneal dessication appeared to be a major contributing factor in the rapid formation of these deposits.

  17. Yes-Associated Protein Inhibits Transcription of Myocardin and Attenuates Differentiation of Vascular Smooth Muscle Cell from Cardiovascular Progenitor Cell Lineage.

    Science.gov (United States)

    Wang, Lunchang; Qiu, Ping; Jiao, Jiao; Hirai, Hiroyuki; Xiong, Wei; Zhang, Jifeng; Zhu, Tianqing; Ma, Peter X; Chen, Y Eugene; Yang, Bo

    2017-02-01

    Vascular smooth muscle cells (VSMCs) derived from cardiovascular progenitor cell (CVPC) lineage populate the tunica media of the aortic root. Understanding differentiation of VSMCs from CVPC will further our understanding of the molecular mechanisms contributing to aortic root aneurysms, and thus, facilitate the development of novel therapeutic agents to prevent this devastating complication. It is established that the yes-associated protein (YAP) and Hippo pathway is important for VSMC proliferation and phenotype switch. To determine the role of YAP in differentiation of VSMCs from CVPCs, we utilized the in vitro monolayer lineage specific differentiation method by differentiating human embryonic stem cells into CVPCs, and then, into VSMCs. We found that expression of YAP decreased during differentiation of VSMC from CVPCs. Overexpression of YAP attenuated expression of VSMC contractile markers and impaired VSMC function. Knockdown of YAP increased expression of contractile proteins during CVPC-VSMCs differentiation. Importantly, expression of YAP decreased transcription of myocardin during this process. Overexpression of YAP in PAC1 SMC cell line inhibited luciferase activity of myocardin proximal promoter in a dose dependent and NKX2.5 dependent manners. YAP protein interacted with NKX2.5 protein and inhibited binding of NKX2.5 to the 5'-proximal promoter region of myocardin in CVPC-derived VSMCs. In conclusion, YAP negatively regulates differentiation of VSMCs from CVPCs by decreasing transcription of myocardin in a NKX2.5-dependent manner. Stem Cells 2017;35:351-361.

  18. Idiopathic arterial calcification in childhood

    Energy Technology Data Exchange (ETDEWEB)

    Patel, Maya [Department of Paediatric Radiology, Red Cross Children' s Hospital, Cape Town (South Africa); Red Cross Children' s Hospital, School of Child and Adolescent Health, University of Cape Town, Klipfontein Road, Rondebosch, Cape Town (South Africa); Andronikou, Savvas; Solomon, Rustum; Sinclair, Paul; McCulloch, Mignon [Department of Paediatric Radiology, Red Cross Children' s Hospital, Cape Town (South Africa)

    2004-08-01

    Idiopathic arterial calcification in infancy is usually fatal with death in early life and diagnosis at post mortem. This report describes a unique, late presentation with hypertension and cardiac failure in a child aged 33 months, found to have widespread arterial calcification at radiological imaging. The calcium-phosphate axis was normal and there was no other demonstrable cause for calcification. Additionally, the histological features of arterial calcification at renal biopsy paralleled the findings in infants with this disorder. The late presentation in this case is unusual and has not been previously reported. Ultrasound and CT are sensitive for calcification, and the disease should be suspected in children presenting with cardiac or respiratory manifestations and features of arterial calcification, where no metabolic cause is established. (orig.)

  19. Medial arterial calcification, calcific aortic stenosis and mitral annular calcification in a diabetic patient with severe autonomic neuropathy.

    LENUS (Irish Health Repository)

    Cronin, C C

    2012-02-03

    Medial arterial calcification (Monckeberg\\'s arteriosclerosis) is well described in diabetic patients with autonomic neuropathy. There is also a high prevalence of diabetes mellitus among subjects with calcific aortic stenosis and mitral annular calcification. We describe a diabetic patient with autonomic neuropathy and extensive medial arterial calcification who also had calcification of the aortic valve and of the mitral valve annulus. We propose that autonomic neuropathy may play a role in calcification of these structures at the base of the heart.

  20. Arterial calcification: Conscripted by collagen

    Science.gov (United States)

    Miller, Jordan D.

    2016-03-01

    In atherosclerotic plaques, patterns of calcification -- which have profound implications for plaque stability and vulnerability to rupture -- are determined by the collagen's content and patterning throughout the plaque.

  1. Intervertebral disc calcifications in children.

    Science.gov (United States)

    Beluffi, G; Fiori, P; Sileo, C

    2009-03-01

    This study was done to assess the presence of both asymptomatic and symptomatic intervertebral disc calcifications in a large paediatric population. We retrospectively reviewed the radiographs taken during the past 26 years in children (age 0-18 years) undergoing imaging of the spine or of other body segments in which the spine was adequately depicted, to determine possible intervertebral disc calcifications. The following clinical evaluation was extrapolated from the patients' charts: presence of spinal symptoms, history of trauma, suspected or clinically evident scoliosis, suspected or clinically evident syndromes, bone dysplasias, and pre- or postoperative chest or abdominal X-rays. We detected intervertebral disc calcifications in six patients only. Five calcifications were asymptomatic (one newborn baby with Patau syndrome; three patients studied to rule out scoliosis, hypochondroplasia and syndromic traits; one for dyspnoea due to sunflower seeds inhalation). Only one was symptomatic, with acute neck pain. Calcifications varied in number from one in one patient to two to five in the others. Apart from the calcification in the patient with cervical pain, all calcifications were asymptomatic and constituted an incidental finding (particularly those detected at the thoracic level in the patient studied for sunflower-seed inhalation). Calcification shapes were either linear or round. Our series confirms that intervertebral disc calcifications are a rare finding in childhood and should not be a source of concern: symptomatic calcifications tend to regress spontaneously within a short time with or without therapy and immobilisation, whereas asymptomatic calcifications may last for years but disappear before the age of 20 years. Only very few cases, such as those of medullary compression or severe dysphagia due to anterior herniation of cervical discs, may require surgical procedures.

  2. Gene expression analysis in calcific tendinopathy of the rotator cuff

    Directory of Open Access Journals (Sweden)

    F Oliva

    2011-06-01

    Full Text Available We evaluated the expression of several genes involved in tissue remodelling and bone development in patients with calcific tendinopathy of the rotator cuff. Biopsies from calcified and non-calcified areas were obtained from 10 patients (8 women and 2 men; average age: 55 years; range: 40-68 with calcific tendinopathy of the rotator cuff. To evaluate the expression of selected genes, RNA extraction, cDNA synthesis and quantitative polymerase chain reaction (PCR were performed. A significantly increased expression of tissue transglutaminase (tTG2 and its substrate, osteopontin, was detected in the calcific areas compared to the levels observed in the normal tissue from the same subject with calcific tendinopathy, whereas a modest increase was observed for catepsin K. There was also a significant decrease in mRNA expression of Bone Morphogenetic Protein (BMP4 and BMP6 in the calcific area. BMP-2, collagen V and vascular endothelial growth factor (VEGF did not show significant differences. Collagen X and matrix metalloproteinase (MMP-9 were not detectable. A variation in expression of these genes could be characteristic of this form tendinopathy, since an increased level of these genes has not been detected in other forms of tendon lesions.

  3. Arterial calcification: A new perspective?

    Science.gov (United States)

    Nicoll, R; Henein, M

    2017-02-01

    Arterial calcification is commonly seen in atherosclerosis, chronic kidney disease (CKD) and diabetes and has long been considered a natural progression of atherosclerosis. Yet it is a systemic condition, occurring in a wide and diverse range of disease states and no medical treatment for cardiovascular disease has yet found a way to regress it; on the contrary, lipid-lowering therapy may worsen its progression. Although numerous studies have found associations between calcification and biomarkers, none has yet found a unifying mechanism that explains the calcification found in atherosclerosis, CKD or diabetes and many of the biomarkers are equally associated with atheroma development and cardiovascular events. Furthermore, both presence and absence of coronary artery calcification appear predictive of plaque rupture and cardiovascular events, indicating that the association is not causal. This suggests that we are no further forward in understanding the true nature of arterial calcification or its pathogenesis, other than noting that it is 'multifactorial'. This is because most researchers view arterial calcification as a progressive pathological condition which must be treated. Instead, we hypothesise that calcification develops as an immune response to endothelial injury, such as shear stress or oxidative stress in diabetics, and is consequently part of the body's natural defences. This would explain why it has been found to be protective of plaque rupture and why it is unresponsive to lipid-lowering agents. We propose that instead of attempting to treat arterial calcification, we should instead be attempting to prevent or treat all causes of endothelial injury.

  4. The role of vitamin K in soft-tissue calcification.

    Science.gov (United States)

    Theuwissen, Elke; Smit, Egbert; Vermeer, Cees

    2012-03-01

    Seventeen vitamin K-dependent proteins have been identified to date of which several are involved in regulating soft-tissue calcification. Osteocalcin, matrix Gla protein (MGP), and possibly Gla-rich protein are all inhibitors of soft-tissue calcification and need vitamin K-dependent carboxylation for activity. A common characteristic is their low molecular weight, and it has been postulated that their small size is essential for calcification inhibition within tissues. MGP is synthesized by vascular smooth muscle cells and is the most important inhibitor of arterial mineralization currently known. Remarkably, the extrahepatic Gla proteins mentioned are only partly carboxylated in the healthy adult population, suggesting vitamin K insufficiency. Because carboxylation of the most essential Gla proteins is localized in the liver and that of the less essential Gla proteins in the extrahepatic tissues, a transport system has evolved ensuring preferential distribution of dietary vitamin K to the liver when vitamin K is limiting. This is why the first signs of vitamin K insufficiency are seen as undercarboxylation of the extrahepatic Gla proteins. New conformation-specific assays for circulating uncarboxylated MGP were developed; an assay for desphospho-uncarboxylated matrix Gla protein and another assay for total uncarboxylated matrix Gla protein. Circulating desphospho-uncarboxylated matrix Gla protein was found to be predictive of cardiovascular risk and mortality, whereas circulating total uncarboxylated matrix Gla protein was associated with the extent of prevalent arterial calcification. Vitamin K intervention studies have shown that MGP carboxylation can be increased dose dependently, but thus far only 1 study with clinical endpoints has been completed. This study showed maintenance of vascular elasticity during a 3-y supplementation period, with a parallel 12% loss of elasticity in the placebo group. More studies, both in healthy subjects and in patients at risk

  5. A small molecule PAI-1 functional inhibitor attenuates neointimal hyperplasia and vascular smooth muscle cell survival by promoting PAI-1 cleavage.

    Science.gov (United States)

    Simone, Tessa M; Higgins, Stephen P; Archambeault, Jaclyn; Higgins, Craig E; Ginnan, Roman G; Singer, Harold; Higgins, Paul J

    2015-05-01

    Plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of urokinase-and tissue-type plasminogen activators (uPA and tPA), is an injury-response gene implicated in the development of tissue fibrosis and cardiovascular disease. PAI-1 mRNA and protein levels were elevated in the balloon catheter-injured carotid and in the vascular smooth muscle cell (VSMC)-enriched neointima of ligated arteries. PAI-1/uPA complex formation and PAI-1 antiproteolytic activity can be inhibited, via proteolytic cleavage, by the small molecule antagonist tiplaxtinin which effectively increased the VSMC apoptotic index in vitro and attenuated carotid artery neointimal formation in vivo. In contrast to the active full-length serine protease inhibitor (SERPIN), elastase-cleaved PAI-1 (similar to tiplaxtinin) also promoted VSMC apoptosis in vitro and similarly reduced neointimal formation in vivo. The mechanism through which cleaved PAI-1 (CL-PAI-1) stimulates apoptosis appears to involve the TNF-α family member TWEAK (TNF-α weak inducer of apoptosis) and it's cognate receptor, fibroblast growth factor (FGF)-inducible 14 (FN14). CL-PAI-1 sensitizes cells to TWEAK-stimulated apoptosis while full-length PAI-1 did not, presumably due to its ability to down-regulate FN14 in a low density lipoprotein receptor-related protein 1 (LRP1)-dependent mechanism. It appears that prolonged exposure of VSMCs to CL-PAI-1 induces apoptosis by augmenting TWEAK/FN14 pro-apoptotic signaling. This work identifies a critical, anti-stenotic, role for a functionally-inactive (at least with regard to its protease inhibitory function) cleaved SERPIN. Therapies that promote the conversion of full-length to cleaved PAI-1 may have translational implications.

  6. Inhibition of angiotensin Ⅱ and blockade of endothelin receptors reduce arterial calcification in rats

    Institute of Scientific and Technical Information of China (English)

    Juxiang LI; Shengying WU; Chunshui PAN; Yongfen QI; Bin GENG; Xiuhua LIU; Chaoshu TANG

    2004-01-01

    Objective To examine whether the two vascular paracrine/autocrine factors, angiotensin Ⅱ (Ang Ⅱ) and endothelin, participate in the pathogenesis of arterial calcification. Methods Nicotine and vitamin D3 treated rats were studied. Vascular calcification was confirmed by using Von Kossa staining, measurement of calcium content,45Ca2+ uptake assay and alkaline phosphatase (ALP) activity. The plasma and vascular Ang Ⅱ and endothelin levels were measured by using radioimmunoassay. Angiotensinogen and endothelin mRNA levels were determined by RTPCR. Results The arterial calcium content, 45Ca2+ uptake and ALP activity were increased in calcification groups compared with control ( P < 0.01 ). Administration of the angiotensin receptor antagonist losartan, the endothelin receptor antagonist bosentan, and the angiotensin-converting enzyme inhibitor captopril reduced significantly the arterial calcium content, 45Ca2+ uptake and ALP activity. In addition, the plasma and aortic Ang Ⅱ and endothelin contents, and vascular angiotensinogen and endothelin mRNA expression were significantly up-regulated ( P <0.05).Conclusions These findings suggest that functional renin-angiotensin system and endothelin pathway are involved in vascular calcification, and that activation of these systems could potentiate pathogenesis of arterial calcification. ( J Geriatr Cardiol 2004;1(2) :108-113. )

  7. [Calcification in nonfunctioning transplanted kidneys].

    Science.gov (United States)

    Peces, R; Sánchez, R J; Fernández, E J; Peces, C

    2007-01-01

    Failed renal allografts often are left in situ in patients who revert to chronic dialysis therapy or who undergo retransplantation. These organs may be the site of massive calcification despite their lack of physiological function. Calcification of an endstage renal allograft is sometimes found incidentally. We report here two patients who developed extensive calcification of the renal graft, one was on chronic hemodialysis and the other had a second renal transplantation with normal renal function. The precise pathogenesis of calcification and the factors which determine its tissue localization are unclear. Factors postulated to promote the development of metastatic calcification include an elevated calcium phosphate product, severe secondary hyperparathyroidism, aluminium toxicity and duration of dialytic therapy. In some cases local factors related with the chronic inflammatory rejection process are probably involved as well. However, the exact relative contribution of these factors remains unresolved. Unless specific clinical indications are present, transplant nephrectomy is not necessary for calcified end-stage renal allografts.

  8. Aortic Arch Calcification Predicts Cardiovascular and All-Cause Mortality in Maintenance Hemodialysis Patients

    OpenAIRE

    Mizuki Komatsu; Masayuki Okazaki; Ken Tsuchiya; Hiroshi Kawaguchi; Kosaku Nitta

    2014-01-01

    Background/Aim: Vascular calcification is associated with cardiovascular risk in maintenance hemodialysis (MHD) patients. Previous reports have shown that simple assessment of aortic arch calcification (AoAC) using plain radiography is associated with cardiovascular mortality in the general population. We conducted a prospective study to investigate factors associated with the presence at baseline and progression of AoAC in MHD patients and examined its prognostic value in a short-term outcom...

  9. Unicentric Castleman's disease of the pancreas with massive central calcification

    Institute of Scientific and Technical Information of China (English)

    Oliver Goetze; Matthias Banasch; Klaus Junker; Wolfgang E. Schmidt; Christian Szymanski

    2005-01-01

    Unicentric Castleman's disease of the pancreas is extremely rare, with only six cases described in the worldwide literature.An asymptomatic case of unicentric, hyaline, vascular-type Castleman's disease (UCD) localized to the tail of the pancreas with central calcification imitating a primary neoplasm of the pancreas is presented. This is the first description of endosonographic and endoscopic retrograde pancreatographic findings of pancreatic UCD. Additionally, computed tomography, histological and serologic findings are reported.

  10. Extra-coronary calcification (aortic valve calcification, mitral annular calcification, aortic valve ring calcification and thoracic aortic calcification) in HIV seropositive and seronegative men: Multicenter AIDS Cohort Study.

    OpenAIRE

    Rezaeian, P.; Miller, PE; Haberlen, SA; Razipour, A; Bahrami, H; Castillo, R.; Witt, MD; Kingsley, L; Palella, FJ; Nakanishi, R; Matsumoto, S.; Alani, A; Jacobson, LP; Post, WS; Budoff, MJ

    2016-01-01

    Previous studies have demonstrated an association between HIV infection and coronary artery disease (CAD); little is known about potential associations between HIV infection and extra-coronary calcification (ECC).We analyzed 621 HIV infected (HIV+) and 384 HIV uninfected (HIV-) men from the Multicenter AIDS Cohort Study who underwent non-contrast computed tomography (CT) from 2010-2013. Agatston scores were calculated for mitral annular calcification (MAC), aortic valve calcification (AVC), a...

  11. [Eight cases of calcific retropharyngeal tendinitis/retropharyngeal calcific tendinitis].

    Science.gov (United States)

    Ohtsuka, Yuichiro; Chazono, Hideaki; Suzuki, Homare; Ohkuma, Yusuke; Sakurai, Toshioki; Hanazawa, Toyoyuki; Okamoto, Yoshitaka

    2013-11-01

    Calcific retropharyngeal tendinitis/retropharyngeal calcific tendinitis is an inflammation of the longus colli muscle caused by calcium hydroxyapatite crystal depositon in the longus colli muscle tendon. The three major symptoms are neck pain, limitations of neck movement, and swallowing pain. We treated 8 cases of calcific retropharyngeal tendinitis/ retropharyngeal calcific tendinitis. Each patient complained of neck pain, limitations of neck movement, and swallowing pain. The only local finding was the smooth swelling of the posterior pharyngeal wall. CT imaging showed calcification of the tendon of the longus colli muscle and a low density area in the retropharyngeal space without ring enhancement, suggesting a retropharyngeal abscess. MR imaging showed the smooth swelling of the retropharyngeal space and an increased signal intensity on T2-weighted MR imaging. Calcific retropharyngeal tendinitis heals spontaneously, and treatment is not usually required. However, the clinical outcomes are similar and can be confused with retropharyngeal abscess and pyogenic spondylitis, so antibiotics are administrated in many cases. In our report, 7 patients were hospitalized and were treated with the intravenous administration of antibiotics, while 1 patient who refused hospitalization was treated with an oral antibiotic. Steroids were administrated in 2 cases. The 7 patients who were hospitalized were cured within 6 to 10 days.

  12. Calcification of multipotent prostate tumor endothelium.

    Science.gov (United States)

    Dudley, Andrew C; Khan, Zia A; Shih, Shou-Ching; Kang, Soo-Young; Zwaans, Bernadette M M; Bischoff, Joyce; Klagsbrun, Michael

    2008-09-01

    Solid tumors require new blood vessels for growth and metastasis, yet the biology of tumor-specific endothelial cells is poorly understood. We have isolated tumor endothelial cells from mice that spontaneously develop prostate tumors. Clonal populations of tumor endothelial cells expressed hematopoietic and mesenchymal stem cell markers and differentiated to form cartilage- and bone-like tissues. Chondrogenic differentiation was accompanied by an upregulation of cartilage-specific col2a1 and sox9, whereas osteocalcin and the metastasis marker osteopontin were upregulated during osteogenic differentiation. In human and mouse prostate tumors, ectopic vascular calcification was predominately luminal and colocalized with the endothelial marker CD31. Thus, prostate tumor endothelial cells are atypically multipotent and can undergo a mesenchymal-like transition.

  13. Arthroscopic Treatment of Calcific Tendonitis

    OpenAIRE

    2014-01-01

    Calcific tendonitis, or calcifying tendonitis, is a common disorder characterized by the multifocal accumulation of basic calcium phosphate crystals within the rotator cuff tendons. In most cases, the multifocal calcifications are located 1 to 2 cm from the insertion of the supraspinatus tendon on the greater tuberosity. The initial treatment should be nonoperative including oral anti-inflammatory medication and physical therapy. If this is unsuccessful, arthroscopic debridement of the deposi...

  14. Calcific tendinopathy of the shoulder.

    Science.gov (United States)

    Bureau, Nathalie J

    2013-02-01

    This review article presents the current knowledge on the epidemiology and the pathogenesis of calcific tendinopathy of the shoulder and discusses the clinical presentation in relation to the stage of the disease process and the appearance of the calcific deposits. The outcome and the available treatment modalities for this common shoulder disorder are also examined, emphasizing the technique of percutaneous lavage and aspiration under ultrasound guidance.

  15. Calcifications simulating peroneus longus tendinitis

    Energy Technology Data Exchange (ETDEWEB)

    Carvalho, A. de; Illum, F.; Joergensen, J.

    1984-06-01

    In two patients with sprains of the ankle joint calcification adjacent to the posterior tibial margin was evident in the lateral projection of a standard radiographic examination. Calcifying peroneus longus tendinitis was suggested. Further tangential views and computed tomography (CT) scan disclosed, however, that the calcifications in both patients were located in the tibial insertion of the posterior and inferior tibio-fibular ligament. In such cases, a correct diagnosis will avoid unnecessary treatment for a non-existent tendinitis.

  16. Calcification prevention tablets

    Science.gov (United States)

    Lindsay, Geoffrey A.; Hasting, Michael A.; Gustavson, Michael A.

    1991-01-01

    Citric acid tablets, which slowly release citric acid when flushed with water, are under development by the Navy for calcification prevention. The citric acid dissolves calcium carbonate deposits and chelates the calcium. For use in urinals, a dispenser is not required because the tablets are non-toxic and safe to handle. The tablets are placed in the bottom of the urinal, and are consumed in several hundred flushes (the release rate can be tailored by adjusting the formulation). All of the ingredients are environmentally biodegradable. Mass production of the tablets on commercial tableting machines was demonstrated. The tablets are inexpensive (about 75 cents apiece). Incidences of clogged pipes and urinals were greatly decreased in long term shipboard tests. The corrosion rate of sewage collection pipe (90/10 Cu/Ni) in citric acid solution in the laboratory is several mils per year at conditions typically found in traps under the urinals. The only shipboard corrosion seen to date is of the yellow brass urinal tail pieces. While this is acceptable, the search for a nontoxic corrosion inhibitor is underway. The shelf life of the tablets is at least one year if stored at 50 percent relative humidity, and longer if stored in sealed plastic buckets.

  17. 高磷对血管平滑肌细胞钙化的影响及阿托伐他汀的干预效应%Study of vascular smooth muscle cell calcification induced by hyperphosphate and intervented by atorvastatin

    Institute of Scientific and Technical Information of China (English)

    战晓丽; 袁伟杰; 于建平; 傅鹏; 郭云珊; 刘凌

    2008-01-01

    目的 观察高磷对大鼠血管平滑肌细胞(RVSMC)钙化的影响,及探讨阿托伐他汀在RVSMC钙化中的保护作用及相关机制.方法 用不同的试剂培养RVSMC,分别为正常磷组(Pi 1.4 mmol/L)、高磷组(Pi 2.0 mmol/L、2.6 mmol/L)、凋亡抑制组(Pi 2.6 mmol/L+ZVAD-FMK 0.1 μmol/L、Pi 2.6 mmol/L+ZVAD-FMK 1.0 μmol/L、Pi 2.6 mmol/L+ZVAD-FMK2.0 μmol/L)和阿托伐他汀组(H 2.6 mmol/L+Statin 1 nmol/L、Pi 2.6 mmol/L+Stain 10 nmol/L、Pi 2.6 mmol/L+Statin 100 nmol/L).甲O-酚酞络合酮方法测定平滑肌细胞钙含量,BCA法测定蛋白含量,用蛋白含量标化钙含量,同时以von Kossa染色观察细胞钙化情况.ELISA方法测定不同时间各组细胞的相对凋亡量.结果 (1)培养第3、6、9天时,Pi 2.0 mmol/L、Pi 2.6mmol/L组与Pi 1.4 mmol/L组相比,RVSMC钙沉积较多(P<0.05).(2)培养第6天时,Pi 2.6mmol/L+ZVAD-FMK 1.0 μmol/L、Pi 2.6 mmol/L+ZVAD-FMK 2.0 μmol/L组与Pi 2.6 mmol/L组相比,RVSMC钙沉积较少(P<0.05);Pi 2.6 mmol/L+Statin 10 nmol/L、Pi 2.6 mmol/L+Statin100 nmol/L组与Pi 2.6 mmol/L组相比,细胞钙沉积较少(P<0.05).von Kossa染色显示Pi2.6 mmol/L组细胞有大量黑色颗粒沉积,而Pi 2.6 mmol/L+Statin 100 nmol/L组较少.(3)培养第3、6、9天时,Pi 2.6 mmol/L与Pi 1.4 mmol/L相比,细胞相对凋亡量较多(P<0.05);培养第12、24小时,Pi 2.0 mmol/L、Pi 2.6 mmol/L组与Pi 1.4 mmol/L组相比,细胞相对凋亡量较多(P<0.05);培养第6天、第24小时时,Pi 2.6 mmol/L+Statin 10 nmol/L、Pi 2.6 mmol/L+Statin100 nmol/L与Pi 2.6 mmol/L组相比,细胞相对凋亡量较少(P<0.05).结论 高磷培养可诱导RVSMC体外钙化.阿托伐他汀对高磷诱导的RVSMC钙化有保护作用,此作用可能与其降低RVSMC凋亡有关.%Objective To investigate the protective effects of atorvastatin on hyperphosphate-induced rat vascular smooth muscle ceils (RVSMCs) calcification and to discuss the mechanism. Methods RVSMCs were placed in various culture media, including normal

  18. Necrotic and apoptotic cells serve as nuclei for calcification on osteoblastic differentiation of human mesenchymal stem cells in vitro.

    Science.gov (United States)

    Fujita, Hirofumi; Yamamoto, Masanao; Ogino, Tetsuya; Kobuchi, Hirotsugu; Ohmoto, Naoko; Aoyama, Eriko; Oka, Takashi; Nakanishi, Tohru; Inoue, Keiji; Sasaki, Junzo

    2014-01-01

    A close relationship between cell death and pathological calcification has recently been reported, such as vascular calcification in atherosclerosis. However, the roles of cell death in calcification by osteoblast lineage have not been elucidated in detail. In this study, we investigated whether cell death is involved in the calcification on osteoblastic differentiation of human bone marrow mesenchymal stem cells (hMSC) under osteogenic culture in vitro. Apoptosis and necrosis occurred in an osteogenic culture of hMSC, and cell death preceded calcification. The generation of intracellular reactive oxygen species, chromatin condensation and fragmentation, and caspase-3 activation increased in this culture. A pan-caspase inhibitor (Z-VAD-FMK) and anti-oxidants (Tiron and n-acetylcysteine) inhibited osteogenic culture-induced cell death and calcification. Furthermore, calcification was significantly promoted by the addition of necrotic dead cells or its membrane fraction. Spontaneously dead cells by osteogenic culture and exogenously added necrotic cells were surrounded by calcium deposits. Induction of localized cell death by photodynamic treatment in the osteogenic culture resulted in co-localized calcification. These findings show that necrotic and apoptotic cell deaths were induced in an osteogenic culture of hMSC and indicated that both necrotic and apoptotic cells of osteoblast lineage served as nuclei for calcification on osteoblastic differentiation of hMSC in vitro.

  19. Survival of Atherosclerotic Calcifications in Skeletonized Material: Forensic and Pathological Implications.

    Science.gov (United States)

    Biehler-Gomez, Lucie; Cappella, Annalisa; Castoldi, Elisa; Martrille, Laurent; Cattaneo, Cristina

    2017-07-18

    Atherosclerosis is a chronic inflammatory disease creating calcifying plaques in the arterial walls. Because its paleopathological diagnosis remains little studied on skeletal remains, its impact on forensic and archeological data is completely underestimated. Here, 24 skeletal remains from the Milano Cemetery Skeletal Collection have been studied to evaluate the chance of atherosclerotic calcification survival, retrieval, and identification. Through direct comparison with a known autopsy collection and literature, the identification and categorization of several types of calcifications were performed. Clothing elements such as tights or socks played a definitive role in the preservation of the calcifications; hence they are more likely to be found in forensic cases than in archeological ones. Therefore, vascular calcifications are possible to collect and identify in skeletal remains if sufficient care is given to their recovery. Consequently and as markers of the disease, such identification can provide valuable pathological information for forensic and archeological cases. © 2017 American Academy of Forensic Sciences.

  20. Sudden death in a captive meerkat (Suricata suricatta with arterial medial and myocardial calcification

    Directory of Open Access Journals (Sweden)

    Laura Bongiovann

    2016-04-01

    Full Text Available A 1-year-old male meerkat was found dead by the owner. The animal was clinically healthy and was regularly vaccinated for distemper virus. Necropsy revealed multifocal to confluent dry white areas in the myocardium, pneumonia and congestive hepatopathy. All the other organs, including gross vessels, were macroscopically normal. The heart showed histologically large, multifocal to confluent areas of mineralization of the myocardium and the wall of small coronary artery. Vascular calcifications were also observed in the hepatic portal tracts and kidneys arteries of small/medium sizes. The arterial lumen appeared narrowed and the wall thickened due to the calcification of the tunica media. In veterinary medicine, arterial mineralization is regarded as a metastatic calcification, as the result of hypercalcemia and/or hyperphosphatemia. However, today, the pathogenesis of medial artery calcification in humans seems to be the results of an active process resembling embryonic osteogenesis, rather than a mere passive process.

  1. The Association Between Serum Magnesium Concentrations and Coronary Artery Calcification Scores in Astronauts

    Science.gov (United States)

    Betcher, Jenna; Zwart, Sara; Smith, Scott M.

    2016-01-01

    Magnesium is a natural calcium antagonist, and is inversely associated with coronary heart disease, cardiovascular mortality rates, and vascular calcification. Coronary artery calcification score is a tool used to evaluate the prognosis of coronary artery disease in individuals. Higher magnesium intake is associated with lower coronary artery calcification scores (CACS), and recent studies have found a significant inverse relationship between serum magnesium concentrations and CACS in Korean and Mexican-mestizo populations. The correlation between serum magnesium concentrations and CACS is not well researched, so our aim was to examine this relationship in astronauts. We found that a higher serum magnesium concentration is significantly related to a higher coronary artery calcification score (p=.0217), and that there is a significant difference in magnesium concentrations of subjects who have a CACS greater than 100 and a CACS less than 100.

  2. 冠状动脉钙化的机制与缺血性心脏病%Mechanism of the calcification in coronary arteries and ischemic heart disease

    Institute of Scientific and Technical Information of China (English)

    Masahiko Kurabayashi

    2010-01-01

    @@ Vascular calcification is a common problem a-mong the elderly and the patients with diabetes and chronic kidney disease(CKD),and may be associated with increased morbidity and mortality of cardiovas-cular disease.

  3. Calcification Transformation of Diasporic Bauxite

    Science.gov (United States)

    Zhao, Qiuyue; Zhu, Xiaofeng; Lv, Guozhi; Zhang, Zimu; Yin, Zhengnan; Zhang, Tingan

    2016-06-01

    The disposal of red mud, which is a solid waste that is generated during the extraction of alumina from bauxite, is one of major problems faced by the aluminum industry. Alkali in red mud seeping under the soil may pollute land and water. The Northeastern University, China, has proposed a calcification-carbonation method to deal with low-grade bauxite or red mud. Its main purpose is to change the equilibrium phase of red mud to 2CaO·SiO2 and CaCO3 hydrometallurgically, so that recomposed alkali-free red mud can be widely used. We conducted calcification transformation experiments using diasporic bauxite sampled from Wenshan, and investigated the effects of parameters such as diasporic bauxite grain size, temperature and treatment time on the calcification transformation digestion rate, which is also termed the calcification transformation rate (CTR). The main phase in the calcification transformation slag (CTS) is hydrogarnet with different grain sizes. The CTR increases with decrease in diasporic bauxite grain size, or increase in temperature or reaction time. The CTR reaches a maximum of 87% after 120 min reaction at 240°C. The Na2O/Al2O3 ratio decreases with increase in temperature and reaches 1.5. The sodium content in the CTS decreases with increasing reaction time and is lower than that in the red mud treated using the Bayer process (4-12%).

  4. Hydrogen-Rich Medium Attenuated Lipopolysaccharide-Induced Monocyte-Endothelial Cell Adhesion and Vascular Endothelial Permeability via Rho-Associated Coiled-Coil Protein Kinase.

    Science.gov (United States)

    Xie, Keliang; Wang, Weina; Chen, Hongguang; Han, Huanzhi; Liu, Daquan; Wang, Guolin; Yu, Yonghao

    2015-07-01

    Sepsis is the leading cause of death in critically ill patients. In recent years, molecular hydrogen, as an effective free radical scavenger, has been shown a selective antioxidant and anti-inflammatory effect, and it is beneficial in the treatment of sepsis. Rho-associated coiled-coil protein kinase (ROCK) participates in junction between normal cells, and regulates vascular endothelial permeability. In this study, we used lipopolysaccharide to stimulate vascular endothelial cells and explored the effects of hydrogen-rich medium on the regulation of adhesion of monocytes to endothelial cells and vascular endothelial permeability. We found that hydrogen-rich medium could inhibit adhesion of monocytes to endothelial cells and decrease levels of adhesion molecules, whereas the levels of transepithelial/endothelial electrical resistance values and the expression of vascular endothelial cadherin were increased after hydrogen-rich medium treatment. Moreover, hydrogen-rich medium could lessen the expression of ROCK, as a similar effect of its inhibitor Y-27632. In addition, hydrogen-rich medium could also inhibit adhesion of polymorphonuclear neutrophils to endothelial cells. In conclusion, hydrogen-rich medium could regulate adhesion of monocytes/polymorphonuclear neutrophils to endothelial cells and vascular endothelial permeability, and this effect might be related to the decreased expression of ROCK protein.

  5. CT of schistosomal calcification of the intestine

    Energy Technology Data Exchange (ETDEWEB)

    Fataar, S.; Bassiony, H.; Satyanath, S.; Rudwan, M.; Hebbar, G.; Khalifa, A.; Cherian, M.J.

    1985-01-01

    The spectrum of schistosomal colonic calcification on abdominal radiographs has been described. The appearance on computed tomography (CT) is equally distinctive and occurs with varying degrees of genitourinary calcification. The authors have experience in three cases with the appearance on CT of intestinal calcification due to schistosomiasis.

  6. Calcification of intracranial vessels in neurocysticercosis

    Energy Technology Data Exchange (ETDEWEB)

    Fernandez-Bouzas, A. [ENEP Iztacala, Universidad Nacional Autonoma de Mexico, Mexico (Mexico); Ballesteros-Maresma, A. [Radiologia Clinica de Cuernavaca (Mexico); Casian, G.; Hernandez-Martinez, P. [Hospital Juarez de Mexico S. S. (Mexico); Martinez-Lopez, M. [Fundacion Clinica Medica Sur (Mexico)

    2000-07-01

    We report calcification of intracranial vessels in neurocysticercosis. Calcification was observed in the middle cerebral arteries in two patients, and the circle of Willis in two others. The patients with middle cerebral artery calcification underwent CT with inhaled stable xenon and an area of mild hypoperfusion was observed in the ipsilateral cerebral hemisphere. (orig.)

  7. Chronic calcific tendinitis of the neck

    Energy Technology Data Exchange (ETDEWEB)

    Newmark, H.; Zee, C.S.; Frankel, P.; Robinson, A.; Blau, L.; Gans, D.C.

    1981-12-01

    The authors present the first three cases of chronic calcific tendinits of the neck. This condition is diagnosed radiologically by the presence of calcification located just inferior to the anterior tubercle of C1. The calcification is at the insertion of the longus colli muscle. No soft tissue swelling is present and the patients are asymptomatic.

  8. Intracranial calcification in central diabetes insipidus.

    Science.gov (United States)

    Al-Kandari, Salwa Ramadan; Pandey, Tarun; Badawi, Mona H

    2008-01-01

    Intracranial calcification is a known but extremely rare complication of diabetes insipidus. To date, only 16 patients have been reported and all had the peripheral (nephrogenic) type of diabetes insipidus. We report a child with intracranial calcification complicating central diabetes insipidus. We also report a child with nephrogenic diabetes insipidus, and compare the patterns of intracranial calcification.

  9. Intracranial calcification in central diabetes insipidus

    Energy Technology Data Exchange (ETDEWEB)

    Al-Kandari, Salwa R. [Al Razi Hospital, Department of Clinical Radiology, Kuwait (Kuwait); Pandey, Tarun [Al Razi Hospital, Department of Clinical Radiology, Kuwait (Kuwait); University of Arkansas for Medical Sciences, Radiology Department, Little Rock, AR (United States); Badawi, Mona H. [Al-Adan Hospital, Department of Paediatrics, Kuwait (Kuwait)

    2008-01-15

    Intracranial calcification is a known but extremely rare complication of diabetes insipidus. To date, only 16 patients have been reported and all had the peripheral (nephrogenic) type of diabetes insipidus. We report a child with intracranial calcification complicating central diabetes insipidus. We also report a child with nephrogenic diabetes insipidus, and compare the patterns of intracranial calcification. (orig.)

  10. Coffee Consumption and Coronary Calcification: The Rotterdam Coronary Calcification Study

    NARCIS (Netherlands)

    Woudenbergh, van G.J.; Vliegenthart, R.; Rooij, van F.J.A.; Hofman, A.; Oudkerk, M.; Witteman, J.C.M.; Geleijnse, J.M.

    2008-01-01

    Background¿ The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. Methods and Results¿ The study involved 1570 older men and women without coronary heart disease who participated in the Ro

  11. Coffee consumption and coronary calcification - The Rotterdam Coronary Calcification Study

    NARCIS (Netherlands)

    van Woudenbergh, Geertruida J.; Vliegenthart, Rozemarijn; van Rooij, Frank J. A.; Hofman, Albert; Oudkerk, Matthijs; Witteman, Jacqueline C. M.; Geleijnse, Johanna M.

    2008-01-01

    Background-The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. Methods and Results-The study involved 1570 older men and women without coronary heart disease who participated in the Rott

  12. Coffee consumption and coronary calcification: The Rotterdam coronary calcification study

    NARCIS (Netherlands)

    G.J. van Woudenbergh (Geertruida); R. Vliegenthart (Rozemarijn); F.J.A. van Rooij (Frank); A. Hofman (Albert); M. Oudkerk (Matthijs); J.C.M. Witteman (Jacqueline); J.M. Geleijnse (Marianne)

    2008-01-01

    textabstractBACKGROUND - The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. METHODS AND RESULTS - The study involved 1570 older men and women without coronary heart disease who particip

  13. Acute retropharyngeal calcific tendinitis: a case report with unusual location of calcification

    Energy Technology Data Exchange (ETDEWEB)

    Park, So Young; Jin, Wook; Yang, Dal Mo [East-West Neo-Medical Center, College of Medicine, Kyung Hee University, Department of Radiology, Seoul (Korea); Lee, Sang Hun [East-West Neo Medical Center, College of Medicine, Kyung Hee University, Department of Orthopedic Surgery, Seoul (Korea); Park, Ji Seon; Ryu, Kyung Nam [Kyung Hee University Medical Center, College of Medicine, Kyung Hee University, Department of Radiology, Seoul (Korea)

    2010-08-15

    Retropharyngeal calcific tendinitis is an inflammatory process caused by calcium hydroxyapatite crystal deposition in the longus colli tendon of the prevertebral space, and it may mimic a retropharyngeal infection or abscess. The diagnosis of retropharyngeal calcific tendinitis will be made radiologically by the detection of calcifications anterior to C1-C3 and prevertebral soft tissue swelling. We present a case of acute retropharyngeal calcific tendinitis with an unusual location of calcification anterior to the C5-C6 disc. (orig.)

