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Sample records for surrounding hypertrophied hepatic

  1. Prevalence of hepatic parasites in Korean wild rats (Rattus norvegicus) and their association with pulmonary arteriolar medial hypertrophy.

    Science.gov (United States)

    Yi, J-Y; Kim, Y-H; Kim, H-C; Hahn, T-W; Jeong, H; Choi, C-U; Woo, G-H; Kim, Y-B; Han, J-H; Yoon, B-I

    2010-03-01

    C hepatica, an important zoonotic parasite, and C fasciolaris are common parasites in rodents. In rodent livers, C hepatica causes sequential morphologic changes that are designated as early, intermediate, or late phase, and C fasciolaris forms cysts surrounded by fibroplasia and granulomatous inflammation. The present study describes the prevalence of these parasites and associated liver and lung lesions in wild rats (Rattus norvegicus) living around pig farms in South Korea. Selected parenchymal organs, including liver and lung, of 89 wild rats were examined. Of 89 rats, 28 (31.5%) were infected with either C hepatica or C fasciolaris or with both parasites. Severe medial hypertrophy of small arterioles was observed in the lungs of 11 of the 28 parasite-infected rats (P parasite-induced hepatitis and pulmonary arteriolar hypertrophy in rodents. Further studies are warranted for the use of C hepatica-infected rats as an animal model to explore the underlying mechanisms of portopulmonary hypertension in humans.

  2. Portal vein embolization for induction of selective hepatic hypertrophy prior to major hepatectomy: rationale, techniques, outcomes and future directions

    Science.gov (United States)

    Li, David; Madoff, David C.

    2016-01-01

    The ability to modulate the future liver remnant (FLR) is a key component of modern oncologic hepatobiliary surgery practice and has extended surgical candidacy for patients who may have been previously thought unable to survive liver resection. Multiple techniques have been developed to augment the FLR including portal vein embolization (PVE), associating liver partition and portal vein ligation (ALPPS), and the recently reported transhepatic liver venous deprivation (LVD). PVE is a well-established means to improve the safety of liver resection by redirecting blood flow to the FLR in an effort to selectively hypertrophy and ultimately improve functional reserve of the FLR. This article discusses the current practice of PVE with focus on summarizing the large number of published reports from which outcomes based practices have been developed. Both technical aspects of PVE including volumetry, approaches, and embolization agents; and clinical aspects of PVE including data supporting indications, and its role in conjunction with chemotherapy and transarterial embolization will be highlighted. PVE remains an important aspect of oncologic care; in large part due to the substantial foundation of information available demonstrating its clear clinical benefit for hepatic resection candidates with small anticipated FLRs. PMID:28154774

  3. Repeated inhalation exposure to octamethylcyclotetrasiloxane produces hepatomegaly, transient hepatic hyperplasia, and sustained hypertrophy in female Fischer 344 rats in a manner similar to phenobarbital.

    Science.gov (United States)

    McKim, J M; Kolesar, G B; Jean, P A; Meeker, L S; Wilga, P C; Schoonhoven, R; Swenberg, J A; Goodman, J I; Gallavan, R H; Meeks, R G

    2001-04-15

    Octamethylcyclotetrasiloxane (D4) has been described as a phenobarbital-like inducer of hepatic enzymes. Phenobarbital (PB) and phenobarbital-like chemicals induce transient hepatic and thyroid hyperplasia and sustained hypertrophy in rats and mice. The extent to which these processes are involved with D4-induced hepatomegaly is not known. The present study has evaluated the effects of repeated inhalation exposure to D4 vapors on hepatic and thyroid cell proliferation and hypertrophy with respect to time and exposure concentration. Female Fischer 344 rats were exposed via whole body inhalation to 0 ppm D4, 700 ppm D4 vapors (6 h/day; 5 days/week), or 0.05% PB in drinking water over a 4-week period. Incorporation of 5'-bromo-2-deoxyuridine (BrdU) and the abundance of proliferating cell nuclear antigen were used as indicators of cell proliferation. Designated animals from each treatment group were euthanized on study days 6, 13, and 27. The effect of D4 exposure concentration on hepatic cell proliferation was evaluated at 0, 7, 30, 70, 150, 300, or 700 ppm. Liver-to-body weight ratios in animals exposed to 700 ppm D4 were increased 18, 20, and 22% over controls while PB-treated animals showed increases of 33, 27, and 27% over controls on days 6, 13, and 27 respectively. Hepatic incorporation of BrdU following exposure to D4 was highest on day 6 (labeling index = 15-22%) and was at or below control values by day 27. This pattern of transient hyperplasia was observed in all hepatic lobes examined and was similar to the pattern observed following treatment with PB.

  4. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    1993-01-01

    930140 Hepatocyte stimulator peptide and itsclinical significance in viral hepatitis.ZHOUWeiping(周卫平),et al.Instit Viral Hepatitis,Chongqing Med Univ,630010.Chin J InternMed 1992;31(10):626-628.Hepatocyte stimulator peptide(HSP)is anewly developed hepatic stimulator substance.Its monoclonal antibodies have been obtained inour laboratory.In this study,HSP was deter-mined in the sera of 315 subjects including pa-

  5. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    2010349 Relationships between serum hepatitis B virus load in mothers,free maternal DNA in peripheral blood of newborns and hepatitis B virus infection of newborns. WEI Junni(魏俊妮),et al. Dept Epidemiol,Shanxi Med Univ,Taiyuan 030001. Chin J Infect Dis 2010;28(5):297-300. Objective To study the relationships between serum hepatitis B virus (HBV) DNA level

  6. Hepatitis

    Science.gov (United States)

    ... inflammation of the liver.” This inflammation can be caused by a wide variety of toxins, drugs, and metabolic diseases, as well as infection. There are at least 5 hepatitis viruses. Hepatitis A is contracted when a child eats food or drinks water that is contaminated with the virus or has ...

  7. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    1997-01-01

    970349 Primary structure and variability of partialsequences in nonstructural gene 5 region of hepatitis Gvirus, CHANG Jinhong(常锦红), et al. Hepatol Instis,People’s Hosp, Beijing Med Univ, Beijing, 100044. NatlMed J China 1997; 77(3): 178-182. Objective: To sequence partial genome of hepatitis G

  8. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2009-01-01

    2009209 Effects of chronic hepatitis B virus infection on human hepatic cytochrome P450 2C9.ZHO Fuping(周福平),et al.Dept Infect Dis,Shanghai Changzheng Hosp,Shanghai 200003.Chin J Infect Dis,2009;27(2):94-98.

  9. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    1992-01-01

    920691 The determination of serum hepa-titis B virus DNA by polymerase chain rea-ction in hepatitis B patients treated withalpha-interferon. XU. Jianye(徐建业), et al.Centr Lab, Chongqing Cancer Instit, 630030.Chin J Intern Med, 1992; 31(5): 278-280. To clarify the status of HBV in serum of

  10. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2005-01-01

    2005226 Characteristics of peripheral blood T lymphocyte subsets in hepatitis B patients. FAN Zhen-ping(范振平),et al. Center Bio Ther, Instit Infect Dis, 302 Hosp Chin PLA, Beijing 100039. World Chin J Digestol, 2005;13(2): 194-197. Objective: To characterize the T-lymphocyte subsets in peripheral blood of patients with acute and chronic hepatitis B, and to explore their relations with the disease state. Methods: Peripheral blood

  11. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    2008312 Impact of hepatitis B virus infection on the activity of hematopoietic stem cell.SHI Yanmei(石雁梅),et al.Dept Infect Dis,1st Clin Coll,Harbin Med Univ,Harbin 150001.Chin J Infect Dis 2008;26(4):197-201.Objective To study the impact of hepatitis B virus (HBV)infection on the activity of cord hematopoieticstem cells.Methods CD34+cells were isolated from healthy human cord blood by mini MACS.Cells were

  12. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    2008449 A cross-sectional survey of occult hepatitis B virus infection in HIV-infected patients. MA Jianxin(马建新), et al.Dept Infect Dis, Shanghai Public Health Clin Center, Shanghai 201508. Chin J Intern Med 2008;47(7):574-577. Objective To assess the prevalence of occult HBV infection in HIV-infected patients.

  13. Periodontitis and myocardial hypertrophy.

    Science.gov (United States)

    Suzuki, Jun-Ichi; Sato, Hiroki; Kaneko, Makoto; Yoshida, Asuka; Aoyama, Norio; Akimoto, Shouta; Wakayama, Kouji; Kumagai, Hidetoshi; Ikeda, Yuichi; Akazawa, Hiroshi; Izumi, Yuichi; Isobe, Mitsuaki; Komuro, Issei

    2017-04-01

    There is a deep relationship between cardiovascular disease and periodontitis. It has been reported that myocardial hypertrophy may be affected by periodontitis in clinical settings. Although these clinical observations had some study limitations, they strongly suggest a direct association between severity of periodontitis and left ventricular hypertrophy. However, the detailed mechanisms between myocardial hypertrophy and periodontitis have not yet been elucidated. Recently, we demonstrated that periodontal bacteria infection is closely related to myocardial hypertrophy. In murine transverse aortic constriction models, a periodontal pathogen, Aggregatibacter actinomycetemcomitans markedly enhanced cardiac hypertrophy with matrix metalloproteinase-2 activation, while another pathogen Porphyromonas gingivalis (P.g.) did not accelerate these pathological changes. In the isoproterenol-induced myocardial hypertrophy model, P.g. induced myocardial hypertrophy through Toll-like receptor-2 signaling. From our results and other reports, regulation of chronic inflammation induced by periodontitis may have a key role in the treatment of myocardial hypertrophy. In this article, we review the pathophysiological mechanism between myocardial hypertrophy and periodontitis.

  14. Hepatitis

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    2008079 Relationship of HBV genotype and bcp and pc mutations with HBV DNA rebound after lamivudine therapy. SU Minghua(苏明华), et al. Dept Infect Dis Clin Hosp, Guangxi Med Univ, Nanning 530027. World Chin J Digestol 2007;15(33):3507-3513. Objective To investigate the relationship of HBV gene mutations with HBV DNA rebound after lamivudine therapy. Methods Twenty-seven hepatitis B patients with HBV DNA rebound after

  15. Premenarchal labia minora hypertrophy

    Directory of Open Access Journals (Sweden)

    Karoon Agrawal

    2016-01-01

    Full Text Available Labia minora hypertrophy is a relatively uncommon surgical entity being popularised in the realm of vulvovaginal plastic surgeries. Apart from the unaesthetic appearance of the hypertrophied minora, these cases are also associated with itching, hygiene problem, pain while sitting down, sports activities, difficulty in wearing tight clothing, bleeding and discomfort while or after sexual intercourse, social embarrassment, insecurity and psychological diminution of confidence and self-esteem. In a country like India, due to sociocultural reasons, patients hesitate to consult a doctor for such deformities. Most of the patients suffer in silence for years. Although common in the west, very few surgeons in the country perform this simple and rewarding surgery. Here, we are presenting a case of premenarchal juvenile labia minora hypertrophy (JLMH in an 8-year-old child. Labial hypertrophy in this age group is uncommon. We were unable to find hypertrophy of labia minora in the eight-year-old child on English literature search.

  16. Left Ventricular Hypertrophy

    Science.gov (United States)

    ... the chamber itself also increases. The enlarged heart muscle loses elasticity and eventually may fail to pump with as much force as needed. Left ventricular hypertrophy is more common in people who have uncontrolled ...

  17. iTRAQ analysis of hepatic proteins in free-living Mus spretus mice to assess the contamination status of areas surrounding Doñana National Park (SW Spain)

    Energy Technology Data Exchange (ETDEWEB)

    Abril, Nieves; Chicano-Gálvez, Eduardo; Michán, Carmen; Pueyo, Carmen; López-Barea, Juan, E-mail: bb1lobaj@uco.es

    2015-08-01

    This work aims to develop and integrate new -omics tools that would be applicable to different ecosystem types for a technological updating of environmental evaluations. We used a 2nd-generation (iTRAQ-8plex) proteomic approach to identify/quantify proteins differentially expressed in the liver of free-living Mus spretus mice from Doñana National Park or its proximities. Mass spectrometry was performed in an LTQ Orbitrap system for iTRAQ reporter ion quantitation and protein identification using a Mus musculus database as reference. A prior IEF step improved the separation of the complex peptide mixture. Over 2000 identified proteins were altered, of which 118 changed by ≥ 2.5-fold in mice from at least two problem sites. Part of the results obtained with the iTRAQ analysis was confirmed by Western blot. Over 75% of the 118 proteins were upregulated in animals captured at polluted sites and only 16 proteins were downregulated. Upregulated proteins were involved in stress response; cell proliferation and apoptosis; signal transduction; metastasis or tumour suppression; xenobiotic export or vesicular trafficking; and metabolism. The downregulated proteins, all potentially harmful, were classified as oncoproteins and proteins favouring genome instability. The iTRAQ results presented here demonstrated that the survival of hepatic cells is compromised in animals living at polluted sites, which showed deep alterations in metabolism and the signalling pathways. The identified proteins may be useful as biomarkers of environmental pollution and provide insight about the metabolic pathways and/or physiological processes affected by pollutants in DNP and its surrounding areas. - Highlights: • iTRAQ quantitation was used for the first time to monitor a wildlife reserve • Over 2,000 proteins with altered expression were identified in problem Doñana sites • Of them, 118 changed over 2.5-fold in, at least, two problem sites • Upregulation of protective proteins

  18. Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy

    Science.gov (United States)

    Kim, Jin Hyun; Jeong, Han-Sin; Kim, Kyung Mi; Lee, Ye Jin; Jung, Myeong Hee; Park, Jung Je; Kim, Jin Pyeong; Woo, Seung Hoon

    2016-01-01

    Background Gastroesophageal reflux is associated with numerous pathologic conditions of the upper aerodigestive tract. Gastric pepsin within reflux contributes to immunologic reactions in the tonsil. In this study, we aimed to find the relationships between pepsin and tonsillar hypertrophy. Methods and finding We explored the notion whether tonsillar hypertrophy was due to pepsin-mediated gastric reflux in tonsil hypertrophy. Fifty-four children with tonsil hypertrophy and 30 adults with tonsillitis were recruited before surgical treatment. Blood and tonsil tissues from each patient were harvested for analysis of changes in lymphocyte and macrophage numbers coupled with histological and biochemical analysis. Pepsin was expressed at different levels in tonsil tissues from each tonsillar hypertrophy. Pepsin-positive cells were found in the crypt epithelium, surrounding the lymphoid follicle with developing fibrosis, and also surrounding the lymphoid follicle that faced the crypt. And also, pepsin staining was well correlated with damaged tonsillar squamous epithelium and TGF-β1 and iNOS expression in the tonsil section. In addition, pepsin and TGF-β1-positive cells were co-localized with CD68-positive cells in the crypt and surrounding germinal centers. In comparison of macrophage responsiveness to pepsin, peripheral blood mononuclear cells (PBMNCs) were noticeably larger in the presence of activated pepsin in the child group. Furthermore, CD11c and CD163-positive cells were significantly increased by activated pepsin. However, this was not seen for the culture of PBMNCs from the adult group. Conclusions The lymphocytes and monocytes are in a highly proliferative state in the tonsillar hypertrophy and associated with increased expression of pro-inflammatory factors as a result of exposure to stomach reflux pepsin. PMID:27058240

  19. Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy.

    Science.gov (United States)

    Kim, Jin Hyun; Jeong, Han-Sin; Kim, Kyung Mi; Lee, Ye Jin; Jung, Myeong Hee; Park, Jung Je; Kim, Jin Pyeong; Woo, Seung Hoon

    2016-01-01

    Gastroesophageal reflux is associated with numerous pathologic conditions of the upper aerodigestive tract. Gastric pepsin within reflux contributes to immunologic reactions in the tonsil. In this study, we aimed to find the relationships between pepsin and tonsillar hypertrophy. We explored the notion whether tonsillar hypertrophy was due to pepsin-mediated gastric reflux in tonsil hypertrophy. Fifty-four children with tonsil hypertrophy and 30 adults with tonsillitis were recruited before surgical treatment. Blood and tonsil tissues from each patient were harvested for analysis of changes in lymphocyte and macrophage numbers coupled with histological and biochemical analysis. Pepsin was expressed at different levels in tonsil tissues from each tonsillar hypertrophy. Pepsin-positive cells were found in the crypt epithelium, surrounding the lymphoid follicle with developing fibrosis, and also surrounding the lymphoid follicle that faced the crypt. And also, pepsin staining was well correlated with damaged tonsillar squamous epithelium and TGF-β1 and iNOS expression in the tonsil section. In addition, pepsin and TGF-β1-positive cells were co-localized with CD68-positive cells in the crypt and surrounding germinal centers. In comparison of macrophage responsiveness to pepsin, peripheral blood mononuclear cells (PBMNCs) were noticeably larger in the presence of activated pepsin in the child group. Furthermore, CD11c and CD163-positive cells were significantly increased by activated pepsin. However, this was not seen for the culture of PBMNCs from the adult group. The lymphocytes and monocytes are in a highly proliferative state in the tonsillar hypertrophy and associated with increased expression of pro-inflammatory factors as a result of exposure to stomach reflux pepsin.

  20. Ventricular hypertrophy--physiological mechanisms.

    Science.gov (United States)

    Vaughan Williams, E M

    1986-01-01

    Adult cardiac myocytes are incapable of mitosis. Dead cells are replaced by connective tissue so that after myocardial infarction (MI), function can only be restored by compensatory hypertrophy of the surviving myocardium. In physiological hypertrophy in response to exercise, high altitude, or mild hypertension, additional myoplasm expands cell diameter in an orderly fashion; Z-lines are in register and the normal ratio of volume densities of contractile elements, mitochondria, and capillaries is conserved. In hypertrophy induced by aortic or pulmonary artery banding or by experimental or congenital hypertension, the borderline between physiological and pathological hypertrophy may be crossed, causing disorganization of fibers and an unfavourable contractile element to capillary ratio. There was, therefore, a need for a graded model of hypertrophy, which involves simulating an altitude of 6,000 m at sea level by supplying rabbits with appropriate nitrogen/oxygen mixtures. In this environment, 50% right ventricular hypertrophy can be achieved without alteration of left ventricular weight or hematocrit. Longer exposures produced 100% right ventricular hypertrophy, with only moderate increases in hematocrit and left ventricular weight. It is well known that adrenergic stimulation causes cardiac hypertrophy, and it has been suggested that release of a trophic factor from sympathetic nerves, either noradrenaline or a protein, might be a necessary stimulus for growth. If so, long-term treatment of post-MI patients with beta-adrenergic blocking agents could inhibit a desirable compensatory hypertrophy of the surviving myocardium. In the above model it has been found, however, that neither beta-blockade nor chemical sympathectomy with guanethidine or 6-hydroxydopamine had any effect on the hypertrophy, nor did treatment with verapamil or nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

  1. Adult adenoid hypertrophy, is it persistent childhood adenoid hypertrophy?

    Directory of Open Access Journals (Sweden)

    Shama Shetty

    2016-01-01

    Full Text Available Objectives: Adult adenoid hypertrophy is not common. More number of cases of adult adenoid hypertrophy is detected in recent years due to the free availability of endoscopes. The aim of this study is to know the etiopathology of adenoid hypertrophy in adults. Materials and Methods: Twenty-five cases of adult adenoid hypertrophy who underwent adenoidectomy were studied in our institution over a period of 5 years from 2008 to 2013. All the patients underwent diagnostic nasal endoscopy, and associated sinus and nasal pathology were studied. Results: Of 25 cases, 12 were males and 13 were females. In our study adult adenoid hypertrophy was more common in second and third decade. Nasal obstruction was main symptom in 80% of our cases. Allergic symptoms were seen in 28%, headache in 24%, and repeated throat infection in 20%. Adenoidectomy with tonsillectomy was done in 5 cases, adenoidectomy with septoplasty in 5 cases, septoplasty with turbinectomy along with adenoidectomy in 7 cases, functional endoscopic sinus surgery with adenoidectomy in 3 cases, adenoidectomy with tympanoplasty in 2 cases, myringotomy with grommet insertion in 2 patients, and isolated adenoidectomy in 1 patient. Conclusion: Since highest number of cases in our study is in early adulthood, we believe that adenoid hypertrophy is persistence of childhood hypertrophy.

  2. Physiological and pathological cardiac hypertrophy.

    Science.gov (United States)

    Shimizu, Ippei; Minamino, Tohru

    2016-08-01

    The heart must continuously pump blood to supply the body with oxygen and nutrients. To maintain the high energy consumption required by this role, the heart is equipped with multiple complex biological systems that allow adaptation to changes of systemic demand. The processes of growth (hypertrophy), angiogenesis, and metabolic plasticity are critically involved in maintenance of cardiac homeostasis. Cardiac hypertrophy is classified as physiological when it is associated with normal cardiac function or as pathological when associated with cardiac dysfunction. Physiological hypertrophy of the heart occurs in response to normal growth of children or during pregnancy, as well as in athletes. In contrast, pathological hypertrophy is induced by factors such as prolonged and abnormal hemodynamic stress, due to hypertension, myocardial infarction etc. Pathological hypertrophy is associated with fibrosis, capillary rarefaction, increased production of pro-inflammatory cytokines, and cellular dysfunction (impairment of signaling, suppression of autophagy, and abnormal cardiomyocyte/non-cardiomyocyte interactions), as well as undesirable epigenetic changes, with these complex responses leading to maladaptive cardiac remodeling and heart failure. This review describes the key molecules and cellular responses involved in physiological/pathological cardiac hypertrophy. Copyright © 2016 Elsevier Ltd. All rights reserved.

  3. Phenylephrine-induced cardiac hypertrophy is attenuated by a histone acetylase inhibitor anacardic acid in mice.

    Science.gov (United States)

    Peng, Chang; Luo, Xiaomei; Li, Shuo; Sun, Huichao

    2017-03-28

    Cardiac hypertrophy is a complex process involving highly coordinated but tight regulation of multiple elements, such as in epigenetics, which make an important contribution to myocardium remodeling and cardiac hypertrophy. Epigenetic regulations, particularly histone acetylation, have been implicated in cardiac hypertrophy, however, the exact mechanism is still largely unknown. In the present study, we explored the potential attenuating effects of Chinese herbal extract anacardic acid on phenylephrine-induced cardiac hypertrophy and the underlying mechanism. The mouse cardiac hypertrophy model was established and the hearts were collected from C57BL/6 mice for further analyses. The data showed that anacardic acid modulated the cardiac genes expression and attenuated the phenylephrine-induced cardiac hypertrophy via the suppression of histone acetylases activity and downstream cardiac genes. In addition, anacardic acid abrogated histone and MEF2A acetylation and DNA-binding activity by blocking p300-HAT and PCAF-HAT activities. In addition, anacardic acid normalized the cardiac hypertrophy-related genes expressions (ANP, BNP, cTnT, cTnI, β-MHC, and Cx43) induced by phenylephrine at the level of transcription and translation. In addition, anacardic acid did not affect the blood routine index, hepatic function, renal function, and myocardial enzymes. Therefore, anacardic acid may prove to be a candidate drug to cure hypertrophic cardiomyopathy.

  4. Practices Surrounding Event Photos

    NARCIS (Netherlands)

    Vyas, Dhaval; Nijholt, Antinus; van der Veer, Gerrit C.; Kotzé, P.; Marsden, G.; Lindgaard, G.; Wesson, J.; Winckler, M.

    Sharing photos through mobile devices has a great potential for creating shared experiences of social events between co-located as well as remote participants. In order to design novel event sharing tools, we need to develop indepth understanding of current practices surrounding these so called

  5. Hepatitis C

    Science.gov (United States)

    ... Events Follow Us Home Health Information Liver Disease Hepatitis (Viral) Hepatitis C Related Topics English English Español Section Navigation Hepatitis (Viral) What Is Viral Hepatitis? Hepatitis A Hepatitis B ...

  6. Inhibition of lipopolysaccharide-induced liver injury in rats treated with a hepatic drug-metabolizing enzyme inducer p,p'-DDT.

    Science.gov (United States)

    Shimada, Yuko; Tomita, Mariko; Yoshida, Toshinori; Fukuyama, Tomoki; Katoh, Yoshitaka; Ohnuma-Koyama, Aya; Takahashi, Naofumi; Soma, Katsumi; Kojima, Sayuri; Ohtsuka, Ryoichi; Takeda, Makio; Kuwahara, Maki; Harada, Takanori

    2015-03-01

    Hepatocellular hypertrophy in association with drug-metabolizing enzyme induction is considered to be an adaptive change associated with drug metabolism. To improve our understanding of liver hypertrophy, we determined the effect of a single ip injection of either lipopolysaccharide (LPS) or vehicle in male F344 rats with hepatocellular hypertrophy induced by oral delivery of p,p'-DDT for 2 weeks. The rats were sacrificed 3h or 24h after LPS or vehicle injection. LPS induced a focal hepatocellular necrosis in rats fed the control diet. When rats pre-treated with p,p'-DDT were injected with LPS, necrotic foci surrounded by ballooned hepatocytes were observed in the liver. The change was consistent with reduced LPS-mediated increases in plasma hepatic biomarkers, neutrophil influx, and apoptosis, and also associated with hepatic mRNA levels of TNF-α, CYPs, and NOS2. By contrast, when combined with p,p'-DDT and LPS, faint hepatocellular fatty change was extended, together with a synergistic increase in total blood cholesterol. These results suggest that hepatocytes exposed to p,p'-DDT are protected from the cell-lethal toxic effects of an exogenous stimulus, resulting in cell ballooning rather than necrosis in association with reduced inflammation and apoptosis, but compromised by an adverse effect on lipid metabolism.

  7. Compensatory Hypertrophy of Skeletal Muscle: Contractile Characteristics

    Science.gov (United States)

    Ianuzzo, C. D.; Chen, V.

    1977-01-01

    Describes an experiment using rats that demonstrates contractile characteristics of normal and hypertrophied muscle. Compensatory hypertrophy of the plantaris muscle is induced by surgical removal of the synergistic gastrocnemium muscle. Includes methods for determination of contractile properties of normal and hypertrophied muscle and…

  8. Compensatory Hypertrophy of Skeletal Muscle: Contractile Characteristics

    Science.gov (United States)

    Ianuzzo, C. D.; Chen, V.

    1977-01-01

    Describes an experiment using rats that demonstrates contractile characteristics of normal and hypertrophied muscle. Compensatory hypertrophy of the plantaris muscle is induced by surgical removal of the synergistic gastrocnemium muscle. Includes methods for determination of contractile properties of normal and hypertrophied muscle and…

  9. Mitochondria and left ventricular hypertrophy

    Institute of Scientific and Technical Information of China (English)

    Haiyan Zhu; Shiwen Wang

    2008-01-01

    @@ Introduction Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension.It contributes a lot to high mortality of essential hypertension due to sudden cardiac death,ventricular arrhythmia and heart failure.Many factors involve in the pathogenesis of hypertension-induced LVH including inherited variants as well as environmental factors.

  10. Biochemical regulators in cardiac hypertrophy.

    Science.gov (United States)

    Kölbel, F; Schreiber, V

    1983-01-01

    In recent years research has shown that muscle is capable of reacting to mechanical stimuli by altering biochemical processes. Myocardium is probably the source of a biochemical factor, or factors which activate myocardial protein synthesis. In experimentally induced cardiac hypertrophy adaptive alterations have been shown to occur not only in the adrenal medulla but also in the adrenal cortex. Finally, detection of cross reactivity between digitalis glycosides and a number of steroid hormones has succeeded. We assume that such cross reactivity indicates the existence of an endogenic factor of steroid character, which is produced in the adrenal gland and functions as an endogenic cardiotonic agent. During experimental cardiac hypertrophy its synthesis is possibly increased. We propose the term "endocardin" or "endocardiotonin" for this agent.

  11. Neurogenic muscle hypertrophy: a case report

    Science.gov (United States)

    Shin, Hyun Ho; Jeon, Young Hoon; Jang, Seung Won

    2016-01-01

    Muscular hypertrophy is caused mainly due to myopathic disorder. But, it is also rarely produced by neurogenic disorder. A 74-year-old woman complained of right calf pain with hypertrophy for several years. Recent lumbar spine magnetic resonance imaging (MRI) showed central and lateral canal narrowing at the L4-L5 intervertebral space. Lower extremity MRI revealed fatty change of right medial head of the gastrocnemius and soleus, causing right calf hypertrophy. Electrodiagnostic examinations including electromyography and nerve conduction velocity testing demonstrated 5th lumbar and 1st sacral polyradiculopathy. Integrating all the results, the diagnosis was neurogenic muscle hypertrophy. Neurogenic muscle hypertrophy is very rare, but we recommend that clinicians consider this problem when a patient complains of lower limb hypertrophy and pain.

  12. Mitochondria in cardiac hypertrophy and heart failure.

    Science.gov (United States)

    Rosca, Mariana G; Tandler, Bernard; Hoppel, Charles L

    2013-02-01

    Heart failure (HF) frequently is the unfavorable outcome of pathological heart hypertrophy. In contrast to physiological cardiac hypertrophy, which occurs in response to exercise and leads to full adaptation of contractility to the increased wall stress, pathological hypertrophy occurs in response to volume or pressure overload, ultimately leading to contractile dysfunction and HF. Because cardiac hypertrophy impairs the relationship between ATP demand and production, mitochondrial bioenergetics must keep up with the cardiac hypertrophic phenotype. We review data regarding the mitochondrial proteomic and energetic remodeling in cardiac hypertrophy, as well as the temporal and causal relationships between mitochondrial failure to match the increased energy demand and progression to cardiac decompensation. We suggest that the maladaptive effect of sustained neuroendocrine signals on mitochondria leads to bioenergetic fading which contributes to the progression from cardiac hypertrophy to failure. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism". Copyright © 2012 Elsevier Ltd. All rights reserved.

  13. Mitochondria in cardiac hypertrophy and heart failure

    Science.gov (United States)

    Rosca, Mariana G.; Tandler, Bernard; Hoppel, Charles L.

    2013-01-01

    Heart failure (HF) frequently is the unfavorable outcome of pathological heart hypertrophy. In contrast to physiological cardiac hypertrophy, which occurs in response to exercise and leads to full adaptation of contractility to the increased wall stress, pathological hypertrophy occurs in response to volume or pressure overload, ultimately leading to contractile dysfunction and HF. Because cardiac hypertrophy impairs the relationship between ATP demand and production, mitochondrial bioenergetics must keep up with the cardiac hypertrophic phenotype. We review data regarding the mitochondrial proteomic and energetic remodeling in cardiac hypertrophy, as well as the temporal and causal relationship between mitochondrial failure to match the increased energy demand and progression to cardiac decompensation. We suggest that the maladaptive effect of sustained neuroendocrine signals on mitochondria leads to bioenergetic fading which contributes to the progression from cardiac hypertrophy to failure. PMID:22982369

  14. Hypertrophied hearts: what of sevoflurane cardioprotection?

    DEFF Research Database (Denmark)

    Larsen, Jens Kjærgaard Rolighed; Smerup, Morten Holdgaard; Hasenkam, John Michael

    2009-01-01

    cardioprotection and more susceptible to ischaemic injury. We investigated whether hypertrophy blocks sevoflurane cardioprotection, and whether tolerance to ischaemia is altered by left ventricular hypertrophy, in an established experimental animal model of ischaemia-reperfusion. METHODS: Anaesthetized juvenile...... in left ventricular hypertrophy development in two further groups and these animals underwent identical ischaemia-reperfusion protocols, with or without sevoflurane cardioprotection. Myocardial infarct sizes were compared post-mortem. RESULTS: The mean myocardial infarct size (% of area...

  15. Masseter and medial pterygoid muscle hypertrophy

    OpenAIRE

    R, Guruprasad; Rishi, Sudhirkumar; Nair, Preeti P; Thomas, Shaji

    2011-01-01

    Hypertrophy refers to an enlargement caused by an increase in the size but not in the number of cells. Generalised masticatory muscle hypertrophy may affect the temporalis muscle, masseters and medial pterygoids in a variety of combinations. Masseteric hypertrophy may present as either unilateral or bilateral painless swelling of unknown origin in the region of angle of mandible. It is a relatively rare condition and presents a diagnostic dilemma. While the history and clinical examination ar...

  16. Neurogenic muscle hypertrophy: a case report

    OpenAIRE

    Shin, Hyun Ho; Jeon, Young Hoon; Jang, Seung Won; Kim, Sae Young

    2016-01-01

    Muscular hypertrophy is caused mainly due to myopathic disorder. But, it is also rarely produced by neurogenic disorder. A 74-year-old woman complained of right calf pain with hypertrophy for several years. Recent lumbar spine magnetic resonance imaging (MRI) showed central and lateral canal narrowing at the L4-L5 intervertebral space. Lower extremity MRI revealed fatty change of right medial head of the gastrocnemius and soleus, causing right calf hypertrophy. Electrodiagnostic examinations ...

  17. [Asymmetric hypertrophy of the masticatory muscles].

    Science.gov (United States)

    Arzul, L; Corre, P; Khonsari, R H; Mercier, J-M; Piot, B

    2012-06-01

    Hypertrophy of the masticatory muscles most commonly affects the masseter. Less common cases of isolated or associated temporalis hypertrophy are also reported. Parafunctional habits, and more precisely bruxism, can favor the onset of the hypertrophy. This condition is generally idiopathic and can require both medical and/or surgical management. A 29-year-old patient was referred to our department for an asymmetric swelling of the masticatory muscles. Physical examination revealed a bilateral hypertrophy of the masticatory muscles, predominantly affecting the right temporalis and the left masseter. Major bruxism was assessed by premature dental wearing. The additional examinations confirmed the isolated muscle hypertrophy. Benign asymmetric hypertrophy of the masticatory muscles promoted by bruxism was diagnosed. Treatment with injections of type A botulinum toxin was conducted in association with a splint and relaxation. Its effectiveness has been observed at six months. Few cases of unilateral or bilateral temporalis hypertrophy have been reported, added to the more common isolated masseter muscles hypertrophy. The diagnosis requires to rule out secondary hypertrophies and tumors using Magnetic Resonance Imaging. The condition is thought to be favoured by parafunctional habits such as bruxism. The conservative treatment consists in reducing the volume of the masticatory muscles using intramuscular injections of type A botulinum toxin. Other potential conservative treatments are wearing splints and muscle relaxant drugs. Surgical procedures aiming to reduce the muscle volume and/or the bone volume (mandibular gonioplasty) can be proposed. Copyright © 2012 Elsevier Masson SAS. All rights reserved.

  18. Genetics Home Reference: myostatin-related muscle hypertrophy

    Science.gov (United States)

    ... Health Conditions myostatin-related muscle hypertrophy myostatin-related muscle hypertrophy Printable PDF Open All Close All Enable Javascript ... view the expand/collapse boxes. Description Myostatin-related muscle hypertrophy is a rare condition characterized by reduced body ...

  19. Regulation of Cardiac Hypertrophy: the nuclear option

    NARCIS (Netherlands)

    D.W.D. Kuster (Diederik)

    2011-01-01

    textabstractCardiac hypertrophy is the response of the heart to an increased workload. After myocardial infarction (MI) the surviving muscle tissue has to work harder to maintain cardiac output. This sustained increase in workload leads to cardiac hypertrophy. Despite its apparent appropriateness, c

  20. Use of intranasal corticosteroids in adenotonsillar hypertrophy.

    Science.gov (United States)

    Sakarya, E U; Bayar Muluk, N; Sakalar, E G; Senturk, M; Aricigil, M; Bafaqeeh, S A; Cingi, C

    2017-05-01

    This review examined the efficacy of intranasal corticosteroids for improving adenotonsillar hypertrophy. The related literature was searched using PubMed and Proquest Central databases. Adenotonsillar hypertrophy causes mouth breathing, nasal congestion, hyponasal speech, snoring, obstructive sleep apnoea, chronic sinusitis and recurrent otitis media. Adenoidal hypertrophy results in the obstruction of nasal passages and Eustachian tubes, and blocks the clearance of nasal mucus. Adenotonsillar hypertrophy and obstructive sleep apnoea are associated with increased expression of various mediators of inflammatory responses in the tonsils, and respond to anti-inflammatory agents such as corticosteroids. Topical nasal steroids most likely affect the anatomical component by decreasing inspiratory upper airway resistance at the nasal, adenoidal or tonsillar levels. Corticosteroids, by their lympholytic or anti-inflammatory effects, might reduce adenotonsillar hypertrophy. Intranasal corticosteroids reduce cellular proliferation and the production of pro-inflammatory cytokines in a tonsil and adenoid mixed-cell culture system. Intranasal corticosteroids have been used in adenoidal hypertrophy and adenotonsillar hypertrophy patients, decreasing rates of surgery for adenotonsillar hypertrophy.

  1. Mammary hypertrophy in an ovariohysterectomized cat.

    Science.gov (United States)

    Pukay, B P; Stevenson, D A

    1983-05-01

    A four year old ovariohysterectomized domestic short-haired cat under treatment for behavioral urine spraying and idiopathic alopecia developed mammary gland hypertrophy following treatment with megestrol acetate. Withdrawal of the progestin and treatment with androgen failed to cause regression of the hypertrophy. The affected mammary gland was surgically excised and recovery was uneventful.

  2. Regulation of Cardiac Hypertrophy: the nuclear option

    NARCIS (Netherlands)

    D.W.D. Kuster (Diederik)

    2011-01-01

    textabstractCardiac hypertrophy is the response of the heart to an increased workload. After myocardial infarction (MI) the surviving muscle tissue has to work harder to maintain cardiac output. This sustained increase in workload leads to cardiac hypertrophy. Despite its apparent appropriateness, c

  3. Regulation of Cardiac Hypertrophy: the nuclear option

    NARCIS (Netherlands)

    D.W.D. Kuster (Diederik)

    2011-01-01

    textabstractCardiac hypertrophy is the response of the heart to an increased workload. After myocardial infarction (MI) the surviving muscle tissue has to work harder to maintain cardiac output. This sustained increase in workload leads to cardiac hypertrophy. Despite its apparent appropriateness,

  4. New frontiers in heart hypertrophy during pregnancy.

    Science.gov (United States)

    Li, Jingyuan; Umar, Soban; Amjedi, Marjan; Iorga, Andrea; Sharma, Salil; Nadadur, Rangarajan D; Regitz-Zagrosek, Vera; Eghbali, Mansoureh

    2012-01-01

    During Pregnancy, heart develops physiological left ventricular hypertrophy as a result of the natural volume overload. Previously we have characterized the molecular and functional signature of heart hypertrophy during pregnancy. Cardiac hypertrophy during pregnancy is a complex process that involves many changes including in the signalling pathways, composition of extracellular matrix as well as the levels of sex hormones. This review summarises the recent advances and the new frontiers in the context of heart hypertrophy during pregnancy. In particular we focus on structural and extracellular matrix remodelling as well as signalling pathways in pregnancy-induced physiological heart hypertrophy. Emerging evidence shows that various microRNAs modulate key components of hypertrophy, therefore the role of microRNAs in the regulation of gene expression in pregnancy induced hypertrophy is also discussed. We also review the role of ubiquitin proteasome system, the major machinery for the degradation of damaged and misfolded proteins, in heart hypertrophy. The role of sex hormones in particular estrogen in cardiac remodeling during pregnancy is also discussed. We also review pregnancy-induced cardiovascular complications such as peripartum cardiomyopathy and pre-eclampsia and how the knowledge from the animal studies may help us to develop new therapeutic strategies for better treatment of cardiovascular diseases during pregnancy. Special emphasis has to be given to the guidelines on disease management in pregnancy.

  5. Masseter and medial pterygoid muscle hypertrophy.

    Science.gov (United States)

    Guruprasad, R; Rishi, Sudhirkumar; Nair, Preeti P; Thomas, Shaji

    2011-09-26

    Hypertrophy refers to an enlargement caused by an increase in the size but not in the number of cells. Generalised masticatory muscle hypertrophy may affect the temporalis muscle, masseters and medial pterygoids in a variety of combinations. Masseteric hypertrophy may present as either unilateral or bilateral painless swelling of unknown origin in the region of angle of mandible. It is a relatively rare condition and presents a diagnostic dilemma. While the history and clinical examination are important in differentiating this benign condition from parotid or dental pathology, they cannot necessarily exclude rare malignant lesion within the muscle. Advanced imaging modalities like CT and MRI are essential to confirm the diagnosis. Here the authors are reporting a unique case of masseter muscle hypertrophy along with medial pterygoid hypertrophy which was missed clinically but confirmed using CT and MRI.

  6. Histopathological image analysis of chemical-induced hepatocellular hypertrophy in mice.

    Science.gov (United States)

    Asaoka, Yoshiji; Togashi, Yuko; Mutsuga, Mayu; Imura, Naoko; Miyoshi, Tomoya; Miyamoto, Yohei

    2016-04-01

    Chemical-induced hepatocellular hypertrophy is frequently observed in rodents, and is mostly caused by the induction of phase I and phase II drug metabolic enzymes and peroxisomal lipid metabolic enzymes. Liver weight is a sensitive and commonly used marker for detecting hepatocellular hypertrophy, but is also increased by a number of other factors. Histopathological observations subjectively detect changes such as hepatocellular hypertrophy based on the size of a hepatocyte. Therefore, quantitative microscopic observations are required to evaluate histopathological alterations objectively. In the present study, we developed a novel quantitative method for an image analysis of hepatocellular hypertrophy using liver sections stained with hematoxylin and eosin, and demonstrated its usefulness for evaluating hepatocellular hypertrophy induced by phenobarbital (a phase I and phase II enzyme inducer) and clofibrate (a peroxisomal enzyme inducer) in mice. The algorithm of this imaging analysis was designed to recognize an individual hepatocyte through a combination of pixel-based and object-based analyses. Hepatocellular nuclei and the surrounding non-hepatocellular cells were recognized by the pixel-based analysis, while the areas of the recognized hepatocellular nuclei were then expanded until they ran against their expanding neighboring hepatocytes and surrounding non-hepatocellular cells by the object-based analysis. The expanded area of each hepatocellular nucleus was regarded as the size of an individual hepatocyte. The results of this imaging analysis showed that changes in the sizes of hepatocytes corresponded with histopathological observations in phenobarbital and clofibrate-treated mice, and revealed a correlation between hepatocyte size and liver weight. In conclusion, our novel image analysis method is very useful for quantitative evaluations of chemical-induced hepatocellular hypertrophy. Copyright © 2015 Elsevier GmbH. All rights reserved.

  7. Signaling Pathways Involved in Cardiac Hypertrophy

    Institute of Scientific and Technical Information of China (English)

    Tao Zewei; Li Longgui

    2006-01-01

    Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress.Traditionally, it has been considered a beneficial mechanism; however, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Delineating intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in potential targets for therapeutic intervention. Generally, there are two types of cardiac hypertrophies, adaptive hypertrophy, including eutrophy (normal growth) and physiological hypertrophy (growth induced by physical conditioning), and maladaptive hypertrophy, including pathologic or reactive hypertrophy (growth induced by pathologic stimuli) and hypertrophic growth caused by genetic mutations affecting sarcomeric or cytoskeletal proteins. Accumulating observations from animal models and human patients have identified a number of intracellular signaling pathways that characterized as important transducers of the hypertrophic response,including calcineurin/nuclear factor of activated Tcells, phosphoinositide 3-kinases/Akt (PI3Ks/Akt),G protein-coupled receptors, small G proteins,MAPK, PKCs, Gp130/STAT'3, Na+/H+ exchanger,peroxisome proliferator-activated receptors, myocyte enhancer factor 2/histone deacetylases, and many others. Furthermore, recent evidence suggests that adaptive cardiac hypertrophy is regulated in large part by the growth hormone/insulin-like growth factors axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive hypertrophy is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phosphorlipase C pathway, leading to an increase in cytosolic calcium and activation of PKC.

  8. Adenoid Hypertrophy in Adults: A case Series.

    Science.gov (United States)

    Rout, Manas Ranjan; Mohanty, Diganta; Vijaylaxmi, Y; Bobba, Kamlesh; Metta, Chakradhar

    2013-07-01

    Adenoid hypertrophy is common in children. Size of the adenoid increases up to the age of 6 years, then slowly atrophies and completely disappears at the age of 16 years. Adenoid hypertrophy in adults is rare. Present study shows that adenoid hypertrophy is now increasing in adults because of various causes. Study has been conducted in the Department of ENT and Head & Neck Surgery, Alluri Sitarama Raju Academy of Medical science, Eluru, Andhra Pradesh, India. Study shows that incidence of adenoid hypertrophy is increasing as the cause of nasal obstruction in adults. This study identified the different causes of adenoid hypertrophy in adult patients. The common causes of adenoid hypertrophy in adults are chronic infection and allergy. Pollution and smoking are also important predisposing factors. Sometimes it is also associated with sinonasal malignancy, lymphoma and HIV infection. Study shows that 21 % of adult nasal obstruction is due to adenoid hypertrophy. But in case of the patient with chronic tonsillitis only 9 % were associated with adenoid hypertrophy. Males are more commonly involved (70 %) then female, may be because of out door activities and more commonly exposed to pollutants. And most commonly involved age group is 16-25 years (60 %). Majority of the cases with adenoid hypertrophy are associated with infection and allergy i.e. descending infection in 33.3 % cases, ascending infection in 20 % cases and allergic rhinitis in 30 % cases. Association of malignant sinonasal tumors, non Hodgkin's lymphoma and HIV infections are rare i.e. 3.3 % each. So any cases of adult adenoid hypertrophy should be treated seriously to exclude the dangerous causes.

  9. Massive hepatic necrosis with toxic liver syndrome following portal vein ligation

    Science.gov (United States)

    Dupré, Aurélien; Gagnière, Johan; Tixier, Lucie; Ines, David Da; Perbet, Sébastien; Pezet, Denis; Buc, Emmanuel

    2013-01-01

    Right portal vein ligation (PVL) is a safe and widespread procedure to induce controlateral liver hypertrophy for the treatment of bilobar colorectal liver metastases. We report a case of a 60-year-old man treated by both right PVL and ligation of the glissonian branches of segment 4 for colorectal liver metastases surrounding the right and median hepatic veins. After surgery, the patient developed massive hepatic necrosis with secondary pulmonary and renal insufficiency requiring transfer to the intensive care unit. This so-called toxic liver syndrome finally regressed after hemofiltration and positive oxygen therapy. Diagnosis of acute congestion of the ligated lobe was suspected. The mechanism suspected was an increase in arterial inflow secondary to portal vein ligation concomitant with a decrease in venous outflow due to liver metastases encircling the right and median hepatic vein. This is the first documented case of toxic liver syndrome in a non-cirrhotic patient with favorable issue, and a rare complication of PVL. PMID:23687421

  10. Portal vein embolization induces compensatory hypertrophy of remnant liver

    Institute of Scientific and Technical Information of China (English)

    Jing-Yao Huang; Wei-Zhu Yang; Jian-Jun Li; Na Jiang; Qu-Bin Zheng

    2006-01-01

    AIM: To evaluate the effectiveness and safety of different portal vein branch embolization agents in inducing compensatory hypertrophy of the remnant liver and to offer a theoretic basis for clinical portal vein branch embolization.METHODS: Forty-one adult dogs were included in the experiment and divided into four groups. Five dogs served as a control group, 12 as a gelfoam group, 12as a coil-gelfoam group and 12 as an absolute ethanol group. Left portal vein embolization was performed in each group. The results from the embolization in each group using different embolic agents were compared.The safety of portal vein embolization (PVE) was evaluated by liver function test, computed tomography (CT) and digital subtraction angiography (DSA) of liver and portal veins. Statistical test of variance was performed to analyze the results.RESULTS: Gelfoam used for PVE was inefficient in recanalization of portal vein branch 4 wk after the procedure. The liver volume in groups of coil-gelfoam and absolute ethanol increased 25.1% and 33.18%,respectively. There was no evidence of recanalization of embolized portal vein, hepatic dysfunction, and portal hypertension in coil-gelfoam group and absolute ethanol group.CONCOUSION: Portal vein branch embolization using absolute ethanol and coil-gelfoam could induce atrophy of the embolized lobes and compensatory hypertrophy of the remnant liver. Gelfoam is an inefficient agent.

  11. The role of autophagy in cardiac hypertrophy

    Science.gov (United States)

    Li, Lanfang; Xu, Jin; He, Lu; Peng, Lijun; Zhong, Qiaoqing; Chen, Linxi; Jiang, Zhisheng

    2016-01-01

    Autophagy is conserved in nature from lower eukaryotes to mammals and is an important self-cannibalizing, degradative process that contributes to the elimination of superfluous materials. Cardiac hypertrophy is primarily characterized by excess protein synthesis, increased cardiomyocyte size, and thickened ventricular walls and is a major risk factor that promotes arrhythmia and heart failure. In recent years, cardiomyocyte autophagy has been considered to play a role in controlling the hypertrophic response. However, the beneficial or aggravating role of cardiomyocyte autophagy in cardiac hypertrophy remains controversial. The exact mechanism of cardiomyocyte autophagy in cardiac hypertrophy requires further study. In this review, we summarize the controversies associated with autophagy in cardiac hypertrophy and provide insights into the role of autophagy in the development of cardiac hypertrophy. We conclude that future studies should emphasize the relationship between autophagy and the different stages of cardiac hypertrophy, as well as the autophagic flux and selective autophagy. Autophagy will be a potential therapeutic target for cardiac hypertrophy. PMID:27084518

  12. The role of autophagy in cardiac hypertrophy.

    Science.gov (United States)

    Li, Lanfang; Xu, Jin; He, Lu; Peng, Lijun; Zhong, Qiaoqing; Chen, Linxi; Jiang, Zhisheng

    2016-06-01

    Autophagy is conserved in nature from lower eukaryotes to mammals and is an important self-cannibalizing, degradative process that contributes to the elimination of superfluous materials. Cardiac hypertrophy is primarily characterized by excess protein synthesis, increased cardiomyocyte size, and thickened ventricular walls and is a major risk factor that promotes arrhythmia and heart failure. In recent years, cardiomyocyte autophagy has been considered to play a role in controlling the hypertrophic response. However, the beneficial or aggravating role of cardiomyocyte autophagy in cardiac hypertrophy remains controversial. The exact mechanism of cardiomyocyte autophagy in cardiac hypertrophy requires further study. In this review, we summarize the controversies associated with autophagy in cardiac hypertrophy and provide insights into the role of autophagy in the development of cardiac hypertrophy. We conclude that future studies should emphasize the relationship between autophagy and the different stages of cardiac hypertrophy, as well as the autophagic flux and selective autophagy. Autophagy will be a potential therapeutic target for cardiac hypertrophy. © The Author 2016. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  13. Clinical Application of Surrounding Puncture

    Institute of Scientific and Technical Information of China (English)

    GUO Yao-jie; HAN Chou-ping

    2003-01-01

    Surrounding puncture can stop pathogenic qi from spreading, consolidate the connection between local meridians and enrich local qi and blood, which can eventually supplement anti-pathogenic qi and remove pathogenic qi, and consequently remedy diseases. The author of this article summrized and analyzed the clinical application of surrounding puncture for the purpose of studying this technique and improving the therapeutic effect.

  14. Regression of altitude-produced cardiac hypertrophy.

    Science.gov (United States)

    Sizemore, D. A.; Mcintyre, T. W.; Van Liere, E. J.; Wilson , M. F.

    1973-01-01

    The rate of regression of cardiac hypertrophy with time has been determined in adult male albino rats. The hypertrophy was induced by intermittent exposure to simulated high altitude. The percentage hypertrophy was much greater (46%) in the right ventricle than in the left (16%). The regression could be adequately fitted to a single exponential function with a half-time of 6.73 plus or minus 0.71 days (90% CI). There was no significant difference in the rates of regression for the two ventricles.

  15. Regression of altitude-produced cardiac hypertrophy.

    Science.gov (United States)

    Sizemore, D. A.; Mcintyre, T. W.; Van Liere, E. J.; Wilson , M. F.

    1973-01-01

    The rate of regression of cardiac hypertrophy with time has been determined in adult male albino rats. The hypertrophy was induced by intermittent exposure to simulated high altitude. The percentage hypertrophy was much greater (46%) in the right ventricle than in the left (16%). The regression could be adequately fitted to a single exponential function with a half-time of 6.73 plus or minus 0.71 days (90% CI). There was no significant difference in the rates of regression for the two ventricles.

  16. Adenoid Hypertrophy in Adults: A case Series

    OpenAIRE

    Rout, Manas Ranjan; Mohanty, Diganta; Y Vijaylaxmi; Bobba, Kamlesh; Metta, Chakradhar

    2012-01-01

    Adenoid hypertrophy is common in children. Size of the adenoid increases up to the age of 6 years, then slowly atrophies and completely disappears at the age of 16 years. Adenoid hypertrophy in adults is rare. Present study shows that adenoid hypertrophy is now increasing in adults because of various causes. Study has been conducted in the Department of ENT and Head & Neck Surgery, Alluri Sitarama Raju Academy of Medical science, Eluru, Andhra Pradesh, India. Study shows that incidence of ade...

  17. Hepatitis A FAQs

    Science.gov (United States)

    ... Policy and Programs Resource Center Viral Hepatitis Hepatitis A Questions and Answers for the Public Recommend on ... Hepatitis C. What is the difference between Hepatitis A, Hepatitis B, and Hepatitis C? Hepatitis A , Hepatitis ...

  18. A Rare Case of Lipomatous Hypertrophy of the Interventricular Septum

    OpenAIRE

    Papadopoulos, Christodoulos E.; Matsiras, Sotirios; Vassilikos, Vassilios

    2016-01-01

    Asymmetrical left ventricular hypertrophy secondary to interventricular septum hypertrophy is usually considered a typical phenotype of hypertrophic cardiomyopathy. In rare cases other conditions such as tumors or lipomatous hypertrophy of the interventricular septum may have a similar presentation. We present a case of a male patient who presented for routine cardiology work up and was diagnosed of having ventricular septal hypertrophy secondary to localized lipomatous hypertrophy.

  19. Hepatitis A

    Science.gov (United States)

    ... care, food, or sewage industry Other common hepatitis virus infections include hepatitis B and hepatitis C. Hepatitis A is the least serious and mildest of these diseases. Symptoms ... most often show up 2 to 6 weeks after being exposed to the hepatitis A virus. They are most often mild, but may last ...

  20. An unusual case of lingual tonsillar hypertrophy.

    Science.gov (United States)

    Hope, Nicholas; Patricia Smith, Caroline; Moran, Michael; Primrose, William

    2016-05-01

    Lingual tonsillar hypertrophy is an unusual presentation of voice change. If managed incorrectly this group of patients has the potential to deteriorate significantly causing airway obstruction and potentially death.

  1. Left ventricular hypertrophy: an initial response to myocardial injury.

    Science.gov (United States)

    Francis, G S; McDonald, K M

    1992-06-04

    The prevailing wisdom generally has been that the failing heart hypertrophies in response to increased wall stress. The increase in myocardial mass observed in heart failure is therefore a relatively late compensatory event geared to normalize wall stress. Although this is undoubtedly true, especially for heart failure resulting from a large anterior myocardial infarction accompanied by rapid left ventricular expansion, it is possible that an important form of hypertrophy occurs much earlier as an initial response to myocardial injury. One can hypothesize that the initial response to injury is a nonspecific phenotypic alteration of the cardiac myocyte to one of growth and development. Such changes may be driven by both trophic and mechanical forces and may be important in altering the architecture of the myocardial cell and surrounding cardiac interstitium. Preliminary data from a variety of models support the concept that neuroendocrine activity is an important component in the ventricular remodeling process, and that pharmacologic interventions designed to block systemic and tissue neuroendocrine activity may prevent excessive cardiac enlargement and its ultimate consequences. Because this concept has important implications for preventive cardiology, the results of several prevention trials, including the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS), Studies of Left Ventricular Dysfunction (SOLVD), and Survival and Ventricular Enlargement (SAVE) are awaited eagerly.

  2. Visual surround suppression in schizophrenia

    Directory of Open Access Journals (Sweden)

    Marc Samuel Tibber

    2013-02-01

    Full Text Available Compared to unaffected observers patients with schizophrenia show characteristic differences in visual perception, including a reduced susceptibility to the influence of context on judgements of contrast - a manifestation of weaker surround suppression. To examine the generality of this phenomenon we measured the ability of 24 individuals with schizophrenia to judge the luminance, contrast, orientation and size of targets embedded in contextual surrounds that would typically influence the target’s appearance. Individuals with schizophrenia demonstrated weaker surround suppression compared to matched controls for stimuli defined by contrast or size, but not for those defined by luminance or orientation. As perceived luminance is thought to be regulated at the earliest stages of visual processing our findings are consistent with a suppression deficit that is predominantly cortical in origin. In addition, we propose that preserved orientation surround suppression in schizophrenia may reflect the sparing of broadly tuned mechanisms of suppression. We attempt to reconcile these data with findings from previous studies.

  3. Educational Success and Surrounding Culture

    Science.gov (United States)

    Walters, Garrison

    2016-01-01

    The curriculum, instruction, and services we provide in schools, colleges, and universities matter a lot, but if we continue to ignore our students' "surrounding culture," progress toward a more educated nation will continue to be disappointing.

  4. Educational Success and Surrounding Culture

    Science.gov (United States)

    Walters, Garrison

    2016-01-01

    The curriculum, instruction, and services we provide in schools, colleges, and universities matter a lot, but if we continue to ignore our students' "surrounding culture," progress toward a more educated nation will continue to be disappointing.

  5. Multichannel spatial surround sound system

    Institute of Scientific and Technical Information of China (English)

    RAO Dan; XIE Bosun

    2004-01-01

    Based on the consideration of being compatible with 5.1 channel horizontal surround sound system, a spatial surround sound system is proposed. Theoretical and experimental results show that the system has a wide listening area. It can not only recreate stable image in the front and rear direction, but also eliminate the defect of poor lateral image of 5.1 channel system. The system can be used to reproduce special 3D sound effect and the spaciousness of hall.

  6. LIGHT regulates inflamed draining lymph node hypertrophy

    Science.gov (United States)

    Zhu, Mingzhao; Yang, Yajun; Wang, Yugang; Wang, Zhongnan; Fu, Yang-Xin

    2011-01-01

    Lymph node (LN) hypertrophy, the increased cellularity of LNs, is the major indication of the initiation and expansion of the immune response against infection, vaccination, cancer or autoimmunity. The mechanisms underlying LN hypertrophy remain poorly defined. Here, we demonstrate that LIGHT (TNFSF14) is a novel factor essential for LN hypertrophy after CFA immunization. Mechanistically, LIGHT is required for the influx of lymphocytes into but not egress out of LNs. In addition, LIGHT is required for DC migration from the skin to draining LNs. Compared with WT mice, LIGHT−/− mice express lower levels of chemokines in skin and addressins in LN vascular endothelial cells after CFA immunization. We unexpectedly observed that LIGHT from radioresistant rather than radiosensitive cells, likely Langerhans cells, is required for LN hypertrophy. Importantly, antigen-specific T cell responses were impaired in DLN of LIGHT−/− mice, suggesting the importance of LIGHT regulation of LN hypertrophy in the generation of an adaptive immune response. Collectively, our data reveal a novel cellular and molecular mechanism for the regulation of LN hypertrophy and its potential impact on the generation of an optimal adaptive immune response. PMID:21572030

  7. Mechanotransduction pathways in skeletal muscle hypertrophy.

    Science.gov (United States)

    Yamada, André Katayama; Verlengia, Rozangela; Bueno Junior, Carlos Roberto

    2012-02-01

    In the last decade, molecular biology has contributed to define some of the cellular events that trigger skeletal muscle hypertrophy. Recent evidence shows that insulin like growth factor 1/phosphatidyl inositol 3-kinase/protein kinase B (IGF-1/PI3K/Akt) signaling is not the main pathway towards load-induced skeletal muscle hypertrophy. During load-induced skeletal muscle hypertrophy process, activation of mTORC1 does not require classical growth factor signaling. One potential mechanism that would activate mTORC1 is increased synthesis of phosphatidic acid (PA). Despite the huge progress in this field, it is still early to affirm which molecular event induces hypertrophy in response to mechanical overload. Until now, it seems that mTORC1 is the key regulator of load-induced skeletal muscle hypertrophy. On the other hand, how mTORC1 is activated by PA is unclear, and therefore these mechanisms have to be determined in the following years. The understanding of these molecular events may result in promising therapies for the treatment of muscle-wasting diseases. For now, the best approach is a good regime of resistance exercise training. The objective of this point-of-view paper is to highlight mechanotransduction events, with focus on the mechanisms of mTORC1 and PA activation, and the role of IGF-1 on hypertrophy process.

  8. Hepatitis E

    Science.gov (United States)

    ... sheets Fact files Questions & answers Features Multimedia Contacts Hepatitis E Fact sheet Updated July 2016 Key facts ... et al. Lancet 2012;380:2095-2128. World Hepatitis Day Know hepatitis - Act now Event notice Key ...

  9. Exercise and the Regulation of Skeletal Muscle Hypertrophy.

    Science.gov (United States)

    McGlory, Chris; Phillips, Stuart M

    2015-01-01

    Skeletal muscle is a critical organ serving as the primary site for postprandial glucose disposal and the generation of contractile force. The size of human skeletal muscle mass is dependent upon the temporal relationship between changes in muscle protein synthesis (MPS) and muscle protein breakdown. The aim of this chapter is to review our current understanding of how resistance exercise influences protein turnover with a specific emphasis on the molecular factors regulating MPS. We also will discuss recent data relating to the prescription of resistance exercise to maximize skeletal muscle hypertrophy. Finally, we evaluate the impact of age and periods of disuse on the loss of muscle mass and the controversy surround the etiology of muscle disuse atrophy.

  10. Hypertrophy of Ligament of Treitz

    Directory of Open Access Journals (Sweden)

    Siddharth P. Dubhashi

    2015-04-01

    Full Text Available Congenital duodenal obstruction commonly occurs due to malrotation, atresia, stenosis and annular pancreas in decreasing order of frequency. This is a case report of a 12 year old male child who presented with complaints of non-projectile vomiting and abdominal distension and pain after meals since 7 years. Barium study showed narrowing of the Duodeno-jejunal(DJ junction due to hypertrophied ligament of Treitz. Exploratory laparotomy revealed a dilated stomach and collapsed bowel loops. There were adhesions at DJ junction and other parts of the small intestine. Adhesiolysis was done. The followup revealed a weight gain of 2 kg. The barium study was repeated which also revealed a normal study. Congenital obstruction of duodeno-jejunal junction due to extrinsic band or due to narrower attachment of ligament of Treitz at duodeno-jejunal flexure is a rare cause of bilious vomiting in the newborn period. A broad attachment of the ligament of Treitz makes a smooth obtuse angle at the duodeno-jejunum junction whereas a narrower insertion creates an acute angle that predisposes to obstruction.Duodenal obstruction may rarely occur in the presence of a normally rotated gut.

  11. Postural control in women with breast hypertrophy

    Directory of Open Access Journals (Sweden)

    Alessandra Ferreira Barbosa

    2012-07-01

    Full Text Available OBJECTIVES: The consequences of breast hypertrophy have been described based on the alteration of body mass distribution, leading to an impact on psychological and physical aspects. The principles of motor control suggest that breast hypertrophy can lead to sensorimotor alterations and the impairment of body balance due to postural misalignment. The aim of this study is to evaluate the postural control of women with breast hypertrophy under different sensory information conditions. METHOD: This cross-sectional study included 14 women with breast hypertrophy and 14 without breast hypertrophy, and the mean ages of the groups were 39 ±15 years and 39±16 years, respectively. A force platform was used to assess the sensory systems that contribute to postural control: somatosensory, visual and vestibular. Four postural conditions were sequentially tested: eyes open and fixed platform, eyes closed and fixed platform, eyes open and mobile platform, and eyes closed and mobile platform. The data were processed, and variables related to the center of pressure were analyzed for each condition. The Kruskal-Wallis test was used to compare the conditions between the groups for the area of center of pressure displacement and the velocity of center of pressure displacement in the anterior-posterior and medial-lateral directions. The alpha level error was set at 0.05. RESULTS: Women with breast hypertrophy presented an area that was significantly higher for three out of four conditions and a higher velocity of center of pressure displacement in the anterior-posterior direction under two conditions: eyes open and mobile platform and eyes closed and mobile platform. CONCLUSIONS: Women with breast hypertrophy have altered postural control, which was demonstrated by the higher area and velocity of center of pressure displacement.

