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Sample records for cortical spreading ischemia

  1. [Cortical spreading depolarization: a new pathophysiological mechanism in neurological diseases].

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    Sánchez-Porras, Renán; Robles-Cabrera, Adriana; Santos, Edgar

    2014-05-20

    Cortical spreading depolarization is a wave of almost complete depolarization of the neuronal and glial cells that occurs in different neurological diseases such as migraine with aura, subarachnoid hemorrhage, intracerebral hemorrhage, head trauma and stroke. These depolarization waves are characterized by a change in the negative potential with an amplitude between -10 and -30mV, duration of ∼1min and changes in the ion homeostasis between the intra- and extracellular space. This results in neuronal edema and dendritic distortion. Under pathologic states of hypoperfusion, cortical spreading depolarization can produce oxidative stress, worsen hypoxia and induce neuronal death. This is due to intense arterial vasoconstriction produced by an inverse response called spreading ischemia. Only in the last years there has been an electrophysiological confirmation of cortical spreading depolarization in human brains. Occurrence of cortical spreading depolarization has been associated with worse outcome in patients. Currently, increased knowledge regarding the pathophysiologic mechanisms supports the hypothetical correlation of cortical spreading depolarization with brain damage in humans. There are diverse therapeutic alternatives that promise inhibition of cortical spreading depolarization and subsequent better outcomes. Copyright © 2013 Elsevier España, S.L. All rights reserved.

  2. The continuum of spreading depolarizations in acute cortical lesion development

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    Hartings, Jed A; Shuttleworth, C William; Kirov, Sergei A;

    2017-01-01

    A modern understanding of how cerebral cortical lesions develop after acute brain injury is based on Aristides Leão's historic discoveries of spreading depression and asphyxial/anoxic depolarization. Treated as separate entities for decades, we now appreciate that these events define a continuum...... of spreading mass depolarizations, a concept that is central to understanding their pathologic effects. Within minutes of acute severe ischemia, the onset of persistent depolarization triggers the breakdown of ion homeostasis and development of cytotoxic edema. These persistent changes are diagnosed....... The causal role of these waves in lesion development has been proven by real-time monitoring of electrophysiology, blood flow, and cytotoxic edema. The spreading depolarization continuum further applies to other models of acute cortical lesions, suggesting that it is a universal principle of cortical lesion...

  3. Cortical spreading depression-induced preconditioning in the brain

    Institute of Scientific and Technical Information of China (English)

    Ping-ping Shen; Shuai Hou; Di Ma; Ming-ming Zhao; Ming-qin Zhu; Jing-dian Zhang; Liang-shu Feng; Li Cui; Jia-chun Feng

    2016-01-01

    Cortical spreading depression is a technique used to depolarize neurons. During focal or global ischemia, cortical spreading depression-induced preconditioning can enhance tolerance of further injury. Howev-er, the underlying mechanism for this phenomenon remains relatively unclear. To date, numerous issues exist regarding the experimental model used to precondition the brain with cortical spreading depression, such as the administration route, concentration of potassium chloride, induction time, duration of the protection provided by the treatment, the regional distribution of the protective effect, and the types of neurons responsible for the greater tolerance. In this review, we focus on the mechanisms underlying cor-tical spreading depression-induced tolerance in the brain, considering excitatory neurotransmission and metabolism, nitric oxide, genomic reprogramming, inlfammation, neurotropic factors, and cellular stress response. Speciifcally, we clarify the procedures and detailed information regarding cortical spreading de-pression-induced preconditioning and build a foundation for more comprehensive investigations in the ifeld of neural regeneration and clinical application in the future.