  14. Association of Ankle-Brachial Index and Aortic Arch Calcification with Overall and Cardiovascular Mortality in Hemodialysis

    OpenAIRE

    Szu-Chia Chen; Mei-Yueh Lee; Jiun-Chi Huang; Ming-Chen Paul Shih; Jer-Ming Chang; Hung-Chun Chen

    2016-01-01

    Peripheral artery occlusive disease and vascular calcification are highly prevalent in hemodialysis (HD) patients, however the association of the combination of ankle-brachial index (ABI) and aortic arch calcification (AoAC) with clinical outcomes in patients undergoing HD is unknown. In this study, we investigated whether the combination of ABI and AoAC is independently associated with overall and cardiovascular mortality in HD patients. The median follow-up period was 5.7 years. Calcificati...

  15. Progression of Aortic Arch Calcification Over 1 Year Is an Independent Predictor of Mortality in Incident Peritoneal Dialysis Patients

    OpenAIRE

    Mi Jung Lee; Dong Ho Shin; Seung Jun Kim; Hyung Jung Oh; Dong Eun Yoo; Kwang Il Ko; Hyang Mo Koo; Chan Ho Kim; Fa Mee Doh; Jung Tak Park; Seung Hyeok Han; Tae-Hyun Yoo; Kyu Hun Choi; Shin-Wook Kang

    2012-01-01

    BACKGROUNDS AND AIMS: The presence and progression of vascular calcification have been demonstrated as important risk factors for mortality in dialysis patients. However, since the majority of subjects included in most previous studies were hemodialysis patients, limited information was available in peritoneal dialysis (PD) patients. Therefore, the aim of this study was to investigate the prevalence of aortic arch calcification (AoAC) and prognostic value of AoAC progression in PD patients. M...

  16. Calcium intake is not associated with increased coronary artery calcification: The Framingham Study

    Science.gov (United States)

    Adequate calcium intake is known to protect the skeleton. However, studies that have reported adverse effects of calcium supplementation on vascular events have raised widespread concern. We assessed the association between calcium intake (from diet and supplements) and coronary artery calcification...

  17. Roscovitine attenuates intimal hyperplasia via inhibiting NF-κB and STAT3 activation induced by TNF-α in vascular smooth muscle cells.

    Science.gov (United States)

    He, Ming; Wang, Chao; Sun, Jia-Huan; Liu, Yu; Wang, Hong; Zhao, Jing-Shan; Li, Yun-Feng; Chang, Hong; Hou, Jian-Ming; Song, Jun-Na; Li, Ai-Ying; Ji, En-Sheng

    2017-08-01

    Roscovitine is a selective CDK inhibitor originally designed as anti-cancer agent, which has also been shown to inhibit proliferation in vascular smooth muscle cells (VSMCs). However, its effect on vascular remodeling and its mechanism of action remain unknown. In our study, we created a new intimal hyperplasia model in male Sprague-Dawley rats by trypsin digestion method, which cause to vascular injury as well as the model of rat carotid balloon angioplasty. Roscovitine administration led to a significant reduction in neointimal formation and VSMCs proliferation after injury in rats. Western blot analysis revealed that, in response to vascular injury, TNF-α stimulation induced p65 and STAT3 phosphorylation and promoted translocation of these molecules into the nucleus. p65 can physically associate with STAT3 and bind to TNF-α-regulated target promoters, such as MCP-1 and ICAM-1, to initiate gene transcription. Roscovitine can interrupt activation of NF-κB and reduce expression of TNF-α-induced proinflammatory gene, thus inhibiting intimal hyperplasia. These findings provide a novel mechanism to explain the roscovitine-mediated inhibition of intimal hyperplasia induced by proinflammatory pathways. Copyright © 2017 Elsevier Inc. All rights reserved.

  18. Arthroscopic treatment of calcific tendonitis.

    Science.gov (United States)

    Barber, F Alan; Cowden, Courtney H

    2014-04-01

    Calcific tendonitis, or calcifying tendonitis, is a common disorder characterized by the multifocal accumulation of basic calcium phosphate crystals within the rotator cuff tendons. In most cases, the multifocal calcifications are located 1 to 2 cm from the insertion of the supraspinatus tendon on the greater tuberosity. The initial treatment should be nonoperative including oral anti-inflammatory medication and physical therapy. If this is unsuccessful, arthroscopic debridement of the deposit is effective. The technique used is an arthroscopic localization and debridement without associated subacromial decompression. The rotator cuff should be evaluated for partial- and full-thickness tears before and after the debridement of calcifications. If a partial- or full-thickness rotator cuff tendon tear is identified, it should be treated in a fashion consistent with those without associated calcium deposits. In our hands, tears 5 mm or greater in depth are repaired using a tendon-to-tendon or tendon-to-bone technique. Tears with less depth are debrided and then left alone. Arthroscopic debridement of calcific tendonitis can yield excellent functional results and high patient satisfaction.

  19. Arterial calcification: friend or foe?

    Science.gov (United States)

    Nicoll, Rachel; Henein, Michael Y

    2013-07-31

    There is a significant relationship between the presence, extent and progression of coronary artery calcification (CAC) and cardiovascular (CV) events and mortality in both CV and renal patients and CAC scoring can provide improved predictive ability over risk factor scoring alone. There is also a close relationship between CAC presence and atherosclerotic plaque burden, with angiography studies showing very high sensitivity but poor specificity of CAC score for predicting obstructive disease. Nevertheless, there are objections to CAC screening because of uncertainties and lack of studies showing improved outcome. Furthermore, histopathology studies indicate that heavily calcified plaque is unlikely to result in a CV event, while the vulnerable plaque tends to be uncalcified or 'mixed', suggesting that calcification may be protective. This scenario highlights a number of paradoxes, which may indicate that the association between CAC and CV events is spurious, following from the adoption of CAC as a surrogate for high plaque burden, which itself is a surrogate for the presence of vulnerable plaque. Since studies indicate that arterial calcification is a complex, organised and regulated process similar to bone formation, there is no particular reason why it should be a reliable indicator of either the plaque burden or the risk of a future CV event. We suggest that it is time to divorce arterial calcification from atherosclerosis and to view it as a distinct pathology in its own right, albeit one which frequently coexists with atherosclerosis and is related to it for reasons which are not yet fully understood.

  20. Specific anti-tumor effect induced by attenuated Salmonella typhimurium vaccine expressing extracellular region of vascular endothelial growth factor receptor 2

    Institute of Scientific and Technical Information of China (English)

    YANG Jun; DONG Jian; PU Ping; WANG ZhiQiang; HONG Min; CHEN MingQing

    2008-01-01

    The purposes of this research were to study the stable expression of exogenous gene encoding therapeutic protein in attenuated Salmonella typhimurium, observe the metabolism of oral gene vac-cine carried by attenuated Salmonella typhimurium in BALB/c mouse, and investigate the feasibility of prevention and treatment of tumors by the recombinant bacteria. Recombinant plasmid pcDNA3.1+ VEGFR2(n1-7) was transformed into competent attenuated Salmonella typhimurium SL3261 to develop oral DNA vaccine SL3261-pcDNA3.1+VEGFR2(n1-7). To observe whether the exogenous gene can be ex-pressed in the recombinant bacteria, PCR was performed to amplify the CMV promoter of the eu-karyotic expression vector as the proof of stable expression of exogenous protein; transmission elec-tron microscopy (TEM) was applied to observe the morphology of the recombinant bacteria to confirm that the exogenous gene has no impact on the growth of the bacteria, and then BALB/c mice were immunized with the gene vaccine. After inoculation of the gene vaccine, the recombinant bacteria SL3261 could be detected in the tissues such as small intestine, colon, liver and spleen. And then, mice in each group were challenged with tumor cells. The results of animal experiment showed that tumor growth of the mice in experimental group was inhibited and survival time of immunized mice was pro-longed compared with control groups. A higher lymphocyte infiltration in tumors from animals treated with DNA vaccine was observed. Immunohistochemical analysis of tumor samples revealed an en-hanced accumulation of CD8+ cytotoxic T lymphocytes, as well as an increase in CD4+ cells in the tu-mors of animals treated with the oral gene vaccine compared to tumors from control group mice. UI-trastructure of the tumor tissue showed that tumor cells in the samples of the immunized mice were well-differentiated. Our research confirmed that the exogenous gene can be stably expressed in the attenuated Salmonella typhimurium and has no

  1. Vitamin K-antagonists accelerate atherosclerotic calcification and induce a vulnerable plaque phenotype.

    Directory of Open Access Journals (Sweden)

    Leon J Schurgers

    Full Text Available BACKGROUND: Vitamin K-antagonists (VKA are treatment of choice and standard care for patients with venous thrombosis and thromboembolic risk. In experimental animal models as well as humans, VKA have been shown to promote medial elastocalcinosis. As vascular calcification is considered an independent risk factor for plaque instability, we here investigated the effect of VKA on coronary calcification in patients and on calcification of atherosclerotic plaques in the ApoE(-/- model of atherosclerosis. METHODOLOGY/PRINCIPAL FINDINGS: A total of 266 patients (133 VKA users and 133 gender and Framingham Risk Score matched non-VKA users underwent 64-slice MDCT to assess the degree of coronary artery disease (CAD. VKA-users developed significantly more calcified coronary plaques as compared to non-VKA users. ApoE(-/- mice (10 weeks received a Western type diet (WTD for 12 weeks, after which mice were fed a WTD supplemented with vitamin K(1 (VK(1, 1.5 mg/g or vitamin K(1 and warfarin (VK(1&W; 1.5 mg/g & 3.0 mg/g for 1 or 4 weeks, after which mice were sacrificed. Warfarin significantly increased frequency and extent of vascular calcification. Also, plaque calcification comprised microcalcification of the intimal layer. Furthermore, warfarin treatment decreased plaque expression of calcification regulatory protein carboxylated matrix Gla-protein, increased apoptosis and, surprisingly outward plaque remodeling, without affecting overall plaque burden. CONCLUSIONS/SIGNIFICANCE: VKA use is associated with coronary artery plaque calcification in patients with suspected CAD and causes changes in plaque morphology with features of plaque vulnerability in ApoE(-/- mice. Our findings underscore the need for alternative anticoagulants that do not interfere with the vitamin K cycle.

  2. Vascular Cures

    Science.gov (United States)

    ... Contact Us Vascular Disease What is Vascular Disease? Education and Awareness Vascular Diseases Abdominal Aortic Aneurysm Aortic Dissection Arteriovenous Malformation Atherosclerosis Buerger's Disease Carotid Artery Disease ...

  3. Are the Symptoms of Calcific Tendinitis Due to Neoinnervation and/or Neovascularization?

    Science.gov (United States)

    Hackett, Lisa; Millar, Neal L; Lam, Patrick; Murrell, George A C

    2016-02-03

    Calcific tendinitis can be a substantial cause of pain and dysfunction in the shoulder, and the pathophysiology is unclear. Recent studies have shown a link among nerve ingrowth, neovascularization, and pain in tendinopathy. The aim of this study was to determine whether there is evidence of neoinnervation and/or neovascularization in calcific tendinitis lesions of the shoulder. At arthroscopy, ultrasound was used to identify calcium within the tendon. Samples were taken from the supraspinatus tendon adjacent to the calcific lesion (in the calcific tendinitis group, with ten patients), the torn supraspinatus tendon of patients undergoing rotator cuff repair (the rotator cuff tear group, with ten patients), and the subscapularis tendon of patients undergoing a stabilization surgical procedure (the control group, with ten patients). Biopsied tendon samples were evaluated immunohistochemically by quantifying the presence of macrophages (using CD68 and CD206), T cells (CD3), mast cells (mast cell tryptase), vascular endothelium (CD34), and peripheral nerve markers (PGP 9.5). There was a twofold to eightfold increase of nerve markers, neovascularization, macrophages, M2 macrophages, and mast cells in the calcific tendinitis group compared with the rotator cuff tear group (p tendinitis lesions of the shoulder along with an eightfold increase in mast cells and macrophages. The findings are consistent with the hypothesis that, in calcific tendinitis, the calcific material is inducing a vigorous inflammatory response within the tendon with formation of new blood vessels and nerves. This study helps to explain why calcific tendinitis is related to substantial pain in the clinical setting. Copyright © 2016 by The Journal of Bone and Joint Surgery, Incorporated.

  4. Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk

    DEFF Research Database (Denmark)

    Blomberg, Björn A; de Jong, Pim A; Thomassen, Anders

    2017-01-01

    /CT imaging), and vascular calcium burden (CT imaging) of the thoracic aorta in a population at low CVD risk. METHODS: Study participants underwent blood pressure measurements, blood analyses, and (18)F-FDG and Na(18)F PET/CT imaging. In addition, the 10-year risk for development of CVD, based......PURPOSE: Arterial inflammation and vascular calcification are regarded as early prognostic markers of cardiovascular disease (CVD). In this study we investigated the relationship between CVD risk and arterial inflammation ((18)F-FDG PET/CT imaging), vascular calcification metabolism (Na(18)F PET...... on the Framingham risk score (FRS), was estimated. CVD risk was compared across quartiles of thoracic aorta (18)F-FDG uptake, Na(18)F uptake, and calcium burden on CT. RESULTS: A total of 139 subjects (52 % men, mean age 49 years, age range 21 - 75 years, median FRS 6 %) were evaluated. CVD risk was, on average, 3...

  5. Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk

    DEFF Research Database (Denmark)

    Blomberg, Björn A; de Jong, Pim A; Thomassen, Anders;

    2016-01-01

    PURPOSE: Arterial inflammation and vascular calcification are regarded as early prognostic markers of cardiovascular disease (CVD). In this study we investigated the relationship between CVD risk and arterial inflammation ((18)F-FDG PET/CT imaging), vascular calcification metabolism (Na(18)F PET....../CT imaging), and vascular calcium burden (CT imaging) of the thoracic aorta in a population at low CVD risk. METHODS: Study participants underwent blood pressure measurements, blood analyses, and (18)F-FDG and Na(18)F PET/CT imaging. In addition, the 10-year risk for development of CVD, based...... on the Framingham risk score (FRS), was estimated. CVD risk was compared across quartiles of thoracic aorta (18)F-FDG uptake, Na(18)F uptake, and calcium burden on CT. RESULTS: A total of 139 subjects (52 % men, mean age 49 years, age range 21 - 75 years, median FRS 6 %) were evaluated. CVD risk was, on average, 3...

  6. Severe aortic arch calcification predicts mortality in patients undergoing peritoneal dialysis

    OpenAIRE

    Ching-Fang Wu; Yee-Fan Lee; Wen-Jeng Lee; Chi-Ting Su; Lukas Jyuhn-Hsiarn Lee; Kwan-Dun Wu; Pau-Chung Chen; Tze-Wah Kao

    2017-01-01

    Vascular calcification can predict cardiovascular (CV) morbidity and mortality in patients with end-stage renal disease. We evaluated the prevalence, association factors, and outcomes of chest X-ray-detected aortic arch calcification (AoAC) in patients undergoing peritoneal dialysis (PD). Methods: We included 190 patients undergoing PD (mean age, 52.6 ± 14.3 years) for whom chest radiographs were available. AoAC revealed by chest X-ray was graded from 0 to 3 according to an AoAC score (AoA...

  7. Coral calcification and ocean acidification

    Science.gov (United States)

    Jokiel, Paul L.; Jury, Christopher P.; Kuffner, Ilsa B.

    2016-01-01

    Over 60 years ago, the discovery that light increased calcification in the coral plant-animal symbiosis triggered interest in explaining the phenomenon and understanding the mechanisms involved. Major findings along the way include the observation that carbon fixed by photosynthesis in the zooxanthellae is translocated to animal cells throughout the colony and that corals can therefore live as autotrophs in many situations. Recent research has focused on explaining the observed reduction in calcification rate with increasing ocean acidification (OA). Experiments have shown a direct correlation between declining ocean pH, declining aragonite saturation state (Ωarag), declining [CO32_] and coral calcification. Nearly all previous reports on OA identify Ωarag or its surrogate [CO32] as the factor driving coral calcification. However, the alternate “Proton Flux Hypothesis” stated that coral calcification is controlled by diffusion limitation of net H+ transport through the boundary layer in relation to availability of dissolved inorganic carbon (DIC). The “Two Compartment Proton Flux Model” expanded this explanation and synthesized diverse observations into a universal model that explains many paradoxes of coral metabolism, morphology and plasticity of growth form in addition to observed coral skeletal growth response to OA. It is now clear that irradiance is the main driver of net photosynthesis (Pnet), which in turn drives net calcification (Gnet), and alters pH in the bulk water surrounding the coral. Pnet controls [CO32] and thus Ωarag of the bulk water over the diel cycle. Changes in Ωarag and pH lag behind Gnet throughout the daily cycle by two or more hours. The flux rate Pnet, rather than concentration-based parameters (e.g., Ωarag, [CO3 2], pH and [DIC]:[H+] ratio) is the primary driver of Gnet. Daytime coral metabolism rapidly removes DIC from the bulk seawater. Photosynthesis increases the bulk seawater pH while providing the energy that drives

  8. Cerebral calcifications and schizophreniform disorder

    Directory of Open Access Journals (Sweden)

    Leonardo Fernandez Meyer

    2013-01-01

    Full Text Available OBJECTIVES: Discuss pathophysiological aspects of cerebral calcifications (CC and highlight its importance related to the occurrence of neuropsychiatric syndromes. METHOD: Single case report. RESULT: Man 52 years old, 20 years after going through a total thyroidectomy, starts showing behavioral disturbance (psychotic syndrome. He was diagnosed as schizophrenic (paranoid subtype and submitted to outpatient psychiatric treatment. During a psychiatric admission to evaluate his progressive cognitive and motor deterioration, we identified a dementia syndrome and extensive cerebral calcifications, derived from iatrogenic hypoparathyroidism. CONCLUSION: The calcium and phosphorus disturbances, including hypoparathyroidism, are common causes of CC. Its symptoms can imitate psychiatric disorders and produce serious and permanent cognitive sequelae. The exclusion of organicity is mandatory in any psychiatric investigative diagnosis in order to avoid unfavorable outcomes, such as in the present case report.

  9. Calcific retropharyngeal tendinitis. [Radiological findings

    Energy Technology Data Exchange (ETDEWEB)

    Karasick, D.; Karasick, S.

    1981-12-01

    Calcific retropharyngeal tendinitis is an imflammation of the longus colli muscle tendon which is located on the anterior surface of the verterbral column extending from the atlas to the third thoracic vertebra. The acute inflammatory condition is selflimiting with symptoms consisting of a gradually increasing neck pain often associated with throat pain and difficulty swallowing. The pain is aggravated by head and neck movement. Clinically the condition can be confused with retropharyngeal absecess, meningitis, infectious spondylitis, and post-traumatic muscle spasm. The radiographic features of this condition consist of pre-vertebral soft tissue swelling from C1 to C4 and amorphous calcific density in the longus colli tendon anterior to the body of C2 and inferior to the anterior arch of C1.

  10. Ultrasound -- Vascular

    Science.gov (United States)

    ... News Physician Resources Professions Site Index A-Z Ultrasound - Vascular Vascular ultrasound uses sound waves to evaluate ... the limitations of Vascular Ultrasound? What is Vascular Ultrasound? Ultrasound is safe and painless, and produces pictures ...

  11. Ultrasound -- Vascular

    Science.gov (United States)

    ... Physician Resources Professions Site Index A-Z Ultrasound - Vascular Vascular ultrasound uses sound waves to evaluate the ... are the limitations of Vascular Ultrasound? What is Vascular Ultrasound? Ultrasound is safe and painless, and produces ...

  12. The retardation of vasculopathy induced by attenuation of insulin resistance in the corpulent JCR:LA-cp rat is reflected by decreased vascular smooth muscle cell proliferation in vivo.

    Science.gov (United States)

    Absher, P M; Schneider, D J; Baldor, L C; Russell, J C; Sobel, B E

    1999-04-01

    Proliferation in vivo of vascular smooth muscle cells occurs early in the course of atherosclerosis. Cultured smooth muscle cells (SMCs) explanted from aortas of JCR:LA-cp corpulent rats known to exhibit metabolic derangements and insulin resistance typical of type II diabetes early in life and to develop atherosclerosis later in life exhibit increased proliferation compared with SMCs from lean, normal rats. Vascular smooth muscle proliferation in vitro was found to be positively and significantly correlated with plasma insulin levels in vivo. Proliferation of aortic SMCs from JCR:LA-cp cp/cp corpulent rats cultured in vitro exhibited increased proliferation in the presence of exogenous insulin. Exercise and diet, selected as interventions designed to ameliorate the insulin resistance and hyperinsulinemia in the JCR:LA-cp cp/cp rat, effectively lowered blood insulin levels and decreased subsequent proliferation in vitro of aortic SMCs explanted from these animals. The results indicate that assessment of proliferation of vascular smooth muscle cells ex vivo may provide insight into the presence and severity of atherogenicity in association with insulin resistance in diverse species under diverse circumstances. Accordingly, with appropriate controls, it may be possible to use SMC proliferation ex vivo as a marker of the extent to which an intervention such as administration of insulin sensitizers to experimental animals and human subjects results in a change in behavior of vessel wall elements potentially indicative of amelioration of atherogenicity and detectable as judged from reduced proliferative rates of the cells ex vivo when they have been harvested from vessels exposed to a milieu in which insulin resistance has been attenuated.

  13. Atypical Steatocystoma Multiplex with Calcification

    Science.gov (United States)

    Rahman, Muhammad Hasibur; Islam, Muhammad Saiful; Ansari, Nazma Parvin

    2011-01-01

    A 60-year-old male reported to us with an atypical case of giant steatocystoma multiplex in the scrotum with calcification. There was no family history of similar lesions. Yellowish, creamy material was expressed from a nodule during punch biopsy. The diagnosis was based on clinical as well as histological findings. Successful surgical excision was done to cure the case without any complications. PMID:22363850

  14. Evaluation and Management of Breast Calcifications

    Directory of Open Access Journals (Sweden)

    Behrooz Zandi

    2010-05-01

    Full Text Available When evaluating mammograms, one looks for masses, areas of asymmetry or architectural distortion and microcalcifications."nCalcification found on screening and diagnostic mammography may be typically benign, of intermediate type, or have a high probability of malignancy."nThe calcifications that most radiologists have prob-lems dealing with are those of "intermediate con-cern.""nOccasionally spot compression-magnification views are necessary to evaluate and analyze the calcification characteristics."nThe morphology and distribution of calcifications are often clues to the differential diagnosis and appropriate management. Calcifications deserve closer scrutiny than those in a regional or diffuse distribution."nIn this article, we discuss the imaging evaluation and management of lesions found on screening and diagnostic mammography, with the focus on commonly encumbered questions and problems. We will also present our interesting cases with breast calcification.

  15. Cardiac calcification in acute intermittent porphyria

    Directory of Open Access Journals (Sweden)

    Tanmoy Ghatak

    2011-01-01

    Full Text Available Aetiology of pericardial calcifications can be multifactorial. Tuberculosis has been reported as the most common cause. Other known causes include uraemia, asbestosis, post-traumatic or postoperative. We report a rare case of pericardial calcification seen in a patient with established acute intermittent porphyria. A direct causal relationship cannot be established between porphyria and pericardial calcification, but it may be due to deposition of the porphyrin in the pericardium.

  16. Calcification of thoracic aorta - solar eclipse sign.

    Science.gov (United States)

    Dhoble, Abhijeet; Puttarajappa, Chethan

    2008-08-29

    Calcification of thoracic aorta is very common in old people, especially ones with hypertension. This can sometime be visible on plain chest radiograph. We present a case of a male patient who had extensive deposition of calcium in the thoracic aorta. The relationship between aortic calcification and coronary atherosclerosis remains contentious. Computed tomography of the thorax can display this calcification which appears like 'solar eclipse'.

  17. Incidental Anterior Cruciate Ligament Calcification: Case Report.

    Science.gov (United States)

    Hayashi, Hisami; Fischer, Hans

    2016-03-01

    The calcification of knee ligaments is a finding noted only in a handful of case reports. The finding of an anterior cruciate ligament calcification has been reported once in the literature. Comparable studies involving the posterior cruciate ligament, medial collateral ligament and an ossicle within the anterior cruciate ligament are likewise discussed in reports of symptomatic patients. We report a case of incidentally discovered anterior cruciate ligament calcification. We discuss the likely etiology and clinical implications of this finding.

  18. Impaired Fasting Glucose and Diabetes as Predictors for Radial Artery Calcification in End Stage Renal Disease Patients

    Directory of Open Access Journals (Sweden)

    Katarzyna Janda

    2013-01-01

    Full Text Available Objective. The objective of the study was to assess the relationship between selected clinical and biochemical parameters of end stage renal disease (ESRD patients and arterial calcification. Materials and Methods. The study comprised 59 stage 5 chronic kidney disease patients (36 hemodialyzed and 23 predialysis. The examined parameters included common carotid artery intima-media thickness (CCA-IMT, BMI, incidence of diabetes and impaired fasting glucose (IFG, dyslipidemia, hypertension, and 3-year mortality. Plasma levels asymmetric dimethylarginine (ADMA, osteopontin (OPN, osteoprotegerin (OPG, and osteocalcin (OC were also measured. Fragments of radial artery obtained during creation of hemodialysis access were stained for calcifications using von Kossa method and alizarin red. Results. Calcification of radial artery was significantly associated with higher prevalence of IFG and diabetes (P=0.0004 and older age (P=0.003, as well as higher OPG (P=0.014 and ADMA concentrations (P=0.022. Fasting glucose >5.6 mmol/l (IFG and diabetes significantly predicted vascular calcification in multiple logistic regression. The calcification was also associated with higher CCA-IMT (P=0.006 and mortality (P=0.004; OR for death 5.39 [1.20–24.1] after adjustment for dialysis status and age. Conclusion. Combination of renal insufficiency and hyperglycemic conditions exerts a synergistic effect on vascular calcification and increases the risk of death.

  19. Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-кB activation

    Institute of Scientific and Technical Information of China (English)

    Hong-wei TAN; Shan-shun XING; Xiu-ping BI; Li LI; Hui-ping GONG; Ming ZHONG; Yun ZHANG; Wei ZHANG

    2008-01-01

    Aim:Metabolic syndrome is associated with an increased incidence of athero-sclerosis. Clinical studies have shown that calcium channel blockers (CCB) inhibit the progression of atherosclerosis. However, the underlying mechanism is unclear. We investigated the inhibitory effect of felodipine on adhesion mo-lecular expression and macrophage infiltration in the aorta of high fructose-fed rats (FFR). Methods: Male Wistar rats were given 10% fructose in drinking water. After 32 weeks of high fructose feeding, they were treated with felodipine (5 mg·kg-1·d-1) for 6 weeks. The control rats were given a normal diet and water. The aortic expression of intercellular adhesion molecule-1 (ICAM-1) and vas-cular cell adhesion molecule-1 (VCAM-1) and the infiltration of macrophages were measured by real-time RT-PCR and/or immunohistochemistry. NF-кB activity was measured by electrophoretic mobility shift assay (EMSA). Results: After 32 weeks of high fructose feeding, FFR displayed increased body weight, systolic blood pressure (SBP), serum insulin, and triglycerides when compared with the control rats. The aortic expressions of ICAM-I and VCAM-1 were significantly increased in FFR than in the control rats and accompanied by the increased activity of NF-кB. FFR also showed significantly increased CD68-positive macrophages in the aortic wall. After treatment with felodipine, SBP, serum insulin, and the homeostasis model assessment decreased significantly. In addition to reducing ICAM-1 and VCAM-1, felodipine decreased macrophages in the aortic wall. EMSA revealed that felodipine inhibited NF-кB activation in FFR. Conclusion: Felodipine inhibited vessel wall inflammation. The inhibition of NF-кB may be involved in the modulation of vascular inflammatory response by CCB in metabolic syndrome.

  20. Matrix stiffness promotes cartilage endplate chondrocyte calcification in disc degeneration via miR-20a targeting ANKH expression.

    Science.gov (United States)

    Liu, Ming-Han; Sun, Chao; Yao, Yuan; Fan, Xin; Liu, Huan; Cui, You-Hong; Bian, Xiu-Wu; Huang, Bo; Zhou, Yue

    2016-05-04

    The mechanical environment is crucial for intervertebral disc degeneration (IDD). However, the mechanisms underlying the regulation of cartilage endplate (CEP) calcification by altered matrix stiffness remain unclear. In this study, we found that matrix stiffness of CEP was positively correlated with the degree of IDD, and stiff matrix, which mimicked the severe degeneration of CEP, promoted inorganic phosphate-induced calcification in CEP chondrocytes. Co-expression analysis of the miRNA and mRNA profiles showed that increasing stiffness resulted in up-regulation of miR-20a and down-regulation of decreased ankylosis protein homolog (ANKH) during inorganic phosphate-induced calcification in CEP chondrocytes. Through a dual luciferase reporter assay, we confirmed that miR-20a directly targets 3'-untranslated regions of ANKH. The inhibition of miR-20a attenuated the calcium deposition and calcification-related gene expression, whereas the overexpression of miR-20a enhanced calcification in CEP chondrocytes on stiff matrix. The rescue of ANKH expression restored the decreased pyrophosphate efflux and inhibited calcification. In clinical samples, the levels of ANKH expression were inversely associated with the degeneration degree of CEP. Thus, our findings demonstrate that the miR-20a/ANKH axis mediates the stiff matrix- promoted CEP calcification, suggesting that miR-20a and ANKH are potential targets in restraining the progression of IDD.

  1. Calcification rates of the massive coral Siderastrea siderea and crustose coralline algae along the Florida Keys (USA) outer-reef tract

    Science.gov (United States)

    Kuffner, I. B.; Hickey, T. D.; Morrison, J. M.

    2013-12-01

    Coral reefs are degrading on a global scale, and rates of reef-organism calcification are predicted to decline due to ocean warming and acidification. Systematic measurements of calcification over space and time are necessary to detect change resulting from environmental stressors. We established a network of calcification monitoring stations at four managed reefs along the outer Florida Keys Reef Tract (FKRT) from Miami to the Dry Tortugas. Eighty colonies (in two sequential sets of 40) of the reef-building coral, Siderastrea siderea, were transplanted to fixed apparatus that allowed repetitive detachment for buoyant weighing every 6 months. Algal-recruitment tiles were also deployed during each weighing interval to measure net calcification of the crustose coralline algal (CCA) community. Coral-calcification rates were an order of magnitude greater than those of CCA. Rates of coral calcification were seasonal (summer calcification was 53 % greater than winter), and corals in the Dry Tortugas calcified 48 % faster than those at the other three sites. Linear extension rates were also highest in the Dry Tortugas, whereas percent area of the coral skeletons excavated by bioeroding fauna was lowest. The spatial patterns in net coral calcification revealed here correlate well with Holocene reef thickness along the FKRT and, in part, support the "inimical waters hypothesis" proposed by Ginsburg, Hudson, and Shinn almost 50 yrs ago to explain reef development in this region. Due to the homogeneity in coral-calcification rates among the three main Keys sites, we recommend refinement of this hypothesis and suggest that water-quality variables (e.g., carbonate mineral saturation state, dissolved and particulate organic matter, light attenuation) be monitored alongside calcification in future studies. Our results demonstrate that our calcification monitoring network presents a feasible and worthwhile approach to quantifying potential impacts of ocean acidification, warming

  2. Calcification rates of the massive coral Siderastrea siderea and crustose coralline algae along the Florida Keys (USA) outer-reef tract

    Science.gov (United States)

    Kuffner, I.B.; Hickey, T.D.; Morrison, J.M.

    2013-01-01

    Coral reefs are degrading on a global scale, and rates of reef-organism calcification are predicted to decline due to ocean warming and acidification. Systematic measurements of calcification over space and time are necessary to detect change resulting from environmental stressors. We established a network of calcification monitoring stations at four managed reefs along the outer Florida Keys Reef Tract (FKRT) from Miami to the Dry Tortugas. Eighty colonies (in two sequential sets of 40) of the reef-building coral, Siderastrea siderea, were transplanted to fixed apparatus that allowed repetitive detachment for buoyant weighing every 6 months. Algal-recruitment tiles were also deployed during each weighing interval to measure net calcification of the crustose coralline algal (CCA) community. Coral-calcification rates were an order of magnitude greater than those of CCA. Rates of coral calcification were seasonal (summer calcification was 53% greater than winter), and corals in the Dry Tortugas calcified 48% faster than those at the other three sites. Linear extension rates were also highest in the Dry Tortugas, whereas percent area of the coral skeletons excavated by bioeroding fauna was lowest. The spatial patterns in net coral calcification revealed here correlate well with Holocene reef thickness along the FKRT and, in part, support the “inimical waters hypothesis” proposed by Ginsburg, Hudson, and Shinn almost 50 yrs ago to explain reef development in this region. Due to the homogeneity in coral-calcification rates among the three main Keys sites, we recommend refinement of this hypothesis and suggest that water-quality variables (e.g., carbonate mineral saturation state, dissolved and particulate organic matter, light attenuation) be monitored alongside calcification in future studies. Our results demonstrate that our calcification monitoring network presents a feasible and worthwhile approach to quantifying potential impacts of ocean acidification

  3. Clinical and imaging features associated with intracranial internal carotid artery calcifications in patients with ischemic stroke

    Energy Technology Data Exchange (ETDEWEB)

    Yilmaz, Arda [Mersin University, Department of Neurology, Faculty of Medicine, Mersin (Turkey); Akpinar, Erhan [Hacettepe University, Department of Radiology, Faculty of Medicine, Ankara (Turkey); Topcuoglu, Mehmet Akif; Arsava, Ethem Murat [Hacettepe University, Department of Neurology, Faculty of Medicine, Ankara (Turkey)

    2015-05-01

    Intracranial internal carotid artery calcifications (ICAC), a frequent finding on imaging studies, are predictive of future stroke risk in population-based studies. The clinical significance of this observation among ischemic stroke patients is however less clear. In this study, we analyzed ICAC burden in relation to vascular risk factor profile, stroke etiology, and extent of craniocervical vascular calcifications in a consecutive series of ischemic stroke patients. The burden of ICAC was determined both on non-contrast CT and CT-angiography source images by semiquantitative scoring algorithms. The distribution of vascular risk factors, etiologic stroke subtype, and calcification burden in other craniocervical arteries was assessed among patients with no ICAC, mild-moderate ICAC, and severe ICAC. Of 319 patients included into the study, 28 % had no ICAC, 35 % had mild-moderate ICAC, and 37 % had severe ICAC on CT angiography. Independent factors associated with ICAC burden in multivariate analysis included age (p < 0.001), diabetes mellitus (p = 0.006), and coronary artery disease (p < 0.001). Furthermore, a stroke etiology of large artery atherosclerosis or cardioaortic embolism was significantly related to higher ICAC burden (p = 0.006). Patients with severe ICAC were more likely to harbor calcifications in other vascular beds (p < 0.001). All of these findings persisted when analyses were repeated with CT-based ICAC burden assessments. ICAC burden reflects a continuum of atherosclerotic disease involving carotid arteries together with other craniocervical vascular beds. ICAC is significantly associated with stroke of large vessel or cardioembolic origin. This information might help the clinician in prioritizing etiologic work-up in the acute period. (orig.)

  4. Clinical studies of the calcification of the basal ganglia as disclosed by computed tomography

    Energy Technology Data Exchange (ETDEWEB)

    Node, Yoji; Nakazawa, Shozo (Nippon Medical School, Tokyo)

    1983-04-01

    One hundred and twenty-nine of the 12,645 patients (1.0%) were found to have attenuating changes suggesting calcification of the basal ganglia. Thirty-seven of those patients were male and 92 were female. The calcification was bilateral and grossly symmetric in 108 of these patients (83.7%), while it was unilateral in 21 (16.3%). In the unilaterally located cases, 15 were on the left side and 6 were on the right side. In 128 of these patients (99.2%), calcification was located in the globus pallidus. Only one patient, whose diagnosis was hypoparathyroidism, had calcification in both the globus pallidus and the head of the caudate nucleus. The patients' ages ranged from 10 to 85 years (mean, 58), but 88.4% of the patients were more than 40 years old at the time of the CT scanning. The attenuation values of the lesions varied from 35 to 375 EMI units (mean, 55.7). Skull radiographs were performed in 120 of the 129 patients. Calcification was detected in only one patient, a 76-year-old woman, whose diagnosis was myasthenia gravis. The clinical diagnoses of the 129 patients were as follows: 37, headache; 22, cerebrovascular diseases (19, occlusive cerebrovascular diseases); 20, vertigo and/or tinnitus; 12, psychiatric disorders; 5, Parkinson's Syndrome; 2, hypopara thyroidism; 2, Fahr's disease; 2, familial basal ganglia calcification; 2, epilepsy, and 25, miscellaneous (including carcinoma, brain tumor, and trauma). Nervous system abnormalities were observed in 41 of the 129 patients (31.2%). Mental signs, such as disturbance of recent memory, mental retardation, and dementia, were noted in 14 patients. Movement disorders were noted in 13 patients. Other nervous-system abnormalities were sensory disturbances (5 patients) and seizures (4 patients). Abnormal EEG activities were noted in 9 patients; three patients showed epileptic activity, and six had a pathologically slow rhythm.

  5. Anagliptin, a DPP-4 inhibitor, suppresses proliferation of vascular smooth muscles and monocyte inflammatory reaction and attenuates atherosclerosis in male apo E-deficient mice.

    Science.gov (United States)

    Ervinna, Nasib; Mita, Tomoya; Yasunari, Eisuke; Azuma, Kosuke; Tanaka, Rica; Fujimura, Satoshi; Sukmawati, Dewi; Nomiyama, Takashi; Kanazawa, Akio; Kawamori, Ryuzo; Fujitani, Yoshio; Watada, Hirotaka

    2013-03-01

    Dipeptyl peptidase-4 (DPP-4) inhibitors modulate the progression of atherosclerosis. To gain insights into their mechanism of action, 9-wk-old male apolipoprotein E (apoE)-deficient mice were fed a DPP-4 inhibitor, anagliptin-containing diet. The effects of anagliptin were investigated in, a monocyte cell line, human THP-1 cells, and rat smooth muscle cells (SMCs). Treatment with anagliptin for 16 wk significantly reduced accumulation of monocytes and macrophages in the vascular wall, SMC content in plaque areas, and oil red O-stained area around the aortic valve without affecting glucose tolerance or body weight. Serum DPP-4 concentrations were significantly higher in apoE-deficient mice than control mice, and the levels increased with aging, suggesting the involvement of DPP-4 in the progression of atherosclerosis. Indeed, soluble DPP-4 augmented cultured SMC proliferation, and anagliptin suppressed the proliferation by inhibiting ERK phosphorylation. In THP-1 cells, anagliptin reduced lipopolysaccharide-induced TNF-α production with inhibiting ERK phosphorylation and nuclear translocation of nuclear factor-κB. Quantitative analysis also showed that anagliptin reduced the area of atherosclerotic lesion in apoE-deficient mice. These results indicated that the anti-atherosclerotic effect of anagliptin is mediated, at least in part, through its direct inhibition of SMC proliferation and inflammatory reaction of monocytes.