  12. The paradox of muscle hypertrophy in muscular dystrophy.

    Science.gov (United States)

    Kornegay, Joe N; Childers, Martin K; Bogan, Daniel J; Bogan, Janet R; Nghiem, Peter; Wang, Jiahui; Fan, Zheng; Howard, James F; Schatzberg, Scott J; Dow, Jennifer L; Grange, Robert W; Styner, Martin A; Hoffman, Eric P; Wagner, Kathryn R

    2012-02-01

    Mutations in the dystrophin gene cause Duchenne and Becker muscular dystrophy in humans and syndromes in mice, dogs, and cats. Affected humans and dogs have progressive disease that leads primarily to muscle atrophy. Mdx mice progress through an initial phase of muscle hypertrophy followed by atrophy. Cats have persistent muscle hypertrophy. Hypertrophy in humans has been attributed to deposition of fat and connective tissue (pseudohypertrophy). Increased muscle mass (true hypertrophy) has been documented in animal models. Muscle hypertrophy can exaggerate postural instability and joint contractures. Deleterious consequences of muscle hypertrophy should be considered when developing treatments for muscular dystrophy.

  13. MRI of nasopharyngeal adenoid hypertrophy.

    Science.gov (United States)

    Surov, Alexey; Ryl, Ina; Bartel-Friedrich, Sylvia; Wienke, Andreas; Kösling, Sabrina

    2016-10-01

    Nasopharyngeal adenoid hypertrophy (NAH) is a typical benign lesion. Due to involution, nasopharyngeal lymphatic tissue usually is not found in adults beyond the 30th to 40th year of life. However, occasionally NAH has been recognized after the 50th or 60th year. The aim of this study is to identify the frequency of NAH and to analyze its MRI findings in different age groups. From 2007 to 2011, 6693 MR investigations of the head were performed at our institution. MRI was obtained with a 1.5 T MRI device. NAH was identified in 18.0% of the patients. The frequency of NAH varied from 60.3% to 1.0% in the different age groups. The mean size of NAH was 23.2 ± 4.5 mm in cranio-caudal, 31.1 ± 5.2 mm in left-right, and 14.2 ± 4.1 mm in the anterior-posterior direction. The left-right and cranio-caudal sizes of NAH were largest in the 0-9 age group and decreased with age. On T1-w images most lesions (95.4%) were hypointense in comparison to the adjacent musculature. On T2-w fat-saturated images 82.4% of the lesions were hyperintense. After intravenous administration of contrast medium most lesions showed a slight enhancement (58.6%). Moderate enhancement was seen in 32.4% and a marked enhancement was identified in 9.0%. In the 0-9 age group most lesions showed a slight enhancement. Cysts within NAH were identified in 433 cases (35.9%). The frequency of cysts increased continuously with age, namely from 10.9% to 65.2%.

  14. Fibrin ring granulomas in hepatitis A.

    Science.gov (United States)

    Ruel, M; Sevestre, H; Henry-Biabaud, E; Courouce, A M; Capron, J P; Erlinger, S

    1992-12-01

    Fibrin ring granuloma is characterized by a fibrinous ring surrounding a central fat vacuole. It has been found in the liver and bone marrow of patients with Q fever, and occasionally with visceral leishmaniasis, cytomegalovirus, Epstein-Barr virus, Staphylococcus epidermidis infections, Hodgkin's lymphoma, and hypersensitivity to allopurinol. We describe a case of serologically confirmed viral hepatitis A with this lesion in the liver biopsy. A false positive anti-hepatitis A virus IgM result has been excluded. This is, to our knowledge, the second reported case of type A hepatitis with hepatic fibrin ring granulomas. It confirms that hepatitis A should be included in the differential diagnosis of this lesion.

  15. Myocardial hypertrophy induces carotid body hyperplasia.

    Science.gov (United States)

    Sivridis, Efthimios; Pavlidis, Pavlos; Fiska, Aliki; Pitsiava, Dimitra; Giatromanolaki, Alexandra

    2011-01-01

    The carotid bodies tend to enlarge after long-standing cardiopulmonary disease. Our objective was to investigate whether cardiac hypertrophy is associated with carotid body hyperplasia. Fifteen autopsy cases with combined left and right ventricular hypertrophy were examined and compared with two control groups (16 cases). The study involved a meticulous dissection of carotid bifurcations, thin serial sections, and morphometric analysis of carotid body volume and cell types (progenitor, dark, light, and sustentacular). There was a significant increase in sustentacular cells in all individuals with cardiac hypertrophy, which was not drug-induced, and accompanied by a similar increase in carotid body volume. Dark or light cell accumulation was detected focally and only in three instances. It appears that the generalized sustentacular cell hyperplasia is the result of long-standing hypoxia, while a superimposed focal prominence of dark or light cells may be proliferative or metaplastic in nature and attributed to short-term hypoxia.

  16. Carpal tunnel syndrome: an unusual presentation of brachial hypertrophy.

    OpenAIRE

    Shenoy, K. T.; Saha, P. K.; Ravindran, M

    1980-01-01

    A patient with carpal tunnel syndrome in association with congenital hypertrophy of right upper limb is described. The median nerve also showed hypertrophy. The symptoms were relieved by decompression of the carpal tunnel.

  17. Lingual Tonsil Hypertrophy: rescuing the airway with videolaryngoscopy.

    Science.gov (United States)

    Souki, Fouad Ghazi; Yemul-Golhar, Shweta Rahul; Zeyed, Yosaf; Pretto, Ernesto A

    2016-12-01

    Lingual tonsils are lymphatic tissues located at the base of the tongue that may hypertrophy causing difficulty and sometimes inability to ventilate or intubate during anesthesia. Routine airway assessment fails to diagnose lingual tonsil hypertrophy. There is limited experience with use of videolaryngoscopy in cases of lingual tonsil hypertrophy. We present a case of difficult airway due to unanticipated lingual tonsil hypertrophy successfully managed by atypical video laryngoscope positioning. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Visual Surround Suppression in Schizophrenia

    Science.gov (United States)

    Tibber, Marc S.; Anderson, Elaine J.; Bobin, Tracy; Antonova, Elena; Seabright, Alice; Wright, Bernice; Carlin, Patricia; Shergill, Sukhwinder S.; Dakin, Steven C.

    2013-01-01

    Compared to unaffected observers patients with schizophrenia (SZ) show characteristic differences in visual perception, including a reduced susceptibility to the influence of context on judgments of contrast – a manifestation of weaker surround suppression (SS). To examine the generality of this phenomenon we measured the ability of 24 individuals with SZ to judge the luminance, contrast, orientation, and size of targets embedded in contextual surrounds that would typically influence the target’s appearance. Individuals with SZ demonstrated weaker SS compared to matched controls for stimuli defined by contrast or size, but not for those defined by luminance or orientation. As perceived luminance is thought to be regulated at the earliest stages of visual processing our findings are consistent with a suppression deficit that is predominantly cortical in origin. In addition, we propose that preserved orientation SS in SZ may reflect the sparing of broadly tuned mechanisms of suppression. We attempt to reconcile these data with findings from previous studies. PMID:23450069

  19. Left ventricular hypertrophy : virtuous intentions, malign consequences

    NARCIS (Netherlands)

    Pokharel, S; Sharma, UC; Pinto, YM

    2003-01-01

    Left ventricular hypertrophy (LVH) is currently the focus of intense cardiovascular research, with the resultant rapid evolution of novel concepts relating to its exceedingly complex pathophysiology. In addition to the alterations in signal transduction and disturbances in Ca2+ homeostasis, there ar

  20. [A girl with congenital hemifacial hypertrophy

    NARCIS (Netherlands)

    Broeke, S.M. van den; Wolvius, E.B.; Adrichem, L.N. van; Baat, C. de

    2006-01-01

    A girl with congenital hemifacial hypertrophy had been observed and treated by a multidisciplinary team for craniofacial disorders in an academic medical centre since birth. At the age of 8 she was treated on account of considerable facial asymmetry and multiple intraoral problems. The two-step surg

  1. Tripartite motif 32 prevents pathological cardiac hypertrophy.

    Science.gov (United States)

    Chen, Lijuan; Huang, Jia; Ji, Yanxiao; Zhang, Xiaojing; Wang, Pixiao; Deng, Keqiong; Jiang, Xi; Ma, Genshan; Li, Hongliang

    2016-05-01

    TRIM32 (tripartite motif 32) is widely accepted to be an E3 ligase that interacts with and eventually ubiquitylates multiple substrates. TRIM32 mutants have been associated with LGMD-2H (limb girdle muscular dystrophy 2H). However, whether TRIM32 is involved in cardiac hypertrophy induced by biomechanical stresses and neurohumoral mediators remains unclear. We generated mice and isolated NRCMs (neonatal rat cardiomyocytes) that overexpressed or were deficient in TRIM32 to investigate the effect of TRIM32 on AB (aortic banding) or AngII (angiotensin II)-mediated cardiac hypertrophy. Echocardiography and both pathological and molecular analyses were used to determine the extent of cardiac hypertrophy and subsequent fibrosis. Our results showed that overexpression of TRIM32 in the heart significantly alleviated the hypertrophic response induced by pressure overload, whereas TRIM32 deficiency dramatically aggravated pathological cardiac remodelling. Similar results were also found in cultured NRCMs incubated with AngII. Mechanistically, the present study suggests that TRIM32 exerts cardioprotective action by interruption of Akt- but not MAPK (mitogen-dependent protein kinase)-dependent signalling pathways. Additionally, inactivation of Akt by LY294002 offset the exacerbated hypertrophic response induced by AB in TRIM32-deficient mice. In conclusion, the present study indicates that TRIM32 plays a protective role in AB-induced pathological cardiac remodelling by blocking Akt-dependent signalling. Therefore TRIM32 could be a novel therapeutic target for the prevention of cardiac hypertrophy and heart failure. © 2016 The Author(s).

  2. Compensatory Hypertrophy After Living Donor Nephrectomy.

    Science.gov (United States)

    Chen, K W; Wu, M W F; Chen, Z; Tai, B C; Goh, Y S B; Lata, R; Vathsala, A; Tiong, H Y

    2016-04-01

    Previous studies have shown that kidney volume enhances the estimation of glomerular filtration rate (eGFR) in kidney donors. This study aimed to describe the phenomenon of compensatory hypertrophy after donor nephrectomy as measured on computerized tomographic (CT) scans. An institutional Domain Specific Review Board (DSRB)-approved study involved approaching kidney donors to have a follow up CT scan from 6 months to 1 year after surgery; 29 patients participated; 55% were female. Clinical chart review was performed, and the patient's remaining kidney volume was measured before and after surgery based on CT scans. eGFR was determined with the use of the Modification of Diet in Renal Disease equation. Mean parenchymal volume of the remaining kidney for this population (mean age, 44.3 ± 8.5 y) was 204.7 ± 82.5 cc before surgery and 250.5 ± 113.3 cc after donor nephrectomy. Compensatory hypertrophy occurred in 79.3% of patients (n = 23). Mean increase in remaining kidney volume was 22.4 ± 23.2% after donor nephrectomy in healthy individuals. Over a median follow-up of 52.9 ± 19.8 months, mean eGFR was 68.9 ± 12.4 mL/min/1.73 m(2), with 24.1% of patients (n = 7) in chronic kidney disease grade 3. Absolute and relative change in kidney volume was not associated with sex, race, surgical approach, or background of hypertension (P = NS). There was a trend of decreased hypertrophy with increasing age (P = .5; Spearman correlation, -0.12). In healthy kidney donors, compensatory hypertrophy of the remaining kidney occurs in 79.3% of the patients, with an average increment of about 22.4%. Older patients may have a blunted compensatory hypertrophy response after surgery. Copyright © 2016 Elsevier Inc. All rights reserved.

  3. Hepatitis C and Incarceration

    Science.gov (United States)

    HEPATITIS C & INCARCERATION What is hepatitis? “Hepatitis” means inflammation or swelling of the liver. The liver is an important ... viral hepatitis: Hepatitis A, Hepatitis B, and Hepatitis C. They are all different from each other and ...

  4. EVALUATION AND COMPARISON OF HYPERTROPHY OF THENONEMBOLIZED LOBE OF THE LIVER AFTER DOUBLE AND SINGLEEMBOLIZATION

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    Objective To evaluate and compare the different result in hypertrophy of remained live lobe after double and single embolization. Methods Combined hepatic arterial embolization(HAE) with portal venous emboliza tion(PVE), HAE and sham operation were carried on the median and left lobes of the livers in normal and cirrhotic rats respectively. Three days later, the volume of the right lobe of the liver and its mitotic index and GPT content per gram protein were measured. Results In hormel rats, the indications mentioned increased significantly in experimen tal rats compared to control rats. The indications mentioned above also increased significantly in HAE+PVE group compared to HAE group. However, they increased more slightly in cirrhotic rats than in normal rats. Enlargement of the nonembolized part of the liver after double embolization is a result of hypertrophy, which enhanced the reserve function of the liver. Considering various degree of hypertrophy of liver cell and enhancement of reserve function, double embolization is more excellent than single embolization when the same volume liver is embolized.

  5. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... of terms Donate Today Enroll in 123 What is Hepatic Encephalopathy? Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy or PSE, is a condition that causes temporary worsening of brain ...

  6. Hepatitis A

    Science.gov (United States)

    ... an inflammation of the liver. One type, hepatitis A, is caused by the hepatitis A virus (HAV). The disease spreads through contact with ... washed in untreated water Putting into your mouth a finger or object that came into contact with ...

  7. Hepatitis B

    Science.gov (United States)

    ... information on hepatitis, both in the context of HIV coinfection and as a separate illness. NATAP provides coverage of key conferences, maintains a selection of hepatitis articles, and features an ask-the-expert forum on ...

  8. Hepatitis B

    Science.gov (United States)

    ... personal items (such as toothbrush, razor, and nail clippers) with a person who has the virus Were ... B virus Digestive system Aggressive hepatitis Gianotti-Crosti syndrome on the leg Hepatitis B References Kim DK, ...

  9. Hepatitis C

    Science.gov (United States)

    ... an inflammation of the liver. One type, hepatitis C, is caused by the hepatitis C virus (HCV). It usually spreads through contact with ... childbirth. Most people who are infected with hepatitis C don't have any symptoms for years. If ...

  10. Hypoksisk hepatitis

    DEFF Research Database (Denmark)

    Amadid, Hanan; Schiødt, Frank Vinholt

    2014-01-01

    Hypoxic hepatitis (HH), also known as ischaemic hepatitis or shock liver, is an acute liver injury caused by hepatic hypoxia. Cardiac failure, respiratory failure and septic shock are the main underlying conditions. In each of these conditions, several haemodynamic mechanisms lead to hepatic...... hypoxia. A shock state is observed in only 50% of cases. Thus, shock liver and ischaemic hepatitis are misnomers. HH can be a diagnostic pitfall but the diagnosis can be established when three criteria are met. Prognosis is poor and prompt identification and treatment of the underlying conditions...

  11. Surgical animal model of ventricular hypertrophy.

    Science.gov (United States)

    Marano, Giuseppe; Ferrari, Alberto U

    2007-01-01

    In response to an increased afterload, the myocardium undergoes a complex adaptation by which wall stress is normalized and cardiac output is maintained. Although the consensus suggests that the increase of the myocardial mass is a necessary adaptive process to accommodate the increased workload, there is growing evidence that hypertrophy ultimately results in pathological remodeling and deterioration of cardiac function. Despite intense investigation, our understanding of the cellular mechanisms that are responsible for the initiation and the maintenance of this adaptation is largely incomplete and preventing or regressing left ventricular hypertrophy (LVH) is a major challenge. This chapter provides a detailed description of the procedures necessary to induce LVH by coarctation of the transverse aorta and to analyze the effects of the increased hemodynamic load on cardiac mass, cardiomyocyte size, and cardiac performance.

  12. [Benign prostatic hypertrophy and prostate cancer].

    Science.gov (United States)

    Mourey, Loïc; Doumerc, Nicolas; Gaudin, Clément; Gérard, Stéphane; Balardy, Laurent

    2014-01-01

    Prostatic diseases are extremely common, especially in older men. Amongst them, benign prostatic hypertrophy may affect significantly the quality of life of patients by the symptoms it causes. It requires appropriate care. Prostate cancer is the second most common cancer in men after lung cancer and the fifth leading cause of cancer deaths in the world. It affects preferentially older men. An oncogeriatric approach is required for personalised care.

  13. Asymptomatic cardiopulmonary changes caused by adenoid hypertrophy.

    Science.gov (United States)

    Abdel-Aziz, Mosaad

    2011-07-01

    Adenoid hypertrophy is the most common cause of pediatric upper airway obstruction, and it can lead to cardiopulmonary complications such as pulmonary hypertension, cor pulmonale, and even heart failure. The aim of this study was to detect the asymptomatic cardiopulmonary changes that could happen in children with adenoid hypertrophy.Eighty children with adenoid hypertrophy were included in this study. Chest x-ray was used to assess the cardiothoracic ratio, whereas echocardiography was used for measuring the pulmonary arterial pressures, right ventricular diastolic filling parameters, and right ventricular end-diastolic diameters. All patients underwent adenoidectomy with or without tonsillectomy, and they were subjected again to echocardiographic assessment 6 months after the operation. No patient showed an increase in the cardiothoracic ratio on x-ray. Preoperative echocardiography showed an increase in pulmonary artery pressure (22.7 [SD, 3.8] mm Hg), a decrease in right ventricular diastolic filling parameters (E/A = 1.03 [SD, 0.17]), and an increase in right ventricular end-diastolic diameters (1.89 [SD, 0.19] cm). Postoperatively, pulmonary artery pressure decreased to 17.2 [SD, 2.1] mm Hg, right ventricular diastolic filling (E/A) increased to 1.25 [SD, 0.11], and right ventricular end-diastolic diameters decreased to 1.68 [SD, 0.12] cm. The comparison between preoperative and postoperative results for each individual parameter was statistically significant. Clinically asymptomatic cardiopulmonary changes due to adenoid hypertrophy are not rare. Early diagnosis and treatment of upper airway obstruction can prevent these serious complications. Echocardiographic examination should be recommended for these patients as a part of preoperative preparation to avoid anesthetic complications.

  14. Hepatitis A through E (Viral Hepatitis)

    Science.gov (United States)

    ... Nutrition Clinical Trials Primary Sclerosing Cholangitis Wilson Disease Hepatitis (Viral) View or Print All Sections What is Viral Hepatitis? Viral hepatitis is an infection that causes liver inflammation ...

  15. Gender and post-ischemic recovery of hypertrophied rat hearts

    Directory of Open Access Journals (Sweden)

    Popov Kirill M

    2006-03-01

    Full Text Available Abstract Background Gender influences the cardiac response to prolonged increases in workload, with differences at structural, functional, and molecular levels. However, it is unknown if post-ischemic function or metabolism of female hypertrophied hearts differ from male hypertrophied hearts. Thus, we tested the hypothesis that gender influences post-ischemic function of pressure-overload hypertrophied hearts and determined if the effect of gender on post-ischemic outcome could be explained by differences in metabolism, especially the catabolic fate of glucose. Methods Function and metabolism of isolated working hearts from sham-operated and aortic-constricted male and female Sprague-Dawley rats before and after 20 min of no-flow ischemia (N = 17 to 27 per group were compared. Parallel series of hearts were perfused with Krebs-Henseleit solution containing 5.5 mM [5-3H/U-14C]-glucose, 1.2 mM [1-14C]-palmitate, 0.5 mM [U-14C]-lactate, and 100 mU/L insulin to measure glycolysis and glucose oxidation in one series and oxidation of palmitate and lactate in the second. Statistical analysis was performed using two-way analysis of variance. The sequential rejective Bonferroni procedure was used to correct for multiple comparisons and tests. Results Female gender negatively influenced post-ischemic function of non-hypertrophied hearts, but did not significantly influence function of hypertrophied hearts after ischemia such that mass-corrected hypertrophied heart function did not differ between genders. Before ischemia, glycolysis was accelerated in hypertrophied hearts, but to a greater extent in males, and did not differ between male and female non-hypertrophied hearts. Glycolysis fell in all groups after ischemia, except in non-hypertrophied female hearts, with the reduction in glycolysis after ischemia being greatest in males. Post-ischemic glycolytic rates were, therefore, similarly accelerated in hypertrophied male and female hearts and higher in

  16. [Autoimmune hepatitis].

    Science.gov (United States)

    Ostojić, Rajko

    2003-01-01

    Autoimmune hepatitis is an unresolving, hepatocellular inflammation of unknown cause that is characterized by the presence of periportal hepatitis on histologic examination, tissue autoantibodies in serum, and hypergammaglobulinemia. By international consensus, the designation autoimmune hepatitis has replaced alternative terms for the condition. Three types of autoimmune hepatitis have been proposed based on immunoserologic findings. Type 1 autoimmune hepatitis is characterized by the presence of antinuclear antibodies (ANA) or smooth muscle antibodies (SMA) (or both) in serum. Seventy percent of patients with type 1 of autoimmune hepatitis are women. This type is the most common form and accounts for at least 80% of cases. Type 2 is characterized by the presence of antibodies to liver-kidney microsome type 1 (anti-LKM1) in serum. Patients with this type of autoimmune hepatitis are predominantly children. Type 3 autoimmune hepatitis is characterized by the presence of antibodies to soluble liver antigen (anti-SLA) in serum. There are no individual features that are pathognomonic of autoimmune hepatitis, and its diagnosis requires the confident exclusion of other conditions. The large majority of patients show satisfactory response to corticosteroid (usually prednisone or prednisolone) therapy. For the past 30 years it has been customary to add azathioprine as a "steroid sparing" agent to allow lower doses of steroids to be used and remission, once achieved, can be sustained in many patients with azathioprine alone after steroid withdrawal. Patients with autoimmune hepatitis who have decompensated during or after corticosteroid therapy are candidates for liver transplantation.

  17. Binaural Rendering in MPEG Surround

    Directory of Open Access Journals (Sweden)

    Kristofer Kjörling

    2008-04-01

    Full Text Available This paper describes novel methods for evoking a multichannel audio experience over stereo headphones. In contrast to the conventional convolution-based approach where, for example, five input channels are filtered using ten head-related transfer functions, the current approach is based on a parametric representation of the multichannel signal, along with either a parametric representation of the head-related transfer functions or a reduced set of head-related transfer functions. An audio scene with multiple virtual sound sources is represented by a mono or a stereo downmix signal of all sound source signals, accompanied by certain statistical (spatial properties. These statistical properties of the sound sources are either combined with statistical properties of head-related transfer functions to estimate “binaural parameters” that represent the perceptually relevant aspects of the auditory scene or used to create a limited set of combined head-related transfer functions that can be applied directly on the downmix signal. Subsequently, a binaural rendering stage reinstates the statistical properties of the sound sources by applying the estimated binaural parameters or the reduced set of combined head-related transfer functions directly on the downmix. If combined with parametric multichannel audio coders such as MPEG Surround, the proposed methods are advantageous over conventional methods in terms of perceived quality and computational complexity.

  18. Reduced surround inhibition in musicians.

    Science.gov (United States)

    Shin, Hae-Won; Kang, Suk Y; Hallett, Mark; Sohn, Young H

    2012-06-01

    To investigate whether surround inhibition (SI) in the motor system is altered in professional musicians, we performed a transcranial magnetic stimulation (TMS) study in 10 professional musicians and 15 age-matched healthy non-musicians. TMS was set to be triggered by self-initiated flexion of the index finger at different intervals ranging from 3 to 1,000 ms. Average motor evoked potential (MEP) amplitudes obtained from self-triggered TMS were normalized to average MEPs of the control TMS at rest and expressed as a percentage. Normalized MEP amplitudes of the abductor digiti minimi (ADM) muscles were compared between the musicians and non-musicians with the primary analysis being the intervals between 3 and 80 ms (during the movement). A mixed-design ANOVA revealed a significant difference in normalized ADM MEPs during the index finger flexion between groups, with less SI in the musicians. This study demonstrated that the functional operation of SI is less strong in musicians than non-musicians, perhaps due to practice of movement synergies involving both muscles. Reduced SI, however, could lead susceptible musicians to be prone to develop task-specific dystonia.

  19. Binaural Rendering in MPEG Surround

    Science.gov (United States)

    Breebaart, Jeroen; Villemoes, Lars; Kjörling, Kristofer

    2008-12-01

    This paper describes novel methods for evoking a multichannel audio experience over stereo headphones. In contrast to the conventional convolution-based approach where, for example, five input channels are filtered using ten head-related transfer functions, the current approach is based on a parametric representation of the multichannel signal, along with either a parametric representation of the head-related transfer functions or a reduced set of head-related transfer functions. An audio scene with multiple virtual sound sources is represented by a mono or a stereo downmix signal of all sound source signals, accompanied by certain statistical (spatial) properties. These statistical properties of the sound sources are either combined with statistical properties of head-related transfer functions to estimate "binaural parameters" that represent the perceptually relevant aspects of the auditory scene or used to create a limited set of combined head-related transfer functions that can be applied directly on the downmix signal. Subsequently, a binaural rendering stage reinstates the statistical properties of the sound sources by applying the estimated binaural parameters or the reduced set of combined head-related transfer functions directly on the downmix. If combined with parametric multichannel audio coders such as MPEG Surround, the proposed methods are advantageous over conventional methods in terms of perceived quality and computational complexity.

  20. Chondrocyte hypertrophy in skeletal development, growth, and disease.

    Science.gov (United States)

    Sun, Margaret Man-Ger; Beier, Frank

    2014-03-01

    Most of our bones form through the process of endochondral ossification, which is tightly regulated by the activity of the cartilage growth plate. Chondrocyte maturation through the various stages of growth plate physiology ultimately results in hypertrophy. Chondrocyte hypertrophy is an essential contributor to longitudinal bone growth, but recent data suggest that these cells also play fundamental roles in signaling to other skeletal cells, thus coordinating endochondral ossification. On the other hand, ectopic hypertrophy of articular chondrocytes has been implicated in the pathogenesis of osteoarthritis. Thus, a better understanding of the processes that control chondrocyte hypertrophy in the growth plate as well as in articular cartilage is required for improved management of both skeletal growth disorders and osteoarthritis. This review summarizes recent findings on the regulation of hypertrophic chondrocyte differentiation, the cellular mechanisms involved in hypertrophy, and the role of chondrocyte hypertrophy in skeletal physiology and pathophysiology.

  1. Cardiac hypertrophy involves both myocyte hypertrophy and hyperplasia in anemic zebrafish.

    Directory of Open Access Journals (Sweden)

    Xiaojing Sun

    Full Text Available BACKGROUND: An adult zebrafish heart possesses a high capacity of regeneration. However, it has been unclear whether and how myocyte hyperplasia contributes to cardiac remodeling in response to biomechanical stress and whether myocyte hypertrophy exists in the zebrafish. To address these questions, we characterized the zebrafish mutant tr265/tr265, whose Band 3 mutation disrupts erythrocyte formation and results in anemia. Although Band 3 does not express and function in the heart, the chronic anemia imposes a sequential biomechanical stress towards the heart. METHODOLOGY/PRINCIPAL FINDINGS: Hearts of the tr265/tr265 Danio rerio mutant become larger than those of the sibling by week 4 post fertilization and gradually exhibit characteristics of human cardiomyopathy, such as muscular disarray, re-activated fetal gene expression, and severe arrhythmia. At the cellular level, we found both increased individual cardiomyocyte size and increased myocyte proliferation can be detected in week 4 to week 12 tr265/tr265 fish. Interestingly, all tr265/tr265 fish that survive after week-12 have many more cardiomyocytes of smaller size than those in the sibling, suggesting that myocyte hyperplasia allows the long-term survival of these fish. We also show the cardiac hypertrophy process can be recapitulated in wild-type fish using the anemia-inducing drug phenylhydrazine (PHZ. CONCLUSIONS/SIGNIFICANCE: The anemia-induced cardiac hypertrophy models reported here are the first adult zebrafish cardiac hypertrophy models characterized. Unlike mammalian models, both cardiomyocyte hypertrophy and hyperplasia contribute to the cardiac remodeling process in these models, thus allowing the effects of cardiomyocyte hyperplasia on cardiac remodeling to be studied. However, since anemia can induce effects on the heart other than biomechanical, non-anemic zebrafish cardiac hypertrophy models shall be generated and characterized.

  2. [Association of post-radiation focal muscular atrophy and hypertrophy].

    Science.gov (United States)

    Serratrice, G; Sangla, I; Pouget, J; Azulay, J P

    1993-01-01

    We report a 48 year old woman who had radiotherapy for uterine carcinoma and who developed amyotrophy and muscle hypertrophy in one lower limb. Very few cases of post-radiation monomelic amyotrophy have been reported. On the other hand denervation hypertrophy was presumed to be well known. The seat of the lesions was presumed to be radicular and spinal. The mechanism of atrophy and hypertrophy is discussed.

  3. Hepatitis B and Hepatitis C in Pregnancy

    Science.gov (United States)

    ... and hepatitis C infections during pregnancy? • How is hepatitis B virus infection spread? • What is acute hepatitis B virus infection? • What is chronic hepatitis B virus infection? • Can ...

  4. Feature Hepatitis: Hepatitis Can Strike Anyone

    Science.gov (United States)

    ... Navigation Bar Home Current Issue Past Issues Feature Hepatitis Hepatitis Can Strike Anyone Past Issues / Spring 2009 Table ... from all walks of life are affected by hepatitis, especially hepatitis C, the most common form of ...

  5. [Viscoelastic properties of relaxed papillary muscle at physiological hypertrophy].

    Science.gov (United States)

    Smoliuk, L T; Lisin, R V; Kuznetsov, D A; Protsenko, Iu L

    2012-01-01

    Viscoelastic properties of relaxed rat papillary muscles at physiological hypertrophy (intensive swimming for 5 weeks) have been obtained. It has been ascertained that viscoelastic properties of hypertrophied muscles are not significantly distinguished from those of control papillary muscles. A three-dimensional model of myocardial fascicle has been verified in compliance with experimental data of biomechanical tests of hypertrophied muscles. Elastic and viscous parameters of structural elements of the model negligibly differ from the parameters of the model of a control muscle. It is shown that physiological hypertrophy has a slight influence on viscoelastic properties of papillary muscles.

  6. Hepatitis (For Parents)

    Science.gov (United States)

    ... of three viruses: the hepatitis A virus the hepatitis B virus the hepatitis C virus In some rare cases, ... also called serum hepatitis) is caused by the hepatitis B virus (HBV). HBV can cause a wide range of ...

  7. Travelers' Health: Hepatitis C

    Science.gov (United States)

    ... 3 - Hepatitis B Chapter 3 - Hepatitis E Hepatitis C Deborah Holtzman INFECTIOUS AGENT Hepatitis C virus (HCV), ... to child. Map 3-05. Prevalence of hepatitis C virus infection 1 PDF Version (printable) 1 Disease ...

  8. Hepatitis (For Parents)

    Science.gov (United States)

    ... Old Feeding Your 1- to 2-Year-Old Hepatitis KidsHealth > For Parents > Hepatitis Print A A A ... to Call the Doctor en español Hepatitis About Hepatitis The word hepatitis simply means an inflammation of ...

  9. Travelers' Health: Hepatitis B

    Science.gov (United States)

    ... Chapter 3 - Hepatitis A Chapter 3 - Hepatitis C Hepatitis B Francisco Averhoff INFECTIOUS AGENT Hepatitis B is ... their exposures. Map 3-04. Prevalence of chronic hepatitis B virus infection among adults PDF Version (printable) ...

  10. Travelers' Health: Hepatitis C

    Science.gov (United States)

    ... Chapter 3 - Hepatitis B Chapter 3 - Hepatitis E Hepatitis C Deborah Holtzman INFECTIOUS AGENT Hepatitis C virus ( ... human blood Map 3-05. Global epidemiology of hepatitis C virus infection 1 PDF Version (printable) 1 ...

  11. Identification of cofactors influencing hypertrophy of the future liver remnant after portal vein embolization-the effect of collaterals on embolized liver volume.

    Science.gov (United States)

    Zeile, Martin; Bakal, Artur; Volkmer, Jan E; Stavrou, Gregor A; Dautel, Philip; Hoeltje, Jan; Stang, Axel; Oldhafer, Karl J; Brüning, Roland

    2016-12-01

    The purpose of this retrospective study was to monitor hypertrophy of future liver remnant following portal vein embolization (PVE) before planned extended right hepatectomy. However, because individual responses to PVE are highly variable, our focus was to identify cofactors of successful hypertrophy. 28 patients with primary or secondary liver tumours, mean age 64.1 ± 12.9 years, underwent PVE. Volumetric analysis of hypertrophy before and after PVE (median 39.0 ± 15.7 days) was performed. The embolized liver segments were investigated for occurrence of reperfusion of their portal branches. Blood parameters before PVE were additionally investigated. Patients were divided into responders (21/28) and non-responders (7/28) by post-PVE standardized future liver remnant being above or below 25%, respectively. No significant differences between the groups were found regarding biometric and volumetric parameters before PVE. In the entire group after PVE, the mean absolute increase of Segments 2 and 3 was 196.0 ± 84.7 cm(3) and the median relative increase was 46.6 ± 98.8%. The formation of left to right hepatic portoportal collaterals exhibited a negative correlation to successful hypertrophy (p = 0.004) as well as low plasma total protein (p = 0.019). Successful embolization of Segment IV showed only a trend to significance (p = 0.098). Cofactors associated with a favourable outcome regarding hypertrophy were the absence of collaterals in the control CT scans and high plasma total protein. Advances in knowledge: Portoportal collaterals negatively influence hypertrophy after PVE. On the other hand, plasma total protein is a positive prognostic indicator on hypertrophy of the liver in our cohort.

  12. Markers of collagen synthesis is related to blood pressure and vascular hypertrophy: a LIFE substudy

    DEFF Research Database (Denmark)

    Olsen, M H; Christensen, M K; Wachtell, K

    2005-01-01

    Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy...

  13. Compensatory renal hypertrophy following uninephrectomy is calcineurin-independent.

    Science.gov (United States)

    Williams, Clintoria R; Wynne, Brandi M; Walker, Makeeva; Hoover, Robert S; Gooch, Jennifer L

    2014-12-01

    Calcineurin is a calcium-dependent phosphatase that is involved in many cellular processes including hypertrophy. Inhibition or genetic loss of calcineurin blocks pathological cardiac hypertrophy and diabetic renal hypertrophy. However, calcineurin does not appear to be involved in physiological cardiac hypertrophy induced by exercise. The role of calcineurin in a compensatory, non-pathological model of renal hypertrophy has not been tested. Therefore, in this study, we examined activation of calcineurin and the effect of calcineurin inhibition or knockout on compensatory hypertrophy following uninephrectomy (UNX). UNX induces ~15% increase in the size of the remaining kidney; the data show no change in the generation of reactive oxygen species (ROS), Nox4 or transforming growth factor-β expression confirming the model as one of compensatory hypertrophy. Next, analyses of the remaining kidney reveal that total calcineurin activity is increased, and, to a lesser extent, transcriptional activity of the calcineurin substrate nuclear factor of activated T cell is up-regulated following UNX. However, inhibition of calcineurin with cyclosporine failed to prevent compensatory renal hypertrophy. Likewise, hypertrophy was comparable to WT in mice lacking either isoform of the catalytic subunit of calcineurin (CnAα-/- or CnAβ-/-). In conclusion, similar to its role in the heart, calcineurin is required for pathological but not compensatory renal hypertrophy. This separation of signalling pathways could therefore help further define key factors necessary for pathological hypertrophy including diabetic nephropathy. © 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

  14. Hepatitis A

    Science.gov (United States)

    ... inflammation of the liver.” This inflammation can be caused by a wide variety of toxins, drugs, and metabolic diseases, as well as infection. There are at least 5 hepatitis viruses. Hepatitis A is contracted when a child eats food or drinks water that is contaminated with the virus or has ...

  15. Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs

    DEFF Research Database (Denmark)

    Smith, Julie; Goetze, Jens Peter; Søndergaard, Lars

    2012-01-01

    peptides were unchanged. CONCLUSIONS: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may be substrate...

  16. Glucose Transporters in Cardiac Metabolism and Hypertrophy

    Science.gov (United States)

    Shao, Dan; Tian, Rong

    2016-01-01

    The heart is adapted to utilize all classes of substrates to meet the high-energy demand, and it tightly regulates its substrate utilization in response to environmental changes. Although fatty acids are known as the predominant fuel for the adult heart at resting stage, the heart switches its substrate preference toward glucose during stress conditions such as ischemia and pathological hypertrophy. Notably, increasing evidence suggests that the loss of metabolic flexibility associated with increased reliance on glucose utilization contribute to the development of cardiac dysfunction. The changes in glucose metabolism in hypertrophied hearts include altered glucose transport and increased glycolysis. Despite the role of glucose as an energy source, changes in other nonenergy producing pathways related to glucose metabolism, such as hexosamine biosynthetic pathway and pentose phosphate pathway, are also observed in the diseased hearts. This article summarizes the current knowledge regarding the regulation of glucose transporter expression and translocation in the heart during physiological and pathological conditions. It also discusses the signaling mechanisms governing glucose uptake in cardiomyocytes, as well as the changes of cardiac glucose metabolism under disease conditions. PMID:26756635

  17. Mechanotransduction in cardiac hypertrophy and failure.

    Science.gov (United States)

    Lyon, Robert C; Zanella, Fabian; Omens, Jeffrey H; Sheikh, Farah

    2015-04-10

    Cardiac muscle cells have an intrinsic ability to sense and respond to mechanical load through a process known as mechanotransduction. In the heart, this process involves the conversion of mechanical stimuli into biochemical events that induce changes in myocardial structure and function. Mechanotransduction and its downstream effects function initially as adaptive responses that serve as compensatory mechanisms during adaptation to the initial load. However, under prolonged and abnormal loading conditions, the remodeling processes can become maladaptive, leading to altered physiological function and the development of pathological cardiac hypertrophy and heart failure. Although the mechanisms underlying mechanotransduction are far from being fully elucidated, human and mouse genetic studies have highlighted various cytoskeletal and sarcolemmal structures in cardiac myocytes as the likely candidates for load transducers, based on their link to signaling molecules and architectural components important in disease pathogenesis. In this review, we summarize recent developments that have uncovered specific protein complexes linked to mechanotransduction and mechanotransmission within the sarcomere, the intercalated disc, and at the sarcolemma. The protein structures acting as mechanotransducers are the first step in the process that drives physiological and pathological cardiac hypertrophy and remodeling, as well as the transition to heart failure, and may provide better insights into mechanisms driving mechanotransduction-based diseases. © 2015 American Heart Association, Inc.

  18. Hypertrophy signaling pathways in experimental chronic aortic regurgitation

    DEFF Research Database (Denmark)

    Olsen, Niels Thue; Dimaano, Veronica L; Fritz-Hansen, Thomas

    2013-01-01

    The development of left ventricular hypertrophy and dysfunction in aortic regurgitation (AR) has only been sparsely studied experimentally. In a new model of chronic AR in rats, we examined activation of molecular pathways involved in myocardial hypertrophy. Chronic AR was produced by damaging one...... at both 2 and 12 weeks, while activation of calcium/calmodulin-dependent protein kinase II and extracellular regulated kinase 1/2 was unchanged. Expression of calcineurin and ANF was also unchanged. Eccentric hypertrophy and early cardiac dysfunction in experimental AR are associated with a pattern...... of activation of intracellular pathways different from that seen with pathological hypertrophy in pressure overload, and more similar to that associated with benign physiological hypertrophy....

  19. El entrenamiento de fuerza reduce la acidosis metabólica y la hipertrofia hepática y renal consecuentes del consumo de una dieta hiperproteica en ratas Resistance training reduces the metabolic acidosis and hepatic and renal hypertrophy caused by the consumption of a high protein diet in rats

    Directory of Open Access Journals (Sweden)

    V. A. Aparicio

    2011-12-01

    Full Text Available Introducción: El consumo de dietas hiperproteicas (HP podría tener un efecto adverso sobre la acidosis metabólica y la salud hepática y renal. Sin embargo, existen pocos estudios que analicen los efectos del entrenamiento de fuerza sobre los parámetros sensibles de ser alterados por dichas dietas. Material y métodos: Un total de 32 ratas Wistar adultas fueron distribuidas de forma aleatoria en 4 grupos experimentales (n = 8: dieta normoproteica o HP, con o sin entrenamiento de fuerza. Las dietas estuvieron basadas en un hidrolizado de proteína de lactosuero (whey. Tras 90 días de diseño experimental los animales fueron sacrificados para los posteriores análisis. Resultados y discusión: El consumo de una dieta HP provocó acidosis metabólica (hipercalcemia e hipocitraturia urinarias, acidificación del pH urinario y niveles elevados de urea plasmática, (P Introduction: High protein (HP diet consumption may adversely affect metabolic acidosis and hepatic and renal health. Despite such potentially adverse effect, there are only few studies analyzing the effects of resistance training on the parameters that could be altered by such diets. Material and methods: A total of 32 adult male Wistar rats were randomly distributed in 4 experimental groups (n = 8: normoprotein or HP diets, with or without resistance training. Diets were based on a whey protein hydrolyzate, and the experimental period lasted for 90 days. Results and discussion: Consumption of HP diets and resistance training significantly affected food intake, body composition and plasmatic levels of total cholesterol and triglycerides. Consumption of HP diets led to a considerable increase in liver and kidney weight (P < 0.001, urinary volume and acidity, as well as in the urinary excretion of Ca, with a parallel reduction in the urinary excretion of citrate (P < 0.05. The buffering action of resistance training on such diet-induced alterations was especially evident in the

  20. Congenital hepatic fibrosis, liver cell carcinoma and adult polycystic kidneys.

    Science.gov (United States)

    Manes, J L; Kissane, J M; Valdes, A J

    1977-06-01

    In reviewing the literature, we found no liver cell carcinoma (LCC) or well-documented adult polycystic kidneys (APK) associated with congenital hepatic fibrosis (CHF). We report a 69-year-old man with CHF, LCC, APK, duplication cyst of distal portion of stomach, two calcified splenic artery aneurysms, myocardial fibrosis and muscular hypertrophy of esophagus. The LCC was grossly predunculated and microscopically showed prominent fibrosis and hyaline intracytoplasmic inclusions in the tumor cells.

  1. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... Symptoms to look for Caregiver Support Caregiver Stories Home › What is Hepatic Encephalopathy? Why Your Liver is ... questions about HE, one step at a time. Home About Us Ways to Give Contact Us Privacy ...

  2. Hepatitis A

    Science.gov (United States)

    ... Hepatitis A is more common in parts of Africa, Asia, Central and South America, and Eastern Europe ... la salud en español Health Statistics Healthy Moments Radio Broadcast Clinical Trials For Health Professionals Diabetes Discoveries & ...

  3. Autoimmune hepatitis.

    Science.gov (United States)

    Heneghan, Michael A; Yeoman, Andrew D; Verma, Sumita; Smith, Alastair D; Longhi, Maria Serena

    2013-10-26

    Autoimmune hepatitis is a disease of the hepatic parenchyma that can present in acute or chronic forms. In common with many autoimmune diseases, autoimmune hepatitis is associated with non-organ-specific antibodies in the context of hepatic autoimmunity. This dichotomy has made definition of a unifying hypothesis in the pathophysiology of the disease difficult, although data from the past 8 years have drawn attention to the role of regulatory T cells. Several triggers have been identified, and the disease arises in genetically susceptible individuals. Clinical and biochemical remission is achievable in up to 85% of cases. For the remaining patients, alternative immunosuppression strategies are an option. Liver transplantation provides an excellent outcome for patients with acute liver failure or complications of end-stage liver disease, including hepatocellular carcinoma. Variant or overlapping syndromes are worthy of consideration when unexpected disease features arise.

  4. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... Get Worse? How is HE Diagnosed? Prior to Treatment Who treats HE? Preparing for your Medical Appointment Hepatic Encephalopathy Treatment Options Treatment Basics Treatment Medications Importance of Adhering ...

  5. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... is a condition that causes temporary worsening of brain function in people with advanced liver disease. When ... travel through your body until they reach your brain, causing mental and physical symptoms of HE. Hepatic ...

  6. Hepatitis B

    Science.gov (United States)

    ... using an infected person’s razor, toothbrush, or nail clippers You can’t get hepatitis B from being ... personal items such as toothbrushes, razors, or nail clippers using a latex or polyurethane condom during sex ...

  7. Hepatic ischemia

    Science.gov (United States)

    ... or oxygen, causing injury to liver cells. Causes Low blood pressure from any condition can lead to hepatic ischemia. ... leading to reduced blood flow (vasculitis) Symptoms If low blood pressure continues for a long time, you may feel ...

  8. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... Get Worse? How is HE Diagnosed? Prior to Treatment Who treats HE? Preparing for your Medical Appointment Hepatic Encephalopathy Treatment Options Treatment Basics Treatment Medications Importance of Adhering ...

  9. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... the Stages of Hepatic Encephalopathy? What Triggers or Can Cause HE to Get Worse? How is HE ... liver disease. When your liver is damaged it can no longer remove toxic substances from your blood. ...

  10. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... to Treatment Who treats HE? Preparing for your Medical Appointment Hepatic Encephalopathy Treatment Options Treatment Basics Treatment ... treatment. Being a fully-informed participant in your medical care is an important factor in staying as ...

  11. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... is a condition that causes temporary worsening of brain function in people with advanced liver disease. When ... travel through your body until they reach your brain, causing mental and physical symptoms of HE. Hepatic ...

  12. Hepatic Encephalopathy

    Medline Plus

    Full Text Available ... Hepatic Encephalopathy so you can tell your doctor right away if you think you may have it. ... American Liver Foundation © 2017 American Liver Foundation. All rights reserved. Funding for the HE123 - Diagnosis, Treatment and ...

  13. Hepatitis autoinmune.

    OpenAIRE

    LOJA OROPEZA, David; VILCA VASQUEZ, Maricela; AVILES GONZAGA, Roberto

    2013-01-01

    Three patients with autoinmune hepatitis type 1 diagnosed at the Hospital Nacional Arzobispo Loayza in Lima-Perú, between 1993 and 1995, are here reported, emphasis is made on the clinical, histological and therapeutical aspects.

  14. Contour detection by surround suppression of texture

    NARCIS (Netherlands)

    Petkov, Nicolai; Tavares, JMRS; Jorge, RMN

    2007-01-01

    Based on a keynote lecture at Complmage 2006, Coimbra, Oct. 20-21, 2006, an overview is given of our activities in modelling and using surround inhibition for contour detection. The effect of suppression of a line or edge stimulus by similar surrounding stimuli is known from visual perception studie

  15. Cardiac Hypertrophy Involves both Myocyte Hypertrophy and Hyperplasia in Anemic Zebrafish

    OpenAIRE

    Xiaojing Sun; Tiffany Hoage; Ping Bai; Yonghe Ding; Zhenyue Chen; Ruilin Zhang; Wei Huang; Ashad Jahangir; Barry Paw; Yi-Gang Li; Xiaolei Xu

    2009-01-01

    BACKGROUND: An adult zebrafish heart possesses a high capacity of regeneration. However, it has been unclear whether and how myocyte hyperplasia contributes to cardiac remodeling in response to biomechanical stress and whether myocyte hypertrophy exists in the zebrafish. To address these questions, we characterized the zebrafish mutant tr265/tr265, whose Band 3 mutation disrupts erythrocyte formation and results in anemia. Although Band 3 does not express and function in the heart, the chroni...

  16. Disruption of mindin exacerbates cardiac hypertrophy and fibrosis

    Science.gov (United States)

    Bian, Zhou-Yan; Wei, Xiang; Deng, Shan; Tang, Qi-Zhu; Feng, Jinghua; Zhang, Yan; Liu, Chen; Jiang, Ding-Sheng; Yan, Ling; Zhang, Lian-Feng; Chen, Manyin; Fassett, John; Chen, Yingjie; He, You-Wen; Yang, Qinglin; Liu, Peter P.

    2013-01-01

    Cardiac hypertrophy is a response of the myocardium to increased workload and is characterised by an increase of myocardial mass and an accumulation of extracellular matrix (ECM). As an ECM protein, an integrin ligand, and an angiogenesis inhibitor, all of which are key players in cardiac hypertrophy, mindin is an attractive target for therapeutic intervention to treat or prevent cardiac hypertrophy and heart failure. In this study, we investigated the role of mindin in cardiac hypertrophy using littermate Mindin knockout (Mindin−/−) and wild-type (WT) mice. Cardiac hypertrophy was induced by aortic banding (AB) or angiotensin II (Ang II) infusion in Mindin−/− and WT mice. The extent of cardiac hypertrophy was quantitated by echocardiography and by pathological and molecular analyses of heart samples. Mindin−/− mice were more susceptible to cardiac hypertrophy and fibrosis in response to AB or Ang II stimulation than wild type. Cardiac function was also markedly exacerbated during both systole and diastole in Mindin−/− mice in response to hypertrophic stimuli. Western blot assays further showed that the activation of AKT/glycogen synthase kinase 3β (GSK3β) signalling in response to hypertrophic stimuli was significantly increased in Mindin−/− mice. Moreover, blocking AKT/GSK3β signalling with a pharmacological AKT inhibitor reversed cardiac abnormalities in Mindin−/− mice. Our data show that mindin, as an intrinsic cardioprotective factor, prevents maladaptive remodelling and the transition to heart failure by blocking AKT/GSK3β signalling. PMID:22367478

  17. Intrinsic-mediated caspase activation is essential for cardiomyocyte hypertrophy

    Science.gov (United States)

    Putinski, Charis; Abdul-Ghani, Mohammad; Stiles, Rebecca; Brunette, Steve; Dick, Sarah A.; Fernando, Pasan; Megeney, Lynn A.

    2013-01-01

    Cardiomyocyte hypertrophy is the cellular response that mediates pathologic enlargement of the heart. This maladaptation is also characterized by cell behaviors that are typically associated with apoptosis, including cytoskeletal reorganization and disassembly, altered nuclear morphology, and enhanced protein synthesis/translation. Here, we investigated the requirement of apoptotic caspase pathways in mediating cardiomyocyte hypertrophy. Cardiomyocytes treated with hypertrophy agonists displayed rapid and transient activation of the intrinsic-mediated cell death pathway, characterized by elevated levels of caspase 9, followed by caspase 3 protease activity. Disruption of the intrinsic cell death pathway at multiple junctures led to a significant inhibition of cardiomyocyte hypertrophy during agonist stimulation, with a corresponding reduction in the expression of known hypertrophic markers (atrial natriuretic peptide) and transcription factor activity [myocyte enhancer factor-2, nuclear factor kappa B (NF-κB)]. Similarly, in vivo attenuation of caspase activity via adenoviral expression of the biologic effector caspase inhibitor p35 blunted cardiomyocyte hypertrophy in response to agonist stimulation. Treatment of cardiomyocytes with procaspase 3 activating compound 1, a small-molecule activator of caspase 3, resulted in a robust induction of the hypertrophy response in the absence of any agonist stimulation. These results suggest that caspase-dependent signaling is necessary and sufficient to promote cardiomyocyte hypertrophy. These results also confirm that cell death signal pathways behave as active remodeling agents in cardiomyocytes, independent of inducing an apoptosis response. PMID:24101493

  18. Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy

    Science.gov (United States)

    Li, Ran; Bai, Jian; Ding, Liang; Gu, Rong; Wang, Lian; Xu, Biao

    2016-01-01

    Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade leading to cardiac hypertrophy is unknown. To evaluate the role of miR-99a in cardiac hypertrophy, we assessed the expression of miR-99a in hypertrophic cardiomyocytes induced by isoprenaline (ISO)/angiotensin-II (Ang II) and in mice model of cardiac hypertrophy induced by transverse aortic constriction (TAC). Expression of miR-99a was evaluated in these hypertrophic cells and hearts. We also found that miR-99a expression was highly correlated with cardiac function of mice with heart failure (8 weeks after TAC surgery). Overexpression of miR-99a attenuated cardiac hypertrophy in TAC mice and cellular hypertrophy in stimuli treated cardiomyocytes through down-regulation of expression of mammalian target of rapamycin (mTOR). These results indicate that miR-99a negatively regulates physiological hypertrophy through mTOR signaling pathway, which may provide a new therapeutic approach for pressure-overload heart failure. PMID:26914935

  19. Regression of Pathological Cardiac Hypertrophy: Signaling Pathways and Therapeutic Targets

    Science.gov (United States)

    Hou, Jianglong; Kang, Y. James

    2012-01-01

    Pathological cardiac hypertrophy is a key risk factor for heart failure. It is associated with increased interstitial fibrosis, cell death and cardiac dysfunction. The progression of pathological cardiac hypertrophy has long been considered as irreversible. However, recent clinical observations and experimental studies have produced evidence showing the reversal of pathological cardiac hypertrophy. Left ventricle assist devices used in heart failure patients for bridging to transplantation not only improve peripheral circulation but also often cause reverse remodeling of the geometry and recovery of the function of the heart. Dietary supplementation with physiologically relevant levels of copper can reverse pathological cardiac hypertrophy in mice. Angiogenesis is essential and vascular endothelial growth factor (VEGF) is a constitutive factor for the regression. The action of VEGF is mediated by VEGF receptor-1, whose activation is linked to cyclic GMP-dependent protein kinase-1 (PKG-1) signaling pathways, and inhibition of cyclic GMP degradation leads to regression of pathological cardiac hypertrophy. Most of these pathways are regulated by hypoxia-inducible factor. Potential therapeutic targets for promoting the regression include: promotion of angiogenesis, selective enhancement of VEGF receptor-1 signaling pathways, stimulation of PKG-1 pathways, and sustention of hypoxia-inducible factor transcriptional activity. More exciting insights into the regression of pathological cardiac hypertrophy are emerging. The time of translating the concept of regression of pathological cardiac hypertrophy to clinical practice is coming. PMID:22750195

  20. Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy.

    Science.gov (United States)

    Li, Qiaoling; Xie, Jun; Wang, Bingjian; Li, Ran; Bai, Jian; Ding, Liang; Gu, Rong; Wang, Lian; Xu, Biao

    2016-01-01

    Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade leading to cardiac hypertrophy is unknown. To evaluate the role of miR-99a in cardiac hypertrophy, we assessed the expression of miR-99a in hypertrophic cardiomyocytes induced by isoprenaline (ISO)/angiotensin-II (Ang II) and in mice model of cardiac hypertrophy induced by transverse aortic constriction (TAC). Expression of miR-99a was evaluated in these hypertrophic cells and hearts. We also found that miR-99a expression was highly correlated with cardiac function of mice with heart failure (8 weeks after TAC surgery). Overexpression of miR-99a attenuated cardiac hypertrophy in TAC mice and cellular hypertrophy in stimuli treated cardiomyocytes through down-regulation of expression of mammalian target of rapamycin (mTOR). These results indicate that miR-99a negatively regulates physiological hypertrophy through mTOR signaling pathway, which may provide a new therapeutic approach for pressure-overload heart failure.

  1. The role of satellite cells in muscle hypertrophy.

    Science.gov (United States)

    Blaauw, Bert; Reggiani, Carlo

    2014-02-01

    The role of satellite cells in muscle hypertrophy has long been a debated issue. In the late 1980s it was shown that proteins remain close to the myonucleus responsible for its synthesis, giving rise to the idea of a nuclear domain. This, together with the observation that during various models of muscle hypertrophy there is an activation of the muscle stem cells, i.e. satellite cells, lead to the idea that satellite cell activation is required for muscle hypertrophy. Thus, satellite cells are not only responsible for muscle repair and regeneration, but also for hypertrophic growth. Further support for this line of thinking was obtained after studies showing that irradiation of skeletal muscle, and therefore elimination of all satellite cells, completely prevented overload-induced hypertrophy. Recently however, using different transgenic approaches, it has become clear that muscle hypertrophy can occur without a contribution of satellite cells, even though in most situations of muscle hypertrophy satellite cells are activated. In this review we will discuss the contribution of satellite cells, and other muscle-resident stem cells, to muscle hypertrophy both in mice as well as in humans.

  2. Beta blockers & left ventricular hypertrophy regression.

    Science.gov (United States)

    George, Thomas; Ajit, Mullasari S; Abraham, Georgi

    2010-01-01

    Left ventricular hypertrophy (LVH) particularly in hypertensive patients is a strong predictor of adverse cardiovascular events. Identifying LVH not only helps in the prognostication but also in the choice of therapeutic drugs. The prevalence of LVH is age linked and has a direct correlation to the severity of hypertension. Adequate control of blood pressure, most importantly central aortic pressure and blocking the effects of cardiomyocyte stimulatory growth factors like Angiotensin II helps in regression of LVH. Among the various antihypertensives ACE-inhibitors and angiotensin receptor blockers are more potent than other drugs in regressing LVH. Beta blockers especially the newer cardio selective ones do still have a role in regressing LVH albeit a minor one. A meta-analysis of various studies on LVH regression shows many lacunae. There have been no consistent criteria for defining LVH and documenting LVH regression. This article reviews current evidence on the role of Beta Blockers in LVH regression.

  3. [Molecular mechanisms of skeletal muscle hypertrophy].

    Science.gov (United States)

    Astratenkova, I V; Rogozkin, V A

    2014-06-01

    Enzymes Akt, AMPK, mTOR, S6K and PGC-1a coactivator take part in skeletal muscles in the regulation of synthesis of proteins. The expression of these proteins is regulated by growth factors, hormones, nutrients, mechanical loading and leads to an increase in muscle mass and skeletal muscle hypertrophy. The review presents the results of studies published in the past four years, which expand knowledge on the effects of various factors on protein synthesis in skeletal muscle. The attention is focused on the achievements that reveal and clarify the signaling pathways involved in the regulation of protein synthesis in skeletal muscle. The central place is taken by mTOR enzyme which controls and regulates the main stages of the cascade of reactions of muscle proteins providing synthesis in the conditions of human life. coactivator PGC-1a.

  4. Cardiac hypertrophy in mice expressing unphosphorylatable phospholemman.

    Science.gov (United States)

    Boguslavskyi, Andrii; Pavlovic, Davor; Aughton, Karen; Clark, James E; Howie, Jacqueline; Fuller, William; Shattock, Michael J

    2014-10-01

    Elevation of intracellular Na in the failing myocardium contributes to contractile dysfunction, the negative force-frequency relationship, and arrhythmias. Although phospholemman (PLM) is recognized to form the link between signalling pathways and Na/K pump activity, the possibility that defects in its regulation contribute to elevation of intracellular Na has not been investigated. Our aim was to test the hypothesis that the prevention of PLM phosphorylation in a PLM(3SA) knock-in mouse (in which PLM has been rendered unphosphorylatable) will exacerbate cardiac hypertrophy and cellular Na overload. Testing this hypothesis should determine whether changes in PLM phosphorylation are simply bystander effects or are causally involved in disease progression. In wild-type (WT) mice, aortic constriction resulted in hypophosphorylation of PLM with no change in Na/K pump expression. This under-phosphorylation of PLM occurred at 3 days post-banding and was associated with a progressive decline in Na/K pump current and elevation of [Na]i. Echocardiography, morphometry, and pressure-volume (PV) catheterization confirmed remodelling, dilation, and contractile dysfunction, respectively. In PLM(3SA) mice, expression of Na/K ATPase was increased and PLM decreased such that net Na/K pump current under quiescent conditions was unchanged (cf. WT myocytes); [Na(+)]i was increased and forward-mode Na/Ca exchanger was reduced in paced PLM(3SA) myocytes. Cardiac hypertrophy and Na/K pump inhibition were significantly exacerbated in banded PLM(3SA) mice compared with banded WT. Decreased phosphorylation of PLM reduces Na/K pump activity and exacerbates Na overload, contractile dysfunction, and adverse remodelling following aortic constriction in mice. This suggests a novel therapeutic target for the treatment of heart failure. © The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.

  5. Hepatitis B Foundation

    Science.gov (United States)

    ... worldwide 2 Billion People have been infected with Hepatitis B Worldwide The Hepatitis B Foundation is working on ... of people living with hepatitis B. Learn About Hepatitis B in 11 Other Languages . Resource Video See More ...

  6. Hepatitis A Test

    Science.gov (United States)

    ... be limited. Home Visit Global Sites Search Help? Hepatitis A Testing Share this page: Was this page ... HAV-Ab total; Anti-HAV Formal name: Viral Hepatitis A Antibody Related tests: Hepatitis B Testing ; Hepatitis ...

  7. Hepatitis Risk Assessment

    Science.gov (United States)

    ... Requirements for Viral Hepatitis Liver Cancer and Viral Hepatitis Viral Hepatitis and Young Persons Who Inject Drugs National Academies’ ... Sources for IG & HBIG About the Division of Viral Hepatitis Contact Us Anonymous Feedback File Formats Help: How ...

  8. Travelers' Health: Hepatitis A

    Science.gov (United States)

    ... 3 - Helminths, Soil-Transmitted Chapter 3 - Hepatitis B Hepatitis A Noele P. Nelson, Trudy V. Murphy INFECTIOUS ... hepatitis/HAV Table 3-02. Vaccines to prevent hepatitis A VACCINE TRADE NAME (MANUFACTURER) AGE (Y) DOSE ...

  9. Delta agent (Hepatitis D)

    Science.gov (United States)

    Hepatitis D virus ... Hepatitis D virus (HDV) is found only in people who carry the hepatitis B virus. HDV may make liver ... B virus but who never had symptoms. Hepatitis D infects about 15 million people worldwide. It occurs ...

  10. Painful unilateral temporalis muscle enlargement: reactive masticatory muscle hypertrophy.

    Science.gov (United States)

    Katsetos, Christos D; Bianchi, Michael A; Jaffery, Fizza; Koutzaki, Sirma; Zarella, Mark; Slater, Robert

    2014-06-01

    An instance of isolated unilateral temporalis muscle hypertrophy (reactive masticatory muscle hypertrophy with fiber type 1 predominance) confirmed by muscle biopsy with histochemical fiber typing and image analysis in a 62 year-old man is reported. The patient presented with bruxism and a painful swelling of the temple. Absence of asymmetry or other abnormalities of the craniofacial skeleton was confirmed by magnetic resonance imaging and cephalometric analyses. The patient achieved symptomatic improvement only after undergoing botulinum toxin injections. Muscle biopsy is key in the diagnosis of reactive masticatory muscle hypertrophy and its distinction from masticatory muscle myopathy (hypertrophic branchial myopathy) and other non-reactive causes of painful asymmetric temporalis muscle enlargement.

  11. Feature Hepatitis: Hepatitis Symptoms, Diagnosis, Treatment & Prevention

    Science.gov (United States)

    ... Navigation Bar Home Current Issue Past Issues Feature Hepatitis Hepatitis: Symptoms, Diagnosis, Treatment & Prevention Past Issues / Spring 2009 ... No appetite Fever Headaches Diagnosis To check for hepatitis viruses, your doctor will test your blood. You ...

  12. Hepatitis C: Diet and Nutrition

    Science.gov (United States)

    ... with Hepatitis » Daily Living: Diet and Nutrition Viral Hepatitis Menu Menu Viral Hepatitis Viral Hepatitis Home For ... have high cholesterol and have fatty liver. How hepatitis C affects diet If you have hepatitis, you ...

  13. Liver Cancer and Hepatitis B

    Science.gov (United States)

    ... Our Accomplishments Annual Reports Our Videos What Is Hepatitis B? What Is Hepatitis B? The ABCs of Viral Hepatitis Liver Cancer and Hepatitis B Hepatitis Delta Coinfection Hepatitis C Coinfection HIV/AIDS ...