  4. Vagus nerve stimulation inhibits cortical spreading depression.

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    Chen, Shih-Pin; Ay, Ilknur; de Morais, Andreia Lopes; Qin, Tao; Zheng, Yi; Sadeghian, Homa; Oka, Fumiaki; Simon, Bruce; Eikermann-Haerter, Katharina; Ayata, Cenk

    2016-04-01

    Vagus nerve stimulation has recently been reported to improve symptoms of migraine. Cortical spreading depression is the electrophysiological event underlying migraine aura and is a trigger for headache. We tested whether vagus nerve stimulation inhibits cortical spreading depression to explain its antimigraine effect. Unilateral vagus nerve stimulation was delivered either noninvasively through the skin or directly by electrodes placed around the nerve. Systemic physiology was monitored throughout the study. Both noninvasive transcutaneous and invasive direct vagus nerve stimulations significantly suppressed spreading depression susceptibility in the occipital cortex in rats. The electrical stimulation threshold to evoke a spreading depression was elevated by more than 2-fold, the frequency of spreading depressions during continuous topical 1 M KCl was reduced by ∼40%, and propagation speed of spreading depression was reduced by ∼15%. This effect developed within 30 minutes after vagus nerve stimulation and persisted for more than 3 hours. Noninvasive transcutaneous vagus nerve stimulation was as efficacious as direct invasive vagus nerve stimulation, and the efficacy did not differ between the ipsilateral and contralateral hemispheres. Our findings provide a potential mechanism by which vagus nerve stimulation may be efficacious in migraine and suggest that susceptibility to spreading depression is a suitable platform to optimize its efficacy.

  5. Neuroprotection and acidosis induced by cortical spreading depression

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    Kwong KK

    2016-12-01

    Full Text Available Kenneth K Kwong, Suk-tak Chan Department of Radiology, MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA We read with interest the article “Cortical spreading depression produces a neuroprotective effect activating mitochondrial uncoupling protein-5” published in Neuropsychiatr Dis Treat by Viggiano et al.1 The authors showed that cerebral spreading depression (CSD triggered uncoupling protein-5 (UCP-5,1 which had been reported to exert a long-term effect upon neuron protection.2 The result is another piece in CSD literature on modifying gene expressions to provide neuroprotection to subsequent ischemic episodes.3,4 Authors' replyGiovanni Messina1,2Emanuela Viggiano1,3Vincenzo Monda1Antonietta Messina1Fiorenzo Moscatelli2Anna Valenzano2Domenico Tafuri4Vincenzo De Luca5Giuseppe Cibelli2Marcellino Monda1 1Section of Human Physiology and Unit of Dietetic and Sport Medicine, Department of Experimental Medicine, Second University of Naples, Caserta, 2Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 3Department of Medicine, University of Padua, Padua, 4Department of Motor Sciences and Wellness, University of Naples “Parthenope,” Napoli, Italy; 5Department of Psychiatry, University of Toronto, Toronto, ON, Canada Thank you for the attention paid to our article entitled: “Cortical spreading depression produces a neuroprotective effect activating mitochondrial uncoupling protein-5”.1 We do agree that cerebral spreading depression (CSD-induced acidosis is an intriguing aspect of the neuroprotection puzzle. It is well known that CSD is involved in the pathophysiology of migraine, cerebral ischemia, subarachnoid hemorrhage, and traumatic brain injury.2–7 View the original paper by Viggiano and colleagues. 

  6. Cortical spreading depression in migraine-time to reconsider?

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    Alan J McComas

    2015-08-01

    Full Text Available New evidence concerning the pathophysiology of migraine has come from the results of therapeutic transcranial magnetic stimulation (tTMS. The instantaneous responses to single pulses applied during the aura or headache phase, together with a number of other observations, make it unlikely that cortical spreading depression is involved in migraine. tTMS is considered to act by abolishing abnormal impulse activity in cortical pyramidal neurons and a suggestion is made as to how this activity could arise.

  7. Cortical spreading depression impairs oxygen delivery and metabolism in mice.

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    Yuzawa, Izumi; Sakadžić, Sava; Srinivasan, Vivek J; Shin, Hwa Kyoung; Eikermann-Haerter, Katharina; Boas, David A; Ayata, Cenk