  6. Niflumic Acid Attenuated Pulmonary Artery Tone and Vascular Structural Remodeling of Pulmonary Arterial Hypertension Induced by High Pulmonary Blood Flow In Vivo.

    Science.gov (United States)

    Wang, Kai; Ma, Jianfa; Pang, Yusheng; Lao, Jinquan; Pan, Xuanren; Tang, Qiaoyun; Zhang, Feng; Su, Danyan; Qin, Suyuan; Shrestha, Arnav Prasad

    2015-10-01

    Calcium-activated chloride channels (CaCCs) play a vital role in regulating pulmonary artery tone during pulmonary arterial hypertension (PAH) induced by high blood flow. The role of CaCCs inhibitor niflumic acid (NFA) in vivo during this process requires further investigation. We established the PAH model by abdominal shunt surgery and treated with NFA in vivo. Fifty rats were randomly divided into normal, sham, shunt, NFA group 1 (0.2 mg/kg), and NFA group 2 (0.4 mg/kg). Pathological changes, right ventricle hypertrophy index, arterial wall area/vessel area, and arterial wall thickness/vessel external diameter were analyzed. Then contraction reactions of pulmonary arteries were measured. Finally, the electrophysiological characteristics of pulmonary arterial smooth muscle cells were investigated using patch-clamp technology. After 11 weeks of shunting, PAH developed, accompanied with increased right ventricle hypertrophy index, arterial wall area/vessel area, and arterial wall thickness/vessel external diameter. In the NFA treatment groups, the pressure and pathological changes were alleviated. The pulmonary artery tone in the shunt group increased, whereas it decreased after NFA treatment. The current density of CaCC was higher in the shunt group, and it was decreased in the NFA treatment groups. In conclusion, NFA attenuated pulmonary artery tone and structural remodeling in PAH induced by high pulmonary blood flow in vivo. CaCCs were involved and the augmented current density was alleviated by NFA treatment.

  7. The Sirt1 activator SRT1720 attenuates angiotensin II-induced atherosclerosis in apoE{sup −/−} mice through inhibiting vascular inflammatory response

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Yi xi; Zhang, Man; Cai, Yuehua; Zhao, Qihui; Dai, Wenjian, E-mail: wjdai@126.com

    2015-10-02

    Activation of the silent mating type information regulation 2 homolog 1 (SIRT1) has been shown consistent antiinflammatory function. However, little information is available on the function of SIRT1 during Angiotensin II (AngII)-induced atherosclerosis. Here we report atheroprotective effects of sirt1 activation in a model of AngII-accelerated atherosclerosis, characterized by suppression pro-inflammatory transcription factors Nuclear transcription factor (NF)-κB and Signal Transducers and Activators of Transcription. (STAT) signaling pathway, and atherosclerotic lesion macrophage content. In this model, administration of the SIRT1 agonist SRT1720 substantially attenuated AngII-accelerated atherosclerosis with decreasing blood pressure and inhibited NF-κB and STAT3 activation, which was associated with suppression of inflammatory factor and atherogenic gene expression in the artery. In vitro studies demonstrated similar changes in AngII-treated VSMCs and macrophages: SIRT1 activation inhibited the expression levels of proinflammatory factor. These studies uncover crucial proinflammatory mechanisms of AngII and highlight actions of SIRT1 activation to inhibit AngII signaling, which is atheroprotective. - Highlights: • SRT1720 reduced atherosclerotic lesion size in aortic arches and atherosclerotic lesion macrophage content. • SRT1720 could inhibit the phosphorylation of STAT3 and p65 phosphorylation and translocation. • SRT1720 could inhibit the expression of proinflammatory factor.

  8. THE MAMMOGRAPHIC CALCIFICATIONS IN BREAST CANCER

    Institute of Scientific and Technical Information of China (English)

    Tang Ruiying; Liu Jingxian; Gaowen

    1998-01-01

    Objective: This study was performed to exam the relativeship between mammographic calcifications and breast cancer. Methods: All of the 184 patients with breast diseases underwent mammography before either an open biopsy or a mastectomy. The presence,morphology, and distribution of calcifications visualized on mammograms for breast cancer were compared with the controls who remained cancer free. Statistical comparisons were made by using the x2 test. Results:Of the 184 patients with breast diaeases, 93 malignant and 91 benign lesions were histologically confirmed.Calcifications were visualized on mammograms in 60(64%) of 93 breast cancers and 26 (28%) of 91 non breast cancers. The estimated odds ratio (OR) of breast cancer was 4.5 in women with calcifications seen on mammograms, compared with those having none (P<0.01). Of the 60 breast carcinomas having mammographic calcifications, 28 (47%) were infiltrating ductal carcinomas.There were only 8 (24%) cases with infiltrating ductal cancers in the group of without calcifications seen on the mammograms (P<0.05). Conclusion: Our finding suggests that mammographic calcification appears to be a risk factor for breast cancer. The granular and linear cast type calcification provide clues to the presence of breast cancer, especially when the carcinomas without associated masses were seen on mammograms.

  9. Vascular Endothelial Growth Factor Receptor Type 1 Signaling Prevents Delayed Wound Healing in Diabetes by Attenuating the Production of IL-1β by Recruited Macrophages.

    Science.gov (United States)

    Okizaki, Shin-Ichiro; Ito, Yoshiya; Hosono, Kanako; Oba, Kazuhito; Ohkubo, Hirotoki; Kojo, Ken; Nishizawa, Nobuyuki; Shibuya, Masabumi; Shichiri, Masayoshi; Majima, Masataka

    2016-06-01

    The persistence of proinflammatory macrophages, which are recruited to the granulation tissue, impairs the healing of diabetic wounds. Herein, we examined the role of vascular endothelial growth factor receptor type 1 (VEGFR1) signaling in streptozotocin (STZ)-induced diabetic wound healing. Angiogenesis, lymphangiogenesis, and the healing of full-thickness skin wounds were impaired in STZ-treated wild-type (WT) mice compared with vehicle-treated WT mice, with attenuated recruitment of VEGFR1-positive macrophages expressing vascular endothelial growth factor (VEGF)-A, VEGF-C, and VEGF-D to the wound granulation tissue. These phenomena were even more prevalent in STZ-treated VEGFR1 tyrosine kinase knockout mice (VEGFR1 TK(-/-) mice). STZ-treated WT mice, but not STZ-treated VEGFR1 TK(-/-) mice, showed accelerated wound healing when treated with placenta growth factor. Compared with that of STZ-treated WT mice, the wound granulation tissue of STZ-treated VEGFR1 TK(-/-) mice contained more VEGFR1-positive cells expressing IL-1β [a classic (M1) activated macrophage marker] and fewer VEGFR1-positive cells expressing the mannose receptor [CD206; an alternatively activated (M2) macrophage marker]. Treatment of STZ-treated VEGFR1 TK(-/-) mice with an IL-1β-neutralizing antibody restored impaired wound healing and angiogenesis/lymphangiogenesis and induced macrophages in the wound granulation tissue to switch to an M2 phenotype. Taken together, these results suggest that VEGFR1 signaling plays a role in regulating the balance between macrophage phenotypes in STZ-induced diabetic wounds, prevents impaired diabetic wound healing, and promotes angiogenesis/lymphangiogenesis.

  10. The Notch pathway attenuates interleukin 1β (IL1β)-mediated induction of adenylyl cyclase 8 (AC8) expression during vascular smooth muscle cell (VSMC) trans-differentiation.

    Science.gov (United States)

    Keuylian, Zela; de Baaij, Jeroen H F; Gueguen, Marie; Glorian, Martine; Rouxel, Clotilde; Merlet, Elise; Lipskaia, Larissa; Blaise, Régis; Mateo, Véronique; Limon, Isabelle

    2012-07-20

    Vascular smooth muscle cell (VSMC) trans-differentiation, or their switch from a contractile/quiescent to a secretory/inflammatory/migratory state, is known to play an important role in pathological vascular remodeling including atherosclerosis and postangioplasty restenosis. Several reports have established the Notch pathway as tightly regulating VSMC response to various stress factors through growth, migration, apoptosis, and de-differentiation. More recently, we showed that alterations of the Notch pathway also govern VSMC acquisition of the inflammatory state, one of the major events accelerating atherosclerosis. We also evidenced that the inflammatory context of atherosclerosis triggers a de novo expression of adenylyl cyclase isoform 8 (AC8), associated with the properties developed by trans-differentiated VSMCs. As an initial approach to understanding the regulation of AC8 expression, we examined the role of the Notch pathway. Here we show that inhibiting the Notch pathway enhances the effect of IL1β on AC8 expression, amplifies its deleterious effects on the VSMC trans-differentiated phenotype, and decreases Notch target genes Hrt1 and Hrt3. Conversely, Notch activation resulted in blocking AC8 expression and up-regulated Hrt1 and Hrt3 expression. Furthermore, overexpressing Hrt1 and Hrt3 significantly decreased IL1β-induced AC8 expression. In agreement with these in vitro findings, the in vivo rat carotid balloon-injury model of restenosis evidenced that AC8 de novo expression coincided with down-regulation of the Notch3 pathway. These results, demonstrating that the Notch pathway attenuates IL1β-mediated AC8 up-regulation in trans-differentiated VSMCs, suggest that AC8 expression, besides being induced by the proinflammatory cytokine IL1β, is also dependent on down-regulation of the Notch pathway occurring in an inflammatory context.

  11. Atypical Radiological Manifestation of Pulmonary Metastatic Calcification

    Energy Technology Data Exchange (ETDEWEB)

    Kang, Eun Hae; Kim, Eun Sun; Kim, Chul Hwan; Ham, Soo Youn; Oh, Yu Whan [Korea University College of Medicine, Seoul (Korea, Republic of)

    2008-04-15

    Metastatic pulmonary calcification is a condition of calcium deposition in the normal pulmonary parenchyma, and this is secondary to abnormal calcium metabolism without any prior soft tissue damage. The predisposing factors for this condition include chronic renal failure, hypercalcemia and increased tissue alkalinity. The most common radiologic manifestation consists of poorly defined nodular opacities in the upper lung zone. These opacities reflect the deposition of calcium salts in the pulmonary interstitium. We present here a case of metastatic pulmonary calcification in a patient who recovered from pneumonia with sepsis and whose high-resolution CT (HRCT) images demonstrated localized parenchymal airspace calcification that was limited to the bilateral lower lobes. These lower lobes had been involved with pneumonic consolidation without calcification, as seen on the previous CT scan. In summary, we report here on an atypical presentation of metastatic pulmonary calcification that showed dense airspace consolidation localized to the bilateral lower lobes in a patient with primary hyperparathyroidism and pneumonia.

  12. Folic Acid Attenuates Vascular Endothelial Cell Injury Caused by Hypoxia via the Inhibition of ERK1/2/NOX4/ROS Pathway.

    Science.gov (United States)

    Cheng, Fei; Lan, Jun; Xia, Wenhao; Tu, Chang; Chen, Benfa; Li, Shicheng; Pan, Weibiao

    2016-06-01

    Coronary artery disease is a disease with high morbidity and mortality, in which vascular endothelial dysfunction plays an important role. Hypoxia leads to the inflammation and oxidative stress in endothelial cells, which results in the endothelial injury. The present study was designed to investigate the protective effect and mechanism of folic acid on hypoxia-induced injury in human umbilical vein endothelial cells (HUVEC). Cell counting Kit was used to detect cell survival rate, and apoptotic cells were detected by Hoechst 33258 staining. Intracellular reactive oxygen species (ROS) level was measured using dichloro-dihydro-fluorescein diacetate staining. Western blot was used to determine the protein expressions of extracellular signal protein kinase 1/2 (ERK1/2) and phosphorylated ERK1/2 (p-ERK1/2), NOX4 subunit of NAPDH and endothelial nitric oxide synthase (eNOS). Folic acid significantly increased the cell survival rate and decreased the apoptosis of HUVECs treated with folic acid compared with hypoxia-treated HUVEC. Folic acid also decreased ROS level, while it increased the nitrite content in HUVECs. In addition, folic acid decreased protein expressions of NOX4 and p-ERK1/2, while it increased the protein expression of eNOS in HUVECs. Furthermore, N-acetyl cysteine (NAC), the antioxidant, had similar effect on the cell survival rate and the apoptosis. In addition, DPI (NOX4 inhibitor) and U0126 (ERK1/2 inhibitor) rather than NAC decreased the protein expression of NOX4. NAC, DPI, and U0126 increased the protein expression of eNOS. Furthermore, U0126 rather than DPI and NAC decreased the protein expression of p-ERK1/2. Taken together, the results suggested that hypoxia decreased the cell survival rate and induced apoptosis via ERK1/2/NOX4/ROS pathway, which could be the target of folic acid in protecting the HUVECs from injury caused by hypoxia.

  13. Chronic vagus nerve stimulation attenuates vascular endothelial impairments and reduces the inflammatory profile via inhibition of the NF-κB signaling pathway in ovariectomized rats.

    Science.gov (United States)

    Li, Ping; Liu, Huaipu; Sun, Peng; Wang, Xiaoyu; Wang, Chen; Wang, Ling; Wang, Tinghuai

    2016-02-01

    Vagus nerve stimulation (VNS), a method for activating cholinergic anti-inflammatory pathways, could suppress endothelial activation and minimize tissue injury during inflammation. The aim of this study was to investigate the effects of chronic VNS on endothelial impairments and the inflammatory profile in ovariectomized (OVX) rats. Sprague-Dawley rats (7-8 months old) were randomly assigned to the following four groups: sham-OVX, OVX, OVX+sham-VNS, and OVX+VNS. Throughout the experimental period, the OVX+VNS group received VNS for 3h (20.0 Hz, 1.0 mA, and 10.00 ms pulse width) at the same time every other day. After 12 weeks of VNS, blood samples and thoracic aortas were collected for further analyses. Light microscopy and electron microscopy analyses showed that chronic VNS prevented endothelial swelling, desquamation and even necrosis in the OVX rats. In addition, it obviously improved endothelial function in the OVX rats by restoring the endothelial nitric oxide synthase (e-NOS) and serum endothelin-1 level. Increased expression of cell adhesion molecules (VCAM-1, ICAM-1 and E-selectin) in the thoracic aortas and increases in the levels of circulating cytokines (TNF-α, IL-6, MCP-1, and CINC/KC) were also observed in the OVX rats. Chronic VNS significantly restored these detrimental changes partly by increasing the ACh concentrations in vascular walls and blocking NF-κB pathway activity. The results of this in vivo study have shown that the administration of chronic VNS during, in the early stage of estrogen deficiency, protects OVX rats from endothelial impairments and the inflammatory profile. These findings indicate that activation of the vagus nerve could be a promising supplemental therapy for reducing the risks of suffering from further CVDs in postmenopausal women.

  14. Physiopathology of intratendinous calcific deposition

    Directory of Open Access Journals (Sweden)

    Oliva Francesco

    2012-08-01

    Full Text Available Abstract In calcific tendinopathy (CT, calcium deposits in the substance of the tendon, with chronic activity-related pain, tenderness, localized edema and various degrees of decreased range of motion. CT is particularly common in the rotator cuff, and supraspinatus, Achilles and patellar tendons. The presence of calcific deposits may worsen the clinical manifestations of tendinopathy with an increase in rupture rate, slower recovery times and a higher frequency of post-operative complications. The aetiopathogenesis of CT is still controversial, but seems to be the result of an active cell-mediated process and a localized attempt of the tendon to compensate the original decreased stiffness. Tendon healing includes many sequential processes, and disturbances at different stages of healing may lead to different combinations of histopathological changes, diverting the normal healing processes to an abnormal pathway. In this review, we discuss the theories of pathogenesis behind CT. Better understanding of the pathogenesis is essential for development of effective treatment modalities and for improvement of clinical outcomes.

  15. Epigallocatechin-3-Gallate Attenuates the Effects of TNF-α in Vascular Endothelial Cells by Causing Ectodomain Shedding of TNF Receptor 1

    Directory of Open Access Journals (Sweden)

    Won Seok Yang

    2016-05-01

    Full Text Available Background/Aims: We investigated the mechanism underlying anti-tumor necrosis factor-α (TNF-α effects of epigallocatechin-3-gallate (EGCG in human aortic endothelial cells. Methods: Tumor necrosis factor receptor 1 (TNFR1 was assessed by Western blot analysis. Cytosolic Ca2+ was measured using Fluo-4 AM. A disintegrin and metalloprotease 10 (ADAM10 was localized by immunofluorescence staining. Results: EGCG caused ectodomain shedding of TNFR1 within 30 min and attenuated TNF-α-induced endothelin-1 (ET-1 expression. EGCG-induced TNFR1 ectodomain shedding was prevented by BAPTA-AM (intracellular Ca2+ chelator, but not by the absence of extracellular Ca2+. In physiologic extracellular Ca2+ concentration, EGCG markedly increased cytosolic Ca2+. Even in the absence of extracellular Ca2+, EGCG raised cytosolic Ca2+, though less potently. siRNA depletion of ADAM10 prevented EGCG-induced ectodomain shedding of TNFR1 and also diminished the inhibitory effect of EGCG on TNF-α-induced ET-1 expression. EGCG caused translocation of ADAM10 to the plasma membrane, and this effect was prevented by BAPTA-AM. Besides extracellular Ca2+ influx, release of intracellular stored Ca2+ caused ADAM10-dependent ectodomain shedding of TNFR1. Conclusion: EGCG decreases the responsiveness of cells to TNF-α by causing ADAM10-dependent ectodomain shedding of TNFR1. This effect was attributed to its property to increase cytosolic Ca2+ through both extracellular Ca2+ influx and release of stored Ca2+.

  16. Progression of aortic calcification is associated with disorders of mineral metabolism and mortality in chronic dialysis patients

    NARCIS (Netherlands)

    M. Noordzij; E.M. Cranenburg; L.F. Engelsman; M.M. Hermans; E.W. Boeschoten; V.M. Brandenburg; W.J.W. Bos; J.P. Kooman; F.W. Dekker; M. Ketteler; L.J. Schurgers; R.T. Krediet; J.C. Korevaar

    2011-01-01

    Previous studies have shown that simple imaging methods may be useful for detection of vascular calcifications in dialysis patients. Based on annual, plain chest X-rays during follow-up on dialysis, we studied the associations of mineral metabolism with the presence and progression of aortic calcifi

  17. Progression of aortic calcification is associated with disorders of mineral metabolism and mortality in chronic dialysis patients.

    NARCIS (Netherlands)

    Noordzij, M.; Cranenburg, E.M.; Engelsman, L.F.; Hermans, M.M.; Boeschoten, E.W.; Brandenburg, V.M.; Bos, W.J.W.; Kooman, J.P.; Dekker, F.W.; Ketteler, M.; Schurgers, L.J.; Krediet, R.T.; Korevaar, J.C.

    2011-01-01

    Background. Previous studies have shown that simple imaging methods may be useful for detection of vascular calcifications in dialysis patients. Based on annual, plain chest X-rays during follow-up on dialysis, we studied the associations of mineral metabolism with the presence and progression of ao

  18. Vascular Cures

    Science.gov (United States)

    ... is Possible EVERY DOLLAR SAVES LIVES. Donate Now Vascular Cures innovates patient-centered research, catalyzes breakthrough collaborations and empowers people in their vascular health journey. what is vascular disease PATIENTS see ...

  19. Vascular ring

    Science.gov (United States)

    ... subclavian and left ligamentum ateriosus; Congenital heart defect - vascular ring; Birth defect heart - vascular ring ... Vascular ring is rare. It accounts for less than 1% of all congenital heart problems. The condition ...

  20. Calcification

    Science.gov (United States)

    ... In: Kumar V, Abbas AK, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease . 9th ed. ... In: Kumar V, Abbas AK, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease . 9th ed. ...

  1. Hydrogen-rich saline attenuates vascular smooth muscle cell proliferation and neointimal hyperplasia by inhibiting reactive oxygen species production and inactivating the Ras-ERK1/2-MEK1/2 and Akt pathways.

    Science.gov (United States)

    Chen, Yali; Jiang, Jinyao; Miao, Huibing; Chen, Xingjuan; Sun, Xuejun; Li, Yongjun

    2013-03-01

    Hydrogen-rich saline has been reported to prevent neointimal hyperplasia induced by carotid balloon injury. The purpose of the present study was to further investigate the molecular mechanisms underlying this phenomenon. Daily injection of a hydrogen-rich saline solution (HRSS) in rats was employed to study the effect of hydrogen on balloon injury-induced neointimal hyperplasia and the neointima/media ratio was assessed. HRSS significantly decreased the neointima area and neointima/media ratio in a dose-dependent manner. In vitro effects of hydrogen on fetal bovine serum (FBS)-induced vascular smooth muscle cell (VSMC) proliferation were also investigated. Hydrogen-rich medium (HRM) inhibited rat VSMC proliferation and migration induced by 10% FBS. FBS-induced reactive oxygen species (ROS) production and activation of intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen (PCNA), Akt were significantly inhibited by HRM. In addition, HRM blocked FBS-induced progression from the G0/G1 to the S-phase and increased the apoptosis rate of VSMCs. These results showed that hydrogen-rich saline was able to attenuate FBS-induced VSMC proliferation and neointimal hyperplasia by inhibiting ROS production and inactivating the Ras-ERK1/2-MEK1/2 and Akt pathways. Thus, HRSS may have potential therapeutic relevance for the prevention of human restenosis.

  2. 慢性肾脏病5期患者桡动脉gremlin表达与血管钙化的关系%Association of vascular calcification and gremlin expression in radial arteries of patients with stage 5 of chronic kidney disease

    Institute of Scientific and Technical Information of China (English)

    龚立峰; 卢景奎; 唐卫刚; 姜维; 马桂香

    2011-01-01

    目的 探讨慢性肾脏病(CKD)5期患者桡动脉中骨形态发生蛋白(BMP)拮抗剂gremlin表达与血管钙化的关系.方法 40例CKD5期患者为试验组,于行首次动静脉内瘘术时取桡动脉标本;38例单纯外伤性脾破裂患者为对照组,取其脾小梁动脉标本.用钙盐特异性染色法( von Kossa)对动脉进行钙化染色;用免疫组化法检测动脉gremlin、BMP-2、-7的表达,并用ELISA法检测血清中3者浓度;用病理图像分析系统(IPP6.0)对组织切片进行半定量化图像分析;用SPSS 19.0统计分析软件进行数据处理.结果 试验组12例(30%)钙盐染色显著阳性,位于中膜的平滑肌细胞层,而对照组无显著钙盐染色.试验组钙盐染色显著阳性的桡动脉均有gremlin、BMP-2显著表达,位于中膜的平滑肌细胞层,且2者的表达量与钙盐染色程度均呈正相关.试验组BMP-7的表达量显著低于对照组.结论 gremlin、BMP-2均可能参与了CKD5期患者桡动脉平滑肌细胞向成骨样细胞表型转化这一过程,而BMP-7可能阻止此过程的进展.%Objective To study the association of the expression of bone morphogenetic protein (BMP) antagonist gremlin and vascular calcification in radial arteries of patients with stage 5 of chronic kidney disease (CKD).Methods Radial arteries of 40 patients with stage 5 of CKD were collected as specimens of the study group,which were trimmed off during arterial venous fistula operations.Splenic trabecular arteries were collected as specimens of the control group,which were removed from 38 patients with simple traumatic splenic rupture.All the arteries were examined histologically for calcification with yon Kossa stain.Expressions of gremlin and BMP-2,-7were detected by immunohistochemistry and their serum concentrations were detected by ELISA.Images of histological sections were semi-quantitatively analyzed by Image-Pro Plus 6.0.SPSS 19.0software was used to perform statistical analysis

  3. Cardiorespiratory Fitness and Coronary Artery Calcification in Young Adults: The CARDIA Study

    OpenAIRE

    Lee, Chong-Do; Jacobs, David R; Hankinson, Arlene; Iribarren, Carlos; SIDNEY, Stephen

    2008-01-01

    Whether cardiorespiratory fitness relates to early subclinical atherosclerotic vascular disease remains unknown. We investigated the relation of cardiorespiratory fitness to coronary artery calcification (CAC) in 2373 African-American and White young adults from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. We measured cardiorespiratory fitness in 1985-1986 (baseline) using a symptom-limited exercise test on a treadmill. Coronary calcium scores were measured in 2001-200...

  4. Calcifications in the breast in Filaria loa infection

    Energy Technology Data Exchange (ETDEWEB)

    Novak, R. (Karolinska Sjukhuset, Stockholm (Sweden). Dept. of Diagnostic Radiology)

    A 40-year-old patient underwent mammography for evaluation of a mass. Atypical calcifications were observed in the opposite breast. Two types of calcification were observed: One type was spiral-shaped and the other type rod-shaped. These calcifications were caused by Filaria loa. Parasitic calcifications in the breast are uncommon. (orig.).

  5. Fetal calcifications are associated with chromosomal abnormalities.

    Directory of Open Access Journals (Sweden)

    Ellika Sahlin

    Full Text Available The biological importance of calcifications occasionally noted in fetal tissues (mainly liver at autopsy or ultrasound is largely unexplored. Previous reports hint at an association to infection, circulatory compromise, malformations or chromosomal abnormalities. To identify factors associated with calcifications, we have performed a case-control study on the largest cohort of fetuses with calcifications described thus far.One-hundred and fifty-one fetuses with calcifications and 302 matched controls were selected from the archives of the Department of Pathology, Karolinska University Hospital. Chromosome analysis by karyotyping or quantitative fluorescence-polymerase chain reaction was performed. Autopsy and placenta reports were scrutinized for presence of malformations and signs of infection.Calcifications were mainly located in the liver, but also in heart, bowel, and other tissues. Fetuses with calcifications showed a significantly higher proportion of chromosomal abnormalities than controls; 50% vs. 20% (p<0.001. The most frequent aberrations among cases included trisomy 21 (33%, trisomy 18 (22%, and monosomy X (18%. A similar distribution was seen among controls. When comparing cases and controls with chromosomal abnormalities, the cases had a significantly higher prevalence of malformations (95% vs. 77%, p=0.004. Analyzed the other way around, cases with malformations had a significantly higher proportion of chromosomal abnormalities compared with controls, (66% vs. 31%, p<0.001.The presence of fetal calcifications is associated with high risk of chromosomal abnormality in combination with malformations. Identification of a calcification together with a malformation at autopsy more than doubles the probability of detecting a chromosomal abnormality, compared with identification of a malformation only. We propose that identification of a fetal tissue calcification at autopsy, and potentially also at ultrasound examination, should infer

  6. An In Vitro Murine Model of Vascular Smooth Muscle Cell Mineralization.

    Science.gov (United States)

    Kelynack, Kristen J; Holt, Stephen G

    2016-01-01

    Vascular calcification (VC) is seen ubiquitously in aging blood vessels and prematurely in disease states like renal failure. It is thought to be driven by a number of systemic and local factors that lead to extra-osseous deposition of mineral in the vascular wall and valves as a common endpoint. The response of resident vascular smooth muscle cell to these dystrophic signals appears to be important in this process. Whilst in vivo models allow the observation of global changes in a pro-calcific environment, identifying the specific cells and mechanisms involved has been largely garnered from in vitro experiments, which provide added benefits in terms of reproducibility, cost, and convenience. Here we describe a 7-21 day cell culture model of calcification developed using immortalized murine vascular smooth muscle cells (MOVAS-1). This model provides a method by which vascular smooth muscle cell involvement and manipulation within a mineralizing domain can be studied.

  7. Imaging findings in acute calcific prevertebral tendinitis

    Energy Technology Data Exchange (ETDEWEB)

    Grassi, Caio Giometti; Diniz, Fabio de Vilhena; Garcia, Marcio Ricardo Taveira; Gomes, Regina Lucia Elia; Daniel, Mauro Miguel; Funari, Marcelo Buarque de Gusmao [Hospital Israelita Albert Einstein (HIAE), Sao Paulo, SP (Brazil). Imaging Dept.

    2011-09-15

    Acute calcific prevertebral tendinitis is a benign and rare condition that presents calcification of the superior oblique fibers of longus colli muscle with local inflammatory reaction. Such condition is one of the less common presentations of calcium hydroxyapatite deposition disease. Clinical signs are usually acute neck pain and odynophagia, and it may be misdiagnosed as retropharyngeal abscess, spondylodiscitis or traumatic injury. The imaging findings in calcific prevertebral tendinitis are pathognomonic. The knowledge of such findings is extremely important to avoid unnecessary interventions in a patient presenting a condition with a good response to conservative treatment. (author)

  8. Atypical calcific tendinitis with cortical erosions

    Energy Technology Data Exchange (ETDEWEB)

    Kraemer, E.J. [College of Medicine, Univ. of Iowa, Iowa City, IA (United States); El-Khoury, G.Y. [Dept. of Radiology and Orthopaedics, Univ. of Iowa, Iowa City, IA (United States)

    2000-12-01

    Objective. To present and discuss six cases of calcific tendinitis in atypical locations (one at the insertion of the pectoralis major and five at the insertion of the gluteus maximus).Patients and results. All cases were associated with cortical erosions, and five had soft tissue calcifications. The initial presentation was confusing and the patients were suspected of having infection or neoplastic disease.Conclusion. Calcific tendinitis is a self-limiting condition. It is important to recognize the imaging features of this condition to avoid unnecessary investigation and surgery. (orig.)

  9. Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.

    Science.gov (United States)

    Stabley, John N; Towler, Dwight A

    2017-02-01

    Diabetes mellitus increasingly afflicts our aging and dysmetabolic population. Type 2 diabetes mellitus and the antecedent metabolic syndrome represent the vast majority of the disease burden-increasingly prevalent in children and older adults. However, type 1 diabetes mellitus is also advancing in preadolescent children. As such, a crushing wave of cardiometabolic disease burden now faces our society. Arteriosclerotic calcification is increased in metabolic syndrome, type 2 diabetes mellitus, and type 1 diabetes mellitus-impairing conduit vessel compliance and function, thereby increasing the risk for dementia, stroke, heart attack, limb ischemia, renal insufficiency, and lower extremity amputation. Preclinical models of these dysmetabolic settings have provided insights into the pathobiology of arterial calcification. Osteochondrogenic morphogens in the BMP-Wnt signaling relay and transcriptional regulatory programs driven by Msx and Runx gene families are entrained to innate immune responses-responses activated by the dysmetabolic state-to direct arterial matrix deposition and mineralization. Recent studies implicate the endothelial-mesenchymal transition in contributing to the phenotypic drift of mineralizing vascular progenitors. In this brief overview, we discuss preclinical disease models that provide mechanistic insights-and point to challenges and opportunities to translate these insights into new therapeutic strategies for our patients afflicted with diabetes mellitus and its arteriosclerotic complications. © 2016 American Heart Association, Inc.

  10. Relationship between the arterial calcification detected in mammography and coronary artery disease

    Energy Technology Data Exchange (ETDEWEB)

    Topal, Ugur [Department of Radiology, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey)], E-mail: utopal@uludag.edu.tr; Kaderli, Aysel [Department of Cardiology, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey); Topal, Naile Bolca [Department of Radiology, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey); Ozdemir, Buelent; Yesilbursa, Dilek; Cordan, Jale [Department of Cardiology, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey); Ediz, Buelent [Department of Statistics, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey); Aydinlar, Ali [Department of Cardiology, Uludag University, Medical School, Goeruekle Campus, 16059 Bursa (Turkey)

    2007-09-15

    Objective: Arterial calcification is frequently encountered in mammography. The frequency of breast arterial calcification (BAC) increases with increasing age. Studies have shown that BAC is seen more frequently among the people who are under the risk of coronary artery diseases (CAD) such as diabetes and hypertension. The objective of this study is to investigate the relationship between the arterial calcification detected in mammography and the CAD. Material and methods: Screening mammography was performed in 123 women above the age of 40 years who had been examined with coronary angiography for the evaluation of CAD. The presence of BAC, number of affected vessels, and the distribution of calcification in the vessel wall were evaluated in the mammography. Subjects were questioned in terms of the cardiovasculary risk factors. The severity of CAD was evaluated according to the Gensini scoring. In addition, the number of blood vessels with stenosis of more than 50% was used as the vascular score. The correlation between Gensini and the vascular scores, and BAC was statistically evaluated using Mann-Whitney U and Kruskal-Wallis tests. Results: Eighty (65%) of 123 patients had CAD. BAC was detected in the mammography of 49 (39.8%) subjects. The ages and duration of menopause of the cases with BAC were significantly higher than those without BAC (p < 0.001). There was an almost significant correlation between the BAC and Gensini scores (p = 0.059). There was a significant increase in the frequency of BAC among subjects with more than two vessels with stenosis (p = 0.033). Conclusion: Frequency of BAC increases with increasing age. BAC is also frequently seen in subjects having severe coronary artery disease. Although increasing age may be a factor increasing the frequency of BAC, BAC may also be an indicator of CAD. Therefore, the mentioning of arterial calcification in mammography reports may be important in warning the clinician in terms of CAD.

  11. In vitro calcification of chemically functionalized carbon nanotubes.

    Science.gov (United States)

    Beuvelot, Johanne; Bergeret, Céline; Mallet, Romain; Fernandez, Vincent; Cousseau, Jack; Baslé, Michel Félix; Chappard, Daniel

    2010-10-01

    Bone is composed of two phases. The organic phase is made of collagen fibrils assembled in broad fibers acting as a template for mineralization. The mineral phase comprises hydroxyapatite (HAP) crystals grown between and inside the collagen fibers. We have developed a biomimetic material using functionalized carbon nanotubes as scaffold to initiate in vitro mineralization. Biomimetic formation of HAP was performed on single-walled carbon nanotubes (SWCNTs) which have been grafted with carboxylic groups. Two types of nanotubes, HiPco(R) and Carbon Solutions(R), were oxidized via various acidic processes, leading to five different groups of carboxylated nanotubes, fully characterized by physical methods (thermogravimetric analysis, attenuated total reflectance infrared spectroscopy and X-ray photoelectron spectroscopy). All samples were dispersed in ultra-pure water and incubated for 2weeks in a synthetic body fluid, in order to induce the calcification of the SWCNTs. Scanning electron microscopy (SEM) and energy-dispersive X-ray analysis studies showed that Ca(2+) and PO(4)(3-) ions were deposited as round-shaped nodules (calcospherites) on the carboxylated SWCNTs. Fourier transform infrared and Raman spectroscopic studies confirmed the HAP formation, and image analysis made on SEM pictures showed that calcospherites and carboxylated SWCNTs were packed together. The size of calcospherites thus obtained in vitro from the HiPco(R) series was close to that issued from calcospherites observed in vivo. Functionalization of SWCNTs with carboxylic groups confers the capacity to induce calcification similar to woven bone.

  12. Intra-Section Analysis of Human Coronary Arteries Reveals a Potential Role for Micro-Calcifications in Macrophage Recruitment in the Early Stage of Atherosclerosis.

    Directory of Open Access Journals (Sweden)

    Martijn L L Chatrou

    Full Text Available Vascular calcification is associated with poor cardiovascular outcome. Histochemical analysis of calcification and the expression of proteins involved in mineralization are usually based on whole section analysis, thereby often ignoring regional differences in atherosclerotic lesions. At present, limited information is available about factors involved in the initiation and progression of atherosclerosis.This study investigates the intra-section association of micro-calcifications with markers for atherosclerosis in randomly chosen section areas of human coronary arteries. Moreover, the possible causal relationship between calcifying vascular smooth muscle cells and inflammation was explored in vitro.To gain insights into the pathogenesis of atherosclerosis, we performed analysis of the distribution of micro-calcifications using a 3-MeV proton microbeam. Additionally, we performed systematic analyses of 30 to 40 regions of 12 coronary sections obtained from 6 patients including histology and immuno-histochemistry. Section areas were classified according to CD68 positivity. In vitro experiments using human vascular smooth muscle cells (hVSMCs were performed to evaluate causal relationships between calcification and inflammation.From each section multiple areas were randomly chosen and subsequently analyzed. Depositions of calcium crystals at the micrometer scale were already observed in areas with early pre-atheroma type I lesions. Micro-calcifications were initiated at the elastica interna concomitantly with upregulation of the uncarboxylated form of matrix Gla-protein (ucMGP. Both the amount of calcium crystals and ucMGP staining increased from type I to IV atherosclerotic lesions. Osteochondrogenic markers BMP-2 and osteocalcin were only significantly increased in type IV atheroma lesions, and at this stage correlated with the degree of calcification. From atheroma area type III onwards a considerable number of CD68 positive cells were observed

  13. Calcification preceding new bone formation induced by demineralized bone matrix gelatin.

    Science.gov (United States)

    Yamashita, K; Takagi, T

    1992-03-01

    Demineralized bone matrix gelatin (BMG) was implanted into the skeletal muscle of Sprague-Dawley (S.D.) rats, and histological changes were examined 3, 5, 7, 10 and 15 days later. Before bone formation, a specific calcification process was found in most of the BMG from day 5 and 7 after implantation. The heterotopic calcified sites were not always consistent with the sites of the alkaline phosphatase activity. It was considered that this calcification progresses without any cellular components, and we distinguished this type of calcification as "acellular mineral deposition" from the calcification which occurs in new bone formation. This "acellular mineral deposition" was first observed as small spherical calcified deposits in the BMG on day 7 after implantation; these deposits then gradually grew and fused with each other. Some multinucleated cells appeared near the site of calcification on day 7 after implantation, but osteoblasts or osteoblast-like cells were scarcely observed around the calcified deposits in BMG until day 7. Vascularization was often observed near the "acellular mineral deposition" and the new bone formation. Fourier transform infrared spectroscopy showed that the calcified deposits in BMG were composed of hydroxyapatite, carbonateapatite and other calcium phosphate components, and that the first two components became prominent with time. It is believed that the "acellular mineral deposition" is due to the deposition of calcium and phosphate into the BMG by a process of heterogenic nucleation that does not involve osteoblasts or matrix vesicles. Bone formation induced by the BMG occurred after the "acellular mineral deposition." The experimental calcification shown in this paper seems a useful model for the study of biocalcification.