  14. Autoimmune hepatitis

    Directory of Open Access Journals (Sweden)

    F Motamed

    2014-04-01

    Full Text Available Autoimmune hepatitis is (AIH is a chronic hepatitis that occurs in children and adults of all ages. It is characterized by immunologic and autoimmune features, including circulating auto antibodies and high serum globulin concentrations. It was first described in the 1950s by term of chronic active hepatitis. It has 2 types with different auto antibodies. Diagnosis is based upon serologic and histologic findings and exclusion of other forms of chronic liver disease.   A scoring system should be used in assessment based upon: 1 Auto anti bodie titer 2 Serum IgG level  3 Liver histology 4 Absence of viral and other causes of hepatitis. Clear indications for treatment: 1   rise of aminotrasferases 2   clinical symptoms of liver disease 3   histological features in liver biopsy 4   Children with AIH initial treatment involve glucocorticoid with or without azathioprine. For patients with fulminant hepatitis liver transplantation, should be kept in mind.   Remission is defined by: 1   Resolution of symptoms 2   Normalization of serum trasaminases 3   Normalization of serum bilirubin and gamma globuline levels. 4   Improvement in liver histology 5   Treatment is continued for at least 2-5 years, glucocorticoids are with drawn first, by tapering over six weeks. Azathioprine will be with drawn.  

  15. [Chronic hepatitis].

    Science.gov (United States)

    Figueroa Barrios, R

    1995-01-01

    Medical literature about chronic hepatitis is reviewed. This unresolving disease caused by viruses, drugs or unknown factors may progress to in cirrhosis and hepatocarcinoma. A classification based on liver biopsy histology into chronic persistent and chronic active types has been largely abandoned and emphasis is placed on recognizing the etiology of the various types. One is associated with continuing hepatitis B virus infection; another is related to chronic hepatitis C virus infection and the third is termed autoinmune, because of the association with positive serum autoantibodies. A fourth type with similar clinical functional and morphologic features is found with some drug reactions. Long term corticoesteroid therapy is usually successful in autoinmune type. Associations between antibodies to liver-kidney microsomes and the hepatitis C virus can cause diagnostic difficulties. Antiviral treatment of chronic hepatitis B and C with interpheron alfa is employed, controlling symptoms and abnormal biochemistry and the progression to cirrhosis and liver cancer in 30 to 40% patients. Alternative therapies or combinations with interpheron are being evaluated waiting for final results.

  16. Agroforestry practice in villages surrounding Nyamure former ...

    African Journals Online (AJOL)

    cntaganda

    Key words: Agroforestry, fuel wood, tree products, woodlot, forest plantation. INTRODUCTION ... The study area included three administrative cells in the surroundings of Nyamure ..... Table 6: Distance and time spent on firewood collection.

  17. Explaining preferences for home surroundings and locations

    Directory of Open Access Journals (Sweden)

    Hans Skifter Andersen

    2011-01-01

    Full Text Available This article is based on a survey carried out in Denmark that asked a random sample of the population about their preferences for home surroundings and locations. It shows that the characteristics of social surroundings are very important and can be divided into three independent dimensions: avoiding social nuisances, preferring social homogeneity and living close to one’s social network and place of origin. The study shows that most people have many detailed preferences, whereas some have very few. This confirms an earlier theory that some people are very connected to certain places with given characteristics and thus do not have priorities regarding home surroundings and locations. For others, mostly young people and singles, home is just a place to sleep and relax, whereas life is lived elsewhere. For this group, there are only preferences for location and there are few specific preferences for surroundings.

  18. left ventricular hypertrophy in renal failure a review

    African Journals Online (AJOL)

    Key words: Left Ventricular hypertrophy (LVH), Renal failure; cardiovascular. INTRODUCTION. Chronic ... of anaemia; age, disturbed elasticity of the central arteries with elevated ..... Arodiwe E. B. Prevalence of and factors associated with LVH ...

  19. Montelukast in Adenoid Hypertrophy: Its Effect on Size and Symptoms

    Directory of Open Access Journals (Sweden)

    Farshid Shokouhi

    2015-11-01

    Conclusion:  Montelukast chewable tablets achieved a significant reduction in adenoid size and improved the related clinical symptoms of AH and can therefore be considered an effective alternative to surgical treatment in children with adenoid hypertrophy.

  20. Myogenic Progenitor Cells Control Extracellular Matrix Production by Fibroblasts during Skeletal Muscle Hypertrophy.

    Science.gov (United States)

    Fry, Christopher S; Kirby, Tyler J; Kosmac, Kate; McCarthy, John J; Peterson, Charlotte A

    2017-01-05

    Satellite cells, the predominant stem cell population in adult skeletal muscle, are activated in response to hypertrophic stimuli and give rise to myogenic progenitor cells (MPCs) within the extracellular matrix (ECM) that surrounds myofibers. This ECM is composed largely of collagens secreted by interstitial fibrogenic cells, which influence satellite cell activity and muscle repair during hypertrophy and aging. Here we show that MPCs interact with interstitial fibrogenic cells to ensure proper ECM deposition and optimal muscle remodeling in response to hypertrophic stimuli. MPC-dependent ECM remodeling during the first week of a growth stimulus is sufficient to ensure long-term myofiber hypertrophy. MPCs secrete exosomes containing miR-206, which represses Rrbp1, a master regulator of collagen biosynthesis, in fibrogenic cells to prevent excessive ECM deposition. These findings provide insights into how skeletal stem and progenitor cells interact with other cell types to actively regulate their extracellular environments for tissue maintenance and adaptation. Copyright © 2017 Elsevier Inc. All rights reserved.

  1. Surround-Masking Affects Visual Estimation Ability

    Science.gov (United States)

    Jastrzebski, Nicola R.; Hugrass, Laila E.; Crewther, Sheila G.; Crewther, David P.

    2017-01-01

    Visual estimation of numerosity involves the discrimination of magnitude between two distributions or perceptual sets that vary in number of elements. How performance on such estimation depends on peripheral sensory stimulation is unclear, even in typically developing adults. Here, we varied the central and surround contrast of stimuli that comprised a visual estimation task in order to determine whether mechanisms involved with the removal of unessential visual input functionally contributes toward number acuity. The visual estimation judgments of typically developed adults were significantly impaired for high but not low contrast surround stimulus conditions. The center and surround contrasts of the stimuli also differentially affected the accuracy of numerosity estimation depending on whether fewer or more dots were presented. Remarkably, observers demonstrated the highest mean percentage accuracy across stimulus conditions in the discrimination of more elements when the surround contrast was low and the background luminance of the central region containing the elements was dark (black center). Conversely, accuracy was severely impaired during the discrimination of fewer elements when the surround contrast was high and the background luminance of the central region was mid level (gray center). These findings suggest that estimation ability is functionally related to the quality of low-order filtration of unessential visual information. These surround masking results may help understanding of the poor visual estimation ability commonly observed in developmental dyscalculia.

  2. Time course of gene expression during mouse skeletal muscle hypertrophy

    Science.gov (United States)

    Lee, Jonah D.; England, Jonathan H.; Esser, Karyn A.; McCarthy, John J.

    2013-01-01

    The purpose of this study was to perform a comprehensive transcriptome analysis during skeletal muscle hypertrophy to identify signaling pathways that are operative throughout the hypertrophic response. Global gene expression patterns were determined from microarray results on days 1, 3, 5, 7, 10, and 14 during plantaris muscle hypertrophy induced by synergist ablation in adult mice. Principal component analysis and the number of differentially expressed genes (cutoffs ≥2-fold increase or ≥50% decrease compared with control muscle) revealed three gene expression patterns during overload-induced hypertrophy: early (1 day), intermediate (3, 5, and 7 days), and late (10 and 14 days) patterns. Based on the robust changes in total RNA content and in the number of differentially expressed genes, we focused our attention on the intermediate gene expression pattern. Ingenuity Pathway Analysis revealed a downregulation of genes encoding components of the branched-chain amino acid degradation pathway during hypertrophy. Among these genes, five were predicted by Ingenuity Pathway Analysis or previously shown to be regulated by the transcription factor Kruppel-like factor-15, which was also downregulated during hypertrophy. Moreover, the integrin-linked kinase signaling pathway was activated during hypertrophy, and the downregulation of muscle-specific micro-RNA-1 correlated with the upregulation of five predicted targets associated with the integrin-linked kinase pathway. In conclusion, we identified two novel pathways that may be involved in muscle hypertrophy, as well as two upstream regulators (Kruppel-like factor-15 and micro-RNA-1) that provide targets for future studies investigating the importance of these pathways in muscle hypertrophy. PMID:23869057

  3. Experimental Mouse Model of Lumbar Ligamentum Flavum Hypertrophy.

    Science.gov (United States)

    Saito, Takeyuki; Yokota, Kazuya; Kobayakawa, Kazu; Hara, Masamitsu; Kubota, Kensuke; Harimaya, Katsumi; Kawaguchi, Kenichi; Hayashida, Mitsumasa; Matsumoto, Yoshihiro; Doi, Toshio; Shiba, Keiichiro; Nakashima, Yasuharu; Okada, Seiji

    2017-01-01

    Lumbar spinal canal stenosis (LSCS) is one of the most common spinal disorders in elderly people, with the number of LSCS patients increasing due to the aging of the population. The ligamentum flavum (LF) is a spinal ligament located in the interior of the vertebral canal, and hypertrophy of the LF, which causes the direct compression of the nerve roots and/or cauda equine, is a major cause of LSCS. Although there have been previous studies on LF hypertrophy, its pathomechanism remains unclear. The purpose of this study is to establish a relevant mouse model of LF hypertrophy and to examine disease-related factors. First, we focused on mechanical stress and developed a loading device for applying consecutive mechanical flexion-extension stress to the mouse LF. After 12 weeks of mechanical stress loading, we found that the LF thickness in the stress group was significantly increased in comparison to the control group. In addition, there were significant increases in the area of collagen fibers, the number of LF cells, and the gene expression of several fibrosis-related factors. However, in this mecnanical stress model, there was no macrophage infiltration, angiogenesis, or increase in the expression of transforming growth factor-β1 (TGF-β1), which are characteristic features of LF hypertrophy in LSCS patients. We therefore examined the influence of infiltrating macrophages on LF hypertrophy. After inducing macrophage infiltration by micro-injury to the mouse LF, we found excessive collagen synthesis in the injured site with the increased TGF-β1 expression at 2 weeks after injury, and further confirmed LF hypertrophy at 6 weeks after injury. Our findings demonstrate that mechanical stress is a causative factor for LF hypertrophy and strongly suggest the importance of macrophage infiltration in the progression of LF hypertrophy via the stimulation of collagen production.

  4. Painful Unilateral Temporalis Muscle Enlargement: Reactive Masticatory Muscle Hypertrophy

    OpenAIRE

    Katsetos, Christos D.; Bianchi, Michael A.; Jaffery, Fizza; Koutzaki, Sirma; Zarella, Mark; Slater, Robert

    2013-01-01

    An instance of isolated unilateral temporalis muscle hypertrophy (reactive masticatory muscle hypertrophy with fiber type 1 predominance) confirmed by muscle biopsy with histochemical fiber typing and image analysis in a 62 year-old man is reported. The patient presented with bruxism and a painful swelling of the temple. Absence of asymmetry or other abnormalities of the craniofacial skeleton was confirmed by magnetic resonance imaging and cephalometric analyses. The patient achieved symptoma...

  5. Raf-mediated cardiac hypertrophy in adult Drosophila.

    Science.gov (United States)

    Yu, Lin; Daniels, Joseph; Glaser, Alex E; Wolf, Matthew J

    2013-07-01

    In response to stress and extracellular signals, the heart undergoes a process called cardiac hypertrophy during which cardiomyocytes increase in size. If untreated, cardiac hypertrophy can progress to overt heart failure that causes significant morbidity and mortality. The identification of molecular signals that cause or modify cardiomyopathies is necessary to understand how the normal heart progresses to cardiac hypertrophy and heart failure. Receptor tyrosine kinase (RTK) signaling is essential for normal human cardiac function, and the inhibition of RTKs can cause dilated cardiomyopathies. However, neither investigations of activated RTK signaling pathways nor the characterization of hypertrophic cardiomyopathy in the adult fly heart has been previously described. Therefore, we developed strategies using Drosophila as a model to circumvent some of the complexities associated with mammalian models of cardiovascular disease. Transgenes encoding activated EGFR(A887T), Ras85D(V12) and Ras85D(V12S35), which preferentially signal to Raf, or constitutively active human or fly Raf caused hypertrophic cardiomyopathy as determined by decreased end diastolic lumen dimensions, abnormal cardiomyocyte fiber morphology and increased heart wall thicknesses. There were no changes in cardiomyocyte cell numbers. Additionally, activated Raf also induced an increase in cardiomyocyte ploidy compared with control hearts. However, preventing increases in cardiomyocyte ploidy using fizzy-related (Fzr) RNAi did not rescue Raf-mediated cardiac hypertrophy, suggesting that Raf-mediated polyploidization is not required for cardiac hypertrophy. Similar to mammals, the cardiac-specific expression of RNAi directed against MEK or ERK rescued Raf-mediated cardiac hypertrophy. However, the cardiac-specific expression of activated ERK(D334N), which promotes hyperplasia in non-cardiac tissues, did not cause myocyte hypertrophy. These results suggest that ERK is necessary, but not sufficient, for

  6. Raf-mediated cardiac hypertrophy in adult Drosophila

    Directory of Open Access Journals (Sweden)

    Lin Yu

    2013-07-01

    In response to stress and extracellular signals, the heart undergoes a process called cardiac hypertrophy during which cardiomyocytes increase in size. If untreated, cardiac hypertrophy can progress to overt heart failure that causes significant morbidity and mortality. The identification of molecular signals that cause or modify cardiomyopathies is necessary to understand how the normal heart progresses to cardiac hypertrophy and heart failure. Receptor tyrosine kinase (RTK signaling is essential for normal human cardiac function, and the inhibition of RTKs can cause dilated cardiomyopathies. However, neither investigations of activated RTK signaling pathways nor the characterization of hypertrophic cardiomyopathy in the adult fly heart has been previously described. Therefore, we developed strategies using Drosophila as a model to circumvent some of the complexities associated with mammalian models of cardiovascular disease. Transgenes encoding activated EGFRA887T, Ras85DV12 and Ras85DV12S35, which preferentially signal to Raf, or constitutively active human or fly Raf caused hypertrophic cardiomyopathy as determined by decreased end diastolic lumen dimensions, abnormal cardiomyocyte fiber morphology and increased heart wall thicknesses. There were no changes in cardiomyocyte cell numbers. Additionally, activated Raf also induced an increase in cardiomyocyte ploidy compared with control hearts. However, preventing increases in cardiomyocyte ploidy using fizzy-related (Fzr RNAi did not rescue Raf-mediated cardiac hypertrophy, suggesting that Raf-mediated polyploidization is not required for cardiac hypertrophy. Similar to mammals, the cardiac-specific expression of RNAi directed against MEK or ERK rescued Raf-mediated cardiac hypertrophy. However, the cardiac-specific expression of activated ERKD334N, which promotes hyperplasia in non-cardiac tissues, did not cause myocyte hypertrophy. These results suggest that ERK is necessary, but not sufficient, for Raf

  7. Raf-mediated cardiac hypertrophy in adult Drosophila

    Science.gov (United States)

    Yu, Lin; Daniels, Joseph; Glaser, Alex E.; Wolf, Matthew J.

    2013-01-01

    SUMMARY In response to stress and extracellular signals, the heart undergoes a process called cardiac hypertrophy during which cardiomyocytes increase in size. If untreated, cardiac hypertrophy can progress to overt heart failure that causes significant morbidity and mortality. The identification of molecular signals that cause or modify cardiomyopathies is necessary to understand how the normal heart progresses to cardiac hypertrophy and heart failure. Receptor tyrosine kinase (RTK) signaling is essential for normal human cardiac function, and the inhibition of RTKs can cause dilated cardiomyopathies. However, neither investigations of activated RTK signaling pathways nor the characterization of hypertrophic cardiomyopathy in the adult fly heart has been previously described. Therefore, we developed strategies using Drosophila as a model to circumvent some of the complexities associated with mammalian models of cardiovascular disease. Transgenes encoding activated EGFRA887T, Ras85DV12 and Ras85DV12S35, which preferentially signal to Raf, or constitutively active human or fly Raf caused hypertrophic cardiomyopathy as determined by decreased end diastolic lumen dimensions, abnormal cardiomyocyte fiber morphology and increased heart wall thicknesses. There were no changes in cardiomyocyte cell numbers. Additionally, activated Raf also induced an increase in cardiomyocyte ploidy compared with control hearts. However, preventing increases in cardiomyocyte ploidy using fizzy-related (Fzr) RNAi did not rescue Raf-mediated cardiac hypertrophy, suggesting that Raf-mediated polyploidization is not required for cardiac hypertrophy. Similar to mammals, the cardiac-specific expression of RNAi directed against MEK or ERK rescued Raf-mediated cardiac hypertrophy. However, the cardiac-specific expression of activated ERKD334N, which promotes hyperplasia in non-cardiac tissues, did not cause myocyte hypertrophy. These results suggest that ERK is necessary, but not sufficient, for

  8. Heart Hypertrophy Caused by Obesity and Physical Exercises

    OpenAIRE

    Zazycki, Sabrina Pereira; Universidade Estadual de Maringá; Gomes, Célia Regina de Godoy; Universidade Estadual de Maringá

    2009-01-01

    The heart is mainly composed of myocytes, blood vessels and collagen interstitial matrix. When these factors are in equilibrium they contribute towards the maintenance of the heart’s form and function. Heart growth after birth mainly occurs through hypertrophy of the cardiomyocyte and the proliferation of interstitial components. This occurs because cardiomyocytes lose their ability to perform complete mitosis resulting in the absence of cell hyperplasia. Cardiomyocyte hypertrophy, the most e...

  9. Time course of gene expression during mouse skeletal muscle hypertrophy.

    Science.gov (United States)

    Chaillou, Thomas; Lee, Jonah D; England, Jonathan H; Esser, Karyn A; McCarthy, John J

    2013-10-01

    The purpose of this study was to perform a comprehensive transcriptome analysis during skeletal muscle hypertrophy to identify signaling pathways that are operative throughout the hypertrophic response. Global gene expression patterns were determined from microarray results on days 1, 3, 5, 7, 10, and 14 during plantaris muscle hypertrophy induced by synergist ablation in adult mice. Principal component analysis and the number of differentially expressed genes (cutoffs ≥2-fold increase or ≥50% decrease compared with control muscle) revealed three gene expression patterns during overload-induced hypertrophy: early (1 day), intermediate (3, 5, and 7 days), and late (10 and 14 days) patterns. Based on the robust changes in total RNA content and in the number of differentially expressed genes, we focused our attention on the intermediate gene expression pattern. Ingenuity Pathway Analysis revealed a downregulation of genes encoding components of the branched-chain amino acid degradation pathway during hypertrophy. Among these genes, five were predicted by Ingenuity Pathway Analysis or previously shown to be regulated by the transcription factor Kruppel-like factor-15, which was also downregulated during hypertrophy. Moreover, the integrin-linked kinase signaling pathway was activated during hypertrophy, and the downregulation of muscle-specific micro-RNA-1 correlated with the upregulation of five predicted targets associated with the integrin-linked kinase pathway. In conclusion, we identified two novel pathways that may be involved in muscle hypertrophy, as well as two upstream regulators (Kruppel-like factor-15 and micro-RNA-1) that provide targets for future studies investigating the importance of these pathways in muscle hypertrophy.

  10. A New Clinical Scoring System for Adenoid Hypertrophy in Children

    OpenAIRE

    Shervin Sharifkashani; Payman Dabirmoghaddam; Maryam Kheirkhah; Rima Hosseinzadehnik

    2015-01-01

    Introduction: Chronic nasal obstruction due to adenoid hypertrophy is a very common disorder. Although the clinical assessment of adenoid hypertrophy is essential, its real value in young children is difficult to evaluate. The purpose of this prospective study was to validate a simple clinical score to predict the severity of adenoid obstruction and to evaluate the relationship between this method of clinical scoring with radiography and nasopharyngeal endoscopy. Materials and Methods: Ninety...

  11. Immune modulation in chronic hepatitis B patients

    NARCIS (Netherlands)

    A.B. van Nunen

    2002-01-01

    textabstractThe hepatitis B virus (HBV) is a 42 nm viral particle and member of the hepadnaviridae family. Its double-shelled structure consists of an outer envelop composed of surface proteins (HBsAg) and an inner capsid formed by core-proteins (HBcAg) surrounding the partially double stranded DNA

  12. Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy.

    Science.gov (United States)

    Abel, E Dale; Doenst, Torsten

    2011-05-01

    Cardiac hypertrophy is a stereotypic response of the heart to increased workload. The nature of the workload increase may vary depending on the stimulus (repetitive, chronic, pressure, or volume overload). If the heart fully adapts to the new loading condition, the hypertrophic response is considered physiological. If the hypertrophic response is associated with the ultimate development of contractile dysfunction and heart failure, the response is considered pathological. Although divergent signalling mechanisms may lead to these distinct patterns of hypertrophy, there is some overlap. Given the close relationship between workload and energy demand, any form of cardiac hypertrophy will impact the energy generation by mitochondria, which are the key organelles for cellular ATP production. Significant changes in the expression of nuclear and mitochondrially encoded transcripts that impact mitochondrial function as well as altered mitochondrial proteome composition and mitochondrial energetics have been described in various forms of cardiac hypertrophy. Here, we review mitochondrial alterations in pathological and physiological hypertrophy. We suggest that mitochondrial adaptations to pathological and physiological hypertrophy are distinct, and we shall review potential mechanisms that might account for these differences.

  13. Network Reconstruction and Systems Analysis of Cardiac Myocyte Hypertrophy Signaling*

    Science.gov (United States)

    Ryall, Karen A.; Holland, David O.; Delaney, Kyle A.; Kraeutler, Matthew J.; Parker, Audrey J.; Saucerman, Jeffrey J.

    2012-01-01

    Cardiac hypertrophy is managed by a dense web of signaling pathways with many pathways influencing myocyte growth. A quantitative understanding of the contributions of individual pathways and their interactions is needed to better understand hypertrophy signaling and to develop more effective therapies for heart failure. We developed a computational model of the cardiac myocyte hypertrophy signaling network to determine how the components and network topology lead to differential regulation of transcription factors, gene expression, and myocyte size. Our computational model of the hypertrophy signaling network contains 106 species and 193 reactions, integrating 14 established pathways regulating cardiac myocyte growth. 109 of 114 model predictions were validated using published experimental data testing the effects of receptor activation on transcription factors and myocyte phenotypic outputs. Network motif analysis revealed an enrichment of bifan and biparallel cross-talk motifs. Sensitivity analysis was used to inform clustering of the network into modules and to identify species with the greatest effects on cell growth. Many species influenced hypertrophy, but only a few nodes had large positive or negative influences. Ras, a network hub, had the greatest effect on cell area and influenced more species than any other protein in the network. We validated this model prediction in cultured cardiac myocytes. With this integrative computational model, we identified the most influential species in the cardiac hypertrophy signaling network and demonstrate how different levels of network organization affect myocyte size, transcription factors, and gene expression. PMID:23091058

  14. Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

    Science.gov (United States)

    Abel, E. Dale; Doenst, Torsten

    2011-01-01

    Cardiac hypertrophy is a stereotypic response of the heart to increased workload. The nature of the workload increase may vary depending on the stimulus (repetitive, chronic, pressure, or volume overload). If the heart fully adapts to the new loading condition, the hypertrophic response is considered physiological. If the hypertrophic response is associated with the ultimate development of contractile dysfunction and heart failure, the response is considered pathological. Although divergent signalling mechanisms may lead to these distinct patterns of hypertrophy, there is some overlap. Given the close relationship between workload and energy demand, any form of cardiac hypertrophy will impact the energy generation by mitochondria, which are the key organelles for cellular ATP production. Significant changes in the expression of nuclear and mitochondrially encoded transcripts that impact mitochondrial function as well as altered mitochondrial proteome composition and mitochondrial energetics have been described in various forms of cardiac hypertrophy. Here, we review mitochondrial alterations in pathological and physiological hypertrophy. We suggest that mitochondrial adaptations to pathological and physiological hypertrophy are distinct, and we shall review potential mechanisms that might account for these differences. PMID:21257612

  15. Novel EGFR inhibitors attenuate cardiac hypertrophy induced by angiotensin II.

    Science.gov (United States)

    Peng, Kesong; Tian, Xinqiao; Qian, Yuanyuan; Skibba, Melissa; Zou, Chunpeng; Liu, Zhiguo; Wang, Jingying; Xu, Zheng; Li, Xiaokun; Liang, Guang

    2016-03-01

    Cardiac hypertrophy is an important risk factor for heart failure. Epidermal growth factor receptor (EGFR) has been found to play a role in the pathogenesis of various cardiovascular diseases. The aim of this current study was to examine the role of EGFR in angiotensin II (Ang II)-induced cardiac hypertrophy and identify the underlying molecular mechanisms. In this study, we observed that both Ang II and EGF could increase the phospohorylation of EGFR and protein kinase B (AKT)/extracellular signal-regulated kinase (ERK), and then induce cell hypertrophy in H9c2 cells. Both pharmacological inhibitors and genetic silencing significantly reduced Ang II-induced EGFR signalling pathway activation, hypertrophic marker overexpression, and cell hypertrophy. In addition, our results showed that Ang II-induced EGFR activation is mediated by c-Src phosphorylation. In vivo, Ang II treatment significantly led to cardiac remodelling including cardiac hypertrophy, disorganization and fibrosis, accompanied by the activation of EGFR signalling pathway in the heart tissues, while all these molecular and pathological alterations were attenuated by the oral administration with EGFR inhibitors. In conclusion, the c-Src-dependent EGFR activation may play an important role in Ang II-induced cardiac hypertrophy, and inhibition of EGFR by specific molecules may be an effective strategy for the treatment of Ang II-associated cardiac diseases. © 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

  16. Resolution of enuresis after adenotsillectomy in children with adenotonsillar hypertrophy

    Directory of Open Access Journals (Sweden)

    Mohammad Naeimi

    2008-06-01

    Full Text Available Introduction: Most of the upper airway obstructions are caused by adenotonsillar hypertrophy. Prevalence of nocturnal enuresis in children accompanied with upper airway obstruction is reported in 8-47% of cases. Considering this fact that adenotonsillar hypertrophy is curable by adenotonsilletomy, in present study the effect of this operation in treatment of children with adenotonsillar hypertrophy has been investigated by comparing the rate of nocturnal enuresis pre and post operation. Materials and Methods: During a period of 18 months, all children referred to otorhinolaryngology department of Ghaem hospital suffering from nocturnal enuresis and adenotonsillar hypertrophy have been surveyed. The patients were evaluated for improvement in nocturnal enuresis after adenotosillectomy for a period of three months. Results: Theaverage age of patients was 6.8 years. 63.8% of children had primary nocturnal enuresis and 36.2% secondary nocturnal enuresis. One month after adenotonsillectomy in 88% of children nocturnal enuresis was completely cured. Using Friedman test we revealed that there was no significant difference in second and third month in comparison with first month. Complete improvement was observed in patients with secondary nocturnal enuresis. Between severity of adenotonsillar hypertrophy and improvement in nocturnal enuresis only in patients with adenoid hypertrophy the result was significant (P

  17. Managing turbinate hypertrophy: coblation vs. radiofrequency treatment.

    Science.gov (United States)

    Passali, D; Loglisci, M; Politi, L; Passali, G C; Kern, E

    2016-06-01

    The role of inferior turbinate hypertrophy in the reduction of nasal airflow is well established. Although chronic nasal obstruction is not life- threatening, it significantly impairs patients' quality of life, affecting many aspects of daily activities; therefore, patients seek medical intervention. 40 patients were selected (27 males and 13 females) between 27 and 64 years of age with a symptom of nasal obstruction. The patients were divided in two groups: Group 1: coblation, 25 patients (18 males and 7 females); Group 2: radiofrequency, 15 patients (7 males and 6 females). These 40 patients were followed for 3 years. Patients were analyzed using both subjective and objective methods. The visual analog scale (VAS) subjective data and objective data including both active anterior rhinomanometry and acoustic rhinometry were recorded and analyzed. Data were collected pre-operatively and at 1 and 3 years post-operatively. According to our data, both coblation and radiofrequency turbinate reduction benefit patients with good results. The complications, found during the follow-up, are limited to minimal bleeding and crusting. Coblation and radiofrequency were significantly less painful than others procedures during the early post-operative period. In our study, both coblation and radiofrequency provide an improvement in nasal airflow with a reduction in nasal obstructive symptoms in the short term, but their efficacy tended to decrease within 3 years.

  18. Arterial baroreflex function and left ventricular hypertrophy

    Institute of Scientific and Technical Information of China (English)

    MIAO Chao-Yu; SU Ding-Feng

    2004-01-01

    It is well known that the arterial baroreflex(ABR)plays a key role in the regulation of heart rate and stabilization of blood pressure.Currently,it appears that ABR dysfunction is involved in the pathophysiology of cardiovascular disease states.Since the mid-1990s,a number of studies have been carried out in our laboratory to explore the pathological significance of ABR function in cardiovascular damage.This minireview summarizes our research work on the topic of ABR and left ventricular hypertrophy(LVH).On the basis of discussion concerning the importance of ABR dysfunction in hypertensive LVH and sinoaortic denervation-induced LVH,we advance a new strategy for reversal of LVH,that is,restoration of impaired ABR function.We tested this hypothesis in animal models with ABR deficiency.It was found that improvement of impaird ABR function with long-term treatment of ketanserin or candesartan was accompanied by reversal of LVH.The preliminary results indicate that it is feasible to target ABR for treatment of LVH.

  19. The problem Of muscle hypertrophy: Revisited.

    Science.gov (United States)

    Buckner, Samuel L; Dankel, Scott J; Mattocks, Kevin T; Jessee, Matthew B; Mouser, J Grant; Counts, Brittany R; Loenneke, Jeremy P

    2016-12-01

    In this paper we revisit a topic originally discussed in 1955, namely the lack of direct evidence that muscle hypertrophy from exercise plays an important role in increasing strength. To this day, long-term adaptations in strength are thought to be primarily contingent on changes in muscle size. Given this assumption, there has been considerable attention placed on programs designed to allow for maximization of both muscle size and strength. However, the conclusion that a change in muscle size affects a change in strength is surprisingly based on little evidence. We suggest that these changes may be completely separate phenomena based on: (1) the weak correlation between the change in muscle size and the change in muscle strength after training; (2) the loss of muscle mass with detraining, yet a maintenance of muscle strength; and (3) the similar muscle growth between low-load and high-load resistance training, yet divergent results in strength. Muscle Nerve 54: 1012-1014, 2016. © 2016 Wiley Periodicals, Inc.

  20. The relation between childhood obesity and adenotonsillar hypertrophy.

    Science.gov (United States)

    Daar, Ghaniya; Sarı, Kamran; Gencer, Zeliha Kapusuz; Ede, Hüseyin; Aydın, Reha; Saydam, Levent

    2016-02-01

    Childhood obesity is a common and significant public health problem all over the world. As a well-known fact obese children have an increased risk of obesity-associated comorbidities, including obstructive sleep apnea, diabetes, and cardiovascular disorders at an earlier age compared to their normal weight peers. They also have an increased risk of poor self-esteem, greater body dissatisfaction, and increased peer teasing that lead to a lower health-related quality of life. While the presence of adenoid hypertrophy and increased rate of obstructive sleep apnea frequently co-exists in majority of cases. We have limited knowledge about the effect of adenotonsillar hypertrophy on development of childhood obesity. In this study, we aimed to investigate the association between obesity, presence of adenotonsillar hypertrophy and the quality of life parameters in obese children as measured by the OSA-18 quality of life questionnaire. Fifty obese children aged between 3 and 18 years and 50 age- and gender-matched otherwise children were enrolled to the study. All subjects were routinely examined by the otolaryngologist before enrollment. The size of adenoid hypertrophy was measured using lateral cephalometric radiographs. The tonsils were also graded using the schema recommended by Brodsky et al. We used OSA-18 questionnaires to evaluate the subjects' quality of life issues. We found, 34 % of obese group had tonsillar hypertrophy while the rate was 6 % in control group. Similarly 16 % of obese group had tonsillar hypertrophy compared to only 4 % in non-obese group. It was also noted that total OSA-18 scores of obese group were significantly higher than those of non-obese group. In subgroup analysis of obese group, total OSA-18 score of obese subjects with either adenoid and/or tonsillar hypertrophy was significantly higher than that of obese subjects without adenoid or tonsillar hypertrophy. As the related literature suggests that the impact of adenotonsillar size on OSA

  1. Autoimmune hepatitis.

    Science.gov (United States)

    Strassburg, Christian P

    2010-10-01

    Autoimmune hepatitis is a chronic inflammatory disease of the liver with a dismal prognosis when left untreated. Key for the improvement of prognosis is a timely diagnosis before cirrhosis has developed. This is reached by the exclusion of other causes of hepatitis, elevated immunoglobulin G, autoantibody profile and histological assessment. Treatment achieves remission rates in 80% of individuals and consists of immunosuppression with corticosteroids and azathioprine. A recent randomised controlled multicenter trial has added budesonide to the effective treatment options in non-cirrhotic patients and leads to a reduction of unwanted steroid side effects. Autoimmune hepatitis is an autoimmune disease of unknown aetiology. Association studies of major histocompatibility complex and other genes demonstrate an influence of immunogenetics. However, apart from the autoimmune polyglandular syndrome type 1, in which 10% of patients suffer from an autoantibody-positive autoimmune hepatitis linked to mutations of the autoimmune regulator gene, there is no clear evidence for a hereditary aetiology of this disease. Copyright © 2010 Elsevier Ltd. All rights reserved.

  2. Hepatitis A vaccine associated with autoimmune hepatitis

    Institute of Scientific and Technical Information of China (English)

    PA Berry; G Smith-Laing

    2007-01-01

    To describe a case of probable relapsing autoimmune hepatitis associated with vaccination against hepatitis A virus (HAV). A case report and review of literature were written concerning autoimmune hepatitis in association with hepatitis A and other hepatotropic viruses. Soon after the administration of formalin-inactivated hepatitis A vaccine, a man who had recently recovered from an uncharacterized but self-limiting hepatitic illness,experienced a severe deterioration (AST 1687 U/L, INR 1.4). Anti-nuclear antibodies were detectable, and liver biopsy was compatible with autoimmune hepatitis. The observation supports the role of HAV as a trigger of autoimmune hepatitis. Studies in helper T-cell activity and antibody expression against hepatic proteins in the context of hepatitis A infection are summarized, and the concept of molecular mimicry with regard to other forms of viral hepatitis and autoimmunity is briefly explored.

  3. Hepatic amebiasis

    Directory of Open Access Journals (Sweden)

    José Maria Salles

    2003-04-01

    Full Text Available Amebiasis can be considered the most aggressive disease of the human intestine, responsible in its invasive form for clinical syndromes, ranging from the classic dysentery of acute colitis to extra-intestinal disease, with emphasis on hepatic amebiasis, unsuitably named amebic liver abscess. Found worldwide, with a high incidence in India, tropical regions of Africa, Mexico and other areas of Central America, it has been frequently reported in Amazonia. The trophozoite reaches the liver through the portal system, provoking enzymatic focal necrosis of hepatocytes and multiple micro-abscesses that coalesce to develop a single lesion whose central cavity contains a homogeneous thick liquid, with typically reddish brown and yellow color similar to "anchovy paste". Right upper quadrant pain, fever and hepatomegaly are the predominant symptoms of hepatic amebiasis. Jaundice is reported in cases with multiple lesions or a very large abscess, and it affects the prognosis adversely. Besides chest radiography, ultrasonography and computerized tomography have brought remarkable contributions to the diagnosis of hepatic abscesses. The conclusive diagnosis is made however by the finding of Entamoeba histolytica trophozoites in the pus and by the detection of serum antibodies to the amoeba. During the evolution of hepatic amebiasis, in spite of the availability of highly effective drugs, some important complications may occur with regularity and are a result of local perforation with extension into the pleural and pericardium cavities, causing pulmonary abscesses and purulent pericarditis, respectively The ruptures into the abdominal cavity may lead to subphrenic abscesses and peritonitis. The treatment of hepatic amebiasis is made by medical therapy, with metronidazole as the initial drug, followed by a luminal amebicide. In patients with large abscesses, showing signs of imminent rupture, and especially those who do not respond to medical treatment, a

  4. Pregnancy restores the regenerative capacity of the aged liver via activation of an mTORC1-controlled hyperplasia/hypertrophy switch.

    Science.gov (United States)

    Gielchinsky, Yuval; Laufer, Neri; Weitman, Efi; Abramovitch, Rinat; Granot, Zvi; Bergman, Yehudit; Pikarsky, Eli

    2010-03-15

    Regenerative capacity is progressively lost with age. Here we show that pregnancy markedly improved liver regeneration in aged mice concomitantly with inducing a switch from proliferation-based liver regeneration to a regenerative process mediated by cell growth. We found that the key mediator of this switch was the Akt/mTORC1 pathway; its inhibition blocked hypertrophy, while increasing proliferation. Moreover, pharmacological activation of this pathway sufficed to induce the hypertrophy module, mimicking pregnancy. This treatment dramatically improved hepatic regenerative capacity and survival of old mice. Thus, cell growth-mediated mass reconstitution, which is relatively resistant to the detrimental effects of aging, is employed in a physiological situation and holds potential as a therapeutic strategy for ameliorating age-related functional deterioration.

  5. Cytoskeletal mechanics in pressure-overload cardiac hypertrophy

    Science.gov (United States)

    Tagawa, H.; Wang, N.; Narishige, T.; Ingber, D. E.; Zile, M. R.; Cooper, G. 4th

    1997-01-01

    We have shown that the cellular contractile dysfunction characteristic of pressure-overload cardiac hypertrophy results not from an abnormality intrinsic to the myofilament portion of the cardiocyte cytoskeleton but rather from an increased density of the microtubule component of the extramyofilament portion of the cardiocyte cytoskeleton. To determine how, in physical terms, this increased microtubule density mechanically overloads the contractile apparatus at the cellular level, we measured cytoskeletal stiffness and apparent viscosity in isolated cardiocytes via magnetic twisting cytometry, a technique by which magnetically induced force is applied directly to the cytoskeleton through integrin-coupled ferromagnetic beads coated with Arg-Gly-Asp (RGD) peptide. Measurements were made in two groups of cardiocytes from cats with right ventricular (RV) hypertrophy induced by pulmonary artery banding: (1) those from the pressure-overloaded RV and (2) those from the normally loaded same-animal control left ventricle (LV). Cytoskeletal stiffness increased almost twofold, from 8.53 +/- 0.77 dyne/cm2 in the normally loaded LV cardiocytes to 16.46 +/- 1.32 dyne/cm2 in the hypertrophied RV cardiocytes. Cytoskeletal apparent viscosity increased almost fourfold, from 20.97 +/- 1.92 poise in the normally loaded LV cardiocytes to 87.85 +/- 6.95 poise in the hypertrophied RV cardiocytes. In addition to these baseline data showing differing stiffness and, especially, apparent viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine was found to return both the stiffness and the apparent viscosity of the pressure overload-hypertrophied RV cells fully to normal. Conversely, microtubule hyperpolymerization by taxol increased the stiffness and apparent viscosity values of normally loaded LV cardiocytes to the abnormal values given above for pressure-hypertrophied RV cardiocytes. Thus, increased microtubule density constitutes primarily a viscous load on

  6. Cytoskeletal mechanics in pressure-overload cardiac hypertrophy

    Science.gov (United States)

    Tagawa, H.; Wang, N.; Narishige, T.; Ingber, D. E.; Zile, M. R.; Cooper, G. 4th

    1997-01-01

    We have shown that the cellular contractile dysfunction characteristic of pressure-overload cardiac hypertrophy results not from an abnormality intrinsic to the myofilament portion of the cardiocyte cytoskeleton but rather from an increased density of the microtubule component of the extramyofilament portion of the cardiocyte cytoskeleton. To determine how, in physical terms, this increased microtubule density mechanically overloads the contractile apparatus at the cellular level, we measured cytoskeletal stiffness and apparent viscosity in isolated cardiocytes via magnetic twisting cytometry, a technique by which magnetically induced force is applied directly to the cytoskeleton through integrin-coupled ferromagnetic beads coated with Arg-Gly-Asp (RGD) peptide. Measurements were made in two groups of cardiocytes from cats with right ventricular (RV) hypertrophy induced by pulmonary artery banding: (1) those from the pressure-overloaded RV and (2) those from the normally loaded same-animal control left ventricle (LV). Cytoskeletal stiffness increased almost twofold, from 8.53 +/- 0.77 dyne/cm2 in the normally loaded LV cardiocytes to 16.46 +/- 1.32 dyne/cm2 in the hypertrophied RV cardiocytes. Cytoskeletal apparent viscosity increased almost fourfold, from 20.97 +/- 1.92 poise in the normally loaded LV cardiocytes to 87.85 +/- 6.95 poise in the hypertrophied RV cardiocytes. In addition to these baseline data showing differing stiffness and, especially, apparent viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine was found to return both the stiffness and the apparent viscosity of the pressure overload-hypertrophied RV cells fully to normal. Conversely, microtubule hyperpolymerization by taxol increased the stiffness and apparent viscosity values of normally loaded LV cardiocytes to the abnormal values given above for pressure-hypertrophied RV cardiocytes. Thus, increased microtubule density constitutes primarily a viscous load on

  7. Shensongyangxin protects against pressure overload‑induced cardiac hypertrophy.

    Science.gov (United States)

    Shen, Di-Fei; Wu, Qing-Qing; Ni, Jian; Deng, Wei; Wei, Cong; Jia, Zhen-Hua; Zhou, Heng; Zhou, Meng-Qiao; Bian, Zhou-Yan; Tang, Qi-Zhu

    2016-01-01

    Shensongyangxin (SSYX) is a medicinal herb, which has long been used in traditional Chinese medicine. Various pharmacological activities of SSYX have been identified. However, the role of SSYX in cardiac hypertrophy remains to be fully elucidated. In present study, aortic banding (AB) was performed to induce cardiac hypertrophy in mice. SSYX (520 mg/kg) was administered by daily gavage between 1 and 8 weeks following surgery. The extent of cardiac hypertrophy was then evaluated by pathological and molecular analyses of heart tissue samples. In addition, in vitro experiments were performed to confirm the in vivo results. The data of the present study demonstrated that SSYX prevented the cardiac hypertrophy and fibrosis induced by AB, as assessed by measurements of heart weight and gross heart size, hematoxylin and eosin staining, cross‑sectional cardiomyocyte area and the mRNA expression levels of hypertrophic markers. SSYX also inhibited collagen deposition and suppressed the expression of transforming growth factor β (TGFβ), connective tissue growth factor, fibronectin, collagen Ⅰα and collagen Ⅲα, which was mediated by the inhibition of the TGFβ/small mothers against decapentaplegic (Smad) signaling pathway. The inhibitory action of SSYX on cardiac hypertrophy was mediated by the inhibition of Akt signaling. In vitro investigations in the rat H9c2 cardiac cells also demonstrated that SSYX attenuated angiotensin II‑induced cardiomyocyte hypertrophy. These findings suggested that SSYX attenuated cardiac hypertrophy and fibrosis in the pressure overloaded mouse heart. Therefore, the cardioprotective effect of SSYX is associated with inhibition of the Akt and TGFβ/Smad signaling pathways.

  8. Smart Chips for Smart Surroundings - 4S

    NARCIS (Netherlands)

    Schuler, Eberhard; König, Ralf; Becker, Jürgen; Rauwerda, Gerard; Burgwal, van de Marcel; Smit, Gerard J.M.; Cardoso, João M.P.; Hübner, Michael

    2011-01-01

    The overall mission of the 4S project (Smart Chips for Smart Surroundings) was to define and develop efficient flexible, reconfigurable core building blocks, including the supporting tools, for future Ambient System Devices. Reconfigurability offers the needed flexibility and adaptability, it provid

  9. Phosphorylation of ribosomal protein S6 mediates compensatory renal hypertrophy

    Science.gov (United States)

    Xu, Jinxian; Chen, Jianchun; Dong, Zheng; Meyuhas, Oded; Chen, Jian-Kang

    2014-01-01

    The molecular mechanism underlying renal hypertrophy and progressive nephron damage remains poorly understood. Here we generated congenic ribosomal protein S6 (rpS6) knockin mice expressing non-phosphorylatable rpS6 and found that uninephrectomy-induced renal hypertrophy was significantly blunted in these knockin mice. Uninephrectomy-induced increases in cyclin D1 and decreases in cyclin E in the remaining kidney were attenuated in the knockin mice compared to their wild-type littermates. Uninephrectomy induced rpS6 phosphorylation in the wild type mice; however, no rpS6 phosphorylation was detected in uninephrectomized or sham-operated knockin mice. Nonetheless, uninephrectomy stimulated comparable 4E-BP1 phosphorylation in both knockin and wild type mice, indicating that mTORC1 was still activated in the knockin mice. Moreover, the mTORC1 inhibitor rapamycin prevented both rpS6 and 4E-BP1 phosphorylation, significantly blunted uninephrectomy-induced renal hypertrophy in wild type mice, but did not prevent residual renal hypertrophy despite inhibiting 4E-BP1 phosphorylation in uninephrectomized knockin mice. Thus, both genetic and pharmacological approaches unequivocally demonstrate that phosphorylated rpS6 is a downstream effector of the mTORC1-S6K1 signaling pathway mediating renal hypertrophy. Hence, rpS6 phosphorylation facilitates the increase in cyclin D1 and decrease in cyclin E1 that underlie the hypertrophic nature of uninephrectomy-induced kidney growth. PMID:25229342

  10. Developmental delays in preschool children with adenotonsillar hypertrophy.

    Science.gov (United States)

    Soylu, Erkan; Soylu, Nusret; Polat, Cahit; Sakallıoğlu, Öner; Uçur, Ömer; Bozdoğan, Gökçe

    2016-01-01

    This study aims to investigate the effects of adenotonsillar hypertrophy on general development, as well as fine and gross motor capabilities, social communication, and language development in children with adenotonsillar hypertrophy by applying the Denver Developmental Screening Test-II. The study included 30 patients (12 boys, 18 girls; mean age 53.3±12.2 months; range 32 to 72 months) who were indicated for adenotonsillectomy due to adenotonsillar hypertrophy between February 2013 and July 2013. The control group comprised 30 children participants (12 boys, 18 girls; mean age 53.1±12.8 months; range 32 to 72 months) with no adenotonsillectomy indication. All participants included in the study were performed routine physical examination, flexible fiberoptic nasopharyngoscopy, and tympanometry. Brodsky scale and fiberendoscopic findings were used to categorize tonsil and adenoid sizes, respectively. Following ear, nose, and throat evaluation, a psychologist conducted Denver Developmental Screening Test-II in all participants blindly. Adenotonsillar hypertrophy patients had higher abnormal levels of general development (c2=7.13, p=0.028). Although patients and controls had similar levels of fine motor, gross motor, and personal-social development levels, there was a statistically borderline difference between them in terms of language development (t=1.82, p=0.074). The possibility of adenotonsillar hypertrophy should definitely be considered in children with delayed general and language developments.

  11. AVE 0991 attenuates cardiac hypertrophy through reducing oxidative stress.

    Science.gov (United States)

    Ma, Yuedong; Huang, Huiling; Jiang, Jingzhou; Wu, Lingling; Lin, Chunxi; Tang, Anli; Dai, Gang; He, Jiangui; Chen, Yili

    2016-06-10

    AVE 0991, the nonpeptide angiotensin-(1-7) (Ang-(1-7)) analog, is recognized as having beneficial cardiovascular effects. However, the mechanisms have not been fully elucidated. This study was designed to investigate the effects of AVE 0991 on cardiac hypertrophy and the mechanisms involved. Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg·day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end-diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers. Furthermore, AVE 0991 inhibited the expression of NOX 2 and NOX 4, meaning that AVE 0991 reduced oxidative stress of cardiac hypertrophy mice. Our data showed that AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress.

  12. Neurogenic muscle hypertrophy in a 12-year-old girl.

    Science.gov (United States)

    Zutelija Fattorini, Matija; Gagro, Alenka; Dapic, Tomislav; Krakar, Goran; Marjanovic, Josip

    2017-01-01

    Muscular hypertrophy secondary to denervation is very rare, but well-documented phenomena in adults. This is the first report of a child with neurogenic unilateral hypertrophy due to S1 radiculopathy. A 12-year-old girl presented with left calf hypertrophy and negative history of low back pain or trauma. The serum creatinine kinase level and inflammatory markers were normal. Magnetic resonance imaging showed muscle hypertrophy of the left gastrocnemius and revealed a protruded lumbar disc at the L5-S1 level. The protruded disc abuts the S1 root on the left side. Electromyography showed mild left S1 radiculopathy. Passive stretching and work load might clarify the origin of neurogenic hypertrophy but there is still a need for further evidence. Clinical, laboratory, magnetic resonance imaging and electromyography findings showed that S1 radiculopathy could be a cause of unilateral calf swelling in youth even in the absence of a history of back or leg pain. Copyright © 2016 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

  13. Phlorizin Prevents Glomerular Hyperfiltration but not Hypertrophy in Diabetic Rats

    Directory of Open Access Journals (Sweden)

    Slava Malatiali

    2008-01-01

    Full Text Available The relationships of renal and glomerular hypertrophies to development of hyperfiltration and proteinuria early in streptozotocin-induced diabetes were explored. Control, diabetic, phlorizin-treated controls, and diabetic male Fischer rats were used. Phlorizin (an Na+-glucose cotransport inhibitor was given at a dose sufficient to normalize blood glucose. Inulin clearance (Cinulin and protein excretion rate (PER were measured. For morphometry, kidney sections were stained with periodic acid Schiff. At one week, diabetes PER increased 2.8-folds (P<.001, Cinulin increased 80% (P<.01. Kidney wet and dry weights increased 10%–12% (P<.05, and glomerular tuft area increased 9.3% (P<.001. Phlorizin prevented proteinuria, hyperfiltration, and kidney hypertrophy, but not glomerular hypertrophy. Thus, hyperfiltration, proteinuria, and whole kidney hypertrophy were related to hyperglycemia but not to glomerular growth. Diabetic glomerular hypertrophy constitutes an early event in the progression of glomerular pathology which occurs in the absence of mesangial expansion and persists even after changes in protein excretion and GFR are reversed through glycemic control.

  14. Hepatic autoregulation

    DEFF Research Database (Denmark)

    Staehr, Peter; Hother-Nielsen, Ole; Beck-Nielsen, Henning

    2007-01-01

    The effect of increased glycogenolysis, simulated by galactose's conversion to glucose, on the contribution of gluconeogenesis (GNG) to hepatic glucose production (GP) was determined. The conversion of galactose to glucose is by the same pathway as glycogen's conversion to glucose, i.e., glucose 1......-phosphate --> glucose 6-phosphate --> glucose. Healthy men (n = 7) were fasted for 44 h. At 40 h, hepatic glycogen stores were depleted. GNG then contributed approximately 90% to a GP of approximately 8 micromol.kg(-1).min(-1). Galactose, 9 g/h, was infused over the next 4 h. The contribution of GNG to GP...... declined from approximately 90% to 65%, i.e., by approximately 2 micromol.kg(-1).min(-1). The rate of galactose conversion to blood glucose, measured by labeling the infused galactose with [1-(2)H]galactose (n = 4), was also approximately 2 micromol.kg(-1).min(-1). The 41st h GP rose by approximately 1...

  15. [Application of philosophy on comprehensive analysis of adenoid hypertrophy space occupying effect in meticulous adenoidectomy].

    Science.gov (United States)

    Lu, Yuanyuan; Zhang, Qingxiang; Yu, Zhenkun

    2015-07-01

    To achieve targeted and meticulous surgery of adenoid hypertrophy, a comprehensive analysis of adenoid hypertrophy space occupying effect and morphological evaluation were conducted and the clinical results were retrospectively analyzed. One hundred and sixty-three children with adenoid hypertrophy were treated in our department from May 2013 to May 2014. All children received three examinations preoperatively, including: Nasopharyngo-fiberoscopy, Audiometry and Tympanometry. Based on the results, space occupying effect of adenoid hypertrophy was divided into three types: vertical hypertrophy type, horizontal hypertrophy type and vertical & horizontal hypertrophy type. We assumed the causal relationship with vertical hypertrophy type to snoring (nasal blockage) and horizontal hypertrophy type to secretory otitis media respectively. All children received transoral endoscopic adenoidectomy with radiofrequency ablation. The postoperative followup of these children for 6 to 12 months showed that the vertical hypertrophy type and horizontal hypertrophy type children all recovered from the syndromes of snoring (nasal blockage) and secretory otitis media respectively. The nasopharyngo-fiberoscopy showed that the nasopharyngeal space was smooth and the bilateral choanas opened well. No recurrence was found. The philosophy of comprehensive analysis on adenoid hypertrophy space occupying effect could help the surgeons understand adenoid hypertrophy better and can guide the adenoidectomy more meticulously.

  16. Hepatitis C Test

    Science.gov (United States)

    ... products and services. Advertising & Sponsorship: Policy | Opportunities Hepatitis C Testing Share this page: Was this page helpful? Also known as: Hepatitis C Antibody; Anti-HCV; HCV-PCR; HCV-RNA; Hepatitis ...

  17. HIV and Hepatitis B

    Science.gov (United States)

    ... AIDS-Related Opportunistic Infections and Coinfections HIV and Hepatitis B (Last updated 8/31/2016; last reviewed ... should be treated for both diseases. What is hepatitis B? Hepatitis B is a liver disease caused ...

  18. Drug-induced hepatitis

    Science.gov (United States)

    Toxic hepatitis ... to get liver damage. Some drugs can cause hepatitis with small doses, even if the liver breakdown ... liver. Many different drugs can cause drug-induced hepatitis. Painkillers and fever reducers that contain acetaminophen are ...

  19. HIV and Hepatitis C

    Science.gov (United States)

    ... AIDS-Related Opportunistic Infections and Coinfections HIV and Hepatitis C (Last updated 8/31/2016; last reviewed ... the medicines for any side effects. What is hepatitis C? Hepatitis C is a liver disease caused ...

  20. Hepatitis B Test

    Science.gov (United States)

    ... helpful? Also known as: HBV Tests; Hep B; anti-HBs; Hepatitis B Surface Antibody; HBsAg; Hepatitis B Surface ... including "HBV carrier" state. Hepatitis B surface antibody (anti-HBs) Detects antibody produced in response to HBV surface ...

  1. Preventing hepatitis A

    Science.gov (United States)

    Hepatitis A is inflammation (irritation and swelling) of the liver caused by the hepatitis A virus. You can take several steps to ... reduce your risk of spreading or catching the hepatitis A virus: Always wash your hands thoroughly after ...

  2. Travelers' Health: Hepatitis E

    Science.gov (United States)

    ... Chapter 3 - Hepatitis C Chapter 3 - Histoplasmosis Hepatitis E Chong-Gee Teo INFECTIOUS AGENT Infection is caused ... for infection. Map 3-06. Distribution of hepatitis E virus infection 1 PDF Version (printable) 1 Disease ...

  3. Hepatitis B virus (image)

    Science.gov (United States)

    Hepatitis B is also known as serum hepatitis and is spread through blood and sexual contact. It is ... population. This photograph is an electronmicroscopic image of hepatitis B virus particles. (Image courtesy of the Centers for ...

  4. Hepatitis C.

    Science.gov (United States)

    Sharara, A I; Hunt, C M; Hamilton, J D

    1996-10-15

    To review the virology, epidemiology, pathogenesis, natural history, clinical manifestations, and current treatment of hepatitis C virus (HCV) infection. The MEDLINE database (1966 to 1996) was searched for English-language articles and abstracts on HCV and non-A, non-B hepatitis. Papers cited in relevant primary articles were also reviewed. More than 500 original and review articles were evaluated, and the most relevant were selected. Data were extracted and reviewed by all authors. In most patients, HCV infection results in chronic hepatitis. The disease is insidious and subclinical but may progress over decades into end-stage liver disease and hepatocellular carcinoma, which makes HCV cirrhosis a leading indication for orthotopic liver transplantation. Current diagnostic methods are highly sensitive and specific, and quantitative assessment of viral load may help to predict and monitor response to treatment. The only available therapeutic option is interferon, and this agent is effective in only a small subset of patients. Infection with HCV is a significant public health problem that has important clinical and financial consequences. The tailoring of specific therapy according to viral load or genotype, better patient selection, and use of combination drug regimens may improve the chance of viral clearance and sustained biochemical and histologic response. Further understanding of the basic virology of HCV and the exact mechanisms of viral persistence and tissue injury is needed to help define future therapeutic and preventive strategies.

  5. [Hepatitis E].

    Science.gov (United States)

    Scotto, Gaetano; Bulla, Fabio; Campanale, Francesca; Tartaglia, Alessandra; Fazio, Vincenzina

    2013-09-01

    Hepatitis E virus (HEV) represents the main aetiological agent of enteric non-A hepatitis and is the only member of a new virus, Hepevirus, belonging to the family of Hepeviridae. HEV is the single most important cause of acute clinical hepatitis among adults in many areas of the developing world, specifically the Indian subcontinent and Southeast Asia, the Middle East and North Africa, where it is a common cause of sporadic and epidemic waterborne outbreaks and results in a high rate of morbidity and death, especially in pregnant women. Once thought of as an infection confined to developing countries, it is now recognized as a geographically widely distributed disease. In low-endemic regions (Western countries), sporadic cases of locally-acquired HEV infection are reported, acquired possibly through zoonotic transmission from pigs, wild boars or deer. In persons with pre-existing chronic liver disease, HEV superinfection can present as acute-on-chronic liver disease. In European countries, chronic infection, which may progress to liver cirrhosis, has been reported among immunosuppressed persons. Two testing vaccines proved to be highly effective in preventing the disease; these vaccines should be of particular use in groups that are at high risk of HEV infection.

  6. Hepatitis Information for the Public

    Science.gov (United States)

    ... Requirements for Viral Hepatitis Liver Cancer and Viral Hepatitis Viral Hepatitis and Young Persons Who Inject Drugs National ... Recommend on Facebook Tweet Share Compartir What is Viral Hepatitis? The word "hepatitis" means inflammation of the liver . ...

  7. Nitric oxide and the enigma of cardiac hypertrophy.

    Science.gov (United States)

    Kempf, Tibor; Wollert, Kai C

    2004-06-01

    In pathological conditions associated with persistent increases in hemodynamic workload (old myocardial infarction, high blood pressure, valvular heart disease), a number of signalling pathways are activated in the heart, all of which promote hypertrophic growth of the heart, characterised at the cellular level by increases in individual cardiac myocyte size. Some of these pathways are required for a successful adaptation to cardiac injury. Other pathways are maladaptive, however, as they lead to progressive contractile dysfunction and heart failure. The free radical gas nitric oxide and natriuretic peptides, both of which are produced in the heart, have emerged as endogenous inhibitors of maladaptive hypertrophy signalling. Overall, it appears that cardiac hypertrophy is controlled by an interplay of pro- and antihypertrophic signalling networks. This delicate balance can tip towards adaptation or heart failure. In the future, patients living with cardiac disease may benefit from therapeutic strategies targeting maladaptive hypertrophy signalling pathways. Copyright 2004 Wiley Periodicals, Inc.

  8. The Interstellar Cloud Surrounding the Solar System

    Science.gov (United States)

    Frisch, P. C.

    Ultraviolet spectral data of nearby stars indicate that the cloud surrounding the solar system has an average neutral density n(HI)~0.1 cm-3, temperature ~6800 K, and turbulence ~1.7 km/s. Comparisons between the anomalous cosmic ray data and ultraviolet data suggest that the electron density is in the range n(e-)~0.22 to 0.44 cm-3. This cloud is flowing past the Sun from a position centered in the Norma-Lupis region. The cloud properties are consistent with interstellar gas which originated as material evaporated from the surfaces of embedded clouds in the Scorpius-Centaurus Association, and which was then displaced towards the Sun by a supernova event about 4 Myrs ago. The Sun and surrounding cloud velocities are nearly perpendicular in space, and this cloud is sweeping past the Sun. The morphology of this cloud can be reconstructed by assuming that the cloud moves in a direction parallel to the surface normal. With this assumption, the Sun entered the surrounding cloud 2000 to 8000 years ago, and is now about 0.05 to 0.16 pc from the cloud surface. Prior to its recent entry into the surrounding cloud complex, the Sun was embedded in a region of space with average density lower than 0.0002 cm-3. If a denser cloud velocity component seen towards alpha Cen A,B is real, it will encounter the solar system within 50,000 yr. The nearby magnetic field seen upwind has a spatial orientation that is parallel to the cloud surface. The nearby star Sirius is viewed through the wake of the solar system, but this direction also samples the hypothetical cloud interface. Comparisons of anomalous cosmic ray and interstellar absorption line data suggest that trace elements in the surrounding cloud are in ionization equilibrium. Data towards nearby white dwarfs indicate partial helium ionization, N(N(HI)(/N(HeI)>~13.7, which is consistent with pickup ion data within the solar system if less than 40% hydrogen ionization occurs in the heliopause region. However, the white dwarfs may

  9. Hepatitis B Vaccine

    Science.gov (United States)

    ... a combination product containing Haemophilus influenzae type b, Hepatitis B Vaccine) ... combination product containing Diphtheria, Tetanus Toxoids, Acellular Pertussis, Hepatitis B, Polio Vaccine)

  10. Association of heart failure hospitalizations with combined electrocardiography and echocardiography criteria for left ventricular hypertrophy

    DEFF Research Database (Denmark)

    Gerdts, Eva; Okin, Peter M; Boman, Kurt

    2012-01-01

    The value of performing echocardiography in hypertensive patients with electrocardiographic left ventricular hypertrophy (LVH) is uncertain.......The value of performing echocardiography in hypertensive patients with electrocardiographic left ventricular hypertrophy (LVH) is uncertain....

  11. Indian hedgehog signals independently of PTHrP to promote chondrocyte hypertrophy

    National Research Council Canada - National Science Library

    Kinglun Kingston Mak; Henry M. Kronenberg; Pao-Tien Chuang; Susan Mackem; Yingzi Yang

    2008-01-01

    .... Indian hedgehog (Ihh) and PTHrP signaling play crucial roles in regulating the onset of chondrocyte hypertrophy by forming a negative feedback loop, in which Ihh signaling regulates chondrocyte hypertrophy by controlling PTHrP expression...

  12. Podocyte hypertrophy precedes apoptosis under experimental diabetic conditions.

    Science.gov (United States)

    Lee, Sun Ha; Moon, Sung Jin; Paeng, Jisun; Kang, Hye-Young; Nam, Bo Young; Kim, Seonghun; Kim, Chan Ho; Lee, Mi Jung; Oh, Hyung Jung; Park, Jung Tak; Han, Seung Hyeok; Yoo, Tae-Hyun; Kang, Shin-Wook

    2015-08-01

    Podocyte hypertrophy and apoptosis are two hallmarks of diabetic glomeruli, but the sequence in which these processes occur remains a matter of debate. Here we investigated the effects of inhibiting hypertrophy on apoptosis, and vice versa, in both podocytes and glomeruli, under diabetic conditions. Hypertrophy and apoptosis were inhibited using an epidermal growth factor receptor inhibitor (PKI 166) and a pan-caspase inhibitor (zAsp-DCB), respectively. We observed significant increases in the protein expression of p27, p21, phospho-eukaryotic elongation factor 4E-binding protein 1, and phospho-p70 S6 ribosomal protein kinase, in both cultured podocytes exposed to high-glucose (HG) medium, and streptozotocin-induced diabetes mellitus (DM) rat glomeruli. These increases were significantly inhibited by PKI 166, but not by zAsp-DCB. In addition, the amount of protein per cell, the relative cell size, and the glomerular volume were all significantly increased under diabetic conditions, and these changes were also blocked by treatment with PKI 166, but not zAsp-DCB. Increased protein expression of cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase, together with increased Bax/Bcl-2 ratios, were also observed in HG-stimulated podocytes and DM glomeruli. Treatment with either zAsp-DCB or PKI 166 resulted in a significant attenuation of these effects. Both PKI 166 and zAsp-DCB also inhibited the increase in number of apoptotic cells, as assessed by Hoechst 33342 staining and TUNEL assay. Under diabetic conditions, inhibition of podocyte hypertrophy results in attenuated apoptosis, whereas blocking apoptosis has no effect on podocyte hypertrophy, suggesting that podocyte hypertrophy precedes apoptosis.