    2012-02-01

    Cortical spreading depression (CSD) is associated with severe hypoperfusion in mice. Using minimally invasive multimodal optical imaging, we show that severe flow reductions during and after spreading depression are associated with a steep decline in cerebral metabolic rate of oxygen. Concurrent severe hemoglobin desaturation suggests that the oxygen metabolism becomes at least in part supply limited, and the decrease in cortical blood volume implicates vasoconstriction as the mechanism. In support of oxygen supply-demand mismatch, cortical nicotinamide adenine dinucleotide (NADH) fluorescence increases during spreading depression for at least 5 minutes, particularly away from parenchymal arterioles. However, modeling of tissue oxygen delivery shows that cerebral metabolic rate of oxygen drops more than predicted by a purely supply-limited model, raising the possibility of a concurrent reduction in oxygen demand during spreading depression. Importantly, a subsequent spreading depression triggered within 15 minutes evokes a monophasic flow increase superimposed on the oligemic baseline, which markedly differs from the response to the preceding spreading depression triggered in naive cortex. Altogether, these data suggest that CSD is associated with long-lasting oxygen supply-demand mismatch linked to severe vasoconstriction in mice.

  8. Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-Nitro-L-arginine induces cortical spreading ischemia when K+0+ is increased in the subarachnoid space

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    Dreier, J.P.; Körner, K.; Ebert, Nathalie

    1998-01-01

    Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)......Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)...

  9. Cortical spreading depression produces a neuroprotective effect activating mitochondrial uncoupling protein-5

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    Viggiano E

    2016-07-01

    Full Text Available Emanuela Viggiano,1,2 Vincenzo Monda,1 Antonietta Messina,1 Fiorenzo Moscatelli,3 Anna Valenzano,3 Domenico Tafuri,4 Giuseppe Cibelli,3 Bruno De Luca,1 Giovanni Messina,1,3 Marcellino Monda1 1Department of Experimental Medicine, Section of Human Physiology and Unit of Dietetics and Sports Medicine, Second University of Naples, Naples, 2Department of Medicine, University of Padua, Padua, 3Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 4Department of Motor Sciences and Wellness, University of Naples “Parthenope”, Naples, Italy Abstract: Depression of electrocorticogram propagating over the cortex surface results in cortical spreading depression (CSD, which is probably related to the pathophysiology of stroke, epilepsy, and migraine. However, preconditioning with CSD produces neuroprotection to subsequent ischemic episodes. Such effects require the expression or activation of several genes, including neuroprotective ones. Recently, it has been demonstrated that the expression of the uncoupling proteins (UCPs 2 and 5 is amplified during brain ischemia and their expression exerts a long-term effect upon neuron protection. To evaluate the neuroprotective consequence of CSD, the expression of UCP-5 in the brain cortex was measured following CSD induction. CSD was evoked in four samples of rats, which were sacrificed after 2 hours, 4 hours, 6 hours, and 24 hours. Western blot analyses were carried out to measure UCP-5 concentrations in the prefrontal cortices of both hemispheres, and immunohistochemistry was performed to determine the localization of UCP-5 in the brain cortex. The results showed a significant elevation in UCP-5 expression at 24 hours in all cortical strata. Moreover, UCP-5 was triggered by CSD, indicating that UCP-5 production can have a neuroprotective effect. Keywords: cortical spreading depression, neuroprotective effect, uncoupling protein-5

  10. In vivo optical imaging of cortical spreading depression in rat

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    Chen, Shangbin; Li, Pengcheng; Luo, Weihua; Gong, Hui; Cheng, Haiying; Luo, Qingming

    2003-12-01

    Intrinsic optical signals imaging (IOSI) and laser speckle imaging (LSI) are both novel techniques for functional neuroimaging in vivo. Combining them to study cortical spreading depression (CSD) which is an important disease model for migraine and other neurological disorders. CSD were induced by pinprick in Sprague-Dawley rats. Intrinsic optical signals (IOS) at 540 nm showed CSD evolution happened in one hemisphere cortex at speeds of 3.7+/-0.4 mm/min, and the vasodilation closely correlated a four-phasic response. By LSI, we observed a transient and significant increase cerebral blood flow (CBF). In this paper, optical imaging would be showed as a powerful tool for describing the hemodynamic character during CSD in rat.

  11. Cerebral blood flow in migraine and cortical spreading depression

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    Lauritzen, M.