  14. Serum Calcification Propensity Predicts All-Cause Mortality in Predialysis CKD

    Science.gov (United States)

    Ford, Martin L.; Tomlinson, Laurie A.; Bodenham, Emma; McMahon, Lawrence P.; Farese, Stefan; Rajkumar, Chakravarthi; Holt, Stephen G.; Pasch, Andreas

    2014-01-01

    Medial arterial calcification is accelerated in patients with CKD and strongly associated with increased arterial rigidity and cardiovascular mortality. Recently, a novel in vitro blood test that provides an overall measure of calcification propensity by monitoring the maturation time (T50) of calciprotein particles in serum was described. We used this test to measure serum T50 in a prospective cohort of 184 patients with stages 3 and 4 CKD, with a median of 5.3 years of follow-up. At baseline, the major determinants of serum calcification propensity included higher serum phosphate, ionized calcium, increased bone osteoclastic activity, and lower free fetuin-A, plasma pyrophosphate, and albumin concentrations, which accounted for 49% of the variation in this parameter. Increased serum calcification propensity at baseline independently associated with aortic pulse wave velocity in the complete cohort and progressive aortic stiffening over 30 months in a subgroup of 93 patients. After adjustment for demographic, renal, cardiovascular, and biochemical covariates, including serum phosphate, risk of death among patients in the lowest T50 tertile was more than two times the risk among patients in the highest T50 tertile (adjusted hazard ratio, 2.2; 95% confidence interval, 1.1 to 5.4; P=0.04). This effect was lost, however, after additional adjustment for aortic stiffness, suggesting a shared causal pathway. Longitudinally, serum calcification propensity measurements remained temporally stable (intraclass correlation=0.81). These results suggest that serum T50 may be helpful as a biomarker in designing methods to improve defenses against vascular calcification. PMID:24179171

  15. Proton pumping accompanies calcification in foraminifera

    Science.gov (United States)

    Toyofuku, Takashi; Matsuo, Miki Y.; de Nooijer, Lennart Jan; Nagai, Yukiko; Kawada, Sachiko; Fujita, Kazuhiko; Reichart, Gert-Jan; Nomaki, Hidetaka; Tsuchiya, Masashi; Sakaguchi, Hide; Kitazato, Hiroshi

    2017-01-01

    Ongoing ocean acidification is widely reported to reduce the ability of calcifying marine organisms to produce their shells and skeletons. Whereas increased dissolution due to acidification is a largely inorganic process, strong organismal control over biomineralization influences calcification and hence complicates predicting the response of marine calcifyers. Here we show that calcification is driven by rapid transformation of bicarbonate into carbonate inside the cytoplasm, achieved by active outward proton pumping. Moreover, this proton flux is maintained over a wide range of pCO2 levels. We furthermore show that a V-type H+ ATPase is responsible for the proton flux and thereby calcification. External transformation of bicarbonate into CO2 due to the proton pumping implies that biomineralization does not rely on availability of carbonate ions, but total dissolved CO2 may not reduce calcification, thereby potentially maintaining the current global marine carbonate production.

  16. Pericardial adipose tissue and coronary artery calcification in the Multi-ethnic Study of Atherosclerosis (MESA).

    Science.gov (United States)

    McClain, Jill; Hsu, Fang; Brown, Elizabeth; Burke, Gregory; Carr, John; Harris, Tamara; Kritchevsky, Stephen; Szklo, Moyses; Tracy, Russell; Ding, Jingzhong

    2013-05-01

    To examine the relationship of pericardial adipose tissue (PAT) with coronary artery calcification in the Multi-Ethnic Study of Atherosclerosis. The baseline cohort comprised 6,814 Caucasian (38%), African-American (28%), Chinese American (12%), and Hispanic (22%) adults aged 45-84, without known clinical cardiovascular disease. Cardiac CT was used to measure PAT (cm(3) ) and calcification (Agatston score). We examined cross-sectional associations of PAT with the presence (score >0) and severity (continuous score if >0) of calcification using prevalence ratio (PR) (n = 6,672) and linear regression (n = 3,362), respectively. Main models were adjusted for age, age(2) , gender, race/ethnicity, field site, smoking, physical activity, alcohol, and education. PAT volume (adjusted for age, height, weight, and site) was greatest in Chinese males, whereas Black males had less PAT than all but Black females. PAT was associated with presence [PR per standard deviation (SD): 1.06 (95% CI: 1.04, 1.08)] and severity [difference in log Agatston score per SD: 0.15 (0.09, 0.21)] of calcification, but neither association varied by race/ethnicity. Adjustment for generalized adiposity attenuated but did not eliminate the associations. With further adjustment for traditional risk factors and inflammatory markers, only the association with severity remained statistically significant [PR: 1.02 (1.00, 1.04); difference: 0.10 (0.03, 0.17)]. Heterogeneity by sex was observed for the presence of calcification (PR in men: 1.04; in women: 1.08; P for interaction PAT was associated with the presence and severity of coronary artery calcification in this cohort, but neither association varied by race/ethnicity. Copyright © 2013 The Obesity Society.

  17. Progressive liver calcifications in neonatal coxsackievirus infection

    Energy Technology Data Exchange (ETDEWEB)

    Konen, O.; Rathaus, V.; Shapiro, M. [Dept. of Diagnostic Imaging, Sapir Medical Center, Meir General Hospital, Kfar Saba (Israel); Bauer, S.; Dolfin, T. [Neonatal Dept. Neonatal intensive Care, Sapir Medical Center, Meir General Hospital Affiliated with the Sackler School of Medicine, Tel-Aviv University, Tel-Aviv (Israel)

    2000-05-01

    Coxsackievirus group B can cause a severe systemic disease in the perinatal period. Severe manifestations like meningitis, encephalitis, hepatitis, and myocarditis have been previously reported. A case of a twin neonate infected by coxsackievirus group B is described, who developed progressive extensive hepatic calcifications demonstrated by ultrasound and computed tomography with follow-up. Hepatic calcifications in coxsackievirus infection have not been previously reported. (orig.)

  18. Coral calcification in a changing ocean

    Science.gov (United States)

    Kuffner, Ilsa B.

    2010-01-01

    Animals and plants that live in the ocean form skeletons and other hard parts by combining calcium ions and carbonate ions to create calcium carbonate. This process is called calcification. In tropical and subtropical oceans, the calcification of corals and other organisms creates reefs that protect islands, produce beautiful white-sand beaches, and create habitat for thousands of species that live on coral reefs.

  19. Gastrointestinal stromal tumor presenting with prominent calcification

    Institute of Scientific and Technical Information of China (English)

    Naoki Izawa; Takeshi Sawada; Ryuichi Abiko; Daisuke Kumon; Mami Hirakawa; Mika Kobayashi; Nobuyuki Obinata

    2012-01-01

    We present a rare case of a gastrointestinal stromal tumor (GIST) in the stomach with prominent calcification at presentation.A 61-year-old woman visited our hospital because of epigastric discomfort.A spherical calcified lesion with a diameter of about 30 mm was incidentally shown in the left upper quadrant on an abdominal X-ray.Computed tomography demonstrated that the tumor was growing from the upper gastric body,with calcification in the peripheral ring area.A laparoscopic partial gastrectomy was performed,and the resected specimen revealed a well-circumscribed tumor with exophytic growth from the gastric muscularis propria.Microscopic examination revealed spindleshaped tumor cells with calcification and hemorrhage.Additionally,positive immunoreactivity of the tumor to KIT and CD34 and a low mitotic index resulted in the diagnosis of very low risk GIST.There are a few case reports of heavily calcified GIST,although solitary or punctate calcification of primary GIST has been reported in several case series.Dystrophic calcification of necrotic or degenerative tissue is the supposed cause of primary calcified GISTs.In contrast,appearance of calcification after administration of imatinib mesylate,which may be one indicator of disease response,is possibly caused by a different mechanism.

  20. Intracranial physiological calcification on computed tomography, 1. Calcification of pineal region

    Energy Technology Data Exchange (ETDEWEB)

    Kwak, Ryungchan; Takeuchi, Fumihiko; Ito, Shotaro; Kadoya, Satoru

    1988-06-01

    Of intracranial physiological calcification, common calcification of pineal region, choroid plexus of lateral ventricles and of basal ganglia was examined based on the frequency of occurence of age and sex and type of CT scanners. Consecutive cases of 2877 (1450 males and 1427 females) underwent plain CT scanning were studied. Pathological calcification was excluded from this study. Three types of CT scanners (SCN-200, Somatom 2 and TCT-10 A) were used. As a whole, calcification was shown in 67.7 % in pineal region, 57.6 % in choroid plexus of lateral ventricles and 7.5 % in basal ganglia. First, we reported in detail the calcification of pineal region, in which calcification occurred most frequently. Calcification in pineal region had a close relation with age by increasing with aging. The youngest patient was 8 years old. There was a striking increase in number of patients aged from 10 to 39 years. There was a gradual increase in those aged over 40 years. Of patients aged from 70 to 79 years, calcification was found in 81.5 %. The incidence was noted no changes in patients aged over 80 years. As for patients aged over 20 years, calcification was observed in 75.1 % (82.6 % males and 68.0 % females). In patients aged from 20 to 79 years, the calcification was significantly higher in male than female. Although there was a different incidence of calcification examined by three types of CT scanners, it was not significant. There was no significant difference between thickness of 8 mm section and 10 mm.

  1. Calcification at orifices of aortic arch branches is a reliable and significant marker of stenosis at carotid bifurcation and intracranial arteries

    Energy Technology Data Exchange (ETDEWEB)

    Yamada, Shigeki, E-mail: shigekiyamada3@gmail.com [Department of Neurosurgery and Stroke Center, Rakuwakai Otowa Hospital, Kyoto (Japan); Interfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, Tokyo (Japan); Department of Neurosurgery, Hamamatsu Rosai Hospital, Shizuoka (Japan); Hashimoto, Kenji, E-mail: hashiken8022@yahoo.co.jp [Department of Neurosurgery, Kishiwada Municipal Hospital, Osaka (Japan); Ogata, Hideki, E-mail: hidogata@gmail.com [Department of Neurosurgery, Hamamatsu Rosai Hospital, Shizuoka (Japan); Watanabe, Yoshihiko, E-mail: ynabe@magic.odn.ne.jp [Department of Neurosurgery, Hamamatsu Rosai Hospital, Shizuoka (Japan); Oshima, Marie, E-mail: marie@iis.u-tokyo.ac.jp [Interfaculty Initiative in Information Studies/Institute of Industrial Science, The University of Tokyo, Tokyo (Japan); Miyake, Hidenori, E-mail: hi-miyake@hamamatsuh.rofuku.go.jp [Department of Neurosurgery, Hamamatsu Rosai Hospital, Shizuoka (Japan)

    2014-02-15

    Purpose: Simple rating scale for calcification in the cervical arteries and the aortic arch on multi-detector computed tomography angiography (MDCTA) was evaluated its reliability and validity. Additionally, we investigated where is the most representative location for evaluating the calcification risk of carotid bifurcation stenosis and atherosclerotic infarction in the overall cervical arteries covering from the aortic arch to the carotid bifurcation. Method: The aortic arch and cervical arteries among 518 patients (292 men, 226 women) were evaluated the extent of calcification using a 4-point grading scale for MDCTA. Reliability, validity and the concomitant risk with vascular stenosis and atherosclerotic infarction were assessed. Results: Calcification was most frequently observed in the aortic arch itself, the orifices from the aortic arch, and the carotid bifurcation. Compared with the bilateral carotid bifurcations, the aortic arch itself had a stronger inter-observer agreement for the calcification score (Fleiss’ kappa coefficients; 0.77), but weaker associations with stenosis and atherosclerotic infarction. Calcification at the orifices of the aortic arch branches had a stronger inter-observer agreement (0.74) and enough associations with carotid bifurcation stenosis and intracranial stenosis. In addition, the extensive calcification at the orifices from the aortic arch was significantly associated with atherosclerotic infarction, similar to the calcification at the bilateral carotid bifurcations. Conclusions: The orifices of the aortic arch branches were the novel representative location of the aortic arch and overall cervical arteries for evaluating the calcification extent. Thus, calcification at the aortic arch should be evaluated with focus on the orifices of 3 main branches.

  2. Acute renal infarction secondary to calcific embolus from mitral annular calcification.

    Science.gov (United States)

    Bande, Dinesh; Abbara, Suhny; Kalva, Sanjeeva P

    2011-06-01

    We report a case of a 62-year-old man who presented with right groin pain who subsequently was found to have a renal infarct secondary to calcific embolus from mitral annular calcification on CT and angiography. We briefly review the literature and discuss the importance of this entity in clinical practice.

  3. Postpartum Acute Liver Dysfunction: A Case of Acute Fatty Liver of Pregnancy Developing Massive Intrahepatic Calcification

    Science.gov (United States)

    Bhat, Khalid Javid; Shovkat, Rabia; Samoon, Hamad Jeelani

    2015-01-01

    The function of the liver is particularly affected by the unique physiologic milieu of the pregnancy. Pregnancy-related liver diseases encompass a spectrum of different etiologies that are related to gestation or one of its complications. Hepatic calcification, a rare entity, is usually associated with infectious, vascular, or neoplastic lesions in the liver. To the best of our knowledge, only one case of rapidly occurring pregnancy-related intrahepatic calcification has been documented in a patient with severe eclampsia or hemolysis, elevated liver enzymes and low platelet count (HELLP) syndrome. Here we present a case of immediate “postpartum” acute fatty liver of pregnancy (AFLP) in a 23-year-old hypertensive primigravida, complicated by acute renal dysfunction who developed dense intrahepatic calcification in less than a month after the initial diagnosis. A multidisciplinary approach for the management was used, to which the patient responded aptly. This case illustrates the first description of intrahepatic calcification in AFLP syndrome and highlights some of the challenges met in making the final diagnosis. PMID:27785315

  4. Sudden death in a captive meerkat(Suricata suricatta) with arterial medial and myocardial calcification

    Institute of Scientific and Technical Information of China (English)

    Laura Bongiovann; Nicola Di Girolamo; Leonardo Della Salda; Marcella Massimi; Mariarita Romanucci; Paolo Selleri

    2016-01-01

    A 1-year-old male meerkat was found dead by the owner.The animal was clinically healthy and was regularly vaccinated for distemper virus.Necropsy revealed multifocal to confluent dry white areas in the myocardium,pneumonia and congestive hepatopathy.All the other organs,including gross vessels,were macroscopically normal.The heart showed histologically large,multifocal to confluent areas of mineralization of the myocardium and the wall of small coronary artery.Vascular calcifications were also observed in the hepatic portal tracts and kidneys arteries of small/medium sizes.The arterial lumen appeared narrowed and the wall thickened due to the calcification of the tunica media.In veterinary medicine,arterial mineralization is regarded as a metastatic calcification,as the result of hypercalcemia and/or hyperphosphatemia.However,today,the pathogenesis of medial artery calcification in humans seems to be the results of an active process resembling embryonic osteogenesis,rather than a mere passive process.

  5. Association of mast cells with calcification in the human pineal gland.

    Science.gov (United States)

    Maślińska, Danuta; Laure-Kamionowska, Milena; Deręgowski, Krzysztof; Maśliński, Sławomir

    2010-01-01

    Increased pineal calcifications and decreased pineal melatonin biosynthesis, both age related, support the notion of a pineal bio-organic timing mechanism. The role of calcification in the pathogenesis of pineal gland dysfunction remains unknown but the available data document that calcification is an organized, regulated process, rather than a passive aging phenomenon. The cellular biology and micro-environmental conditions required for calcification remain poorly understood but most studies have demonstrated evidence that mast cells are strongly implicated in this process. The aim of the present study was to examine the phenotype of mast cells associated with early stages and with the progressive development of calcification in the human pineal gland. The study was performed on pineal samples of 170 fetuses and children whose brains were autopsied and diagnosed during 1998-2002. The representative cerebral and pineal specimens were stained with haematoxylin and eosin or the von Kossa staining technique and for the distribution of mast cell tryptase, mast cell chymase, histamine H4 receptor and vascular network using biotinylated Ulex europaeus agglutinin. Tryptase mast cells were found in all stages of pineal gland development independently of the presence of local tissue lesions. All of them were always localized in the close vicinity of the blood vessels and expressed immunoreactivity to histamine H4 receptor antibody. Immunolocalization of mast cells by chymase antibody (and following dual immunostaining with both chymase and tryptase antibodies) demonstrated that these cells were few in number and were located in the subcapsular region of the gland. In our study, all functional mast cells that underwent activation and were co-localized with deposits of calcium did not contain chymase. All of them were stained with tryptase and represent the MC-T phenotype. Tryptase mast cells and extracellular tryptase were often associated with areas of early and more

  6. Vascular Diseases

    Science.gov (United States)

    The vascular system is the body's network of blood vessels. It includes the arteries, veins and capillaries that carry ... to and from the heart. Problems of the vascular system are common and can be serious. Arteries ...

  7. Imaging patterns of intratumoral calcification in the abdominopelvic cavity

    Energy Technology Data Exchange (ETDEWEB)

    Yu, Mi Hye; Kim, Young Jun; Park, Hee Sun; Jung, Sung Il; Jeon, Hae Jeong [Dept. of Radiology, Konkuk University Medical Center, Seoul(Korea, Republic of)

    2017-04-15

    Intratumoral calcification is one of the most noticeable of radiologic findings. It facilitates detection and provides information important for correctly diagnosing tumors. In the abdominopelvic cavity, a wide variety of tumors have calcifications with various imaging features, though the majority of such calcifications are dystrophic in nature. In this article, we classify the imaging patterns of intratumoral calcification according to number, location, and morphology. Then, we describe commonly-encountered abdominopelvic tumors containing typical calcification patterns, focusing on their differentiable characteristics using the imaging patterns of intratumoral calcification.

  8. Imaging Patterns of Intratumoral Calcification in the Abdominopelvic Cavity

    Science.gov (United States)

    Yu, Mi Hye; Park, Hee Sun; Jung, Sung Il; Jeon, Hae Jeong

    2017-01-01

    Intratumoral calcification is one of the most noticeable of radiologic findings. It facilitates detection and provides information important for correctly diagnosing tumors. In the abdominopelvic cavity, a wide variety of tumors have calcifications with various imaging features, though the majority of such calcifications are dystrophic in nature. In this article, we classify the imaging patterns of intratumoral calcification according to number, location, and morphology. Then, we describe commonly-encountered abdominopelvic tumors containing typical calcification patterns, focusing on their differentiable characteristics using the imaging patterns of intratumoral calcification. PMID:28246512

  9. Vascular Vertigo

    OpenAIRE

    Mazyar Hashemilar; Masoud Nikanfar; Dariush Savadi Oskoui

    2017-01-01

    Vertigo is a common complaint in neurology and medicine. The most common causes of vertigo are benign paroxysmal positional vertigo, vestibular neuritis, Meniere’s disease, and vascular disorders. Vertigo of vascular origin is usually limited to migraine, transient ischemic attacks, and ischemic or hemorrhagic stroke. Vascular causes lead to various central or peripheral vestibular syndromes with vertigo. This review provides an overview of epidemiology and clinical syndromes of vascular vert...

  10. 氧化苦参碱对人脐静脉平滑肌细胞钙化的影响及其可能机制%Effect of oxymatrine on vascular calcification of humans umbilical vein smooth muscle cells and its underlying mechanism

    Institute of Scientific and Technical Information of China (English)

    王秀梅; 张娟; 张鸣号; 刘爽; 李桂忠; 曹军

    2012-01-01

    Objective: To observe the effect of oxymatrine (OMT) on calcification of humans umbilical vein smooth muscle cells and its underlying mechanism. Method: Human umbilical vein smooth muscle cells (HUSMCs) were calcified by β-giycerophos-phosphate (β-GP) and then divided into 6 groups: the control group, the calcification group, the pure OMT group, and lower, middle and higher-dosage OMT groups. Cell calcification were observed by Von Kossa staining, calcium content in HUSMCs were determined by the colorimetric method, the alkaline phosphatase (ALP) activity in HUSMCs were determined by phenyl diphosphate-2-sodium, the osteocalcin (OC) level in HUSMCs were determined by radioimmunossay, the transforming growth factor-β1 (TGF-β1) level in HUSMC culture medium and the content changes in psmad2/3 and smad2/3 were determined by the ELISA method, and the expression of Core binding factor a, (Cbfa, ) protein in HUSMCs were determined by western blot method. Result: Compared with the control group, the calcification group showed a great number of black granules among the smooth muscle cells and significant increase in the content of calcium and OC and the activity of ALP; OMT intervention can decrease the content of calcium, OC, TGF-β1, psmad2/3 and Cbfα1 and the activity of ALP. And high-dosage OMT group had better effect than middle and low-dosage groups. Conclusion: OMT can effectively inhibit 0-GP-induced HUSMC calcification and its effect on reducing TGF-β1, psmad2/3 and Cbfα1 may be one of its mechanisms in inhibiting HVSMC calcification.%目的:观察氧化苦参碱(oxymatrine,OMT)对人脐静脉平滑肌细胞(humans umbilical vein smooth muscle cells,HUSMCs)钙化的影响及其可能机制.方法:以β-甘油磷酸盐诱导HUSMCs钙化,实验分为对照组、钙化组、单纯OMT组、OMT干预高、中、低剂量组.采用Von Kossa染色鉴定细胞钙化,比色法检测细胞钙含量,磷酸苯二钠法测定ALP活性,放射免疫法测定骨钙素(OC)

  11. Long-term effect of cinacalcet hydrochloride on abdominal aortic calcification in patients on hemodialysis with secondary hyperparathyroidism

    Science.gov (United States)

    Nakayama, Kazunori; Nakao, Kazushi; Takatori, Yuji; Inoue, Junko; Kojo, Shoichirou; Akagi, Shigeru; Fukushima, Masaki; Wada, Jun; Makino, Hirofumi

    2014-01-01

    Background Secondary hyperparathyroidism (SHPT) is one of the common complications in dialysis patients, and is associated with increased risk of vascular calcification. The effects of cinacalcet hydrochloride treatment on bone and mineral metabolism have been previously reported, but the benefit of cinacalcet on vascular calcification remains uncertain. The aim of this study was to evaluate the impact of cinacalcet on abdominal aortic calcification in dialysis patients. Subjects and methods Patients were on maintenance hemodialysis with insufficiently controlled SHPT (intact parathyroid hormone [PTH] >180 pg/mL) by conventional therapies. All subjects were initially administered 25 mg cinacalcet daily, with concomitant use of calcitriol analogs. Abdominal aortic calcification was annually evaluated by calculating aortic calcification area index (ACAI) using multidetector computed tomography (MDCT), from 12 months before to 36 months after the initiation of cinacalcet therapy. Results Twenty-three patients were analyzed in this study. The mean age was 59.0±8.7 years, 34.8% were women, and the mean dialysis duration was 163.0±76.0 months. After administration of cinacalcet, serum levels of intact PTH, phosphorus, and calcium significantly decreased, and mean Ca × P values significantly decreased from 67.4±7.9 mg2/dL2 to 52±7.7 mg2/dL2. Although the ACAI value did not decrease during the observation period, the increase in ACAI between 24 months and 36 months after cinacalcet administration was significantly suppressed. Conclusion Long-term administration of cinacalcet was associated with reduced progression of abdominal aortic calcification, and achieving appropriate calcium and phosphorus levels may reduce the rates of cardiovascular events and mortality in patients on hemodialysis. PMID:24379691

  12. Vitamin D receptor deficiency and low vitamin D diet stimulate aortic calcification and osteogenic key factor expression in mice.

    Directory of Open Access Journals (Sweden)

    Nadine Schmidt

    Full Text Available Low levels of 25-hydroxy vitamin D (25(OHD are associated with cardiovascular diseases. Herein, we tested the hypothesis that vitamin D deficiency could be a causal factor in atherosclerotic vascular changes and vascular calcification. Aortic root sections of vitamin D receptor knockout (VDR(-/- mice that were stained for vascular calcification and immunostained for osteoblastic differentiation factors showed more calcified areas and a higher expression of the osteogenic key factors Msx2, Bmp2, and Runx2 than the wild-type mice (P<0.01. Data from LDL receptor knockout (LDLR(-/- mice that were fed western diet with either low (50 IU/kg, recommended (1,000 IU/kg, or high (10,000 IU/kg amounts of vitamin D(3 over 16 weeks revealed increasing plasma concentrations of 25(OHD (P<0.001 with increasing intake of vitamin D, whereas levels of calcium and phosphorus in plasma and femur were not influenced by the dietary treatment. Mice treated with the low vitamin D diet had more calcified lesions and a higher expression of Msx2, Bmp2, and Runx2 in aortic roots than mice fed recommended or high amounts of vitamin D (P<0.001. Taken together, these findings indicate vitamin D deficiency as a risk factor for aortic valve and aortic vessel calcification and a stimulator of osteogenic key factor expression in these vascular areas.

  13. Genetics Home Reference: familial idiopathic basal ganglia calcification

    Science.gov (United States)

    ... idiopathic basal ganglia calcification ( FIBGC , formerly known as Fahr disease) is a condition characterized by abnormal deposits of ... on chromosome 14q for idiopathic basal ganglia calcification (Fahr disease). Am J Hum Genet. 1999 Sep;65(3): ...

  14. Genetic associations with valvular calcification and aortic stenosis

    DEFF Research Database (Denmark)

    Thanassoulis, George; Campbell, Catherine Y; Owens, David S

    2013-01-01

    Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease.......Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease....

  15. FIBROBLAST INVOLVEMENT IN SOFT CONNECTIVE TISSUE CALCIFICATION

    Directory of Open Access Journals (Sweden)

    Ivonne eRonchetti

    2013-03-01

    Full Text Available Soft connective tissue calcification is not a passive process, but the consequence of metabolic changes of local mesenchymal cells that, depending on both genetic and environmental factors, alter the balance between pro- and anti-calcifying pathways. While the role of smooth muscle cells and pericytes in ectopic calcifications has been widely investigated, the involvement of fibroblasts is still elusive. Fibroblasts isolated from the dermis of PXE patients and of patients exhibiting PXE-like clinical and histopathological findings offer an attractive model to investigate the mechanisms leading to the precipitation of mineral deposits within elastic fibres and to explore the influence of the genetic background and of the extracellular environment on fibroblast-associated calcifications, thus improving the knowledge on the role of mesenchymal cells on pathologic mineralization.

  16. Calcification detection of abdominal aorta in CT images and 3D visualization in VR devices.

    Science.gov (United States)

    Garcia-Berna, Jose A; Sanchez-Gomez, Juan M; Hermanns, Judith; Garcia-Mateos, Gines; Fernandez-Aleman, Jose L

    2016-08-01

    Automatic calcification detection in abdominal aorta consists of a set of computer vision techniques to quantify the amount of calcium that is found around this artery. Knowing that information, it is possible to perform statistical studies that relate vascular diseases with the presence of calcium in these structures. To facilitate the detection in CT images, a contrast is usually injected into the circulatory system of the patients to distinguish the aorta from other body tissues and organs. This contrast increases the absorption of X-rays by human blood, making it easier the measurement of calcifications. Based on this idea, a new system capable of detecting and tracking the aorta artery has been developed with an estimation of the calcium found surrounding the aorta. Besides, the system is complemented with a 3D visualization mode of the image set which is designed for the new generation of immersive VR devices.

  17. RAGE deficiency alleviates aortic valve calcification in ApoE(-/-) mice via the inhibition of endoplasmic reticulum stress.

    Science.gov (United States)

    Wang, Bo; Cai, Zhejun; Liu, Baoqing; Liu, Zongtao; Zhou, Xianming; Dong, Nianguo; Li, Fei

    2017-03-01

    Receptor for advanced glycation end products (RAGE) and endoplasmic reticulum (ER) stress have been shown to be involved in calcific aortic valve disease (CAVD). However, the association between RAGE and ER stress remains unknown in the pathogenesis of CAVD. The current study aims to test the hypothesis that RAGE deficiency alleviates aortic valve calcification via the inhibition of ER stress. Up-regulation of RAGE and ER stress markers in calcified human aortic valves were confirmed by immunoblotting. Aortic valve calcification was evaluated in atherosclerotic prone ApoE(-/-) mice or in mice with dual deficiencies of ApoE and RAGE (ApoE(-/-)RAGE(-/-)) fed with high cholesterol diet for 24weeks. Echocardiography and histological examination show that genetic deficiency of RAGE attenuates aortic valve calcification in ApoE(-/-) mice. Meanwhile, RAGE deficiency inhibited the osteogenic signaling and ER stress activation as well as suppressed macrophage infiltration in vivo. Cultured human aortic valve interstitial cells (AVICs) were treated with high molecular group box 1 protein (HMGB1) as in vitro model. We found that HMGB1 induced osteoblastic differentiation and calcification through RAGE/ER stress. Furthermore, Sox9 up-regulation and intranuclear translocation mediated the pro-osteogenic effect of HMGB1 on AVICs. RAGE or ER stress knockdown reduced the up-regulation of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α) in human AVICs exposed to HMGB1.These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE(-/-) mice via inhibition of ER stress. HMGB1 induces AVIC osteoblastic differentiation and calcification through RAGE/ER stress/Sox9 pathway. Copyright © 2016. Published by Elsevier B.V.

  18. Intracranial arterial calcification is highly prevalent in hemodialysis patients but does not associate with acute ischemic stroke.

    Science.gov (United States)

    Power, Albert; Chan, Kakit; Haydar, Ali; Hamady, Mohamed; Cairns, Tom; Taube, David; Duncan, Neill

    2011-04-01

    Intracranial arterial calcification (IAC) is associated with ischemic stroke in the general population but this relationship has not been examined in hemodialysis patients. We examined the factors associated with IAC and its relationship with acute ischemic stroke in this population. We retrospectively studied 490 head computed tomographic scans from 2225 hemodialysis patients presenting with neurological symptoms at our center (October 2005-May 2009). Intracranial arterial calcification was graded using a validated scoring system. Multivariate regression was used to examine the factors associated with the presence of IAC, its severity, and its ability to predict acute ischemic stroke. Weibull's survival models analyzed the relationship between IAC severity and survival. Ninety-five percent of patients with ischemic stroke had IAC vs. 83% in the nonstroke group (P=0.02). Intracranial arterial calcification severity increased with age (Pacute ischemic stroke (P=0.05) on logistic regression analysis. High-grade and not low-grade IAC was associated with worse survival (P=0.008). Intracranial arterial calcification is highly prevalent in hemodialysis patients, especially in those with acute ischemic stroke. Its severity is prognostically significant and associated with risk factors for vascular calcification and may confer a greater risk of acute ischemic stroke. The mechanisms underlying the high incidence of ischemic stroke in this patient group require further comprehensive study. © 2011 The Authors. Hemodialysis International © 2011 International Society for Hemodialysis.

  19. High-Flux Hemodialysis and High-Volume Hemodiafiltration Improve Serum Calcification Propensity.

    Directory of Open Access Journals (Sweden)

    Marijke Dekker

    Full Text Available Calciprotein particles (CPPs may play an important role in the calcification process. The calcification propensity of serum (T50 is highly predictive of all-cause mortality in chronic kidney disease patients. Whether T50 is therapeutically improvable, by high-flux hemodialysis (HD or hemodiafiltration (HDF, has not been studied yet.We designed a cross-sectional single center study, and included stable prevalent in-center dialysis patients on HD or HDF. Patients were divided into two groups based on dialysis modality, were on a thrice-weekly schedule, had a dialysis vintage of > 3 months and vascular access providing a blood flow rate > 300 ml/min. Calcification propensity of serum was measured by the time of transformation from primary to secondary CPP (T50 test, by time-resolved nephelometry.We included 64 patients, mean convective volume was 21.7L (SD 3.3L. In the pooled analysis, T50 levels increased in both the HD and HDF group with pre- and post-dialysis (mean (SD of 244(64 - 301(57 and 253(55 - 304(61 min respectively (P = 0.43(HD vs. HDF. The mean increase in T50 was 26.29% for HD and 21.97% for HDF patients (P = 0.61 (HD vs. HDF. The delta values (Δ of calcium, phosphate and serum albumin were equal in both groups. Baseline T50 was negatively correlated with phosphate, and positively correlated with serum magnesium and fetuin-A. The ΔT50 was mostly influenced by Δ phosphate (r = -0.342; P = 0.002 HD and r = -0.396; P<0.001 HDF in both groups.HD and HDF patients present with same baseline T50 calcification propensity values pre-dialysis. Calcification propensity is significantly improved during both HD and HDF sessions without significant differences between both modalities.

  20. Dystrophic calcification of the prostate after cryotherapy.

    Science.gov (United States)

    Dru, Christopher; Bender, Leon

    2014-01-01

    We present a previously undocumented complication of dystrophic calcification of the prostate after cryotherapy. An 87-year-old male presented with recurrent lower urinary tract infections and was found to have an obstructing large calcified mass in the right lobe of the prostate. Subsequently, he underwent transurethral resection of the prostate (TURP) and bladder neck with laser lithotripsy to remove the calculus. We propose that chronic inflammation and necrosis of the prostate from cryotherapy resulted in dystrophic calcification of the prostate. As the use of cryotherapy for the treatment of localized prostate cancer continues to increase, it is important that clinicians be aware of this scenario and the technical challenges it poses.

  1. Calcific tendinitis of the gluteus maximus tendon (Gluteus maximus tendinitis)

    Energy Technology Data Exchange (ETDEWEB)

    Wepfer, J.F.; Reed, J.G.; Cullen, G.M.; McDevitt, W.P.

    1983-02-01

    Seven cases of calcific tendinitis of the gluteus maximus tendon are presented. Awareness of the precise anatomic location of the calcific deposit is essential for the accurate diagnosis of this uncommon site of tendinitis. Clinically, the presenting complaint is that of pain. In some instances, however, the patients are asymptomatic and the calcification is an incidental finding.

  2. The Notch pathway attenuates interleukin 1beta (IL1beta)-mediated induction of adenylyl cyclase 8 (AC8) expression during vascular smooth muscle cell (VSMC) trans-differentiation

    NARCIS (Netherlands)

    Keuylian, Z.; Baaij, J.H. de; Glorian, M.; Rouxel, C.; Merlet, E.; Lipskaia, L.; Blaise, R.; Mateo, V.; Limon, I.

    2012-01-01

    Vascular smooth muscle cell (VSMC) trans-differentiation, or their switch from a contractile/quiescent to a secretory/inflammatory/migratory state, is known to play an important role in pathological vascular remodeling including atherosclerosis and postangioplasty restenosis. Several reports have

  3. The Notch pathway attenuates interleukin 1beta (IL1beta)-mediated induction of adenylyl cyclase 8 (AC8) expression during vascular smooth muscle cell (VSMC) trans-differentiation

    NARCIS (Netherlands)

    Keuylian, Z.; Baaij, J.H. de; Glorian, M.; Rouxel, C.; Merlet, E.; Lipskaia, L.; Blaise, R.; Mateo, V.; Limon, I.

    2012-01-01

    Vascular smooth muscle cell (VSMC) trans-differentiation, or their switch from a contractile/quiescent to a secretory/inflammatory/migratory state, is known to play an important role in pathological vascular remodeling including atherosclerosis and postangioplasty restenosis. Several reports have es

  4. Direct Promotion of Collagen Calcification by Alkaline Phosphatase

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    Alkaline phosphatase promotes hydrolysis of phosphate containing substrates, causes a rise in inorganic phosphate and, therefore, enhances calcification of biological tissues. In this work, the calcification of collagen in a model serum was used as a model of collagenous tissue biomaterials to study the possible calcification promotion mechanism of alkaline phosphatase. In the enzyme concentration range of 0.10.5mg/mL, the enzyme shows a direct calcification promoting effect which is independent of the hydrolysis of its phosphate containing substrates but proportional to the enzyme concentration. Potassium pyrophosphate somewhat inhibits the calcification promotion.

  5. Sclerosing peritonitis with gross calcification: case report

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Cheung Sook; Kim, Young Jae; Min, Seon Jeong; Cho, Seong Whi; Lee, Gyung Kyu; Lee, Eil Seong; Kang, Ik Won [Hallym University College of Medicine, Seoul (Korea, Republic of)

    2003-09-01

    Sclerosing peritonitis is an uncommon complication of continuous ambulatory peritoneal dialysis (CAPD) and can lead to small bowel dysfunction involving abdominal pain, progressive loss of ultrafiltration, and small intestinal obstruction. Peritoneal thickening, in which calcification can develop, often starts as al small plaque which gradually becomes larger. We report a case of CAPD-related calcifying peritonitis.

  6. Retropharyngeal Calcific Tendonitis Mimics a Retropharyngeal Abscess

    Directory of Open Access Journals (Sweden)

    Natasha Pollak

    2013-01-01

    Full Text Available Retropharyngeal calcific tendonitis (RCT is an uncommon, self-limiting condition that is often omitted in the differential diagnosis of a retropharyngeal fluid collection. This condition mimics a retropharyngeal abscess and should be considered when evaluating a fluid collection in the retropharyngeal space. Although calcific tendonitis at other sites has been well described in the medical literature, it appears that this entity has been underreported in the otolaryngology literature where only a few case reports have been identified. Presumably, the actual incidence is higher than the reported incidence, due to lack of familiarity with this disorder. As an otolaryngologist’s scope of practice includes the managements of retropharyngeal lesions, it is important for the otolaryngologist to recognize the presentation of acute RCT and be familiar with appropriate treatment strategies. Retropharyngeal calcific tendonitis presents with neck pain, limitation of neck range of motion and includes inflammation, calcifications, and a sterile effusion within the longus colli muscle. Treatment is medical with nonsteroidal anti-inflammatory medications. RCT does not require surgical treatment, and an accurate diagnosis can prevent unnecessary attempts at operative drainage. In this study, we discuss two cases of RCT, summarize the salient features in diagnosis, including key radiologic features, discuss treatment options, and review the literature.

  7. Differential diagnosis of disseminated periventricular calcifications

    Energy Technology Data Exchange (ETDEWEB)

    Rieger, P.; Piepgras, U.

    1986-08-01

    Juvenile disseminated periventricular calcifications may occur in tuberous sclerosis, toxoplasmosis, cytomegaly, and in tuberculous meningitis. Cysticercosis, by contrast, does not result in corresponding intracerebral foci until an older age. Differential diagnosis is no problem if clinical findings are typical (tuberous sclerosis) or if serological verification is positive. However, any unclear clinical diagnosis can often be secured by CT.

  8. What Is Vascular Disease?

    Science.gov (United States)

    ... Donors Corporate Sponsors Donor Privacy Policy What Is Vascular Disease? What Is Vascular Disease? Vascular disease is any abnormal condition of ... steps to prevent vascular disease here. Understanding the Vascular System Your vascular system – the highways of the ...

  9. The Involvement of miR-29b-3p in Arterial Calcification by Targeting Matrix Metalloproteinase-2

    Science.gov (United States)

    Jiang, Wenhong; Zhang, Zhanman; Yang, Han; Lin, Qiuning; Han, Chuangye

    2017-01-01

    Vascular calcification is a risk predictor and common pathological change in cardiovascular diseases that are associated with elastin degradation and phenotypic transformation of vascular smooth muscle cells via gelatinase matrix metalloproteinase-2 (MMP2). However, the mechanisms involved in this process remain unclear. In this study, we investigated the relationships between miR-29b-3p and MMP2, to confirm miR-29b-3p-mediated MMP2 expression at the posttranscriptional level in arterial calcification. In male Sprague Dawley rats, arterial calcification was induced by subcutaneous injection of a toxic dose of cholecalciferol. In vivo, the quantitative real-time polymerase chain reaction (qRT-PCR) showed that MMP2 expression was upregulated in calcified arterial tissues, and miR-29b-3p expression was downregulated. There was a negative correlation between MMP2 mRNA expression and miR-29b-3p levels (P = 0.0014, R2 = 0.481). Western blotting showed that MMP2 expression was significantly increased in rats treated with cholecalciferol. In vitro, overexpression of miR-29b-3p led to decreased MMP2 expression in rat vascular smooth muscle cells, while downregulation of miR-29b-3p expression led to increased MMP2 expression. Moreover, the luciferase reporter assay confirmed that MMP2 is the direct target of miR-29b-3p. Together, our results demonstrated that a role of miR-29b-3p in vascular calcification involves targeting MMP2. PMID:28164126

  10. The Involvement of miR-29b-3p in Arterial Calcification by Targeting Matrix Metalloproteinase-2

    Directory of Open Access Journals (Sweden)

    Wenhong Jiang

    2017-01-01

    Full Text Available Vascular calcification is a risk predictor and common pathological change in cardiovascular diseases that are associated with elastin degradation and phenotypic transformation of vascular smooth muscle cells via gelatinase matrix metalloproteinase-2 (MMP2. However, the mechanisms involved in this process remain unclear. In this study, we investigated the relationships between miR-29b-3p and MMP2, to confirm miR-29b-3p-mediated MMP2 expression at the posttranscriptional level in arterial calcification. In male Sprague Dawley rats, arterial calcification was induced by subcutaneous injection of a toxic dose of cholecalciferol. In vivo, the quantitative real-time polymerase chain reaction (qRT-PCR showed that MMP2 expression was upregulated in calcified arterial tissues, and miR-29b-3p expression was downregulated. There was a negative correlation between MMP2 mRNA expression and miR-29b-3p levels (P=0.0014, R2=0.481. Western blotting showed that MMP2 expression was significantly increased in rats treated with cholecalciferol. In vitro, overexpression of miR-29b-3p led to decreased MMP2 expression in rat vascular smooth muscle cells, while downregulation of miR-29b-3p expression led to increased MMP2 expression. Moreover, the luciferase reporter assay confirmed that MMP2 is the direct target of miR-29b-3p. Together, our results demonstrated that a role of miR-29b-3p in vascular calcification involves targeting MMP2.