  13. Supra-physiological dose of testosterone induces pathological cardiac hypertrophy.

    Science.gov (United States)

    Pirompol, Prapawadee; Teekabut, Vassana; Weerachatyanukul, Wattana; Bupha-Intr, Tepmanas; Wattanapermpool, Jonggonnee

    2016-04-01

    Testosterone and androgenic anabolic steroids have been misused for enhancement of physical performance despite many reports on cardiac sudden death. Although physiological level of testosterone provided many regulatory benefits to human health, including the cardiovascular function, supra-physiological levels of the hormone induce hypertrophy of the heart with unclear contractile activation. In this study, dose- and time-dependent effects of high-testosterone treatment on cardiac structure and function were evaluated. Adult male rats were divided into four groups of testosterone treatment for 0, 5, 10, and 20 mg/kg BW for 4, 8, or 12 weeks. Increases in both percentage heart:body weight ratio and cardiomyocyte cross-sectional area in representing hypertrophy of the heart were significantly shown in all testosterone-treated groups to the same degree. In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation. In contrast, pathological cardiac hypertrophy was observed in 8- and 12-week testosterone-treated groups, as indicated by suppression of myofilament activation and myocardial collagen deposition without transition of MHC isoforms. Only in 12-week testosterone-treated group, eccentric cardiac hypertrophy was demonstrated with unaltered myocardial stiffness, but significant reductions in the phosphorylation signals of ERK1/2 and mTOR. Results of our study suggest that the outcome of testosterone-induced cardiac hypertrophy is not dose dependent but is rather relied on the factor of exposure to duration in inducing maladaptive responses of the heart. © 2016 Society for Endocrinology.

  14. Airway smooth muscle growth in asthma: proliferation, hypertrophy, and migration.

    Science.gov (United States)

    Bentley, J Kelley; Hershenson, Marc B

    2008-01-01

    Increased airway smooth muscle mass is present in fatal and non-fatal asthma. However, little information is available regarding the cellular mechanism (i.e., hyperplasia vs. hypertrophy). Even less information exists regarding the functional consequences of airway smooth muscle remodeling. It would appear that increased airway smooth muscle mass would tend to increase airway narrowing and airflow obstruction. However, the precise effects of increased airway smooth muscle mass on airway narrowing are not known. This review will consider the evidence for airway smooth muscle cell proliferation and hypertrophy in asthma, potential functional effects, and biochemical mechanisms.

  15. Investigating the Mechanism of Hyperglycemia-Induced Fetal Cardiac Hypertrophy

    Science.gov (United States)

    Ma, Zheng-lai; Jia, Wei-jing; Wu, Xia; Wang, Xiao-yu; He, Mei-yao; Cheng, Xin; Li, Wei-jing; Yang, Xuesong; Liu, Guo-sheng

    2015-01-01

    Hyperglycemia in diabetic mothers enhances the risk of fetal cardiac hypertrophy during gestation. However, the mechanism of high-glucose-induced cardiac hypertrophy is not largely understood. In this study, we first demonstrated that the incidence rate of cardiac hypertrophy dramatically increased in fetuses of diabetic mothers using color ultrasound examination. In addition, human fetal cardiac hypertrophy was successfully mimicked in a streptozotocin (STZ)-induced diabetes mouse model, in which mouse cardiac hypertrophy was diagnosed using type-M ultrasound and a histological assay. PH3 immunofluorescent staining of mouse fetal hearts and in vitro-cultured H9c2 cells indicated that cell proliferation decreased in E18.5, E15.5 and E13.5 mice, and cell apoptosis in H9c2 cells increased in the presence of high glucose in a dose-dependent manner. Next, we found that the individual cardiomyocyte size increased in pre-gestational diabetes mellitus mice and in response to high glucose exposure. Meanwhile, the expression of β-MHC and BMP-10 was up-regulated. Nkx2.5 immunofluorescent staining showed that the expression of Nkx2.5, a crucial cardiac transcription factor, was suppressed in the ventricular septum, left ventricular wall and right ventricular wall of E18.5, E15.5 and E13.5 mouse hearts. However, cardiac hypertrophy did not morphologically occur in E13.5 mouse hearts. In cultured H9c2 cells exposed to high glucose, Nkx2.5 expression decreased, as detected by both immunostaining and western blotting, and the expression of KCNE1 and Cx43 was also restricted. Taken together, alterations in cell size rather than cell proliferation or apoptosis are responsible for hyperglycemia-induced fetal cardiac hypertrophy. The aberrant expression of Nkx2.5 and its regulatory target genes in the presence of high glucose could be a principal component of pathogenesis in the development of fetal cardiac hypertrophy. PMID:26418041

  16. Congenital hypertrophy of multiple intrinsic muscles of the foot.

    Science.gov (United States)

    Shiraishi, Tomohiro; Park, Susam; Niu, Atushi; Hasegawa, Hiromi

    2014-12-01

    Congenital hypertrophy of a single intrinsic muscle of the foot is rare, and as far as we know, only six cases have been reported. We describe a case of congenital anomaly that showed hypertrophy of multiple intrinsic muscles of the foot; the affected muscles were all the intrinsic muscles of the foot except the extensor digitorum brevis or extensor hallucis. Other tissues such as adipose tissue, nervous tissue, or osseous tissue showed no abnormalities. To reduce the volume of the foot we removed parts of the enlarged muscles.

  17. Bacterial meningitis after radiofrequency diathermy for adenoid hypertrophy.

    Science.gov (United States)

    Nagasaki, Azusa; Sato, Atsuo; Shiro, Hiroyuki

    2014-06-01

    A 6-year-old otherwise healthy girl who underwent radiofrequency diathermy for adenoid hypertrophy presented with fever on the same day and was diagnosed as having bacterial meningitis 2 days later. Culture of cerebrospinal fluid indicated that the pathogens were penicillin-sensitive Streptococcus pneumoniae and methicillin-sensitive Staphylococcus aureus. The serotype of the causative pneumococcus, 11A, was not covered by the 7-valent pneumococcal conjugate vaccine the patient had been inoculated with. Although not previously reported, radiofrequency diathermy for adenoid hypertrophy can be considered a risk factor for bacteremia and meningitis.

  18. Persistent Confusion and Controversy Surrounding Gene Patents

    Science.gov (United States)

    Guerrini, Christi J.; Majumder, Mary A.; McGuire, Amy L.

    2016-01-01

    There is persistent confusion and controversy surrounding basic issues of patent law relevant to the genomics industry. Uncertainty and conflict can lead to the adoption of inefficient practices and exposure to liability. The development of patent-specific educational resources for industry members, as well as the prompt resolution of patentability rules unsettled by recent U.S. Supreme Court decisions, are therefore urgently needed. PMID:26849516

  19. Cardiac hypertrophy induced by active Raf depends on Yorkie-mediated transcription

    OpenAIRE

    Yu, Lin; Daniels, Joseph P.; Wu, Huihui; Wolf, Matthew J.

    2015-01-01

    Organ hypertrophy can result from enlargement of individual cells or from cell proliferation or both. Activating mutations in the serine-threonine kinase Raf cause cardiac hypertrophy and contribute to Noonan syndrome in humans. Cardiac-specific expression of activated Raf also causes hypertrophy in Drosophila melanogaster. We found that Yorkie (Yki), a transcriptional coactivator in the Hippo pathway that regulates organ size, is required for Raf-induced cardiac hypertrophy in flies. Althoug...

  20. The Akt-mTOR axis is a pivotal regulator of eccentric hypertrophy during volume overload

    OpenAIRE

    Masataka Ikeda; Tomomi Ide; Takeo Fujino; Yuka Matsuo; Shinobu Arai; Keita Saku; Takamori Kakino; Yasuhiro Oga; Akiko Nishizaki; Kenji Sunagawa

    2015-01-01

    The heart has two major modalities of hypertrophy in response to hemodynamic loads: concentric and eccentric hypertrophy caused by pressure and volume overload (VO), respectively. However, the molecular mechanism of eccentric hypertrophy remains poorly understood. Here we demonstrate that the Akt-mammalian target of rapamycin (mTOR) axis is a pivotal regulator of eccentric hypertrophy during VO. While mTOR in the heart was activated in a left ventricular end-diastolic pressure (LVEDP)-depende...

  1. Speckle Tracking Based Strain Analysis Is Sensitive for Early Detection of Pathological Cardiac Hypertrophy

    OpenAIRE

    Xiangbo An; Jingjing Wang; Hao Li; Zhizhen Lu; Yan Bai; Han Xiao; Youyi Zhang; Yao Song

    2016-01-01

    Cardiac hypertrophy is a key pathological process of many cardiac diseases. However, early detection of cardiac hypertrophy is difficult by the currently used non-invasive method and new approaches are in urgent need for efficient diagnosis of cardiac malfunction. Here we report that speckle tracking-based strain analysis is more sensitive than conventional echocardiography for early detection of pathological cardiac hypertrophy in the isoproterenol (ISO) mouse model. Pathological hypertrophy...

  2. Prolonged acute hepatitis A mimicking autoimmune hepatitis

    Institute of Scientific and Technical Information of China (English)

    Rintaro Mikata; Osamu Yokosuka; Fumio Imazeki; Kenichi Fukai; Tatsuo Kanda; Hiromitsu Saisho

    2005-01-01

    AIM: We report a case with a prolonged course of hepatitisA, with alanine aminotransferase (ALT) higher than 500 IU/Lfor more than 2 mo.METHODS: A middle-aged woman had an elevated IgG level of more than 2 000 mg/dL, positive arti-nudear antibodies (ANA) and anti-smooth muscle antibodies (ASMA), but no evidence of persistent hepatitis A virus (HAV) infection. Liver biopsy findings were compatible with prolonged acute hepatitis, although acute onset of autoimmune hepatitis could not be ruled out.RESULTS: It was assumed that she developed a course of hepatitis similar to autoimmune hepatitis triggered by HAV infection. Ursodeoxycholic acid (UDCA) treatment was initiated and a favorable outcome was obtained. CONCLUSION: We describe a case of a middle-aged woman who showed a prolonged course of acute hepatitis A mimicking autoimmune hepatitis. Treatment with UDCAproved to be effective.

  3. The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy

    NARCIS (Netherlands)

    Buitrago, M; Lorenz, K; Maass, AH; Maass, SO; Keller, U; Schmitteckert, EM; Ivashchenko, Y; Lohse, MJ; Engelhardt, S

    2005-01-01

    Hypertrophy represents the major physiological response of the heart to adapt to chronically enhanced workload, but is also crucial in the development of heart failure. Although we know of numerous inducers of cardiac hypertrophy, little is known about mechanisms that limit cardiac hypertrophy. Here

  4. Through thick and thin: A circulating growth factor inhibits age-related cardiac hypertrophy

    OpenAIRE

    McPherron, Alexandra C.

    2013-01-01

    In an intriguing new study, Loffredo et al., report that joining the circulation of old mice with that of young mice reduces age-related cardiac hypertrophy. They also found that the growth factor GDF11 is a circulating negative regulator of cardiac hypertrophy which suggests that raising GDF11 levels may be useful to treat cardiac hypertrophy associated with aging.

  5. Identification of -SiC surrounded by relatable surrounding diamond medium using weak Raman surface phonons

    Indian Academy of Sciences (India)

    Mohan Kumar Kuntumalla; Harish Ojha; Vadali Venkata Satya Siva Srikanth

    2013-11-01

    It is difficult to detect -SiC using micro-Raman scattering, if it is surrounded by carbon medium. Here, -SiC is identified in the presence of a relatable surrounding diamond medium using subtle, but discernible Raman surface phonons. In this study, diamond/-SiC nanocomposite thin film system is considered in which nanosized -SiC crystallites are surrounded by a relatable nanodiamond medium that leads to the appearance of a weak Raman surface phonon band at about 855 cm-1. Change in the nature of the surrounding material structure and its volume content when relatable, will affect the resultant Raman response of -SiC phase as seen in the present case of diamond/-SiC nanocomposite thin films.

  6. Antileukotrienes in adenotonsillar hypertrophy: a review of the literature.

    Science.gov (United States)

    Kar, Murat; Altıntoprak, Niyazi; Muluk, Nuray Bayar; Ulusoy, Seckin; Bafaqeeh, Sameer Ali; Cingi, Cemal

    2016-12-01

    We assessed the use of antileukotrienes for treating adenotonsillar hypertrophy. We reviewed the current literature on the anatomy of adenotonsillar tissue, adenotonsillar hypertrophy/hyperplasia (and the associated pathophysiology and symptoms), and the effects of antileukotrienes used to treat adenotonsillar hypertrophy. Leukotrienes (LTs) are inflammatory mediators produced by a number of cell types, including mast cells, eosinophils, basophils, macrophages, and monocytes. There are several types (e.g., LTA4, LTB4, LTC4, LTD4, and LTE4). By competitive binding to the cysLT1 receptor, LT-receptor antagonist drugs such as montelukast, zafirlukast, and pranlukast block the effects of cySHLTs, improving the symptoms of some chronic respiratory diseases. High numbers of LT receptors have been found in the tonsils of children with obstructive sleep apnea. Antileukotrienes reduce the apnea-hypopnea index and adenotonsillar inflammation. Antileukotrienes may be useful for children with adenotonsillar hypertrophy due to their anti-inflammatory effects, which help to reduce adenotonsillar inflammation.

  7. Electrocardiographic criteria for left ventricular hypertrophy in children.

    NARCIS (Netherlands)

    Rijnbeek, P.R.; Herpen, G van; Kapusta, L.; Harkel, AD Ten; Witsenburg, M.; Kors, J.A.

    2008-01-01

    Previous studies to determine the sensitivity of the electrocardiogram (ECG) for left ventricular hypertrophy (LVH) in children had their imperfections: they were not done on an unselected hospital population, several criteria used in adults were not applied to children, and obsolete limits of norma

  8. Salt and left ventricular hypertrophy: what are the links?

    Science.gov (United States)

    Langenfeld, M R; Schmieder, R E

    1995-11-01

    Left ventricular hypertrophy is a frequent and prognostically unfavourable finding in patients with essential hypertension and has been found to be a predictor for the development of essential hypertension in normotensive subjects. Among various genetic, haemodynamic and humoral determinants, dietary salt intake has been demonstrated to influence left ventricular mass in hypertensive disease. Several cross-sectional studies have shown a close relation between dietary salt intake and parameters of left ventricular hypertrophy. Moreover, reduction of dietary sodium intake was associated with a decrease of left ventricular mass in a prospective study. The underlying mechanism of how salt intake modulates myocardial structure has not been explained yet. Three possible explanations are discussed: (1) sodium influences left ventricular mass via raised preload, (2) the sympathetic nervous system acts as a mediator, and (3) the renin-angiotensin-aldosterone system is the responsible link. Recent animal experiments and clinical studies suggest that the renin-angiotensin-aldosterone system may mediate both the cardiotrophic and the blood pressure raising effects of salt. However, not all individuals have a similar high susceptibility to blood pressure elevation develop left ventricular hypertrophy when exposed to high salt intake. We suggest that the underlying mechanism is a dysregulation of the renin-angiotensin-aldosterone system. Some individuals may have an impaired downregulation of angiotensin II synthesis when challenged with high salt intake. Accordingly, we found that relatively too high levels of angiotensin II in relation to urinary sodium excretion were associated with left ventricular hypertrophy in these individuals on high salt intake.

  9. Synovial hypertrophy causing recurrent hemarthrosis after total knee replacement.

    Science.gov (United States)

    Gajjar, Shreyash M; Platts, Andrew; Dowd, George

    2010-03-01

    Recurrent hemarthrosis following total knee replacement is relatively uncommon and can result from causes that may not always be easy to diagnose. We report three patients with late-onset recurrent hemarthrosis following total knee replacement due to synovial hypertrophy and impingement, which were successfully treated by embolization.

  10. Hyperplasia and Hypertrophy of Pacinian Corpuscles: A Case Report.

    Science.gov (United States)

    García, Fernando Cano; Acosta, Dalia Rodríguez; Diaz González, José Manuel; Lima, Marcela Saeb

    2015-08-01

    The proliferation of Pacinian corpuscles is a rare benign lesion that occurs frequently in the fingers of hands, with the only clinical sign of pain when a drastic temperature change happens. A case of an extremely rare lesion in which we observed hypertrophy and hyperplasia of Pacinian corpuscles has been reported.

  11. Congenital monomelic muscular hypertrophy of the upper extremity.

    NARCIS (Netherlands)

    Gilhuis, H.J.; Zophel, O.T.; Lammens, M.M.Y.; Zwarts, M.J.

    2009-01-01

    Pathological muscular hypertrophy results from either muscular or neurogenic damage. Rarely, it is caused by a congenital malformation consisting of a unilateral muscular hyperplasia of the upper extremity. We report on a young woman with an enlargement of the right upper extremity. Electromyography

  12. Muscle hypertrophy in prepubescent tennis players: a segmentation MRI study.

    Directory of Open Access Journals (Sweden)

    Joaquin Sanchis-Moysi

    Full Text Available PURPOSE: To asses if tennis at prepubertal age elicits the hypertrophy of dominant arm muscles. METHODS: The volume of the muscles of both arms was determined using magnetic resonance imaging (MRI in 7 male prepubertal tennis players (TP and 7 non-active control subjects (CG (mean age 11.0 ± 0.8 years, Tanner 1-2. RESULTS: TP had 13% greater total muscle volume in the dominant than in the contralateral arm. The magnitude of inter-arm asymmetry was greater in TP than in CG (13 vs 3%, P<0.001. The dominant arm of TP was 16% greater than the dominant arm of CG (P<0.01, whilst non-dominant arms had similar total muscle volumes in both groups (P = 0.25, after accounting for height as covariate. In TP, dominant deltoid (11%, forearm supinator (55% and forearm flexors (21% and extensors (25% were hypertrophied compared to the contralateral arm (P<0.05. In CG, the dominant supinator muscle was bigger than its contralateral homonimous (63%, P<0.05. CONCLUSIONS: Tennis at prepubertal age is associated with marked hypertrophy of the dominant arm, leading to a marked level of asymmetry (+13%, much greater than observed in non-active controls (+3%. Therefore, tennis particpation at prepubertal age is associated with increased muscle volumes in dominant compared to the non-dominant arm, likely due to selectively hypertrophy of the loaded muscles.

  13. Satellite cell depletion prevents fiber hypertrophy in skeletal muscle.

    Science.gov (United States)

    Egner, Ingrid M; Bruusgaard, Jo C; Gundersen, Kristian

    2016-08-15

    The largest mammalian cells are the muscle fibers, and they have multiple nuclei to support their large cytoplasmic volumes. During hypertrophic growth, new myonuclei are recruited from satellite stem cells into the fiber syncytia, but it was recently suggested that such recruitment is not obligatory: overload hypertrophy after synergist ablation of the plantaris muscle appeared normal in transgenic mice in which most of the satellite cells were abolished. When we essentially repeated these experiments analyzing the muscles by immunohistochemistry and in vivo and ex vivo imaging, we found that overload hypertrophy was prevented in the satellite cell-deficient mice, in both the plantaris and the extensor digitorum longus muscles. We attribute the previous findings to a reliance on muscle mass as a proxy for fiber hypertrophy, and to the inclusion of a significant number of regenerating fibers in the analysis. We discuss that there is currently no model in which functional, sustainable hypertrophy has been unequivocally demonstrated in the absence of satellite cells; an exception is re-growth, which can occur using previously recruited myonuclei without addition of new myonuclei. © 2016. Published by The Company of Biologists Ltd.

  14. Congenital monomelic muscular hypertrophy of the upper extremity.

    NARCIS (Netherlands)

    Gilhuis, H.J.; Zophel, O.T.; Lammens, M.M.Y.; Zwarts, M.J.

    2009-01-01

    Pathological muscular hypertrophy results from either muscular or neurogenic damage. Rarely, it is caused by a congenital malformation consisting of a unilateral muscular hyperplasia of the upper extremity. We report on a young woman with an enlargement of the right upper extremity. Electromyography

  15. The terminology of hepatitis*

    Science.gov (United States)

    1973-01-01

    It is proposed that the diseases formerly known as “infectious hepatitis” and “serum hepatitis” be referred to as viral hepatitis type A and viral hepatitis type B, respectively. It is further recommended that the “Australia” antigen be referred to as hepatitis B antigen (HB Ag) and the corresponding antibody as hepatitis B antibody (HB Ab). PMID:4544683

  16. Hepatitis A and HIV

    Science.gov (United States)

    ... Hepatitis B and Hepatitis C . Hepatitis A and HIV Hepatitis A is preventable with a vaccine, and ... Notice Network blog.aids.gov • locator.aids.gov • HIV/AIDS Service Locator Locator Widgets • Instructions • API Find ...

  17. Hepatitis B (HBV)

    Science.gov (United States)

    ... Loss Surgery? A Week of Healthy Breakfasts Shyness Hepatitis B (HBV) KidsHealth > For Teens > Hepatitis B (HBV) Print A A A What's in this ... poisons). There are several different types of hepatitis . Hepatitis B is a type that can move from one ...

  18. Hepatitis B (HBV)

    Science.gov (United States)

    ... Loss Surgery? A Week of Healthy Breakfasts Shyness Hepatitis B (HBV) KidsHealth > For Teens > Hepatitis B (HBV) A A A What's in this article? ... poisons). There are several different types of hepatitis . Hepatitis B is a type that can move from one ...

  19. Explaining preferences for home surroundings and locations

    DEFF Research Database (Denmark)

    Andersen, Hans Skifter

    2011-01-01

    : avoiding social nuisances, preferring social homogeneity and living close to one’s social network and place of origin. The study shows that most people have many detailed preferences, whereas some have very few. This confirms an earlier theory that some people are very connected to certain places...... with given characteristics and thus do not have priorities regarding home surroundings and locations. For others, mostly young people and singles, home is just a place to sleep and relax, whereas life is lived elsewhere. For this group, there are only preferences for location and there are few specific...

  20. Phosphorylation of ribosomal protein S6 mediates compensatory renal hypertrophy.

    Science.gov (United States)

    Xu, Jinxian; Chen, Jianchun; Dong, Zheng; Meyuhas, Oded; Chen, Jian-Kang

    2015-03-01

    The molecular mechanism underlying renal hypertrophy and progressive nephron damage remains poorly understood. Here we generated congenic ribosomal protein S6 (rpS6) knock-in mice expressing nonphosphorylatable rpS6 and found that uninephrectomy-induced renal hypertrophy was significantly blunted in these knock-in mice. Uninephrectomy-induced increases in cyclin D1 and decreases in cyclin E in the remaining kidney were attenuated in the knock-in mice compared with their wild-type littermates. Uninephrectomy induced rpS6 phosphorylation in the wild-type mice; however, no rpS6 phosphorylation was detected in uninephrectomized or sham-operated knock-in mice. Nonetheless, uninephrectomy stimulated comparable 4E-BP1 phosphorylation in both knock-in and wild-type mice, indicating that mTORC1 was still activated in the knock-in mice. Moreover, the mTORC1 inhibitor rapamycin prevented both rpS6 and 4E-BP1 phosphorylation, significantly blunted uninephrectomy-induced renal hypertrophy in wild-type mice, but did not prevent residual renal hypertrophy despite inhibiting 4E-BP1 phosphorylation in uninephrectomized knock-in mice. Thus, both genetic and pharmacological approaches unequivocally demonstrate that phosphorylated rpS6 is a downstream effector of the mTORC1-S6K1 signaling pathway mediating renal hypertrophy. Hence, rpS6 phosphorylation facilitates the increase in cyclin D1 and decrease in cyclin E1 that underlie the hypertrophic nature of uninephrectomy-induced kidney growth.

  1. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle.

    Science.gov (United States)

    McCarthy, John J; Mula, Jyothi; Miyazaki, Mitsunori; Erfani, Rod; Garrison, Kelcye; Farooqui, Amreen B; Srikuea, Ratchakrit; Lawson, Benjamin A; Grimes, Barry; Keller, Charles; Van Zant, Gary; Campbell, Kenneth S; Esser, Karyn A; Dupont-Versteegden, Esther E; Peterson, Charlotte A

    2011-09-01

    An important unresolved question in skeletal muscle plasticity is whether satellite cells are necessary for muscle fiber hypertrophy. To address this issue, a novel mouse strain (Pax7-DTA) was created which enabled the conditional ablation of >90% of satellite cells in mature skeletal muscle following tamoxifen administration. To test the hypothesis that satellite cells are necessary for skeletal muscle hypertrophy, the plantaris muscle of adult Pax7-DTA mice was subjected to mechanical overload by surgical removal of the synergist muscle. Following two weeks of overload, satellite cell-depleted muscle showed the same increases in muscle mass (approximately twofold) and fiber cross-sectional area with hypertrophy as observed in the vehicle-treated group. The typical increase in myonuclei with hypertrophy was absent in satellite cell-depleted fibers, resulting in expansion of the myonuclear domain. Consistent with lack of nuclear addition to enlarged fibers, long-term BrdU labeling showed a significant reduction in the number of BrdU-positive myonuclei in satellite cell-depleted muscle compared with vehicle-treated muscle. Single fiber functional analyses showed no difference in specific force, Ca(2+) sensitivity, rate of cross-bridge cycling and cooperativity between hypertrophied fibers from vehicle and tamoxifen-treated groups. Although a small component of the hypertrophic response, both fiber hyperplasia and regeneration were significantly blunted following satellite cell depletion, indicating a distinct requirement for satellite cells during these processes. These results provide convincing evidence that skeletal muscle fibers are capable of mounting a robust hypertrophic response to mechanical overload that is not dependent on satellite cells.

  2. Stimulus specific changes of energy metabolism in hypertrophied heart.

    Science.gov (United States)

    Rimbaud, S; Sanchez, H; Garnier, A; Fortin, D; Bigard, X; Veksler, V; Ventura-Clapier, R

    2009-06-01

    Cardiac energy metabolism is a determinant of the response to hypertrophic stimuli. To investigate how it responds to physiological or pathological stimuli, we compared the energetic status in models of hypertrophy induced by physiological stimuli (pregnancy or treadmill running) and by pathological stimulus (spontaneously hypertensive rats, SHR) in 15 week-old female rats, leading to a 10% cardiac hypertrophy. Late stage of compensated hypertrophy was also studied in 25 week-old SHR (35% of hypertrophy). Markers of cardiac remodelling did not follow a unique pattern of expression: in trained rats, only ANF was increased; in gravid rats, calcineurin activation and BNP expression were reduced while beta-MHC expression was enhanced; all markers were clearly up-regulated in 25 week-old SHR. Respiration of permeabilized fibers revealed a 17% increase in oxidative capacity in trained rats only. Mitochondrial enzyme activities, expression of the master regulator PGC-1alpha and mitochondrial transcription factor A, and content of mitochondrial DNA were not consistently changed, suggesting that compensated hypertrophy does not involve alterations of mitochondrial biogenesis. Mitochondrial fatty acid utilization tended to increase in trained rats and decreased by 14% in 15 week-old SHR. Expression of markers of lipid oxidation, PPARalpha and its down-stream targets MCAD and CPTI, was up-regulated after training and tended to decrease in gravid and 15 week-old SHR rats. Taken together these results show that there is no univocal pattern of cardiac adaptation in response to physiological or pathological hypertrophic stimuli, suggesting that other factors could play a role in determining adaptation of energy metabolism to increased workload.

  3. Reversible compensatory hypertrophy in rat kidneys: morphometric characterization.

    Science.gov (United States)

    Schwartz, M M; Churchill, M; Bidani, A; Churchill, P C

    1993-03-01

    Functional renal compensatory hypertrophy (RCH) in the uninephrectomized rat is completely reversible by transplantation in Brown Norway (BN) rats, while anatomic RCH is not. To determine the nephron element(s) responsible for persistent anatomic RCH, we performed morphometric analysis on perfusion fixed rat kidneys following renal function studies. In this model the function of renal transplants is not different from contralateral and unmanipulated control kidneys, and there is no histological evidence of rejection. Rats uninephrectomized for three or six weeks had larger glomeruli than controls, and after transplantation of a previously hypertrophied kidney into a rat with a normal or a solitary hypertrophied kidney, glomerular size returned to control levels. Increased glomerular capillary volume (CVCP) in kidneys with RCH was due to increased capillary length (LCP; 13.1 +/- 1.0 mm cf. 10.3 +/- 0.9, P < 0.01) without increase in capillary radius (RCP; 3.26 +/- 0.33 microM cf. 3.28 +/- 0.24). In contrast, return of CVCP to control levels in kidneys undergoing regression was associated with persistently elevated LCP (13.0 +2- 2.9 mm; native previously hypertrophied kidney; 12.2 +/- 0.9; transplanted previously hypertrophied kidney vs. 10.3 +/- 0.9, P < 0.01) and decreased RCP (2.79 +/- 0.10 microM and 2.73 +/- 0.09, cf 3.28 +/- 0.24, P < 0.01). RCH was associated with proportional increases in glomerular, tubular, and vascular-interstitial volumes while only elevated tubular volume persisted during regression. Altered glomerular capillary dimensions and increased tubular volumes acquired during renal RCH induced by unilateral nephrectomy persisted during complete functional regression.(ABSTRACT TRUNCATED AT 250 WORDS)

  4. Cinnamaldehyde attenuates pressure overload-induced cardiac hypertrophy.

    Science.gov (United States)

    Yang, Liu; Wu, Qing-Qing; Liu, Yuan; Hu, Zhe-Fu; Bian, Zhou-Yan; Tang, Qi-Zhu

    2015-01-01

    Cinnamaldehyde is a major bioactive compound isolated from the leaves of Cinnamomum osmophloeum. Studies have demonstrated that cinnamaldehyde has anti-bacterial activity, anti-tumorigenic effect, immunomodulatory effect, anti-fungal activity, anti-oxidative effect, anti-inflammatory and anti-diabetic effect. It has been proven that Cinnamaldehyde improves ischemia/reperfusion injury of pre-treatment. However, little is known about the effect of cinnamaldehyde on cardiac hypertrophy. Aortic banding (AB) was performed to induce cardiac hypertrophy in mice. Cinnamaldehyde premixed in diets was administered to mice after one week of AB. Echocardiography and catheter-based measurements of hemodynamic parameters were performed at week 7 after starting cinnamaldehyde (8 weeks after surgery). The extent of cardiac hypertrophy was evaluated by pathological and molecular analyses of heart samples. Meanwhile, the effect of cinnamaldehyde on myocardial hypertrophy, fibrosis and dysfunction induced by AB was investigated, as was assessed by heart weigh/body weight, lung weight/body weight, heart weight/tibia length, echocardiographic and haemodynamic parameters, histological analysis, and gene expression of hypertrophic and fibrotic markers. Our data demonstrated that echocardiography and catheter-based measurements of hemodynamic parameters at week 7 revealed the amelioration of systolic and diastolic abnormalities by cinnamaldehyde intervention. Cardiac fibrosis in AB mice was also decreased by cinnamaldehyde. Moreover, the beneficial effect of cinnamaldehyde was associated with the normalization in gene expression of hypertrophic and fibrotic markers. Further studies showed that pressure overload significantly induced the activation of extracellular signal-regulated kinase (ERK) signaling pathway, which was blocked by cinnamaldehyde. Cinnamaldehyde may be able to retard the progression of cardiac hypertrophy and fibrosis, probably via blocking ERK signaling pathway.

  5. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle

    Science.gov (United States)

    McCarthy, John J.; Mula, Jyothi; Miyazaki, Mitsunori; Erfani, Rod; Garrison, Kelcye; Farooqui, Amreen B.; Srikuea, Ratchakrit; Lawson, Benjamin A.; Grimes, Barry; Keller, Charles; Van Zant, Gary; Campbell, Kenneth S.; Esser, Karyn A.; Dupont-Versteegden, Esther E.; Peterson, Charlotte A.

    2011-01-01

    An important unresolved question in skeletal muscle plasticity is whether satellite cells are necessary for muscle fiber hypertrophy. To address this issue, a novel mouse strain (Pax7-DTA) was created which enabled the conditional ablation of >90% of satellite cells in mature skeletal muscle following tamoxifen administration. To test the hypothesis that satellite cells are necessary for skeletal muscle hypertrophy, the plantaris muscle of adult Pax7-DTA mice was subjected to mechanical overload by surgical removal of the synergist muscle. Following two weeks of overload, satellite cell-depleted muscle showed the same increases in muscle mass (approximately twofold) and fiber cross-sectional area with hypertrophy as observed in the vehicle-treated group. The typical increase in myonuclei with hypertrophy was absent in satellite cell-depleted fibers, resulting in expansion of the myonuclear domain. Consistent with lack of nuclear addition to enlarged fibers, long-term BrdU labeling showed a significant reduction in the number of BrdU-positive myonuclei in satellite cell-depleted muscle compared with vehicle-treated muscle. Single fiber functional analyses showed no difference in specific force, Ca2+ sensitivity, rate of cross-bridge cycling and cooperativity between hypertrophied fibers from vehicle and tamoxifen-treated groups. Although a small component of the hypertrophic response, both fiber hyperplasia and regeneration were significantly blunted following satellite cell depletion, indicating a distinct requirement for satellite cells during these processes. These results provide convincing evidence that skeletal muscle fibers are capable of mounting a robust hypertrophic response to mechanical overload that is not dependent on satellite cells. PMID:21828094

  6. Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.

    Directory of Open Access Journals (Sweden)

    Shaon Naskar

    Full Text Available A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy or detrimental (pathological hypertrophy. This study was undertaken to establish the role of different protein kinase-C (PKC isoforms in the regulation of cardiac adaptation during two types of cardiac hypertrophy. Phosphorylation of specific PKC-isoforms and expression of their downstream proteins were studied during physiological and pathological hypertrophy in 24 week male Balb/c mice (Mus musculus models, by reverse transcriptase-PCR, western blot analysis and M-mode echocardiography for cardiac function analysis. PKC-δ was significantly induced during pathological hypertrophy while PKC-α was exclusively activated during physiological hypertrophy in our study. PKC-δ activation during pathological hypertrophy resulted in cardiomyocyte apoptosis leading to compromised cardiac function and on the other hand, activation of PKC-α during physiological hypertrophy promoted cardiomyocyte growth but down regulated cellular apoptotic load resulting in improved cardiac function. Reversal in PKC-isoform with induced activation of PKC-δ and simultaneous inhibition of phospho-PKC-α resulted in an efficient myocardium to deteriorate considerably resulting in compromised cardiac function during physiological hypertrophy via augmentation of apoptotic and fibrotic load. This is the first report where PKC-α and -δ have been shown to play crucial role in cardiac adaptation during physiological and pathological hypertrophy respectively thereby rendering compromised cardiac function to an otherwise efficient heart by conditional reversal of their activation.

  7. Differential and Conditional Activation of PKC-Isoforms Dictates Cardiac Adaptation during Physiological to Pathological Hypertrophy

    Science.gov (United States)

    Naskar, Shaon; Datta, Kaberi; Mitra, Arkadeep; Pathak, Kanchan; Datta, Ritwik; Bansal, Trisha; Sarkar, Sagartirtha

    2014-01-01

    A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of cardiac adaptation during two types of cardiac hypertrophy. Phosphorylation of specific PKC-isoforms and expression of their downstream proteins were studied during physiological and pathological hypertrophy in 24 week male Balb/c mice (Mus musculus) models, by reverse transcriptase-PCR, western blot analysis and M-mode echocardiography for cardiac function analysis. PKC-δ was significantly induced during pathological hypertrophy while PKC-α was exclusively activated during physiological hypertrophy in our study. PKC-δ activation during pathological hypertrophy resulted in cardiomyocyte apoptosis leading to compromised cardiac function and on the other hand, activation of PKC-α during physiological hypertrophy promoted cardiomyocyte growth but down regulated cellular apoptotic load resulting in improved cardiac function. Reversal in PKC-isoform with induced activation of PKC-δ and simultaneous inhibition of phospho-PKC-α resulted in an efficient myocardium to deteriorate considerably resulting in compromised cardiac function during physiological hypertrophy via augmentation of apoptotic and fibrotic load. This is the first report where PKC-α and -δ have been shown to play crucial role in cardiac adaptation during physiological and pathological hypertrophy respectively thereby rendering compromised cardiac function to an otherwise efficient heart by conditional reversal of their activation. PMID:25116170

  8. Differential and conditional activation of PKC-isoforms dictates cardiac adaptation during physiological to pathological hypertrophy.

    Science.gov (United States)

    Naskar, Shaon; Datta, Kaberi; Mitra, Arkadeep; Pathak, Kanchan; Datta, Ritwik; Bansal, Trisha; Sarkar, Sagartirtha

    2014-01-01

    A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of cardiac adaptation during two types of cardiac hypertrophy. Phosphorylation of specific PKC-isoforms and expression of their downstream proteins were studied during physiological and pathological hypertrophy in 24 week male Balb/c mice (Mus musculus) models, by reverse transcriptase-PCR, western blot analysis and M-mode echocardiography for cardiac function analysis. PKC-δ was significantly induced during pathological hypertrophy while PKC-α was exclusively activated during physiological hypertrophy in our study. PKC-δ activation during pathological hypertrophy resulted in cardiomyocyte apoptosis leading to compromised cardiac function and on the other hand, activation of PKC-α during physiological hypertrophy promoted cardiomyocyte growth but down regulated cellular apoptotic load resulting in improved cardiac function. Reversal in PKC-isoform with induced activation of PKC-δ and simultaneous inhibition of phospho-PKC-α resulted in an efficient myocardium to deteriorate considerably resulting in compromised cardiac function during physiological hypertrophy via augmentation of apoptotic and fibrotic load. This is the first report where PKC-α and -δ have been shown to play crucial role in cardiac adaptation during physiological and pathological hypertrophy respectively thereby rendering compromised cardiac function to an otherwise efficient heart by conditional reversal of their activation.

  9. Identification of a core set of genes that signifies pathways underlying cardiac hypertrophy

    DEFF Research Database (Denmark)

    Strom, C.C.; Kruhoffer, M.; Knudsen, Steen

    2004-01-01

    Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic...... gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved...... in hypertrophic signalling. From gene expression analyses (8740 probe sets, n = 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61...

  10. Identification of a core set of genes that signifies pathways underlying cardiac hypertrophy

    DEFF Research Database (Denmark)

    Strøm, Claes C; Kruhøffer, Mogens; Knudsen, Steen

    2004-01-01

    Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic...... gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved...... in hypertrophic signalling. From gene expression analyses (8740 probe sets, n = 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61...

  11. Inhalation of diesel exhaust does not exacerbate cardiac hypertrophy or heart failure in two mouse models of cardiac hypertrophy.

    Science.gov (United States)

    Liu, Yonggang; Chien, Wei-Ming; Medvedev, Ivan O; Weldy, Chad S; Luchtel, Daniel L; Rosenfeld, Michael E; Chin, Michael T

    2013-10-05

    Strong associations have been observed between exposure to fine ambient particulate matter (PM2.5) and adverse cardiovascular outcomes. In particular, exposure to traffic related PM2.5 has been associated with increases in left ventricular hypertrophy, a strong risk factor for cardiovascular mortality. As much of traffic related PM2.5 is derived from diesel exhaust (DE), we investigated the effects of chronic DE exposure on cardiac hypertrophy and heart failure in the adult mouse by exposing mice to DE combined with either of two mouse models of cardiac hypertrophy: angiotensin II infusion or pressure overload induced by transverse aortic banding. Wild type male C57BL/6 J mice were either infused with angiotensin II (800 ng/kg/min) via osmotic minipump implanted subcutaneously for 1 month, or underwent transverse aortic banding (27 gauge needle 1 week for observing acute reactions, 26 gauge needle 3 months or 6 months for observing chronic reactions). Vehicle (saline) infusion or sham surgery was used as a control. Shortly after surgery, mice were transferred to our exposure facility and randomly assigned to either diesel exhaust (300 or 400 μg/m(3)) or filtered air exposures. After reaching the end of designated time points, echocardiography was performed to measure heart structure and function. Gravimetric analysis was used to measure the ventricular weight to body weight ratio. We also measured heart rate by telemetry using implanted ambulatory ECG monitors. Both angiotensin II and transverse aortic banding promoted cardiac hypertrophy compared to vehicle or sham controls. Transverse aortic banding for six months also promoted heart failure in addition to cardiac hypertrophy. In all cases, DE failed to exacerbate the development of hypertrophy or heart failure when compared to filtered air controls. Prolonged DE exposure also led to a decrease in average heart rate. Up to 6-months of DE exposure had no effect on cardiac hypertrophy and heart function induced by

  12. Hepatic Encephalopathy-the Old and the New.

    Science.gov (United States)

    Kandiah, Prem A; Kumar, Gagan

    2016-07-01

    Hepatic encephalopathy occurs ubiquitously in all causes of advanced liver failure, however, its implications on mortality diverge and vary depending upon acuity and severity of liver failure. This associated mortality has decreased in subsets of liver failure over the last 20 years. Aside from liver transplantation, this improvement is not attributable to a single intervention but likely to a combination of practical advances in critical care management. Misconceptions surrounding many facets of hepatic encephalopathy exists due to heterogeneity in presentation, pathophysiology and outcome. This review is intended to highlight the important concepts, rationales and strategies for managing hepatic encephalopathy.

  13. Segmental Difference of the Hepatic Fibrosis from Chronic Viral Hepatitis due to Hepatitis B versus C Virus Infection: Comparison Using Dual Contrast Material-Enhanced MRI

    Energy Technology Data Exchange (ETDEWEB)

    Shin, Jae Ho; Yu, Jeong Sik; Chung, Jae Joon; Kim, Joo Hee; Kim, Ki Whang [Gangnam Severance Hospital, Yensei University College of Medicine, Seoul (Korea, Republic of)

    2011-08-15

    We wanted to identify the geographic differences in hepatic fibrosis and their associations with the atrophy-hypertrophy complex in patients with chronic viral hepatitis using the dual-contrast material-enhanced MRI (DC-MRI) with gadopentetate dimeglumine and ferucarbotran. Patients with chronic C (n = 22) and B-viral hepatitis (n = 35) were enrolled for determining the subjective grade of fibrosis (the extent and thickness of fibrotic reticulations) in the right lobe (RL), the caudate lobe (CL), the medial segment (MS) and the lateral segment (LS) of the liver, with using a 5-grade scale, on the gradient echo T2-weighted images of DC-MRI. The fibrosis grades of different segments were compared using the Kruskal-Wallis test followed by post-hoc analysis to establish the segment-by-segment differences. The incidences of two pre-established morphologic signs of cirrhosis were also compared with each other between the two groups of patients. There were significant intersegmental differences in fibrosis grades of the C-viral group (p = 0.005), and the CL showed lower fibrosis grades as compared with the grades of the RL and MS, whereas all lobes were similarly affected in the B-viral group (p = 0.221). The presence of a right posterior hepatic notch was significantly higher in the patients with intersegmental differences of fibrosis between the RL and the CL (19 out of 25, 76%) than those without such differences (6 out of 32, 19%) (p < 0.001). An expanded gallbladder fossa showed no significant relationship (p = 0.327) with the segmental difference of the fibrosis grades between the LS and the MS. The relative lack of fibrosis in the CL with more advanced fibrosis in the RL can be a distinguishing feature to differentiate chronic C-viral hepatitis from chronic B-viral hepatitis and this is closely related to the presence of a right posterior hepatic notch.

  14. Compromised epidermal barrier stimulates Harderian gland activity and hypertrophy in ACBP−/− mice[S

    Science.gov (United States)

    Bek, Signe; Neess, Ditte; Dixen, Karen; Bloksgaard, Maria; Marcher, Ann-Britt; Chemnitz, John; Færgeman, Nils J.; Mandrup, Susanne

    2015-01-01

    Acyl-CoA binding protein (ACBP) is a small, ubiquitously expressed intracellular protein that binds C14-C22 acyl-CoA esters with very high affinity and specificity. We have recently shown that targeted disruption of the Acbp gene leads to a compromised epidermal barrier and that this causes delayed adaptation to weaning, including the induction of the hepatic lipogenic and cholesterogenic gene programs. Here we show that ACBP is highly expressed in the Harderian gland, a gland that is located behind the eyeball of rodents and involved in the production of fur lipids and lipids used for lubrication of the eye lid. We show that disruption of the Acbp gene leads to a significant enlargement of this gland with hypertrophy of the acinar cells and increased de novo synthesis of monoalkyl diacylglycerol, the main lipid species produced by the gland. Mice with conditional targeting of the Acbp gene in the epidermis recapitulate this phenotype, whereas generation of an artificial epidermal barrier during gland development reverses the phenotype. Our findings indicate that the Harderian gland is activated by the compromised epidermal barrier as an adaptive and protective mechanism to overcome the barrier defect. PMID:26142722

  15. Essential role of constitutive androstane receptor in Ginkgo biloba extract induced liver hypertrophy and hepatocarcinogenesis.

    Science.gov (United States)

    Maeda, Jun; Inoue, Kaoru; Ichimura, Ryohei; Takahashi, Miwa; Kodama, Yukio; Saito, Naoaki; Yoshida, Midori

    2015-09-01

    Ginkgo biloba extract (GBE) is commonly used as a herbal supplement. The National Toxicology Program (NTP) study of GBE reported clear evidence of hepatocarcinogenicity in mice. To clarify the mode of action (MOA) for hepatocarcinogenesis by GBE, we investigated the involvement of the constitutive androstane receptor (CAR) in hepatocarcinogenesis induced by GBE using CAR-knockout (CARKO) and wild type (WT) mice. We used the same lot of GBE that was used for the NTP study. In 1-week GBE dietary treatment, hepatocellular DNA replication was increased in WT mice but not in CARKO mice. In 4- or 13-week treatment, greater hepatic Cyp2b10 induction and hepatocellular hypertrophy were observed in WT mice, whereas these effects of GBE were much smaller in CARKO mice. In a two-stage hepatocarcinogenesis model initiated by diethylnitrosamine, 27-week treatment with GBE resulted in an increase of eosinophilic altered foci and adenomas in WT mice. By contrast, foci and adenomas were clearly less evident in CARKO mice. These results indicate that GBE-induced hepatocarcinogenesis is mainly CAR-mediated. Since CAR-mediated MOA for hepatocarcinogenesis in rodents is considered to be qualitatively implausible for humans, our findings would be helpful to evaluate the carcinogenic characterization of GBE to humans.

  16. Characterizing the Microenvironment Surrounding Phosphorylated Protein Sites

    Institute of Scientific and Technical Information of China (English)

    Shi-Cai Fan; Xue-Gong Zhang

    2005-01-01

    Protein phosphorylation plays an important role in various cellular processes. Due to its high complexity, the mechanism needs to be further studied. In the last few years, many methods have been contributed to this field, but almost all of them investigated the mechanism based on protein sequences around protein sites. In this study, we implement an exploration by characterizing the microenvironment surrounding phosphorylated protein sites with a modified shell model, and obtain some significant properties by the rank-sum test, such as the lack of some classes of residues, atoms, and secondary structures. Furthermore, we find that the depletion of some properties affects protein phosphorylation remarkably. Our results suggest that it is a meaningful direction to explore the mechanism of protein phosphorylation from microenvironment and we expect further findings along with the increasing size of phosphorylation and protein structure data.

  17. Opportunity's Surroundings After Sol 1820 Drive

    Science.gov (United States)

    2009-01-01

    NASA's Mars Exploration Rover Opportunity used its navigation camera to take the images combined into this full-circle view of the rover's surroundings during the 1,820th to 1,822nd Martian days, or sols, of Opportunity's surface mission (March 7 to 9, 2009). South is at the center; north at both ends. The rover had driven 20.6 meters toward the northwest on Sol 1820 before beginning to take the frames in this view. Tracks from that drive recede southwestward. For scale, the distance between the parallel wheel tracks is about 1 meter (about 40 inches). The terrain in this portion of Mars' Meridiani Planum region includes dark-toned sand ripples and small exposures of lighter-toned bedrock. This view is presented as a cylindrical projection with geometric seam correction.

  18. Exploiting Surrounding Text for Retrieving Web Images

    Directory of Open Access Journals (Sweden)

    S. A. Noah

    2008-01-01

    Full Text Available Web documents contain useful textual information that can be exploited for describing images. Research had been focused on representing images by means of its content (low level description such as color, shape and texture, little research had been directed to exploiting such textual information. The aim of this research was to systematically exploit the textual content of HTML documents for automatically indexing and ranking of images embedded in web documents. A heuristic approach for locating and assigning weight surrounding web images and a modified tf.idf weighting scheme was proposed. Precision-recall measures of evaluation had been conducted for ten queries and promising results had been achieved. The proposed approach showed slightly better precision measure as compared to a popular search engine with an average of 0.63 and 0.55 relative precision measures respectively.

  19. Diabetes and Hepatitis B Vaccination

    Science.gov (United States)

    Diabetes and Hepatitis B Vaccination Information for Diabetes Educators What is hepatitis B? Hepatitis B is a contagious liver disease that results from infection with the hepatitis B virus. When first infected, a person can develop ...

  20. Microbiological diagnostics of viral hepatitis

    OpenAIRE

    HASDEMİR, Ufuk

    2016-01-01

    Viral hepatitis is an infection that primarily affects the liverbut may also have systemic clinical manifestations. The vastmajority of viral hepatitis are caused by one of five hepatotropicviruses: hepatitis A virus (HAV), hepatitis B virus (HBV),hepatitis C virus (HCV), hepatitis D (delta) virus (HDV), andhepatitis E virus (HEV) (Table I) [1]. HBV, HCV, and HDValso cause chronic hepatitis, whereas HAV does not. HEVcauses acute hepatitis in normal hosts but can cause protractedand chronic he...

  1. Microbiological diagnostics of viral hepatitis

    OpenAIRE

    HASDEMİR, Ufuk

    2016-01-01

    Viral hepatitis is an infection that primarily affects the liverbut may also have systemic clinical manifestations. The vastmajority of viral hepatitis are caused by one of five hepatotropicviruses: hepatitis A virus (HAV), hepatitis B virus (HBV),hepatitis C virus (HCV), hepatitis D (delta) virus (HDV), andhepatitis E virus (HEV) (Table I) [1]. HBV, HCV, and HDValso cause chronic hepatitis, whereas HAV does not. HEVcauses acute hepatitis in normal hosts but can cause protractedand chronic he...

  2. The Natural History of Soft Tissue Hypertrophy, Bony Hypertrophy, and Nodule Formation in Patients With Untreated Head and Neck Capillary Malformations.

    Science.gov (United States)

    Lee, Jeong Woo; Chung, Ho Yun; Cerrati, Eric W; O, Teresa M; Waner, Milton

    2015-11-01

    A percentage of patients with capillary malformation (CM) develop soft tissue hypertrophy, bony hypertrophy, and/or nodule formation. To determine the incidence, age of onset, anatomic distribution of soft tissue/bony hypertrophy, and nodule formation in patients with untreated CM. A retrospective medical records review of head and neck CM patients presenting to a tertiary referral center over a 7-year period (2004-2011) was performed. Of the 160 patients with CM, 96 demonstrated progression of disease to include either soft tissue/bony hypertrophy or nodule formation. Of these, 87 patients had not received previous treatment and met the inclusion criteria for analysis. On average, soft tissue hypertrophy began at 9 years of age. The V2/maxillary segment was most commonly involved with upper lip hypertrophy being the most prominent. Fourteen percent of the patients also presented with bony hypertrophy, which began at an average age of 15 years. Nodules were present in 38/87 (44%) of patients with an average age of onset of 22 years. This study demonstrates the nature progression of CM and quantifies the clinical characteristics of hypertrophy and nodule formation with untreated head and neck CM. Early and continuous treatment is recommended in hopes of preventing CM progression.

  3. Speckle Tracking Based Strain Analysis Is Sensitive for Early Detection of Pathological Cardiac Hypertrophy.

    Science.gov (United States)

    An, Xiangbo; Wang, Jingjing; Li, Hao; Lu, Zhizhen; Bai, Yan; Xiao, Han; Zhang, Youyi; Song, Yao

    2016-01-01

    Cardiac hypertrophy is a key pathological process of many cardiac diseases. However, early detection of cardiac hypertrophy is difficult by the currently used non-invasive method and new approaches are in urgent need for efficient diagnosis of cardiac malfunction. Here we report that speckle tracking-based strain analysis is more sensitive than conventional echocardiography for early detection of pathological cardiac hypertrophy in the isoproterenol (ISO) mouse model. Pathological hypertrophy was induced by a single subcutaneous injection of ISO. Physiological cardiac hypertrophy was established by daily treadmill exercise for six weeks. Strain analysis, including radial strain (RS), radial strain rate (RSR) and longitudinal strain (LS), showed marked decrease as early as 3 days after ISO injection. Moreover, unlike the regional changes in cardiac infarction, strain analysis revealed global cardiac dysfunction that affects the entire heart in ISO-induced hypertrophy. In contrast, conventional echocardiography, only detected altered E/E', an index reflecting cardiac diastolic function, at 7 days after ISO injection. No change was detected on fractional shortening (FS), E/A and E'/A' at 3 days or 7 days after ISO injection. Interestingly, strain analysis revealed cardiac dysfunction only in ISO-induced pathological hypertrophy but not the physiological hypertrophy induced by exercise. Taken together, our study indicates that strain analysis offers a more sensitive approach for early detection of cardiac dysfunction than conventional echocardiography. Moreover, multiple strain readouts distinguish pathological cardiac hypertrophy from physiological hypertrophy.

  4. Speckle Tracking Based Strain Analysis Is Sensitive for Early Detection of Pathological Cardiac Hypertrophy

    Science.gov (United States)

    An, Xiangbo; Wang, Jingjing; Li, Hao; Lu, Zhizhen; Bai, Yan; Xiao, Han; Zhang, Youyi; Song, Yao

    2016-01-01

    Cardiac hypertrophy is a key pathological process of many cardiac diseases. However, early detection of cardiac hypertrophy is difficult by the currently used non-invasive method and new approaches are in urgent need for efficient diagnosis of cardiac malfunction. Here we report that speckle tracking-based strain analysis is more sensitive than conventional echocardiography for early detection of pathological cardiac hypertrophy in the isoproterenol (ISO) mouse model. Pathological hypertrophy was induced by a single subcutaneous injection of ISO. Physiological cardiac hypertrophy was established by daily treadmill exercise for six weeks. Strain analysis, including radial strain (RS), radial strain rate (RSR) and longitudinal strain (LS), showed marked decrease as early as 3 days after ISO injection. Moreover, unlike the regional changes in cardiac infarction, strain analysis revealed global cardiac dysfunction that affects the entire heart in ISO-induced hypertrophy. In contrast, conventional echocardiography, only detected altered E/E’, an index reflecting cardiac diastolic function, at 7 days after ISO injection. No change was detected on fractional shortening (FS), E/A and E’/A’ at 3 days or 7 days after ISO injection. Interestingly, strain analysis revealed cardiac dysfunction only in ISO-induced pathological hypertrophy but not the physiological hypertrophy induced by exercise. Taken together, our study indicates that strain analysis offers a more sensitive approach for early detection of cardiac dysfunction than conventional echocardiography. Moreover, multiple strain readouts distinguish pathological cardiac hypertrophy from physiological hypertrophy. PMID:26871457

  5. Malondialdehyde in benign prostate hypertrophy: a useful marker?

    Directory of Open Access Journals (Sweden)

    Rosaria Alba Merendino

    2003-01-01

    Full Text Available Benign prostate hypertrophy (BPH is the most common benign tumor in men due to obstruction of the urethra and, finally, uremia. Malondialdehyde (MDA is a product derived from peroxidation of polyunsaturated fatty acids and related esters. Evaluation of MDA in serum represents a non-invasive biomarker of oxidative stress. Prostate-specific antigen (PSA is a sensitive marker for prostatic hypertrophy and cancer. We analyzed MDA serum levels to evaluate the oxidative stress in BPH. To this end, 22 BPH patients and 22 healthy donors were enrolled. Data show an increase of MDA level in BPH patients and a positive correlation between PSA and MDA levels. In conclusion, we describe a previously unknown relationship between PSA and MDA as an index of inflammation and oxidative stress in BPH.

  6. Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs

    DEFF Research Database (Denmark)

    Smith, Julie; Goetze, Jens Peter; Søndergaard, Lars;

    2012-01-01

    BACKGROUND: Patients may suffer from right ventricular (RV) failure and malignant cardiac arrhythmias after late pulmonary valve replacement correcting pulmonary regurgitation (PR). But the underlying mechanisms of the refractory arrhythmias are not well understood. METHODS: The aim of present...... study was to characterize the RV myocardium after percutaneous pulmonary valve implantation (PPVI) in a porcine model after severe PR for 3months. RV histology was evaluated with morphometric methods and RV function was assessed with electrophysiology, echocardiography, and biochemical measures...... and plasma natriuretic peptides were unchanged. CONCLUSIONS: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may...

  7. Bilateral masseter and internal pterygoid muscle hypertrophy: a diagnostic challenge.

    Science.gov (United States)

    Andreadis, Dimitrios; Stylianou, Florentia; Link-Tsatsouli, Iris; Markopoulos, Anastasios

    2014-01-01

    To describe an unusual case of bilateral masseter and pterygoid muscle hypertrophy. A 53-year-old female patient presented with a bilateral, painless swelling at the parotid areas without improvement after using antibiotics/systemic corticosteroids/nonsteroidal anti-inflammatory agents. Her medical history included thyroid nodules, but no dental/occlusal disorders were observed. The initial differential diagnosis included salivary gland/jaw bone/masseter pathology, but the CT/MRI revealed only an increase in the size of the masseter and pterygoid muscles. The patient was informed of the benign nature of the swelling and was advised to discontinue the use of nonsteroidal anti-inflammatory agents. The bilateral hypertrophy of masseter muscles should be considered in differential diagnosis in cases of unilateral or bilateral swelling of the parotid or lateral mandible area. © 2013 S. Karger AG, Basel.

  8. Region specific patella tendon hypertrophy in humans following resistance training

    DEFF Research Database (Denmark)

    Kongsgaard, M.; Reitelseder, S; Pedersen, T.G.

    2007-01-01

    AIM: To examine if cross-sectional area (CSA) differs along the length of the human patellar tendon (PT), and if there is PT hypertrophy in response to resistance training. METHODS: Twelve healthy young men underwent baseline and post-training assessments. Maximal isometric knee extension strength...... (MVC) was determined unilaterally in both legs. PT CSA was measured at the proximal-, mid- and distal PT level and quadriceps muscle CSA was measured at mid-thigh level using magnetic resonance imaging. Mechanical properties of the patellar tendons were determined using ultrasonography. Subsequently....... CONCLUSIONS: To our knowledge, this study is the first to report tendon hypertrophy following resistance training. Further, the data show that the human PT CSA varies along the length of the tendon....

  9. Repeated blood flow restriction induces muscle fiber hypertrophy.

    Science.gov (United States)

    Sudo, Mizuki; Ando, Soichi; Kano, Yutaka

    2017-02-01

    We recently developed an animal model to investigate the effects of eccentric contraction (ECC) and blood flow restriction (BFR) on muscle tissue at the cellular level. This study clarified the effects of repeated BFR, ECC, and BFR combined with ECC (BFR+ECC) on muscle fiber hypertrophy. Male Wistar rats were assigned to 3 groups: BFR, ECC, and BFR+ECC. The contralateral leg in the BFR group served as a control (CONT). Muscle fiber cross-sectional area (CSA) of the tibialis anterior was determined after the respective treatments for 6 weeks. CSA was greater in the BFR+ECC group than in the CONT (P muscle fiber hypertrophy at the cellular level. Muscle Nerve 55: 274-276, 2017. © 2016 Wiley Periodicals, Inc.

  10. A New Clinical Scoring System for Adenoid Hypertrophy in Children

    Directory of Open Access Journals (Sweden)

    Shervin Sharifkashani

    2015-01-01

    Full Text Available Introduction: Chronic nasal obstruction due to adenoid hypertrophy is a very common disorder. Although the clinical assessment of adenoid hypertrophy is essential, its real value in young children is difficult to evaluate. The purpose of this prospective study was to validate a simple clinical score to predict the severity of adenoid obstruction and to evaluate the relationship between this method of clinical scoring with radiography and nasopharyngeal endoscopy.   Materials and Methods: Ninety symptomatic children were enrolled into this study. The clinical score included difficulty of breathing during sleep, apnea, and snoring. We investigated the relationship between clinical scoring, nasal endoscopy, and radiographic findings.   Results: The clinical score correlated very well with endoscopic findings (P0.05 and endoscopic findings and imaging (P>0.05 was weak.    Conclusion:  Clinical findings could be used to select children for adenoidectomy, especially when endoscopic examination is not available or cannot be performed.

  11. Reversible compensatory hypertrophy in transplanted brown Norway rat kidneys.

    Science.gov (United States)

    Churchill, M; Churchill, P C; Schwartz, M; Bidani, A; McDonald, F

    1991-07-01

    Recently we described methods for optimizing the function of transplanted rat kidneys. In unilaterally nephrectomized recipients, one week after surgery, the left transplanted kidney was identical to the right native kidney with respect to wet weight and the clearances of inulin and para-aminohippuric acid (PAH). The goals of the present experiments were first, to extend the post-surgery period to three weeks (sufficient to allow hypertrophic changes), and second, to study function of transplanted hypertrophied kidneys. Genetically identical Brown Norway rats were used as donor and recipients. Three weeks after transplanting a normal kidney into a unilaterally-nephrectomized recipient, the transplanted kidney had a normal plasma flow and was identical to the contralateral native kidney with respect to wet weight and the clearances of inulin and PAH. Three weeks after transplanting a normal kidney into a bilaterally-nephrectomized recipient, the wet weight, inulin and PAH clearances, and plasma flow of the transplanted kidney were all higher than control, and not significantly different from those observed in unilaterally-nephrectomized control rats. Thus, transplanted and native kidneys exhibited the same degree of compensatory hypertrophy. Hypertrophied donor kidneys (that is, the donor rat had been unilaterally-nephrectomized three weeks previously) remained hypertrophied in bilaterally-nephrectomized recipients, but in unilaterally-nephrectomized recipients, they regressed towards normal (that is, the values of wet weight, inulin and PAH clearances and plasma flow were significantly less than those in rats with only one kidney) while the contralateral native kidney remained normal (values of wet weight and inulin and PAH clearances were not different from control).(ABSTRACT TRUNCATED AT 250 WORDS)

  12. Elucidation of MRAS-mediated Noonan syndrome with cardiac hypertrophy

    Science.gov (United States)

    Higgins, Erin M.; Bos, J. Martijn; Tester, David J.; Ackerman, Jaeger P.; Sol-Church, Katia; Urrutia, Raul; Ackerman, Michael J.