    1987-01-01

    In a series of migraine patients, carotid arteriography was carried out as part of the clinical evalution. Nine patients developed a migrainous attack with focal neurological symptoms and headache after the angiography and during the subsequent, ongoing regional cerebral blood flow rCBF study. rCBF was measured by bolus injection of Xenon/sup 133/ into the internal carotid artery and a gamma camera with 254 collimated scintillation detectors covering the lateral aspect of the hemisphere. This technique depicts rCBF mainly at the level of the superficial cortex, with no depth resolution. The resolution is 1 cm/sup 2/ providing detailed spatial information of the cortical blood flow. Other methods for measuring local blood flow in animal and man employ a radioactive, freely diffusible tracer, in combination with an autoradiographic technique for the assessment of the tissue concentration, the so-called autoradiographic methods. In the series of patients with spontaneous migraine, rCBF was estimated using an in-vivo application of the autoradiographic principle. Xenon/sup 133/ was administered by inhalation and the time course of the arterial concentration curve was assessed by a scintillation detector over the upper right lung, since the arterial curve has been found to follow the shape of the lung curve. The rCBF was studied accompanying cortical spreading depression in rat experiments to evaluate wheter this phenomenon could explain the blood flow changes in migraine. (/sup 14/C) iodoantipyrine was given as an intravenous bolus injection and the brain content of indicator was determined by tissue sample or autoradiography after 10 or 20 seconds of isotope circulation. The conditions of the autoradiographic methods are that the flow remains constant within the period of measuring, and that the region under study is homogenous with regard to flow and lambda. (EG).

  12. Cortical spreading depolarization increases adult neurogenesis, and alters behavior and hippocampus-dependent memory in mice.

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    Urbach, Anja; Baum, Eileen; Braun, Falko; Witte, Otto W

    2017-05-01

    Cortical spreading depolarizations are an epiphenomenon of human brain pathologies and associated with extensive but transient changes in ion homeostasis, metabolism, and blood flow. Previously, we have shown that cortical spreading depolarization have long-lasting consequences on the brains transcriptome and structure. In particular, we found that cortical spreading depolarization stimulate hippocampal cell proliferation resulting in a sustained increase in adult neurogenesis. Since the hippocampus is responsible for explicit memory and adult-born dentate granule neurons contribute to this function, cortical spreading depolarization might influence hippocampus-dependent cognition. To address this question, we induced cortical spreading depolarization in C57Bl/6 J mice by epidural application of 1.5 mol/L KCl and evaluated neurogenesis and behavior at two, four, or six weeks thereafter. Congruent with our previous findings in rats, we found that cortical spreading depolarization increases numbers of newborn dentate granule neurons. Moreover, exploratory behavior and object location memory were consistently enhanced. Reference memory in the water maze was virtually unaffected, whereas memory formation in the Barnes maze was impaired with a delay of two weeks and facilitated after four weeks. These data show that cortical spreading depolarization produces lasting changes in psychomotor behavior and complex, delay- and task-dependent changes in spatial memory, and suggest that cortical spreading depolarization-like events affect the emotional and cognitive outcomes of associated brain pathologies.

  13. Cortical spreading depression occurs during elective neurosurgical procedures.

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    Carlson, Andrew P; William Shuttleworth, C; Mead, Brittany; Burlbaw, Brittany; Krasberg, Mark; Yonas, Howard