  11. [Vascular dementia

    NARCIS (Netherlands)

    Leeuw, H.F. de; Gijn, J. van

    2004-01-01

    Vascular dementia is one of the most frequently occurring dementia syndromes. Its prevalence is about 5% among subjects above 85 years of age. Elevated blood pressure and atherosclerosis are the most important risk factors. According to international criteria, vascular dementia usually occurs within

  12. Activating transcription factor-4 promotes mineralization in vascular smooth muscle cells

    Science.gov (United States)

    Masuda, Masashi; Miyazaki-Anzai, Shinobu; Keenan, Audrey L.; Shiozaki, Yuji; Okamura, Kayo; Chick, Wallace S.; Williams, Kristina; Zhao, Xiaoyun; Rahman, Shaikh Mizanoor; Tintut, Yin; Adams, Christopher M.

    2016-01-01

    Emerging evidence indicates that upregulation of the ER stress–induced pro-osteogenic transcription factor ATF4 plays an important role in vascular calcification, a common complication in patients with aging, diabetes, and chronic kidney disease (CKD). In this study, we demonstrated the pathophysiological role of ATF4 in vascular calcification using global Atf4 KO, smooth muscle cell–specific (SMC-specific) Atf4 KO, and transgenic (TG) mouse models. Reduced expression of ATF4 in global ATF4-haplodeficient and SMC-specific Atf4 KO mice reduced medial and atherosclerotic calcification under normal kidney and CKD conditions. In contrast, increased expression of ATF4 in SMC-specific Atf4 TG mice caused severe medial and atherosclerotic calcification. We further demonstrated that ATF4 transcriptionally upregulates the expression of type III sodium-dependent phosphate cotransporters (PiT1 and PiT2) by interacting with C/EBPβ. These results demonstrate that the ER stress effector ATF4 plays a critical role in the pathogenesis of vascular calcification through increased phosphate uptake in vascular SMCs. PMID:27812542

  13. Vascular rings.

    Science.gov (United States)

    Backer, Carl L; Mongé, Michael C; Popescu, Andrada R; Eltayeb, Osama M; Rastatter, Jeffrey C; Rigsby, Cynthia K

    2016-06-01

    The term vascular ring refers to congenital vascular anomalies of the aortic arch system that compress the esophagus and trachea, causing symptoms related to those two structures. The most common vascular rings are double aortic arch and right aortic arch with left ligamentum. Pulmonary artery sling is rare and these patients need to be carefully evaluated for frequently associated tracheal stenosis. Another cause of tracheal compression occurring only in infants is the innominate artery compression syndrome. In the current era, the diagnosis of a vascular ring is best established by CT imaging that can accurately delineate the anatomy of the vascular ring and associated tracheal pathology. For patients with a right aortic arch there recently has been an increased recognition of a structure called a Kommerell diverticulum which may require resection and transfer of the left subclavian artery to the left carotid artery. A very rare vascular ring is the circumflex aorta that is now treated with the aortic uncrossing operation. Patients with vascular rings should all have an echocardiogram because of the incidence of associated congenital heart disease. We also recommend bronchoscopy to assess for additional tracheal pathology and provide an assessment of the degree of tracheomalacia and bronchomalacia. The outcomes of surgical intervention are excellent and most patients have complete resolution of symptoms over a period of time. Copyright © 2016 Elsevier Inc. All rights reserved.

  14. Calcification by reef-building sclerobionts.

    Directory of Open Access Journals (Sweden)

    Jennie Mallela

    Full Text Available It is widely accepted that deteriorating water quality associated with increased sediment stress has reduced calcification rates on coral reefs. However, there is limited information regarding the growth and development of reef building organisms, aside from the corals themselves. This study investigated encruster calcification on five fore-reefs in Tobago subjected to a range of sedimentation rates (1.2 to 15.9 mg cm(-2 d(-1. Experimental substrates were used to assess rates of calcification in sclerobionts (e.g. crustose coralline algae, bryozoans and barnacles across key reef microhabitats: cryptic (low-light, exposed (open-horizontal and vertical topographic settings. Sedimentation negatively impacted calcification by photosynthesising crustose coralline algae in exposed microhabitats and encrusting foram cover (% in exposed and cryptic substrates. Heterotrophs were not affected by sedimentation. Fore-reef, turbid water encruster assemblages calcified at a mean rate of 757 (SD ±317 g m(-2 y(-1. Different microhabitats were characterised by distinct calcareous encruster assemblages with different rates of calcification. Taxa with rapid lateral growth dominated areal cover but were not responsible for the majority of CaCO3 production. Cryptobiont assemblages were composed of a suite of calcifying taxa which included sciaphilic cheilostome bryozoans and suspension feeding barnacles. These calcified at mean rates of 20.1 (SD ±27 and 4.0 (SD ±3.6 g m(-2 y(-1 respectively. Encruster cover (% on exposed and vertical substrates was dominated by crustose coralline algae which calcified at rates of 105.3 (SD ±67.7 g m(-2 y(-1 and 56.3 (SD ±8.3 g m(-2 y(-1 respectively. Globally, encrusting organisms contribute significant amounts of carbonate to the reef framework. These results provide experimental evidence that calcification rates, and the importance of different encrusting organisms, vary significantly according to topography and sediment

  15. Calcification by reef-building sclerobionts.

    Science.gov (United States)

    Mallela, Jennie

    2013-01-01

    It is widely accepted that deteriorating water quality associated with increased sediment stress has reduced calcification rates on coral reefs. However, there is limited information regarding the growth and development of reef building organisms, aside from the corals themselves. This study investigated encruster calcification on five fore-reefs in Tobago subjected to a range of sedimentation rates (1.2 to 15.9 mg cm(-2) d(-1)). Experimental substrates were used to assess rates of calcification in sclerobionts (e.g. crustose coralline algae, bryozoans and barnacles) across key reef microhabitats: cryptic (low-light), exposed (open-horizontal) and vertical topographic settings. Sedimentation negatively impacted calcification by photosynthesising crustose coralline algae in exposed microhabitats and encrusting foram cover (%) in exposed and cryptic substrates. Heterotrophs were not affected by sedimentation. Fore-reef, turbid water encruster assemblages calcified at a mean rate of 757 (SD ±317) g m(-2) y(-1). Different microhabitats were characterised by distinct calcareous encruster assemblages with different rates of calcification. Taxa with rapid lateral growth dominated areal cover but were not responsible for the majority of CaCO3 production. Cryptobiont assemblages were composed of a suite of calcifying taxa which included sciaphilic cheilostome bryozoans and suspension feeding barnacles. These calcified at mean rates of 20.1 (SD ±27) and 4.0 (SD ±3.6) g m(-2) y(-1) respectively. Encruster cover (%) on exposed and vertical substrates was dominated by crustose coralline algae which calcified at rates of 105.3 (SD ±67.7) g m(-2) y(-1) and 56.3 (SD ±8.3) g m(-2) y(-1) respectively. Globally, encrusting organisms contribute significant amounts of carbonate to the reef framework. These results provide experimental evidence that calcification rates, and the importance of different encrusting organisms, vary significantly according to topography and sediment

  16. VASCULAR SURGERY

    African Journals Online (AJOL)

    Thromboses can result from venous stasis, vascular injury or hypercoagulability, and those involving the deep veins proximal to the knee are linked to an increased risk of PE.2 .... tool for DVT in hospitalised patients, where higher scores.

  17. Vascular Dementia

    Science.gov (United States)

    ... that includes enjoyable activities well within the comfort zone of the person with vascular dementia. New situations, ... your cholesterol in check. A healthy, low-fat diet and cholesterol-lowering medications if you need them ...

  18. The relationship between aortic calcification volume and obstructive coronary artery disease: comparison with coronary calcification volume

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Dae Seok; Kim, Jeong Ho; Park, Chul Hi; Park, Seon Young; Choe, Soo Jin; Hwang, Hee Young; Kim, Hyung Sik [Gachon University Gil Medical Center, Incheon (Korea, Republic of)

    2007-12-15

    We compared the diagnostic performance of aortic calcification volume with that of coronary artery calcification volume at CT in diagnosing obstructive coronary artery disease (OCAD). A total of 308 patients (M: F 141: 167) underwent coronary CT angiography using a 64-slice MDCT. We measured the calcification volume (mm{sup 3}) of coronary artery (CAC), thoracic aorta (TAC), abdominal aorta (AAC), and whole aorta (AC) at unenhanced CT. OCAD was defined as the significant stenosis ({>=} 50%) in any coronary artery at CT angiography. The diagnostic performance for OCAD was evaluated by calculating the area under the receiver operating characteristic (ROC) curve. Among the 308 patients studied, 45 patients were diagnosed with OCAD. The mean volumes of TAC, AAC, AC, and CAC were 518.8 mm{sup 3}, 551.5 mm{sup 3}, 1069.9 mm{sup 3}, 57.6 mm{sup 3} respectively. The areas under the ROC curve of TAC, AAC, AC, and CAC for OCAD were 0.766 (0.694 < 95% confidence interval < 0.838), 0.837 (0.784 < 95% confidence interval < 0.892), 0.814 (0.755 < 95% confidence interval < 0.873), 0.871 (0.812 < 95% confidence interval < 0.930), respectively. The volume of aortic calcification as well as coronary artery calcification is associated with obstructive coronary artery disease.

  19. Dystrophic Calcification of the Prostate after Cryotherapy

    Directory of Open Access Journals (Sweden)

    Christopher Dru

    2014-01-01

    Full Text Available We present a previously undocumented complication of dystrophic calcification of the prostate after cryotherapy. An 87-year-old male presented with recurrent lower urinary tract infections and was found to have an obstructing large calcified mass in the right lobe of the prostate. Subsequently, he underwent transurethral resection of the prostate (TURP and bladder neck with laser lithotripsy to remove the calculus. We propose that chronic inflammation and necrosis of the prostate from cryotherapy resulted in dystrophic calcification of the prostate. As the use of cryotherapy for the treatment of localized prostate cancer continues to increase, it is important that clinicians be aware of this scenario and the technical challenges it poses.

  20. Unusual ganglioglioma with extensive calcification and ossification

    Directory of Open Access Journals (Sweden)

    Vikas Shashikant Kavishwar

    2016-01-01

    Full Text Available Ganglioglioma is a slow-growing relatively low-grade mixed glioneuronal tumor with most cases corresponding to the WHO Grade I category. It frequently presents with seizures. The temporal lobe is the most common location followed by frontal, parietal, and occipital lobes. These generally behave in a benign fashion and have a favorable prognosis. We describe a case of a 24-year-old male presenting with convulsions and a calcified parieto-occipital mass. This mass removed from the parietal lobe showed neoplastic glial and dysplastic neuronal tissue amidst extensive areas of calcification and foci of ossification. On immunohistochemistry, the glial component expressed glial fibrillary acidic protein whereas the dysplastic neuronal component expressed synaptophysin and CD34. Epithelial membrane antigen was negative and Ki-67 showed a low proliferative index. After the surgery, the patient is free of neurological symptoms. Widespread calcification and ossification are very unusual in ganglioglioma, which prompted us to report this case.

  1. Dystrophic Calcification of the Prostate after Cryotherapy

    Science.gov (United States)

    2014-01-01

    We present a previously undocumented complication of dystrophic calcification of the prostate after cryotherapy. An 87-year-old male presented with recurrent lower urinary tract infections and was found to have an obstructing large calcified mass in the right lobe of the prostate. Subsequently, he underwent transurethral resection of the prostate (TURP) and bladder neck with laser lithotripsy to remove the calculus. We propose that chronic inflammation and necrosis of the prostate from cryotherapy resulted in dystrophic calcification of the prostate. As the use of cryotherapy for the treatment of localized prostate cancer continues to increase, it is important that clinicians be aware of this scenario and the technical challenges it poses. PMID:25548712

  2. Intervertebral disc calcification in a child

    Directory of Open Access Journals (Sweden)

    Ahemad Athar

    2008-01-01

    Full Text Available Disc calcification in children is a rare condition of which only approximately 200 cases have been reported worldwide and one from India and we report one such case. A five year-old boy presented with neck pain, torticollis and limitations of cervical motions following a fall while playing 3 months back. He had low grade fever cervical lymphadenopthy, paraspinal muscle spasm. His blood counts and ESR was raised. Fine needle aspiration cytology of lymph node revealed reactive lymphadenitis. His cervical radiograph slowed calcification of C 6-7. MRI scan showed hypointense signals in C6-C7 and D5-D6 disc on both T1 and T2 W images. Cerebrospinal fluid examination was normal. He improved on analgesics, bed rest and cervical traction.

  3. vascular hemiplegia

    OpenAIRE

    Voto Bernales, Jorge; Facultad de Medicina, Universidad Nacional Mayor de San Marcos, Lima, Perú

    2014-01-01

    The vascular hemiplegia is the functional disorder of a lateral half of the body produced by alterations of cerebral vessels. Should review the concepts of this common condition, with the dual aim of expanding its nosographic value and considering the hemiplegic patient as worthy of the highest professional care La hemiplejia vascular, es el trastorno funcional de una mitad lateral del cuerpo producido por alteraciones de los vasos cerebrales. Conviene revisar los conceptos sobre esta frec...

  4. vascular hemiplegia

    OpenAIRE

    Voto Bernales, Jorge; Facultad de Medicina, Universidad Nacional Mayor de San Marcos, Lima, Perú

    2014-01-01

    The vascular hemiplegia is the functional disorder of a lateral half of the body produced by alterations of cerebral vessels. Should review the concepts of this common condition, with the dual aim of expanding its nosographic value and considering the hemiplegic patient as worthy of the highest professional care La hemiplejia vascular, es el trastorno funcional de una mitad lateral del cuerpo producido por alteraciones de los vasos cerebrales. Conviene revisar los conceptos sobre esta frec...

  5. Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk: results of the CAMONA study

    Energy Technology Data Exchange (ETDEWEB)

    Blomberg, Bjoern A. [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); University Medical Center Utrecht, Department of Radiology and Nuclear Medicine, Utrecht (Netherlands); Jong, Pim A. de; Lam, Marnix G.E.; Mali, Willem P.T.M. [University Medical Center Utrecht, Department of Radiology and Nuclear Medicine, Utrecht (Netherlands); Thomassen, Anders [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); Vach, Werner [University Medical Center Freiburg, Clinical Epidemiology, Institute of Medical Biometry and Medical Informatics, Freiburg (Germany); Olsen, Michael H. [Odense University Hospital, The Cardiovascular and Metabolic Preventive Clinic, Department of Endocrinology, Center for Individualized Medicine in Arterial Diseases, Odense (Denmark); Narula, Jagat [Mount Sinai Hospital, Icahn School of Medicine, New York, NY (United States); Alavi, Abass [Hospital of the University of Pennsylvania, Department of Radiology, Philadelphia, PA (United States); Hoeilund-Carlsen, Poul F. [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); University of Southern Denmark, Institute of Clinical Research, Odense (Denmark)

    2017-02-15

    Arterial inflammation and vascular calcification are regarded as early prognostic markers of cardiovascular disease (CVD). In this study we investigated the relationship between CVD risk and arterial inflammation ({sup 18}F-FDG PET/CT imaging), vascular calcification metabolism (Na{sup 18}F PET/CT imaging), and vascular calcium burden (CT imaging) of the thoracic aorta in a population at low CVD risk. Study participants underwent blood pressure measurements, blood analyses, and {sup 18}F-FDG and Na{sup 18}F PET/CT imaging. In addition, the 10-year risk for development of CVD, based on the Framingham risk score (FRS), was estimated. CVD risk was compared across quartiles of thoracic aorta {sup 18}F-FDG uptake, Na{sup 18}F uptake, and calcium burden on CT. A total of 139 subjects (52 % men, mean age 49 years, age range 21 - 75 years, median FRS 6 %) were evaluated. CVD risk was, on average, 3.7 times higher among subjects with thoracic aorta Na{sup 18}F uptake in the highest quartile compared with those in the lowest quartile of the distribution (15.5 % vs. 4.2 %; P < 0.001). CVD risk was on average, 3.7 times higher among subjects with a thoracic aorta calcium burden on CT in the highest quartile compared with those in the lowest two quartiles of the distribution (18.0 % vs. 4.9 %; P < 0.001). CVD risk was similar in subjects in all quartiles of thoracic aorta {sup 18}F-FDG uptake. Our findings indicate that an unfavourable CVD risk profile is associated with marked increases in vascular calcification metabolism and vascular calcium burden of the thoracic aorta, but not with arterial inflammation. (orig.)

  6. Neurological manifestations of calcific aortic stenosis

    Directory of Open Access Journals (Sweden)

    I. V. Egorov

    2014-01-01

    Full Text Available Despite being thoroughly studied, senile aortic stenosis (AS remains a disease that is frequently underestimated by Russian clinicians. Meanwhile, its manifestations can not only deteriorate quality of life in patients, but can also be poor prognostic signs. The most common sequels of this disease include heart failure and severe arrhythmias. However, there may be also rare, but no less dangerous complications: enteric bleeding associated with common dysembriogenetic backgrounds, infarctions of various organs, the basis for which is spontaneous calcium embolism, and consciousness loss episodes. The latter are manifestations of cardiocerebral syndrome. Apart from syncope, embolic stroke may develop within this syndrome. There is evidence that after syncope occurs, life expectancy averages 3 years. Global practice is elaborating approaches to the intracardiac calcification prevention based on the rapid development of new pathogenetic ideas on this disease. In particular, it is clear that valvular calcification is extraskeletal leaflet ossification rather than commonplace impregnation with calcium salts, i.e. the case in point is the reverse of osteoporosis. This is the basis for a new concept of drug prevention of both calcification and the latter-induced heart disease. But the view of senile AS remains more than conservative in Russia. The paper describes a clinical case of a rare complication as cerebral calcium embolism and discusses the nature of neurological symptoms of the disease, such as vertigo and syncope.

  7. Calcification of intraocular implant lens surfaces.

    Science.gov (United States)

    Wu, Wenju; Guan, Xiangying; Tang, Ruikang; Hook, Daniel; Yan, Wenyan; Grobe, George; Nancollas, George H

    2004-02-17

    Calcification of octacalcium phosphate [Ca8H2(PO4)6 x 5H2O, OCP] on differently packaged "Ultem" and "Surefold" intraocular implant lens surfaces has been studied in vitro in solutions supersaturated with respect to OCP at pH = 7.10 and 37 degrees C. No mineral deposition was observed on the lenses packaged in Ultem vials even after treatment with behenic acid, one of the fatty acids identified on explanted lenses. Following treatment with behenic acid, nucleation of OCP occurred on the lenses from Surefold vials, which incorporate silicone gaskets; induction periods preceding calcification were about 6 h. No mineralization was found on the lenses in vials with other gasket materials, including polytetrafluoroethylene, fluorocarbon elastomer, and polypropylene. The results of this study indicate that both silicone and fatty acids such as behenic acid play important roles in inducing the in vivo calcification of OCP on IOL lenses; all of the lens treatment steps were necessary for nucleation induction.

  8. Retropharyngeal calcific tendonitis: report of two cases.

    Science.gov (United States)

    Razon, Rhea Victoria B; Nasir, Asad; Wu, George S; Soliman, Manal; Trilling, Jeffrey

    2009-01-01

    Retropharyngeal calcific tendonitis is an inflammatory process of the superior oblique tendons of the longus colli muscle, a neck flexor in the upper cervical spine, caused by deposition of calcium hydroxyapatite crystals; the definitive diagnostic test is computed tomography (CT). Presented in this article are two cases seen at our institution. Patients typically present with acute onset of neck pain/spasm, odynophagia, dysphagia, and/or low grade fevers. Leukocytosis and elevated erythrocyte sedimentation rate may be noted. It is important to understand this entity because its signs and symptoms are mimickers of those of the more serious condition of retropharyngeal space abscess. Calcific tendonitis is managed conservatively whereas retropharyngeal abscess requires incision and drainage. Some may argue that this entity is a zebra because its reported incidence in the literature is low. However, most of these studies were done in an era when CT was not yet in vogue. With today's widespread use of CT and its superb ability to visualize the calcification, the true incidence of this condition is probably higher and, thus, it is important for the family practitioner to be aware of this entity. The astute clinician may save the patient from unnecessary diagnostic workup, undue anxiety, and delays in hospital discharge.

  9. Aortic Arch Calcification Predicts Cardiovascular and All-Cause Mortality in Maintenance Hemodialysis Patients

    Directory of Open Access Journals (Sweden)

    Mizuki Komatsu

    2014-12-01

    Full Text Available Background/Aim: Vascular calcification is associated with cardiovascular risk in maintenance hemodialysis (MHD patients. Previous reports have shown that simple assessment of aortic arch calcification (AoAC using plain radiography is associated with cardiovascular mortality in the general population. We conducted a prospective study to investigate factors associated with the presence at baseline and progression of AoAC in MHD patients and examined its prognostic value in a short-term outcome. Methods: We prospectively evaluated chest X-rays in 301 asymptomatic MHD patients. The extent of AoAC was divided into three Grades (0, 1, 2+3. Demographic data including age, gender, dialysis vintage, co-morbidity and biochemical data were assessed and the patients were then followed for 3 years. Results: AoAC was observed in 126 patients (41.9% as Grade 0, in 112 patients (37.2% as Grade 1, and in 63 patients (20.9% as Grade 2 and 3 at baseline. An increase in the severity of calcification was associated with older male patients who had lower serum albumin levels. During the follow-up period of 3 years, multivariate Cox proportional hazards analysis revealed that high-grade calcification was associated with cardiovascular and all-cause mortality. Patients with AoAC were associated with a worse outcome in survival analysis and the grade of AAC also influenced their survival. Moreover, all-cause death rates were significantly higher in the progression groups than in the non-progression groups. Conclusions: The presence and progression of AoAC assessed by chest X-ray were independently associated with mortality in MHD patients. Regular follow-up by chest X-ray could be a simple and useful method to stratify mortality risk in MHD patients.

  10. Calcifications of the thoracic aorta on extended non-contrast-enhanced cardiac CT.

    Directory of Open Access Journals (Sweden)

    Damian Craiem

    Full Text Available BACKGROUND: The presence of calcified atherosclerosis in different vascular beds has been associated with a higher risk of mortality. Thoracic aorta calcium (TAC can be assessed from computed tomography (CT scans, originally aimed at coronary artery calcium (CAC assessment. CAC screening improves cardiovascular risk prediction, beyond standard risk assessment, whereas TAC performance remains controversial. However, the curvilinear portion of the thoracic aorta (TA, that includes the aortic arch, is systematically excluded from TAC analysis. We investigated the prevalence and spatial distribution of TAC all along the TA, to see how those segments that remain invisible in standard TA evaluation were affected. METHODS AND RESULTS: A total of 970 patients (77% men underwent extended non-contrast cardiac CT scans including the aortic arch. An automated algorithm was designed to extract the vessel centerline and to estimate the vessel diameter in perpendicular planes. Then, calcifications were quantified using the Agatston score and associated with the corresponding thoracic aorta segment. The aortic arch and the proximal descending aorta, "invisible" in routine CAC screening, appeared as two vulnerable sites concentrating 60% of almost 11000 calcifications. The aortic arch was the most affected segment per cm length. Using the extended measurement method, TAC prevalence doubled from 31% to 64%, meaning that 52% of patients would escape detection with a standard scan. In a stratified analysis for CAC and/or TAC assessment, 111 subjects (46% women were exclusively identified with the enlarged scan. CONCLUSIONS: Calcium screening in the TA revealed that the aortic arch and the proximal descending aorta, hidden in standard TA evaluations, concentrated most of the calcifications. Middle-aged women were more prone to have calcifications in those hidden portions and became candidates for reclassification.

  11. Long-term effect of cinacalcet hydrochloride on abdominal aortic calcification in patients on hemodialysis with secondary hyperparathyroidism

    Directory of Open Access Journals (Sweden)

    Nakayama K

    2013-12-01

    Full Text Available Kazunori Nakayama,1,2 Kazushi Nakao,1,2 Yuji Takatori,1,2 Junko Inoue,1 Shoichirou Kojo,1 Shigeru Akagi,1,2 Masaki Fukushima,2 Jun Wada,1 Hirofumi Makino11Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2Shigei Medical Research Hospital, Okayama, JapanBackground: Secondary hyperparathyroidism (SHPT is one of the common complications in dialysis patients, and is associated with increased risk of vascular calcification. The effects of cinacalcet hydrochloride treatment on bone and mineral metabolism have been previously reported, but the benefit of cinacalcet on vascular calcification remains uncertain. The aim of this study was to evaluate the impact of cinacalcet on abdominal aortic calcification in dialysis patients.Subjects and methods: Patients were on maintenance hemodialysis with insufficiently controlled SHPT (intact parathyroid hormone [PTH] >180 pg/mL by conventional therapies. All subjects were initially administered 25 mg cinacalcet daily, with concomitant use of calcitriol analogs. Abdominal aortic calcification was annually evaluated by calculating aortic calcification area index (ACAI using multidetector computed tomography (MDCT, from 12 months before to 36 months after the initiation of cinacalcet therapy.Results: Twenty-three patients were analyzed in this study. The mean age was 59.0±8.7 years, 34.8% were women, and the mean dialysis duration was 163.0±76.0 months. After administration of cinacalcet, serum levels of intact PTH, phosphorus, and calcium significantly decreased, and mean Ca × P values significantly decreased from 67.4±7.9 mg2/dL2 to 52±7.7 mg2/dL2. Although the ACAI value did not decrease during the observation period, the increase in ACAI between 24 months and 36 months after cinacalcet administration was significantly suppressed.Conclusion: Long-term administration of cinacalcet was associated with reduced progression of

  12. Plant phosphates, phytate and pathological calcifications in chronic kidney disease.

    Science.gov (United States)

    Buades Fuster, Juan Manuel; Sanchís Cortés, Pilar; Perelló Bestard, Joan; Grases Freixedas, Félix

    Phytate, or myo-inositol 1,2,3,4,5,6-hexakis dihydrogen phosphate (InsP6), is a naturally occurring phosphorus compound that is present in many foods, mainly legumes, whole grains and nuts. Patients with chronic kidney disease (CKD) have cardiovascular disease mortality up to 30times higher than the general population. Vascular calcifications (VCs) directly contribute to overall morbidity and mortality, especially in CKD. In part, this high mortality is due to elevated levels of phosphorus in the blood. Therefore, control of dietary phosphorus is essential. Dietary phosphorus can be classified according to its structure in organic phosphorus (plant and animal) and inorganic (preservatives and additives). Plant-phosphorus (legumes and nuts), mainly associated with InsP6, is less absorbable by the human gastrointestinal tract as the bioavailability of phosphorous from plant-derived foods is very low. Recent data indicate that restriction of foods containing plant phosphates may compromise the adequate supply of nutrients that have a beneficial effect in preventing cardiovascular events, such as InsP6 or fibre found in legumes and nuts. Experimental studies in animals and observational studies in humans suggest that InsP6 can prevent lithiasis and VCs and protect from osteoporosis. In conclusion, we need prospective studies to elucidate the potential benefits and risks of phytate (InsP6) through the diet and as an intravenous drug in patients on haemodialysis.

  13. Corals concentrate dissolved inorganic carbon to facilitate calcification.

    Science.gov (United States)

    Allison, Nicola; Cohen, Itay; Finch, Adrian A; Erez, Jonathan; Tudhope, Alexander W

    2014-01-01

    The sources of dissolved inorganic carbon (DIC) used to produce scleractinian coral skeletons are not understood. Yet this knowledge is essential for understanding coral biomineralization and assessing the potential impacts of ocean acidification on coral reefs. Here we use skeletal boron geochemistry to reconstruct the DIC chemistry of the fluid used for coral calcification. We show that corals concentrate DIC at the calcification site substantially above seawater values and that bicarbonate contributes a significant amount of the DIC pool used to build the skeleton. Corals actively increase the pH of the calcification fluid, decreasing the proportion of DIC present as CO2 and creating a diffusion gradient favouring the transport of molecular CO2 from the overlying coral tissue into the calcification site. Coupling the increases in calcification fluid pH and [DIC] yields high calcification fluid [CO3(2-)] and induces high aragonite saturation states, favourable to the precipitation of the skeleton.

  14. Medial arterial calcification in diabetes and its relationship to neuropathy

    DEFF Research Database (Denmark)

    Jeffcoate, W J; Rasmussen, Lars Melholt; Hofbauer, L C

    2009-01-01

    Calcification of the media of arterial walls is common in diabetes and is particularly associated with distal symmetrical neuropathy. Arterial calcification also complicates chronic kidney disease and is an independent risk factor for cardiovascular and all-cause mortality. The term calcification...... factor linked to the development of arterial calcification is distal symmetrical neuropathy; indeed, it has been suggested that neuropathy explains the distal distribution of arterial calcification in diabetes. It has also been suggested that the link with neuropathy results from loss of neuropeptides......, such as calcitonin gene-related peptide, which are inherently protective. The association between distal symmetrical neuropathy and calcification of the arterial wall highlights the fact that neuropathy may be an independent risk factor for cardiovascular mortality....

  15. An unusual case of neonatal peritoneal calcifications associated with hydrometrocolpos

    Energy Technology Data Exchange (ETDEWEB)

    Hu, M.X.; Methratta, S. [College of Medicine and Dentistry of New Jersey - New Jersey Medical School, Newark (United States). Dept. of Radiology

    2001-10-01

    Neonatal peritoneal calcifications usually suggest a diagnosis of meconium peritonitis, but in this case, a premature baby girl, peritoneal calcifications were caused by hydrometrocolpos secondary to imperforate hymen, a rare association. The patient presented with respiratory distress and ascites and demonstrated abdominal calcifications on plain film. Other radiographic work-up revealed hydrometrocolpos without evidence of gastrointestinal tract obstruction. The patient was diagnosed and treated for imperforate hymen; she was recovered fully. (orig.)

  16. Calcific tendonitis of pectoralis major: CT and MRI findings

    Energy Technology Data Exchange (ETDEWEB)

    Cahir, John [Royal National Orthopaedic Hospital NHS Trust, Department of Radiology, Middlesex (United Kingdom); Saifuddin, Asif [Royal National Orthopaedic Hospital NHS Trust, Department of Radiology, Middlesex (United Kingdom); University College London, The Institute of Orthopaedics and Musculoskeletal Sciences, London (United Kingdom); London Bone and Soft Tissue Tumour Service, London (United Kingdom)

    2005-04-01

    The shoulder is the most common location for calcific tendonitis. Presentation of calcific tendonitis at other sites is unusual and may lead to diagnostic difficulty. We report a case of calcific tendonitis of the pectoralis major insertion and describe the CT and MRI findings. The presence of an associated cortical defect at the site of tendon insertion may lead to the incorrect diagnosis of neoplastic process. (orig.)

  17. Significance of density and demarcation of calcifications in calcifying tendinitis

    Energy Technology Data Exchange (ETDEWEB)

    Uhthoff, H.K.; Sarkar, K.; Hammond, I.

    1982-04-01

    Calcification of tendons can be either degenerative and progressive in nature or reactive and selfhealing. Radiologic examinations permit to distinguish between both kinds. The reactive calcification, known also as calcifying tendinitis, passes through two main phases, the formative and the resorptive phase. Since treatment is different for each phase, their roentgenologic distinction is important. Dense, well demarcated and homogenous calcifications indicate the presence of a formative phase whereas less dense, ill defined and fluffy deposits point toward an ongoing resorption.

  18. Atraumatic quadriceps tendon tear associated with calcific tendonitis.

    Science.gov (United States)

    Abram, Simon G F; Sharma, Akash D; Arvind, Chinnakonda

    2012-11-27

    Calcific tendonitis of the quadriceps tendon is an uncommon condition. We present the first case of a quadriceps tendon tear associated with calcific tendonitis. In this case, the patient presented with symptoms mimicking a rupture of the quadriceps tendon. This case illustrates that although calcific tendonitis of the quadriceps is a rare condition it is not benign and should be considered when investigating acute symptoms associated with the extensor mechanism of the knee.

  19. Eggshell calcification of the heart in constrictive pericarditis

    Institute of Scientific and Technical Information of China (English)

    Rajesh; Vijayvergiya; Ramalingam; Vadivelu; Sachin; Mahajan; Sandeep; S; Rana; Manphool; Singhal

    2015-01-01

    Constrictive pericarditis(CP) is an inflammatory disease of pericardium. Pericardial calcification in X-ray provides a clue for the diagnosis of CP. An extensive "eggshell" type of calcification is rarely seen in CP. We hereby report a case of CP with eggshell calcification of pericardium, encircling whole of the heart. A need for multimodality imaging and hemodynamic assessment followed by surgical pericardiectomy is discussed.

  20. Familial idiopathic basal ganglia calcification (Fahr’s disease)

    OpenAIRE

    Mufaddel, Amir A.; Al-Hassani, Ghanem A.

    2014-01-01

    Familial idiopathic basal ganglia calcification (Fahr’s disease) is a rare neurodegenerative disorder characterized by symmetrical and bilateral calcification of the basal ganglia. Calcifications may also occur in other brain regions such as dentate nucleus, thalamus, and cerebral cortex. Both familial and non-familial cases of Fahr’s disease have been reported, predominantly with autosomal-dominant fashion. The disease has a wide range of clinical presentations, predominantly with neuropsych...

  1. Calcification of thoracic aorta – solar eclipse sign

    Science.gov (United States)

    Dhoble, Abhijeet; Puttarajappa, Chethan

    2008-01-01

    Background Calcification of thoracic aorta is very common in old people, especially ones with hypertension. This can sometime be visible on plain chest radiograph. Case Presentation We present a case of a male patient who had extensive deposition of calcium in the thoracic aorta. Conclusion The relationship between aortic calcification and coronary atherosclerosis remains contentious. Computed tomography of the thorax can display this calcification which appears like 'solar eclipse'. PMID:18759981

  2. Progressive pulmonary calcification in a child after orthotopic liver transplantation

    Energy Technology Data Exchange (ETDEWEB)

    Weaver, Olena O.; Stazzone, Madelyn M.; Bhalla, Sanjeev [Washington University School of Medicine, Department of Radiology, 660 S. Euclid Ave., Campus Box 8131, St. Louis, MO (United States)

    2006-06-15

    We present a case of progressive pulmonary calcification associated with prolonged respiratory insufficiency in a 2-year-old boy with a history of orthotopic liver transplantation. This case demonstrates the potentially progressive nature of pulmonary calcification and that it can present with respiratory insufficiency at a later period after transplantation than previously thought. We describe radiological findings and discuss established as well as plausible pathological mechanisms contributing to the development of calcifications in these patients. (orig.)

  3. Calcification Changes of Mesozoic Calcareous Nannofossils

    Science.gov (United States)

    Bornemann, A.; Mutterlose, J.

    2003-12-01

    Studies on plankton samples and cultures revealed a variety factors which presumably control calcification and the size of coccoliths. Among others temperature, nutrients and seawater pH are thought to influence nannoplankton calcification. Whereas these studies only provide information of very short time intervals from hours to years, global climatic and oceanographic changes occur, however, on geological timescales. Thus their impact on nannofossil calcification and carbonate production can only be studied from the fossil record. We investigated DSDP sites from the western Atlantic of late Jurassic to early Cretaceous age in order to better understand long-term variations of the size of common nannofossil taxa and the resulting carbonate accumulation. The studied interval is characterized by two events in the pelagic carbonate record: (1) the onset of pelagic carbonate accumulation in the Tithonian, and (2) the Valanginian 'nannoconid crisis'. The Tithonian event went along with high abundances of strongly calcified nannofossils which presumably have an affinity to more oligotrophic surface water conditions. The mid Valanginian is marked by a positive carbon isotope excursion (CIE). This coincides with a sea level rise, volcanic activity and elevated atmospheric pCO2 levels. Greenhouse climate and an accelerated hydrological cycle presumably intensified weathering processes causing enhanced nutrient transfer from the continents into the oceans. Increasing surface water fertility is indicated by high abundances of nannofossils which possibly indicate more eutrophic conditions. In the western Tethys the CIE is predated by a sharp decrease in the abundance of rockforming nannoconids. This event is less pronounced in the western Atlantic due to a general scarcity of nannoconids. Low nannofossil carbonate accumulation rates and a dominance of less calcified taxa were observed and may reflect a general marine biocalcification crisis. Possible factors, which may have

  4. Calcific tendinitis of the gluteus maximus tendon: CT findings

    Energy Technology Data Exchange (ETDEWEB)

    Hottat, N.; Fumiere, E.; Delcour, C. [C. H. U. de Charleroi (Belgium). Dept. of Radiology

    1999-08-01

    Two cases of calcific tendinitis of gluteus maximus muscle are presented. The CT findings, including amorphous calcification without soft tissue mass and possible cortical erosion at the femoral enthesis of the gluteus maximus muscle, are highly suggestive of calcific tendinitis at this unusual but classical location. Ossifying entheses with well-defined cortical defect are frequent at the femoral insertion of the gluteus maximus muscle in asymptomatic subjects and must be differentiated from a real cortical erosion sometimes associated with these calcific tendinitis. (orig.) With 3 figs., 7 refs.

  5. Association of gastrocnemius tendon calcification with chondrocalcinosis of the knee

    Energy Technology Data Exchange (ETDEWEB)

    Foldes, K. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States)]|[National Institute of Rheumatology and Physiotherapy, Budapest (Hungary); Lenchik, L. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Jaovisidha, S. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Clopton, P. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States); Sartoris, D.J. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Resnick, D. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States)

    1996-10-01

    Objective. Chondrocalcinosis of the knee is a common radiological finding in the elderly. However, visualization of chondrocalcinosis may be difficult in patients with advanced cartilage loss.The purpose of this study was to determine sensitivity, specificity, and accuracy of gastrocnemius tendon calcification that might serve as a radiographic marker of chondrocalcinosis in patients with painful knees. Design and patients. We prospectively evaluated 37 knee radiographs in 30 consecutive patients (29 men, 8 women; mean age 67 years, age range 37-90 years) with painful knees who had radiographic evidence of chondrocalcinosis. The frequency of fibrocartilage, hyaline cartilage, and gastrocnemius tendon calcification was determined. For a control group, we evaluated knee radiographs in 65 consecutive patients with knee pain (54 men, 11 women; mean age 59 years, age range 40-93 years) who had no radiological signs of chondrocalcinosis. The frequency of gastrocnemius tendon calcification in the control group was determined. Results. Gastrocnemius tendon calcification was 41% sensitive, 100% specific, and 78% accurate in predicting chondrocalcinosis. The gastrocnemius tendon was calcified on 15 of 37 (41%) radiographs in the experimental group and on 0 of 67 radiographs in the control group. In the chondrocalcinosis group, 23 (62%) had posterior hyaline cartilage calcification, 14 (38%) had anterior hyaline cartilage calcification, 31 (84%) had medial meniscus calcification, and 36 (97%) had lateral meniscus calcification. Conclusions. Our results show that gastrocnemius tendon calcification is an accurate radiographic marker of chondrocalcinosis in patients with knee pain. (orig.). With 2 figs., 2 tabs.