    2017-01-01

    Noonan syndrome (NS; MIM 163950) is an autosomal dominant disorder and a member of a family of developmental disorders termed “RASopathies,” which are caused mainly by gain-of-function mutations in genes encoding RAS/MAPK signaling pathway proteins. Whole exome sequencing (WES) and trio-based genomic triangulation of a 15-year-old female with a clinical diagnosis of NS and concomitant cardiac hypertrophy and her unaffected parents identified a de novo variant in MRAS-encoded RAS-related protein 3 as the cause of her disease. Mutation analysis using in silico mutation prediction tools and molecular dynamics simulations predicted the identified variant, p.Gly23Val-MRAS, to be damaging to normal protein function and adversely affect effector interaction regions and the GTP-binding site. Subsequent ectopic expression experiments revealed a 40-fold increase in MRAS activation for p.Gly23Val-MRAS compared with WT-MRAS. Additional biochemical assays demonstrated enhanced activation of both RAS/MAPK pathway signaling and downstream gene expression in cells expressing p.Gly23Val-MRAS. Mutational analysis of MRAS in a cohort of 109 unrelated patients with phenotype-positive/genotype-negative NS and cardiac hypertrophy yielded another patient with a sporadic de novo MRAS variant (p.Thr68Ile, c.203C>T). Herein, we describe the discovery of mutations in MRAS in patients with NS and cardiac hypertrophy, establishing MRAS as the newest NS with cardiac hypertrophy-susceptibility gene. PMID:28289718

  13. Estrogens Mediate Cardiac Hypertrophy in a Stimulus-Dependent Manner

    Science.gov (United States)

    Haines, Christopher D.; Harvey, Pamela A.

    2012-01-01

    The incidence of cardiac hypertrophy, an established risk factor for heart failure, is generally lower in women compared with men, but this advantage is lost after menopause. Although it is widely believed that estrogens are cardioprotective, there are contradictory reports, including increased cardiac events in postmenopausal women receiving estrogens and enhanced cardiac protection from ischemic injury in female mice without estrogens. We exposed aromatase knockout (ArKO) mice, which produce no estrogens, to both pathologic and physiologic stimuli. This model allows an investigation into the effects of a complete, chronic lack of estrogens in male and female hearts. At baseline, female ArKO mice had normal-sized hearts but decreased cardiac function and paradoxically increased phosphorylation of many progrowth kinases. When challenged with the pathological stimulus, isoproterenol, ArKO females developed 2-fold more hypertrophy than wild-type females. In contrast, exercise-induced physiological hypertrophy was unaffected by the absence of estrogens in either sex, although running performance was blunted in ArKO females. Thus, loss of estrogen signaling in females, but not males, impairs cardiac function and sensitizes the heart to pathological insults through up-regulation of multiple hypertrophic pathways. These findings provide insight into the apparent loss of cardioprotection after menopause and suggest that caution is warranted in the long-term use of aromatase inhibitors in the setting of breast cancer prevention. PMID:22759381

  14. Wasabi leaf extracts attenuate adipocyte hypertrophy through PPARγ and AMPK.

    Science.gov (United States)

    Oowatari, Yasuo; Ogawa, Tetsuro; Katsube, Takuya; Iinuma, Kiyohisa; Yoshitomi, Hisae; Gao, Ming

    2016-08-01

    Hypertrophy of adipocytes in obese adipose tissues causes metabolic abnormality by adipocytokine dysregulation, which promotes type 2 diabetes mellitus, hypertension, and dyslipidemia. We investigated the effects of wasabi (Wasabia japonica Matsum) leaf extracts on metabolic abnormalities in SHRSP.Z-Leprfa/IzmDmcr rats (SHRSP/ZF), which are a model of metabolic syndrome. Male SHRSP/ZF rats aged 7 weeks were divided into two groups: control and wasabi leaf extract (WLE) groups, which received water or oral treatment with 4 g/kg/day WLE for 6 weeks. WLE improved the body weight gain and high blood pressure in SHRSP/ZF rats, and the plasma triglyceride levels were significantly lower in the WLE group. Adipocyte hypertrophy was markedly prevented in adipose tissue. The expression of PPARγ and subsequent downstream genes was suppressed in the WLE group adipose tissues. Our data suggest that WLE inhibits adipose hypertrophy by suppressing PPARγ expression in adipose tissue and stimulating the AMPK activity by increased adiponectin.

  15. Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Clark Robinson

    2016-01-01

    Full Text Available Traumatic brain injury (TBI is a widespread epidemic with severe cognitive, affective, and behavioral consequences. TBIs typically result in a relatively rapid inflammatory and neuroinflammatory response. A major component of the neuroinflammatory response is astrocytes, a type of glial cell in the brain. Astrocytes are important in maintaining the integrity of neuronal functioning, and it is possible that astrocyte hypertrophy after TBIs might contribute to pathogenesis. The hippocampus is a unique brain region, because neurogenesis persists in adults. Accumulating evidence supports the functional importance of these newborn neurons and their associated astrocytes. Alterations to either of these cell types can influence neuronal functioning. To determine if hypertrophied astrocytes might negatively influence immature neurons in the dentate gyrus, astrocyte and newborn neurons were analyzed at 30 days following a TBI in mice. The results demonstrate a loss of radial glial-like processes extending through the granule cell layer after TBI, as well as ectopic growth and migration of immature dentate neurons. The results further show newborn neurons in close association with hypertrophied astrocytes, suggesting a role for the astrocytes in aberrant neurogenesis. Future studies are needed to determine the functional significance of these alterations to the astrocyte/immature neurons after TBI.

  16. The Effects of Singal Protein SMADs on Rat Cardiocyte Hypertrophy

    Institute of Scientific and Technical Information of China (English)

    Huang Jun; Wang Menghong; Xiao Jing; Peng Jingtian; Zheng Zeqi; Peng Xiaoping

    2005-01-01

    Objectives To investigate the role of signal protein SMADs in rat cardiac hypertrophy.Methods The rat models of cardiac hypertrophy were produced by constriction of the abdominal aorta. The left vertricular mass index (LVMI) was investigated.The expression of transforming growth factor-β1 mRNA (TGF-β1) and Smad 2,3,7 mRNA were assessed by RT-PCR. Reslutes The LVMI and the expression of TGF-β1 and Smad 2,3,7mRNA in hypertrophic left ventricule were increased on day 3 after the operation and continued to 4th weeks. The peak expression of TGF-β1 and Smad 2,3 mRNA were in 2 weeks after operation. The expression of Smad 7 was increased in 3day after operation, but the peak was in 1 week after operation, then decreased. Conclusions The TGF-31and signal protein Smad 2,3,7 were included in the progress of rat cardiac hypertrophy produced by constriction of abdominal aorta.

  17. Lean heart: Role of leptin in cardiac hypertrophy and metabolism

    Institute of Scientific and Technical Information of China (English)

    Michael; E; Hall; Romain; Harmancey; David; E; Stec

    2015-01-01

    Leptin is an adipokine that has been linked with the cardiovascular complications resulting from obesity such as hypertension and heart disease. Obese patients have high levels of circulating leptin due to increased fat mass. Clinical and population studies have correlated high levels of circulating leptin with the development of cardiac hypertrophy in obesity. Leptin has also been demonstrated to increase the growth of cultured cardiomyocytes. However, several animal studies of obese leptin deficient mice have not supported a role for leptin in promoting cardiac hypertrophy so the role of leptin in this pathological process remains unclear. Leptin is also an important hormone in the regulation of cardiac metabolism where it supports oxidation of glucose and fatty acids. In addition, leptin plays a critical role in protecting the heart from excess lipid accumulation and the formation of toxic lipids in obesity a condition known as cardiac lipotoxicity. This paper focuses on the data supporting and refuting leptin’s role in promoting cardiac hypertrophy as well as its important role in the regulation of cardiac metabolism and protection against cardiac lipotoxicity.

  18. Effect of prophylactic digitalization on the development of myocardial hypertrophy.

    Science.gov (United States)

    Cutilletta, A F; Rudnik, M; Arcilla, R A; Straube, R

    1977-11-01

    The effect of prophylactic digitalization on the development of left ventricular hypertrophy was studied in adult rats. Digitoxin, 0.1 mg/100 g body wt or solvent was given daily for 1 wk prior to either aortic constriction or sham operation and was continued until the animals were killed, either 1 or 4 wk after surgery. A hemodynamic study was done in those animals killed 1 wk after surgery; hearts of all animals were examined for evidence of myocardial hypertrophy. Constriction of the ascending aorta had no significant effect on cardiac output but did reduce peak flow velocity and flow acceleration. An increase in left ventricular mass, RNA, and hydroxyproline was found in the animals with aortic constriction. Digitoxin treatment did not alter peak flow velocity or flow acceleration, but did significantly increase isovolumic (dP/dt)P-1. Digitoxin had no effect on body weight, heart weight, RNA, or hydroxyproline in either the sham-operated animals or in the animals with aortic constriction. Therefore, despite plasma digitoxin levels sufficient to affect myocardial contractility, left ventricular hypertrophy still developed after aortic constriction.

  19. Role of Histone Demethylases in Cardiomyocytes Induced to Hypertrophy

    Directory of Open Access Journals (Sweden)

    Wendy Rosales

    2016-01-01

    Full Text Available Epigenetic changes induced by histone demethylases play an important role in differentiation and pathological changes in cardiac cells. However, the role of the jumonji family of demethylases in the development of cardiac hypertrophy remains elusive. In this study, the presence of different histone demethylases in cardiac cells was evaluated after hypertrophy was induced with neurohormones. A cell line from rat cardiomyocytes was used as a biological model. The phenotypic profiles of the cells, as well as the expression of histone demethylases, were studied through immunofluorescence, transient transfection, western blot, and qRT-PCR analysis after inducing hypertrophy by angiotensin II and endothelin-1. An increase in fetal gene expression (ANP, BNP, and β-MHC was observed in cardiomyocytes after treatment with angiotensin II and endothelin-1. A significant increase in JMJD2A expression, but not in UTX or JMJD2C expression, was observed. When JMJD2A was overexpressed in cardiomyocytes through transient transfection, the effect of neurohormones on fetal cardiac gene expression was increased. We conclude that JMJD2A plays a principal role in the regulation of fetal cardiac genes, which increase in expression during the pathological hypertrophic process.

  20. Mouse models for the study of postnatal cardiac hypertrophy

    Directory of Open Access Journals (Sweden)

    A. Del Olmo-Turrubiarte

    2015-06-01

    Full Text Available The main objective of this study was to create a postnatal model for cardiac hypertrophy (CH, in order to explain the mechanisms that are present in childhood cardiac hypertrophy. Five days after implantation, intraperitoneal (IP isoproterenol (ISO was injected for 7 days to pregnant female mice. The fetuses were obtained at 15, 17 and 19 dpc from both groups, also newborns (NB, neonates (7–15 days and young adults (6 weeks of age. Histopathological exams were done on the hearts. Immunohistochemistry and western blot demonstrated GATA4 and PCNA protein expression, qPCR real time the mRNA of adrenergic receptors (α-AR and β-AR, alpha and beta myosins (α-MHC, β-MHC and GATA4. After the administration of ISO, there was no change in the number of offsprings. We observed significant structural changes in the size of the offspring hearts. Morphometric analysis revealed an increase in the size of the left ventricular wall and interventricular septum (IVS. Histopathological analysis demonstrated loss of cellular compaction and presence of left ventricular small fibrous foci after birth. Adrenergic receptors might be responsible for changing a physiological into a pathological hypertrophy. However GATA4 seemed to be the determining factor in the pathology. A new animal model was established for the study of pathologic CH in early postnatal stages.

  1. The frequency of benign prostate hypertrophy in Calabar.

    Science.gov (United States)

    Umezurike, B I; Ekanem, T B; Eluwa, M A; Etta, K K; Udo-Affah, G A; Aligwekwe, A U

    2006-09-01

    The present study was to find out through histopathological records the most frequently occurring disease of the prostate from suspected prostate diseases in Calabar, Cross River State, Nigeria. A total number of 324 cases of prostatic biopsies and autopsy materials recorded in the histopathology laboratory of the University of Calabar Teaching Hospital (UCTH), Calabar between 1986 and 1995 were used for this study. Benign prostatic hypertrophy was observed as the major pathology among all the diseases of the prostate gland recorded in UCTH in Calabar having accounted for 76.3% (261 out of 342) while prostatic carcinoma accounted for 19% (65 out of 324), rest 4.7% (16 out of 342) were inflammatory lesions. The result indicated that benign prostatic hypertrophy occurs in men from 40 years and above. The frequency increased with age, reaching a maximum of 34.5% (90 out of 261) in the age group (70-79) years old. The people in Cross River State should be informed of the high frequency of benign prostatic hypertrophy and should be advised to seek health care promptly in suspected prostate related illness.

  2. The lithosphere-asthenosphere Italy and surroundings

    CERN Document Server

    Panza, G F; Chimera, G; Pontevivo, A; Raykova, R

    2003-01-01

    The velocity-depth distribution of the lithosphere-asthenosphere in the Italian region and surroundings is imaged, with a lateral resolution of about 100 km, by surface wave velocity tomography and non-linear inversion. Maps of the Moho depth, of the thickness of the lithosphere and of the shear-wave velocities, down to depths of 200 km and more, are constructed. A mantle wedge, identified in the uppermost mantle along the Apennines and the Calabrian Arc, underlies the principal recent volcanoes, and partial melting can be relevant in this part of the uppermost mantle. In Calabria a lithospheric doubling is seen, in connection with the subduction of the Ionian lithosphere. The asthenosphere is shallow in the Southern Tyrrhenian Sea. High velocity bodies, cutting the asthenosphere, outline the Adria-lonian subduction in the Tyrrhenian Sea and the deep-reaching lithospheric root in the Western Alps. Less deep lithospheric roots are seen in the Central Apennines. The lithosphere-asthenosphere properties delineat...

  3. The lithosphere-asthenosphere: Italy and surroundings

    Institute of Scientific and Technical Information of China (English)

    GiulianoF.Panza; AntonellaPontevivo; GiordanoChimera; RenetaRaykova; AbdelkrimAoudia

    2003-01-01

    The velocity-depth distribution of the lithosphere-asthenosphere in the Italian region and surroundings is imaged, with a lateral resolution of about 100 km, by sur-face wave velocity tomography and non-linear inversion.Maps of the Moho depth, of the thickness of the lithos-phere and of the shear-wave velocities, down to depths of 200 km and more, are constructed. A mantle wedge, iden-tified in the uppermost mantle along the Apennines and the Calabrian Arc, underlies the prmctpat recent votca-noes, and partial melting can be relevant in this part of the uppermost mantle. In Calabria, a lithospheric dou-bling is seen, in connection with the subduction of the Ionian lithosphere. The asthenosphere is shallow in the Southern Tyrrhenian Sea. High velocity bodies, cutting the asthenosphere, outline the Adria-lonian subduction in the Tyrrhenian Sea and the deep-reaching lithospheric root in the Western Alps. Less deep lithospheric roots are seen in the Central Apennines. The lithosphere-asthenos-phere properties delineate a differentiation between the northern and the southern sectors of the Adriatic Sea,likely attesting the fragmentation of Adria.

  4. Preliminary design of surrounding heliostat fields

    Energy Technology Data Exchange (ETDEWEB)

    Collado, Francisco J. [Zaragoza University, Dpto. de Ingenieria Mecanica, CPS-B, Maria de Luna 3, 50018 Zaragoza (Spain)

    2009-05-15

    Recently, the author has shown elsewhere a simplified model that allows quick evaluations of the annual overall energy collected by a surrounding heliostat field. This model is the combination of an analytical flux density function produced by a heliostat, developed by the own author, and an optimized mirror density distribution developed by University of Houston for the Solar One Project. As main conclusion of this previous work, it was recognized that such pseudo-continuous simplified model should not substitute much more accurate discrete evaluations, which manage thousands of individual heliostat coordinates. Here in this work, the difficulty of generating a preliminary discrete layout of a large number of heliostats is addressed. The main novelty is the direct definition of thousands of heliostat coordinates through basically two parameters i.e. a simplified blocking factor and an additional security distance. Such procedure, which was formerly theoretically suggested by the author, is put into practice here, showing examples and commenting their problems and advantages. Getting a previous set of thousands of heliostat coordinates would be a major first step in the complex process of designing solar power tower (SPT). (author)

  5. Hepatitis C FAQs for the Public

    Science.gov (United States)

    ... Requirements for Viral Hepatitis Liver Cancer and Viral Hepatitis Viral Hepatitis and Young Persons Who Inject Drugs National ... Hepatitis Contact Us Anonymous Feedback Quick Links to Hepatitis … A | B | C | D | E Viral Hepatitis Home Statistics & ...

  6. Hepatitis B Foundation Newsletter: B Informed

    Science.gov (United States)

    ... Our Accomplishments Annual Reports Our Videos What Is Hepatitis B? What Is Hepatitis B? The ABCs of Viral Hepatitis Liver Cancer and Hepatitis B Hepatitis Delta Coinfection Hepatitis C Coinfection HIV/AIDS ...

  7. Hepatitis B - children

    Science.gov (United States)

    ... care provider will perform blood tests called the hepatitis viral panel . These tests can help diagnose: A new ... 07, 2016. Jensen MK, William F, Balistreri WF. Viral hepatitis. In: Kliegman RM, Stanton BF, St Geme JW ...

  8. Hepatitis Foundation International

    Science.gov (United States)

    ... million people globally. admin / 03/17/2015 Viral Hepatitis An estimated 4.4 million Americans from all ... Events section below. EVENTS FULL CALENDAR Loading… VIRAL HEPATITIS DISPARITIES HARD TO REACH, HARD TO TREAT™ AFRICAN ...

  9. Hepatitis B Vaccination Protection

    Science.gov (United States)

    Fact Sheet Hepatitis B Vaccination Protection Hepatitis B virus (HBV) is a pathogenic microorganism that can cause potentially life- threatening disease in humans. HBV infection is transmitted through exposure ...

  10. Hepatitis C (image)

    Science.gov (United States)

    Hepatitis C is a virus-caused liver inflammation which may cause jaundice, fever and cirrhosis. Persons who are most at risk for contracting and spreading hepatitis C are those who share needles for injecting drugs ...

  11. Hepatitis virus panel

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/article/003558.htm Hepatitis virus panel To use the sharing features on this page, please enable JavaScript. The hepatitis virus panel is a series of blood tests used ...

  12. C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB.

    Science.gov (United States)

    Zou, Jian; Li, Hong; Chen, Xi; Zeng, Siyu; Ye, Jiantao; Zhou, Changhua; Liu, Min; Zhang, Luankun; Yu, Na; Gan, Xiaohong; Zhou, Houfeng; Xian, Zhiwei; Chen, Shaorui; Liu, Peiqing

    2014-06-05

    C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy.

  13. Hepatitis C and HIV

    Science.gov (United States)

    ... Hepatitis A and Hepatitis B . Hepatitis C and HIV About 25% of people living with HIV in ... Notice Network blog.aids.gov • locator.aids.gov • HIV/AIDS Service Locator Locator Widgets • Instructions • API Find ...

  14. Hepatitis B and HIV

    Science.gov (United States)

    ... Hepatitis A and Hepatitis C . Hepatitis B and HIV About 10% of people living with HIV in ... Notice Network blog.aids.gov • locator.aids.gov • HIV/AIDS Service Locator Locator Widgets • Instructions • API Find ...

  15. What Is Hepatitis?

    Science.gov (United States)

    ... عربي 中文 English Français Русский Español What is hepatitis? Online Q&A Reviewed July 2016 Q: What ... Question and answer archives Submit a question World Hepatitis Day Know hepatitis - Act now Event notice Key ...

  16. Hepatic (Liver) Function Panel

    Science.gov (United States)

    ... 1- to 2-Year-Old Blood Test: Hepatic (Liver) Function Panel KidsHealth > For Parents > Blood Test: Hepatic (Liver) Function Panel Print A A A What's in ... Is The hepatic function panel, also known as liver function tests, is a group of seven tests ...

  17. Asymmetric left ventricular hypertrophy associated with morbid obesity mimicking familial hypertrophic cardiomyopathy.

    Science.gov (United States)

    Wong, Raymond Ching-Chiew; Tan, Kong Bing

    2014-12-01

    Asymmetric septal hypertrophy with systolic anterior motion of the mitral valve is frequently a phenotypic, but not pathognomonic, expression of genetic hypertrophic cardiomyopathy (HCM) with or without obstruction. It can, however, be associated nonspecifically with other forms of increased left ventricular (LV) afterload. We herein report the case of a young man with obesity cardiomyopathy and heart failure who presented with asymmetric septal hypertrophy and marked LV hypertrophy, and endomyocardial biopsy ruled out genetic HCM.

  18. Biomechanical implications of skeletal muscle hypertrophy and atrophy: a musculoskeletal model

    OpenAIRE

    Andrew D. Vigotsky; Bret Contreras; Chris Beardsley

    2015-01-01

    Muscle hypertrophy and atrophy occur frequently as a result of mechanical loading or unloading, with implications for clinical, general, and athletic populations. The effects of muscle hypertrophy and atrophy on force production and joint moments have been previously described. However, there is a paucity of research showing how hypertrophy and atrophy may affect moment arm (MA) lengths. The purpose of this model was to describe the mathematical relationship between the anatomical cross-secti...

  19. Myocardial hypertrophy in the recipient with twin-to-twin transfusion syndrome

    DEFF Research Database (Denmark)

    Jeppesen, D.L.; Jorgensen, F.S.; Pryds, O.A.

    2008-01-01

    In a set of monochorionic-diamniotic twins with twin-to-twin transfusion syndrome, systemic hypertension and biventricular myocardial hypertrophy were found in the recipient. The infant developed mild respiratory distress. A partial exchange transfusion was performed because of polycytaemia. Blood...... pressure measurements revealed persistent systemic hypertension. Biventricular hypertrophy was demonstrated by echocardiography. Blood pressure normalised after treatment with Nifedipine and the cardiac hypertrophy subsided over the following weeks. A potential contributing mechanism is intrauterine...

  20. Lingual tonsil hypertrophy causing severe dysphagia: treatment with plasma-mediated radiofrequency-based ablation (Coblation).

    Science.gov (United States)

    Mowry, Sarah E; Ament, Marvin; Shapiro, Nina L

    2010-03-01

    Lingual tonsil hypertrophy is an uncommon cause of upper aerodigestive tract pathology. We present the case of a 17-year-old boy who developed severe dysphagia and subsequent weight loss as a result of lingual tonsil hypertrophy. He was successfully treated with plasma-mediated radiofrequency-based ablation (Coblation). In the past, traditional surgical procedures for lingual tonsil hypertrophy were difficult to perform and recovery was difficult, but the introduction of Coblation has made lingual tonsillectomy much easier.

  1. Myocardial hypertrophy in the recipient with twin-to-twin transfusion syndrome

    DEFF Research Database (Denmark)

    Jeppesen, D.L.; Jorgensen, F.S.; Pryds, O.A.

    2008-01-01

    pressure measurements revealed persistent systemic hypertension. Biventricular hypertrophy was demonstrated by echocardiography. Blood pressure normalised after treatment with Nifedipine and the cardiac hypertrophy subsided over the following weeks. A potential contributing mechanism is intrauterine......In a set of monochorionic-diamniotic twins with twin-to-twin transfusion syndrome, systemic hypertension and biventricular myocardial hypertrophy were found in the recipient. The infant developed mild respiratory distress. A partial exchange transfusion was performed because of polycytaemia. Blood...

  2. Asymmetric adenoid hypertrophy in a patient with ipsilateral rhinolithiasis: an overlooked entity?

    OpenAIRE

    Kazikdas, C; Gode, S; Demirci, M.

    2011-01-01

    The aim of this article is to present a rhinolithiasis patient with a significant asymmetric adenoid hypertrophy on the same side and to describe possible mechanisms for this clinical entity. Careful nasopharyngoscopy after removal of rhinolith is mandatory not to overlook significant adenoid hypertrophy which may interfere with patients’ symptoms. The role of paranasal CT scan in the diagnosis of an asymmetric adenoid hypertrophy in rhinolithiasis patients is also discussed.

  3. Tympanometric Findings among Children with Adenoid Hypertrophy in Port Harcourt, Nigeria

    OpenAIRE

    Chibuike Nwosu; Mathilda Uju Ibekwe; Lucky Obukowho Onotai

    2016-01-01

    Introduction. Adenoid hypertrophy (AH) is a common childhood disorder. Adenoid plays a significant role in the pathogenesis of otitis media with effusion (OME). The aim of this study is to critically appraise the tympanometric finding among children with adenoid hypertrophy in Port Harcourt, Nigeria. Methodology. A Prospective, controlled study carried out among newly diagnosed cases of adenoid hypertrophy at the ENT clinic of the UPTH, between November 2014 and June 2015. Tympanometry was do...

  4. Cardiac hypertrophy: a risk factor for QT-prolongation and cardiac sudden death.

    Science.gov (United States)

    Kang, Y James

    2006-01-01

    Cardiac hypertrophy was viewed as a compensatory response to hemodynamic stress. However, cumulative evidence obtained from studies using more advanced technologies in human patients and animal models suggests that cardiac hypertrophy is a maladaptive process of the heart in response to intrinsic and extrinsic stimuli. Although hypertrophy can normalize wall tension, it is a risk factor for QT-prolongation and cardiac sudden death. Studies using molecular biology techniques such as transgenic and knockout mice have revealed many important molecules that are involved in the development of heart hypertrophy and have demonstrated signaling pathways leading to the pathogenesis. With the same approach, the consequence of heart hypertrophy has been examined. The significance of hypertrophy in the development of overt heart failure has been demonstrated and several critical molecular pathways involved in the process were revealed. A comprehensive understanding of the threats of heart hypertrophy to patients has helped to develop novel treatment strategies. The recognition of hypertrophy as a major risk factor for QT-prolongation and cardiac sudden death is an important advance in cardiac medicine. Cellular and molecular mechanisms of this risk aspect are currently under extensively exploring. These studies would lead to more comprehensive approaches to prevention of potential life threatening arrhythmia and cardiac sudden death. The adaptation of new approaches such as functional genomics and proteomics will further advance our knowledge of heart hypertrophy.

  5. Cardiac hypertrophy induced by active Raf depends on Yorkie-mediated transcription.

    Science.gov (United States)

    Yu, Lin; Daniels, Joseph P; Wu, Huihui; Wolf, Matthew J

    2015-02-03

    Organ hypertrophy can result from enlargement of individual cells or from cell proliferation or both. Activating mutations in the serine-threonine kinase Raf cause cardiac hypertrophy and contribute to Noonan syndrome in humans. Cardiac-specific expression of activated Raf also causes hypertrophy in Drosophila melanogaster. We found that Yorkie (Yki), a transcriptional coactivator in the Hippo pathway that regulates organ size, is required for Raf-induced cardiac hypertrophy in flies. Although aberrant activation of Yki orthologs stimulates cardiac hyperplasia in mice, cardiac-specific expression of an activated mutant form of Yki in fruit flies caused cardiac hypertrophy without hyperplasia. Knockdown of Yki caused cardiac dilation without loss of cardiomyocytes and prevented Raf-induced cardiac hypertrophy. In flies, Yki-induced cardiac hypertrophy required the TEA domain-containing transcription factor Scalloped, and, in mammalian cells, expression of mouse Raf(L613V), an activated form of Raf with a Noonan syndrome mutation, increased Yki-induced Scalloped activity. Furthermore, overexpression of Tgi (a Tondu domain-containing Scalloped-binding corepressor) in the fly heart abrogated Yki- or Raf-induced cardiac hypertrophy. Thus, crosstalk between Raf and Yki occurs in the heart and can influence Raf-mediated cardiac hypertrophy.

  6. Management of Unilateral Masseter Hypertrophy and Hypertrophic Scar—A Case Report

    Directory of Open Access Journals (Sweden)

    Naresh Shetty

    2012-01-01

    Full Text Available Masseter muscle hypertrophy is a rare condition of idiopathic cause. It clinically presents as an enlargement of one or both masseter muscles. Most patients complain of facial asymmetry; however, symptoms such as trismus, protrusion, and bruxism may also occur. Several treatment options reported for masseter hypertrophy are present, which range from simple pharmacotherapy to more invasive surgical reduction. Keloid scar with unilateral masseter hypertrophy is a rarely seen in clinical practice. This paper reports a case of unilateral masseter hypertrophy with keloid scar in the angle of the mandible for which surgical treatment was rendered to the patient by using a single approach.

  7. Selumetinib, an Oral Anti-Neoplastic Drug, May Attenuate Cardiac Hypertrophy via Targeting the ERK Pathway.

    Science.gov (United States)

    Li, Chen; Chen, Zhongxiu; Yang, Hao; Luo, Fangbo; Chen, Lihong; Cai, Huawei; Li, Yajiao; You, Guiying; Long, Dan; Li, Shengfu; Zhang, Qiuping; Rao, Li

    2016-01-01

    Although extracellular-regulated kinases (ERK) are a well-known central mediator in cardiac hypertrophy, no clinically available ERK antagonist has been tested for preventing cardiac hypertrophy. Selumetinib is a novel oral MEK inhibitor that is currently under Phase II and Phase III clinical investigation for advanced solid tumors. In this study, we investigated whether Selumetinib could inhibit the aberrant ERK activation of the heart in response to stress as well as prevent cardiac hypertrophy. In an in vitro model of PE-induced cardiac hypertrophy, Selumetinib significantly inhibited the ERK activation and prevented enlargement of cardiomyocytes or reactivation of certain fetal genes. In the pathologic cardiac hypertrophy model of ascending aortic constriction, Selumetinib provided significant ERK inhibition in the stressed heart but not in the other organs. This selective ERK inhibition prevented left ventricular (LV) wall thickening, LV mass increase, fetal gene reactivation and cardiac fibrosis. In another distinct physiologic cardiac hypertrophy model of a swimming rat, Selumetinib provided a similar anti-hypertrophy effect, except that no significant fetal gene reactivation or cardiac fibrosis was observed. Selumetinib, a novel oral anti-cancer drug with good safety records in a number of Phase II clinical trials, can inhibit ERK activity in the heart and prevent cardiac hypertrophy. These promising results indicate that Selumetinib could potentially be used to treat cardiac hypertrophy. However, this hypothesis needs to be validated in human clinical trials.

  8. Isorhamnetin protects against cardiac hypertrophy through blocking PI3K-AKT pathway.

    Science.gov (United States)

    Gao, Lu; Yao, Rui; Liu, Yuzhou; Wang, Zheng; Huang, Zhen; Du, Binbin; Zhang, Dianhong; Wu, Leiming; Xiao, Lili; Zhang, Yanzhou

    2017-05-01

    Isorhamnetin, a flavonoid compound extracted from the Chinese herb Hippophae rhamnoides L., is well known for its anti-inflammatory, anti-oxidative, anti-adipogenic, anti-proliferative, and anti-tumor activities. However, the role of isorhamnetin in cardiac hypertrophy has not been reported. The aims of the present study were to find whether isorhamnetin could alleviate cardiac hypertrophy and to define the underlying molecular mechanisms. Here, we investigated the effects of isorhamnetin (100 mg/kg/day) on cardiac hypertrophy induced by aortic banding in mice. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. Our data demonstrated that isorhamnetin could inhibit cardiac hypertrophy and fibrosis 8 weeks after aortic banding. The results further revealed that the effect of isorhamnetin on cardiac hypertrophy was mediated by blocking the activation of phosphatidylinositol 3-kinase-AKT signaling pathway. In vitro studies performed in neonatal rat cardiomyocytes confirmed that isorhamnetin could attenuate cardiomyocyte hypertrophy induced by angiotensin II, which was associated with phosphatidylinositol 3-kinase-AKT signaling pathway. In conclusion, these data indicate for the first time that isorhamnetin has protective potential for targeting cardiac hypertrophy by blocking the phosphatidylinositol 3-kinase-AKT signaling pathway. Thus, our study suggests that isorhamnetin may represent a potential therapeutic strategy for the treatment of cardiac hypertrophy and heart failure.

  9. Cardiac‐specific Hexokinase 2 Overexpression Attenuates Hypertrophy by Increasing Pentose Phosphate Pathway Flux

    Science.gov (United States)

    McCommis, Kyle S.; Douglas, Diana L.; Krenz, Maike; Baines, Christopher P.

    2013-01-01

    Background The enzyme hexokinase‐2 (HK2) phosphorylates glucose, which is the initiating step in virtually all glucose utilization pathways. Cardiac hypertrophy is associated with a switch towards increased glucose metabolism and decreased fatty acid metabolism. Recent evidence suggests that the increased glucose utilization is compensatory to the down‐regulated fatty acid metabolism during hypertrophy and is, in fact, beneficial. Therefore, we hypothesized that increasing glucose utilization by HK2 overexpression would decrease cardiac hypertrophy. Methods and Results Mice with cardiac‐specific HK2 overexpression displayed decreased hypertrophy in response to isoproterenol. Neonatal rat ventricular myocytes (NRVMs) infected with an HK2 adenovirus similarly displayed decreased hypertrophy in response to phenylephrine. Hypertrophy increased reactive oxygen species (ROS) levels, which were attenuated by HK2 overexpression, thereby decreasing NRVM hypertrophy and death. HK2 appears to modulate ROS via the pentose phosphate pathway, as inhibition of glucose‐6‐phosphate dehydrogenase with dehydroepiandrosterone decreased the ability of HK2 to diminish ROS and hypertrophy. Conclusions These results suggest that HK2 attenuates cardiac hypertrophy by decreasing ROS accumulation via increased pentose phosphate pathway flux. PMID:24190878

  10. Selumetinib, an Oral Anti-Neoplastic Drug, May Attenuate Cardiac Hypertrophy via Targeting the ERK Pathway.

    Directory of Open Access Journals (Sweden)

    Chen Li

    Full Text Available Although extracellular-regulated kinases (ERK are a well-known central mediator in cardiac hypertrophy, no clinically available ERK antagonist has been tested for preventing cardiac hypertrophy. Selumetinib is a novel oral MEK inhibitor that is currently under Phase II and Phase III clinical investigation for advanced solid tumors. In this study, we investigated whether Selumetinib could inhibit the aberrant ERK activation of the heart in response to stress as well as prevent cardiac hypertrophy.In an in vitro model of PE-induced cardiac hypertrophy, Selumetinib significantly inhibited the ERK activation and prevented enlargement of cardiomyocytes or reactivation of certain fetal genes. In the pathologic cardiac hypertrophy model of ascending aortic constriction, Selumetinib provided significant ERK inhibition in the stressed heart but not in the other organs. This selective ERK inhibition prevented left ventricular (LV wall thickening, LV mass increase, fetal gene reactivation and cardiac fibrosis. In another distinct physiologic cardiac hypertrophy model of a swimming rat, Selumetinib provided a similar anti-hypertrophy effect, except that no significant fetal gene reactivation or cardiac fibrosis was observed.Selumetinib, a novel oral anti-cancer drug with good safety records in a number of Phase II clinical trials, can inhibit ERK activity in the heart and prevent cardiac hypertrophy. These promising results indicate that Selumetinib could potentially be used to treat cardiac hypertrophy. However, this hypothesis needs to be validated in human clinical trials.

  11. Selumetinib, an Oral Anti-Neoplastic Drug, May Attenuate Cardiac Hypertrophy via Targeting the ERK Pathway

    Science.gov (United States)

    Yang, Hao; Luo, Fangbo; Chen, Lihong; Cai, Huawei; Li, Yajiao; You, Guiying; Long, Dan; Li, Shengfu; Zhang, Qiuping; Rao, Li

    2016-01-01

    Aims Although extracellular-regulated kinases (ERK) are a well-known central mediator in cardiac hypertrophy, no clinically available ERK antagonist has been tested for preventing cardiac hypertrophy. Selumetinib is a novel oral MEK inhibitor that is currently under Phase II and Phase III clinical investigation for advanced solid tumors. In this study, we investigated whether Selumetinib could inhibit the aberrant ERK activation of the heart in response to stress as well as prevent cardiac hypertrophy. Methods and Results In an in vitro model of PE-induced cardiac hypertrophy, Selumetinib significantly inhibited the ERK activation and prevented enlargement of cardiomyocytes or reactivation of certain fetal genes. In the pathologic cardiac hypertrophy model of ascending aortic constriction, Selumetinib provided significant ERK inhibition in the stressed heart but not in the other organs. This selective ERK inhibition prevented left ventricular (LV) wall thickening, LV mass increase, fetal gene reactivation and cardiac fibrosis. In another distinct physiologic cardiac hypertrophy model of a swimming rat, Selumetinib provided a similar anti-hypertrophy effect, except that no significant fetal gene reactivation or cardiac fibrosis was observed. Conclusions Selumetinib, a novel oral anti-cancer drug with good safety records in a number of Phase II clinical trials, can inhibit ERK activity in the heart and prevent cardiac hypertrophy. These promising results indicate that Selumetinib could potentially be used to treat cardiac hypertrophy. However, this hypothesis needs to be validated in human clinical trials. PMID:27438013

  12. Relative etiological importance of adenoid hypertrophy versus sinusitis in children with persistent rhinorrhoea.

    Science.gov (United States)

    Maheswaran, S; Rupa, V; Ebenezer, Jareen; Manoharan, Anand; Irodi, Aparna

    2015-03-01

    Persistent rhinorrhoea is a common, yet often neglected, problem among Indian children. This study was designed to evaluate the relative etiological importance of adenoid hypertrophy versus sinusitis in children with persistent rhinorrhea. Additionally, the association between S. pneumoniae colonization and adenoid hypertrophy was studied. Children aged 1-14 years with persistent rhinorrhea underwent clinical evaluation, rigid nasal endoscopy and xrays of the nasopharynx and paranasal sinuses to ascertain the presence of adenoid hypertrophy and sinusitis using standard criteria. Nasopharyngeal swabbing to ascertain the presence of nasopharyngeal colonization with S. pneumoniae was also performed. Adenoid hypertrophy was more consistently associated with persistent rhinorrhea than sinusitis (p adenoid hypertrophy and sinusitis occurred in 57 %. S. pneumoniae was cultured in only 29 % of children. Up to 47 % of patients had features of nasal allergy. There was no association between S. pneumoniae colonization and adenoid hypertrophy (p = 0.1). Adenoid hypertrophy is an important cause of persistent rhinorrhea in children. Measures to evaluate for and treat adenoid hypertrophy should be instituted early to alleviate the problem of persistent rhinorrhoea in children. S. pneumoniae colonization of the nasopharynx is not a major etiological factor for persistent rhinorrhoea in these children. Nasal allergy may be a cause of adenoid hypertrophy in roughly half the children.

  13. VIRAL HEPATITIS E DIAGNOSTICS

    Directory of Open Access Journals (Sweden)

    E. Yu. Malinnikova

    2013-01-01

    Full Text Available Abstract. The results of clinical and epidemiological studies conducted in the M.P. Chumakov’ Research Institute of Poliomyelitis and Viral Encephalitis and in the different research institutions of the world have been summarized in the current article. Data on etiology, pathogenesis, clinical symptoms, epidemiology and prevention of hepatitis E are presented. Increasing of significance of this infection for health care system in Russia is emphasized . The actual problems of hepatitis E (autochthonic hepatitis E, hepatitis E as zoonosis, chronic hepatitis E are discussed.

  14. Pathogenesis of Hepatic Encephalopathy

    Directory of Open Access Journals (Sweden)

    Irena Ciećko-Michalska

    2012-01-01

    Full Text Available Hepatic encephalopathy can be a serious complication of acute liver failure and chronic liver diseases, predominantly liver cirrhosis. Hyperammonemia plays the most important role in the pathogenesis of hepatic encephalopathy. The brain-blood barrier disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, GABA-ergic or benzodiazepine pathway abnormalities, manganese neurotoxicity, brain energetic disturbances, and brain blood flow abnormalities are considered to be involved in the development of hepatic encephalopathy. The influence of small intestine bacterial overgrowth (SIBO on the induction of minimal hepatic encephalopathy is recently emphasized. The aim of this paper is to present the current views on the pathogenesis of hepatic encephalopathy.

  15. Impacts of Artificial Reefs on Surrounding Ecosystems

    Science.gov (United States)

    Manoukian, Sarine

    Artificial reefs are becoming a popular biological and management component in shallow water environments characterized by soft seabed, representing both important marine habitats and tools to manage coastal fisheries and resources. An artificial reef in the marine environment acts as an open system with exchange of material and energy, altering the physical and biological characteristics of the surrounding area. Reef stability will depend on the balance of scour, settlement, and burial resulting from ocean conditions over time. Because of the unstable nature of sediments, they require a detailed and systematic investigation. Acoustic systems like high-frequency multibeam sonar are efficient tools in monitoring the environmental evolution around artificial reefs, whereas water turbidity can limit visual dive and ROV inspections. A high-frequency multibeam echo sounder offers the potential of detecting fine-scale distribution of reef units, providing an unprecedented level of resolution, coverage, and spatial definition. How do artificial reefs change over time in relation to the coastal processes? How accurately does multibeam technology map different typologies of artificial modules of known size and shape? How do artificial reefs affect fish school behavior? What are the limitations of multibeam technology for investigating fish school distribution as well as spatial and temporal changes? This study addresses the above questions and presents results of a new approach for artificial reef seafloor mapping over time, based upon an integrated analysis of multibeam swath bathymetry data and geoscientific information (backscatter data analysis, SCUBA observations, physical oceanographic data, and previous findings on the geology and sedimentation processes, integrated with unpublished data) from Senigallia artificial reef, northwestern Adriatic Sea (Italy) and St. Petersburg Beach Reef, west-central Florida continental shelf. A new approach for observation of fish

  16. Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling.

    Science.gov (United States)

    Gitau, Samuel Chege; Li, Xuelian; Zhao, Dandan; Guo, Zhenfeng; Liang, Haihai; Qian, Ming; Lv, Lifang; Li, Tianshi; Xu, Bozhi; Wang, Zhiguo; Zhang, Yong; Xu, Chaoqian; Lu, Yanjie; Du, Zhiming; Shan, Hongli; Yang, Baofeng

    2015-12-01

    Ventricular hypertrophy is a powerful and independent predictor of cardiovascular morbid events. The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail. In this study, healthy wild-type male mice were randomly divided into three groups and subjected to transverse aortic constriction (TAC) or sham operation. The TAC-operated mice were treated with the human equivalent of low-dose aspirin (10 mg·kg(-1)·d(-1)); the remaining mice received an equal amount of phosphate buffered saline with 0.65% ethanol, which was used as a vehicle. A cardiomyocyte hypertrophy model induced by angiotensin II (10 nmol·L(-1)) was treated with the human equivalent of low (10 or 100 μmol·L(-1)) and high (1000 μmol·L(-1)) aspirin concentrations in plasma. Changes in the cardiac structure and function were assessed through echocardiography and transmission electron microscopy. Gene expression was determined through RT-PCR and western blot analysis. Results indicated that aspirin treatment abrogated the increased thickness of the left ventricular anterior and posterior walls, the swelling of mitochondria, and the increased surface area in in vivo and in vitro hypertrophy models. Aspirin also normalized the upregulated hypertrophic biomarkers, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP). Aspirin efficiently reversed the upregulation of β-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3β. Therefore, low-dose aspirin possesses significant anti-hypertrophic properties at clinically relevant concentrations for anti-thrombotic therapy. The downregulation of β-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.

  17. The Molecular Basis for Load-Induced Skeletal Muscle Hypertrophy

    Science.gov (United States)

    Marcotte, George R.; West, Daniel W.D.; Baar, Keith

    2016-01-01

    In a mature (weight neutral) animal, an increase in muscle mass only occurs when the muscle is loaded sufficiently to cause an increase in myofibrillar protein balance. A tight relationship between muscle hypertrophy, acute increases in protein balance, and the activity of the mechanistic target of rapamycin complex 1 (mTORC1) was demonstrated 15 years ago. Since then, our understanding of the signals that regulate load-induced hypertrophy has evolved considerably. For example, we now know that mechanical load activates mTORC1 in the same way as growth factors, by moving TSC2 (a primary inhibitor of mTORC1) away from its target (the mTORC activator) Rheb. However, the kinase that phosphorylates and moves TSC2 is different in the two processes. Similarly, we have learned that a distinct pathway exists whereby amino acids activate mTORC1 by moving it to Rheb. While mTORC1 remains at the forefront of load-induced hypertrophy, the importance of other pathways that regulate muscle mass are becoming clearer. Myostatin, is best known for its control of developmental muscle size. However, new mechanisms to explain how loading regulates this process are suggesting that it could play an important role in hypertrophic muscle growth as well. Lastly, new mechanisms are highlighted for how β2 receptor agonists could be involved in load-induced muscle growth and why these agents are being developed as non-exercise-based therapies for muscle atrophy. Overall, the results highlight how studying the mechanism of load-induced skeletal muscle mass is leading the development of pharmaceutical interventions to promote muscle growth in those unwilling or unable to perform resistance exercise. PMID:25359125

  18. Hyperplasia vs hypertrophy in tissue regeneration after extensive liver resection.

    Science.gov (United States)

    Marongiu, Fabio; Marongiu, Michela; Contini, Antonella; Serra, Monica; Cadoni, Erika; Murgia, Riccardo; Laconi, Ezio

    2017-03-14

    To address to what extent hypertrophy and hyperplasia contribute to liver mass restoration after major tissue loss. The ability of the liver to regenerate is remarkable on both clinical and biological grounds. Basic mechanisms underlying this process have been intensively investigated. However, it is still debated to what extent hypertrophy and hyperplasia contribute to liver mass restoration after major tissue loss. We addressed this issue using a genetically tagged system. We were able to follow the fate of single transplanted hepatocytes during the regenerative response elicited by 2/3 partial surgical hepatectomy (PH) in rats. Clusters of transplanted cells were 3D reconstructed and their size distribution was evaluated over time after PH. Liver size and liver DNA content were largely recovered 10 d post-PH, as expected (e.g., total DNA/liver/100 g b.w. was 6.37 ± 0.21 before PH and returned to 6.10 ± 0.36 10 d after PH). Data indicated that about 2/3 of the original residual hepatocytes entered S-phase in response to PH. Analysis of cluster size distribution at 24, 48, 96 h and 10 d after PH revealed that about half of the remnant hepatocytes completed at least 2 cell cycles. Average size of hepatocytes increased at 24 h (248.50 μm(2) ± 7.82 μm(2), P = 0.0015), but returned to control values throughout the regenerative process (up to 10 d post-PH, 197.9 μm(2) ± 6.44 μm(2), P = 0.11). A sizeable fraction of the remnant hepatocyte population does not participate actively in tissue mass restoration. Hyperplasia stands as the major mechanism contributing to liver mass restoration after PH, with hypertrophy playing a transient role in the process.

  19. The Association Between Adenoid Hypertrophy and Enuresis in Children

    Directory of Open Access Journals (Sweden)

    Neshat

    2016-02-01

    Full Text Available Background Considering that enuresis is a common health problem among Iranian children, identifying the frequency of enuresis among children with adenoid hypertrophy (AH and its related factors could help us design appropriate management plans as well as preventative and interventional studies. Objectives We aimed to evaluate the prevalence of enuresis among children with AH and its associations with different characteristics of the disease. Patients and Methods This study was designed as a cross-sectional study. Children aged 5 - 12 years diagnosed with adenoid hypertrophy and as well as a group of normal children were studied (2010 - 2011 in Shariati hospital. The prevalence of enuresis was determined and compared in the two groups. The frequencies of different symptoms related to AH were compared in AH patients with and without enuresis. Results During this study, children with (n = 60 and without (n = 60 adenoid hypertrophy were investigated. The prevalence of enuresis was significantly higher in patients with AH compared with the control group (40% vs. 15%, P = 0.004, OR = 8.19. Enuresis was more prevalent among patients with AH who had a severe form of the disease, the signs of which are obstructive sleep apnea (OSA, growth impairment, and irritability (P < 0.05. Conclusions The results of our study indicated that enuresis was a common health problem among children with AH and it is associated with some symptoms of AH such as OSA, growth retardation and irritability. Using these findings as baseline data, we could determine the appropriate treatment approach for improving the course of the disease as well as the quality of the affected patients’ lives.

  20. The molecular basis for load-induced skeletal muscle hypertrophy.

    Science.gov (United States)

    Marcotte, George R; West, Daniel W D; Baar, Keith

    2015-03-01

    In a mature (weight neutral) animal, an increase in muscle mass only occurs when the muscle is loaded sufficiently to cause an increase in myofibrillar protein balance. A tight relationship between muscle hypertrophy, acute increases in protein balance, and the activity of the mechanistic target of rapamycin complex 1 (mTORC1) was demonstrated 15 years ago. Since then, our understanding of the signals that regulate load-induced hypertrophy has evolved considerably. For example, we now know that mechanical load activates mTORC1 in the same way as growth factors, by moving TSC2 (a primary inhibitor of mTORC1) away from its target (the mTORC activator) Rheb. However, the kinase that phosphorylates and moves TSC2 is different in the two processes. Similarly, we have learned that a distinct pathway exists whereby amino acids activate mTORC1 by moving it to Rheb. While mTORC1 remains at the forefront of load-induced hypertrophy, the importance of other pathways that regulate muscle mass are becoming clearer. Myostatin, is best known for its control of developmental muscle size. However, new mechanisms to explain how loading regulates this process are suggesting that it could play an important role in hypertrophic muscle growth as well. Last, new mechanisms are highlighted for how β2 receptor agonists could be involved in load-induced muscle growth and why these agents are being developed as non-exercise-based therapies for muscle atrophy. Overall, the results highlight how studying the mechanism of load-induced skeletal muscle mass is leading the development of pharmaceutical interventions to promote muscle growth in those unwilling or unable to perform resistance exercise.

  1. Muscle hypertrophy induced by myostatin inhibition accelerates degeneration in dysferlinopathy.

    Science.gov (United States)

    Lee, Yun-Sil; Lehar, Adam; Sebald, Suzanne; Liu, Min; Swaggart, Kayleigh A; Talbot, C Conover; Pytel, Peter; Barton, Elisabeth R; McNally, Elizabeth M; Lee, Se-Jin

    2015-10-15

    Myostatin is a secreted signaling molecule that normally acts to limit muscle growth. As a result, there is extensive effort directed at developing drugs capable of targeting myostatin to treat patients with muscle loss. One potential concern with this therapeutic approach in patients with muscle degenerative diseases like muscular dystrophy is that inducing hypertrophy may increase stress on dystrophic fibers, thereby accelerating disease progression. To investigate this possibility, we examined the effect of blocking the myostatin pathway in dysferlin-deficient (Dysf(-/-)) mice, in which membrane repair is compromised, either by transgenic expression of follistatin in skeletal muscle or by systemic administration of the soluble form of the activin type IIB receptor (ACVR2B/Fc). Here, we show that myostatin inhibition by follistatin transgene expression in Dysf(-/-) mice results in early improvement in histopathology but ultimately exacerbates muscle degeneration; this effect was not observed in dystrophin-deficient (mdx) mice, suggesting that accelerated degeneration induced by follistatin transgene expression is specific to mice lacking dysferlin. Dysf(-/-) mice injected with ACVR2B/Fc showed significant increases in muscle mass and amelioration of fibrotic changes normally seen in 8-month-old Dysf(-/-) mice. Despite these potentially beneficial effects, ACVR2B/Fc treatment caused increases in serum CK levels in some Dysf(-/-) mice, indicating possible muscle damage induced by hypertrophy. These findings suggest that depending on the disease context, inducing muscle hypertrophy by myostatin blockade may have detrimental effects, which need to be weighed against the potential gains in muscle growth and decreased fibrosis. © The Author 2015. Published by Oxford University Press.

  2. Tomoregulin-1 prevents cardiac hypertrophy after pressure overload in mice by inhibiting TAK1-JNK pathways

    Directory of Open Access Journals (Sweden)

    Dan Bao

    2015-08-01

    Full Text Available Cardiac hypertrophy is associated with many forms of heart disease, and identifying important modifier genes involved in the pathogenesis of cardiac hypertrophy could lead to the development of new therapeutic strategies. Tomoregulin-1 is a growth factor that is primarily involved in embryonic development and adult central nervous system (CNS function, and it is expressed abnormally in a variety of CNS pathologies. Tomoregulin-1 is also expressed in the myocardium. However, the effects of tomoregulin-1 on the heart, particularly on cardiac hypertrophy, remains unknown. The aim of the study is to examine whether and by what mechanism tomoregulin-1 regulates the development of cardiac hypertrophy induced by pressure overload. In this study, we found that tomoregulin-1 was significantly upregulated in two cardiac hypertrophy models: cTnTR92Q transgenic mice and thoracic aorta constriction (TAC-induced cardiac hypertrophy mice. The transgenic overexpression of tomoregulin-1 increased the survival rate, improved the cardiac geometry and functional parameters of echocardiography, and decreased the degree of cardiac hypertrophy of the TAC mice, whereas knockdown of tomoregulin-1 expression resulted in an opposite phenotype and exacerbated phenotypes of cardiac hypertrophy induced by TAC. A possible mechanism by which tomoregulin-1 regulates the development of cardiac hypertrophy in TAC-induced cardiac hypertrophy is through inhibiting TGFβ non-canonical (TAK1-JNK pathways in the myocardium. Tomoregulin-1 plays a protective role in the modulation of adverse cardiac remodeling from pressure overload in mice. Tomoregulin-1 could be a therapeutic target to control the development of cardiac hypertrophy.

  3. Tomoregulin-1 prevents cardiac hypertrophy after pressure overload in mice by inhibiting TAK1-JNK pathways.

    Science.gov (United States)

    Bao, Dan; Lu, Dan; Liu, Ning; Dong, Wei; Lu, Ying-Dong; Qin, Chuan; Zhang, Lian-Feng

    2015-08-01

    Cardiac hypertrophy is associated with many forms of heart disease, and identifying important modifier genes involved in the pathogenesis of cardiac hypertrophy could lead to the development of new therapeutic strategies. Tomoregulin-1 is a growth factor that is primarily involved in embryonic development and adult central nervous system (CNS) function, and it is expressed abnormally in a variety of CNS pathologies. Tomoregulin-1 is also expressed in the myocardium. However, the effects of tomoregulin-1 on the heart, particularly on cardiac hypertrophy, remains unknown. The aim of the study is to examine whether and by what mechanism tomoregulin-1 regulates the development of cardiac hypertrophy induced by pressure overload. In this study, we found that tomoregulin-1 was significantly upregulated in two cardiac hypertrophy models: cTnT(R92Q) transgenic mice and thoracic aorta constriction (TAC)-induced cardiac hypertrophy mice. The transgenic overexpression of tomoregulin-1 increased the survival rate, improved the cardiac geometry and functional parameters of echocardiography, and decreased the degree of cardiac hypertrophy of the TAC mice, whereas knockdown of tomoregulin-1 expression resulted in an opposite phenotype and exacerbated phenotypes of cardiac hypertrophy induced by TAC. A possible mechanism by which tomoregulin-1 regulates the development of cardiac hypertrophy in TAC-induced cardiac hypertrophy is through inhibiting TGFβ non-canonical (TAK1-JNK) pathways in the myocardium. Tomoregulin-1 plays a protective role in the modulation of adverse cardiac remodeling from pressure overload in mice. Tomoregulin-1 could be a therapeutic target to control the development of cardiac hypertrophy. © 2015. Published by The Company of Biologists Ltd.

  4. Acute colonic obstruction due to benign prostatic hypertrophy.

    LENUS (Irish Health Repository)

    Mac Giobuin, S

    2012-02-01

    A seventy two year old man presented to the Emergency Department with clinical features of colonic obstruction. Subsequent radiological investigations confirmed this impression and revealed the aetiology to be compression of the sigmoid colon against the sacrum by a massively distended urinary bladder. Chronic urinary retention due to benign prostatic hypertrophy is an extremely unusual cause of large bowel obstruction. Little in this patient\\'s clinical findings suggested this aetiology. We reviewed the literature in this area and highlight the benefits of CT scanning over contrast studies.

  5. 58 CASES OF PROSTATIC HYPERTROPHY TREATED BY ELECTROACUPUNCTURE

    Institute of Scientific and Technical Information of China (English)

    李兰敏; 欧阳颀; 张立夫

    2001-01-01

    In the present paper, 58 prostatic hypertrophy patients were treated with electroacupuncture (EA) therapy. Their ages ranged from 50 to above 70 years in 38 cases and above 80 years in 20 cases. Main acupoints were Qugu (CV 2), Henggu (KI 11), Shuidao (ST 28) and Guanyuan (CV 4) in combination with auxiliary acupoints Zhonglushu (BL 29), Huiyang (BL 35) and Sanyinjiao (SP 6) which were stimulated with EA Therapeutic Apparatus for 30min. After treatment, of the 58 cases, 36 were cured, accounting for 62 %, 20 had marked effect, accounting for 34%, and 2 had no any effectiveness, accounting for 3%. The total effective rate was 96%.

  6. The early days of prostatectomy for benign prostatic hypertrophy.

    Science.gov (United States)

    Ellis, Harold

    2011-10-01

    The syndrome of bladder neck obstruction, often leading to retention of urine, in ageing men has been recognised since earliest times. Catheterisation for the relief of urinary retention was used by the ancient Chinese and Egyptians and is described in the writings of the Indian surgeon Susrata, who flourished in Benares sometime after Christ. Although many of these cases were the result of urethral stricture from trauma or gonorrhoea, we can assume that, in older men, the cause was often benign prostatic hypertrophy (BPH).

  7. [A new outlook on adenoid hypertrophy: adenoids or adenoid disease?].

    Science.gov (United States)

    Antoniv, V F; Aksenov, V M; Antoniv, T V; Portianoĭ, M N; Perekrest, A I

    2004-01-01

    Hypertrophy of the pharyngeal tonsil affects functions of some organs and systems producing negative effects on physical and mental development of the child. The existing classification based of the tonsil size does not reflect the complexity of the pathological process. "Adenoid disease" is thought to be a more adequate term. A new classification of adenoid disease is proposed. Indications for conservative and surgical treatments can be well formulated with the new classification. The authors prefer adenotomy as, in their opinion, adenectomy is not safe for health.

  8. A functional insulin-like growth factor receptor is not necessary for load-induced skeletal muscle hypertrophy

    National Research Council Canada - National Science Library

    Espen E. Spangenburg; Derek Le Roith; Chris W. Ward; Sue C. Bodine

    2008-01-01

    ...-I), which is thought to be a critical step in the induction of muscle hypertrophy. To determine the role of the IGF-I receptor in load-induced skeletal muscle hypertrophy, we utilized a transgenic mouse model (MKR...

  9. Second statement of the working group on electrocardiographic diagnosis of left ventricular hypertrophy

    DEFF Research Database (Denmark)

    Bacharova, Ljuba; Estes, E Harvey; Bang, Lia E

    2011-01-01

    The Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy, appointed by the Editor of the Journal of Electrocardiology, presents the alternative conceptual model for the ECG diagnosis of left ventricular hypertrophy (LVH). It is stressed that ECG is a record of electrical...

  10. The 4th Report of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy

    DEFF Research Database (Denmark)

    Bacharova, Ljuba; Estes, Harvey E; Schocken, Douglas D

    2016-01-01

    The 4th Report provides a brief review of publications focused on the electrocardiographic diagnosis of left ventricular hypertrophy published during the period of 2010 to 2016 by the members of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy. The Working Group recommended...

  11. Changes in cardiac phenotype in hypertrophy and failure: From receptor to gene

    NARCIS (Netherlands)

    H.A. van Heugten (Han); J.M.J. Lamers (Jos)

    1997-01-01

    textabstractThe terminally differentiated adult cardiac myocyte cannot undergo cellular division. Growth of the heart in response to chronic hemodynamic overload therefore occurs through hypertrophy of the myocytes. The adaptation of the myocyte during hypertrophy not only involves an increase in ce

  12. Body-building without power training : Endogenously regulated pectoral muscle hypertrophy in confined shorebirds

    NARCIS (Netherlands)

    Dietz, MW; Piersma, T; Dekinga, A

    1999-01-01

    Shorebirds such as red knots Calidris canutus routinely make migratory flights of 3000 km or more. Previous studies on this species, based on compositional analyses, suggest extensive pectoral muscle hypertrophy in addition to fat storage before take-off. Such hypertrophy could be due to power

  13. Body-building without power training : Endogenously regulated pectoral muscle hypertrophy in confined shorebirds

    NARCIS (Netherlands)

    Dietz, MW; Piersma, T; Dekinga, A

    1999-01-01

    Shorebirds such as red knots Calidris canutus routinely make migratory flights of 3000 km or more. Previous studies on this species, based on compositional analyses, suggest extensive pectoral muscle hypertrophy in addition to fat storage before take-off. Such hypertrophy could be due to power train

  14. Decreased KCNE2 expression participates in the development of cardiac hypertrophy

    Institute of Scientific and Technical Information of China (English)

    DENG Jian-xin; LIU Wen-juan; DING Wen-wen; WANG Gang; LIU Jie

    2016-01-01

    AIM:To investigate whether KCNE 2 participates in the development of pathological hypertrophy .METHODS:Bidirectional ma-nipulations of KCNE2 expression were performed by adenoviral overexpression of KCNE 2 or knockdown of KCNE2 with RNA interfer-ence in PE-induced neonatal rat ventricular myocytes .Then overexpression of KCNE 2 in mouse model of left ventricular hypertrophy in-duced by transverse aortic constriction (TAC) by ultrasound microbubble-mediated gene transfer were used to detect the therapeutic function of KCNE2 in the development of hypertrophy .RESULTS:KCNE2 expression was significantly decreased in PE-induced hy-pertrophic cardiomyocytes and in hypertrophic hearts produced by TAC .Knockdown of KCNE2 in cardiomyocytes reproduced hypertro-phy, whereas overexpression of KCNE2 attenuated PE-induced cardiomyocyte hypertrophy .Knockdown of KCNE2 increased calcineurin activity and nuclear NFAT protein level , and pretreatment with nifedipine or FK 506 attenuated decreased KCNE 2-induced cardiomyo-cyte hypertrophy .Overexpression of KCNE 2 in heart by ultrasound microbubble-mediated gene transfer suppressed the development of hypertrophy and activation of calcineurin-NFAT and MAPK pathways in TAC mice .CONCLUSION:These findings demonstrate that cardiac KCNE2 expression is decreased and contributes to the development of hypertrophy via activation of calcineurin -NFAT and MAPK pathways .

  15. Regression of Copper-Deficient Heart Hypertrophy: Reduction in the Size of Hypertrophic Cardiomyocytes

    Science.gov (United States)

    Dietary copper deficiency causes cardiac hypertrophy and its transition to heart failure in a mouse model. Copper repletion results in a rapid regression of cardiac hypertrophy and prevention of heart failure. The present study was undertaken to understand dynamic changes of cardiomyocytes in the hy...

  16. Effect of miR-29a inhibition on ventricular hypertrophy induced by pressure overload.

    Science.gov (United States)

    Han, Wei; Han, Yancong; Liu, Xiaokun; Shang, Xiaoming

    2015-03-01

    To investigate whether inhibition of miR-29a functioning prevents the hypertension-induced ventricular hypertrophy and fibrosis. Patients diagnosed with hypertension and left ventricular hypertrophy were recruited for the study. Serum levels of miR-29a were determined by RT-PCR. Levels of serum matrix metalloproteinase-9 (MMP-9), collagen type I and III (PINP and PIIINP) were determined by double-antibody enzyme-linked immunosorbent assay. Mouse model of transverse aortic constriction (TAC) was established. 7 days after surgery, TAC mice were injected intraperitoneally with antagomir miR-29a or vehicle once a day for 3 days. After 4 weeks of surgery, animals were sacrificed and cross-sections of the hearts were stained and evaluated for hypertrophy and fibrosis. The expression of the protein markers of hypertrophy and fibrosis was determined by immunoblotting. The serum level of miR-29a in hypertensive patients with left ventricular hypertrophy was significantly higher than those in patients with hypertension alone (p hypertrophy of cardiomyocytes and the expression of ANP and β-MHC, the hypertrophy indices. Also, the ventricular fibrosis and expression of the marker proteins were blocked in antagomir treated mice. The inhibition of miR-29a was found to be effective in improving the ventricular remodeling and hypertrophy caused by pressure overload.