    2017-01-01

    OBJECTIVE Cortical spreading depression (CSD) has been observed with relatively high frequency in the period following human brain injury, including traumatic brain injury and ischemic/hemorrhagic stroke. These events are characterized by loss of ionic gradients through massive cellular depolarization, neuronal dysfunction (depression of electrocorticographic [ECoG] activity) and slow spread (2-5 mm/min) across the cortical surface. Previous data obtained in animals have suggested that even in the absence of underlying injury, neurosurgical manipulation can induce CSD and could potentially be a modifiable factor in neurosurgical injury. The authors report their initial experience with direct intraoperative ECoG monitoring for CSD. METHODS The authors prospectively enrolled patients undergoing elective craniotomy for supratentorial lesions in cases in which the surgical procedure was expected to last > 2 hours. These patients were monitored for CSD from the time of dural opening through the time of dural closure, using a standard 1 × 6 platinum electrode coupled with an AC or full-spectrum DC amplifier. The data were processed using standard techniques to evaluate for slow potential changes coupled with suppression of high-frequency ECoG propagating across the electrodes. Data were compared with CSD validated in previous intensive care unit (ICU) studies, to evaluate recording conditions most likely to permit CSD detection, and identify likely events during the course of neurosurgical procedures using standard criteria. RESULTS Eleven patients underwent ECoG monitoring during elective neurosurgical procedures. During the periods of monitoring, 2 definite CSDs were observed to occur in 1 patient and 8 suspicious events were detected in 4 patients. In other patients, either no events were observed or artifact limited interpretation of the data. The DC-coupled amplifier system represented an improvement in stability of data compared with AC-coupled systems. Compared

  14. Ischemia-Induced Neural Stem/Progenitor Cells in the Pia Mater Following Cortical Infarction

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    Nakagomi, Takayuki; Molnar, Zoltan; Nakano-Doi, Akiko; Taguchi, Akihiko; Saino, Orie; Kubo, Shuji; Clausen, Martijn; Yoshikawa, Hiroo; Nakagomi, Nami; Matsuyama, Tomohiro

    2011-01-01

    Increasing evidence shows that neural stem/ progenitor cells (NSPCs) can be activated in the nonconventional neurogenic zones such as the cortex following ischemic stroke. However, the precise origin, identity, and subtypes of the ischemia-induced NSPCs (iNSPCs), which can contribute to cortical

  15. Ischemia-Induced Neural Stem/Progenitor Cells in the Pia Mater Following Cortical Infarction

    NARCIS (Netherlands)

    Nakagomi, Takayuki; Molnar, Zoltan; Nakano-Doi, Akiko; Taguchi, Akihiko; Saino, Orie; Kubo, Shuji; Clausen, Martijn; Yoshikawa, Hiroo; Nakagomi, Nami; Matsuyama, Tomohiro

    2011-01-01

    Increasing evidence shows that neural stem/ progenitor cells (NSPCs) can be activated in the nonconventional neurogenic zones such as the cortex following ischemic stroke. However, the precise origin, identity, and subtypes of the ischemia-induced NSPCs (iNSPCs), which can contribute to cortical neu

  16. Mathematical approaches to modeling of cortical spreading depression

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    Miura, Robert M.; Huang, Huaxiong; Wylie, Jonathan J.

    2013-12-01

    Migraine with aura (MwA) is a debilitating disease that afflicts about 25%-30% of migraine sufferers. During MwA, a visual illusion propagates in the visual field, then disappears, and is followed by a sustained headache. MwA was conjectured by Lashley to be related to some neurological phenomenon. A few years later, Leão observed electrophysiological waves in the brain that are now known as cortical spreading depression (CSD). CSD waves were soon conjectured to be the neurological phenomenon underlying MwA that had been suggested by Lashley. However, the confirmation of the link between MwA and CSD was not made until 2001 by Hadjikhani et al. [Proc. Natl. Acad. Sci. U.S.A. 98, 4687-4692 (2001)] using functional MRI techniques. Despite the fact that CSD has been studied continuously since its discovery in 1944, our detailed understandings of the interactions between the mechanisms underlying CSD waves have remained elusive. The connection between MwA and CSD makes the understanding of CSD even more compelling and urgent. In addition to all of the information gleaned from the many experimental studies on CSD since its discovery, mathematical modeling studies provide a general and in some sense more precise alternative method for exploring a variety of mechanisms, which may be important to develop a comprehensive picture of the diverse mechanisms leading to CSD wave instigation and propagation. Some of the mechanisms that are believed to be important include ion diffusion, membrane ionic currents, osmotic effects, spatial buffering, neurotransmitter substances, gap junctions, metabolic pumps, and synaptic connections. Discrete and continuum models of CSD consist of coupled nonlinear differential equations for the ion concentrations. In this review of the current quantitative understanding of CSD, we focus on these modeling paradigms and various mechanisms that are felt to be important for CSD.