  6. The roentgenographic study of placental calcifications in Korean pregnant

    Energy Technology Data Exchange (ETDEWEB)

    Cho, Chung Che [Chungang Univ., Seoul (Korea, Republic of)

    1980-12-15

    Calcifications in the placenta have been considered as a sign of the maturity because it is found frequently in variable degrees in full-term placentas. The placentas studied were those from deliveries at Chung-Ang University Hospital during the period of January 1978 to June 1980 and were excluded if their deliveries were by Caesarean section. Roentgenographic studies of placenta were performed postnatally in 135 cases delivered from normal pregnant. The results were as follows: 1. The incidence of calcification in the placenta was 53.3%. 2. The tendency of placenta calcification was increased as progress of maturity but not indicated as postmaturity. 3. Calcifications were less correlated with increasing gravidity or maternal age. 4. Calcifications occurred more frequently with increasing birth weight. 5. Calcifications in placentas were more frequently in the neonates with 10 scores of Apgar and normal level of maternal hemoglobin. 6. No significant correlation between incidence of calcification and maternal toxemia was observed. In the pregnant with an episode of previous abortion or S. P. R. M., incidence of calcification was apparently increased but statistically not significant. On the whole, placental calcifications are not harmful and identified as normal or proper aging process.

  7. Chronic parotitis with multiple calcifications: Clinical and sialendoscopic findings.

    Science.gov (United States)

    Jáuregui, Emmanuel; Kiringoda, Ruwan; Ryan, William R; Eisele, David W; Chang, Jolie L

    2017-07-01

    To characterize clinical, imaging, and sialendoscopy findings in patients with chronic parotitis and multiple parotid calcifications. Retrospective review. Clinical history, radiographic images and reports, lab tests, and operative reports were reviewed for adult patients with chronic parotitis and multiple parotid calcifications who underwent parotid sialendoscopy. Thirteen of 133 (10%) patients undergoing parotid sialendoscopy for chronic sialadenitis had more than one calcification in the region of the parotid gland. Seven patients (54%) were diagnosed with immune-mediated disease from autoimmune parotitis (positive Sjögren's antibodies or antinuclear antibodies) or human immunodeficiency virus (HIV) disease. The six patients (46%) who did not have an immune-mediated disorder had most calcifications located anterior or along the masseter muscle. Eight of 13 patients (61%) had at least one calculus found in the parotid duct on sialendoscopy. Four patients (38%) had multiple punctate calcifications within the parotid gland, all of whom had either autoimmune parotitis or HIV. None of the proximal or punctate parotid calcifications posterior to the masseter were visualized on sialendoscopy. Chronic parotitis in conjunction with multiple parotid calcifications is uncommon and was identified in 10% of our cohort. We contrast two classifications of parotid calcifications: 1) intraductal stones that cause recurrent duct obstruction and are often located within the main parotid duct along or anterior to the masseter and 2) punctate intraparenchymal parotid gland calcifications that are not visualized on sialendoscopy and may represent underlying inflammatory disease. 4 Laryngoscope, 127:1565-1570, 2017. © 2016 The American Laryngological, Rhinological and Otological Society, Inc.

  8. Effect of medial arterial calcification on O2 supply to exercising diabetic feet.

    Science.gov (United States)

    Chantelau, E; Ma, X Y; Herrnberger, S; Dohmen, C; Trappe, P; Baba, T

    1990-08-01

    We investigated whether medial arterial calcification (MAC) impairs O2 supply to the exercising foot in diabetic patients with foot lesions. Transcutaneous O2 tension (tcPO2) was monitored at the dorsum of the foot before and after bicycle exercise in 11 diabetic patients with peripheral ischemic vascular disease (PIVD) with or without concomitant existence of MAC, 10 patients with MAC but without PIVD, 10 diabetic control subjects, and 6 nondiabetic control subjects. The mean preexercise tcPO2 level was comparable in these four groups. However, tcPO2 decreased significantly with exercise in feet with PIVD (mean +/- SE -17.9 +/- 2.7%, P less than 0.01, n = 11), regardless of presence or absence of vascular calcification. On the other hand, the value increased significantly with exercise in feet with MAC but without PIVD (21.2 +/- 3.5%, P less than 0.01, n = 10) and in those of diabetic control subjects (14.9 +/- 3.6%, P less than 0.01), respectively. The tcPO2 remained unchanged in the feet of nondiabetic control subjects (1.7 +/- 1.1%). The results suggest that MAC is not associated with reduced O2 supply to the exercising foot in diabetic patients.

  9. Magnesium intake is inversely associated with coronary artery calcification: the Framingham Heart Study

    Science.gov (United States)

    OBJECTIVES: The aim of this study was to examine whether magnesium intake is associated with coronary artery calcification (CAC) and abdominal aortic calcification (AAC). BACKGROUND: Animal and cell studies suggest that magnesium may prevent calcification within atherosclerotic plaques underlying c...

  10. Calcification and photosynthesis of the coral acropora cervicornis under calcium limited conditions

    Science.gov (United States)

    Rathfon, Megan; Brewer, Debbie

    1997-01-01

    Differing hypothesis about the function of calcification are based on an interesting dilemma. Is the purpose of calcification mainly a structural and protective one or does calcification serve other functions? Does photosynthesis increase carbonate ion activity and cause calcification or does calcification increase CO2 levels and stimulate photsynthesis? It is proposed that calcification in corals is not dependent upon photosynthesis but upon calcium levels in the water. Under normal ocean conditions, corals convert a certain percentage of energy to photosynthesis and respiration and another percentage to calcification. As corals become nutrient stressed, particularly calcium limited, the ratio of photosynthesis to calcification shifts towards calcification in order to generate protons. The protons generated during calcification may stimulate photosynthesis and aid in the uptake of nutrients and biocarbonates. The results of the calcification experiment show a trend towards increased calcification and decreased photosynthesis when the coral Acropora cervicornis is calcium limited, but the data are inconclusive and further research is needed.

  11. [Kidney and bone update : the 5-year history and future of CKD-MBD. Disorders of musculoskeletal system in CKD ; bone fracture and periarticular calcification].

    Science.gov (United States)

    Yamada, Shunsuke; Taniguchi, Masatomo

    2012-07-01

    Chronic kidney disease-mineral and bone disorder (CKD-MBD) affects life expectancy through vascular calcification, and impairs patient's activity of daily living (ADL) and quality of life (QOL) through bone fracture and periarticular calcification. In CKD patients, vitamin D deficiency and secondary hyperparathyroidism impairs bone strength, and muscle dysfunction related to vitamin D deficiency also causes easy fall, leading to the high risk of bone fracture. Bone fracture not only aggravates ADL and QOL but increases the risk of mortality. Periarticular calcification such as tumoral calcinosis in relation to CKD-MBD causes restricted range of articular motion, leading to the deterioration of patient's ADL and QOL. Because bone fragility and tumoral calcinosis occurs in relation to CKD-MBD, the appropriate management of CKD-MBD is madatory.

  12. Dystrophic calcification and stone formation on the entire bladder neck after potassium-titanyl phosphate laser vaporization for the prostate: a case report.

    Science.gov (United States)

    Jeon, Sang-Wohn; Park, Yong-Koo; Chang, Sung-Goo

    2009-08-01

    Dystrophic calcification can be defined as a calcification that occurs in degenerated or necrotic tissue. It is associated with multiple clinical conditions, such as collagen vascular diseases. It involves the deposition of calcium in soft tissues despite no generalized disturbance in the calcium or phosphorus metabolism, and this is often seen at sites of previous inflammation or damage. Potassium-titanyl phosphate (KTP) laser vaporization of the prostate is safe and relatively bloodless procedure that results in a shorter catheterization, immediate symptomatic improvement, and less severe postoperative irritative symptoms. However, longer follow-up studies or reports about complications are lacking. Here in we report a case of dystrophic calcification and stone formation on the entire bladder neck after performing KTP laser vaporization of benign prostate hyperplasia. That was treated by lithotripsy and transurethral resection.

  13. Clinical decision-making for vitamin K-1 and K-2 deficiency and coronary artery calcification with warfarin therapy: are diet, factor Xa inhibitors or both the answer?

    Science.gov (United States)

    Wahlqvist, Mark L; Tanaka, Kiyoshi; Tzeng, Bing-Hsiean

    2013-01-01

    Coronary artery calcification is a recognised risk factor for ischaemic heart disease and mortality. Evidence is now strong that Mönckeberg's arteriosclerosis, a form of vascular calcification, can be attributable to vitamin K deficiency, but that vitamin K-2, especially the MK-4 form from foods like cheese can be protective. Warfarin blocks the recycling of hepatic and peripheral vitamin K leading to secondary vitamin K deficiency with adverse effects on vasculature, bone, kidneys, brain and other tissues and systems (inflammatory, immune function and neoplasia at least). There is individual susceptibility to vitamin K deficiency and warfarin sensitivity, partly explicable in terms of genetic polymorphisms, epigenetics, diet and pharmacotherapy. The emergence of extensive coronary calcification in a man with atrial fibrillation treated for a decade with warfarin is described by way of illustration and to raise the present clinical management conundrums. Finally, a putative set of recommendations is provided.

  14. Predictive value of osteoprotegerin for detecting coronary artery calcification in symptomatic patients: correlation with extent of calcification detected by multidetector computed tomography

    Directory of Open Access Journals (Sweden)

    Naser Aslanabadi

    2016-02-01

    Full Text Available Introduction: Osteoprotegerin (OPG could be a marker of vascular calcification extent. The purpose of this study was to evaluate relationships between OPG and coronary artery calcification (CAC extent in an Iranian population. Methods: A total of 151 patients with chest pain [107 males/44 females, mean age: 57.23 (30-85] were enrolled, excluding patients with previously established coronary artery diseases. All underwent chest multidetector computed tomography (MDCT for CAC scoring. Blood samples were collected for measurement of OPG. A potential relationship between CAC, OPG, age and number of involved coronary arteries was investigated, and a receiver-operating characteristic (ROC curve was designed thereafter to identify a cut-off value of OPG that best predicted the presence of CAC. Results: A total of 93 patients did not have CAC, who were younger than others. The mean age of patients with a different number of involved arteries was significantly different and is significantly correlated with a number of involved coronary arteries. The mean level of OPG differed by the number of calcified coronary arteries and is significantly correlated with the number of involved coronary arteries. The level of OPG had a weak but positive correlation with Ca score. ROC curve analysis showed that plasma OPG level had a fair prediction of CAC score, with an area under ROC curve of 0.62. The cut-off value best predicting CAC score was 59.1 pg/ml. Conclusion: This study suggests that a serum level of OPG can fairly predict extent of coronary retry calcification in symptomatic population.

  15. Pre-existing Arterial Micro-Calcification Predicts Primary Unassisted Arteriovenous Fistula Failure in Incident Hemodialysis Patients.

    Science.gov (United States)

    Choi, Su Jin; Yoon, Hye Eun; Kim, Young Soo; Yoon, Sun Ae; Yang, Chul Woo; Kim, Yong-Soo; Park, Sun Cheol; Kim, Young Ok

    2015-01-01

    Vascular access micro-calcification is a risk factor for cardiovascular morbidity and mortality in hemodialysis (HD) patients but its influence on vascular access patency is still undetermined. Our study aimed to determine the impact of arterial micro-calcification (AMiC) on the patency of vascular access in HD patients. One-hundred fourteen HD patients receiving arteriovenous fistula (AVF) operation were included in this study. During the operation, we obtained partial arterial specimen and performed pathological examination by von Kossa stain to identify AMiC. We compared primary unassisted AVF failure within 1 year between positive and negative AMiC groups, and performed Cox regression analysis for evaluating risk factor of AVF failure. The incidence of AMiC was 37.7% and AVF failure occurred in 45 patients (39.5%). The AVF failure rate within 1 year was greater in the positive AMiC group than those in the negative AMiC group (53.5% vs. 31.0%, p = 0.02). Kaplan-Meier analysis showed that the positive AMiC group had a lower AVF patency rate than the negative AMiC group (p = 0.02). The presence of AMiC was an independent risk factor for AVF failure. In conclusion, preexisting AMiC of the vascular access is associated with primary unassisted AVF failure in incident HD patients.

  16. The Relation between Calcium Supplement Consumption and Calcific Shoulder Tendonitis

    Directory of Open Access Journals (Sweden)

    Alireza Rouhani

    2015-10-01

    Full Text Available Background: Calcific tendonitis is a common cause of non-traumatic shoulder pain. Previous studies have suggested a relation between minerals and endocrine and calcium deposition. Thus, hypercalcemia is probably related to calcific tendonitis. This study aims at evaluating the relation found between calcium supplement consumption and calcific shoulder tendonitis. Methods: This analytical-descriptive study was conducted on 250 patients with shoulder pain referring to clinics and emergency department of Shohada Orthopedics Hospital during one year for considering calcific shoulder tendonitis and calcium supplement consumption. Patients with calcific tendonitis were treated and their functional ability was evaluated using DASH questionnaire, pain severity and range of motion (ROM before and after treatment and their correlation with calcium supplement consumption. Results: Calcific tendonitis and calcium consumption were generally seen in 30 (12% and 73 (29.2% cases, respectively. Calcium consumption frequency in patients with calcific tendonitis was significantly higher than the patients who did not consume calcium supplements (76.7% vs. 22.7%. Patients with calcific tendonitis who did not consume calcium supplements suffered from significantly longer periods of shoulder pain. All patients having consumed calcium supplement were female. The group who consumed calcium supplement had significantly severe pain and higher DASH score before and after treatment, while there was no significant difference in number of impaired ROM before and after treatment. Also, there was a negative correlation between calcium supplement consumption, pain severity and DASH score before and after treatment. Conclusion: Calcium supplement consumption is related to calcific tendonitis and is also accompanied with more pain and lower functional ability in patients with calcific tendonitis.    Keywords: Calcific tendonitis; Shoulder; Calcium supplement; Pain

  17. Substrate properties influence calcification in valvular interstitial cell culture.

    Science.gov (United States)

    Benton, Julie A; Kern, Hanna B; Anseth, Kristi S

    2008-11-01

    Valvular calcification is an active, cell-mediated process that results in significant morbidity and mortality. In standard culture, valvular interstitial cells (VICs) elicit significant calcification as a result of myofibroblast activation, and this limits their use in characterization studies. The study aim was to identify culturing substrates that would suppress atypical VIC calcification, and to investigate culture substrates representing a more physiological system. Several culture platforms were selected to compare and contrast the influence of biochemical and mechanical properties on VIC calcification. Substrates investigated included: tissue culture polystyrene (TCPS), TCPS coated with either fibronectin or fibrin, and an elastic poly(ethylene glycol) (PEG) hydrogel, also with fibronectin or fibrin coupled to the surface. Experiments were repeated with profibrotic growth factor transforming growth factor-beta 1 (TGF-beta1). VIC calcification was characterized by calcific nodule formation, alkaline phosphatase activity and calcium accumulation. Gene and protein expression of alpha smooth muscle actin (aSMA) and core binding factor-1 (CBFa-1) were analyzed with qRT-PCR and immunostaining. Unmodified TCPS substrates had an innate ability to promote the markers of calcification studied. The addition of TGF-beta1 enhanced levels of all osteoblastic markers studied. When TCPS surfaces were modified with fibronectin, all markers for calcification were repressed, but alphaSMA - a marker for myofibroblastic activity was unchanged. Meanwhile, fibrin-modified TCPS surfaces enhanced calcification over unmodified TCPS substrates. On soft PEG hydrogels, all markers for calcification were repressed, regardless of the surface chemistry, while alphaSMA expression remained unaffected. Collectively, VIC properties are highly linked to the culture microenvironment. Both, the biochemical and mechanical environment of tissue culture has an effect on the spontaneous calcification

  18. The time of onset of abnormal calcification in spondylometaepiphyseal dysplasia, short limb-abnormal calcification type

    Energy Technology Data Exchange (ETDEWEB)

    Tueysuez, Beyhan [Istanbul University, Department of Pediatric Genetics, Cerrahpasa Medical School, Istanbul (Turkey); Gazioglu, Nurperi [Istanbul University, Department of Neurosurgery, Cerrahpasa Medical School, Istanbul (Turkey); Uenguer, Savas [Istanbul University, Department of Pediatric Radiology, Cerrahpasa Medical School, Istanbul (Turkey); Aji, Dolly Yafet [Istanbul University, Department of Pediatrics, Cerrahpasa Medical School, Istanbul (Turkey); Tuerkmen, Seval [Istanbul University, Department of Pediatric Genetics, Cerrahpasa Medical School, Istanbul (Turkey); Universitatsklinikum Berlin, Charite Virchow-Klinik, Berlin (Germany)

    2009-01-15

    A 1-month-old boy with shortness of extremities on prenatal US was referred to our department with a provisional diagnosis of achondroplasia. His height was normal but he had short extremities and platyspondyly, premature carpal epiphyses on both hands, and short tubular bones with irregular metaphyses on radiographs. Re-evaluation of the patient at the age of 1 year revealed very short height and premature calcification of the costal cartilages and epiphyses. Spondylometaepiphyseal dysplasia (SMED), short limb-abnormal calcification type was diagnosed. This condition is a very rare autosomal recessively inherited disorder, and most of the patients die in early childhood due to neurological involvement. At the age of 2 years and 5 months, a CT scan showed narrowing of the cervical spinal canal. One month later he died suddenly because of spinal cord injury. In conclusion early diagnosis is very important because the recurrence risk is high and patients may die due to early neurological complications. The time of onset of abnormal calcifications, a diagnostic finding of the disease, is at the age of around 1 year in most patients. When abnormal calcifications are not yet present, but radiological changes associated with SMED are present, this rare disease must be considered. (orig.)

  19. Aortic root, not valve, calcification correlates with coronary artery calcification in patients with severe aortic stenosis

    DEFF Research Database (Denmark)

    Henein, Michael; Hällgren, Peter; Holmgren, Anders

    2015-01-01

    calcification (AVC), due to tissue similarity between the two types of vessel rather than with the valve leaflet tissue. MATERIAL AND METHODS: We studied 212 consecutive patients (age 72.5 ± 7.9 years, 91 females) with AS requiring aortic valve replacement (AVR) in two Heart Centers, who underwent multidetector...

  20. The time of onset of abnormal calcification in spondylometaepiphyseal dysplasia, short limb-abnormal calcification type.

    Science.gov (United States)

    Tüysüz, Beyhan; Gazioğlu, Nurperi; Ungür, Savaş; Aji, Dolly Yafet; Türkmen, Seval

    2009-01-01

    A 1-month-old boy with shortness of extremities on prenatal US was referred to our department with a provisional diagnosis of achondroplasia. His height was normal but he had short extremities and platyspondyly, premature carpal epiphyses on both hands, and short tubular bones with irregular metaphyses on radiographs. Re-evaluation of the patient at the age of 1 year revealed very short height and premature calcification of the costal cartilages and epiphyses. Spondylometaepiphyseal dysplasia (SMED), short limb-abnormal calcification type was diagnosed. This condition is a very rare autosomal recessively inherited disorder, and most of the patients die in early childhood due to neurological involvement. At the age of 2 years and 5 months, a CT scan showed narrowing of the cervical spinal canal. One month later he died suddenly because of spinal cord injury. In conclusion early diagnosis is very important because the recurrence risk is high and patients may die due to early neurological complications. The time of onset of abnormal calcifications, a diagnostic finding of the disease, is at the age of around 1 year in most patients. When abnormal calcifications are not yet present, but radiological changes associated with SMED are present, this rare disease must be considered.

  1. Lipoprotein-associated phospholipase A2 and coronary calcification - The Rotterdam coronary calcification study

    NARCIS (Netherlands)

    Kardys, Isabella; Oei, Hok-Hay S.; Hofman, Albert; Oudkerk, Matthijs; Witteman, Jacqueline C. M.

    2007-01-01

    Objectives: Although several studies have recently suggested that lipoprotein-associated phospholipase A2 (Lp-PLA2) is an independent predictor of coronary events, only one study has examined the association between Lp-PLA2 and coronary calcification, using young adults. We investigated the associat

  2. Mitral annular calcification and aortic valve calcification may help in predicting significant coronary artery disease.

    Science.gov (United States)

    Acartürk, Esmeray; Bozkurt, Abdi; Cayli, Murat; Demir, Mesut

    2003-01-01

    Mitral annular calcification (MAC) and aortic valve calcification (AVC) are manifestations of atherosclerosis. To determine whether mitral annular calcification and aortic valve calcification detected by transthoracic echocardiography (TTE) might help in predicting significant coronary artery disease (CAD), 123 patients with significant CAD and 93 patients without CAD detected by coronary angiography were investigated. MAC and AVC identified CAD with a sensitivity and specificity of 60.2%, 55.9% and 74.8%, 52.7%, respectively, and with a negative and a positive predictive values of 51.5%, 64.3% and 61.3% and 67.6%, respectively. The positive predictive value of MAC was greater than gender, hypertension, and hypercholesterolemia. AVC showed a positive predictive value greater than gender, hypertension, family history, and hypercholesterolemia. The negative predictive values of MAC and AVC for CAD were greater than those of all risk factors except diabetes mellitus. In conclusion, presence of MAC and AVC on TTE may help in predicting CAD and should be added to conventional risk factors. Absence of MVC and AVC is a stronger predictor for absence of CAD than all conventional risk factors, except diabetes mellitus. Patients with MAC and AVC should be taken into consideration for the presence of significant CAD and thereby for diagnostic and therapeutic interventions in order to improve the prognosis.

  3. 维生素 D、非含钙的磷结合剂与含钙的磷结合剂对慢性肾脏病患者血管钙化进展的影响%Examination of the Effect of Vitamin D,Non-Calcium Phosphate Binders,and Calcium Phosphate ;Binders on the Progress of Vascular Calcification in Patients with Chronic Kidney Disease

    Institute of Scientific and Technical Information of China (English)

    李幕军; 卜荣亮

    2016-01-01

    Objective]To analyze the effect of vitamin D,non-calcium phosphate binders,and calcium phosphate binders on the progress of vascular calcification in patients with chronic kidney disease.[Methods]Seventy-eight cases of patients with chronic kidney disease treated in our hospital from January 2010 to December 2014 were randomly selected as the research ob-jects.According to the order of admission,the patients were numbered and,with reference to the random number table meth-od,divided into two Groups,A and B,with 39 cases in each group.All of the patients were treated with vitamin D.Patients in group A were also treated with non-calcium phosphate binder (lanthanum carbonate),while patients in group B were also treated with routine calcium phosphate binder (calcium acetate).The changes in blood calcium,serum phosphorus,calcium-phosphorus product,and intact parathyroid hormone (iPTH)levels were compared between the two groups before and after the treatment.The use of vitamin D and phosphorus binder in the two groups was compared.Imaging examinations showed the changes in coronary artery calcium score (CACs),which were evaluated and statistically analyzed along with the incidence rates of adverse events during the treatment.[Results]①After the treatment,serum phosphorus,calcium-phosphorus prod-uct,and iPTH levels in the two group decreased significantly,but the differences between groups were not statistically signifi-cant (P >0.05).Blood calcium level in group A was reduced to(2.24±0.17)mmol/L and the decreased amplitude was higher than that in Group B (P 0.05),A 组血钙水平降低至(2.24±0.17)mmol/L,降低幅度高于 B 组,两组相比较差异有显著性(P <0.05);②A 组磷结合剂摄入量为(1719.21±410.22)mg/d,明显低于 B 组的(4913.34±1332.26)mg/d,两组相比较差异有显著性(P <0.05);③B 组中重度钙化分别占20.51%、10.26%,均高于 A 组(P <0.05);④A 组不良事件发生率为10.26%,明显低于 B 组的48.72%,两组

  4. Leptin promotes osteoblast differentiation and mineralization of primary cultures of vascular smooth muscle cells by inhibiting glycogen synthase kinase (GSK)-3{beta}

    Energy Technology Data Exchange (ETDEWEB)

    Zeadin, Melec G.; Butcher, Martin K.; Shaughnessy, Stephen G. [Department of Medicine, McMaster University, Hamilton, ON (Canada); Thrombosis and Atherosclerosis Research Institute, Hamilton, ON (Canada); Werstuck, Geoff H., E-mail: Geoff.Werstuck@taari.ca [Department of Medicine, McMaster University, Hamilton, ON (Canada); Thrombosis and Atherosclerosis Research Institute, Hamilton, ON (Canada)

    2012-09-07

    Highlights: Black-Right-Pointing-Pointer Leptin promotes osteoblast differentiation of primary smooth muscle cells. Black-Right-Pointing-Pointer Leptin regulates the expression of genes involved in osteoblast differentiation. Black-Right-Pointing-Pointer Constitutively active GSK-3{beta} attenuates leptin-induced osteoblast differentiation. Black-Right-Pointing-Pointer This suggests that leptin signals through GSK-3{beta} to promote osteoblast differentiation. -- Abstract: In this study, we begin to investigate the underlying mechanism of leptin-induced vascular calcification. We found that treatment of cultured bovine aortic smooth muscle cells (BASMCs) with leptin (0.5-4 {mu}g/ml) induced osteoblast differentiation in a dose-dependent manner. Furthermore, we found that leptin significantly increased the mRNA expression of osteopontin and bone sialoprotein, while down-regulating matrix gla protein (MGP) expression in BASMCs. Key factors implicated in osteoblast differentiation, including members of the Wnt signaling pathway, were examined. Exposure to leptin enhanced phosphorylation of GSK-3{beta} on serine-9 thereby inhibiting activity and promoting the nuclear accumulation of {beta}-catenin. Transfection of BASMCs with an adenovirus that expressed constitutively active GSK-3{beta} (Ad-GSK-3{beta} S9A) resulted in a >2-fold increase in GSK-3{beta} activity and a significant decrease in leptin-induced alkaline phosphatase (ALP) activity. In addition, qRT-PCR analysis showed that GSK-3{beta} activation resulted in a significant decrease in the expression of osteopontin and bone sialoprotein, but a marked increase in MGP mRNA expression. When taken together, our results suggest a mechanism by which leptin promotes osteoblast differentiation and vascular calcification in vivo.

  5. Taurine inhibits osteoblastic differentiation of vascular smooth muscle cells via the ERK pathway.

    Science.gov (United States)

    Liao, Xiao-bo; Zhou, Xin-min; Li, Jian-ming; Yang, Jin-fu; Tan, Zhi-ping; Hu, Zhuo-wei; Liu, Wei; Lu, Ying; Yuan, Ling-qing

    2008-05-01

    Vascular calcification develops within atherosclerotic lesions and results from a process similar to osteogenesis. Taurine is a free beta-amino acid and plays an important physiological role in mammals. We have recently demonstrated that vascular smooth muscle cells (VSMCs) express a functional taurine transporter. To evaluate the possible role of taurine in vascular calcification, we assessed its effects on osteoblastic differentiation of VSMCs in vitro. The results showed that taurine inhibited the beta-glycerophosphate-induced osteoblastic differentiation of VSMCs as evidenced by both the decreasing alkaline phosphate (ALP) activity and expression of the core binding factor alpha1 (Cbfalpha1). Taurine also activated the extracellular signal-regulated protein kinase (ERK) pathway. Inhibition of ERK pathway reversed the effect of taurine on ALP activity and Cbfalpha1 expression. These results suggested that taurine inhibited osteoblastic differentiation of vascular cells via the ERK pathway.

  6. Vascular emergencies.

    Science.gov (United States)

    Semashko, D C

    1997-01-01

    This article reviews the initial assessment and emergent management of several common as well as uncommon vascular emergencies. Aortic dissection, aneurysms, and arterial occlusive disease are familiar but challenging clinical entities. Less frequently encountered conditions are also discussed including an aortic enteric fistula, mesenteric venous thrombosis, phlegmasia alba dolens, and subclavian vein thrombosis.

  7. Vascular Disease Foundation

    Science.gov (United States)

    ... Contact Us Vascular Disease What is Vascular Disease? Education and Awareness Vascular Diseases Abdominal Aortic Aneurysm Aortic Dissection Arteriovenous Malformation Atherosclerosis Buerger's Disease Carotid Artery Disease ...

  8. What Is Vascular Disease?

    Science.gov (United States)

    ... Contact Us Vascular Disease What is Vascular Disease? Education and Awareness Vascular Diseases Abdominal Aortic Aneurysm Aortic Dissection Arteriovenous Malformation Atherosclerosis Buerger's Disease Carotid Artery Disease ...

  9. Tanshinone IIA attenuates interleukin-17A-induced systemic sclerosis patient-derived dermal vascular smooth muscle cell activation via inhibition of the extracellular signal-regulated kinase signaling pathway

    Directory of Open Access Journals (Sweden)

    Mengguo Liu

    2015-04-01

    Full Text Available OBJECTIVE: Salvia miltiorrhiza has long been used to treat systemic sclerosis. Tanshinone IIA, one of the phytochemicals derived from the roots of Salvia miltiorrhiza, exhibits multiple biological activities. The present study aimed to investigate whether tanshinone IIA has an effect on the interleukin-17A-induced functional activation of systemic sclerosis patient-derived dermal vascular smooth muscle cells. METHODS: Systemic sclerosis patient-derived dermal vascular smooth muscle cells were incubated with various dosages of tanshinone IIA in the presence of interleukin-17A or the serum of systemic sclerosis patients. Cell proliferation was assessed using Cell Counting Kit-8. The expression of collagen 1 and 3 in cells was evaluated by immunofluorescence. Cell migration was measured using a transwell assay. The expression of phospho-extracellular signal-regulated kinase was detected by Western blotting. RESULTS: Our data demonstrate that tanshinone IIA exerts an inhibitory effect on interleukin-17A-induced systemic sclerosis patient-derived dermal vascular smooth muscle cell proliferation, collagen synthesis and migration. CONCLUSION: These findings suggest that tanshinone IIA might serve as a promising therapeutic agent for the treatment of systemic sclerosis.

  10. Liposarcoma of the thigh with mixed calcification and ossification

    Directory of Open Access Journals (Sweden)

    Jeremy R. Child, MD

    2016-09-01

    Full Text Available Liposarcoma is one of the most common soft-tissue sarcomas. Calcification and ossification can occur in liposarcoma; however, the presence of both ossification and calcification is a very rare entity. We present a case of a partially calcified and ossified dedifferentiated liposarcoma of the thigh in a 76-year-old woman, which contained heterologous elements of chondrosarcoma and rhabdomyosarcoma.

  11. Acute calcific tendinitis of the finger--a case report.

    LENUS (Irish Health Repository)

    Ali, S N

    2004-07-01

    Acute calcific tendinitis of the hand is rare and often misdiagnosed as infection, fracture or periarthritis. It frequently occurs in peri-menopausal women and is caused by deposits of hydroxyapatite crystals. We describe acute calcific tendinitis of the flexor digitorum superficialis insertion in an elderly man taking oral anticoagulants. The differential diagnoses and recommended treatment are discussed.

  12. Hyperprolactinemia associated to calcification of the pituitary stalk: case report

    Directory of Open Access Journals (Sweden)

    OLIVEIRA MIRIAM DA COSTA

    1998-01-01

    Full Text Available In this work, the authors report the case of a female patient with 24 years of age with hyperprolactinemia, who presented a pituitary stalk calcification as seen by CT scan. Once other possible etiologies were excluded, we concluded that the calcification was probably related to hyperprolactinemia caused by interruption of the input of dopamine to the pituitary gland.

  13. Umbilical and portal vein calcification following umbilical vein catheterization

    Energy Technology Data Exchange (ETDEWEB)

    Schneider, K.; Fendel, H.; Hartl, M.

    1989-07-01

    Calcifications of the umbilical vein and intrahepatic branches of the portal vein developed in a newborn who had inserted an umbilical vein catheter for 11 days postnatally. The calcified intrahepatic portal veins can still be demonstrated sonographically at the age of three years, whereby these calcifications were no longer detectable radiologically. (orig.).

  14. [Endomyocardial fibrosis with massive calcification of the left ventricle].

    Science.gov (United States)

    Trigo, Joana; Camacho, Ana; Gago, Paula; Candeias, Rui; Santos, Walter; Marques, Nuno; Matos, Pedro; Brandão, Victor; Gomes, Veloso

    2010-03-01

    Endomyocardial fibrosis is a rare disease, endemic in tropical countries. It is characterized by fibrosis of the endocardium that can extend to myocardium. Important calcification of the endocardium is rare with only a few cases reported in the literature. We report a case of endomyocardial fibrosis in a european caucasian patient, associated with massive calcification of left ventricle.

  15. Left atrial calcification in a hemodialysis patient with cor triatriatum.

    Science.gov (United States)

    Peces, R; Pobes, A; Rodriguez, M; Simarro, C; Iglesias, G; Simarro, E

    2000-05-01

    Myocardial calcification is a rare manifestation of abnormal calcium metabolism seen in some patients with chronic renal failure. This report describes the transesophageal echocardiographic and spiral computed tomography (CT) findings in a young hemodialysis female with severe secondary hyperparathyroidism. These findings included calcification of the multiperforated membrane of a cor triatriatum and the wall of the left atrium.

  16. Susceptibility weighted imaging: differentiating between calcification and hemosiderin

    Energy Technology Data Exchange (ETDEWEB)

    Barbosa, Jeam Haroldo Oliveira; Salmon, Carlos Ernesto Garrido, E-mail: jeamharoldo@hotmail.com [Universidade de Sao Paulo (FFCLRP/USP), Ribeirao Preto, SP (Brazil). Faculdade de Filosofia, Ciencias e Letras; Santos, Antonio Carlos [Universidade de Sao Paulo (FMRP/USP), Ribeirao Preto, SP (Brazil). Faculdade de Medicina

    2015-03-15

    Objective: to present a detailed explanation on the processing of magnetic susceptibility weighted imaging (SWI), demonstrating the effects of echo time and sensitive mask on the differentiation between calcification and hemosiderin. Materials and methods: computed tomography and magnetic resonance (magnitude and phase) images of six patients (age range 41-54 years; four men) were retrospectively selected. The SWI images processing was performed using the Matlab's own routine. Results: four out of the six patients showed calcifications at computed tomography images and their SWI images demonstrated hyperintense signal at the calcification regions. The other patients did not show any calcifications at computed tomography, and SWI revealed the presence of hemosiderin deposits with hypointense signal. Conclusion: the selection of echo time and of the mask may change all the information on SWI images, and compromise the diagnostic reliability. Amongst the possible masks, the authors highlight that the sigmoid mask allows for contrasting calcifications and hemosiderin on a single SWI image. (author)

  17. Basal ganglia calcification on computed tomography in systemic lupus erythematosus

    Energy Technology Data Exchange (ETDEWEB)

    Nagaoka, Shohei; Tani, Kenji; Ishigatsubo, Yoshiaki and others

    1988-09-01

    The development of basal ganglia calcification was studied in 85 patients with systemic lupus erythematosus (SLE) by computed tomography (CT). Bilateral calcification of the basal ganglia was found to occur in 5 patients (5.9 %) with SLE, but was not seen in patients with rheumatoid arthritis and progressive systemic sclerosis. All were female with a mean age of 42 years (range 29 - 49). The patients with calcification of the basal ganglia had neurological symptoms, such as psychiatric problems (3 cases), grand mal seizures (1 case), CSF abnormalities (2 cases), and EEG changes (4 cases). There were significantly higher incidences of alopecia, cutaneous vasculitis, leukopenia, and thrombocytopenia in the group with calcifications than those in the group with normal CT findings. Circulating immune complexes were detected and LE tests were positive in 2 patients. Endocrinological examination showed no abnormality in any. We suggest that basal ganglia calcification in SLE might be related to cerebral vasculitis.

  18. Osteoprotegerin and biomarkers of vascular inflammation in type 2 diabetes.

    LENUS (Irish Health Repository)

    O'Sullivan, Eoin P

    2010-09-01

    Osteoprotegerin (OPG), receptor activator for nuclear factor kappa beta ligand (RANKL) and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) are newly discovered members of the tumour necrosis factor-alpha receptor superfamily. While their role in bone metabolism is well described, their function within the vasculature is poorly understood. OPG inhibits vascular calcification in vitro and high serum levels have been demonstrated in type 2 diabetes, but serum RANKL and TRAIL and their potential correlation with well-established biomarkers of subclinical vascular inflammation such as high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) have not been described.

  19. Endovascular Access for Challenging Anatomies in Peripheral Vascular Interventions.

    Science.gov (United States)

    Vatakencherry, Geogy; Gandhi, Ripal; Molloy, Christopher

    2016-06-01

    Vascular interventionalists continue to expand the scope and breadth of endovascular procedures that we offer to our patients. However, we often have to overcome various anatomical and technical challenges to deliver an endovascular device. This article should give the modern interventionalist an array of technical tips and tricks to enable them to overcome various challenging anatomical features such as vessel tortuosity, vascular calcifications, and increasing abdominal pannus. We also hope to elucidate alternative accesses such as radial access, pedal access, popliteal access, and direct stent access as well as direct aortic access.

  20. Treatment with recombinant lubricin attenuates osteoarthritis by positive feedback loop between articular cartilage and subchondral bone in ovariectomized rats.

    Science.gov (United States)

    Cui, Zhuang; Xu, Changpeng; Li, Xue; Song, Jinqi; Yu, Bin

    2015-05-01

    Osteoarthritis (OA) is a most commonly multifactorial degenerative joint disease along with the aging population, particularly in postmenopausal women. During the onset of OA, articular cartilage and subchondral bone act in concert as a functional unit. This present study is to investigate the effects of early or late treatment with recombinant lubricin on the onset of osteoarthritis (OA) in ovariectomized (OVX) rats. We found that both early and late recombinant lubricin treatments attenuated the onset of OA by positive feedback loop between articular cartilage and subchondral bone, although late treatment contributed to a lesser effect compared with early treatment. Specifically, treatment with recombinant lubricin protected articular cartilage from degeneration, demonstrated by lower proteoglycan loss, lower OARSI scores, less calcification cartilage zone and reduced immunostaining for collagen X (Col X) and matrix metalloproteinase (MMP-13) but increased the expression of lubricin, in comparison with vehicle-treated OVX rat group. Further, chondroprotective effects of lubricin normalized bone remodeling in subchondral bone underneath. It's suggested that treatment with recombinant lubricin inhibited the elevation of TRAP and Osterix positive cells in OVX rats and led to the normalization of subchondral bone microarchitectures with the suppression of subsidence of bone volume ratio (BV/TV) and trabecular thickness (Tb.Th) and the increase of trabecular separation (Tb.Sp) in vehicle-treated OVX rats. What's more, the normalization of subchondral bone in turn attenuated the articular cartilage erosion by inhibiting vascular invasion from subchondral bone to calcified cartilage zone, exemplified by inhibiting the elevation of CD31 positive cells in calcified cartilage and angiography in subchondral bone. Together, these results shed light that both early and late recombinant lubricin treatments attenuate the onset of OA by balancing the interplay between articular

  1. Feedbacks and responses of coral calcification on the Bermuda reef system to seasonal changes in biological processes and ocean acidification

    Science.gov (United States)

    Bates, N. R.; Amat, A.; Andersson, A. J.