  17. Gastrodin Inhibits Store-Operated Ca2+ Entry and Alleviates Cardiac Hypertrophy

    Directory of Open Access Journals (Sweden)

    Xiaoqiang Yao

    2017-04-01

    Full Text Available Cardiac hypertrophy is a major risk factor for heart failure, which are among the leading causes of human death. Gastrodin is a small molecule that has been used clinically to treat neurological and vascular diseases for many years without safety issues. In the present study, we examined protective effect of gastrodin against cardiac hypertrophy and explored the underlying mechanism. Phenylephrine and angiotensin II were used to induce cardiac hypertrophy in a mouse model and a cultured cardiomyocyte model. Gastrodin was found to alleviate the cardiac hypertrophy in both models. Mechanistically, gastrodin attenuated the store-operated Ca2+ entry (SOCE by reducing the expression of STIM1 and Orai1, two key proteins in SOCE, in animal models as well as in cultured cardiomyocyte model. Furthermore, suppressing SOCE by RO2959, Orai1-siRNAs or STIM1-siRNAs markedly attenuated the phenylephrine-induced hypertrophy in cultured cardiomyocyte model. Together, these results showed that gastrodin inhibited cardiac hypertrophy and it also reduced the SOCE via its action on the expression of STIM1 and Orai1. Furthermore, suppression of SOCE could reduce the phenylephrine-induced cardiomyocyte hypertrophy, suggesting that SOCE-STIM1-Orai1 is located upstream of hypertrophy.

  18. Relationship between electrocardiographic features and distribution of hypertrophy in patients with hypertrophic cardiomyopathy

    Energy Technology Data Exchange (ETDEWEB)

    Sato, Tetsuya; Nakamura, Kazufumi; Yamanari, Hiroshi; Ohe, Tohru [Okayama Univ. (Japan). School of Medicine; Yoshinouchi, Takeo

    1998-07-01

    To evaluate the relationship between the distribution of hypertrophy and the electrocardiographic findings in patients with hypertrophic cardiomyopathy (HCM), 54 HCM patients were studied using magnetic resonance imaging. The patients were divided into 4 groups according to hypertrophic patterns: hypertrophy only at the apex (group I, n=12); hypertrophy in both the apex and base (group II, n=20); hypertrophy only at the base with asymmetric septal hypertrophy (ASH) (group IIIa, n=17); and hypertrophy only at the base without ASH (group IIIb, n=5). Abnormal Q waves in leads II, III and aV{sub F} were found in 1/12, 3/20, 10/17 and 0/5, respectively, and in leads I and aV{sub L} they were found in 1/12, 8/20, 4/17 and 1/5, respectively. The largest negative T waves (mm) were found in group I (group I vs group II vs group IIIa vs group IIIb: 15.2{+-}5.3, 8.2{+-}6.1, 1.6{+-}2.0, 0.8{+-}1.3, respectively). The largest positive T waves (mm) were identified in group IIIb (3.8{+-}3.0, 6.8{+-}3.2, 5.8{+-}3.6, 9.3{+-}2.1, respectively). The presence of abnormal Q waves reflected regional hypertrophy in HCM patients but the configuration of T waves represented the difference in the localization of hypertrophy between the basal and apical segments. (author)

  19. Muscular and systemic correlates of resistance training-induced muscle hypertrophy.

    Science.gov (United States)

    Mitchell, Cameron J; Churchward-Venne, Tyler A; Bellamy, Leeann; Parise, Gianni; Baker, Steven K; Phillips, Stuart M

    2013-01-01

    To determine relationships between post-exercise changes in systemic [testosterone, growth hormone (GH), insulin like grow factor 1 (IGF-1) and interleukin 6 (IL-6)], or intramuscular [skeletal muscle androgen receptor (AR) protein content and p70S6K phosphorylation status] factors in a moderately-sized cohort of young men exhibiting divergent resistance training-mediated muscle hypertrophy. Twenty three adult males completed 4 sessions•wk⁻¹ of resistance training for 16 wk. Muscle biopsies were obtained before and after the training period and acutely 1 and 5 h after the first training session. Serum hormones and cytokines were measured immediately, 15, 30 and 60 minutes following the first and last training sessions of the study. Mean fiber area increased by 20% (range: -7 to 80%; Pmuscle fiber hypertrophy; however, the magnitude of the post exercise IL-6 response was correlated with muscle hypertrophy (r=0.48, P=0.019). Post-exercise increases in circulating hormones are not related to hypertrophy following training. Exercise-induced changes in IL-6 correlated with hypertrophy, but the mechanism for the role of IL-6 in hypertrophy is not known. Acute increases, in p70S6K phosphorylation and changes in muscle AR protein content correlated with muscle hypertrophy implicating intramuscular rather than systemic processes in mediating hypertrophy.

  20. Lactosylceramide promotes hypertrophy through ROS generation and activation of ERK1/2 in cardiomyocytes

    Science.gov (United States)

    Mishra, Sumita; Chatterjee, Subroto

    2014-01-01

    Hypertrophy is central to several heart diseases; however, not much is known about the role of glycosphingolipids (GSLs) in this phenotype. Since GSLs have been accorded several physiological functions, we sought to determine whether these compounds affect cardiac hypertrophy. By using a rat cardiomyoblast cell line, H9c2 cells and cultured primary neonatal rat cardiomyocytes, we have determined the effects of GSLs on hypertrophy. Our study comprises (a) measurement of [3H]-leucine incorporation into protein, (b) measurement of cell size and morphology by immunofluorescence microscopy and (c) real-time quantitative mRNA expression assay for atrial natriuretic peptide and brain natriuretic peptide. Phenylephrine (PE), a well-established agonist of cardiac hypertrophy, served as a positive control in these studies. Subsequently, mechanistic studies were performed to explore the involvement of various signaling transduction pathways that may contribute to hypertrophy in these cardiomyocytes. We observed that lactosylceramide specifically exerted a concentration- (50–100 µM) and time (48 h)-dependent increase in hypertrophy in cardiomyocytes but not a library of other structurally related GSLs. Further, in cardiomyocytes, LacCer generated reactive oxygen species, stimulated the phosphorylation of p44 mitogen activated protein kinase and protein kinase-C, and enhanced c-jun and c-fos expression, ultimately leading to hypertrophy. In summary, we report here that LacCer specifically induces hypertrophy in cardiomyocytes via an “oxygen-sensitive signal transduction pathway.” PMID:24658420

  1. Dose-dependent difference of nuclear receptors involved in murine liver hypertrophy by piperonyl butoxide.

    Science.gov (United States)

    Sakamoto, Yohei; Yoshida, Midori; Tamura, Kei; Takahashi, Miwa; Kodama, Yukio; Inoue, Kaoru

    2015-12-01

    Nuclear receptors play important roles in chemically induced liver hypertrophy in rodents. To clarify the involvement of constitutive androstane receptor (CAR) and other nuclear receptors in mouse liver hypertrophy induced by different doses of piperonyl butoxide (PBO), wild-type and CAR-knockout mice were administered PBO (200, 1,000, or 5,000 ppm) in the basal diet for 1 week. Increased liver weight and diffuse hepatocellular hypertrophy were observed at 5,000 ppm for both genotypes, accompanied by increased Cyp3a11 mRNA and CYP3A protein expression, suggesting that CAR-independent pathway, possibly pregnane X receptor (PXR), plays a major role in the induction of hypertrophy. Moreover, wild-type mice at 5,000 ppm showed enhanced hepatocellular hypertrophy and strong positive staining for CYP2B in the centrilobular area, suggesting the localized contribution of CAR. At 1,000 ppm, only wild-type mice showed liver weight increase and centrilobular hepatocellular hypertrophy concurrent with elevated Cyp2b10 mRNA expression and strong CYP2B staining, indicating that CAR was essential at 1,000 ppm. We concluded that high-dose PBO induced hypertrophy via CAR and another pathway, while lower dose of PBO induced a pathway mediated predominantly by CAR. The dose-responsiveness on liver hypertrophy is important for understanding the involvement of nuclear receptors.

  2. Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid.

    Science.gov (United States)

    Zhao, Mingyue; Lu, Lihui; Lei, Song; Chai, Hua; Wu, Siyuan; Tang, Xiaoju; Bao, Qinxue; Chen, Li; Wu, Wenchao; Liu, Xiaojing

    2016-01-01

    Palmitic acid (PA) is known to cause cardiomyocyte dysfunction. Cardiac hypertrophy is one of the important pathological features of PA-induced lipotoxicity, but the mechanism by which PA induces cardiomyocyte hypertrophy is still unclear. Therefore, our study was to test whether necroptosis, a receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3-) dependent programmed necrosis, was involved in the PA-induced cardiomyocyte hypertrophy. We used the PA-treated primary neonatal rat cardiac myocytes (NCMs) or H9c2 cells to study lipotoxicity. Our results demonstrated that cardiomyocyte hypertrophy was induced by PA treatment, determined by upregulation of hypertrophic marker genes and cell surface area enlargement. Upon PA treatment, the expression of RIPK1 and RIPK3 was increased. Pretreatment with the RIPK1 inhibitor necrostatin-1 (Nec-1), the PA-induced cardiomyocyte hypertrophy, was attenuated. Knockdown of RIPK1 or RIPK3 by siRNA suppressed the PA-induced myocardial hypertrophy. Moreover, a crosstalk between necroptosis and endoplasmic reticulum (ER) stress was observed in PA-treated cardiomyocytes. Inhibition of RIPK1 with Nec-1, phosphorylation level of AKT (Ser473), and mTOR (Ser2481) was significantly reduced in PA-treated cardiomyocytes. In conclusion, RIPKs-dependent necroptosis might be crucial in PA-induced myocardial hypertrophy. Activation of mTOR may mediate the effect of necroptosis in cardiomyocyte hypertrophy induced by PA.

  3. Satellite Cells Contribution to Exercise Mediated Muscle Hypertrophy and Repair

    Science.gov (United States)

    Bazgir, Behzad; Fathi, Rouhollah; Rezazadeh Valojerdi, Mojtaba; Mozdziak, Paul; Asgari, Alireza

    2017-01-01

    Satellite cells (SCs) are the most abundant skeletal muscle stem cells. They are widely recognized for their contributions to maintenance of muscle mass, regeneration and hypertrophy during the human life span. These cells are good candidates for cell therapy due to their self-renewal capabilities and presence in an undifferentiated form. Presently, a significant gap exists between our knowledge of SCs behavior and their application as a means for human skeletal muscle tissue repair and regeneration. Both physiological and pathological stimuli potentially affect SCs activation, proliferation, and terminal differentiation the former category being the focus of this article. Activation of SCs occurs following exercise, post-training micro-injuries, and electrical stimulation. Exercise, as a potent and natural stimulus, is at the center of numerous studies on SC activation and relevant fields. According to research, different exercise modalities end with various effects. This review article attempts to picture the state of the art of the SCs life span and their engagement in muscle regeneration and hypertrophy in exercise. PMID:28042532

  4. Brain renin angiotensin system in cardiac hypertrophy and failure

    Directory of Open Access Journals (Sweden)

    Luciana eCampos

    2012-01-01

    Full Text Available Brain renin-angiotensin system (RAS is significantly involved in the roles of the endocrine RAS in cardiovascular regulation. Our studies indicate that the brain RAS participates in the development of cardiac hypertrophy and fibrosis through sympathetic activation. Inhibition of sympathetic hyperactivity after myocardial infarction through suppression of the brain RAS appears beneficial. The brain RAS is involved in the modulation of circadian rhythms of arterial pressure, contributing to nondipping hypertension. We conclude that the brain RAS in pathophysiological states interacts synergistically with the chronically overactive RAS through a positive biofeedback in order to maintain a state of alert diseased conditions, such as cardiac hypertrophy and failure. Therefore, targeting brain RAS with drugs such as angiotensin converting inhibitors or receptor blockers having increased brain penetrability could be of advantage. These RAS-targeting drugs are first-line therapy for all heart failure patients. Since the RAS has both endocrine and local tissue components, RAS drugs are being developed to attain increased tissue penetrability and volume of distribution and consequently an efficient inhibition of both RAS components.

  5. Role of microRNAs in skeletal muscle hypertrophy

    Directory of Open Access Journals (Sweden)

    Keisuke eHitachi

    2014-01-01

    Full Text Available Skeletal muscle comprises approximately 40% of body weight, and is important for locomotion, as well as for metabolic homeostasis. Adult skeletal muscle mass is maintained by a fine balance between muscle protein synthesis and degradation. In response to cytokines, nutrients, and mechanical stimuli, skeletal muscle mass is increased (hypertrophy, whereas skeletal muscle mass is decreased (atrophy in a variety of conditions, including cancer cachexia, starvation, immobilization, aging, and neuromuscular disorders. Recent studies have determined two important signaling pathways involved in skeletal muscle mass. The insulin-like growth factor-1 (IGF-1/Akt pathway increases skeletal muscle mass via stimulation of protein synthesis and inhibition of protein degradation. By contrast, myostatin signaling negatively regulates skeletal muscle mass by reducing protein synthesis. In addition, the discovery of microRNAs as novel regulators of gene expression has provided new insights into a multitude of biological processes, especially in skeletal muscle physiology. We summarize here the current knowledge of microRNAs in the regulation of skeletal muscle hypertrophy, focusing on the IGF-1/Akt pathway and myostatin signaling.

  6. Satellite Cells Contribution to Exercise Mediated Muscle Hypertrophy and Repair

    Directory of Open Access Journals (Sweden)

    Behzad Bazgir

    2016-10-01

    Full Text Available Satellite cells (SCs are the most abundant skeletal muscle stem cells. They are widely recognized for their contributions to maintenance of muscle mass, regeneration and hypertrophy during the human life span. These cells are good candidates for cell therapy due to their self-renewal capabilities and presence in an undifferentiated form. Presently, a significant gap exists between our knowledge of SCs behavior and their application as a means for human skeletal muscle tissue repair and regeneration. Both physiological and pathological stimuli potentially affect SCs activation, proliferation, and terminal differentiation - the former category being the focus of this article. Activation of SCs occurs following exercise, post-training micro-injuries, and electrical stimulation. Exercise, as a potent and natural stimulus, is at the center of numerous studies on SC activation and relevant fields. According to research, different exercise modalities end with various effects. This review article attempts to picture the state of the art of the SCs life span and their engagement in muscle regeneration and hypertrophy in exercise.

  7. Skin Sodium Concentration Correlates with Left Ventricular Hypertrophy in CKD.

    Science.gov (United States)

    Schneider, Markus P; Raff, Ulrike; Kopp, Christoph; Scheppach, Johannes B; Toncar, Sebastian; Wanner, Christoph; Schlieper, Georg; Saritas, Turgay; Floege, Jürgen; Schmid, Matthias; Birukov, Anna; Dahlmann, Anke; Linz, Peter; Janka, Rolf; Uder, Michael; Schmieder, Roland E; Titze, Jens M; Eckardt, Kai-Uwe

    2017-06-01

    The pathogenesis of left ventricular hypertrophy in patients with CKD is incompletely understood. Sodium intake, which is usually assessed by measuring urinary sodium excretion, has been inconsistently linked with left ventricular hypertrophy. However, tissues such as skin and muscle may store sodium. Using (23)sodium-magnetic resonance imaging, a technique recently developed for the assessment of tissue sodium content in humans, we determined skin sodium content at the level of the calf in 99 patients with mild to moderate CKD (42 women; median [range] age, 65 [23-78] years). We also assessed total body overhydration (bioimpedance spectroscopy), 24-hour BP, and left ventricular mass (cardiac magnetic resonance imaging). Skin sodium content, but not total body overhydration, correlated with systolic BP (r=0.33, P=0.002). Moreover, skin sodium content correlated more strongly than total body overhydration did with left ventricular mass (r=0.56, Pskin sodium content is a strong explanatory variable for left ventricular mass, unaffected by BP and total body overhydration. In conclusion, we found skin sodium content to be closely linked to left ventricular mass in patients with CKD. Interventions that reduce skin sodium content might improve cardiovascular outcomes in these patients. Copyright © 2017 by the American Society of Nephrology.

  8. Proteinuria and glomerular hypertrophy in extremely low-birthweight children.

    Science.gov (United States)

    Hayashi, Asako; Santo, Yoko; Satomura, Kenichi

    2014-12-01

    Of late, there is an increased awareness of the frequent occurrence of hypertension or proteinuria in adults born at low birthweight. We retrospectively studied five children born with extremely low birthweight (ELBW) who were first diagnosed with proteinuria in a school urinary screening program. These children were born at 23-25 weeks of gestation, and their birthweight was 532-732 g. Proteinuria was identified in all the subjects in a school urinary screening program when they were 6-15 years old. Renal biopsy showed diffuse increase in glomerular size, consistent with glomerular hypertrophy. There were no findings of mesangial proliferation or glomerular sclerosis. All the subjects had a marked decrease in proteinuria after angiotensin receptor blocker (ARB) treatment. Reduced number of glomeruli associated with prematurity was speculated to have caused compensatory glomerular hyperfiltration, hypertrophy, and hypertension in children born with ELBW when they developed proteinuria. ARB could have been effective for proteinuria by reducing glomerular hypertension. Physicians should be aware of proteinuria in children born with ELBW because there is an increasing number of ELBW survivors as a result of advances in medical technology. © 2014 Japan Pediatric Society.

  9. Autophagy modulation: a potential therapeutic approach in cardiac hypertrophy.

    Science.gov (United States)

    Wang, Xuejun; Cui, Taixing

    2017-08-01

    Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload. Copyright © 2017 the American Physiological Society.

  10. Photoperiodic regulation of compensatory testicular hypertrophy in hamsters.

    Science.gov (United States)

    Paul, Matthew J; Park, Jin Ho; Horton, Teresa H; Alvarez, Maria I; Burke, Morgan K; Place, Ned J; Zucker, Irving

    2006-08-01

    In mammals, removal of one testis results in compensatory testicular hypertrophy (CTH) of the remaining gonad. Although CTH is ubiquitous among juveniles of many species, laboratory rats, laboratory mice, and humans unilaterally castrated in adulthood fail to display CTH. We documented CTH in pre- and postpubertally hemi-castrated Syrian and Siberian hamsters and tested whether day length affects CTH in juvenile and adult Siberian hamsters. Robust CTH was evident in long-day hemi-castrates of both species and was preceded by increased serum FSH concentrations in juvenile Siberian hamsters. In sharp contrast, CTH was undetectable in short-day hemi-castrated Siberian hamsters for several months and only made its appearance with the development of neuroendocrine refractoriness to short day lengths; serum FSH concentrations of juveniles also did not increase above sham-castrate values until the onset of refractoriness. Long-day hemi-castrated Siberian hamsters with hypertrophied testes underwent complete gonadal regression after transfer to short days, albeit at a reduced rate for the first 3 weeks of treatment. Blood testosterone concentrations of adult hamsters did not differ between long-day hemicastrates and sham-castrates 9-12 weeks after surgery. We conclude that CTH is suppressed by short day lengths in Siberian hamsters at all ages and stages of reproductive development; in short day lengths, but not long day lengths, the remaining testis produces sufficient negative feedback inhibition to restrain FSH hypersecretion and prevent CTH.

  11. Autophagy in Hepatic Fibrosis

    Directory of Open Access Journals (Sweden)

    Yang Song

    2014-01-01

    Full Text Available Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that degrades damaged organelles or protein aggregation, which participates in many pathological processes including liver diseases. Autophagy participates in hepatic fibrosis by activating hepatic stellate cells and may participate as well through influencing other fibrogenic cells. Besides that, autophagy can induce some liver diseases to develop while it may play a protective role in hepatocellular abnormal aggregates related liver diseases and reduces fibrosis. With a better understanding of the potential effects of autophagy on hepatic fibrosis, targeting autophagy might be a novel therapeutic strategy for hepatic fibrosis in the near future.

  12. Molecular switches under TGFβ signalling during progression from cardiac hypertrophy to heart failure.

    Science.gov (United States)

    Heger, J; Schulz, R; Euler, G

    2016-01-01

    Cardiac hypertrophy is a mechanism to compensate for increased cardiac work load, that is, after myocardial infarction or upon pressure overload. However, in the long run cardiac hypertrophy is a prevailing risk factor for the development of heart failure. During pathological remodelling processes leading to heart failure, decompensated hypertrophy, death of cardiomyocytes by apoptosis or necroptosis and fibrosis as well as a progressive dysfunction of cardiomyocytes are apparent. Interestingly, the induction of hypertrophy, cell death or fibrosis is mediated by similar signalling pathways. Therefore, tiny changes in the signalling cascade are able to switch physiological cardiac remodelling to the development of heart failure. In the present review, we will describe examples of these molecular switches that change compensated hypertrophy to the development of heart failure and will focus on the importance of the signalling cascades of the TGFβ superfamily in this process. In this context, potential therapeutic targets for pharmacological interventions that could attenuate the progression of heart failure will be discussed.

  13. New approaches to the quantitation of hypertrophy and hyperplasia in hepatomegaly.

    Science.gov (United States)

    Carthew, P; Edwards, R E; Nolan, B M

    1998-12-28

    A histological method utilizing the optical dissector principle has been developed for determining the contribution of hypertrophy and hyperplasia to the hepatomegaly induced by the peroxisome proliferator gemfibrozil. The optical dissector is a technique derived from the 'new stereology' and has been used to estimate the number of hepatocyte nuclear profiles, that are present in a reference volume of tissue. The overall changes due to hypertrophy and hyperplasia in the rat liver after gemfibrozil treatment, did not reach significance, although the zonal hypertrophy change did. This indicated that although there was a 20% increase in liver weight with treatment, the hepatomegaly was caused by a combination of hypertrophy and hyperplasia, neither of which, on its own, was significantly different from the control values. The distinction of hyperplasia from hypertrophy, using a purely histological method, will be useful in assessing whether treatment related sustained hyperplasia is occurring in the liver.

  14. Tear me down: Role of calpain in the development of cardiac ventricular hypertrophy

    Science.gov (United States)

    Patterson, Cam; Portbury, Andrea; Schisler, Jonathan C.; Willis, Monte S.

    2011-01-01

    Cardiac hypertrophy develops most commonly in response to hypertension and is an independent risk factor for the development of heart failure. The mechanisms by which cardiac hypertrophy may be reversed to reduce this risk have not been fully determined to the point where mechanism-specific therapies have been developed. Recently, proteases in the calpain family have been implicated in regulating the development of cardiac hypertrophy in preclinical animal models. In this review, we summarize the molecular mechanisms by which calpain inhibition has been shown to modulate the development of cardiac (specifically ventricular) hypertrophy. The context within which calpain inhibition might be developed for therapeutic intervention of cardiac hypertrophy is then discussed. PMID:21817165

  15. Effect of strength training on regional hypertrophy of the elbow flexor muscles.

    Science.gov (United States)

    Drummond, Marcos D M; Szmuchrowski, Leszek A; Goulart, Karine N O; Couto, Bruno P

    2016-10-01

    Muscle hypertrophy is the main structural adaptation to strength training. We investigated the chronic effects of strength training on muscle hypertrophy in different regions of the elbow flexor muscles. Eleven untrained men (21.8 ± 1.62 years) underwent magnetic resonance imaging to determine the proximal, medial, distal, and mean cross-sectional areas (CSA) of the elbow flexors. The volunteers completed 12 weeks of strength training. The training protocol consisted of 4 sets of 8-10 maximum repetitions of unilateral elbow flexion. The interval between sets was 120 s. The training frequency was 3 sessions per week. The magnetic resonance images verified the presence of significant and similar hypertrophy in the distal, medial, and proximal portions of the elbow flexor muscles. Muscle hypertrophy may be assessed using only the medial CSA. We should not expect different degrees of hypertrophy among the regions of the elbow flexor muscles. Muscle Nerve 54: 750-755, 2016. © 2016 Wiley Periodicals, Inc.

  16. Hepatitis isquémica Ischemic hepatitis

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    Marcos Amuchástegui (h

    2006-10-01

    Full Text Available La hepatitis isquémica es una complicación sumamente infrecuente de cirugía cardiovascular. Las biopsias muestran necrosis centrolobulillar. El término de "hepatitis" fue propuesto debido al aumento de transaminasas similar a aquellas de origen infeccioso, e "isquémica" por falla en la perfusión hepática. Posteriormente se definió el término de hepatitis isquémica como cuadro de elevación aguda y reversible (dentro de las 72 horas de transaminasas de hasta 20 veces el valor normal, asociado a trastornos en la perfusión hepática, luego de haber excluido otras causas de hepatitis aguda o daño hepatocelular. Se describe el caso de un paciente de 53 años que consulta por dolor epigástrico de 12 h de evolución sin fiebre, náuseas ni vómitos, resistente a la medicación. Tenía antecedentes inmediatos de reemplazo de válvula aórtica, y estaba anticoagulado. Evolucionó con shock y fallo multiorgánico. El examen evidenció marcada ictericia y signos de taponamiento pericárdico, asociado a un aumento considerable de enzimas hepáticas. Un ecocardiograma informó signos de taponamiento cardíaco y ausencia de disección aórtica. Se decidió pericardiocentesis, extrayéndose 970 cc. de líquido sanguinolento, y hemodiálisis, con notable mejoría de su estado hemodinámico. Los valores enzimáticos disminuyeron. Los marcadores virales fueron negativos.Ischemic hepatitis is an uncommon cardiovascular surgery complication. Hepatic biopsies show centrolobulillar necrosis. The term "hepatitis" was proposed because of a raise in hepatic enzymes similar with infectious disease, and "ischemic" because of failure in hepatic perfusion. Ischemic hepatitis was then defined as an acute and reversible elevation of hepatic enzymes (within 72 h, associated with disturbance in hepatic perfusion after excluding other causes of acute hepatitis. A 53 year-old male presented complaining of a 12 h epigastric pain, without nausea or vomiting, resistant

  17. Preventing hepatitis B or C

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/patientinstructions/000401.htm Preventing hepatitis B or C To use the sharing features on this page, please enable JavaScript. Hepatitis B and hepatitis C infections cause irritation and swelling ...

  18. Hepatitis C Virus Genotypes

    OpenAIRE

    Kayhan Azadmanesh; Safie Amini; Seyed-Moayed Alavian; Malek Hossein Ahmadipour

    2005-01-01

    IntroductionHepatitis C virus (HCV) is an important cause of chronic liver disease. HCV causes 20% of acute hepatitis cases, 70% of all chronic hepatitis cases, 40% of all cases of liver cirrhosis, 60% of hepatocellular carcinomas, and 30% of liver transplants in Europe(1). It is also recognized as the leading cause of liver transplantation in the world(2). Only 20% of infected individuals will recover from this viral infection, while the rest become chronically infected(3). While the majorit...

  19. MYBPH acts as modifier of cardiac hypertrophy in hypertrophic cardiomyopathy (HCM) patients.

    Science.gov (United States)

    Mouton, J M; van der Merwe, L; Goosen, A; Revera, M; Brink, P A; Moolman-Smook, J C; Kinnear, C

    2016-05-01

    Left ventricular hypertrophy is a risk factor for cardiovascular morbidity and mortality. Hypertrophic cardiomyopathy (HCM) is considered a model disease to study causal molecular factors underlying isolated cardiac hypertrophy. However, HCM manifests with various clinical symptoms, even in families bearing the same genetic defects, suggesting that additional factors contribute to hypertrophy. The gene encoding the cardiac myosin binding protein C (cMYBPC) is one of the most frequently implicated genes in HCM. Recently another myosin binding protein, myosin binding protein H (MYBPH) was shown to function in concert with cMYBPC in regulating cardiomyocyte contraction. Given the similarity in sequence, structure and the critical role MYBPH plays in sarcomere contraction, we proposed that MYBPH may be involved in HCM pathogenesis. Family-based genetic association analysis was employed to investigate the contribution of MYBPH in modifying hypertrophy. Seven single nucleotide polymorphisms and haplotypes in MYBPH were investigated for hypertrophy modifying effects in 388 individuals (27 families), in which three unique South African HCM-causing founder mutations (p.R403W and pA797T in β-myosin heavy chain gene (MYH7) and p.R92W in the cardiac troponin T gene (TNNT2)) segregate. We observed a significant association between rs2250509 and hypertrophy traits in the p.A797T MYH7 mutation group. Additionally, haplotype GGTACTT significantly affected hypertrophy within the same mutation group. MYBPH was for the first time assessed as a candidate hypertrophy modifying gene. We identified a novel association between MYBPH and hypertrophy traits in HCM patients carrying the p.A797T MYH7 mutation, suggesting that variation in MYBPH can modulate the severity of hypertrophy in HCM.

  20. Indian hedgehog signals independently of PTHrP to promote chondrocyte hypertrophy.

    Science.gov (United States)

    Mak, Kinglun Kingston; Kronenberg, Henry M; Chuang, Pao-Tien; Mackem, Susan; Yang, Yingzi

    2008-06-01

    Chondrocyte hypertrophy is an essential process required for endochondral bone formation. Proper regulation of chondrocyte hypertrophy is also required in postnatal cartilage homeostasis. Indian hedgehog (Ihh) and PTHrP signaling play crucial roles in regulating the onset of chondrocyte hypertrophy by forming a negative feedback loop, in which Ihh signaling regulates chondrocyte hypertrophy by controlling PTHrP expression. To understand whether there is a PTHrP-independent role of Ihh signaling in regulating chondrocyte hypertrophy, we have both activated and inactivated Ihh signaling in the absence of PTHrP during endochondral skeletal development. We found that upregulating Ihh signaling in the developing cartilage by treating PTHrP(-/-) limb explants with sonic hedgehog (Shh) protein in vitro, or overexpressing Ihh in the cartilage of PTHrP(-/-) embryos or inactivating patched 1 (Ptch1), a negative regulator of hedgehog (Hh) signaling, accelerated chondrocyte hypertrophy in the PTHrP(-/-) embryos. Conversely, when Hh signaling was blocked by cyclopamine or by removing Smoothened (Smo), a positive regulator of Hh signaling, chondrocyte hypertrophy was delayed in the PTHrP(-/-) embryo. Furthermore, we show that upregulated Hh signaling in the postnatal cartilage led to accelerated chondrocyte hypertrophy during secondary ossification, which in turn caused reduction of joint cartilage. Our results revealed a novel role of Ihh signaling in promoting chondrocyte hypertrophy independently of PTHrP, which is particularly important in postnatal cartilage development and homeostasis. In addition, we found that bone morphogenetic protein (Bmp) and Wnt/beta-catenin signaling in the cartilage may both mediate the effect of upregulated Ihh signaling in promoting chondrocyte hypertrophy.

  1. Global microRNA profiles and signaling pathways in the development of cardiac hypertrophy

    Energy Technology Data Exchange (ETDEWEB)

    Feng, H.J.; Ouyang, W.; Liu, J.H.; Sun, Y.G.; Hu, R.; Huang, L.H.; Xian, J.L. [Southern Medical University, Department of Nuclear Medicine, Zhujiang Hospital, Guangzhou, China, Department of Nuclear Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou (China); Jing, C.F.; Zhou, M.J. [Sun Yat-Sen University, South China Sea Marine Biotechnology, National Engineering Research Center, Guangzhou, China, National Engineering Research Center, South China Sea Marine Biotechnology, Sun Yat-Sen University, Guangzhou (China)

    2014-04-11

    Hypertrophy is a major predictor of progressive heart disease and has an adverse prognosis. MicroRNAs (miRNAs) that accumulate during the course of cardiac hypertrophy may participate in the process. However, the nature of any interaction between a hypertrophy-specific signaling pathway and aberrant expression of miRNAs remains unclear. In this study, Spague Dawley male rats were treated with transverse aortic constriction (TAC) surgery to mimic pathological hypertrophy. Hearts were isolated from TAC and sham operated rats (n=5 for each group at 5, 10, 15, and 20 days after surgery) for miRNA microarray assay. The miRNAs dysexpressed during hypertrophy were further analyzed using a combination of bioinformatics algorithms in order to predict possible targets. Increased expression of the target genes identified in diverse signaling pathways was also analyzed. Two sets of miRNAs were identified, showing different expression patterns during hypertrophy. Bioinformatics analysis suggested the miRNAs may regulate multiple hypertrophy-specific signaling pathways by targeting the member genes and the interaction of miRNA and mRNA might form a network that leads to cardiac hypertrophy. In addition, the multifold changes in several miRNAs suggested that upregulation of rno-miR-331*, rno-miR-3596b, rno-miR-3557-5p and downregulation of rno-miR-10a, miR-221, miR-190, miR-451 could be seen as biomarkers of prognosis in clinical therapy of heart failure. This study described, for the first time, a potential mechanism of cardiac hypertrophy involving multiple signaling pathways that control up- and downregulation of miRNAs. It represents a first step in the systematic discovery of miRNA function in cardiovascular hypertrophy.

  2. Atorvastatin prevents connexin43 remodeling in hypertrophied left ventricular myocardium of spontaneously hypertensive rats

    Institute of Scientific and Technical Information of China (English)

    CHEN Hong-juan; YAO Lei; CHEN Tu-gang; YU Min; WANG Li-hong; CHEN Jun-zhu

    2007-01-01

    Background Connexin43 (Cx43) is the predominant gap junction protein in heart and is involved in the control of cell-to-cell communication to modulate the contractility and the electrical coupling of cardiac myocytes. Left ventricular(LV) hypertrophy is accompanied by changes of Cx43 expression. Recent studies have demonstrated that statins reduced cardiac hypertrophy. However, it is unknown whether statins can affect Cx43 expression in hypertrophied left ventricular myocardium. This study was designed to assess the effects of atorvastatin on LV hypertrophy and Cx43 expression in spontaneously hypertensive rats (SHR).Methods Nine-week old SHRs were randomly divided into two groups. Some received atorvastatin at 30 mg/kg by oral gavage once daily for 8 weeks (SHR-A); others received vehicle. Age-matched Wistar-Kyoto rats (WKY) received atorvastatin or vehicle for 8 weeks were used as controls. At the end of the experiment, we investigated LV hypertrophy and the expression of Cx43 in LV myocardium in four groups. Cx43 expression was investigated by the methods of Western blotting, immunohistochemistry, and transmission electron microscope. LV hypertrophy was accessed by pathological analysis and plasma brain natriuretic peptide (BNP) level.Results LV hypertrophy was prominent in untreated SHR. In SHR, LV myocardium Cx43 level was upregulated, and the distribution of Cx43 was displaced from their usual locations to other sites at various distances away from the intercalated disks. After atorvastatin treatment, myocardium Cx43 level was reduced in SHR-A, and the distribution of Cx43 gap junction became much regular and confined to intercalated disk. Statins also prevented LV hypertrophy in SHR.Conclusions These results provide novel in vivo evidence for the key role of Cx43 gap junctions in LV hypertrophy and the possible mechanism in anti-hypertrophic effect of statins. Atorvastatin treatment may have beneficial effects on LV hypertrophy in spontaneously hypertensive

  3. BMP type I receptor ALK2 is required for angiotensin II-induced cardiac hypertrophy

    Science.gov (United States)

    Spagnolli, Ester; Ernande, Laura; Thoonen, Robrecht; Kolodziej, Starsha A.; Leyton, Patricio A.; Cheng, Juan; Tainsh, Robert E. T.; Mayeur, Claire; Rhee, David K.; Wu, Mei. X.; Scherrer-Crosbie, Marielle; Buys, Emmanuel S.; Zapol, Warren M.; Bloch, Kenneth D.; Bloch, Donald B.

    2016-01-01

    Bone morphogenetic protein (BMP) signaling contributes to the development of cardiac hypertrophy. However, the identity of the BMP type I receptor involved in cardiac hypertrophy and the underlying molecular mechanisms are poorly understood. By using quantitative PCR and immunoblotting, we demonstrated that BMP signaling increased during phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes (NRCs), as evidenced by increased phosphorylation of Smads 1 and 5 and induction of Id1 gene expression. Inhibition of BMP signaling with LDN193189 or noggin, and silencing of Smad 1 or 4 using small interfering RNA diminished the ability of phenylephrine to induce hypertrophy in NRCs. Conversely, activation of BMP signaling with BMP2 or BMP4 induced hypertrophy in NRCs. Luciferase reporter assay further showed that BMP2 or BMP4 treatment of NRCs repressed atrogin-1 gene expression concomitant with an increase in calcineurin protein levels and enhanced activity of nuclear factor of activated T cells, providing a mechanism by which BMP signaling contributes to cardiac hypertrophy. In a model of cardiac hypertrophy, C57BL/6 mice treated with angiotensin II (A2) had increased BMP signaling in the left ventricle. Treatment with LDN193189 attenuated A2-induced cardiac hypertrophy and collagen deposition in left ventricles. Cardiomyocyte-specific deletion of BMP type I receptor ALK2 (activin-like kinase 2), but not ALK1 or ALK3, inhibited BMP signaling and mitigated A2-induced cardiac hypertrophy and left ventricular fibrosis in mice. The results suggest that BMP signaling upregulates the calcineurin/nuclear factor of activated T cell pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis. PMID:26873969

  4. BMP type I receptor ALK2 is required for angiotensin II-induced cardiac hypertrophy.

    Science.gov (United States)

    Shahid, Mohd; Spagnolli, Ester; Ernande, Laura; Thoonen, Robrecht; Kolodziej, Starsha A; Leyton, Patricio A; Cheng, Juan; Tainsh, Robert E T; Mayeur, Claire; Rhee, David K; Wu, Mei X; Scherrer-Crosbie, Marielle; Buys, Emmanuel S; Zapol, Warren M; Bloch, Kenneth D; Bloch, Donald B

    2016-04-15

    Bone morphogenetic protein (BMP) signaling contributes to the development of cardiac hypertrophy. However, the identity of the BMP type I receptor involved in cardiac hypertrophy and the underlying molecular mechanisms are poorly understood. By using quantitative PCR and immunoblotting, we demonstrated that BMP signaling increased during phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes (NRCs), as evidenced by increased phosphorylation of Smads 1 and 5 and induction of Id1 gene expression. Inhibition of BMP signaling with LDN193189 or noggin, and silencing of Smad 1 or 4 using small interfering RNA diminished the ability of phenylephrine to induce hypertrophy in NRCs. Conversely, activation of BMP signaling with BMP2 or BMP4 induced hypertrophy in NRCs. Luciferase reporter assay further showed that BMP2 or BMP4 treatment of NRCs repressed atrogin-1 gene expression concomitant with an increase in calcineurin protein levels and enhanced activity of nuclear factor of activated T cells, providing a mechanism by which BMP signaling contributes to cardiac hypertrophy. In a model of cardiac hypertrophy, C57BL/6 mice treated with angiotensin II (A2) had increased BMP signaling in the left ventricle. Treatment with LDN193189 attenuated A2-induced cardiac hypertrophy and collagen deposition in left ventricles. Cardiomyocyte-specific deletion of BMP type I receptor ALK2 (activin-like kinase 2), but not ALK1 or ALK3, inhibited BMP signaling and mitigated A2-induced cardiac hypertrophy and left ventricular fibrosis in mice. The results suggest that BMP signaling upregulates the calcineurin/nuclear factor of activated T cell pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis.

  5. THE CLASSIFICATION OF THE SURROUNDINGS OF COAL MINING ROADWAYS

    Institute of Scientific and Technical Information of China (English)

    邹喜正; 侯朝炯; 李华祥

    1996-01-01

    This introduces the calculation of opaper the deformationg .the Surroundings of coaowaysand the divisi of surroundings into 5 levels by means or !fuzzy integral assess mairrx, wnlcnserves-asthe scientific basis for selecting supporting pattern of roadways and determining the, pa-rameters of support.

  6. Perioperative hepatocyte growth factor (HGF) infusions improve hepatic regeneration following portal branch ligation (PBL) in rodents.

    Science.gov (United States)

    Mangieri, Christopher W; McCartt, Jason C; Strode, Matthew A; Lowry, John E; Balakrishna, Prasad M

    2017-07-01

    As hepatic surgery has become safer and more commonly performed, the extent of hepatic resections has increased. When there is not enough expected hepatic reserve to facilitate primary resection of hepatic tumors, a clinical adjunct to facilitating primary resection is portal vein embolization (PVE). PVE allows the hepatic remnant to increase to an appropriate size prior to resection via hepatocyte regeneration; however, PVE is not always successful in facilitating adequate regeneration. One of the strongest trophic factors for hepatocyte regeneration is hepatocyte growth factor (HGF). The purpose of this study was to improve hepatic regeneration with perioperative HGF infusions in an animal model that mimics PVE. Portal branch ligation (PBL) in rodents is equivalent to PVE in humans. We performed left-sided PBL in Sprague-Dawley rodents with the experimental group receiving perioperative HGF infusions. Baseline and postoperative liver volumetrics were obtained with CT scanning methods as performed in clinical practice. Baseline and postoperative liver functions were assessed via indocyanine green (ICG) elimination testing. HGF infused rodents had statistically significant increase in all postoperative liver volumetrics. Most clinically relevant were increased right liver volumes (RLV), 14.10 versus 7.85 cm(3) (p value 0.0001), and increased degree of hypertrophy (DH %), 159.23 versus 47.11 % (p value 0.0079). HGF infused rodents also had a quick return to baseline liver function, 2.38 days compared to 6.13 days (p value 0.0001). Perioperative HGF infusions significantly increase hepatic regeneration following PBL in rodents. Perioperative HGF infusions following PVE are a possible adjunct to increase the amount of patients able to successfully undergo primary resection for hepatic tumors. Further basic science is warranted in examining the use of HGF infusions to increase hepatic regeneration and translating that basic science work to clinical practice.

  7. Mechanisms of nascent fiber formation during avian skeletal muscle hypertrophy

    Science.gov (United States)

    McCormick, K. M.; Schultz, E.

    1992-01-01

    This study examined two putative mechanisms of new fiber formation in postnatal skeletal muscle, namely longitudinal fragmentation of existing fibers and de novo formation. The relative contributions of these two mechanisms to fiber formation in hypertrophying anterior latissimus dorsi (ALD) muscle were assessed by quantitative analysis of their nuclear populations. Muscle hypertrophy was induced by wing-weighting for 1 week. All nuclei formed during the weighting period were labeled by continuous infusion of 5-bromo-2'-deoxyuridine (BrdU), a thymidine analog, and embryonic-like fibers were identified using an antibody to ventricular-like embryonic (V-EMB) myosin. The number of BrdU-labeled and unlabeled nuclei in V-EMB-positive fibers were counted. Wing-weighting resulted in significant muscle enlargement and the appearance of many V-EMB+ fibers. The majority of V-EMB+ fibers were completely independent of mature fibers and had a nuclear density characteristics of developing fibers. Furthermore, nearly 100% of the nuclei in independent V-EMB+ fibers were labeled. These findings strongly suggest that most V-EMB+ fibers were nascent fibers formed de novo during the weighting period by satellite cell activation and fusion. Nascent fibers were found primarily in the space between fascicles where they formed a complex anastomosing network of fibers running at angles to one another. Although wing-weighting induced an increase in the number of branched fibers, there was no evidence that V-EMB+ fibers were formed by longitudinal fragmentation. The location of newly formed fibers in wing-weighted and regenerating ALD muscle was compared to determine whether satellite cells in the ALD muscle were unusual in that, if stimulated to divide, they would form fibers in the inter- and intrafascicular space. In contrast to wing-weighted muscle, nascent fibers were always found closely associated with necrotic fibers. These results suggest that wing-weighting is not simply another

  8. Mechanisms of nascent fiber formation during avian skeletal muscle hypertrophy

    Science.gov (United States)

    McCormick, K. M.; Schultz, E.

    1992-01-01

    This study examined two putative mechanisms of new fiber formation in postnatal skeletal muscle, namely longitudinal fragmentation of existing fibers and de novo formation. The relative contributions of these two mechanisms to fiber formation in hypertrophying anterior latissimus dorsi (ALD) muscle were assessed by quantitative analysis of their nuclear populations. Muscle hypertrophy was induced by wing-weighting for 1 week. All nuclei formed during the weighting period were labeled by continuous infusion of 5-bromo-2'-deoxyuridine (BrdU), a thymidine analog, and embryonic-like fibers were identified using an antibody to ventricular-like embryonic (V-EMB) myosin. The number of BrdU-labeled and unlabeled nuclei in V-EMB-positive fibers were counted. Wing-weighting resulted in significant muscle enlargement and the appearance of many V-EMB+ fibers. The majority of V-EMB+ fibers were completely independent of mature fibers and had a nuclear density characteristics of developing fibers. Furthermore, nearly 100% of the nuclei in independent V-EMB+ fibers were labeled. These findings strongly suggest that most V-EMB+ fibers were nascent fibers formed de novo during the weighting period by satellite cell activation and fusion. Nascent fibers were found primarily in the space between fascicles where they formed a complex anastomosing network of fibers running at angles to one another. Although wing-weighting induced an increase in the number of branched fibers, there was no evidence that V-EMB+ fibers were formed by longitudinal fragmentation. The location of newly formed fibers in wing-weighted and regenerating ALD muscle was compared to determine whether satellite cells in the ALD muscle were unusual in that, if stimulated to divide, they would form fibers in the inter- and intrafascicular space. In contrast to wing-weighted muscle, nascent fibers were always found closely associated with necrotic fibers. These results suggest that wing-weighting is not simply another

  9. Cytomegalovirus Hepatitis During Pregnancy

    Directory of Open Access Journals (Sweden)

    Ying Chan

    1995-01-01

    Full Text Available Background: Although cytomegalovirus (CMV is an uncommon cause of viral hepatitis during pregnancy, a definitive diagnosis is important because of the potential for congenital CMV. In the case reported here, a diagnosis of hepatitis caused by CMV was made after the more common viral pathogens had been ruled out.

  10. Hepatic angiosarcoma: CT findings

    Institute of Scientific and Technical Information of China (English)

    余日胜; 章士正; 华建明

    2003-01-01

    @@ Hepatic angiosarcoma is a rare malignant vascular tumor. Accurate preoperative diagnosis of this tumor is very difficult if the patient does not have any history of exposure to specific carcinogens including thorotrast, arsenicals and vinyl chloride monomer. We describe CT findings in two cases of hepatic angiosarcoma in combination with a review of the literature.

  11. Hepatitis E og graviditet

    DEFF Research Database (Denmark)

    Mannheimer, Ebba Elisabeth; Harritshøj, Lene Holm; Katzenstein, Terese Lea

    2016-01-01

    Hepatitis E virus (HEV) infection among pregnant women is severe, often leading to fulminant hepatic failure and death, with mortality rates up to 15-25%. Studies suggest that differences in genotypes/subgenotypes, hormonal and immunological changes during pregnancy may contribute to the severe...

  12. Proteasome activation during cardiac hypertrophy by the chaperone H11 Kinase/Hsp22.

    Science.gov (United States)

    Hedhli, Nadia; Wang, Li; Wang, Qian; Rashed, Eman; Tian, Yimin; Sui, Xiangzhen; Madura, Kiran; Depre, Christophe

    2008-02-01

    The regulation of protein degradation by the proteasome during cardiac hypertrophy remains largely unknown. Also, the proteasome translocates to the nuclear periphery in response to cellular stress in yeast, which remains unexplored in mammals. The purpose of this study was to determine the quantitative and qualitative adaptation of the proteasome during stable cardiac hypertrophy. We measured proteasome activity, expression and sub-cellular distribution in a model of chronic cardiac hypertrophy induced by the stress-response chaperone H11 Kinase/Hsp22 (Hsp22). Over-expression of Hsp22 in a transgenic (TG) mouse leads to a 30% increase in myocyte cross-sectional area compared to wild-type (WT) mice (P hypertrophy in TG by 50% (P hypertrophy. Proteasome inhibitors also prevented the increase in rate of protein synthesis observed after over-expression of Hsp22 or upon addition of pro-hypertrophic stimuli. Hsp22-mediated cardiac hypertrophy promotes an increased expression and activity, and a subcellular redistribution of the proteasome. Inhibition of the proteasome reverses cardiac hypertrophy upon Hsp22 over-expression or upon stimulation by pro-hypertrophic hormones, and also blocks the stimulation of protein synthesis in these conditions.

  13. Role of Nodal-PITX2C signaling pathway in glucose-induced cardiomyocyte hypertrophy.

    Science.gov (United States)

    Su, Dongmei; Jing, Sun; Guan, Lina; Li, Qian; Zhang, Huiling; Gao, Xiaobo; Ma, Xu

    2014-06-01

    Pathological cardiac hypertrophy is a major cause of morbidity and mortality in cardiovascular disease. Recent studies have shown that cardiomyocytes, in response to high glucose (HG) stimuli, undergo hypertrophic growth. While much work still needs to be done to elucidate this important mechanism of hypertrophy, previous works have showed that some pathways or genes play important roles in hypertrophy. In this study, we showed that sublethal concentrations of glucose (25 mmol/L) could induce cardiomyocyte hypertrophy with an increase in the cellular surface area and the upregulation of the atrial natriuretic peptide (ANP) gene, a hypertrophic marker. High glucose (HG) treatments resulted in the upregulation of the Nodal gene, which is under-expressed in cardiomyocytes. We also determined that the knockdown of the Nodal gene resisted HG-induced cardiomyocyte hypertrophy. The overexpression of Nodal was able to induce hypertrophy in cardiomyocytes, which was associated with the upregulation of the PITX2C gene. We also showed that increases in the PITX2C expression, in response to Nodal, were mediated by the Smad4 signaling pathway. This study is highly relevant to the understanding of the effects of the Nodal-PITX2C pathway on HG-induced cardiomyocyte hypertrophy, as well as the related molecular mechanisms.

  14. Herbal Supplement Ameliorates Cardiac Hypertrophy in Rats with CCl4-Induced Liver Cirrhosis

    Directory of Open Access Journals (Sweden)

    Ping-Chun Li

    2012-01-01

    Full Text Available We used the carbon tetrachloride (CCl4 induced liver cirrhosis model to test the molecular mechanism of action involved in cirrhosis-associated cardiac hypertrophy and the effectiveness of Ocimum gratissimum extract (OGE and silymarin against cardiac hypertrophy. We treated male wistar rats with CCl4 and either OGE (0.02 g/kg B.W. or 0.04 g/kg B.W. or silymarin (0.2 g/kg B.W.. Cardiac eccentric hypertrophy was induced by CCl4 along with cirrhosis and increased expression of cardiac hypertrophy related genes NFAT, TAGA4, and NBP, and the interleukin-6 (IL-6 signaling pathway related genes MEK5, ERK5, JAK, and STAT3. OGE or silymarin co-treatment attenuated CCl4-induced cardiac abnormalities, and lowered expression of genes which were elevated by this hepatotoxin. Our results suggest that the IL-6 signaling pathway may be related to CCl4-induced cardiac hypertrophy. OGE and silymarin were able to lower liver fibrosis, which reduces the chance of cardiac hypertrophy perhaps by lowering the expressions of IL-6 signaling pathway related genes. We conclude that treatment of cirrhosis using herbal supplements is a viable option for protecting cardiac tissues against cirrhosis-related cardiac hypertrophy.

  15. MicroRNA-1 and-16 inhibit cardiomyocyte hypertrophy by targeting cyclins/Rb pathway

    Institute of Scientific and Technical Information of China (English)

    SHAN Zhi-xin; ZHU Jie-ning; TANG Chun-mei; ZHU Wen-si; LIN Qiu-xiong; HU Zhi-qin; FU Yong-heng; ZHANG Meng-zhen

    2016-01-01

    AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

  16. Tumor necrosis factor receptor-associated factor 3 is a positive regulator of pathological cardiac hypertrophy.

    Science.gov (United States)

    Jiang, Xi; Deng, Ke-Qiong; Luo, Yuxuan; Jiang, Ding-Sheng; Gao, Lu; Zhang, Xiao-Fei; Zhang, Peng; Zhao, Guang-Nian; Zhu, Xueyong; Li, Hongliang

    2015-08-01

    Cardiac hypertrophy, a common early symptom of heart failure, is regulated by numerous signaling pathways. Here, we identified tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein in tumor necrosis factor-related signaling cascades, as a key regulator of cardiac hypertrophy in response to pressure overload. TRAF3 expression was upregulated in hypertrophied mice hearts and failing human hearts. Four weeks after aortic banding, cardiac-specific conditional TRAF3-knockout mice exhibited significantly reduced cardiac hypertrophy, fibrosis, and dysfunction. Conversely, transgenic mice overexpressing TRAF3 in the heart developed exaggerated cardiac hypertrophy in response to pressure overload. TRAF3 also promoted an angiotensin II- or phenylephrine-induced hypertrophic response in isolated cardiomyocytes. Mechanistically, TRAF3 directly bound to TANK-binding kinase 1 (TBK1), causing increased TBK1 phosphorylation in response to hypertrophic stimuli. This interaction between TRAF3 and TBK1 further activated AKT signaling, which ultimately promoted the development of cardiac hypertrophy. Our findings not only reveal a key role of TRAF3 in regulating the hypertrophic response but also uncover TRAF3-TBK1-AKT as a novel signaling pathway in the development of cardiac hypertrophy and heart failure. This pathway may represent a potential therapeutic target for this pathological process.

  17. Ubiquitin-specific protease 14 regulates cardiac hypertrophy progression by increasing GSK-3β phosphorylation.

    Science.gov (United States)

    Liu, Ningning; Chai, Renjie; Liu, Bin; Zhang, Zhenhui; Zhang, Shuangwei; Zhang, Jingzhi; Liao, Yuning; Cai, Jianyu; Xia, Xiaohong; Li, Aiqun; Liu, Jinbao; Huang, Hongbiao; Liu, Shiming

    2016-09-23

    Cardiac hypertrophy, a compensatory response to various stimuli in the heart, independently predicts cardiovascular ailments and related deaths. Increasing evidence indicates ubiquitin-proteasome signaling contributes to cardiac hypertrophy regulation. Here, we identified ubiquitin-specific protease 14 (USP14), a 19S proteasome associated deubiquitinase (DUB), as a novel target for cardiac hypertrophy therapy via inhibition of the GSK-3β pathway. Indeed, USP14 expression was increased in an animal model of abdominal aorta constriction. In an angiotensin II (AngII) induced primary neonatal rat cardiomyocyte hypertrophy model, USP14 expression was increased in a time-dependent manner, and reduced USP14 deubiquitinase activity or USP14 knockdown resulted in lower expression levels of the myocardial hypertrophy specific marker β-MHC, and subsequent decreased GSK-3β phosphorylation. In conclusion, USP14 mediates the development of cardiac hypertrophy by promoting GSK-3β phosphorylation, suggesting that USP14 might represent a novel therapeutic target for cardiac hypertrophy treatment. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Kallikrein-related peptidase 8 is expressed in myocardium and induces cardiac hypertrophy

    Science.gov (United States)

    Cao, Buqing; Yu, Qing; Zhao, Wei; Tang, Zhiping; Cong, Binghai; Du, Jiankui; Lu, Jianqiang; Zhu, Xiaoyan; Ni, Xin

    2016-01-01

    The tissue kallikrein-related peptidase family (KLK) is a group of trypsin- and chymotrypsin-like serine proteases that share a similar homology to parent tissue kallikrein (KLK1). KLK1 is identified in heart and has anti-hypertrophic effects. However, whether other KLK family members play a role in regulating cardiac function remains unknown. In the present study, we demonstrated for the first time that KLK8 was expressed in myocardium. KLK8 expression was upregulated in left ventricle of cardiac hypertrophy models. Both intra-cardiac adenovirus-mediated and transgenic-mediated KLK8 overexpression led to cardiac hypertrophy in vivo. In primary neonatal rat cardiomyocytes, KLK8 knockdown inhibited phenylephrine (PE)-induced cardiomyocyte hypertrophy, whereas KLK8 overexpression promoted cardiomyocyte hypertrophy via a serine protease activity-dependent but kinin receptor-independent pathway. KLK8 overexpression increased epidermal growth factor (EGF) production, which was blocked by the inhibitors of serine protease. EGF receptor (EGFR) antagonist and EGFR knockdown reversed the hypertrophy induced by KLK8 overexpression. KLK8-induced cardiomyocyte hypertrophy was also significantly decreased by blocking the protease-activated receptor 1 (PAR1) or PAR2 pathway. Our data suggest that KLK8 may promote cardiomyocyte hypertrophy through EGF signaling- and PARs-dependent but a kinin receptor-independent pathway. It is implied that different KLK family members can subtly regulate cardiac function and remodeling. PMID:26823023

  19. Transient receptor potential vanilloid 2 function regulates cardiac hypertrophy via stretch-induced activation.

    Science.gov (United States)

    Koch, Sheryl E; Mann, Adrien; Jones, Shannon; Robbins, Nathan; Alkhattabi, Abdullah; Worley, Mariah C; Gao, Xu; Lasko-Roiniotis, Valerie M; Karani, Rajiv; Fulford, Logan; Jiang, Min; Nieman, Michelle; Lorenz, John N; Rubinstein, Jack

    2017-03-01

    Hypertension (increased afterload) results in cardiomyocyte hypertrophy leading to left ventricular hypertrophy and subsequently, heart failure with preserved ejection fraction. This study was performed to test the hypothesis that transient receptor potential vanilloid 2 subtype (TRPV2) function regulates hypertrophy under increased afterload conditions. We used functional (pore specific) TRPV2 knockout mice to evaluate the effects of increased afterload-induced stretch on cardiac size and function via transverse aortic constriction (TAC) as well as hypertrophic stimuli including adrenergic and angiotensin stimulation via subcutaneous pumps. Wild-type animals served as control for all experiments. Expression and localization of TRPV2 was investigated in wild-type cardiac samples. Changes in cardiac function were measured in vivo via echocardiography and invasive catheterization. Molecular changes, including protein and real-time PCR markers of hypertrophy, were measured in addition to myocyte size. TRPV2 is significantly upregulated in wild-type mice after TAC, though not in response to beta-adrenergic or angiotensin stimulation. TAC-induced stretch stimulus caused an upregulation of TRPV2 in the sarcolemmal membrane. The absence of functional TRPV2 resulted in significantly reduced left ventricular hypertrophy after TAC, though not in response to beta-adrenergic or angiotensin stimulation. The decreased development of hypertrophy was not associated with significant deterioration of cardiac function. We conclude that TRPV2 function, as a stretch-activated channel, regulates the development of cardiomyocyte hypertrophy in response to increased afterload.

  20. [Preliminary Study of Necroptosis in Cardiac Hypertrophy Induced by Pressure Overload].

    Science.gov (United States)

    Zhao, Mingyue; Qin, Yupei; Lu, Lihui; Tang, Xiaoju; Wu, Wenchao; Fu, Hua; Liu, Xiaojing

    2015-06-01

    The aim of this study was to observe whether necroptosis is involved in the process of cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and protein expression of receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for cardiac hypertrophy was established. The experimental data showed that the gene and protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the sham group. HE staining showed cardiomyocytes injury and hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with losartan used, the selective antagonist of angiotensin II type I receptor could improve the cardiac function of TAC rats. Moreover, losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of cardiac hypertrophy with pressure overload, and losartan could alleviate the cardiac hypertrophy and inhibit necroptosis.

  1. Consideration of Drug Therapy in Benign Prostatic Hypertrophy

    Directory of Open Access Journals (Sweden)

    G. Diamantis

    2015-01-01

    Full Text Available Benign prostatic hypertrophy (BPH has become a major global health problem both in its frequency by which it determines the complications and the problems of diagnosis and treatment it requires. BPH is a heterogeneous disease. The symptoms attributed to BPH may have other coexisting causes and growth factors both androgen-dependent and independent, which promotes prostate enlargement. It is well known that prostate size correlates poorly with the symptoms so that reducing prostate using 5-alphareductase or alphablocants inhibitors may not always be sufficient. A better understanding of the pathophysiology of BPH and its interactions with other drugs will help the development of new substances with a better efficiency. This present work aims to be a modest contribution related to medical treatment in benign prostatic hyperplasia and the role that the generalist practitioner should play in managing of this urinary disease quite common in elderly men.

  2. Hepatitis G virus

    Institute of Scientific and Technical Information of China (English)

    Vasiliy Ivanovich Reshetnyak; Tatiana Igorevna Karlovich; Ljudmila Urievna Ilchenko

    2008-01-01

    A number of new hepatitis viruses (G,TT,SEN) were discovered late in the past century.We review the data available in the literature and our own findings suggesting that the new hepatitis G virus (HGV),disclosed in the late 1990s,has been rather well studied.Analysis of many studies dealing with HGV mainly suggests the lymphotropicity of this virus.HGV or GBV-C has been ascertained to influence course and prognosis in the HIV-infected patient.Until now,the frequent presence of GBV-C in coinfections,hematological diseases,and biliary pathology gives no grounds to determine it as an "accidental tourist" that is of no significance.The similarity in properties of GBV-C and hepatitis C virus (HCV) offers the possibility of using HGV,and its induced experimental infection,as a model to study hepatitis C and to develop a hepatitis C vaccine.

  3. The relationship of enuresis nocturna and adenoid hypertrophy

    Directory of Open Access Journals (Sweden)

    Muhsin Balaban

    2016-07-01

    Full Text Available Objectives: This study was organized to assess the relationship of enuresis nocturna (EN and upper airway obstruction (UAO in children. Material and Methods: This study was multi-centrically and prospectively designed including 79 children who presented to a urology clinic with symptoms of EN between January 2013 and February 2014. Sixty-four age-matched children with no history of urological complaints were randomly recruited from children admitted to a pediatric clinic as a control group. All children and parents were asked to fill out a dysfunctional elimination syndrome (DES questionnaire and children were examined by an ear, nose and throat (ENT specialist to evaluate the UAO. Descriptive statistics, chisquare and Mann-Whitney-U tests were used to compare variables. Results: The mean ages of the 79 children (48 male, 31 female in the study group and the 64 children (41 male, 23 female in the control group were 10.14+/-3.38 and 9.17+/- 2.85, respectively. Family history of the study showed that 19% of the children’s mothers, 10% of the children’s fathers and 37% of the children’s siblings had experienced EN. There was a significant difference between the study and the control groups in terms of urge to urinate, bladder emptying, bowel symptoms and psychological stress. There was also a significant difference between rates of tonsillar hypertrophy and nasopharynx obstruction in the EN group (p = 0.009. Conclusion: In this study we found that half of the children with EN had tonsillar hypertrophy, which was significantly higher than in the control group. Further studies are needed to clarify the exact relationship between UAO and EN.

  4. Association between routine and standardized blood pressure measurements and left ventricular hypertrophy among patients on hemodialysis

    Directory of Open Access Journals (Sweden)

    Walsh Michael

    2010-06-01

    Full Text Available Abstract Background Left ventricular (LV hypertrophy is common among patients on hemodialysis. While a relationship between blood pressure (BP and LV hypertrophy has been established, it is unclear which BP measurement method is the strongest correlate of LV hypertrophy. We sought to determine agreement between various blood pressure measurement methods, as well as identify which method was the strongest correlate of LV hypertrophy among patients on hemodialysis. Methods This was a post-hoc analysis of data from a randomized controlled trial. We evaluated the agreement between seven BP measurement methods: standardized measurement at baseline; single pre- and post-dialysis, as well as mean intra-dialytic measurement at baseline; and cumulative pre-, intra- and post-dialysis readings (an average of 12 monthly readings based on a single day per month. Agreement was assessed using Lin's concordance correlation coefficient (CCC and the Bland Altman method. Association between BP measurement method and LV hypertrophy on baseline cardiac MRI was determined using receiver operating characteristic curves and area under the curve (AUC. Results Agreement between BP measurement methods in the 39 patients on hemodialysis varied considerably, from a CCC of 0.35 to 0.94, with overlapping 95% confidence intervals. Pre-dialysis measurements were the weakest predictors of LV hypertrophy while standardized, post- and inter-dialytic measurements had similar and strong (AUC 0.79 to 0.80 predictive power for LV hypertrophy. Conclusions A single standardized BP has strong predictive power for LV hypertrophy and performs just as well as more resource intensive cumulative measurements, whereas pre-dialysis blood pressure measurements have the weakest predictive power for LV hypertrophy. Current guidelines, which recommend using pre-dialysis measurements, should be revisited to confirm these results.

  5. Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants.

    Science.gov (United States)

    Fernandes, T; Soci, U P R; Oliveira, E M

    2011-09-01

    Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, β-myosin heavy chain and α-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.