  17. Therapeutic potential of the novel hybrid molecule JM-20 against focal cortical ischemia in rats

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    Yanier Núñez Figueredo

    2016-08-01

    Full Text Available Context: Despite the great mortality and morbidity of stroke, treatment options remain limited. We previously showed that JM-20, a novel synthetic molecule, possessed a strong neuroprotective effect in rats subjected to transient middle cerebral artery occlusion. However, to verify the robustness of the pre-clinical neuroprotective effects of JM-20 to get good prognosis in the translation to the clinic, it is necessary to use other experimental models of brain ischemia. Aims: To evaluate the neuroprotective effects of JM-20 following the onset of permanent focal cerebral ischemia induced in rats by thermocoagulation of blood into pial blood vessels of cerebral cortices. Methods: Ischemic lesion was induced by thermocoagulation of blood into pial blood vessels of primary motor and somatosensory cortices. Behavioral performance was evaluated by the cylinder testing for a period of 2, 3 and 7 days after surgery, and was followed by histopathological study in brain cortex stained with hematoxylin- eosin. Results: Ischemic injury resulted in impaired function of the forelimb evidenced by high asymmetry punctuation, and caused histopathological alterations indicative of tissue damage at cerebral cortex. JM-20 treatment (4 and 8 mg/kg significantly decreased asymmetry scores and histological alterations with a marked preservation of cortical neurons. Conclusions: The effects of permanent brain ischemia were strongly attenuated by JM-20 administration, which expands and improves the current preclinical data of JM-20 as neuroprotector against cerebral ischemia, and strongly support the examination of its translation to the clinic to treat acute ischemic stroke.

  18. Continuous nimodipine treatment attenuates cortical infarction in rats subjected to 24 hours of focal cerebral ischemia.

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    Jacewicz, M; Brint, S; Tanabe, J; Pulsinelli, W A

    1990-01-01

    Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 micrograms/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10-15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20-60% smaller cortical infarct volumes than controls (p less than 0.002). Cortical edema was reduced proportionately to the decrease in infarct volume and constituted approximately 36% of the infarct volume. Nimodipine caused a mild hypotensive response that did not aggravate ischemic brain damage. The results indicate that continuous nimodipine treatment, started before induction of focal cerebral ischemia, can attenuate ischemic brain damage and edema as late as 24 h after the onset of ischemia.

  19. Cortico-cortical evoked potentials for sites of early versus late seizure spread in stereoelectroencephalography.

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    Lega, Bradley; Dionisio, Sasha; Flanigan, Patrick; Bingaman, William; Najm, Imad; Nair, Dileep; Gonzalez-Martinez, Jorge

    2015-09-01

    Cortico-cortical evoked potentials offer the possibility of understanding connectivity within seizure networks to improve diagnosis and more accurately identify candidates for seizure surgery. We sought to determine if cortico-cortical evoked potentials and post-stimulation oscillatory changes differ for sites of EARLY versus LATE ictal spread. 37 patients undergoing stereoelectroencephalography were tested using a cortico-cortical evoked potential paradigm. All electrodes were classified according to the speed of ictal spread. EARLY spread sites were matched to a LATE spread site equidistant from the onset zone. Root-mean-square was used to quantify evoked responses and post-stimulation gamma band power and coherence were extracted and compared. Sites of EARLY spread exhibited significantly greater evoked responses after stimulation across all patients (t(36)=2.973, p=0.004). Stimulation elicited enhanced gamma band activity at EARLY spread sites (t(36)=2.61, p=0.03, FDR corrected); this gamma band oscillation was highly coherent with the onset zone. Cortico-cortical evoked potentials and post-stimulation changes in gamma band activity differ between sites of EARLY versus LATE ictal spread. The oscillatory changes can help visualize connectivity within the seizure network.