    2010-08-01

    Despite the potential impact of ocean acidification on ecosystems such as coral reefs, surprisingly, there is very limited field data on the relationships between calcification and seawater carbonate chemistry. In this study, contemporaneous in situ datasets of seawater carbonate chemistry and calcification rates from the high-latitude coral reef of Bermuda over annual timescales provide a framework for investigating the present and future potential impact of rising carbon dioxide (CO2) levels and ocean acidification on coral reef ecosystems in their natural environment. A strong correlation was found between the in situ rates of calcification for the major framework building coral species Diploria labyrinthiformis and the seasonal variability of [CO32-] and aragonite saturation state Ωaragonite, rather than other environmental factors such as light and temperature. These field observations provide sufficient data to hypothesize that there is a seasonal "Carbonate Chemistry Coral Reef Ecosystem Feedback" (CREF hypothesis) between the primary components of the reef ecosystem (i.e., scleractinian hard corals and macroalgae) and seawater carbonate chemistry. In early summer, strong net autotrophy from benthic components of the reef system enhance [CO32-] and Ωaragonite conditions, and rates of coral calcification due to the photosynthetic uptake of CO2. In late summer, rates of coral calcification are suppressed by release of CO2 from reef metabolism during a period of strong net heterotrophy. It is likely that this seasonal CREF mechanism is present in other tropical reefs although attenuated compared to high-latitude reefs such as Bermuda. Due to lower annual mean surface seawater [CO32-] and Ωaragonite in Bermuda compared to tropical regions, we anticipate that Bermuda corals will experience seasonal periods of zero net calcification within the next decade at [CO32-] and Ωaragonite thresholds of ~184 μmoles kg-1 and 2.65. However, net autotrophy of the reef

  2. Feedbacks and responses of coral calcification on the Bermuda reef system to seasonal changes in biological processes and ocean acidification

    Directory of Open Access Journals (Sweden)

    N. R. Bates

    2010-08-01

    Full Text Available Despite the potential impact of ocean acidification on ecosystems such as coral reefs, surprisingly, there is very limited field data on the relationships between calcification and seawater carbonate chemistry. In this study, contemporaneous in situ datasets of seawater carbonate chemistry and calcification rates from the high-latitude coral reef of Bermuda over annual timescales provide a framework for investigating the present and future potential impact of rising carbon dioxide (CO2 levels and ocean acidification on coral reef ecosystems in their natural environment. A strong correlation was found between the in situ rates of calcification for the major framework building coral species Diploria labyrinthiformis and the seasonal variability of [CO32-] and aragonite saturation state Ωaragonite, rather than other environmental factors such as light and temperature. These field observations provide sufficient data to hypothesize that there is a seasonal "Carbonate Chemistry Coral Reef Ecosystem Feedback" (CREF hypothesis between the primary components of the reef ecosystem (i.e., scleractinian hard corals and macroalgae and seawater carbonate chemistry. In early summer, strong net autotrophy from benthic components of the reef system enhance [CO32-] and Ωaragonite conditions, and rates of coral calcification due to the photosynthetic uptake of CO2. In late summer, rates of coral calcification are suppressed by release of CO2 from reef metabolism during a period of strong net heterotrophy. It is likely that this seasonal CREF mechanism is present in other tropical reefs although attenuated compared to high-latitude reefs such as Bermuda. Due to lower annual mean surface seawater [CO32-] and Ωaragonite in Bermuda compared to tropical regions, we anticipate that Bermuda corals will experience seasonal periods

  3. Ligustrazine attenuates the platelet-derived growth factor-BB-induced proliferation and migration of vascular smooth muscle cells by interrupting extracellular signal-regulated kinase and P38 mitogen-activated protein kinase pathways.

    Science.gov (United States)

    Yu, Lifei; Huang, Xiaojing; Huang, Kai; Gui, Chun; Huang, Qiaojuan; Wei, Bin

    2015-07-01

    The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) leads to intimal thickening of the aorta and is, therefore, important in the development of arteriosclerosis. As a result, the use of antiproliferative and antimigratory agents for VSMCs offers promise for the treatment of vascular disorders. Although several studies have demonstrated that ligustrazine may be used to treat heart and blood vessel diseases, the detailed mechanism underlying its actions remain to be elucidated. In the present study, the inhibitory effect of ligustrazine on platelet-derived growth factor (PDGF)-BB-stimulated VSMC proliferation and migration, and the underlying mechanisms were investigated. The findings demonstrated that ligustrazine significantly inhibited PDGF-BB-stimulated VSMC proliferation. VSMCs dedifferentiated into a proliferative phenotype under PDGF-BB stimulation, which was effectively reversed by the administration of ligustrazine. In addition, ligustrazine also downregulated the production of nitric oxide and cyclic guanine monophosphate, induced by PDGF-BB. Additionally, ligustrazine significantly inhibited PDGF-BB-stimulated VSMC migration. Mechanistic investigation indicated that the upregulation of cell cycle-associated proteins and the activation of the extracellular signal-regulated kinase (ERK) and P38 mitogen-activated protein kinase (MAPK) signaling induced by PDGF-BB was suppressed by the administration of ligustrazine. In conclusion, the present study, demonstrated for the first time, to the best of our knowledge, that ligustrazine downregulated PDGF-BB-induced VSMC proliferation and migration partly, at least, through inhibiting the activation of the ERK and P38 MAPK signaling.

  4. Association of Advanced Glycation End Products with coronary Artery Calcification in Japanese Subjects with Type 2 Diabetes as Assessed by Skin Autofluorescence

    OpenAIRE

    Hangai, Mari; Takebe, Noriko; Honma, Hiroyuki; Sasaki, Atsumi; Chida, Ai; Nakano, Rieko; Togashi, Hirobumi; Nakagawa, Riyuki; Oda, Tomoyasu; Matsui, Mizue; Yashiro, Satoshi; Nagasawa, Kan; Kajiwara, Takashi; Takahashi, Kazuma; Takahashi, Yoshihiko

    2016-01-01

    Aim: Advanced glycation end products (AGE) are considered to be among the critical pathogenic factors involved in the progression of diabetic complications. Skin autofluorescence (AF), a noninvasive measurement of AGE accumulation, has been recognized as a useful and convenient marker for diabetic vascular diseases in Caucasians. This study aimed to evaluate the association of tissue AGE, assessed using skin AF, with coronary artery calcification in Japanese subjects with type 2 diabetes. Met...

  5. Incidental orbital calcifications on computed tomography scans; Calcificacoes orbitarias incidentais na tomografia computadorizada

    Energy Technology Data Exchange (ETDEWEB)

    Fugita, Dalton Yukio A.; Cruz, Daniela Nogueira; Cappucci, Alessandro; Arakava, Marcia Mayumi; Guimaraes, Maria Carolina; Wolosker, Angela Maria B.; Yamashita, Helio Kiitiro [Universidade Federal de Sao Paulo (UNIFESP), SP (Brazil). Dept. de Diagnostico por Imagem; Manso, Paulo Goes [Universidade Federal de Sao Paulo (UNIFESP), SP (Brazil). Dept. de Oftalmologia

    2001-02-01

    We retrospectively studied the computed tomography scans of the orbit in 75 patients in order to identify the presence of incidental calcifications (scleral and trochlear apparatus calcifications.). These imaging findings should integrate the vast list of differential diagnosis of orbital calcifications, as they may help radiologists to distinguish these calcifications from orbital foreign bodies. (author)

  6. Idiopathic calcification of the seminal vesicles: a rare cause for prostate cancer overstaging.

    Science.gov (United States)

    Pannek, J; Senge, T

    2001-01-01

    Calcification of the seminal vesicles is a rare phenomenon. We present 2 cases in whom calcification of the seminal vesicles led to preoperative overstaging of prostate cancer. Although idiopathic calcifications are extremely rare, calcifications appear more frequently in diabetic patients. Therefore, knowledge of these formations is essential to prevent overstaging, namely infiltration of the seminal vesicles.

  7. Observer study to evaluate the simulation of mammographic calcification clusters

    Science.gov (United States)

    Sousa, Maria A. Z.; Marcomini, Karem D.; Bakic, Predrag R.; Maidment, Andrew D. A.; Schiabel, Homero

    2016-03-01

    Numerous breast phantoms have been developed to be as realistic as possible to ensure the accuracy of image quality analysis, covering a greater range of applications. In this study, we simulated three different densities of the breast parenchyma using paraffin gel, acrylic plates and PVC films. Hydroxyapatite was used to simulate calcification clusters. From the images acquired with a GE Senographe DR 2000D mammography system, we selected 68 regions of interest (ROIs) with and 68 without a simulated calcification cluster. To validate the phantom simulation, we selected 136 ROIs from the University of South Florida's Digital Database for Screening Mammography (DDSM). Seven trained observers performed two observer experiments by using a high-resolution monitor Barco mod. E-3620. In the first experiment, the observers had to distinguish between real or phantom ROIs (with and without calcification). In the second one, the observers had to indicate the ROI with calcifications between a pair of ROIs. Results from our study show that the hydroxyapatite calcifications had poor contrast in the simulated breast parenchyma, thus observers had more difficulty in identifying the presence of calcification clusters in phantom images. Preliminary analysis of the power spectrum was conducted to investigate the radiographic density and the contrast thresholds for calcification detection. The values obtained for the power spectrum exponent (β) were comparable with those found in the literature.

  8. Acromial morphology in patients with calcific tendinitis of the shoulder.

    Science.gov (United States)

    Balke, Maurice; Banerjee, Marc; Vogler, Tim; Akoto, Ralph; Bouillon, Bertil; Liem, Dennis

    2014-02-01

    The purpose of this study was to evaluate whether the morphology of the acromion in calcific tendinitis differs from controls without subacromial pathology and matches subacromial impingement. Digital radiographs of 150 shoulders were evaluated with the open source DICOM-Viewer OsiriX. 50 patients had symptomatic calcific tendinitis of the shoulder, 50 had subacromial impingement without calcifications or rotator cuff tears, 50 with bruised shoulder that were previously asymptomatic served as controls. Acromial shape according to Bigliani et al. acromial tilt (AT) according to Kitay et al. and Aoki et al. acromion index (AI) according to Nyffeler et al. and lateral acromial angle (LAA) according to Banas et al. were measured. Both calcific (0.72; P = 0.001) and impingement groups (0.73; P = 0.008) were significantly different from controls (0.67) using AI measure, while only the calcific group (79.5°) was different from controls (84.1°) using LAA (P tendinitis. The hypothesis of this study was that the morphology of the acromion in calcific tendinitis differs from controls without subacromial pathology and matches subacromial impingement was only confirmed for the AI. The AI of shoulders with calcific tendinitis is comparable to that of shoulders with subacromial impingement.

  9. In-vitro calcification study of polyurethane heart valves.

    Science.gov (United States)

    Boloori Zadeh, Parnian; Corbett, Scott C; Nayeb-Hashemi, Hamid

    2014-02-01

    Tri-leaflet polyurethane heart valves have been considered as a potential candidate in heart valve replacement surgeries. In this study, polyurethane (Angioflex(®)) heart valve prostheses were fabricated using a solvent-casting method to evaluate their calcification resistance. These valves were subjected to accelerated life testing (continuous opening and closing of the leaflets) in a synthetic calcification solution. Results showed that Angioflex(®) could be considered as a potential material for fabricating prosthetic heart valves with possibly a higher calcification resistance compared to tissue valves. In addition, calcification resistance of bisphosphonate-modified Angioflex(®) valves was also evaluated. Bisphosphonates are considered to enhance the calcification resistance of polymers once covalently bonded to the bulk of the material. However, our in-vitro results showed that bisphosphonate-modified Angioflex(®) valves did not improve the calcification resistance of Angioflex(®) compared to its untreated counterparts. The results also showed that cyclic loading of the valves' leaflets resulted in formation of numerous cracks on the calcified surface, which were not present when calcification study did not involve mechanical loading. Further study of these cracks did not result in enough evidence to conclude whether these cracks have penetrated to the polymeric surface.

  10. Management of rotator cuff calcific tendinosis guided by ultrasound elastography.

    Science.gov (United States)

    Lin, Yen-Huai; Chiou, Hong-Jen; Wang, Hsin-Kai; Lai, Yi-Chen; Chou, Yi-Hong; Chang, Cheng-Yen

    2015-10-01

    Ultrasound (US) elastography can provide information about the hardness of calcification and might help decide treatment strategy. The purpose of this study was to evaluate the hardness of the calcific area within rotator cuffs by US elastography as an aid for the selection of aspiration or fine-needle repeated puncture for the treatment of rotator cuff calcific tendinosis. This prospective study included 39 patients (32 males, 7 females; mean age, 52.9 years) who received US elastography and gray-scale ultrasonography before US-guided treatment for rotator cuff calcific tendinosis. The morphology of the calcifications was classified as arc, fragmented, nodular, and cystic types. US elastography using virtual touch imaging (acoustic radiation force impulse) technique was performed to examine the calcified region to obtain an elastogram that was graded dark, intermediate, or bright. The hardness of the calcifications were recorded, and graded as hard, sand-like, or fluid-like tactile patterns during the US-guided treatment, and the tactile patterns were compared with the results of US elastography and gray-scale ultrasonography. Though the morphologies of the calcifications were significantly related to the tactile pattern of the needle punctures (p tendinosis, and as an aid to guide management. If elastography shows the calcified area as a non-dark pattern, then fine-needle aspiration should be performed. Copyright © 2015. Published by Elsevier Taiwan.

  11. Trochlear calcification and intraorbital foreign body in ocular trauma patients

    Institute of Scientific and Technical Information of China (English)

    XIAO Tian-lin; Nileshkumar M Kalariya; YAN Zhi-han; CHEN Wei; LIU Xiao-qiang; ZHAO Zhen-quan; ZHOU Ye-hui; XU Dan

    2009-01-01

    Objective: To distinguish trochlear calcification and intraorbital foreign body after eye injury in order to avoid misdiagnosis as well as mistreatment. Methods: The orbital CT images of 403 patients, who visited the Eye Hospital or the Second Affiliated Hospital of Wenzhou Medical College during May 2005-April 2007, were reviewed. The diagnosis of trochlear calcification and in-traorbital foreign body was made together by a skilled radi-ologist as well as an ophthalmologist. General information and CT characteristics in the patients with trochlear calcifi-cation were collected.Results: Using CT scan images, 27 among 403 pa-tients (6.69%) were identified with trochlear calcification. Three patients (3/27, 11.11%) were misdiagnosed by radi-ologists as intraorbital foreign body. Among the 27 patients with trochlear calcification, 23 (85.19%) were male and 4 (14.81%)were female, with an unilateral calcification in 7 patients (7/27, 25.93%) and bilateral in 20(74.07%). The highest occurrence of trochlear calcification was in 31-40 years old group (13/403, 3.23%) which reached to 12.87% (13/101) after age-correction. There were 3 types of trochlear calcification on the basis of CT images: commas, dot and inverted "U".Conclusions: The trochlear calcification is not an un-common phenomenon and should not be diagnosed as in-traorbital foreign body, especially when it co-exists with eye injury in 31-40 years old group. Injury history and our classification method on the basis of CT images could help to avoid misdiagnosis.

  12. In vascular smooth muscle cells paricalcitol prevents phosphate-induced Wnt/β-catenin activation.

    Science.gov (United States)

    Martínez-Moreno, Julio M; Muñoz-Castañeda, Juan R; Herencia, Carmen; Oca, Addy Montes de; Estepa, Jose C; Canalejo, Rocio; Rodríguez-Ortiz, Maria E; Perez-Martinez, Pablo; Aguilera-Tejero, Escolástico; Canalejo, Antonio; Rodríguez, Mariano; Almadén, Yolanda

    2012-10-15

    The present study investigates the differential effect of two vitamin D receptor agonists, calcitriol and paricalcitol, on human aortic smooth muscle cells calcification in vitro. Human vascular smooth muscle cells were incubated in a high phosphate (HP) medium alone or supplemented with either calcitriol 10(-8)M (HP + CTR) or paricalcitol 3·10(-8) M (HP + PC). HP medium induced calcification, which was associated with the upregulation of mRNA expression of osteogenic factors such as bone morphogenetic protein 2 (BMP2), Runx2/Cbfa1, Msx2, and osteocalcin. In these cells, activation of Wnt/β-catenin signaling was evidenced by the translocation of β-catenin into the nucleus and the increase in the expression of direct target genes as cyclin D1, axin 2, and VCAN/versican. Addition of calcitriol to HP medium (HP + CTR) further increased calcification and also enhanced the expression of osteogenic factors together with a significant elevation of nuclear β-catenin levels and the expression of cyclin D1, axin 2, and VCAN. By contrast, the addition of paricalcitol (HP + PC) not only reduced calcification but also downregulated the expression of BMP2 and other osteoblastic phenotype markers as well as the levels of nuclear β-catenin and the expression of its target genes. The role of Wnt/β-catenin on phosphate- and calcitriol-induced calcification was further demonstrated by the inhibition of calcification after addition of Dickkopf-related protein 1 (DKK-1), a specific natural antagonist of the Wnt/β-catenin signaling pathway. In conclusion, the differential effect of calcitriol and paricalcitol on vascular calcification appears to be mediated by a distinct regulation of the BMP and Wnt/β-catenin signaling pathways.

  13. Maximal conservative therapy of calcific uremic ateriolopathy.

    Science.gov (United States)

    Van Noten, Charlotte; Janssen van Doorn, Karin; Vermander, Evert; Vlayen, Sonja; Verpooten, Gert A; Couttenye, Marie-Madeleine

    2012-07-01

    We present the case of a 61-year- old female patient in long-term hemodialysis who developed calcific uremic arteriolopathy (CUA) upon administration of the oral calcimimetic agent cinacalcet for treatment of secondary hyperparathyroidism. In May 2009, the baseline serum values were parathormone (PTH) 310 pg/ml, calcium 9.1 mg/dl and phosphorous 6.9 mg/dl. Necrotic wounds in the suprapubic fat tissue were successfully treated first, by correcting the calcium phosphorous product; second, through treatment with sodium thiosulfate and third, through intensive wound care with hyperbaric oxygen therapy and vacuum-assisted closure therapy, with no need for parathyroidectomy. Multiple factors have been described to play a role in the development of CUA. Based on the findings of this case, the treatment of CUA should be aimed at correcting different causes simultaneously.

  14. Orbital melanoma with calcification: A diagnostic dilemma

    Directory of Open Access Journals (Sweden)

    Sukhdeep Bains

    2016-01-01

    Full Text Available Primary orbital melanoma is rare and has varied initial presentation. A 28-year-old female presented with proptosis and decreased vision in the left eye. Computed tomography scan showed an orbital mass with contrast enhancement and calcification around the optic nerve leading to a diagnosis of meningioma. The patient chose to be on observation. Loss of vision with an increase in proptosis was seen at 6 months follow-up. On surgical exploration, a well-defined pigmented mass was seen encasing the optic nerve. Histopathological analysis revealed a malignant melanoma. Metastatic workup was negative. Left eye lid sparing exenteration was done. A high index of suspicion is necessary in a rapidly growing suspected optic nerve sheath meningioma and a differential diagnosis including orbital melanoma be considered.

  15. [Effect of sodium thiosulfate on coronary artery calcification in maintenance hemodialysis patients].

    Science.gov (United States)

    Yu, Y; Bi, Z M; Wang, Y; Chen, Z Q; Xu, S W

    2016-12-13

    Objective: To investigate the factors correlated to coronary artery calcification (CAC)in maintenance hemodialysis (MHD) patients and observe the effect of sodium thiosulfate (STS) on the progression of vascular calcification and its safety. Methods: Thirty-eight subjects from Fuzhou Genernal Hospital who underwent coronary artery CT scan using Philip's spiral CT were enrolled and the calcification degree was evaluated by CAC scores from December 2013 to December 2014. The hemodialysis patients were divided into CAC group (CAC scores>10, 27 cases) and non-CAC group (CAC scores≤10, 11 cases)according to the CT scan results.The differences of age, duration of dialysis, blood pressure and other hematological indices between the two groups were analyzed to investigate the factors correlated to CAC. Next, those with CAC (CAC scores≥50) received intravenous 0.18 g/kg STS (dissolved in 100 ml saline) in 30 minutes after each dialysis for 3 months (n=17, only 15 patients completed STS treatment) or received conventional treatment (n=10). Baseline data between the two groups before treatment had no significant statistical difference. All examination indices were evaluated before and after the treatment course. The changes of vascular calcification imaging, CAC scores, biochemical indices and bone mineral density were compared between two groups before and after the treatment. Besides, adverse reactions were observed during the treatment of STS. This study was approved by the Ethics Committee of Fuzhou General Hospital(2013No1). Results: Twenty-seven out of 38 patients (71.05%) had CAC, and the patients with CAC had significantly higher age, phosphate, the product of calcium and phosphate, intact parathyroid hormone (hPTH), hypersensitive C-reactive protein (hsCRP), and longer duration of dialysis (P=0.017, 0.038, 0.037, 0.012, 0.002, 0.037) and lower serum albumin (P=0.026) than patients without CAC.There was no significant statistical difference in the baseline

  16. Relationship between intra thyroid calcifications and thyroglobulin in endemic goiter

    Energy Technology Data Exchange (ETDEWEB)

    Zaccheroni, V.; Iagulli, M.P.; Vescini, F.; Bianchi, G.P.; Menini, S.; Vacirca, A.; Vallese, M.; Lodi, A. [Bologna Univ., Bologna (Italy). Dipt. di medicina interna, cardioangiologia e epatologia

    1999-06-01

    The authors have been looking for the presence of parameters associated with thyroid calcifications in patients affected by simple or nodular goiter, either sporadic or endemic. A multistep discriminant analysis taking the presence-absence of calcifications as dependent variant was applied and a new variable (TG1) was created to differentiate normal from supra physiologic concentrations of hTG. In conclusion, as far as a follicular hyperstimulation can be assumed, especially if long-lasting, the presence intra thyroid calcifications should rise clinical suspect toward an old goiter rather than a neoplastic lesion.

  17. Intraocular Lens Calcification; a Clinicopathologic Report

    Directory of Open Access Journals (Sweden)

    Mozhgan Rezaei-Kanavi

    2009-04-01

    Full Text Available

    PURPOSE: To describe the clinical and pathological features of a case of hydrogel intraocular lens (IOL calcification. CASE REPORT: A 48-year-old man underwent explantation of a single-piece hydrophilic acrylic intraocular lens in his left eye because of decreased visual acuity and milky white opalescence of the IOL. The opacified lens was exchanged uneventfully with a hydrophobic acrylic IOL. Gross examination of the explanted IOL disclosed opacification of the optic and haptics. Full-thickness sections of the lens optic were stained with hematoxylin and eosin (H&E, von Kossa and Gram Tworts'. Microscopic examination of the sections revealed fine and diffuse basophilic granular deposits of variable size within the lens optic parallel to the lens curvature but separated from the surface by a moderately clear zone. The deposits were of high calcium content as evident by dark brown staining with von Kossa. Gram Tworts' staining disclosed no microorganisms. CONCLUSION: This report further contributes to the existing literature on hydrogel IOL calcification.

  18. Calcification of the stylohyoid ligament and elongated styloid process: a finding during a medical-legal autopsy for sudden death

    OpenAIRE

    Pareja-Pineda, Jorge Iván

    2015-01-01

    Purpose: The relationship between Eagle syndrome and both sudden death andforensic sciences has been rarely described in the literature; then, it is necessary to consider this anatomical-pathological alteration both from a clinical and forensic point of view, since its few symptoms do not allow an early diagnosis, which can lead to death due to certain pre-existing physical conditions such as heart or vascular disease. Topics: Elongation of the styloid process and calcification of the stylohy...

  19. Dystrophic calcifications and Raynaud’s phenomenon in an eight-year old girl

    Directory of Open Access Journals (Sweden)

    Grebeldinger Slobodan P.

    2014-01-01

    Full Text Available Introduction. Dystrophic calcifications are the most common subtype of skin calcinosis. Tumorous soft tissue calcium deposits usually contain hydroxyapatite and amorphous calcium phosphate. Differential diagnosis of skin calcinosis encompasses Thibierge-Weissenbach syndrome, systemic sclerosis, scleroderma, CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia, dermatomyositis, systemic lupus erythematosus, ad myositis ossificans progressiva. Case Outline. We present the case of an eight-year old girl with tumorous soft tissue calcium deposits and Raynaud’s phenomenon. At the age of 3.5 years, our patient was admitted to Pediatric Surgery Clinic because of bilateral acrocyanosis localized at the fingertips area of hands, with the signs of vascular trauma. Therapy with vasodilators and hyperbaric oxygen treatment were completed. This therapy resulted in improvement. At the age of eight, the patient was admitted again due to intermittent, painful cramps localized in both hands. Punctiform deposits were present at the tips of fingers and toes, which looked like calcifications and were spontaneously eliminated, with the remnants of crater-shaped defects. A hard tumorous deformity localized in soft tissue was present in the extensor area of the right elbow. Laboratory indicators of inflammation were within the reference values, and antinuclear antibodies were positive. A nodus localized at the right elbow was extirpated. Pathohistological findings: connective and fat tissue with large deposits of calcium. Conclusion. Further follow-up of our patient is necessary due to possible development of complete picture of CREST syndrome or systemic sclerosis.

  20. Dystrophic calcifications and Raynaud's phenomenon in an eight-year old girl.

    Science.gov (United States)

    Grebeldinger, Slobodan P; Tomić, Jelena M; Vijatov-Djurić, Gordana V; Radojcić, Branka S; Vucković, Nada M; Culafić, Jelena N

    2014-01-01

    Dystrophic calcifications are the most common subtype of skin calcinosis. Tumorous soft tissue calcium deposits usually contain hydroxyapatite and amorphous calcium phosphate. Differential diagnosis of skin calcinosis encompasses Thibierge-Weissenbach syndrome, systemic sclerosis, scleroderma, CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia), dermatomyositis, systemic lupus erythematosus, ad myositis ossificans progressiva. We present the case of an eight-year old girl with tumorous soft tissue calcium deposits and Raynaud's phenomenon. At the age of 3.5 years, our patient was admitted to Pediatric Surgery Clinic because of bilateral acrocyanosis localized at the fingertips area of hands, with the signs of vascular trauma. Therapy with vasodilators and hyperbaric oxygen treatment were completed. This therapy resulted in improvement. At the age of eight, the patient was admitted again due to intermittent, painful cramps localized in both hands. Punctiform deposits were present at the tips of fingers and toes, which looked like calcifications and were spontaneously eliminated, with the remnants of crater-shaped defects. A hard tumorous deformity localized in soft tissue was present in the extensor area of the right elbow. Laboratory indicators of inflammation were within the reference values, and antinuclear antibodies were positive. A nodus localized at the right elbow was extirpated. Pathohistological findings: connective and fat tissue with large deposits of calcium. Further follow-up of our patient is necessary due to possible development of complete picture of CREST syndrome or systemic sclerosis.

  1. Vascular biology of ageing-Implications in hypertension.

    Science.gov (United States)

    Harvey, Adam; Montezano, Augusto C; Touyz, Rhian M

    2015-06-01

    Ageing is associated with functional, structural and mechanical changes in arteries that closely resemble the vascular alterations in hypertension. Characteristic features of large and small arteries that occur with ageing and during the development of hypertension include endothelial dysfunction, vascular remodelling, inflammation, calcification and increased stiffness. Arterial changes in young hypertensive patients mimic those in old normotensive individuals. Hypertension accelerates and augments age-related vascular remodelling and dysfunction, and ageing may impact on the severity of vascular damage in hypertension, indicating close interactions between biological ageing and blood pressure elevation. Molecular and cellular mechanisms underlying vascular alterations in ageing and hypertension are common and include aberrant signal transduction, oxidative stress and activation of pro-inflammatory and pro-fibrotic transcription factors. Strategies to suppress age-associated vascular changes could ameliorate vascular damage associated with hypertension. An overview on the vascular biology of ageing and hypertension is presented and novel molecular mechanisms contributing to these processes are discussed. The complex interaction between biological ageing and blood pressure elevation on the vasculature is highlighted. This article is part of a Special Issue entitled: CV Ageing. Copyright © 2015 Elsevier Ltd. All rights reserved.

  2. Prevalence of carotid and pulp calcifications: a correlation using digital panoramic radiographs

    Energy Technology Data Exchange (ETDEWEB)

    Clark, Stephen J. [School of Dentistry, University of Louisville, Department of Periodontics, Endodontics and Dental Hygiene, Louisville, KY (United States); Scheetz, James P.; Khan, Zafrulla [University of Louisville, Department of Diagnostic Sciences, Prosthodontics and Restorative Dentistry, School of Dentistry, Louisville, KY (United States); Farman, Allan G. [School of Dentistry, University of Louisville, Department of Periodontics, Endodontics and Dental Hygiene, Louisville, KY (United States); Horsley, Scott H.; Beckstrom, Brice

    2009-03-15

    To compare the prevalence of pulp calcification with that of carotid calcification using digital panoramic dental radiographs. Digital panoramic radiographs of patients at a dental oncology clinic were included if (1) the carotid artery bifurcation region was visible bilaterally and (2) the patient had non-restored or minimally restored molars and/or canines. An endodontist evaluated the images for pulpal calcifications in the selected teeth. An oral and maxillofacial radiologist independently evaluated the same images for calcifications in the carotid bifurcation region. Odds-ratio and Pearson {chi}{sup 2} were used for data analysis. Presence of pulpal calcification was also evaluated as a screening test for the presence of carotid calcification. A total of 247 panoramic radiographs were evaluated. 32% (n=80) had pulpal calcifications and 25% (n=61) had carotid calcifications with 12% (n=29) having both carotid and pulp calcifications. A significantly higher prevalence of both pulp and carotid calcification was found in subjects older than age 60 years compared to younger age groups. Accuracy of pulpal calcification in screening for carotid calcification was 66.4%. Both pulp and carotid calcifications were more prevalent in older individuals. The presence of pulp calcification was not a strong predictor for the presence of carotid calcification. (orig.)

  3. Osteoprotegerin Serum Level is Associated with Severity of Coronary Artery Calcification in Non Diabetic Centrally Obese Men

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    Trilis Yulianti

    2012-04-01

    Full Text Available BACKGROUND: Osteoprotegerin (OPG is produced by a variety of tissues including those of the cardiovascular system. Recent clinical studies have suggested a significant correlation between elevated OPG serum level and cardiovascular mortality. Since coronary artery calcification (CAC is positively associated with cardiovascular disease (CVD events, we carried out a study to investigate whether OPG serum level is associated with the severity of CAC in non diabetic centrally obese men. METHODS: A cross sectional study was done on seventy non diabetic centrally obese men. CAC score was determined by using dual source computed tomography (DSCT. OPG serum level was measured by enzyme-linked immunosorbent assay (ELISA method. Statistical analysis was done with SPSS for windows ver 16. ANOVA was performed to analyze mean, maximum, minimum value, and standard deviation. Spearman correlation test was performed to determine the correlation between OPG serum level and CAC score. Significance value was defined as alpha level=0.05 based on two-tailed tests. RESULTS: OPG serum level was significantly correlated with CAC score. The severity of CAC increased with the increase of OPG level. Age was significantly correlated with OPG serum level and CAC score. CONCLUSIONS: Our data show that serum OPG level was associated with the severity of CAC, which highlights that OPG could be involved in the progression of CAC in non diabetic obese men. KEYWORDS: obesity, vascular calcification, osteoprotegerin, coronary artery calcification.

  4. Calcified plaque resorptive status as determined by high-resolution ultrasound is predictive of successful conservative management of calcific tendinosis.

    Science.gov (United States)

    Lin, Chien-Hung; Chao, Hai-Lun; Chiou, Hong-Jen

    2012-08-01

    In patients with calcific tendinosis, the morphology of calcified plaques is associated with response to conservative management. We aimed to determine changes in pain and morphology of plaques in patients with calcific tendinosis and non-arc-shaped plaques identified by high-resolution ultrasonography who received only conservative treatment. A total of 33 patients with a mean age of 63.3±10.3 years were included. Pain scores at the time of first and follow-up ultrasound were recorded, and the degree of plaque resolution was calculated. At follow-up, 90.9% (30 of 33) of patients reported improvement in pain, and 84.8% (28 of 33) patient had more than 50% elimination of plaques. Most of increased vascularity observed in color Doppler ultrasonography during 1st visit disappeared at follow-up. In patients with calcific tendinosis, non-arc-shaped plaques determined by high-resolution ultrasonography are likely to resolve and conservative management is warranted. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  5. Calcified plaque resorptive status as determined by high-resolution ultrasound is predictive of successful conservative management of calcific tendinosis

    Energy Technology Data Exchange (ETDEWEB)

    Lin, Chien-Hung [Department of Diagnostic Radiology, Chi-Mei Medical Center, Yung Kang City, Tainan, Taiwan (China); Department of Health Care Administration, Chung-Hwa University of Medical Technology, Tainan, Taiwan (China); Chao, Hai-Lun [Department of Health Care Administration, Chung-Hwa University of Medical Technology, Tainan, Taiwan (China); Chiou, Hong-Jen, E-mail: hjchiou@vghtpe.gov.tw [Department of Radiology, Taipei Veterans General Hospital, National Yang Ming University, School of Medicine, and National Defense Medical Center, No. 201, Sec. 2, Shih-Pai Rd., Taipei 11217, Taiwan (China)

    2012-08-15

    Objective: In patients with calcific tendinosis, the morphology of calcified plaques is associated with response to conservative management. We aimed to determine changes in pain and morphology of plaques in patients with calcific tendinosis and non-arc-shaped plaques identified by high-resolution ultrasonography who received only conservative treatment. Methods: A total of 33 patients with a mean age of 63.3 {+-} 10.3 years were included. Pain scores at the time of first and follow-up ultrasound were recorded, and the degree of plaque resolution was calculated. Results: At follow-up, 90.9% (30 of 33) of patients reported improvement in pain, and 84.8% (28 of 33) patient had more than 50% elimination of plaques. Most of increased vascularity observed in color Doppler ultrasonography during 1st visit disappeared at follow-up. Conclusions: In patients with calcific tendinosis, non-arc-shaped plaques determined by high-resolution ultrasonography are likely to resolve and conservative management is warranted.

  6. Magnesium inhibits Wnt/β-catenin activity and reverses the osteogenic transformation of vascular smooth muscle cells.

    Science.gov (United States)

    Montes de Oca, Addy; Guerrero, Fatima; Martinez-Moreno, Julio M; Madueño, Juan A; Herencia, Carmen; Peralta, Alan; Almaden, Yolanda; Lopez, Ignacio; Aguilera-Tejero, Escolastico; Gundlach, Kristina; Büchel, Janine; Peter, Mirjam E; Passlick-Deetjen, Jutta; Rodriguez, Mariano; Muñoz-Castañeda, Juan R

    2014-01-01

    Magnesium reduces vascular smooth muscle cell (VSMC) calcification in vitro but the mechanism has not been revealed so far. This work used only slightly increased magnesium levels and aimed at determining: a) whether inhibition of magnesium transport into the cell influences VSMC calcification, b) whether Wnt/β-catenin signaling, a key mediator of osteogenic differentiation, is modified by magnesium and c) whether magnesium can influence already established vascular calcification. Human VSMC incubated with high phosphate (3.3 mM) and moderately elevated magnesium (1.4 mM) significantly reduced VSMC calcification and expression of the osteogenic transcription factors Cbfa-1 and osterix, and up-regulated expression of the natural calcification inhibitors matrix Gla protein (MGP) and osteoprotegerin (OPG). The protective effects of magnesium on calcification and expression of osteogenic markers were no longer observed in VSMC cultured with an inhibitor of cellular magnesium transport (2-aminoethoxy-diphenylborate [2-APB]). High phosphate induced activation of Wnt/β-catenin pathway as demonstrated by the translocation of β-catenin into the nucleus, increased expression of the frizzled-3 gene, and downregulation of Dkk-1 gene, a specific antagonist of the Wnt/β-catenin signaling pathway. The addition of magnesium however inhibited phosphate-induced activation of Wnt/β-catenin signaling pathway. Furthermore, TRPM7 silencing using siRNA resulted in activation of Wnt/β-catenin signaling pathway. Additional experiments were performed to test the ability of magnesium to halt the progression of already established VSMC calcification in vitro. The delayed addition of magnesium decreased calcium content, down-regulated Cbfa-1 and osterix and up-regulated MGP and OPG, when compared with a control group. This effect was not observed when 2-APB was added. In conclusion, magnesium transport through the cell membrane is important to inhibit VSMC calcification in vitro

  7. Coronary calcification improves cardiovascular risk prediction in the elderly

    NARCIS (Netherlands)

    Vliegenthart, R; Oudkerk, M; Hofman, A; Oei, HHS; van Dijck, W; van Rooij, FJA; Witteman, JCM

    2005-01-01

    Background - Coronary calcification detected by electron beam tomography may improve cardiovascular risk prediction. The technique is particularly promising in the elderly because the predictive power of cardiovascular risk factors weakens with age. We investigated the prognostic value of coronary c

  8. CT imaging of metastatic liver cancer with calcification

    Energy Technology Data Exchange (ETDEWEB)

    Kanazawa, Susumu; Kido, Choichiro (Aichi Cancer Center, Nagoya (Japan). Hospital)

    1983-05-01

    In 15 out of 20 cases of hepatic metastases with calcication, the primary focal lesion was found to be colonic cancer (10 of which were rectal cancer). The rate of calcification of metastatic liver lesions from colorectal cancer was as high as 17.9%. According to pathological classification, the primary lesion was a differentiated adenocarcinoma in 16 cases. Calcification was found to be large and to have a tendency to occur more easily in a person with multiple metastatic liver lesions. The forms of calcification from ''disperse punctate''- ''collective punctate''-''central mass''-to'' vermicular'' were inferred to represent the changes in development of the calcification.

  9. [Calcifications of the prostate: a transrectal echographic study].

    Science.gov (United States)

    Bock, E; Calugi, V; Stolfi, V; Rossi, P; D'Ascenzo, R; Solivetti, F M

    1989-05-01

    Prostatic lithiasis is a well know phenomenon. It has little clinical significance and is not easily shown by conventional radiography, which has poor sensitivity and specificity. The authors have studied 612 patients with both suprapubic and transrectal US in order to 1) assess US sensitivity and specificity and 2) report the frequency, spatial distribution, number and features of prostatic calcifications with special emphasis on differential diagnosis between prostatic neoplasms and chronic prostatitis. The authors have also studied the relationship between morphology and symptoms and the results agree with those reported in the scanty literature. The authors conclude that the parameters studied are directly related to age, except for a younger group with clear evidence of genital inflammation. The authors emphasize the impossibility to correlate morphology of prostatic calcifications with pathologic conditions: there are no specific symptoms clearly connected with calcification even though the inflammation is often associated with calcifications.

  10. [The hemodynamic characterization of the diabetic patient with arterial calcifications].

    Science.gov (United States)

    Vega Gómez, M E; Ley Pozo, J; Aldama Figueroa, A; Lima Santana, B; Montalvo Diago, J; Bustillo, C; Fernández Boloña, A; Gutiérrez Jiménez, O; Ramirez Muñoz, O; Martínez Hernández, R

    1993-01-01

    This study was designed to describe the presence of calcifications according to the clinical features of the diabetic patient and the hemodynamics of the calcified arteries. With this purpose, 197 lower limbs from diabetic patients (type I and II) and carbon-hydrate intolerant patients, were studied. In all of the patients, the pressure ratio leg/arm was measured. On the same way, the arterial flow velocity was recorded using the Doppler ultrasonography on the pedia and postero-tibial arteries. The arterial calcifications, evident on the radiography of the foot, were more frequent between the type I patients and the neuro-infections diabetic foot. According to the hemodynamics point of view, we found a trend of association of more pathologic arterial flow velocity curves with the presence of calcifications (specially on the intima layer). It was also remarkable that an arterial incomprensibility was always associated with arterial calcifications.