  6. Calcium Signaling Regulates Ventricular Hypertrophy During Development Independent of Contraction or Blood Flow

    Science.gov (United States)

    Andersen, Nicholas D.; Ramachandran, Kapil V.; Bao, Michelle M.; Kirby, Margaret L.; Pitt, Geoffrey S.; Hutson, Mary R.

    2014-01-01

    In utero interventions aimed at restoring left ventricular hemodynamic forces in fetuses with prenatally diagnosed hypoplastic left heart syndrome failed to stimulate ventricular myocardial growth during gestation, suggesting chamber growth during development may not rely upon fluid forces. We therefore hypothesized that ventricular hypertrophy during development may depend upon fundamental Ca2+-dependent growth pathways that function independent of hemodynamic forces. To test this hypothesis, zebrafish embryos were treated with inhibitors or activators of Ca2+ signaling in the presence or absence of contraction during the period of chamber development. Abolishment of contractile function alone in the setting of preserved Ca2+ signaling did not impair ventricular hypertrophy. In contrast, inhibition of L-type voltage-gated Ca2+ influx abolished contraction and led to reduced ventricular hypertrophy, whereas increasing L-type voltage-gated Ca2+ influx led to enhanced ventricular hypertrophy in either the presence or absence of contraction. Similarly, inhibition of the downstream Ca2+-sensitive phosphatase calcineurin, a known regulator of adult cardiac hypertrophy, led to reduced ventricular hypertrophy in the presence or absence of contraction, whereas hypertrophy was rescued in the absence of L-type voltage-gated Ca2+ influx and contraction by expression of a constitutively active calcineurin. These data suggest ventricular cardiomyocyte hypertrophy during chamber formation is dependent upon Ca2+ signaling pathways that are unaffected by heart function or hemodynamic forces. Disruption of Ca2+-dependent hypertrophy during heart development may therefore represent one mechanism for impaired chamber formation that is not related to impaired blood flow. PMID:25536179

  7. Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants

    Directory of Open Access Journals (Sweden)

    T. Fernandes

    2011-09-01

    Full Text Available Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, β-myosin heavy chain and α-skeletal actin are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1 receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.

  8. MiR-30-regulated autophagy mediates angiotensin II-induced myocardial hypertrophy.

    Science.gov (United States)

    Pan, Wei; Zhong, Yun; Cheng, Chuanfang; Liu, Benrong; Wang, Li; Li, Aiqun; Xiong, Longgen; Liu, Shiming

    2013-01-01

    Dysregulated autophagy may lead to the development of disease. Role of autophagy and the diagnostic potential of microRNAs that regulate the autophagy in cardiac hypertrophy have not been evaluated. A rat model of cardiac hypertrophy was established using transverse abdominal aortic constriction (operation group). Cardiomyocyte autophagy was enhanced in rats from the operation group, compared with those in the sham operation group. Moreover, the operation group showed up-regulation of beclin-1 (an autophagy-related gene), and down-regulation of miR-30 in cardiac tissue. The effects of inhibition and over-expression of the beclin-1 gene on the expression of hypertrophy-related genes and on autophagy were assessed. Angiotensin II-induced myocardial hypertrophy was found to be mediated by over-expression of the beclin-1 gene. A dual luciferase reporter assay confirmed that beclin-1 was a target gene of miR-30a. miR-30a induced alterations in beclin-1 gene expression and autophagy in cardiomyocytes. Treatment of cardiomyocytes with miR-30a mimic attenuated the Angiotensin II-induced up-regulation of hypertrophy-related genes and decreased in the cardiomyocyte surface area. Conversely, treatment with miR-30a inhibitor enhanced the up-regulation of hypertrophy-related genes and increased the surface area of cardiomyocytes induced by Angiotensin II. In addition, circulating miR-30 was elevated in patients with left ventricular hypertrophy, and circulating miR-30 was positively associated with left ventricular wall thickness. Collectively, these above-mentioned results suggest that Angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy. Circulating miR-30 may be an important marker for the diagnosis of left ventricular hypertrophy.

  9. Mechanisms of Ca2+-dependent calcineurin activation in mechanical stretch-induced hypertrophy.

    Science.gov (United States)

    Zobel, Carsten; Rana, Obaida R; Saygili, Erol; Bölck, Birgit; Saygili, Esra; Diedrichs, Holger; Reuter, Hannes; Frank, Konrad; Müller-Ehmsen, Jochen; Pfitzer, Gabriele; Schwinger, Robert H G

    2007-01-01

    Pressure overload is the major stimulus for cardiac hypertrophy. Accumulating evidence suggests an important role for calcium-induced activation of calcineurin in mediating hypertrophic signaling. Hypertrophy is an important risk factor for cardiovascular morbidity and mortality. We therefore employed an in vitro mechanical stretch model of cultured neonatal cardiomyocytes to evaluate proposed mechanisms of calcium-induced calcineurin activation in terms of inhibition of calcineurin activity and hypertrophy. The protein/DNA ratio and ANP gene expression were used as markers for stretch-induced hypertrophy. Stretch increased the calcineurin activity, MCIP1 gene expression and DNA binding of NFATc as well as the protein/DNA ratio and ANP mRNA in a significant manner. The specific inhibitor of calcineurin, cyclosporin A, inhibited the stretch-induced increase in calcineurin activity, MCIP1 gene expression and hypertrophy. The L-type Ca2+ channel blocker nifedipine and a blocker of the Na+/H+ exchanger (cariporide) both suppressed stretch-dependent enhanced calcineurin activity and hypertrophy. Also application of a blocker of the Na+/Ca2+ exchanger (KB-R7943) was effective in preventing calcineurin activation and increases in the protein/DNA ratio. Inhibition of capacitative Ca2+ entry with SKF 96365 was also sufficient to abrogate calcineurin activation and hypertrophy. The blocker of stretch-activated ion channels, streptomycin, was without effect on stretch-induced hypertrophy and calcineurin activity. The present work suggests that of the proposed mechanisms for the calcium-induced activation of calcineurin (L-type Ca2+ channels, capacitative Ca2+ entry, Na+/H+ exchanger, Na+/Ca2+ exchanger and stretch-activated channels) all but stretch-activated channels are possible targets for the inhibition of hypertrophy. 2007 S. Karger AG, Basel

  10. Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload.

    Science.gov (United States)

    Li, Wei-Ming; Zhao, Yi-Fan; Zhu, Guo-Fu; Peng, Wen-Hui; Zhu, Meng-Yun; Yu, Xue-Jing; Chen, Wei; Xu, Da-Chun; Xu, Ya-Wei

    2017-01-01

    Pathological cardiac hypertrophy is an independent risk factor of heart failure. However, we still lack effective methods to reverse cardiac hypertrophy. DUSP12 is a member of the dual specific phosphatase (DUSP) family, which is characterized by its DUSP activity to dephosphorylate both tyrosine and serine/threonine residues on one substrate. Some DUSPs have been identified as being involved in the regulation of cardiac hypertrophy. However, the role of DUSP12 during pathological cardiac hypertrophy is still unclear. In the present study, we observed a significant decrease in DUSP12 expression in hypertrophic hearts and cardiomyocytes. Using a genetic loss-of-function murine model, we demonstrated that DUSP12 deficiency apparently aggravated pressure overload-induced cardiac hypertrophy and fibrosis as well as impaired cardiac function, whereas cardiac-specific overexpression of DUPS12 was capable of reversing this hypertrophic and fibrotic phenotype and improving contractile function. Furthermore, we demonstrated that JNK1/2 activity but neither ERK1/2 nor p38 activity was increased in the DUSP12 deficient group and decreased in the DUSP12 overexpression group both in vitro and in vivo under hypertrophic stress conditions. Pharmacological inhibition of JNK1/2 activity (SP600125) is capable of reversing the hypertrophic phenotype in DUSP12 knockout (KO) mice. DUSP12 protects against pathological cardiac hypertrophy and related pathologies. This regulatory role of DUSP12 is primarily through c-Jun N-terminal kinase (JNK) inhibition. DUSP12 could be a promising therapeutic target of pathological cardiac hypertrophy. DUSP12 is down-regulated in hypertrophic hearts. An absence of DUSP12 aggravated cardiac hypertrophy, whereas cardiomyocyte-specific DUSP12 overexpression can alleviate this hypertrophic phenotype with improved cardiac function. Further study demonstrated that DUSP12 inhibited JNK activity to attenuate pathological cardiac hypertrophy. © 2016 The

  11. MiR-30-regulated autophagy mediates angiotensin II-induced myocardial hypertrophy.

    Directory of Open Access Journals (Sweden)

    Wei Pan

    Full Text Available Dysregulated autophagy may lead to the development of disease. Role of autophagy and the diagnostic potential of microRNAs that regulate the autophagy in cardiac hypertrophy have not been evaluated. A rat model of cardiac hypertrophy was established using transverse abdominal aortic constriction (operation group. Cardiomyocyte autophagy was enhanced in rats from the operation group, compared with those in the sham operation group. Moreover, the operation group showed up-regulation of beclin-1 (an autophagy-related gene, and down-regulation of miR-30 in cardiac tissue. The effects of inhibition and over-expression of the beclin-1 gene on the expression of hypertrophy-related genes and on autophagy were assessed. Angiotensin II-induced myocardial hypertrophy was found to be mediated by over-expression of the beclin-1 gene. A dual luciferase reporter assay confirmed that beclin-1 was a target gene of miR-30a. miR-30a induced alterations in beclin-1 gene expression and autophagy in cardiomyocytes. Treatment of cardiomyocytes with miR-30a mimic attenuated the Angiotensin II-induced up-regulation of hypertrophy-related genes and decreased in the cardiomyocyte surface area. Conversely, treatment with miR-30a inhibitor enhanced the up-regulation of hypertrophy-related genes and increased the surface area of cardiomyocytes induced by Angiotensin II. In addition, circulating miR-30 was elevated in patients with left ventricular hypertrophy, and circulating miR-30 was positively associated with left ventricular wall thickness. Collectively, these above-mentioned results suggest that Angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy. Circulating miR-30 may be an important marker for the diagnosis of left ventricular hypertrophy.

  12. Autoimmune hepatitis triggered by acute hepatitis A

    Institute of Scientific and Technical Information of China (English)

    Hiroto Tanaka; Hiroto Tujioka; Hiroki Ueda; Hiroko Hamagami; Youhei Kida; Masakazu Ichinose

    2005-01-01

    The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003.Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (×320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized,so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy,levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized.The present case was thus considered to represent AIH triggered by acute HA.

  13. Black hole solutions surrounded by perfect fluid in Rastall theory

    Science.gov (United States)

    Heydarzade, Y.; Darabi, F.

    2017-08-01

    In this work, we obtain uncharged∖charged Kiselev-like black holes as a new class of black hole solutions surrounded by perfect fluid in the context of Rastall theory. Then, we study the specific cases of the uncharged∖charged black holes surrounded by regular matter like dust and radiation, or exotic matter like quintessence, cosmological constant and phantom fields. By comparing the Kiselev-like black hole solutions in Rastall theory with the Kiselev black hole solutions in GR, we find an effective perfect fluid behavior for the black hole's surrounding field. It is shown that the corresponding effective perfect fluid has interesting characteristic features depending on the different ranges of the parameters in Rastall theory. For instance, Kiselev-like black holes surrounded by regular matter in Rastall theory may be considered as Kiselev black holes surrounded by exotic matter in GR, or Kiselev-like black holes surrounded by exotic matter in Rastall theory may be considered as Kiselev black holes surrounded by regular matter in GR.

  14. Surround suppression and sparse coding in visual and barrel cortices

    Directory of Open Access Journals (Sweden)

    Robert N S Sachdev

    2012-07-01

    Full Text Available During natural vision the entire retina is stimulated. Likewise, during natural tactile behaviors, spatially extensive regions of the somatosensory surface are co-activated. The large spatial extent of naturalistic stimulation means that surround suppression, a phenomenon whose neural mechanisms remain a matter of debate, must arise during natural behavior. To identify common neural motifs that might instantiate surround suppression across modalities, we review models of surround suppression and compare the evidence supporting the competing ideas that surround suppression has either cortical or sub-cortical origins in visual and barrel cortex. In the visual system there is general agreement lateral inhibitory mechanisms contribute to surround suppression, but little direct experimental evidence that intracortical inhibition plays a major role. Two intracellular recording studies of V1, one using naturalistic stimuli (Haider et al., 2010, the other sinusoidal gratings (Ozeki et al., 2009, sought to identify the causes of reduced activity in V1 with increasing stimulus size, a hallmark of surround suppression. The former attributed this effect to increased inhibition, the latter to largely balanced withdrawal of excitation and inhibition. In rodent primary somatosensory barrel cortex, multi-whisker responses are generally weaker than single whisker responses, suggesting multi-whisker stimulation engages similar surround suppressive mechanisms. The origins of suppression in S1 remain elusive: studies have implicated brainstem lateral/internuclear interactions and both thalamic and cortical inhibition. Although the anatomical organization and instantiation of surround suppression in the visual and somatosensory systems differ, we consider the idea that one common function of surround suppression, in both modalities, is to remove the statistical redundancies associated with natural stimuli by increasing the sparseness or selectivity of sensory

  15. Markers of collagen synthesis is related to blood pressure and vascular hypertrophy: a LIFE substudy

    DEFF Research Database (Denmark)

    Olsen, M H; Christensen, M K; Wachtell, K;

    2005-01-01

    , we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment......Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy...

  16. Simultaneous Bilateral Hypertrophies of the Parotid Gland and Masseter Muscle: Case Report.

    Science.gov (United States)

    Prabhu, Rohan; Mandel, Louis

    2017-01-01

    Increased salivary demand can lead to enlarged parotid salivary glands, and increased activity of the masseter muscles can cause masseter hypertrophy. This report describes a most unusual case of simultaneous bilateral hypertrophies of the parotid gland and masseter muscle originating from the very extensive habit of chewing gum. An extensive literature review uncovered many cases of the independent existence of masseteric or parotid hypertrophy, but no example of the simultaneous occurrence of these 2 conditions. Copyright © 2016 American Association of Oral and Maxillofacial Surgeons. Published by Elsevier Inc. All rights reserved.

  17. Development of left ventricular hypertrophy in a novel porcine model of mitral regurgitation

    DEFF Research Database (Denmark)

    Ravn, Nathja; Zois, Nora Elisabeth; Moesgaard, Sophia Gry

    2014-01-01

    OBJECTIVES: We aimed to develop a porcine model for chronic nonischemic mitral regurgitation (MR) to investigate left ventricular (LV) enlargement and eccentric hypertrophy. DESIGN: Nonischemic MR was induced in 30 pigs by open-chest immobilization of the posterior mitral leaflet by transannular...... traction sutures that where applied in transmyocardial fashion. A sham operated control group (n = 13) was included. Echocardiographic LV size and heart weight assessed at euthanasia were used to evaluate the development of LV enlargement and eccentric hypertrophy after 8 weeks follow-up. RESULTS: Eight...... for chronic moderate to severe nonischemic MR with development of LV enlargement and eccentric hypertrophy within 8 weeks has been established in pigs....

  18. Becker muscular dystrophy with widespread muscle hypertrophy and a non-sense mutation of exon 2

    DEFF Research Database (Denmark)

    Witting, Nanna; Duno, M; Vissing, J

    2013-01-01

    Becker muscular dystrophy features progressive proximal weakness, wasting and often focal hypertrophy. We present a patient with pain and cramps from adolescence. Widespread muscle hypertrophy, preserved muscle strength and a 10-20-fold raised CPK were noted. Muscle biopsy was dystrophic......, and Western blot showed a 95% reduction of dystrophin levels. Genetic analyses revealed a non-sense mutation in exon 2 of the dystrophin gene. This mutation is predicted to result in a Duchenne phenotype, but resulted in a mild Becker muscular dystrophy with widespread muscle hypertrophy. We suggest...

  19. [Impacts of physical exercise on remodeling and hypertrophy of skeletal muscle.

    Science.gov (United States)

    Sakashita, Yoshihiro; Uchida, Takayuki; Nikawa, Takeshi

    The skeletal muscle has high sensitivity for the mechanical stress. Because it is enlarged by training, whereas it is easily withered by lack of exercise. When we exercise, skeletal muscle cells per se sense mechanical loading, and muscular remodeling and the muscular hypertrophy occur. It has been revealed that the intracellular signaling through PGC-1α participates in the remodeling of the skeletal muscle, while PGC-1α4, an isoform of PGC-1α, and the dystrophin-glycoprotein complex play important roles in muscular hypertrophy. This review describes the impact of physical exercise gives on the remodeling and hypertrophy of muscle through the signaling.

  20. Occult hepatitis B among Iranian hepatitis C patients

    OpenAIRE

    Ahmad shavakhi; Babak Norinaier; Fatomeh Esteghamat; Mohamad Seghatoleslami; Mahsa Khodadustan; Mohamad hossein Somi; Mohsen Masoodi; Mohamad reza Zali

    2009-01-01

    • BACKGROUND: Occult hepatitis B is defined as presence of HBV DNA in tissue or serum without hepatitis B surface antigen. The aim of this study is to determine frequency of occult hepatitis B among hepatitis C patients in Tehran and compare the route of transmission and liver enzymes between positive and negative HBV DNA patients.
    • METHODS: In a cross sectional study, serum of 103 hepatitis C cas...

  1. [The ABC of viral hepatitis].

    Science.gov (United States)

    Van Bambeke, F

    2008-03-01

    Viral hepatitis has long been under-diagnosed. Hepatitis A is an acute disease, while patients infected by hepatitis B and hepatitis C viruses are likely to develop chronical infections and severe complications (cancer, cirrhosis). The current treatment of hepatitis B and C consists in alpha interferon (preferably under its pegylated form), in combination with ribavirin for hepatitis C. The frequent and severe adverse effects of interferon-based therapy constitute, however, a major limiting factor (reactions at the injection site, flu-like syndrome, neurological disorders, ...). For hepatitis B, two alternatives are available so far, namely lamivudine and adefovir (used as a prodrug with highe oral bioavailability).

  2. Surrounding Moving Obstacle Detection for Autonomous Driving Using Stereo Vision

    Directory of Open Access Journals (Sweden)

    Hao Sun

    2013-06-01

    Full Text Available Detection and tracking surrounding moving obstacles such as vehicles and pedestrians are crucial for the safety of mobile robotics and autonomous vehicles. This is especially the case in urban driving scenarios. This paper presents a novel framework for surrounding moving obstacles detection using binocular stereo vision. The contributions of our work are threefold. Firstly, a multiview feature matching scheme is presented for simultaneous stereo correspondence and motion correspondence searching. Secondly, the multiview geometry constraint derived from the relative camera positions in pairs of consecutive stereo views is exploited for surrounding moving obstacles detection. Thirdly, an adaptive particle filter is proposed for tracking of multiple moving obstacles in surrounding areas. Experimental results from real‐world driving sequences demonstrate the effectiveness and robustness of the proposed framework.

  3. Surrounding Moving Obstacle Detection for Autonomous Driving Using Stereo Vision

    Directory of Open Access Journals (Sweden)

    Hao Sun

    2013-06-01

    Full Text Available Detection and tracking surrounding moving obstacles such as vehicles and pedestrians are crucial for the safety of mobile robotics and autonomous vehicles. This is especially the case in urban driving scenarios. This paper presents a novel framework for surrounding moving obstacles detection using binocular stereo vision. The contributions of our work are threefold. Firstly, a multiview feature matching scheme is presented for simultaneous stereo correspondence and motion correspondence searching. Secondly, the multiview geometry constraint derived from the relative camera positions in pairs of consecutive stereo views is exploited for surrounding moving obstacles detection. Thirdly, an adaptive particle filter is proposed for tracking of multiple moving obstacles in surrounding areas. Experimental results from real-world driving sequences demonstrate the effectiveness and robustness of the proposed framework.

  4. Traditional Indian custOInS surrounding birth

    African Journals Online (AJOL)

    traditional custOIns surrounding birth in Indian culture. ... conception, pregnancy, birth and the early months ofparenthood. .... house attended by a traditional birth attendant of a ..... Spiritual components play a dominant role in traditional.

  5. Glow phenomenon surrounding the vertical stabilizer and OMS pods

    Science.gov (United States)

    1994-01-01

    This 35mm frame, photographed as the Space Shuttle Columbia was orbiting Earth during a 'night' pass, documents the glow phenomenon surrounding the vertical stabilizer and the Orbital Maneuvering System (OMS) pods of the spacecraft.

  6. Surrounding Moving Obstacle Detection for Autonomous Driving Using Stereo Vision

    OpenAIRE

    Hao Sun; Huanxin Zou; Shilin Zhou; Cheng Wang; Naser El-Sheimy

    2013-01-01

    Detection and tracking surrounding moving obstacles such as vehicles and pedestrians are crucial for the safety of mobile robotics and autonomous vehicles. This is especially the case in urban driving scenarios. This paper presents a novel framework for surrounding moving obstacles detection using binocular stereo vision. The contributions of our work are threefold. Firstly, a multiview feature matching scheme is presented for simultaneous stereo correspondence and motion correspondence searc...

  7. "Tilt" in color space: Hue changes induced by chromatic surrounds.

    Science.gov (United States)

    Klauke, Susanne; Wachtler, Thomas

    2015-01-01

    The perceived color of a chromatic stimulus is influenced by the chromaticity of its surround. To investigate these influences along the dimension of hue, we measured hue changes induced in stimuli of different hues by isoluminant chromatic surrounds. Generally, induced hue changes were directed in color space away from the hue of the inducing surround and depended on the magnitude on the hue difference between stimulus and surround. With increasing difference in hue between stimulus and surround, induced hue changes increased up to a maximum and then decreased for larger differences. This qualitative pattern was similar for different inducers, but quantitatively, induction was weaker along some directions in cone-opponent color space than along other directions. The strongest induction effects were found along an oblique, blue-yellow axis that corresponds to the daylight axis. The overall pattern of the induction effect shows similarities to the well-known tilt effect, where shifts in perceived angle of oriented stimuli are induced by oriented surrounds. This suggests analogous neural representations and similar mechanisms of contextual processing for different visual features such as orientation and color.

  8. Control of Formation of Lithological Reservoirs by Surrounding Mudstone

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    Taking the Jiyang depression as an example, this paper discusses the control of the formation of lithological reservoir by surrounding rocks by integrated application of geological analysis, physical simulation, and the analysis of oil & gas accumulation mechanism. Geological statistical shows that the major burial depth and interval of lithological reservoirs in the Jiyang depression are related to the hydrocarbon generation in and expulsion from the Lower Tertiary source rocks and the time of the formation of most lithological reservoirs coincides with the peak of hydrocarbon generation and expulsion. The lithological traps located in the center of effective source rocks are propitious to high oil saturation than those located on the margin of effective source rocks. The hydrocarbon charge degree of the lithological reservoir has a positive correlation with the intensity of hydrocarbon expulsion from surrounding source rocks.Geological analyses and NMR experiments also show that the oil saturation of surrounding source rocks control the hydrocarbon potential of lithological traps, and a critical value for oil saturation of surrounding mudstone is required, that is, when the oil saturation of surrounding mudstone is lower than this critical value, no oil and gas accumulate in the lithological trap. The control of surrounding mudstone on the oil-bearing properties of lithological reservoirs is also analyzed by the mechanisms of hydrocarbon generation and expulsion as well as accumulation.

  9. Asymmetric septal hypertrophy - a marker of hypertension in aortic stenosis (a SEAS substudy)

    DEFF Research Database (Denmark)

    Tuseth, Nora; Cramariuc, Dana; Rieck, Ashild E

    2010-01-01

    Some patients with aortic stenosis develop asymmetric septal hypertrophy (ASH) that may influence the surgical approach and is associated with higher perioperative morbidity. The aim of this analysis was to characterize further this subtype of aortic stenosis patients....

  10. Premature osteoarthritis of the knee associated with cartilage hypertrophy and phalangeal dysgenesis

    Energy Technology Data Exchange (ETDEWEB)

    Vital, E.M.J.; Hutton, C.W. [Derriford Hospital, Medical Directorate, Plymouth (United Kingdom); Hughes, P.M. [Derriford Hospital, Radiology Department, Plymouth (United Kingdom)

    2005-08-01

    A woman presented with premature knee osteoarthritis associated with marked femoral cartilage hypertrophy. She also exhibited phalangeal dysgenesis, suggesting this may be an unrecognised syndrome that may predispose to knee osteoarthritis. (orig.)

  11. Muscle memory and a new cellular model for muscle atrophy and hypertrophy

    National Research Council Canada - National Science Library

    Gundersen, Kristian

    2016-01-01

    .... This review describes a cellular memory in skeletal muscle in which hypertrophy is 'remembered' such that a fibre that has previously been large, but subsequently lost its mass, can regain mass faster than naive fibres...

  12. Terazosin versus alfuzosin in treatment of acute urinary retention in patients with benign prostatic hypertrophy

    National Research Council Canada - National Science Library

    Tang, HN; Lui, CT; Tsui, KL; Fung, HT

    2015-01-01

    Objective: To compare the efficacy and adverse reactions of terazosin and alfuzosin in treatment of acute urinary retention in patients with benign prostatic hypertrophy. Design: Case control study. Setting...

  13. Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation

    Institute of Scientific and Technical Information of China (English)

    Yong-nan FU; Han XIAO; Xiao-wei MA; Sheng-yang JIANG; Ming XU; You-yi ZHANG

    2011-01-01

    Aim: To identify the role of metformin in cardiac hypertrophy and investigate the possible mechanism underlying this effect.Methods: Wild type and AMPKα2 knockout (AMPKα2-/-) littermates were subjected to left ventricular pressure overload caused by evaluated using echocardiography and anatomic and histological methods. The antihypertrophic mechanism of metformin was analyzed using Western blotting.Results: Metformin significantly attenuated cardiac hypertrophy induced by pressure overload in wild type mice, but the antihypertrophic actions of metformin were ablated in AMPKx2-/- mice. Furthermore, metformin suppressed the phosphorylation of Akt/protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in response to pressure overload in wild type mice, but not in AMPKα2-/-mice.Conclusion: Long-term administration of metformin may attenuate cardiac hypertrophy induced by pressure overload in nondiabetic mice, and this attenuation is highly dependent on AMPK activation. These findings may provide a potential therapy for patients at risk of developing pathological cardiac hypertrophy.

  14. Hypertrophic cardiomyopathy: Prevalence, hypertrophy patterns, and their clinical and ECG findings in a hospital at Qatar

    Directory of Open Access Journals (Sweden)

    Sherif M Helmy

    2011-01-01

    Conclusion: The prevalence of HCM in our population group is 0.13% with a male predominance (12:1. There was a diversity of clinical presentation, ECG abnormalities and patterns of LV hypertrophy among HCM patients.

  15. Factors associated with diagnostic discrepancy for left ventricular hypertrophy between electrocardiography and echocardiography

    DEFF Research Database (Denmark)

    Sandager Petersen, Søren; Reinholdt Pedersen, Line; Pareek, Manan

    2017-01-01

    OBJECTIVE: To investigate the influence of cardiovascular risk factors, including fasting plasma glucose (FPG), on the association between electrocardiographic (ECG) and echocardiographic left ventricular hypertrophy (LVH) in an elderly population. METHODS: We tested cross-sectional associations...

  16. A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle.

    Science.gov (United States)

    Nishi, Masumi; Yasue, Akihiro; Nishimatu, Shinichirou; Nohno, Tsutomu; Yamaoka, Takashi; Itakura, Mitsuo; Moriyama, Keiji; Ohuchi, Hideyo; Noji, Sumihare

    2002-04-26

    Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle development in a dominant negative manner, we generated transgenic mice overexpressing the mutated gene. The transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In contrast, it has been reported that a myostatin mutated at its cleavage site produces hypertrophy without hyperplasia in the muscle. Thus, these results suggest that (1) the myostatin containing the missense mutation exhibits a dominant negative activity and that (2) there are two types in the dominant negative form of myostatin, causing either hypertrophy or hyperplasia.

  17. Impact of fasting glucose on electrocardiographic left ventricular hypertrophy in an elderly general population

    DEFF Research Database (Denmark)

    Diederichsen, Søren Z; Pareek, Manan; Nielsen, Mette L

    2015-01-01

    OBJECTIVE: To evaluate relationships between fasting plasma glucose (FPG), other cardiovascular risk markers and left ventricular hypertrophy (LVH) as detected by electrocardiography. METHODS: Subjects were selected randomly from groups defined by FPG. Traditional risk markers were assessed. LVH...

  18. Heterogeneity of capillary spacing in the hypertrophied plantaris muscle from young-adult and old rats.

    NARCIS (Netherlands)

    Degens, H.; Morse, C.I.; Hopman, M.T.E.

    2009-01-01

    Heterogeneity of capillary spacing may affect tissue oxygenation. The determinants of heterogeneity of capillary spacing are, however, unknown. To investigate whether 1) impaired angiogenesis and increased heterogeneity of capillary spacing delays development of hypertrophy during aging and 2)

  19. Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure

    Science.gov (United States)

    Experimental and clinical investigations have demonstrated that reactive oxygen species (ROS) production is increased during cardiac hypertrophy and heart failure. Excess ROS can directly impair cardiac contraction through modification of Ca2+ handling proteins or activate multiple effectors and sig...

  20. Isolated papillary muscle hypertrophy: A gap in our knowledge of hypertrophic cardiomyopathy?

    Science.gov (United States)

    Ferreira, Catarina; Delgado, Carlos; Vázquez, María; Trinidad, Carmen; Vilar, Manuel

    2014-06-01

    Increased thickness of left ventricular walls is the predominant characteristic and one of the diagnostic criteria of hypertrophic cardiomyopathy (HCM). This case illustrates an uncommon but important finding of isolated hypertrophy of the papillary muscles (PMs), observed in a young woman in whom an abnormal electrocardiogram was initially detected. During the investigation isolated PM hypertrophy was identified. The structural characteristics of the PMs have received scant attention in this setting and there is little information in the literature on this entity, whose real prevalence and clinical significance remain to be determined. The available information relates solitary PM hypertrophy with an early form or a different pattern of HCM. In this case PM hypertrophy was only detected due to the finding of an abnormal electrocardiogram, which prompted further diagnostic tests and a search for possible etiologies. Copyright © 2013 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.

  1. A Case of Painful Hemimasticatory Spasm with Masseter Muscle Hypertrophy Responsive to Botulinum Toxin

    Directory of Open Access Journals (Sweden)

    Jin-Hyuck Kim

    2009-10-01

    Full Text Available Hemimasticatory spasm (HMS is a rare disorder of the trigeminal nerve characterized by paroxysmal involuntary contractions of the unilateral jaw-closing muscles. HMS has been frequently described in association with facial hemiatrophy or localized scleroderma. A 42-year-old female presented with involuntary paroxysmal spasms of the left face, of 6 months duration. Her lower face on the left was markedly hypertrophied without skin lesions. An electrophysiological study indicated that the masseter reflexes and masseteric silent period were attenuated on the affected side. Surface electromyography demonstrated irregular bursts of motor unit potentials at high frequencies up to 200 Hz. Magnetic resonance imaging of the head showed marked hypertrophy of the left masseter muscle. Biopsy of the hypertrophied masseter muscle was normal. Repeated local injections of botulinum toxin noticeably reduced the size of the hypertrophied muscle as well as improved the patient’s symptoms.

  2. [Obstructive sleep apnea-hypopnea syndrome in children: beyond adenotonsillar hypertrophy].

    Science.gov (United States)

    Esteller, Eduard

    2015-01-01

    The prevalence of obstructive sleep apnea-hypopnea syndrome in the general childhood population is 1-2% and the most common cause is adenotonsillar hypertrophy. However, beyond adenotonsillar hypertrophy, there are other highly prevalent causes of this syndrome in children. The causes are often multifactorial and include muscular hypotonia, dentofacial abnormalities, soft tissue hypertrophy of the airway, and neurological disorders). Collaboration between different specialties involved in the care of these children is essential, given the wide variability of conditions and how frequently different factors are involved in their genesis, as well as the different treatments to be applied. We carried out a wide literature review of other causes of obstructive sleep apnea-hypopnea syndrome in children, beyond adenotonsillar hypertrophy. We organised the prevalence of this syndrome in each pathology and the reasons that cause it, as well as their interactions and management, in a consistent manner.

  3. Feature Hepatitis: The Dangers of Hepatitis: What you should know from A to E

    Science.gov (United States)

    ... Navigation Bar Home Current Issue Past Issues Feature Hepatitis The Dangers of Hepatitis: What you should know from A to E ... drugs. In some cases, hepatitis lasts a lifetime. Hepatitis: Acute or Chronic? Acute hepatitis is the initial ...

  4. Viral hepatitis and hepatitis B antigen: recent advances

    Science.gov (United States)

    Krugman, Saul

    1974-01-01

    Recent advances in hepatitis research have shed new light on the etiology, pathogenesis, epidemiology and prevention of type B hepatitis infection. The so-called ‘Dane’ particle is probably the complete hepatitis B virion; its outer coat is the hepatitis B (Australia) antigen (HB Ag) and its inner core is an immunologically distinct particle. Subtypes of HB Ag (a, d, y, w and r) are useful indices for epidemiological surveys. Concepts of epidemiology have changed: type B hepatitis is transmissible by contact as well as by inoculation. The presence of HB Ag in blood is indicative of the presence of hepatitis B virus. Tests to detect antigen and use of voluntary blood donors have played a major role in the decreased incidence of post transfusion hepatitis. A special hepatitis B gammaglobulin preparation and a heat-inactivated hepatitis B vaccine have proved to be effective in preliminary studies. PMID:4219230

  5. Hepatic microcirculatory disturbances in patients with chronic hepatitis B

    Institute of Scientific and Technical Information of China (English)

    郝菁华; 石军; 任万华; 韩国庆; 朱菊人; 王书运; 谢英渤

    2002-01-01

    Objective To document morphological changes in hepatic microcirculation in liver tissue with hepatitis B and the pathogenesis of hepatic microcirculatory disturbances. Methods Liver tissue samples were obtained from patients with hepatitis B by liver biopsy. These samples were examined with a light microscope and transmission electron microscope. Results Hepatic microcirculatory disturbances existed in patients with hepatitis B, including those with normal liver function, manifested by red blood cell aggregation in sinusoids seen under light microscope and sinusoidal capillarization seen under electron microscope. Weibel-Palade bodies in sinusoidal endothelial cells were seen in 26 out of 53 cases. Intimate contacts were found between lymphocyte/Kupffer cells and sinusoidal endothelial cells. Conclusions Hepatic microcirculatory disturbances exist in patients with hepatitis B .The appearance of Weibel-Palade bodies in sinusoidal endothelial cells may be a key step in the development of hepatic microcirculatory disturbances.

  6. Acute hepatitis due to brucellosis: case report

    Directory of Open Access Journals (Sweden)

    Nevil AYKIN

    2009-06-01

    Full Text Available Brucella infection is a systemic disease. It rarely causes local infections like hepatitis in gastrointestinal system. In this article we would like to present an acute hepatitis case related to brucella infection that followed up in our clinic. A male, 30 year-old patient hospitalized due to common muscle pain, high fever and vomiting. During the physical examination the patient’s skin, scleras and mucosal membranes were icteric, the liver was 2-3 cm palpable and tender. Laboratory findings were as follows: AST:1190 U/L; ALT:715 U/L; GGT:961 U/L; ALP:369 U/L; total bilirubin:4.6 mg/dL; direct bilirubin:2.1 mg/dL. Viral markers were found to be negative. We started treatment with streptomicine and doxicycline since, the patient’s standard brucella tube agglutination test was positive (1/60 and brucella spp produced in his blood culture. From the second day of the treatment, we started to get clinical response. On the 17th day of the treatment, he discharged from the hospital because ALT, AST and bilirubine level were found normal and his treatment was completed to the 8 weeks. Brucella is continuing to be an important health problem especially who live in surrounding countryside and have to keep in mind in the differential diagnosis of the acute hepatitis.

  7. Chronic high-fat diet-induced obesity decreased survival and increased hypertrophy of rats with experimental eccentric hypertrophy from chronic aortic regurgitation.

    Science.gov (United States)

    Dhahri, Wahiba; Drolet, Marie-Claude; Roussel, Elise; Couet, Jacques; Arsenault, Marie

    2014-09-24

    The composition of a diet can influence myocardial metabolism and development of left ventricular hypertrophy (LVH). The impact of a high-fat diet in chronic left ventricular volume overload (VO) causing eccentric LVH is unknown. This study examined the effects of chronic ingestion of a high-fat diet in rats with chronic VO caused by severe aortic valve regurgitation (AR) on LVH, function and on myocardial energetics and survival. Male Wistar rats were divided in four groups: Shams on control or high-fat (HF) diet (15 rats/group) and AR rats fed with the same diets (ARC (n = 56) and ARHF (n = 32)). HF diet was started one week before AR induction and the protocol was stopped 30 weeks later. As expected, AR caused significant LV dilation and hypertrophy and this was exacerbated in the ARHF group. Moreover, survival in the ARHF group was significantly decreased compared the ARC group. Although the sham animals on HF also developed significant obesity compared to those on control diet, this was not associated with heart hypertrophy. The HF diet in AR rats partially countered the expected shift in myocardial energy substrate preference usually observed in heart hypertrophy (from fatty acids towards glucose). Systolic function was decreased in AR rats but HF diet had no impact on this parameter. The response to HF diet of different fatty acid oxidation markers as well as the increase in glucose transporter-4 translocation to the plasma membrane compared to ARC was blunted in AR animals compared to those on control diet. HF diet for 30 weeks decreased survival of AR rats and worsened eccentric hypertrophy without affecting systolic function. The expected adaptation of myocardial energetics to volume-overload left ventricle hypertrophy in AR animals seemed to be impaired by the high-fat diet suggesting less metabolic flexibility.

  8. P38 mitogen-activated protein kinase pathways are involved in the hypertrophy and apoptosis of cardiomyocytes induced by Porphyromonas gingivalis conditioned medium.

    Science.gov (United States)

    Wu, Hsi-Chin; Yeh, Yu-Lan; Kuo, Wei-Wen; Huang, Shu-Kuei; Kuo, Wu-Hsien; Hsieh, Dennis Jine-Yuan; Wu, Ching-Lin; Tsai, Chang-Hai; Lee, Shin-Da; Huang, Chih-Yang

    2008-01-01

    The surrounding medium of periodontal pathogen Porphyromonas gingivalis (P. gingivalis) increased cardiomyocyte hypertrophy and apoptosis whereas Actinobaeillus actinomycetemcomitans and Prevotella intermedia had no effects. The purpose of this study is to clarify the role of p38 pathway in P. gingivalis conditioned medium-induced H9c2 myocardial cell hypertrophy and apoptosis. DNA fragmentation, cellular morphology, nuclear condensation, p38 protein products, and mitochondrial-dependent apoptotic related proteins in cultured H9c2 myocardial cell were measured by agarose gel electrophoresis, immunofluorescence, DAPI, and western blotting following P. gingivalis conditioned medium and/or pre-administration of SB203580 (p38 inhibitor). The p38 protein products and associated activities in H9c2 cells were both upregulated by P. gingivalis conditioned medium. P. gingivalis conditioned medium increased cellular sizes, DNA fragmentation, nuclear condensation, mitochondrial Bcl2-associated death promoter (Bad), cytosolic cytochrome c (cyt c), and the activated form of caspase-9 proteins in H9c2 cells. The increased cellular sizes, DNA fragmentation, nuclear condensation, Bad, cyt c, and caspase-9 activities of H9c2 cells treated with P. gingivalis conditioned medium were all significantly reduced after pre-administration of SB203580. Our findings suggest that the activity of p38 signal pathway may be initiated by P. gingivalis conditioned medium and further activate mitochondrial-dependent apoptotic pathways leading to cell death in cultured H9c2 myocardial cells.

  9. Lower facial remodeling with botulinum toxin type A for the treatment of masseter hypertrophy*

    OpenAIRE

    Klein,Fernanda Homem de Mello de Souza; Brenner,Fabiane Mulinari; Sato,Maurício Shigeru; Robert,Fernanda Manfron Batista Rosas; Helmer, Karin Adriane

    2014-01-01

    BACKGROUND: Masseter hypertrophy has been treated with botulinum toxin injections because of esthetic complaints especially in Asians. OBJECTIVES: The goal of the present study was to evaluate the efficacy of abobotulin toxin use in masseter hipertrophy treatment in Brazilians. METHODS: Ten Brazilian female patients with masseter hypertrophy were subjected to injections of 90U of abobotulinum toxin A applied on each side respecting the safety zone stabilished in literature and were followed u...

  10. Calhex231 Ameliorates Cardiac Hypertrophy by Inhibiting Cellular Autophagy in Vivo and in Vitro

    Directory of Open Access Journals (Sweden)

    Lei Liu

    2015-07-01

    Full Text Available Background/Aims: Intracellular calcium concentration ([Ca2+]i homeostasis, an initial factor of cardiac hypertrophy, is regulated by the calcium-sensing receptor (CaSR and is associated with the formation of autolysosomes. The aim of this study was to investigate the role of Calhex231, a CaSR inhibitor, on the hypertrophic response via autophagy modulation. Methods: Cardiac hypertrophy was induced by transverse aortic constriction (TAC in 40 male Wistar rats, while 10 rats underwent a sham operation and served as controls. Cardiac function was monitored by transthoracic echocardiography, and the hypertrophy index was calculated. Cardiac tissue was stained with hematoxylin and eosin (H&E or Masson's trichrome reagent and examined by transmission electron microscopy. An angiotensin II (Ang II-induced cardiomyocyte hypertrophy model was established and used to test the involvement of active molecules. Intracellular calcium concentration ([Ca2+]i was determined by the introduction of Fluo-4/AM dye followed by confocal microscopy. The expression of various active proteins was analyzed by western blot. Results: The rats with TAC-induced hypertrophy had an increased heart size, ratio of heart weight to body weight, myocardial fibrosis, and CaSR and autophagy levels, which were suppressed by Calhex231. Experimental results using Ang II-induced hypertrophic cardiomyocytes confirmed that Calhex231 suppressed CaSR expression and downregulated autophagy by inhibiting the Ca2+/calmodulin-dependent-protein kinase-kinase-β (CaMKKβ- AMP-activated protein kinase (AMPK-mammalian target of rapamycin (mTOR pathway to ameliorate cardiomyocyte hypertrophy. Conclusions: Calhex231 ameliorates myocardial hypertrophy induced by pressure-overload or Ang II via inhibiting CaSR expression and autophagy. Our results may support the notion that Calhex231 can become a new therapeutic agent for the treatment of cardiac hypertrophy.

  11. Haemochromatosis genotype and iron overload: association with hypertension and left ventricular hypertrophy

    DEFF Research Database (Denmark)

    Ellervik, C; Tybjaerg-Hansen, A; Appleyard, M

    2010-01-01

    We hypothesized that there is an association between haemochromatosis genotype C282Y/C282Y and/or iron overload and risk of hypertension and/or left ventricular hypertrophy (LVH).......We hypothesized that there is an association between haemochromatosis genotype C282Y/C282Y and/or iron overload and risk of hypertension and/or left ventricular hypertrophy (LVH)....

  12. Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants

    OpenAIRE

    Fernandes, T.; Soci, U.P.R.; E.M. Oliveira

    2011-01-01

    Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of th...

  13. UCH-L1 induces podocyte hypertrophy in membranous nephropathy by protein accumulation.

    Science.gov (United States)

    Lohmann, Frithjof; Sachs, Marlies; Meyer, Tobias N; Sievert, Henning; Lindenmeyer, Maja T; Wiech, Thorsten; Cohen, Clemens D; Balabanov, Stefan; Stahl, R A K; Meyer-Schwesinger, Catherine

    2014-07-01

    Podocytes are terminally differentiated cells of the glomerular filtration barrier that react with hypertrophy in the course of injury such as in membranous nephropathy (MGN). The neuronal deubiquitinase ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed and activated in podocytes of human and rodent MGN. UCH-L1 regulates the mono-ubiquitin pool and induces accumulation of poly-ubiquitinated proteins in affected podocytes. Here, we investigated the role of UCH-L1 in podocyte hypertrophy and in the homeostasis of the hypertrophy associated "model protein" p27(Kip1). A better understanding of the basic mechanisms leading to podocyte hypertrophy is crucial for the development of specific therapies in MGN. In human and rat MGN, hypertrophic podocytes exhibited a simultaneous up-regulation of UCH-L1 and of cytoplasmic p27(Kip1) content. Functionally, inhibition of UCH-L1 activity and knockdown or inhibition of UCH-L1 attenuated podocyte hypertrophy by decreasing the total protein content in isolated glomeruli and in cultured podocytes. In contrast, UCH-L1 levels and activity increased podocyte hypertrophy and total protein content in culture, specifically of cytoplasmic p27(Kip1). UCH-L1 enhanced cytoplasmic p27(Kip1) levels by nuclear export and decreased poly-ubiquitination and proteasomal degradation of p27(Kip1). In parallel, UCH-L1 increased podocyte turnover, migration and cytoskeletal rearrangement, which are associated with known oncogenic functions of cytoplasmic p27(Kip1) in cancer. We propose that UCH-L1 induces podocyte hypertrophy in MGN by increasing the total protein content through altered degradation and accumulation of proteins such as p27(Kip1) in the cytoplasm of podocytes. Modification of both UCH-L1 activity and levels could be a new therapeutic avenue to podocyte hypertrophy in MGN. Copyright © 2014 Elsevier B.V. All rights reserved.

  14. Asymmetric septal hypertrophy - a marker of hypertension in aortic stenosis (a SEAS substudy)

    DEFF Research Database (Denmark)

    Tuseth, Nora; Cramariuc, Dana; Rieck, Ashild E

    2010-01-01

    Some patients with aortic stenosis develop asymmetric septal hypertrophy (ASH) that may influence the surgical approach and is associated with higher perioperative morbidity. The aim of this analysis was to characterize further this subtype of aortic stenosis patients.......Some patients with aortic stenosis develop asymmetric septal hypertrophy (ASH) that may influence the surgical approach and is associated with higher perioperative morbidity. The aim of this analysis was to characterize further this subtype of aortic stenosis patients....

  15. MicroRNA-297 promotes cardiomyocyte hypertrophy via targeting sigma-1 receptor.

    Science.gov (United States)

    Bao, Qinxue; Zhao, Mingyue; Chen, Li; Wang, Yu; Wu, Siyuan; Wu, Wenchao; Liu, Xiaojing

    2017-04-15

    Sigma-1 receptor (Sig-1R) is a ligand-regulated endoplasmic reticulum (ER) chaperone involved in cardiac hypertrophy, but it is not known whether Sig-1R is regulated by microRNAs (miRNAs). According to bioinformatic analysis, miR-297 was suggested as a potential target miRNA for Sig-1R. Therefore, we verified whether miR-297 could target Sig-1R and investigated the possible mechanisms underlying the role of miR-297 in cardiac hypertrophy. Bioinformatic analysis combined with laboratory experiments, including quantitative RT-PCR, Western blotting, and luciferase assay, were performed to identify the target miRNA of Sig-1R. Transverse aortic constriction (TAC) model and neonatal rat cardiomyocytes (NCMs) stimulated with angiotensin II (AngII) were used to explore the relationship between miR-297 and Sig-1R. Additionally, the function of miR-297 in cardiomyocyte hypertrophy and ER stress/unfolded protein response (UPR) signaling pathway was investigated by transfecting miR-297 mimics/inhibitor. miR-297 levels were increased in both TAC-induced hypertrophic heart tissue and AngII-induced cardiomyocyte hypertrophy. Up-regulation of miR-297 by specific mimics exacerbated AngII-induced cardiomyocyte hypertrophy, whereas inhibition of miR-297 suppressed the process. During cardiomyocyte hypertrophy, Sig-1R expression, which was negatively regulated by miR-297 by directly targeting its 3'untranslated region (UTR), was decreased. Furthermore, attenuation of miR-297 inhibited the activation of X-box binding protein 1 (Xbp1) and activating transcriptional factor 4 (ATF4) signaling pathways in NCMs. Our data demonstrate that miR-297 promotes cardiomyocyte hypertrophy by inhibiting the expression of Sig-1R and activation of ER stress signaling, which provides a novel interpretation for cardiac hypertrophy. Copyright © 2017 Elsevier Inc. All rights reserved.

  16. Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

    OpenAIRE

    Olivetti, G; R. Ricci; Anversa, P.

    1987-01-01

    In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic...

  17. Testicular compensatory hypertrophy in the unilaterally adrenalectomized lizard Mabuya carinata (Schn.).

    Science.gov (United States)

    Yajurvedi, H N; Chandramohan, K

    1994-05-15

    Unilateral adrenalectomy in recrudescent and breeding phases of the reproductive cycle caused atrophic changes in the ipsilateral testis, shown by inhibition of spermatogenic and steroidogenic activity of the ipsilateral testis. The contralateral testis showed compensatory hypertrophy. Unilateral adrenalectomy in regressing and quiescent phases of the reproductive cycle did not induce compensatory hypertrophy in the contralateral testis although there were atrophic changes in the ipsilateral testis.

  18. Angiotensin II-induced cardiac hypertrophy and fibrosis are promoted in mice lacking Fgf16

    OpenAIRE

    Matsumoto, Emi; Sasaki, Sayaka; Kinoshita, Hideyuki; Kito, Takuya; Ohta, Hiroya; Konishi, Morichika; Kuwahara, Koichiro; Nakao, Kazuwa; Itoh, Nobuyuki

    2013-01-01

    Fibroblast growth factors (Fgfs) are pleiotropic proteins involved in development, repair and metabolism. Fgf16 is predominantly expressed in the heart. However, as the heart function is essentially normal in Fgf16 knockout mice, its role has remained unclear. To elucidate the pathophysiological role of Fgf16 in the heart, we examined angiotensin II-induced cardiac hypertrophy and fibrosis in Fgf16 knockout mice. Angiotensin II-induced cardiac hypertrophy and fibrosis were significantly promo...

  19. Left ventricular hypertrophy in children, adolescents and young adults with sickle cell anemia

    Directory of Open Access Journals (Sweden)

    Gustavo Baptista de Almeida Faro

    2015-10-01

    Full Text Available OBJECTIVE: The aims of this study were to estimate the frequency of left ventricular hypertrophy and to identify variables associated with this condition in under 25-year-old patients with sickle cell anemia.METHODS: A cross-sectional study was performed of children, adolescents and young adults with sickle cell anemia submitted to a transthoracic Doppler echocardiography. The mass of the left ventricle was determined by the formula of Devereux et al. with correction for height, and the percentile curves of gender and age were applied. Individuals with rheumatic and congenital heart disease were excluded. The patients were divided into two groups according to the presence or absence of left ventricular hypertrophy and compared according to clinical, echocardiographic and laboratory variables.RESULTS: A total of 37.6% of the patients had left ventricular hypertrophy in this sample. There was no difference between the groups of patients with and without hypertrophy according to pathological history or clinical characteristics, except possibly for the use of hydroxyurea, more often used in the group without left ventricular hypertrophy. Patients with left ventricular hypertrophy presented larger left atria and lower hemoglobin and hematocrit levels, reticulocyte index and a higher albumin:creatinine ratio in urine.CONCLUSION: Left ventricular hypertrophy was observed in more than one-third of the young patients with sickle cell anemia with this finding being inversely correlated to the hemoglobin and hematocrit levels, and reticulocyte index and directly associated to a higher albumin/creatinine ratio. It is possible that hydroxyurea had had a protective effect on the development of left ventricular hypertrophy.

  20. Ubiquitin-Specific Protease 4 Is an Endogenous Negative Regulator of Pathological Cardiac Hypertrophy.

    Science.gov (United States)

    He, Ben; Zhao, Yi-Chao; Gao, Ling-Chen; Ying, Xiao-Ying; Xu, Long-Wei; Su, Yuan-Yuan; Ji, Qing-Qi; Lin, Nan; Pu, Jun

    2016-06-01

    Dysregulation of the ubiquitin proteasome system components ubiquitin ligases and proteasome plays an important role in the pathogenesis of cardiac hypertrophy. However, little is known about the role of another ubiquitin proteasome system component, the deubiquitinating enzymes, in cardiac hypertrophy. Here, we revealed a crucial role of ubiquitin specific protease 4 (USP4), a deubiquitinating enzyme prominently expressed in the heart, in attenuating pathological cardiac hypertrophy and dysfunction. USP4 levels were consistently decreased in human failing hearts and in murine hypertrophied hearts. Adenovirus-mediated gain- and loss-of-function approaches indicated that deficiency of endogenous USP4 promoted myocyte hypertrophy induced by angiotensin II in vitro, whereas restoration of USP4 significantly attenuated the prohypertrophic effect of angiotensin II. To corroborate the role of USP4 in vivo, we generated USP4 global knockout mice and mice with cardiac-specific overexpression of USP4. Consistent with the in vitro study, USP4 depletion exacerbated the hypertrophic phenotype and cardiac dysfunction in mice subjected to pressure overload, whereas USP4 transgenic mice presented ameliorated pathological cardiac hypertrophy compared with their control littermates. Molecular analysis revealed that USP4 deficiency augmented the activation of the transforming growth factor β-activated kinase 1 (TAK1)-(JNK1/2)/P38 signaling in response to hypertrophic stress, and blockage of TAK1 activation abolished the pathological effects of USP4 deficiency in vivo. These findings provide the first evidence for the involvement of USP4 in cardiac hypertrophy, and shed light on the therapeutic potential of targeting USP4 in the treatment of cardiac hypertrophy.

  1. Beneficial effect of isradipine on the development of left ventricular hypertrophy in mild hypertension

    DEFF Research Database (Denmark)

    Mehlsen, J; Fornitz, Gitte Gleerup; Haedersdal, C

    1993-01-01

    The objective of this study was to analyze the long-term hemodynamic effects of the calcium antagonist isradipine in mild hypertension compared with those of the beta 1-selective adrenoceptor antagonist atenolol, focusing in particular on the development of cardiac hypertrophy. Ten male patients...... with isradipine (254 +/- 55 g). The results indicate that antihypertensive treatment with isradipine as monotherapy may prevent the development of left ventricular hypertrophy whereas treatment with atenolol as monotherapy does not appear to offer this possibility....

  2. Calhex₂₃₁ Ameliorates Cardiac Hypertrophy by Inhibiting Cellular Autophagy in Vivo and in Vitro.

    Science.gov (United States)

    Liu, Lei; Wang, Chao; Sun, Dianjun; Jiang, Shuangquan; Li, Hong; Zhang, Weihua; Zhao, Yajun; Xi, Yuhui; Shi, Sa; Lu, Fanghao; Tian, Ye; Xu, Changqing; Wang, Lina

    2015-01-01

    Intracellular calcium concentration ([Ca2+]i) homeostasis, an initial factor of cardiac hypertrophy, is regulated by the calcium-sensing receptor (CaSR) and is associated with the formation of autolysosomes. The aim of this study was to investigate the role of Calhex231, a CaSR inhibitor, on the hypertrophic response via autophagy modulation. Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in 40 male Wistar rats, while 10 rats underwent a sham operation and served as controls. Cardiac function was monitored by transthoracic echocardiography, and the hypertrophy index was calculated. Cardiac tissue was stained with hematoxylin and eosin (H&E) or Masson’s trichrome reagent and examined by transmission electron microscopy. An angiotensin II (Ang II)-induced cardiomyocyte hypertrophy model was established and used to test the involvement of active molecules. Intracellular calcium concentration ([Ca2+]i) was determined by the introduction of Fluo-4/AM dye followed by confocal microscopy. The expression of various active proteins was analyzed by western blot. The rats with TAC-induced hypertrophy had an increased heart size, ratio of heart weight to body weight, myocardial fibrosis, and CaSR and autophagy levels, which were suppressed by Calhex231. Experimental results using Ang II-induced hypertrophic cardiomyocytes confirmed that Calhex231 suppressed CaSR expression and downregulated autophagy by inhibiting the Ca2+/calmodulin-dependent-protein kinase-kinase-β (CaMKKβ)– AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway to ameliorate cardiomyocyte hypertrophy. Calhex231 ameliorates myocardial hypertrophy induced by pressure-overload or Ang II via inhibiting CaSR expression and autophagy. Our results may support the notion that Calhex231 can become a new therapeutic agent for the treatment of cardiac hypertrophy. © 2015 S. Karger AG, Basel.

  3. Cardiac-Specific EPI64C Blunts Pressure Overload-Induced Cardiac Hypertrophy.

    Science.gov (United States)

    Zhu, Xuehai; Fang, Jing; Gong, Jun; Guo, Jun-Hong; Zhao, Guang-Nian; Ji, Yan-Xiao; Liu, Hong-Yun; Wei, Xiang; Li, Hongliang

    2016-05-01

    The calcium-responsive molecule, calcineurin, has been well characterized to play a causal role in pathological cardiac hypertrophy over the past decade. However, the intrinsic negative regulation of calcineurin signaling during the progression of cardiomyocyte hypertrophy remains enigmatic. Herein, we explored the role of EPI64C, a dual inhibitor of both Ras and calcineurin signaling during T-cell activation, in pressure overload-induced cardiac hypertrophy. We generated a cardiac-specific Epi64c conditional knockout mouse strain and showed that loss of Epi64c remarkably exacerbates pressure overload-induced cardiac hypertrophy. In contrast, EPI64C gain-of-function in cardiomyocyte-specific Epi64c transgenic mice exerts potent protective effects against cardiac hypertrophy. Mechanistically, the cardioprotective effects of EPI64C are largely attributed to the disrupted calcineurin signaling but are independent of its Ras suppressive capability. Molecular studies have indicated that the 406 to 446 C-terminal amino acids in EPI64C directly bind to the 287 to 337 amino acids in the catalytic domain of calcineurin, which is responsible for the EPI64C-mediated suppressive effects. We further extrapolated our studies to cynomolgus monkeys and showed that gene therapy based on lentivirus-mediated EPI64C overexpression in the monkey hearts blunted pressure overload-induced cardiac hypertrophy. Our study thus identified EPI64C as a novel negative regulator in cardiac hypertrophy by targeting calcineurin signaling and demonstrated the potential of gene therapy and drug development for treating cardiac hypertrophy. © 2016 American Heart Association, Inc.

  4. miR-206 Mediates YAP-Induced Cardiac Hypertrophy and Survival.

    Science.gov (United States)

    Yang, Yanfei; Del Re, Dominic P; Nakano, Noritsugu; Sciarretta, Sebastiano; Zhai, Peiyong; Park, Jiyeon; Sayed, Danish; Shirakabe, Akihiro; Matsushima, Shoji; Park, Yongkyu; Tian, Bin; Abdellatif, Maha; Sadoshima, Junichi

    2015-10-23

    In Drosophila, the Hippo signaling pathway negatively regulates organ size by suppressing cell proliferation and survival through the inhibition of Yorkie, a transcriptional cofactor. Yes-associated protein (YAP), the mammalian homolog of Yorkie, promotes cardiomyocyte growth and survival in postnatal hearts. However, the underlying mechanism responsible for the beneficial effect of YAP in cardiomyocytes remains unclear. We investigated whether miR-206, a microRNA known to promote hypertrophy in skeletal muscle, mediates the effect of YAP on promotion of survival and hypertrophy in cardiomyocytes. Microarray analysis indicated that YAP increased miR-206 expression in cardiomyocytes. Increased miR-206 expression induced cardiac hypertrophy and inhibited cell death in cultured cardiomyocytes, similar to that of YAP. Downregulation of endogenous miR-206 in cardiomyocytes attenuated YAP-induced cardiac hypertrophy and survival, suggesting that miR-206 plays a critical role in mediating YAP function. Cardiac-specific overexpression of miR-206 in mice induced hypertrophy and protected the heart from ischemia/reperfusion injury, whereas suppression of miR-206 exacerbated ischemia/reperfusion injury and prevented pressure overload-induced cardiac hypertrophy. miR-206 negatively regulates Forkhead box protein P1 expression in cardiomyocytes and overexpression of Forkhead box protein P1 attenuated miR-206-induced cardiac hypertrophy and survival, suggesting that Forkhead box protein P1 is a functional target of miR-206. YAP increases the abundance of miR-206, which in turn plays an essential role in mediating hypertrophy and survival by silencing Forkhead box protein P1 in cardiomyocytes. © 2015 American Heart Association, Inc.

  5. Whey protein hydrolysate augments tendon and muscle hypertrophy independent of resistance exercise contraction mode

    DEFF Research Database (Denmark)

    Farup, Jean; Rahbek, S K; Vendelbo, M H

    2014-01-01

    In a comparative study, we investigated the effects of maximal eccentric or concentric resistance training combined with whey protein or placebo on muscle and tendon hypertrophy. 22 subjects were allocated into either a high-leucine whey protein hydrolysate + carbohydrate group (WHD...... or contraction mode effects. In conclusion, high-leucine whey protein hydrolysate augments muscle and tendon hypertrophy following 12 weeks of resistance training – irrespective of contraction mode....

  6. The metabolic and temporal basis of muscle hypertrophy in response to resistance exercise.

    Science.gov (United States)

    Brook, Matthew S; Wilkinson, Daniel J; Smith, Kenneth; Atherton, Philip J

    2016-09-01

    Constituting ∼40% of body mass, skeletal muscle has essential locomotory and metabolic functions. As such, an insight into the control of muscle mass is of great importance for maintaining health and quality-of-life into older age, under conditions of cachectic disease and with rehabilitation. In healthy weight-bearing individuals, muscle mass is maintained by the equilibrium between muscle protein synthesis (MPS) and muscle protein breakdown; when this balance tips in favour of MPS hypertrophy occurs. Despite considerable research into pharmacological/nutraceutical interventions, resistance exercise training (RE-T) remains the most potent stimulator of MPS and hypertrophy (in the majority of individuals). However, the mechanism(s) and time course of hypertrophic responses to RE-T remain poorly understood. We would suggest that available data are very much in favour of the notion that the majority of hypertrophy occurs in the early phases of RE-T (though still controversial to some) and that, for the most part, continued gains are hard to come by. Whilst the mechanisms of muscle hypertrophy represent the culmination of mechanical, auto/paracrine and endocrine events, the measurement of MPS remains a cornerstone for understanding the control of hypertrophy - mainly because it is the underlying driving force behind skeletal muscle hypertrophy. Development of sophisticated isotopic techniques (i.e. deuterium oxide) that lend to longer term insight into the control of hypertrophy by sustained RE-T will be paramount in providing insights into the metabolic and temporal regulation of hypertrophy. Such technologies will have broad application in muscle mass intervention for both athletes and for mitigating disease/age-related cachexia and sarcopenia, alike.

  7. Negative feedback regulation of Homer 1a on norepinephrine-dependent cardiac hypertrophy

    Energy Technology Data Exchange (ETDEWEB)

    Chiarello, Carmelina; Bortoloso, Elena; Carpi, Andrea; Furlan, Sandra; Volpe, Pompeo, E-mail: pompeo.volpe@unipd.it

    2013-07-15

    Homers are scaffolding proteins that modulate diverse cell functions being able to assemble signalling complexes. In this study, the presence, sub-cellular distribution and function of Homer 1 was investigated. Homer 1a and Homer 1b/c are constitutively expressed in cardiac muscle of both mouse and rat and in HL-1 cells, a cardiac cell line. As judged by confocal immunofluorescence microscopy, Homer 1a displays sarcomeric and peri-nuclear localization. In cardiomyocytes and cultured HL-1 cells, the hypertrophic agonist norepinephrine (NE) induces α{sub 1}-adrenergic specific Homer 1a over-expression, with a two-to-three-fold increase within 1 h, and no up-regulation of Homer 1b/c, as judged by Western blot and qPCR. In HL-1 cells, plasmid-driven over-expression of Homer 1a partially antagonizes activation of ERK phosphorylation and ANF up-regulation, two well-established, early markers of hypertrophy. At the morphometric level, NE-induced increase of cell size is likewise and partially counteracted by exogenous Homer 1a. Under the same experimental conditions, Homer 1b/c does not have any effect on ANF up-regulation nor on cell hypertrophy. Thus, Homer 1a up-regulation is associated to early stages of cardiac hypertrophy and appears to play a negative feedback regulation on molecular transducers of hypertrophy. -- Highlights: • Homer 1a is constitutively expressed in cardiac tissue. • In HL-1 cells, norepinephrine activates signaling pathways leading to hypertrophy. • Homer 1a up-regulation is an early event of norepinephrine-induced hypertrophy. • Homer 1a plays a negative feedback regulation modulating pathological hypertrophy. • Over-expression of Homer 1a per se does not induce hypertrophy.