  20. The effect of a gap-junction blocker, carbenoxolone, on ischemic brain injury and cortical spreading depression.

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    Tamura, K; Alessandri, B; Heimann, A; Kempski, O

    2011-10-27

    Cortical spreading depression (CSD) has been shown to cause secondary cell loss in experimental models of brain injury and in patients, and blocking of CSD is a potential neuroprotective strategy. Here we tested the hypothesis that gap junctions affect CSD under physiological conditions as well as infarct development in a rat two-vein occlusion model suited to study pathophysiology of the penumbra (n = 71). We applied the gap junction blocker carbenoxolone (CBX) or saline intra-ventricularly. Interestingly, CBX temporarily increased systemic blood pressure and cortical blood flow (41% and 53%, 15 min after 250 μg CBX). We induced CSD with cortical microinjection of potassium chloride (KCl), counted how many spontaneous CSDs after CSD induction were elicited and measured the propagation velocity. After 250 μg CBX administration, significant 37.5 ± 6.5 additional CSDs were seen. CSD velocity increased significantly after 50 μg and 250 μg CBX. Occlusion of two adjacent cortical veins using Rose Bengal dye and fiberoptic illumination followed by 250 μg CBX or saline showed a significant more than doubling of infarct volumes 7 days after CBX. The current experiments provide evidence that CBX can accelerate the initiation and propagation of CSD suggesting opening of gap junctions is not required for CSD propagation. Blocking gap junctions worsens outcome from focal cerebral ischemia. Hence, measures intended to improve spatial buffering via astroglial gap junctions could have therapeutic potential in disease processes involving CSD. Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

  1. Effects of ketamine, midazolam, thiopental, and propofol on brain ischemia injury in rat cerebral cortical slices

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    Qing-shengXUE; Bu-weiYU; Ze-jianWANG; Hong-zhuanCHEN

    2004-01-01

    AIM: To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices. METHODS: Cerebral cortical slices were incu-bated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine,midazolam, thiopental, and propofol were quantitativlye evaluated by ELISA reader of absorbance (A) at 490 nm,which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured. RESULTS: Progressive prolongation of OGD resulted in decreases of TTC staining.The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P<0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD(P<0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited thedecrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 μmol/L) and thiopental (400μmol/L) partly attenuated this decrease. Propofol at high concentration (100 μmol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P<0.01). CONCLUSION; Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.

  2. PSD-95 uncoupling from NMDA receptors by Tat-N-dimer ameliorates neuronal depolarisation in cortical spreading depression

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    Kucharz, Krzysztof; Søndergaard Rasmussen, Ida; Bach, Anders;

    2017-01-01

    of the negative shift in direct current potential by 33% (4.1 mV). Furthermore, the compound diminished the average depression of spontaneous electrocorticographic activity by 11% during first 40 min of post-cortical spreading depression recovery, but did not mitigate the suppressing effect of cortical spreading...... during the first hour after i.v. injection. The Tat-N-dimer suppressed stimulation-evoked synaptic activity by 2-20%, while cortical blood flow and cerebral oxygen metabolic (CMRO2) responses were preserved. During cortical spreading depression, the Tat-N-dimer reduced the average amplitude...

  3. Caffeine/nutrition interaction in the rat brain: Influence on latent inhibition and cortical spreading depression.

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    de Aguiar, Márlison José Lima; de Aguiar, Cilene Rejane Ramos Alves; Guedes, Rubem Carlos Araújo

    2011-01-10

    Caffeine, like malnutrition, can produce behavioral and electrophysiological alterations. However, the interaction of both factors remains unclear. Here this interaction has been studied in male Wistar rats previously malnourished during the lactation period by feeding their dams the "regional basic diet" of Northeast Brazil, containing about 8% protein, predominantly from vegetable sources (RBD(8)). At 70-75days of life, a subset of the pups was treated intraperitoneally with 30mg/kg caffeine for 4days while being tested according to the behavioral model of latent inhibition. Another group was subjected to an electrophysiological recording of the phenomenon known as cortical spreading depression, and the effects of caffeine injected during the recording session were evaluated. Caffeine did not affect cortical spreading depression, but antagonized latent inhibition in both the RBD(8)-malnourished rats and in the well-nourished control group fed a chow diet with 22% protein. This effect of caffeine was not seen in malnourished rats fed a protein-supplemented RBD (protein increased to 22% by increasing the proportion of foodstuffs from vegetable origin; RBD(22) group), suggesting that the amino acid imbalance of this diet may modulate the caffeine effects on latent inhibition. The results indicate a differential effect of caffeine in the latent inhibition behavioral model, as compared to the cortical spreading depression phenomenon, and this effect is influenced by the early nutritional status of the animal. We suggest that caffeine may modulate dopaminergic subcortical receptors participating in attention processes, but does not interact at the cortical level, in a way that would affect cortical spreading depression.