  11. Calcification of vestibular schwannoma: a case report and literature review

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    Zhang Yang

    2012-10-01

    Full Text Available Abstract Calcification rarely occurs in vestibular schwannoma (VS, and only seven cases of calcified VS have been reported in the literature. Here, we report a 48-year-old man with VS, who had a history of progressive left-sided hearing loss for 3 years. Neurological examination revealed that he had left-sided hearing loss and left cerebellar ataxia. Magnetic resonance imaging and computerized tomography angiography showed a mass with calcification in the left cerebellopontine angle (CPA. The tumor was successfully removed via suboccipital craniotomy, and postoperative histopathology showed that the tumor was a schwannoma. We reviewed seven cases of calcified VS that were previously reported in the literature, and we analyzed and summarized the characteristics of these tumors, including the calcification, texture, and blood supply. We conclude that calcification in VS is associated with its texture and blood supply, and these characteristics affect the surgical removal of the tumor.

  12. Clinical significance of intramammary arterial calcifications in diabetic women

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    Milošević Zorica

    2004-01-01

    Full Text Available Background. It is well known that intramammary arterial calcifications diagnosed by mammography as a part of generalized diabetic macroangiopathy may be an indirect sign of diabetes mellitus. Hence, the aim of this study was to determine the incidence of intramammary arterial calcifications, the patient’s age when the calcifications occur, as well as to observe the influence of diabetic polineuropathy, type, and the duration of diabetes on the onset of calcifications, in comparison with nondiabetic women. Methods. Mammographic findings of 113 diabetic female patients (21 with type 1 diabetes and 92 with type 2, as well as of 208 nondiabetic women (the control group were analyzed in the prospective study. The data about the type of diabetes, its duration, and polineuropathy were obtained using the questionnaire. Statistical differences were determined by Mann-Whitney test. Results. Intramammary arterial calcifications were identified in 33.3% of the women with type 1 diabetes, in 40.2% with type 2, and in 8.2% of the women from the control group, respectively. The differences comparing the women with type 1, as well as type 2 diabetes and the controls were statistically significant (p=0.0001. Women with intramammary arterial calcifications and type 1 diabetes were younger comparing to the control group (median age 52 years, comparing to 67 years of age, p=0.001, while there was no statistically significant difference in age between the women with calcifications and type 2 diabetes (61 years of age in relation to the control group (p=0.176. The incidence of polineuropathy in diabetic women was higher in the group with intramammary arterial calcifications (52.3% in comparison to the group without calcifications (26.1%, (p=0.005. The association between intramammary arterial calcifications and the duration of diabetes was not found. Conclusion. The obtained results supported the theory that intramammary arterial calcifications, detected by

  13. Late calcific mitral stenosis after MitraClip procedure in a dialysis-dependent patient.

    Science.gov (United States)

    Pope, Nicolas H; Lim, Scott; Ailawadi, Gorav

    2013-05-01

    The EVEREST II trial investigated the MitraClip (Abbott Vascular, Menlo Park, CA) in patients with severe mitral regurgitation (MR) undergoing surgical procedures. Although mitral stenosis was not reported in this cohort, this trial excluded patients receiving dialysis. We report a case of a 43-year-old HIV-positive, dialysis-dependent patient with nonischemic cardiomyopathy and severe MR, who was considered at high operative risk because of frailty. She was treated with a MitraClip as part of the REALISM high-risk registry. Her symptomatic MR improved but severe symptomatic mitral stenosis developed 28 months after the MitraClip procedure. At that point, she was felt to be a better operative candidate but required open mitral valve replacement. Pathologic examination demonstrated significant calcification of the leaflets around the MitraClip devices.

  14. A Review of the Effect of Diet on Cardiovascular Calcification

    Directory of Open Access Journals (Sweden)

    Rachel Nicoll

    2015-04-01

    Full Text Available Cardiovascular (CV calcification is known as sub-clinical atherosclerosis and is recognised as a predictor of CV events and mortality. As yet there is no treatment for CV calcification and conventional CV risk factors are not consistently correlated, leaving clinicians uncertain as to optimum management for these patients. For this reason, a review of studies investigating diet and serum levels of macro- and micronutrients was carried out. Although there were few human studies of macronutrients, nevertheless transfats and simple sugars should be avoided, while long chain ω-3 fats from oily fish may be protective. Among the micronutrients, an intake of 800 μg/day calcium was beneficial in those without renal disease or hyperparathyroidism, while inorganic phosphorus from food preservatives and colas may induce calcification. A high intake of magnesium (≥380 mg/day and phylloquinone (500 μg/day proved protective, as did a serum 25(OHD concentration of ≥75 nmol/L. Although oxidative damage appears to be a cause of CV calcification, the antioxidant vitamins proved to be largely ineffective, while supplementation of α-tocopherol may induce calcification. Nevertheless other antioxidant compounds (epigallocatechin gallate from green tea and resveratrol from red wine were protective. Finally, a homocysteine concentration >12 µmol/L was predictive of CV calcification, although a plasma folate concentration of >39.4 nmol/L could both lower homocysteine and protect against calcification. In terms of a dietary programme, these recommendations indicate avoiding sugar and the transfats and preservatives found in processed foods and drinks and adopting a diet high in oily fish and vegetables. The micronutrients magnesium and vitamin K may be worthy of further investigation as a treatment option for CV calcification.

  15. Calcific periarthritis of the elbow presenting as acute tennis elbow.

    Science.gov (United States)

    Jawad, F; Jawad, A S M

    2014-01-01

    A 28-year-old woman presented with sudden acute lateral epicondylitis. There was no history of preceding trauma or repetitive use of the arm. Because of the acute onset and signs of acute inflammation, an X-ray was arranged. The X-ray showed a hyperdense calcified elongated globule distal to the lateral epicondyle. A diagnosis of calcific periarthritis (calcium apatite) of the elbow was made. Calcific periarthritis has rarely been reported as a cause of acute elbow pain.

  16. US-guided percutaneous treatment of chronic calcific tendinitis of the shoulder; Trattamento percutaneo eco-guidato della tendinite calcifica cronica della spalla

    Energy Technology Data Exchange (ETDEWEB)

    Giacomoni, P. [Ospedale S. Camillo, Trient (Italy). Servizio di Radiologia; Siliotto, R. [Ospedale S. Camillo, Trient (Italy). Fisiatria e Riabilitazione

    1999-11-01

    The purpose of this work is to report on the personal technique and the results of US-guided percutaneous treatment of chronic calcific tendinitis. January 1997 to March 1999, 70 patients with known chronic calcific supraspinatus tendinitis were submitted to the US-guided treatment. All patients had undergone plain radiography, US, and physical and psychiatric examination. Plain radiography and aspiration biopsy demonstrated hard and radiopaque calcification in 59 patients and soft and faintly milky calcification in 11 cases; calcification diameter ranged 6-30 mm. US showed tendon thickening, with bulging of the outer tendon surface; 10 patients also had moderate dilatation of the subacromial bursa. Physiatric examination revealed chronic pain exacerbated at night, which was always associated with motion impairment. The selection criteria for treatment were calcification diameter >6 mm, integrity of the tendon, and chronic pain. After superficial planes were anesthetized, a 16 G needle was positioned inside the calcification under US guidance and the calcific deposits were fragmented and aspirated. Then, 0.5-1 mL triamcinolone acetonide (40 mg) was injected in the soft tissues or subacromial bursa. The US-guided technique always allowed easy location of calcific deposits and complete aspiration of all soft calcifications. Splintering of hard calcifications helped migration of residual deposits to vascularized soft tissues, which accelerated the - frequently complete - resorption process. It has been privileged extensive and prolonged fragmentation of the calcifications using a single needle, versus the technique using a second needle, saline lavage and aspiration of residual deposits. US-guided percutaneous treatment with aspiration and splintering of chronic calcific supraspinatus tendinitis is a conservative, simple, well-tolerated procedure which can be considered the method of choice after the failure of medical treatment. [Italian] Vengono presentati la

  17. Dual energy subtraction method for breast calcification imaging

    Science.gov (United States)

    Koukou, Vaia; Martini, Niki; Fountos, George; Michail, Christos; Sotiropoulou, Panagiota; Bakas, Athanasios; Kalyvas, Nektarios; Kandarakis, Ioannis; Speller, Robert; Nikiforidis, George

    2017-03-01

    The aim of this work was to present an experimental dual energy (DE) method for the visualization of microcalcifications (μCs). A modified radiographic X-ray tube combined with a high resolution complementary metal-oxide-semiconductor (CMOS) active pixel sensor (APS) X-ray detector was used. A 40/70 kV spectral combination was filtered with 100 μm cadmium (Cd) and 1000 μm copper (Cu) for the low/high-energy combination. Homogenous and inhomogeneous breast phantoms and two calcification phantoms were constructed with various calcification thicknesses, ranging from 16 to 152 μm . Contrast-to-noise ratio (CNR) was calculated from the DE subtracted images for various entrance surface doses. A calcification thickness of 152 μm was visible, with mean glandular doses (MGD) in the acceptable levels (below 3 mGy). Additional post-processing on the DE images of the inhomogeneous breast phantom resulted in a minimum visible calcification thickness of 93 μm (MGD=1.62 mGy). The proposed DE method could potentially improve calcification visibility in DE breast calcification imaging.

  18. Limbal and corneal calcification in patients with chronic renal failure.

    Science.gov (United States)

    Klaassen-Broekema, N; van Bijsterveld, O P

    1993-09-01

    In patients with chronic renal failure on regular dialysis treatment, limboconjunctival degenerations and calcifications are commonly observed. In this study three groups of patients were followed over a period of 6 years. The first group consisted of 47 patients with renal failure, the second group of 17 patients with renal failure and hyperparathyroidism not controlled by drugs, and the third group seven patients with primary hyperparathyroidism without renal failure. The aim of this study was to determine the progression of the limboconjunctival changes over time. The hypothesis that an increase in serum calcium and phosphorus concentrations, as a result of tertiary hyperparathyroidism, could possibly add a corneal component to the limbal calcification was also tested. All patients with renal failure (in as much as the degenerative limbal features were not obscured by deposits of lime salts), had a type II white limbus girdle of Vogt. This limbal degeneration was observed in only 45% of controls. In all 47 patients with renal failure conjunctival calcification was observed; 26 of them also had limbal calcification. After 6 years 41 patients had developed limbal calcification. This progression was statistically significant. In 15 out of 17 patients with tertiary hyperparathyroidism a band-shaped keratopathy developed in addition to the limboconjunctival calcification.

  19. Ocean acidification reduces growth and calcification in a marine dinoflagellate.

    Science.gov (United States)

    Van de Waal, Dedmer B; John, Uwe; Ziveri, Patrizia; Reichart, Gert-Jan; Hoins, Mirja; Sluijs, Appy; Rost, Björn

    2013-01-01

    Ocean acidification is considered a major threat to marine ecosystems and may particularly affect calcifying organisms such as corals, foraminifera and coccolithophores. Here we investigate the impact of elevated pCO2 and lowered pH on growth and calcification in the common calcareous dinoflagellate Thoracosphaera heimii. We observe a substantial reduction in growth rate, calcification and cyst stability of T. heimii under elevated pCO2. Furthermore, transcriptomic analyses reveal CO2 sensitive regulation of many genes, particularly those being associated to inorganic carbon acquisition and calcification. Stable carbon isotope fractionation for organic carbon production increased with increasing pCO2 whereas it decreased for calcification, which suggests interdependence between both processes. We also found a strong effect of pCO2 on the stable oxygen isotopic composition of calcite, in line with earlier observations concerning another T. heimii strain. The observed changes in stable oxygen and carbon isotope composition of T. heimii cysts may provide an ideal tool for reconstructing past seawater carbonate chemistry, and ultimately past pCO2. Although the function of calcification in T. heimii remains unresolved, this trait likely plays an important role in the ecological and evolutionary success of this species. Acting on calcification as well as growth, ocean acidification may therefore impose a great threat for T. heimii.

  20. Bone biomarkers help grading severity of coronary calcifications in non dialysis chronic kidney disease patients.

    Directory of Open Access Journals (Sweden)

    Marion Morena

    Full Text Available BACKGROUND: Osteoprotegerin (OPG and fibroblast growth factor-23 (FGF23 are recognized as strong risk factors of vascular calcifications in non dialysis chronic kidney disease (ND-CKD patients. The aim of this study was to investigate the relationships between FGF23, OPG, and coronary artery calcifications (CAC in this population and to attempt identification of the most powerful biomarker of CAC: FGF23? OPG? METHODOLOGY/PRINCIPAL FINDINGS: 195 ND-CKD patients (112 males/83 females, 70.8 [27.4-94.6] years were enrolled in this cross-sectional study. All underwent chest multidetector computed tomography for CAC scoring. Vascular risk markers including FGF23 and OPG were measured. Logistic regression analyses were used to study the potential relationships between CAC and these markers. The fully adjusted-univariate analysis clearly showed high OPG (≥10.71 pmol/L as the only variable significantly associated with moderate CAC ([100-400[ (OR = 2.73 [1.03;7.26]; p = 0.04. Such association failed to persist for CAC scoring higher than 400. Indeed, severe CAC was only associated with high phosphate fractional excretion (FEPO(4 (≥38.71% (OR = 5.47 [1.76;17.0]; p = 0.003 and high FGF23 (≥173.30 RU/mL (OR = 5.40 [1.91;15.3]; p = 0.002. In addition, the risk to present severe CAC when FGF23 level was high was not significantly different when OPG was normal or high. Conversely, the risk to present moderate CAC when OPG level was high was not significantly different when FGF23 was normal or high. CONCLUSIONS: Our results strongly suggest that OPG is associated to moderate CAC while FGF23 rather represents a biomarker of severe CAC in ND-CKD patients.

  1. Relation of heart rate recovery after exercise testing to coronary artery calcification.

    Science.gov (United States)

    Jae, Sae Young; Kurl, Sudhir; Laukkanen, Jari A; Yoon, Eun Sun; Choi, Yoon-Ho; Fernhall, Bo; Franklin, Barry A

    2017-08-01

    We examined whether slow heart rate recovery (HRR) after exercise testing as an estimate of impaired autonomic function is related to coronary artery calcification (CAC), an emerging marker of coronary atherosclerosis. We evaluated 2088 men who participated in a health-screening program that included measures of CAC and peak or symptom-limited cardiopulmonary exercise testing. HRR was calculated as the difference between peak heart rate (HR) during exercise testing and the HR at 2 min of recovery after peak exercise. We measured CAC using multidetector computed tomography to calculate the Agatston coronary artery calcium score. Advanced CAC was defined as a mean CAC >75th percentile for each age group. HRR was negatively correlated with CAC (r = -.14, p 52 bpm). Each 1 bpm decrease in HRR was associated with 1% increase in advanced CAC after adjusting for potential confounders. An attenuated HRR after exercise testing is associated with advanced CAC, independent of coronary risk factors and other related hemodynamic response. KEY MESSAGES Slow heart rate recovery (HRR) after maximal exercise testing, indicating decreased autonomic function, is associated with an increased risk of cardiovascular event and mortality. Slow HRR has been linked with the occurrence of malignant ventricular arrhythmias, but it remains unclear whether slow HRR is associated with an increased risk of coronary artery calcification (CAC), an emerging marker of coronary atherosclerosis. An attenuated HRR after exercise testing was associated with advanced CAC, independent of coronary risk factors and other potential hemodynamic confounder, supporting the hypothesis that slow HRR is related to the burden of atherosclerotic coronary artery disease.

  2. Abdominal calcification in cystic fibrosis with meconium ileus: radiologic-pathologic correlation

    Energy Technology Data Exchange (ETDEWEB)

    Lang, I. [Department of Diagnostic Imaging, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario M5G 1X8 (Canada); Daneman, A. [Department of Diagnostic Imaging, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario M5G 1X8 (Canada); Cutz, E. [Department of Pathology, University of Toronto, Hospital for Sick Children, Toronto, Ontario (Canada); Hagen, P. [Department of Pathology, University of Toronto, Hospital for Sick Children, Toronto, Ontario (Canada); Shandling, B. [Division of General Surgery, University of Toronto, Hospital for Sick Children, Toronto, Ontario (Canada)

    1997-06-01

    Background. There is confusion in the radiological literature as to the site of abdominal calcification in cystic fibrosis (CF) with meconium ileus (MI) in neonates. Purpose. To correlate the site of radiographic abdominal calcification with histologic and operative findings. Materials and methods. A review of clinical, radiographic, surgical and histologic data in 58 neonates with CF and MI. Results. Abdominal calcification was identified in 15 (26 %) neonates: on an abdominal radiograph in 8 (13 %), at laparotomy in 3 and histologically in 10 (37 %) of the 27 resected specimens. The radiographic pattern of calcification varied from small specks in three cases to small, better-defined areas in two. In the other three patients, the calcification was more extensive and curvilinear. Histologically, calcification was found to be intramural in ten resected specimens, of which two also had intraluminal and one serosal calcification. The more extensive, curvilinear calcification identified radiographically correlated with histologically proven dystrophic intramural calcification. The less marked flecks or discrete areas of radiographic calcification may represent intramural, serosal or intraluminal calcification. Conclusion. Intramural calcification is common microscopically in CF with MI. Extensive radiographic calcification in these patients is more likely to represent intramural rather than serosal or intraluminal calcification. (orig.). With 4 figs.

  3. Breast arterial calcifications are correlated with subsequent development of coronary artery calcifications, but their aetiology is predominantly different

    Energy Technology Data Exchange (ETDEWEB)

    Maas, Angela H.E.M. [Department of Cardiology, Isala Klinieken, Groot Wezenland 20, 8011 JW Zwolle (Netherlands)], E-mail: a.maas@diagram-zwolle.nl; Schouw, Yvonne T. van der; Atsma, Femke [Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands); Beijerinck, David; Deurenberg, Jan J.M. [Preventicon Breast Cancer Screening Center, Stationsplein 91, 3511ED Utrecht (Netherlands); Mali, Willem P.Th.M. [Department of Radiology, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands); Graaf, Y. van der [Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands)

    2007-09-15

    Objective: To study whether calcifications in breast arteries, as seen on mammograms, predict future development of coronary artery calcifications. Methods: We studied 499 women, aged 49-70 years, participating in a breast cancer screening program and investigated whether arterial calcifications in the breast (BAC) are associated with coronary arterial calcifications (CAC) after 9 years follow-up. Mammograms were reviewed for the presence of BAC. CAC was assessed by multi slice computed tomography (MSCT). With logistic regression analysis the independent effect of various risk factors on BAC and CAC was measured. Results: BAC was present in 58 of 499 women (12%) and CAC score > 0 was present in 262 of 499 women (53%). BAC was strongly associated with CAC (OR 3.2, 95% CI 1.71-6.04) and this remained significant after adjustment for age at baseline and the duration of follow-up (OR 2.1, 95% CI 1.10-4.23). Most CV risk factors were associated with CAC but not with BAC. Only parity was significantly associated with both increased CAC (OR 2.1, 95% CI 1.21-3.60) and increased BAC (OR 5.3, 95% CI 1.23-22.43). Breastfeeding was associated with BAC (OR 3.4, 95% CI 1.40-8.23) but not with CAC (OR 1.3, 95% CI 0.84-1.93). Conclusion: Breast arterial calcifications are predictive of subsequent development of calcifications in the coronary arteries.

  4. Bovine pericardium coated with biopolymeric films as an alternative to prevent calcification: In vitro calcification and cytotoxicity results

    Energy Technology Data Exchange (ETDEWEB)

    Nogueira, Grinia M. [Faculdade de Engenharia Quimica, Universidade Estadual de Campinas, CP: 6066, CEP: 13083-970, Campinas, SP (Brazil); Rodas, Andrea C.D. [Instituto de Pesquisas Energeticas e Nucleares (IPEN), Sao Paulo, SP (Brazil); Weska, Raquel F.; Aimoli, Cassiano G. [Faculdade de Engenharia Quimica, Universidade Estadual de Campinas, CP: 6066, CEP: 13083-970, Campinas, SP (Brazil); Higa, Olga Z. [Instituto de Pesquisas Energeticas e Nucleares (IPEN), Sao Paulo, SP (Brazil); Maizato, Marina; Leiner, Adolfo A. [Divisao de Bioengenharia do Instituto do Coracao (InCor) HC-FMUSP (Brazil); Pitombo, Ronaldo N.M.; Polakiewicz, Bronislaw [Faculdade de Ciencias Farmaceuticas, Universidade de Sao Paulo, Sao Paulo (SP) (Brazil); Beppu, Marisa M., E-mail: beppu@feq.unicamp.br [Faculdade de Engenharia Quimica, Universidade Estadual de Campinas, CP: 6066, CEP: 13083-970, Campinas, SP (Brazil)

    2010-05-10

    Bovine pericardium, for cardiac valve fabrication, was coated with either chitosan or silk fibroin film. In vitro calcification tests of coated and non coated bovine pericardium were performed in simulated body fluid solution in order to investigate potential alternatives to minimize calcification on implanted heart valves. Complementary, morphology was assessed by scanning electron microscopy - SEM; X-ray diffraction (XRD) and infrared spectroscopy (FTIR-ATR) were performed for structural characterization of coatings and biocompatibility of chitosan. Silk fibroin films were assayed by in vitro cytotoxicity and endothelial cell growth tests. Bovine pericardium coated with silk fibroin or chitosan did not present calcification during in vitro calcification tests, indicating that these biopolymeric coatings do not induce bovine pericardium calcification. Chitosan and silk fibroin films were characterized as non cytotoxic and silk fibroin films presented high affinity to endothelial cells. The results indicate that bovine pericardium coated with silk fibroin is a potential candidate for cardiac valve fabrication, since the affinity of silk fibroin to endothelial cells can be explored to induce the tissue endothelization and therefore, increase valve durability by increasing their mechanical resistance and protecting them against calcification.

  5. Energetic costs of calcification under ocean acidification

    Science.gov (United States)

    Spalding, Christopher; Finnegan, Seth; Fischer, Woodward W.

    2017-05-01

    Anthropogenic ocean acidification threatens to negatively impact marine organisms that precipitate calcium carbonate skeletons. Past geological events, such as the Permian-Triassic Mass Extinction, together with modern experiments generally support these concerns. However, the physiological costs of producing a calcium carbonate skeleton under different acidification scenarios remain poorly understood. Here we present an idealized mathematical model to quantify whole-skeleton costs, concluding that they rise only modestly (up to ˜10%) under acidification expected for 2100. The modest magnitude of this effect reflects in part the low energetic cost of inorganic, calcium carbonate relative to the proteinaceous organic matrix component of skeletons. Our analysis does, however, point to an important kinetic constraint that depends on seawater carbonate chemistry, and we hypothesize that the impact of acidification is more likely to cause extinctions within groups where the timescale of larval development is tightly constrained. The cheapness of carbonate skeletons compared to organic materials also helps explain the widespread evolutionary convergence upon calcification within the metazoa.

  6. Retropharyngeal Calcific Tendinitis Mimicking a Retropharyngeal Phlegmon

    Directory of Open Access Journals (Sweden)

    Nathalie Gabra

    2013-01-01

    Full Text Available Background. Acute retropharyngeal tendinitis is a little known but not an uncommon condition. It was first described by Hartley in 1964 as an inflammation of the longus colli muscle secondary to calcium crystals deposition on its insertion. The calcifications are mostly located on the oblique portion of the muscle at the level of C1-C2. Methods. We will describe this disease through 4 cases that presented in our institution. Results. The most common symptoms are severe neck pain, odynophagia, and a painful restriction of neck movement. It is associated with mild fever and inflammatory lab findings such as a slight elevation of white blood cell count, erythrocyte sedimentation rate, and C-reactive protein. CT scan is recommended as the first-line imaging modality to establish a diagnosis. Treatments consist of NSAIDs and analgesics to accelerate the healing process. If symptoms are severe, a course of corticosteroids is required. Conclusion. Since the clinical and laboratory findings of this condition and those of a retropharyngeal abscess overlap, it is important to establish the right diagnosis in order to prevent more invasive procedures. A good knowledge of this clinical entity by otolaryngologists would prevent delays in hospital discharge and unnecessary anxiety.

  7. Experimental evidence for foraminiferal calcification under anoxia

    Directory of Open Access Journals (Sweden)

    M. P. Nardelli

    2014-03-01

    Full Text Available Benthic foraminiferal tests are widely used for paleoceanographic reconstructions. There is ample evidence that foraminifera can live in anoxic sediments. For some species, this is explained by a switch to facultative anaerobic metabolism (i.e. denitrification. Here we show for the first time that adult specimens of three benthic foraminiferal species are not only able to survive but are also able to calcify in anoxic conditions, at various depths in the sediment, with and without nitrates. This demonstrates ongoing metabolic processes, even in micro-environments where denitrification is not possible. Earlier observations suggest that the disappearance of foraminiferal communities after prolonged anoxia is not due to instantaneous or strongly increased adult mortality. Here we show that it cannot be explained by an inhibition of growth through chamber addition either. Our observations of ongoing calcification under anoxic conditions means that geochemical proxy data obtained from benthic foraminifera in settings experiencing intermittent anoxia have to be reconsidered. The analysis of whole single specimens or of their successive chambers may provide essential information about short-term environmental variability and/or the causes of anoxia.

  8. Molecular signal transduction in vascular cell apoptosis

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Apoptosis is a form of genetically programmed cell death, which plays a key role in regulation of cellularity in a variety of tissue and cell types including the cardiovascular tissues. Under both physiological and pathophysiological conditions, various biophysiological and biochemical factors, including mechanical forces, reactive oxygen and nitrogen species, cytokines, growth factors, oxidized lipoproteins, etc., may influence apoptosis of vascular cells. The Fas/Fas ligand/caspase death-signaling pathway, Bcl-2 protein family/mitochondria, the tumor suppressive gene p53, and the proto-oncogene c-myc may be activated in atherosclerotic lesions, and mediates vascular apoptosis during the development of atherosclerosis. Abnormal expression and dysfunction of these apoptosis-regulating genes may attenuate or accelerate vascular cell apoptosis and affect the integrity and stability of atherosclerotic plaques. Clarification of the molecular mechanism that regulates apoptosis may help design a new strategy for treatment of atherosclerosis and its major complication, the acute vascular syndromes.

  9. Paroxysmal vascular events in Sturge– Weber syndrome: Role of aspirin

    Directory of Open Access Journals (Sweden)

    Jyoti Sanghvi

    2014-01-01

    Full Text Available Sturge-Weber syndrome (SWS is a rare, sporadically occurring neurocutaneous disorder with a frequency of approximately 1 per 50,000. The hallmark is an intracranial leptomeningeal vascular angioma in association with a port wine nevus, usually involving ophthalmic or maxillary distribution of trigeminal nerve. Other clinical findings associated with SWS are seizures, glaucoma, hemiparesis and mental retardation. The radiological hallmark is "Tram-line" or "Gyri-form" calcification. 25 to 56% of patients experience recurrent episodes of paroxysmal focal neurological deficits in form of transient hemiparesis, which may be due to vascular ischemia or postictal in origin. EEG helps to differentiate the exact etiology, as it is normal in former. Aspirin prophylaxis in those, due to ischemia decreases their recurrences and improves overall neurological prognosis. We report a 25-month-old child of SWS with recurrent episodes of transient hemiparesis and atypical midline location of facial vascular nevus.

  10. The association of breast arterial calcification and metabolic syndrome

    Directory of Open Access Journals (Sweden)

    Seyma Yildiz

    2014-01-01

    Full Text Available OBJECTIVES: We investigated the relationship between metabolic syndrome and breast arterial calcification detected via mammography in a cohort of postmenopausal subjects. METHODS: Among 837 patients referred to our radiology department for mammographic screening, 310 postmenopausal females (105 patients with and 205 patients without breast arterial calcification aged 40 to 73 (mean 55.9±8.4 years were included in this study. The groups were compared with respect to clinical characteristics and metabolic syndrome criteria. Univariate and multivariate analyses identified the factors related to breast arterial calcification. RESULTS: Age, postmenopausal duration and the frequencies of diabetes mellitus, hypertension and metabolic syndrome were significantly higher in the subjects with breast arterial calcification than in those without (p<0.05. Multivariate analysis indicated that age (OR = 1.3, 95% CI = 1.1-1.6, p = 0.001 and metabolic syndrome (OR = 4.0, 95% CI = 1.5−10.4, p = 0.005 were independent predictors of breast arterial calcification detected via mammography. The independent predictors among the features of metabolic syndrome were low levels of high-density lipoproteins (OR = 8.1, 95% CI = 1.0−64.0, p = 0.047 and high blood pressure (OR = 8.7, 95% CI = 1.5−49.7, p = 0.014. CONCLUSIONS: The likelihood of mammographic detection of breast arterial calcification increases with age and in the presence of hypertension or metabolic syndrome. For patients undergoing screening mammography who present with breast arterial calcification, the possibility of metabolic syndrome should be considered. These patients should be informed of their cardiovascular risk factors and counseled on appropriate lifestyle changes.

  11. Oral Magnesium Supplementation in Chronic Kidney Disease Stages 3 and 4: Efficacy, Safety, and Effect on Serum Calcification Propensity—A Prospective Randomized Double-Blinded Placebo-Controlled Clinical Trial

    DEFF Research Database (Denmark)

    Bressendorff, Iain; Hansen, Ditte; Schou, Morten

    2016-01-01

    propensity (T50) is a novel functional test, which is associated with all-cause mortality in CKD and measures the ability of serum to delay the formation of crystalline nanoparticles. Theoretically, increasing serum Mg should improve T50 and thereby reduce the propensity towards ectopic calcification......Introduction Chronic kidney disease (CKD) is associated with high cardiovascular morbidity and mortality. Recent evidence suggests that increases in both serum and intracellular magnesium (Mg) can slow or even prevent the development of vascular calcification seen in CKD. Serum calcification....... Methods We conducted a randomized placebo-controlled double-blinded clinical trial to investigate the safety of 2 different doses of oral Mg supplementation in subjects with CKD stages 3 and 4 as well as their effects on intracellular Mg and T50. Thirty-six subjects with CKD stages 3 and 4 were randomized...

  12. Management of acute calcific tendinitis around the hip joint.

    Science.gov (United States)

    Park, Sang-Min; Baek, Ji-Hoon; Ko, Young-Bong; Lee, Han-Jun; Park, Ki Jeong; Ha, Yong-Chan

    2014-11-01

    Although the natural history of calcific tendinitis within the rotator cuff of the shoulder is established, the natural history of calcific tendinitis around the hip joint remains unknown. To examine the duration of symptoms including pain, the location of calcific tendinitis around the hip joint, the radiologic course of calcium phosphate crystals, and the proportion of patients who required surgical treatment. Case series; Level of evidence, 4. Thirty hips (29 patients) with acute calcific tendinitis were treated between January 2010 and December 2012. Level of subjective hip pain using the visual analog scale pain score, radiologic type, and the location and size of calcium deposits were measured during a follow-up period of 12 to 32 months. The 29 patients included 7 men (24%) and 22 women (76%) with a mean age of 51.5 years (range, 28-78 years). All visual analog scale pain scores significantly improved from a mean of 7.1 to 0.8 at the latest follow-up (P 3 months) of severe pain, solid type, and large size (range, 96-416 mm(2)) were treated with arthroscopic excision. Nonoperative treatment in patients with acute calcific tendinitis of the hip joint might be successful in most patients. Surgical treatment is of value for patients experiencing prolonged severe pain, solid type, and large size. © 2014 The Author(s).

  13. Radiographic and histologic patterns of calcification in chondromyxoid fibroma

    Energy Technology Data Exchange (ETDEWEB)

    Yamaguchi, Takehiko [Section of Orthopaedic Pathology, Montefiore Medical Center/ Albert Einstein College of Medicine, Bronx, NY (United States)]|[Department of Pathology, Dokkyo University School of Medicine, Mibu (Japan); Dorfman, H.D. [Section of Orthopaedic Pathology, Montefiore Medical Center/ Albert Einstein College of Medicine, Bronx, NY (United States)

    1998-10-01

    Objective. To evaluate the frequency of radiologic and histologic manifestations of matrix calcification in chondromyxoid fibromas. Patients. Forty-four cases of chondromyxoid fibroma were reviewed. The age range of the patients was 3-70 years (average 29 years). Results. Calcification was found microscopically in 15 cases (34.1%). In five cases (12.5%) it was demonstrated on plain films or CT. The age range of the patients with microscopic evidence of calcified matrix was 14-70 years (mean 46 years), while that of the patients with non-calcified lesions was 3-59 years (average 21 years). All but two of the patients who showed microscopic calcification in the tumors were over 40 years of age. Four microscopic patterns of calcification were observed: coarse granular, circumscribed, trabecular, and ``chicken-wire.``Conclusions. Calcification in chondromyxoid fibroma was found more frequently than in previously reported studies. There was a tendency for this phenomenon to occur in the tumors of older patients, particularly those over 40 years old, and in chondromyxoid fibromas situated in flat bones, including ribs. (orig.) With 6 figs., 3 tabs., 11 refs.

  14. Smoking and morphology of calcific deposits affect the outcome of needle aspiration of calcific deposits (NACD) for calcific tendinitis of the rotator cuff.

    Science.gov (United States)

    Oudelaar, Bart W; Ooms, Edwin M; Huis In 't Veld, Rianne M H A; Schepers-Bok, Relinde; Vochteloo, Anne J

    2015-11-01

    Although NACD has proven to be an effective minimal invasive treatment for calcific tendinitis of the rotator cuff, little is known about the factors associated with treatment failure or the need for multiple procedures. Patients with symptomatic calcific tendinitis who were treated by NACD were evaluated in a retrospective cohort study. Demographic details, medical history, sonographic and radiographic findings were collected from patient files. Failure of NACD was defined as the persistence of symptoms after a follow-up of at least six months. NACD procedures performed within six months after a previous NACD procedure were considered repeated procedures. Multivariate logistic regression analysis was used to determine factors associated with treatment failure and multiple procedures. 431 patients (277 female; mean age 51.4±9.9 years) were included. Smoking (adjusted odds ratio (AOR): 1.7, 95% CI 1.0-2.7, p=0.04) was significantly associated with failure of NACD. Patients with Gärtner and Heyer (GH) type I calcific deposits were more likely to need multiple NACD procedures (AOR: 3.4, 95% CI 1.6-7.5, p<0.01) compared to patients with type III calcific deposits. Partial thickness rotator cuff tears were of no influence on the outcome of NACD or the number of treatments necessary. Smoking almost doubled the chance of failure of NACD and the presence of GH type I calcific deposits significantly increased the chance of multiple procedures. Partial thickness rotator cuff tears did not seem to affect the outcome of NACD. Based on the findings in this study, the importance of quitting smoking should be emphasized prior to NACD and partial thickness rotator cuff tears should not be a reason to withhold patients NACD. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  15. Drinking citrus fruit juice inhibits vascular remodeling in cuff-induced vascular injury mouse model.

    Science.gov (United States)

    Ohnishi, Arika; Asayama, Rie; Mogi, Masaki; Nakaoka, Hirotomo; Kan-No, Harumi; Tsukuda, Kana; Chisaka, Toshiyuki; Wang, Xiao-Li; Bai, Hui-Yu; Shan, Bao-Shuai; Kukida, Masayoshi; Iwanami, Jun; Horiuchi, Masatsugu

    2015-01-01

    Citrus fruits are thought to have inhibitory effects on oxidative stress, thereby attenuating the onset and progression of cancer and cardiovascular disease; however, there are few reports assessing their effect on vascular remodeling. Here, we investigated the effect of drinking the juice of two different citrus fruits on vascular neointima formation using a cuff-induced vascular injury mouse model. Male C57BL6 mice were divided into five groups as follows: 1) Control (water) (C), 2) 10% Citrus unshiu (CU) juice (CU10), 3) 40% CU juice (CU40), 4) 10% Citrus iyo (CI) juice (CI10), and 5) 40% CI juice (CI40). After drinking them for 2 weeks from 8 weeks of age, cuff injury was induced by polyethylene cuff placement around the femoral artery. Neointima formation was significantly attenuated in CU40, CI10 and CI40 compared with C; however, no remarkable preventive effect was observed in CU10. The increases in levels of various inflammatory markers including cytokines such as monocyte chemotactic protein-1, interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α in response to vascular injury did not differ significantly between C, CU10 and CI10. The increases in cell proliferation and superoxide anion production were markedly attenuated in CI10, but not in CU10 compared with C. The increase in phosphorylated ERK expression was markedly attenuated both in CU10 and CI10 without significant difference between CU10 and CI10. Accumulation of immune cells did not differ between CU10 and CI10. These results indicate that drinking citrus fruit juice attenuates vascular remodeling partly via a reduction of oxidative stress. Interestingly, the preventive efficacy on neointima formation was stronger in CI than in CU at least in part due to more prominent inhibitory effects on oxidative stress by CI.

  16. Sida rhomboidea.Roxb aqueous extract down-regulates in vivo expression of vascular cell adhesion molecules in atherogenic rats and inhibits in vitro macrophage differentiation and foam cell formation.

    Science.gov (United States)

    Thounaojam, Menaka C; Jadeja, Ravirajsinh N; Salunke, Sunita P; Devkar, Ranjitsinh V; Ramachandran, A V

    2012-10-01

    The present study evaluates efficacy of Sida rhomboidea.Roxb (SR) leaves extract in ameliorating experimental atherosclerosis using in vitro and in vivo experimental models. Atherogenic (ATH) diet fed rats recorded significant increment in the serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), very LDL (VLDL), autoantibody against oxidized LDL (Ox-LDL), markers of LDL oxidation and decrement in high-density lipoprotein (HDL) along with increment in aortic TC and TG. The ex vivo LDL oxidation assay revealed an increased susceptibility of LDL isolated from ATH rats to undergo copper mediated oxidation. These set of changes were minimized by simultaneous co-supplementation of SR extract to ATH diet fed rats. Histopathology of aorta and immunolocalization studies recorded pronounced atheromatous plaque formation, vascular calcification, significant elastin derangements and higher expression of macrophage surface marker (F4/80), vascular cell adhesion molecule-1 (VCAM-1) and p-selectin in ATH rats. Whereas, ATH+SR rats depicted minimal evidence of atheromatous plaque formation, calcium deposition, distortion/defragmentation of elastin and accumulation of macrophages along with lowered expression of VCAM-1 and P-selectin compared to ATH rats. Further, monocyte to macrophage differentiation and in vitro foam cell formation were significantly attenuated in presence of SR extract. In conclusion, SR extract has the potency of controlling experimental atherosclerosis and can be used as promising herbal supplement in combating atherosclerosis.

  17. Vascular development in Arabidopsis.

    Science.gov (United States)

    Ye, Zheng-Hua; Freshour, Glenn; Hahn, Michael G; Burk, David H; Zhong, Ruiqin

    2002-01-01

    Vascular tissues, xylem and phloem, form a continuous network throughout the plant body for transport of water, minerals, and food. Characterization of Arabidopsis mutants defective in various aspects of vascular formation has demonstrated that Arabidopsis is an ideal system for