  8. Atopy does not affect the frequency of adenotonsillar hypertrophy and sleep apnoea in children who snore.

    Science.gov (United States)

    Alexopoulos, Emmanouel I; Bizakis, John; Gourgoulianis, Konstantinos; Kaditis, Athanasios G

    2014-12-01

    Viral respiratory infections and atopy have been implicated in the pathogenesis of adenotonsillar hypertrophy and obstructive sleep apnoea (OSA), but the role of atopy is controversial. We aimed to test our hypothesis that atopy, expressed as physician-diagnosed eczema, was associated with adenotonsillar hypertrophy and OSA among children who snored. Data on children who snored and were referred for polysomnography were reviewed. The primary outcome measures were adenotonsillar hypertrophy and OSA. We analysed data on 855 children with a mean age (±standard deviation) of 6.3 (±2.5) years and median obstructive apnoea-hypopnea index of 2.1 episodes per hour. Of the 855 subjects, 133 (15.6%) had physician-diagnosed eczema, 591 (69.1%) had adenoidal hypertrophy, 605 (70.8%) had tonsillar hypertrophy, 219 (25.6%) were obese and 470 (55%) had OSA. Eczema was not related to adenoidal or tonsillar hypertrophy after adjustment for gender and age, with odds ratios (OR) of 1.00 (95% confidence interval 0.67-1.49; p = 0.98) and 0.88 (95% confidence interval 0.59-1.32; p = 0.54), respectively. Similarly, eczema did not affect OSA frequency after adjustment for adenoidal and tonsillar hypertrophy, obesity, gender and age, with an adjusted OR of 0.82 (0.56-1.21; p = 0.32). Atopy was not related to adenotonsillar hypertrophy or OSA in children who snore. ©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

  9. Health-related quality of life among children with adenoid hypertrophy in Xi'an, China.

    Science.gov (United States)

    Jiang, Xun; Ren, Xiaoyong; Liu, Haiqin; Tian, Jiao; Du, Chunyan; Luo, Huanan; Cheng, Ying; Shang, Lei

    2015-12-01

    The aim of this study was to investigate the health-related quality of life (HRQOL) in 5-7-year-old children diagnosed with adenoid hypertrophy and the impact of adenoid hypertrophy on affected families. This is a cross-sectional case-control study evaluating 5-7-year-old children with adenoid hypertrophy (n=195), 5-7-year-old healthy children (n=156), and associated caregivers (parents and/or grandparents). A Chinese version of the PedsQL™ 4.0 Generic Core Scale was used to assess childhood HRQOL, and a Chinese version of the Family Impact Module (FIM) was used to assess the impact of adenoid hypertrophy on family members. HRQOL scores were compared between the children with adenoid hypertrophy and healthy children. In addition, a multiple step-wise regression with demographic variables of children and their caregivers, family economic status, and caregiver's HRQOL as independent variables were referenced to determine the factors that may influence HRQOL in children with adenoid hypertrophy. Children with adenoid hypertrophy showed significantly lower physical, emotional, social, and school functioning scores than healthy children (phypertrophy also scored significantly lower than caregivers for healthy children on physical, emotional, social, cognitive, and communication functioning (phypertrophy-affected children also exhibited significantly higher levels of worry than healthy children (phypertrophy (phypertrophy were associated with lower HRQOL in both children and their caregivers, and may negatively influence family functioning. In addition, caregivers' social characteristics may also significantly affect the HRQOL in children with adenoid hypertrophy. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  10. Evaluation of carotid intima-media thickness and carotid arterial stiffness in children with adenotonsillar hypertrophy.

    Science.gov (United States)

    Çiftel, Murat; Demir, Berrin; Kozan, Günay; Yılmaz, Osman; Kahveci, Hasan; Kılıç, Ömer

    2016-02-01

    Adenotonsillar hypertrophy can produce cardiopulmonary disease in children. However, it is unclear whether adenotonsillar hypertrophy causes atherosclerosis. This study evaluated carotid intimamedia thickness and carotid arterial stiffness in children with adenotonsillar hypertrophy. The study included 40 children with adenotonsillar hypertrophy (age: 5-10 years) and 36 healthy children with similar age and body mass index. Systolic blood pressure, diastolic blood pressure, and pulse pressure were measured in all subjects. Carotid intima-media thickness, carotid arterial systolic diameter, and carotid arterial diastolic diameter were measured using a high-resolution ultrasound device. Based on these measurements, carotid arterial strain, carotid artery distensibility, beta stiffness index, and elasticity modulus were calculated. Carotid intima-media thickness was greater in children with adenotonsillar hypertrophy (0.36±0.05 mm vs. 0.34±0.04 mm, P=0.02) compared to healthy controls. Beta stiffness index (3.01±1.22 vs. 2.98±0.98, P=0.85), elasticity modulus (231.39±99.23 vs. 226.46±83.20, P=0.88), carotid arterial strain (0.17±0.06 vs. 0.17±0.04, P=0.95), and carotid artery distensibility (13.14±3.88 vs. 12.92±3.84, P=0.75) were similar between children with adenotonsillar hypertrophy and the healthy controls. The present study revealed increased carotid intima-media thickness in children with adenotonsillar hypertrophy. The risk of subclinical atherosclerosis may be higher in children with adenotonsillar hypertrophy.

  11. Relative Etiological Importance of Adenoid Hypertrophy Versus Sinusitis in Children with Persistent Rhinorrhoea

    OpenAIRE

    Maheswaran, S; Rupa, V.; Ebenezer, Jareen; Manoharan, Anand; Irodi, Aparna

    2014-01-01

    Persistent rhinorrhoea is a common, yet often neglected, problem among Indian children. This study was designed to evaluate the relative etiological importance of adenoid hypertrophy versus sinusitis in children with persistent rhinorrhea. Additionally, the association between S. pneumoniae colonization and adenoid hypertrophy was studied. Children aged 1–14 years with persistent rhinorrhea underwent clinical evaluation, rigid nasal endoscopy and xrays of the nasopharynx and paranasal sinuses...

  12. Concordance of Lateral Radiological Measurements and Quality of Life in Adenoid Hypertrophy

    OpenAIRE

    Ziya Salturk

    2013-01-01

    Aim: The aim of the study is to investigate the relationship between lateral radiological measurements and quality of life in children with adenoid hypertrophy. Material and Method: 22 children with adenoid hypertrophy were included in study. Survey obstructive sleep apnea 18 was used to assess the quality of life. Adenoid nasopharynx ratio was used to asses lateral radiological measurements. Results were analyzed statistically. Results: The mean value of obstructive sleep apnea 18 survey was...

  13. Forest Fragments Surrounded by Sugar Cane Are More Inhospitable to Terrestrial Amphibian Abundance Than Fragments Surrounded by Pasture

    Directory of Open Access Journals (Sweden)

    Paula Eveline Ribeiro D’Anunciação

    2013-01-01

    Full Text Available In recent years, there has been increasing interest in matrix-type influence on forest fragments. Terrestrial amphibians are good bioindicators for this kind of research because of low vagility and high philopatry. This study compared richness, abundance, and species composition of terrestrial amphibians through pitfall traps in two sets of semideciduous seasonal forest fragments in southeastern Brazil, according to the predominant surrounding matrix (sugar cane and pasture. There were no differences in richness, but fragments surrounded by sugar cane had the lowest abundance of amphibians, whereas fragments surrounded by pastures had greater abundance. The most abundant species, Rhinella ornata, showed no biometric differences between fragment groups but like many other amphibians sampled showed very low numbers of individuals in fragments dominated by sugar cane fields. Our data indicate that the sugar cane matrix negatively influences the community of amphibians present in fragments surrounded by this type of land use.

  14. Minimal hepatic encephalopathy.

    Science.gov (United States)

    Zamora Nava, Luis Eduardo; Torre Delgadillo, Aldo

    2011-06-01

    The term minimal hepatic encephalopathy (MHE) refers to the subtle changes in cognitive function, electrophysiological parameters, cerebral neurochemical/neurotransmitter homeostasis, cerebral blood flow, metabolism, and fluid homeostasis that can be observed in patients with cirrhosis who have no clinical evidence of hepatic encephalopathy; the prevalence is as high as 84% in patients with hepatic cirrhosis. Physician does generally not perceive cirrhosis complications, and neuropsychological tests and another especial measurement like evoked potentials and image studies like positron emission tomography can only make diagnosis. Diagnosis of minimal hepatic encephalopathy may have prognostic and therapeutic implications in cirrhotic patients. The present review pretends to explore the clinic, therapeutic, diagnosis and prognostic aspects of this complication.

  15. Hepatitis A - children

    Science.gov (United States)

    ... fulminant hepatitis (liver failure) is rare in healthy children. The symptoms are often easy to manage and include: Dark urine Tiredness Loss of appetite Fever Nausea and vomiting Pale stools Abdominal pain ( ...

  16. Human hereditary hepatic porphyrias.

    Science.gov (United States)

    Nordmann, Yves; Puy, Hervé

    2002-11-01

    The human hereditary hepatic porphyrias are diseases due to marked deficiencies of enzymes in the heme biosynthetic pathway. Porphyrias can be classified as either hepatic or erythroid, depending on the major production site of porphyrins or their precursors. The pathogenesis of inherited hepatic porphyrias has now been defined at the molecular level. Some gene carriers are vulnerable to a range of exogenous and endogenous factors, which may trigger neuropsychiatric and/or cutaneous symptoms. Early diagnosis is of prime importance since it makes way for counselling. In this article we present an overview of recent advances on hepatic porphyrias: 5-aminolevulinic acid dehydratase deficiency porphyria, acute intermittent porphyria (AIP), porphyria cutanea tarda (PCT), hereditary coproporphyria (HC), and variegate porphyria (VP).

  17. Imaging of hepatic infections

    Energy Technology Data Exchange (ETDEWEB)

    Doyle, D.J. [Department of Medical Imaging, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ont. (Canada)]. E-mail: doyledj@hotmail.com; Hanbidge, A.E. [Department of Medical Imaging, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ont. (Canada); O' Malley, M.E. [Department of Medical Imaging, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ont. (Canada)

    2006-09-15

    Imaging plays a significant role in the detection, characterization and treatment of hepatic infections. Infectious diseases of the liver include pyogenic and amoebic abscesses and parasitic, fungal, viral and granulomatous infections. With increases in worldwide travel, immunosuppression and changing population demographics, identification of cases of hepatic infection is becoming more common in daily practice. Knowledge of the imaging features seen with hepatic infections can assist in early diagnosis and timely initiation of appropriate therapy. This review presents the imaging appearances of hepatic infections, emphasizing specific features that may contribute to the diagnosis. Examples of the imaging findings seen with pyogenic and amoebic abscesses, infection with Echinococcus granulosus (Hydatid), schistosomiasis, candidiasis and tuberculosis (TB) are presented.

  18. Aggressive hepatitis (image)

    Science.gov (United States)

    Chronic active hepatitis is a liver disease caused by infection, drug ingestion, metabolic or autoimmune disorders. Necrosis (death) of liver cells, inflammation and fibrosis may lead to liver failure. Death within 5 years of onset occurs in ...

  19. Pentoxifylline for alcoholic hepatitis

    DEFF Research Database (Denmark)

    Whitfield, Kate; Rambaldi, Andrea; Wetterslev, Jørn

    2009-01-01

    -cause mortality and mortality due to hepatorenal syndrome, and conversely, an increase in serious and non-serious adverse events. However, the evidence is not firm; no conclusions can be drawn regarding whether pentoxifylline has a positive, negative, or neutral effect on participants with alcoholic hepatitis....... analysis did not support this result. Data from one trial suggests that pentoxifylline may increase the occurrence of serious and non-serious adverse events compared to control. AUTHORS' CONCLUSIONS: The current available data may indicate a possible positive intervention effect of pentoxifylline on all......BACKGROUND: Alcoholic hepatitis is a life-threatening disease, with an average mortality of approximately 40%. There is no widely accepted, effective treatment for alcoholic hepatitis. Pentoxifylline is used to treat alcoholic hepatitis, but there has been no systematic review to assess its effects...

  20. Hepatitis C - children

    Science.gov (United States)

    ... sexual contact with a person with HCV Getting tattoos or acupuncture therapy with infected needles Hepatitis C ... for chronic HCV. These medicines: Have fewer side effects Are easier to take Are taken by mouth ...

  1. Alcohol and Hepatitis

    Science.gov (United States)

    ... code here Enter ZIP code here Daily Living: Alcohol for Veterans and the Public Alcohol and Hepatitis: Entire Lesson Overview Alcohol is one ... related to choices you make about your lifestyle . Alcohol and fibrosis Fibrosis is the medical term for ...

  2. Hepatitis C and sex.

    Science.gov (United States)

    Page, Emma E; Nelson, Mark

    2016-04-01

    An outbreak of acute hepatitis C among HIV-positive men who have sex with men (MSM) in the last decade has been shown to be sexually transmitted. Initially recreational drug use, in particular drug injection, was not prevalent among those becoming infected with hepatitis C. However more recently chemsex (the use of drugs to enhance sexual experience) and its associated drugs, which are not uncommonly injected, have become more frequently reported among those diagnosed with hepatitis C. It is hoped that the widespread -introduction of direct-acting antivirals and upscaling of numbers treated may have a positive impact on this epidemic. However their introduction may negatively impact on the perceived risk of acquiring hepatitis C and in conjunction with the introduction of HIV transmission prevention strategies may result in increased transmissions and spread to the HIV-negative MSM population.

  3. Inhibition of Uncoupling Protein 2 Attenuates Cardiac Hypertrophy Induced by Transverse Aortic Constriction in Mice

    Directory of Open Access Journals (Sweden)

    Xiao-Bing Ji

    2015-07-01

    Full Text Available Background: Uncoupling protein 2 (UCP2 is critical in regulating energy metabolism. Due to the significant change in energy metabolism of myocardium upon pressure overload, we hypothesize that UCP2 could contribute to the etiology of cardiac hypertrophy. Methods: Adult male C57BL/6J mice were subjected to pressure overload by using transverse aortic constriction (TAC, and then received genipin (a UCP2 selective inhibitor; 25 mg/kg/d, ip or vehicle for three weeks prior to histologic assessment of myocardial hypertrophy. ATP concentration, ROS level, and myocardial apoptosis were also examined. A parallel set of experiments was also conducted in UCP2-/- mice. Results: TAC induced left ventricular hypertrophy, as reflected by increased ventricular weight/thickness and increased size of myocardial cell (vs. sham controls. ATP concentration was decreased; ROS level was increased. Apoptosis and fibrosis markers were increased. TAC increased mitochondrial UCP2 expression in the myocardium at both mRNA and protein levels. Genipin treatment attenuated cardiac hypertrophy and the histologic/biochemical changes described above. Hypertrophy and associated changes induced by TAC in UCP2-/- mice were much less pronounced than in WT mice. Conclusions: Blocking UCP2 expression attenuates cardiac hypertrophy induced by pressure overload.

  4. Syndecan-4 Signaling Is Required for Exercise-Induced Cardiac Hypertrophy

    Science.gov (United States)

    Xie, Jun; He, Guixin; Chen, Qinhua; Sun, Jiayin; Dai, Qin; Lu, Jianrong; Li, Guannan; Wu, Han; Li, Ran; Chen, Jianzhou; Xu, Wei; Xu, Biao

    2016-01-01

    Cardiac hypertrophy can be broadly classified as either physiological or pathological. Physiological stimuli such as exercise cause adaptive cardiac hypertrophy and normal heart function. Pathological stimuli including hypertension and aortic valvular stenosis cause maladaptive cardiac remodeling and ultimately heart failure. Syndecan-4 (synd4) is a transmembrane proteoglycan identified as being involved in cardiac adaptation after injury, but whether it takes part in physiological cardiac hypertrophy is unclear. We observed upregulation of synd4 in exercise-induced hypertrophic myocardium. To evaluate the role of synd4 in the physiological form of cardiac hypertrophy, mice lacking synd4 (synd4–/–) were exercised by swimming for 4 wks. Ultrasonic cardiogram (UCG) and histological analysis revealed that swimming induced the hypertrophic phenotype but was blunted in synd4–/– compared with wild-type (WT) mice. The swimming-induced activation of Akt, a key molecule in physiological hypertrophy was also more decreased than in WT controls. In cultured cardiomyocytes, synd4 overexpression could induce cell enlargement, protein synthesis and distinct physiological molecular alternation. Akt activation also was observed in synd4-overexpressed cardiomyocytes. Furthermore, inhibition of protein kinase C (PKC) prevented the synd4-induced hypertrophic phenotype and Akt phosphorylation. This study identified an essential role of synd4 in mediation of physiological cardiac hypertrophy. PMID:26835698

  5. Proteasome inhibitors attenuated cholesterol-induced cardiac hypertrophy in H9c2 cells

    Science.gov (United States)

    Lee, Hyunjung; Park, Jinyoung; Kim, Eunice EunKyeong; Yoo, Young Sook; Song, Eun Joo

    2016-01-01

    The Ubiquitin proteasome system (UPS) plays roles in protein degradation, cell cycle control, and growth and inflammatory cell signaling. Dysfunction of UPS in cardiac diseases has been seen in many studies. Cholesterol acts as an inducer of cardiac hypertrophy. In this study, the effect of proteasome inhibitors on the cholesterol-induced hypertrophic growth in H9c2 cells is examined in order to observe whether UPS is involved in cardiac hypertrophy. The treatment of proteasome inhibitors MG132 and Bortezomib markedly reduced cellular surface area and mRNA expression of β-MHC in cholesterol-induced cardiac hypertrophy. In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol-induced cardiac hypertrophy. We demonstrated that cholesterol-induced cardiac hypertrophy was suppressed by proteasome inhibitors. Thus, regulatory mechanism of cholesterol-induced cardiac hypertrophy by proteasome inhibitors may provide a new therapeutic strategy to prevent the progression of heart failure. [BMB Reports 2016; 49(5): 270-275] PMID:26592933

  6. Consequences of reversal of hypertensive cardiac hypertrophy by captopril on left ventricular pumping ability and performance.

    Science.gov (United States)

    Saragoça, M A; Cezaretti, M L; Bessa, A M; Casarini, D; Almeida, J B; Amorim, M P; Ramos, O L

    1987-12-01

    Left ventricular hypertrophy can be reversed by treatment of hypertension with captopril but the consequences of this regression are not yet fully described. We studied the maximal capacity of the hypertrophied and hypertrophy-reversed ventricle to generate pressure during transient total occlusion of the aorta, and also the left ventricular end-diastolic pressure required to meet this maximal effort. Two-kidney, one clip Goldblatt (renal hypertensive rats; RHR) hypertension was induced in 17 Wistar rats, eight of which were treated with captopril (RHR-C: 50 mg/kg given orally) from the fourth to the eighth week. Sham-operated controls (SC) remained untreated, or were treated with similar doses of captopril (SC-C). Significantly lower heart weights were found in RHR-C than in RHR (2.88 +/- 0.15 versus 2.38 +/- 0.04; P less than 0.001). During transient total occlusion of the aorta, the maximal intraventricular pressure developed in RHR-C was not significantly different from that in RHR, but left ventricular end-diastolic pressure was significantly less in RHR-C than in RHR (21.4 +/- 2.2 versus 34.3 +/- 3.8; P less than 0.01). The analysis of pressure-volume characteristics of the hypertrophied left ventricles and those in which hypertrophy was reversed revealed similar compliances between these two groups. Our data suggest that there was a mechanical improvement in the heart function after reversal of left ventricular hypertrophy.

  7. Sulforaphane protects H9c2 cardiomyocytes from angiotensin II-induced hypertrophy.

    Science.gov (United States)

    Wu, Q-Q; Zong, J; Gao, L; Dai, J; Yang, Z; Xu, M; Fang, Y; Ma, Z-G; Tang, Q-Z

    2014-05-01

    Cardiac hypertrophy is an adaptive process of the heart in response to various stimuli, but sustained cardiac hypertrophy will finally lead to heart failure. Sulforaphane-extracted from cruciferous vegetables of the genus Brassica such as broccoli, brussels sprouts, and cabbage-has been evaluated for its anticarcinogenic and antioxidant effects. To investigate the effect of sulforaphane on angiotensin II (Ang II)-induced cardiac hypertrophy in vitro. Embryonic rat heart-derived H9c2 cells were co-incubated with sulforaphane and Ang II. The cell surface area and mRNA levels of hypertrophic markers were measured to clarify the effect of sulforaphane on cardiac hypertrophy. The underlying mechanism was further investigated by detecting the activation of Akt and NF-κB signaling pathways. We found that H9c2 cells pretreated with sulforaphane were protected from Ang II-induced hypertrophy. The increasing mRNA levels of ANP, BNP, and β-MHC in Ang II-stimulated cells were also down-regulated after sulforaphane treatment. Moreover, sulforaphane repressed the Ang II-induced phosphorylation of Akt, GSK3β, mTOR, eIF4e, as well as of IκBα and NF-κB. Based on our results, sulforaphane attenuates Ang II-induced hypertrophy of H9c2 cardiomyocytes mediated by the inhibition of intracellular signaling pathways including Akt and NF-κB.

  8. The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy.

    Science.gov (United States)

    Wang, Zhihua; Zhang, Xiao-Jing; Ji, Yan-Xiao; Zhang, Peng; Deng, Ke-Qiong; Gong, Jun; Ren, Shuxun; Wang, Xinghua; Chen, Iris; Wang, He; Gao, Chen; Yokota, Tomohiro; Ang, Yen Sin; Li, Shen; Cass, Ashley; Vondriska, Thomas M; Li, Guangping; Deb, Arjun; Srivastava, Deepak; Yang, Huang-Tian; Xiao, Xinshu; Li, Hongliang; Wang, Yibin

    2016-10-01

    Epigenetic reprogramming is a critical process of pathological gene induction during cardiac hypertrophy and remodeling, but the underlying regulatory mechanisms remain to be elucidated. Here we identified a heart-enriched long noncoding (lnc)RNA, named cardiac-hypertrophy-associated epigenetic regulator (Chaer), which is necessary for the development of cardiac hypertrophy. Mechanistically, Chaer directly interacts with the catalytic subunit of polycomb repressor complex 2 (PRC2). This interaction, which is mediated by a 66-mer motif in Chaer, interferes with PRC2 targeting to genomic loci, thereby inhibiting histone H3 lysine 27 methylation at the promoter regions of genes involved in cardiac hypertrophy. The interaction between Chaer and PRC2 is transiently induced after hormone or stress stimulation in a process involving mammalian target of rapamycin complex 1, and this interaction is a prerequisite for epigenetic reprogramming and induction of genes involved in hypertrophy. Inhibition of Chaer expression in the heart before, but not after, the onset of pressure overload substantially attenuates cardiac hypertrophy and dysfunction. Our study reveals that stress-induced pathological gene activation in the heart requires a previously uncharacterized lncRNA-dependent epigenetic checkpoint.

  9. The alpha1-adrenergic receptors in cardiac hypertrophy: signaling mechanisms and functional implications.

    Science.gov (United States)

    Cotecchia, Susanna; Del Vescovo, Cosmo Damiano; Colella, Matilde; Caso, Stefania; Diviani, Dario

    2015-10-01

    Cardiac hypertrophy is a complex remodeling process of the heart induced by physiological or pathological stimuli resulting in increased cardiomyocyte size and myocardial mass. Whereas cardiac hypertrophy can be an adaptive mechanism to stressful conditions of the heart, prolonged hypertrophy can lead to heart failure which represents the primary cause of human morbidity and mortality. Among G protein-coupled receptors, the α1-adrenergic receptors (α1-ARs) play an important role in the development of cardiac hypertrophy as demonstrated by numerous studies in the past decades, both in primary cardiomyocyte cultures and genetically modified mice. The results of these studies have provided evidence of a large variety of α1-AR-induced signaling events contributing to the defining molecular and cellular features of cardiac hypertrophy. Recently, novel signaling mechanisms have been identified and new hypotheses have emerged concerning the functional role of the α1-adrenergic receptors in the heart. This review will summarize the main signaling pathways activated by the α1-AR in the heart and their functional implications in cardiac hypertrophy. Copyright © 2015 Elsevier Inc. All rights reserved.

  10. Overexpression of mitofilin in the mouse heart promotes cardiac hypertrophy in response to hypertrophic stimuli.

    Science.gov (United States)

    Zhang, Yuan; Xu, Jing; Luo, Yu-Xuan; An, Xi-Zhou; Zhang, Ran; Liu, Guang; Li, Hongliang; Chen, Hou-Zao; Liu, De-Pei

    2014-10-20

    Mitofilin was originally described as a heart muscle protein because of its abundance in the heart tissue; however, its function in the heart is still to be elucidated. Thus, this study aims at investigating the role of mitofilin in the heart in response to hypertrophic stimuli. In this study, a significant increase in mitofilin expression was observed in the hearts of patients with hypertrophic cardiomyopathy. Transgenic (TG) mice with cardiomyocyte-specific overexpression of mitofilin were generated, and cardiac hypertrophy was introduced by transverse aortic constriction (TAC) or chronic infusion of isoproterenol (ISO). In TG mice overexpressing mitofilin, the level of cardiac hypertrophy was significantly greater than that in wild-type (WT) mice after TAC and ISO stimulation. A detailed analysis showed that compared with WT mice, the level of reactive oxygen species was increased after TAC and ISO induction and mitochondrial oxidative phosphorylation (OXPHOS) activity in the TG hearts was lower. These alterations may contribute to the aggravated cardiac hypertrophy observed in response to TAC and ISO stimulation. Over-expression of mitofilin promotes cardiac hypertrophy under pathological conditions both in vivo and in vitro. Mitofilin, a mitochondria protein, is shown to be related to cardiac hypertrophy for the first time, which enhances our understanding of the role of mitochondria in cardiac hypertrophy.

  11. Systematic review of the synergist muscle ablation model for compensatory hypertrophy.

    Science.gov (United States)

    Terena, Stella Maris Lins; Fernandes, Kristianne Porta Santos; Bussadori, Sandra Kalill; Deana, Alessandro Melo; Mesquita-Ferrari, Raquel Agnelli

    2017-02-01

    The aim was to evaluate the effectiveness of the experimental synergists muscle ablation model to promote muscle hypertrophy, determine the period of greatest hypertrophy and its influence on muscle fiber types and determine differences in bilateral and unilateral removal to reduce the number of animals used in this model. Following the application of the eligibility criteria for the mechanical overload of the plantar muscle in rats, nineteen papers were included in the review. The results reveal a greatest hypertrophy occurring between days 12 and 15, and based on the findings, synergist muscle ablation is an efficient model for achieving rapid hypertrophy and the contralateral limb can be used as there was no difference between unilateral and bilateral surgery, which reduces the number of animals used in this model. This model differs from other overload models (exercise and training) regarding the characteristics involved in the hypertrophy process (acute) and result in a chronic muscle adaptation with selective regulation and modification of fast-twitch fibers in skeletal muscle. This is an efficient and rapid model for compensatory hypertrophy.

  12. G protein-coupled receptor 56 regulates mechanical overload-induced muscle hypertrophy.

    Science.gov (United States)

    White, James P; Wrann, Christiane D; Rao, Rajesh R; Nair, Sreekumaran K; Jedrychowski, Mark P; You, Jae-Sung; Martínez-Redondo, Vicente; Gygi, Steven P; Ruas, Jorge L; Hornberger, Troy A; Wu, Zhidan; Glass, David J; Piao, Xianhua; Spiegelman, Bruce M

    2014-11-04

    Peroxisome proliferator-activated receptor gamma coactivator 1-alpha 4 (PGC-1α4) is a protein isoform derived by alternative splicing of the PGC1α mRNA and has been shown to promote muscle hypertrophy. We show here that G protein-coupled receptor 56 (GPR56) is a transcriptional target of PGC-1α4 and is induced in humans by resistance exercise. Furthermore, the anabolic effects of PGC-1α4 in cultured murine muscle cells are dependent on GPR56 signaling, because knockdown of GPR56 attenuates PGC-1α4-induced muscle hypertrophy in vitro. Forced expression of GPR56 results in myotube hypertrophy through the expression of insulin-like growth factor 1, which is dependent on Gα12/13 signaling. A murine model of overload-induced muscle hypertrophy is associated with increased expression of both GPR56 and its ligand collagen type III, whereas genetic ablation of GPR56 expression attenuates overload-induced muscle hypertrophy and associated anabolic signaling. These data illustrate a signaling pathway through GPR56 which regulates muscle hypertrophy associated with resistance/loading-type exercise.

  13. The effect of inter-set rest intervals on resistance exercise-induced muscle hypertrophy.

    Science.gov (United States)

    Henselmans, Menno; Schoenfeld, Brad J

    2014-12-01

    Due to a scarcity of longitudinal trials directly measuring changes in muscle girth, previous recommendations for inter-set rest intervals in resistance training programs designed to stimulate muscular hypertrophy were primarily based on the post-exercise endocrinological response and other mechanisms theoretically related to muscle growth. New research regarding the effects of inter-set rest interval manipulation on resistance training-induced muscular hypertrophy is reviewed here to evaluate current practices and provide directions for future research. Of the studies measuring long-term muscle hypertrophy in groups employing different rest intervals, none have found superior muscle growth in the shorter compared with the longer rest interval group and one study has found the opposite. Rest intervals less than 1 minute can result in acute increases in serum growth hormone levels and these rest intervals also decrease the serum testosterone to cortisol ratio. Long-term adaptations may abate the post-exercise endocrinological response and the relationship between the transient change in hormonal production and chronic muscular hypertrophy is highly contentious and appears to be weak. The relationship between the rest interval-mediated effect on immune system response, muscle damage, metabolic stress, or energy production capacity and muscle hypertrophy is still ambiguous and largely theoretical. In conclusion, the literature does not support the hypothesis that training for muscle hypertrophy requires shorter rest intervals than training for strength development or that predetermined rest intervals are preferable to auto-regulated rest periods in this regard.

  14. Systematic review of the synergist muscle ablation model for compensatory hypertrophy

    Directory of Open Access Journals (Sweden)

    Stella Maris Lins Terena

    Full Text Available Summary Objective: The aim was to evaluate the effectiveness of the experimental synergists muscle ablation model to promote muscle hypertrophy, determine the period of greatest hypertrophy and its influence on muscle fiber types and determine differences in bilateral and unilateral removal to reduce the number of animals used in this model. Method: Following the application of the eligibility criteria for the mechanical overload of the plantar muscle in rats, nineteen papers were included in the review. Results: The results reveal a greatest hypertrophy occurring between days 12 and 15, and based on the findings, synergist muscle ablation is an efficient model for achieving rapid hypertrophy and the contralateral limb can be used as there was no difference between unilateral and bilateral surgery, which reduces the number of animals used in this model. Conclusion: This model differs from other overload models (exercise and training regarding the characteristics involved in the hypertrophy process (acute and result in a chronic muscle adaptation with selective regulation and modification of fast-twitch fibers in skeletal muscle. This is an efficient and rapid model for compensatory hypertrophy.

  15. Effect of adenoid hypertrophy and pulmonary function tests in children with mild asthma.

    Science.gov (United States)

    Aykan, Merve; Aydın, Sedat; Öktem, Sedat; Demir, Mehmet Gökhan; Tutar, Engin

    2016-01-01

    This study aims to assess the effect of adenoid hypertrophy on asthma in children with mild asthma. Between September 2010 and September 2012, 63 children (42 males, 21 females; median age 10.5 years; range 6 to 14 years) admitted to our clinic with asthma complaint were included in this study. These children were evaluated for adenoid hypertrophy, symptoms of asthma, medical treatment, pulmonary function tests at the beginning of the study and at the end of second month. There was no correlation between initial pulmonary function tests and adenoid hypertrophy. But we observed significantly lower forced vital capacity values in children with prominent adenoid hypertrophy (p=0.033). While there was no significant difference in pulmonary function tests in terms of inhaled steroid usage (p>0.05), final forced mid-expiratory flow rate (FEF25-75) values were statistically higher in patients who were using nasal steroids (p=0.015). Consequently, significantly higher values of FEF25-75 in the group that used nasal steroid suggest that adenoid hypertrophy affects the airway obstruction. Moreover, absence of airway obstruction symptoms in patients with mild adenoid hypertrophy suggests pulmonary function tests may help to decide performing adenoidectomy.

  16. Adenotonsillar hypertrophy as a risk factor of dentofacial abnormality in Korean children.

    Science.gov (United States)

    Kim, Dong-Kyu; Rhee, Chae Seo; Yun, Pil-Young; Kim, Jeong-Whun

    2015-11-01

    No studies for the role of adenotonsillar hypertrophy in development of dentofacial abnormalities have been performed in Asian pediatric population. Thus, we aimed to investigate the relationship between adenotonsillar hypertrophy and dentofacial abnormalities in Korean children. The present study included consecutive children who visited a pediatric clinic for sleep-disordered breathing due to habitual mouth breathing, snoring or sleep apnea. Their palatine tonsils and adenoids were graded by oropharyngeal endoscopy and lateral cephalometry. Anterior open bite, posterior crossbite, and Angle's class malocclusions were evaluated for dentofacial abnormality. The receiver-operating characteristic curve analysis was used to identify age cutoffs to predict dentofacial abnormality. A total of 1,083 children were included. The presence of adenotonsillar hypertrophy was significantly correlated with the prevalence of dentofacial abnormality [adjusted odds ratio = 4.587, 95% CI (2.747-7.658)] after adjusting age, sex, body mass index, allergy, and Korean version of obstructive sleep apnea-18 score. The cutoff age associated with dentofacial abnormality was 5.5 years (sensitivity = 75.5%, specificity = 67%) in the children with adenotonsillar hypertrophy and 6.5 years (sensitivity = 70.6%, specificity = 57%) in those without adenotonsillar hypertrophy. In conclusion, adenotonsillar hypertrophy may be a risk factor for dentofacial abnormalities in Korean children and early surgical intervention could be considered with regards to dentofacial abnormality.

  17. Hepatitis C pada Anak

    Directory of Open Access Journals (Sweden)

    Yusri Dianne Jurnalis

    2014-05-01

    Full Text Available AbstrakInfeksi virus hepatitis C saat ini masih merupakan persoalan yang serius. Penularan infeksi HCV pada anak yang utama adalah melalui transfusi darah atau produk darah yang saat ini bertanggung jawab menyebabkan kasus hepatitis C kronis. Selain itu infeksi HCV pada anak dapat disebabkan oleh transmisi perinatal (vertikal. Infeksi HCV akut dapat berakhir dengan sirosis dan karsinoma hepatoselular setelah dekade ketiga (sekitar 20%, karena progresivitas infeksi HCV lebih lambat dari infeksi hepatitis B virus. Pada umumnya infeksi HCV bersifat asimptomatik termasuk pada anak. Karena tidak ada gejala yang jelas pada infeksi HCV tersebut maka diagnosis infeksi HCV hanya dapat ditegakkan dengan pemeriksaan awal laboratorium dan uji serologi, dan bila perlu dengan uji molekuler pada pasien dengan risiko tinggi. Kebijakan kuratif khusus terhadap HCV adalah terapi antivirus berupa interferon dan ribavirin yang diberikan bila diagnosis HCV sudah ditegakkanKata kunci: Hepatitis C, diagnosis and management problem, childrenAbstractHepatitis C virus infection is still a serious problem. Transmission of HCV infection in children is a major blood transfusion or blood products that are currently responsible for causing chronic hepatitis C cases. Additionally HCV infection in children can be caused by perinatal transmission (vertical. Acute HCV infection may end up with cirrhosis and hepatocellular carcinoma after the third decade (around 20%, due to a slower progression of HCV infection of hepatitis B virus infection. In most cases of HCV infection are asymptomatic, including in children. Since there are no obvious symptoms in the diagnosis of HCV infection HCV infection can only be confirmed by laboratory examinations and serologic testing early, and if necessary with molecular testing in patients at high risk. Curative policy is specific to HCV antiviral therapy such as interferon and ribavirin are given when the diagnosis of HCV has been establishedKeywords:Hepatitis

  18. Immigration and viral hepatitis.

    Science.gov (United States)

    Sharma, Suraj; Carballo, Manuel; Feld, Jordan J; Janssen, Harry L A

    2015-08-01

    WHO estimates reveal that the global prevalence of viral hepatitis may be as high as 500 million, with an annual mortality rate of up to 1.3 million individuals. The majority of this global burden of disease is borne by nations of the developing world with high rates of vertical and iatrogenic transmission of HBV and HCV, as well as poor access to healthcare. In 2013, 3.2% of the global population (231 million individuals) migrated into a new host nation. Migrants predominantly originate from the developing countries of the south, into the developed economies of North America and Western Europe. This mass migration of individuals from areas of high-prevalence of viral hepatitis poses a unique challenge to the healthcare systems of the host nations. Due to a lack of universal standards for screening, vaccination and treatment of viral hepatitis, the burden of chronic liver disease and hepatocellular carcinoma continues to increase among migrant populations globally. Efforts to increase case identification and treatment among migrants have largely been limited to small outreach programs in urban centers, such that the majority of migrants with viral hepatitis continue to remain unaware of their infection. This review summarizes the data on prevalence of viral hepatitis and burden of chronic liver disease among migrants, current standards for screening and treatment of immigrants and refugees, and efforts to improve the identification and treatment of viral hepatitis among migrants.

  19. FELINE HEPATIC LIPIDOSIS

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    C. Masotti

    2016-11-01

    Full Text Available Since the first description of feline hepatic lipidosis occurred in 1977, it becames the most diagnosed liver disease in cats. Several factors have been proposed as causes of disease, and obesity being a predisposing factor. The disease can be considered primary or idiopathic when its underlying cause is unknown, or secondary when there is another concomitant disease lipidosis. Cats with hepatic lipidosis have anorexia usually ranging from several days to weeks and weight loss, followed by jaundice and varying degrees of dehydration, diarrhea and vomiting episodes may occur. A worsening of the disease shows signs of hepatic encephalopathy, drooling and retroflexion of the neck. In clinical examination can be observed depression, lethargy and hepatomegaly. The definitive diagnosis of the disease can be performed by fine needle aspiration biopsy guided by ultrasound and cytology or biopsy. The treatment of hepatic lipidosis is based on stabilizing the patient by supplying water and electrolyte losses and provide adequate nutritional support. The diet is usually provided through feeding tubes for a period ranging from 4 to 6 weeks may occur depending on the patient's condition. The prognosis for cats with hepatic lipidosis is favored in cases of identification followed by intensive treatment of underlying causes and for patients receiving therapy necessary in cases of idiopathic hepatic lipidosis.

  20. Migraine increases centre-surround suppression for drifting visual stimuli.

    Directory of Open Access Journals (Sweden)

    Josephine Battista

    Full Text Available BACKGROUND: The pathophysiology of migraine is incompletely understood, but evidence points to hyper-responsivity of cortical neurons being a key feature. The basis of hyper-responsiveness is not clear, with an excitability imbalance potentially arising from either reduced inhibition or increased excitation. In this study, we measure centre-surround contrast suppression in people with migraine as a perceptual analogue of the interplay between inhibition and excitation in cortical areas responsible for vision. We predicted that reduced inhibitory function in migraine would reduce perceptual surround suppression. Recent models of neuronal surround suppression incorporate excitatory feedback that drives surround inhibition. Consequently, an increase in excitation predicts an increase in perceptual surround suppression. METHODS AND FINDINGS: Twenty-six people with migraine and twenty approximately age- and gender-matched non-headache controls participated. The perceived contrast of a central sinusoidal grating patch (4 c/deg stationary grating, or 2 c/deg drifting at 2 deg/sec, 40% contrast was measured in the presence and absence of a 95% contrast annular grating (same orientation, spatial frequency, and drift rate. For the static grating, similar surround suppression strength was present in control and migraine groups with the presence of the surround resulting in the central patch appearing to be 72% and 65% of its true contrast for control and migraine groups respectively (t(44 = 0.81, p = 0.42. For the drifting stimulus, the migraine group showed significantly increased surround suppression (t(44 = 2.86, p<0.01, with perceived contrast being on average 53% of actual contrast for the migraine group and 68% for non-headache controls. CONCLUSIONS: In between migraines, when asymptomatic, visual surround suppression for drifting stimuli is greater in individuals with migraine than in controls. The data provides evidence for a

  1. Hepatitis B FAQs for the Public

    Science.gov (United States)

    ... Professional Resources Patient Education Resources Quick Links to Hepatitis … A | B | C | D | E Viral Hepatitis Home ... Grantees Policy and Programs Resource Center Viral Hepatitis Hepatitis B FAQs for the Public Recommend on Facebook ...

  2. Kidney transplant complications from undiagnosed benign prostatic hypertrophy.

    Science.gov (United States)

    Lubetzky, Michelle; Ajaimy, Maria; Kamal, Layla; de Boccardo, Graciela; Akalin, Enver; Kayler, Liise

    2015-06-01

    It is estimated that approximately 50% of males over 50 have benign prostatic hypertrophy (BPH). BPH is underappreciated in anuric patients with end stage renal disease, and failure of diagnosis in this population can lead to complications after kidney transplantation. A single-center retrospective review of male patients over 50 yr of age transplanted from January 1, 2010, until September 30, 2013, was performed. Outcomes assessed were as follows: graft survival, urinary retention, discharge with Foley catheter, and urinary tract infection (UTI). Of 147 patients, 17.0% were diagnosed with BPH before transplant, 19.0% received a BPH diagnosis after transplant, and 64% did not have BPH. Compared to those without BPH, a post-transplant BPH diagnosis was associated with urinary retention during the transplant admission (0% vs. 46.4%, p < 0.01), discharge with Foley catheter (0% vs. 21.4%, p < 0.01), readmission related to urinary retention (0% vs. 46.4%, p < 0.01), and UTI (18.0% vs. 64.3%, p < 0.01). Patients with prior diagnosis of BPH and on therapy had similar outcomes to those without BPH. Following kidney transplant, urinary tract complications are more common in patients with BPH; however, being on medical therapy prior to transplantation diminishes the incidence of these complications significantly. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  3. PERIOPERATIVE PERIOD FOLLOWING HEART TRANSPLANTATION WITH SEVERE LEFT VENTRICULAR HYPERTROPHY

    Directory of Open Access Journals (Sweden)

    V. N. Poptsov

    2012-01-01

    Full Text Available Use donor hearts with left ventricular hypertrophy (LVH is controversial. This category of heart recipients has increasing risk of early graft failure. We proposed that heart transplantation (HT with LVH ≥1.5 cm may be successful if performed in selective category patients from alternate transplant list. This study included 10 pati- ents (2 female and 8 male at the age 26–62 (44 ± 3, who needed urgent HT. This study showed that recipients with LVH ≥1.5 cm demanded more high and long inotropic support with adrenalin and dopamine, more fre- quent use of levosimendan infusion (in 40% of cases and intraaortic balloon conterpulsation (in 50% of cases. However we didn’t observed any difference in survival rate (90.0% vs 89.0% and ICU time (4.8 ± 0.6 days vs 4.1 ± 0.4 days between HT recipients with and without LVH. Our study showed that HT from donor with LVH ≥1.5 cm may be performed in patients, demanding urgent HT, with acceptable early posttransplant results. 

  4. Asymmetrical septal hypertrophy in newborn infants of diabetic mothers.

    Science.gov (United States)

    Vela-Huerta, M M; Vargas-Origel, A; Olvera-López, A

    2000-01-01

    The objective of this paper is to determine the frequency and outcome of asymmetrical septal hypertrophy (ASH) in large-for-gestational-age infants (LGA) born to diabetic (DM) and nondiabetic mothers (NDM), and to establish the relationship between ASH and maternal diabetes control. A comparative study was design to assess ASH in infants born to DM and NDM. The study was conducted in the Departments of Neonatology and Pediatric Cardiology of the "Hospital de Gineco-Pediatria 48", Instituto Mexicano del Seguro Social from January to December 1997. Eighty-five full-term infants of DM (group A) and 85 LGA infants of NDM (group B) were included. As a control group (group C), we studied 85 healthy, full-term infants. In all cases a Doppler echocardiogram was obtained in the first 48 h after birth, and for the ASH infants, at 2 and 4 months. Chest X ray, electrocardiogram, and laboratory tests were performed as complementary studies. ASH was present in 38.8% of LGA infants of DM and in 7.1% of NDM. The difference was significant (p < 0.01). Interventricular septum (IVS) and IVS/ posterior wall of left ventricle ratio were significantly different between groups A and B with C. There was no correlation between Hb A1 level and the presence of ASH in group A. ASH is a common finding in infants of DM. We could not find a relationship between the degree of metabolic control during pregnancy and the incidence and severity of ASH.

  5. Hypertrophy of chronically unloaded muscle subjected to resistance exercise.

    Science.gov (United States)

    Tesch, P A; Trieschmann, J T; Ekberg, A

    2004-04-01

    In an effort to simulate the compromised function and atrophy of lower limb muscles experienced by astronauts after spaceflight, 21 men and women age 30-56 yr were subjected to unilateral lower limb unloading for 5 wk. Whereas 10 of these subjects performed unilateral knee extensor resistance exercise (ULRE) two or three times weekly, 11 subjects (UL) refrained from training. The exercise regimen consisted of four sets of seven maximal actions, using an apparatus that offers concentric and eccentric resistance by utilizing the inertia of rotating flywheel(s). Knee extensor muscle strength was measured before and after UL and ULRE, and knee extensor and ankle plantar flexor muscle volumes were determined by means of magnetic resonance imaging. Surface electromyographic activity measured after UL inferred increased muscle use to perform a given motor task. UL induced an 8.8% decrease (P 0.05) strength. Ankle plantar flexor muscle volume of the unloaded limb decreased (P 0.05) in muscle volume or strength. The results of this study provide evidence that resistance exercise not only may offset muscle atrophy but is in fact capable of promoting marked hypertrophy of chronically unloaded muscle.

  6. Integrin activation and focal complex formation in cardiac hypertrophy

    Science.gov (United States)

    Laser, M.; Willey, C. D.; Jiang, W.; Cooper, G. 4th; Menick, D. R.; Zile, M. R.; Kuppuswamy, D.

    2000-01-01

    Cardiac hypertrophy is characterized by both remodeling of the extracellular matrix (ECM) and hypertrophic growth of the cardiocytes. Here we show increased expression and cytoskeletal association of the ECM proteins fibronectin and vitronectin in pressure-overloaded feline myocardium. These changes are accompanied by cytoskeletal binding and phosphorylation of focal adhesion kinase (FAK) at Tyr-397 and Tyr-925, c-Src at Tyr-416, recruitment of the adapter proteins p130(Cas), Shc, and Nck, and activation of the extracellular-regulated kinases ERK1/2. A synthetic peptide containing the Arg-Gly-Asp (RGD) motif of fibronectin and vitronectin was used to stimulate adult feline cardiomyocytes cultured on laminin or within a type-I collagen matrix. Whereas cardiocytes under both conditions showed RGD-stimulated ERK1/2 activation, only collagen-embedded cells exhibited cytoskeletal assembly of FAK, c-Src, Nck, and Shc. In RGD-stimulated collagen-embedded cells, FAK was phosphorylated only at Tyr-397 and c-Src association occurred without Tyr-416 phosphorylation and p130(Cas) association. Therefore, c-Src activation is not required for its cytoskeletal binding but may be important for additional phosphorylation of FAK. Overall, our study suggests that multiple signaling pathways originate in pressure-overloaded heart following integrin engagement with ECM proteins, including focal complex formation and ERK1/2 activation, and many of these pathways can be activated in cardiomyocytes via RGD-stimulated integrin activation.

  7. Absence of left ventricular hypertrophy in elite college basketball players.

    Science.gov (United States)

    Wolfe, L A; Martin, R P; Seip, R L

    1985-09-01

    Left ventricular dimensions of 11 successful male college basketball players engaged in pre-season conditioning (mean age, 20.3 years) and 13 tall healthy male controls (mean age, 21.6 years) were studied by echocardiography. Left ventricular internal dimension (LVIDd, mm), posterior wall thickness (PWT, mm), septal thickness (ST, mm), and calculated left ventricular mass (LV mass, g) in the athletes were within or only slightly in excess of echocardiographic normal limits and mean values were not significantly different from the control group. LVIDd (mm/m2 body surface area) was significantly lower in the athletes. However, five guard-type players displayed significantly greater mean values for PWT and LV mass compared to six taller forwards/centers with linear body builds. It was concluded that left ventricular hypertrophy is not a common characteristic of college basketball players. It was hypothesized that cardiac dimensions of young men may vary independently of gross body size in relation to somatotype or other anthropometric variables.

  8. Integrin activation and focal complex formation in cardiac hypertrophy

    Science.gov (United States)

    Laser, M.; Willey, C. D.; Jiang, W.; Cooper, G. 4th; Menick, D. R.; Zile, M. R.; Kuppuswamy, D.

    2000-01-01

    Cardiac hypertrophy is characterized by both remodeling of the extracellular matrix (ECM) and hypertrophic growth of the cardiocytes. Here we show increased expression and cytoskeletal association of the ECM proteins fibronectin and vitronectin in pressure-overloaded feline myocardium. These changes are accompanied by cytoskeletal binding and phosphorylation of focal adhesion kinase (FAK) at Tyr-397 and Tyr-925, c-Src at Tyr-416, recruitment of the adapter proteins p130(Cas), Shc, and Nck, and activation of the extracellular-regulated kinases ERK1/2. A synthetic peptide containing the Arg-Gly-Asp (RGD) motif of fibronectin and vitronectin was used to stimulate adult feline cardiomyocytes cultured on laminin or within a type-I collagen matrix. Whereas cardiocytes under both conditions showed RGD-stimulated ERK1/2 activation, only collagen-embedded cells exhibited cytoskeletal assembly of FAK, c-Src, Nck, and Shc. In RGD-stimulated collagen-embedded cells, FAK was phosphorylated only at Tyr-397 and c-Src association occurred without Tyr-416 phosphorylation and p130(Cas) association. Therefore, c-Src activation is not required for its cytoskeletal binding but may be important for additional phosphorylation of FAK. Overall, our study suggests that multiple signaling pathways originate in pressure-overloaded heart following integrin engagement with ECM proteins, including focal complex formation and ERK1/2 activation, and many of these pathways can be activated in cardiomyocytes via RGD-stimulated integrin activation.

  9. Surgical therapy for benign prostatic hypertrophy/bladder outflow obstruction

    Directory of Open Access Journals (Sweden)

    Nikesh Thiruchelvam

    2014-01-01

    Full Text Available Monopolar transurethral resection of the prostate (TURP with endoscopic electrocautery remains the gold standard surgical technique for benign prostatic hypertrophy (BPH by which all new procedures are compared. We reviewed the current literature, and international urological guidelines and consensus opinion on various surgical options for BPH and present a brief overview of alternative techniques including bipolar TURP, transurethral incision of the prostate, transurethral vaporization of the prostate, laser prostatectomy (with holmium, thulium and potassium titanyl phosphate greenlight lasers and open prostatectomy (with mention of new techniques including laparoscopic and robotic prostatectomy. Emerging, experimental and less established techniques are also described including endoscopic heat generation (transurethral microwave thermotherapy, radiofrequency transurethral needle ablation of the prostate, high intensity focused ultrasound, hot water induced thermotherapy, pulsed electromagnetic radiofrequency, injection therapy (transurethral ethanol ablation and botulinum toxin and mechanical devices (intraprostatic stents and urethral lift devices. Despite a plethora of surgical options, none have realistically improved outcomes in the long-term compared with TURP. Improvements have been made on improving surgical morbidity and time in hospital. Questions remain in this area, including what specific elements of bladder outflow obstruction (BOO result in damage to the urinary tract, how does BPH contribute to BOO and how much prostate volume reduction is necessary to relieve BOO or lower urinary tract symptoms. Given these unanswered questions and the multitude of procedures available, it is clear that appropriate counselling is necessary in all men who undergo BPH surgery.

  10. Surgical therapy for benign prostatic hypertrophy/bladder outflow obstruction.

    Science.gov (United States)

    Thiruchelvam, Nikesh

    2014-04-01

    Monopolar transurethral resection of the prostate (TURP) with endoscopic electrocautery remains the gold standard surgical technique for benign prostatic hypertrophy (BPH) by which all new procedures are compared. We reviewed the current literature, and international urological guidelines and consensus opinion on various surgical options for BPH and present a brief overview of alternative techniques including bipolar TURP, transurethral incision of the prostate, transurethral vaporization of the prostate, laser prostatectomy (with holmium, thulium and potassium titanyl phosphate greenlight lasers) and open prostatectomy (with mention of new techniques including laparoscopic and robotic prostatectomy). Emerging, experimental and less established techniques are also described including endoscopic heat generation (transurethral microwave thermotherapy, radiofrequency transurethral needle ablation of the prostate, high intensity focused ultrasound, hot water induced thermotherapy, pulsed electromagnetic radiofrequency), injection therapy (transurethral ethanol ablation and botulinum toxin) and mechanical devices (intraprostatic stents and urethral lift devices). Despite a plethora of surgical options, none have realistically improved outcomes in the long-term compared with TURP. Improvements have been made on improving surgical morbidity and time in hospital. Questions remain in this area, including what specific elements of bladder outflow obstruction (BOO) result in damage to the urinary tract, how does BPH contribute to BOO and how much prostate volume reduction is necessary to relieve BOO or lower urinary tract symptoms. Given these unanswered questions and the multitude of procedures available, it is clear that appropriate counselling is necessary in all men who undergo BPH surgery.

  11. Contact laser vaporization of the prostate for benign prostatic hypertrophy

    Science.gov (United States)

    Gomella, Leonard G.; Lotfi, M. A.; Milam, Douglas F.; Albala, David; Reagan, Gary

    1994-05-01

    The contact laser applications for the removal of the enlarged prostate are distinctly different than the majority of non-contact Nd:YAG lasers that rely on coagulation necrosis and delayed sloughing. Contact Nd:YAG laser allows cutting, coagulation and vaporization of tissue with minimal penetration beyond the contact surface. Using the contact laser prostatectomy technique, the contact laser probe directly touches and immediately vaporizes the prostatic tissue under the probe. The net result is the immediate removal of the obstructing tissue, in a manner similar to the standard electrosurgical TURP. This immediate removal of tissue offers the patient treated with the contact laser the potential for decreased catheter time and a more rapid resolution of symptoms. Our initial experience suggests that the contact technique may be better suited for the smaller prostate gland (i.e. less than 30 gm). The contact laser may also be used for a procedure termed the `laser assisted TURP': a standard electrosurgical TURP is performed and the contact laser is used for hemostasis. Several investigators have reported non-randomized results of the contact technique with good outcomes. A prospective randomized trial of the contact laser prostatectomy vrs the electrosurgical TURP is underway. The contact laser vaporization of the prostate holds great promise for the treatment of symptomatic benign prostatic hypertrophy: it is virtually bloodless and allows immediate visualization of the TUR defect.

  12. Active palpation sensor for detecting prostatic cancer and hypertrophy

    Science.gov (United States)

    Tanaka, Mami; Furubayashi, Mitsuyuki; Tanahashi, Yoshikatsu; Chonan, Seiji

    2001-03-01

    This paper is concerned with the development of an active palpation sensor for detecting the prostatic cancer and hypertrophy. The receptor of the sensor is a polyvinylidene fluoride (PVDF) film placed on the surface of a sponge rubber layer. It is mounted on a linear z-translation bar and inserted into the examinee's rectum being protected by a medical rubber glove. After positioned faced to the prostate gland, the sensor probe is driven sinusoidally at about 50Hz with peak-to-peak amplitude 2mm. The voltage signal from the PVDF film is integrated over the sampling period and used as the output of sensor for extracting the features of the collected data. The evaluation of stiffness by the sensor on 27 normal and unhealthy prostate glands are compared with the results of diagnosis by the doctor's palpation. It is shown that the output of sensor becomes greater with an increase of the stiffness of the prostate gland, which has good correlation with the doctor's evaluation on the stiffness. Further results on the laboratory test reconfirm that the present sensor well discriminates the stiffness of the prostate glands in vivo and non-invasively.

  13. Mean platelet volume levels in children with adenoid hypertrophy.

    Science.gov (United States)

    Kucur, Cuneyt; Kulekci, Semra; Zorlu, Aylin; Savran, Bircan; Oghan, Fatih; Yildirim, Nadir

    2014-01-01

    Adenoid hypertrophy (AH) is a common disorder in children, resulting in chronic nasal congestion. This chronic congestion should be evaluated carefully because it can lead to chronic upper airway obstruction. Many authors have suggested that increased nasal resistance to respiration may cause disturbances in the pulmonary ventilation and carry the risk of cardiopulmonary diseases. Mean platelet volume (MPV) is a marker of platelet function and is positively associated with indicators of platelet activity. Mean platelet volume is an indicator of larger and more reactive platelets and has been shown to be increased in patients with vascular disease, including peripheral, pulmonary, and coronary artery disease. Recently, MPV levels have also been shown to be increased in patients with severe obstructive sleep apnea, and marked nasal septal deviation. Moreover, increased MPV has also been shown to have a prognostic role in cardiovascular disease. We investigated whether MPV is higher in patients with AH and whether higher MPV levels can be reduced by adenoidectomy. To the best of our knowledge, this is the first study to investigate MPV in patients with AH. Our results suggest that MPV, a determinant of platelet activation, is elevated in patients with AH and adenoidectomy is an effective therapeutic measure in such patients. Increased platelet activation may be related to an increase of cardiopulmonary risk in patients with AH.

  14. Hepatitis C Virus, Cholesterol and Lipoproteins — Impact for the Viral Life Cycle and Pathogenesis of Liver Disease

    Directory of Open Access Journals (Sweden)

    Thomas F. Baumert

    2013-05-01

    Full Text Available Hepatitis C virus (HCV is a leading cause of chronic liver disease, including chronic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Hepatitis C infection associates with lipid and lipoprotein metabolism disorders such as hepatic steatosis, hypobetalipoproteinemia, and hypocholesterolemia. Furthermore, virus production is dependent on hepatic very-low-density lipoprotein (VLDL assembly, and circulating virions are physically associated with lipoproteins in complexes termed lipoviral particles. Evidence has indicated several functional roles for the formation of these complexes, including co-opting of lipoprotein receptors for attachment and entry, concealing epitopes to facilitate immune escape, and hijacking host factors for HCV maturation and secretion. Here, we review the evidence surrounding pathogenesis of the hepatitis C infection regarding lipoprotein engagement, cholesterol and triglyceride regulation, and the molecular mechanisms underlying these effects.

  15. Hepatic manifestations of celiac disease

    Directory of Open Access Journals (Sweden)

    Hugh James Freeman

    2010-05-01

    Full Text Available Hugh James FreemanDepartment of Medicine (Gastroenterology, University of British Columbia, Vancouver, British Columbia, CanadaAbstract: Different hepatic and biliary tract disorders may occur with celiac disease. Some have been hypothesized to share genetic or immunopathogenetic factors, such as primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis. Other hepatic changes in celiac disease may occur with malnutrition resulting from impaired nutrient absorption, including hepatic steatosis. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma.Keywords: celiac disease, autoimmune liver disease, primary biliary cirrhosis, fatty liver, gluten-free diet

  16. Diagnosis of bacterial hepatic abscess by CT

    Institute of Scientific and Technical Information of China (English)

    Cheng-Lin Wang; Xue-Jun Guo; Shui-Bo Qiu; Yi Lei; Zhi-Dong Yuan; Han-Bin Dong; Hui-An Liu

    2007-01-01

    BACKGROUND: Bacterial hepatic abscess usually is acute and progressive, often resulting in sepsis, impairment of liver function and disseminated intravascular coagulation. The mortality rate was as high as 80%in the past. For the purpose of early diagnosis and differential diagnosis of this disease, we probed the imaging manifestations and their characteristics in bacterial hepatic abscesses by CT scan. METHODS:Twenty-four lesions from 21 patients with bacterial hepatic abscesses that were conifrmed by clinical features, puncture and culture were reviewed for CT manifestations. Fourteen patients were male and 7 were female, with an average age of 56.2 years. All lesions underwent CT plain scan and three-phase enhanced scan and 15 patients underwent delayed-phase imaging. Three senior radiologists read the iflms in accordance with a standard. RESULTS: Among 24 lesions, 18 (75%) were situated in the right liver with diameters of 1.4-9.3 cm (average 4.5 cm). Nineteen (79.2%) lesions were round or sub-round in shape, and 22 (91.7%) had smooth, uninterrupted and sharp edges. All lesions showed low attenuation of less than 20 Hu. Twenty-two enhanced lesions (91.7%) had rim-shaped enhancement in the abscess wall, and 13 (54.2%) showed single or double-ring signs. Eighteen (75%) displayed honeycomb-like, grid-like or strip-like enhancement. Eighteen (75%) were regionally enhanced in the surroundings or upper or lower layers. Only 2 (8.3%) displayed a gas-liquid surface sign. CONCLUSIONS:  The CT ifndings of bacterial hepatic abscess are usually typical, and the diagnosis of the abscess is not dififcult. To precisely diagnose atypical cases, it is necessary to combine CT with clinical observations and follow-up.

  17. Epidemiology of Hepatitis B and Hepatitis C Virus infections among ...

    African Journals Online (AJOL)

    Abstract. Hepatitis B and hepatitis C virus infection are common in Nigeria; where they ... the epidemiology of HBV and HCV infection among HIV Counseling and Testing (HCT) ... Clients who declined to sign the consent form were excluded.

  18. Gall-forming root-knot nematodes hijack key plant cellular functions to induce multinucleate and hypertrophied feeding cells.

    Science.gov (United States)

    Favery, Bruno; Quentin, Michaël; Jaubert-Possamai, Stéphanie; Abad, Pierre

    2016-01-01

    Among plant-parasitic nematodes, the root-knot nematodes (RKNs) of the Meloidogyne spp. are the most economically important genus. RKN are root parasitic worms able to infect nearly all crop species and have a wide geographic distribution. During infection, RKNs establish and maintain an intimate relationship with the host plant. This includes the creation of a specialized nutritional structure composed of multinucleate and hypertrophied giant cells, which result from the redifferentiation of vascular root cells. Giant cells constitute the sole source of nutrients for the nematode and are essential for growth and reproduction. Hyperplasia of surrounding root cells leads to the formation of the gall or root-knot, an easily recognized symptom of plant infection by RKNs. Secreted effectors produced in nematode salivary glands and injected into plant cells through a specialized feeding structure called the stylet play a critical role in the formation of giant cells. Here, we describe the complex interactions between RKNs and their host plants. We highlight progress in understanding host plant responses, focusing on how RKNs manipulate key plant processes and functions, including cell cycle, defence, hormones, cellular scaffold, metabolism and transport.

  19. Surveillance for Viral Hepatitis - United States, 2014

    Science.gov (United States)

    ... and Programs Resource Center Viral Hepatitis Surveillance for Viral Hepatitis – United States, 2014 Recommend on Facebook Tweet Share ... Cases Hepatitis A Hepatitis B Hepatitis C Discussion Hepatitis A virus Index PAGE DESCRIPTION Table 2.1 Reported ...

  20. Viral kinetics of the Hepatitis C virus

    NARCIS (Netherlands)

    F.C. Bekkering (Frank)

    2001-01-01

    textabstractHepatitis A virus and hepatitis B virus were identified as the cause of infectious hepatitis and serum hepatitis respectively in the beginning of the seventies. After introduction of screening tests for hepatitis A and B 4 only 25% of the cases of post transfusion hepatitis were found to