  4. Cortical and brain stem changes in neural activity during static handgrip and postexercise ischemia in humans

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    Sander, Mikael; Macefield, Vaughan G; Henderson, Luke A

    2010-01-01

    Static isometric exercise increases muscle sympathetic nerve activity (MSNA) and mean arterial pressure, both of which can be maintained at the conclusion of the exercise by occlusion of the arterial supply [postexercise ischemia (PEI)]. To identify the cortical and subcortical sites involved......, and to differentiate between central command and reflex inputs, we used blood oxygen level-dependent (BOLD) functional MRI (fMRI) of the whole brain (3 T). Subjects performed submaximal static handgrip exercise for 2 min followed by 6 min of PEI; MSNA was recorded on a separate day. During the contraction phase......, parallel increases in BOLD signal intensity occurred in the contralateral primary motor cortex and cerebellar nuclei and cortex; these matched the effort profile and ceased at the conclusion of the contraction. Progressive increases in the contralateral insula and primary and secondary somatosensory...

  5. Homocysteine Aggravates Cortical Neural Cell Injury through Neuronal Autophagy Overactivation following Rat Cerebral Ischemia-Reperfusion

    Directory of Open Access Journals (Sweden)

    Yaqian Zhao

    2016-07-01

    Full Text Available Elevated homocysteine (Hcy levels have been reported to be involved in neurotoxicity after ischemic stroke. However, the underlying mechanisms remain incompletely understood to date. In the current study, we hypothesized that neuronal autophagy activation may be involved in the toxic effect of Hcy on cortical neurons following cerebral ischemia. Brain cell injury was determined by hematoxylin-eosin (HE staining and TdT-mediated dUTP Nick-End Labeling (TUNEL staining. The level and localization of autophagy were detected by transmission electron microscopy, western blot and immunofluorescence double labeling. The oxidative DNA damage was revealed by immunofluorescence of 8-Hydroxy-2′-deoxyguanosine (8-OHdG. Hcy treatment aggravated neuronal cell death, significantly increased the formation of autophagosomes and the expression of LC3B and Beclin-1 in the brain cortex after middle cerebral artery occlusion-reperfusion (MCAO. Immunofluorescence analysis of LC3B and Beclin-1 distribution indicated that their expression occurred mainly in neurons (NeuN-positive and hardly in astrocytes (GFAP-positive. 8-OHdG expression was also increased in the ischemic cortex of Hcy-treated animals. Conversely, LC3B and Beclin-1 overexpression and autophagosome accumulation caused by Hcy were partially blocked by the autophagy inhibitor 3-methyladenine (3-MA. Hcy administration enhanced neuronal autophagy, which contributes to cell death following cerebral ischemia. The oxidative damage-mediated autophagy may be a molecular mechanism underlying neuronal cell toxicity of elevated Hcy level.

  6. Nimodipine posttreatment does not increase blood flow in rats with focal cortical ischemia.

    Science.gov (United States)

    Dirnagl, U; Jacewicz, M; Pulsinelli, W

    1990-09-01

    We used laser-Doppler flowmetry to study the effect of nimodipine administered after the onset of focal cortical ischemia on regional cerebral blood flow in 16 halothane-anesthetized, mechanically ventilated Wistar rats. We selected the Wistar rats strain since it would provide a wide range of ischemia severities to test the vascular response to nimodipine. Laser-Doppler probes continuously recorded regional cerebral blood flow at two or three sites over the parietal cortex (dura intact) while brain temperature was regulated at 37 degrees C. Occlusion of the right middle cerebral and common carotid arteries reduced cerebral blood flow to a mean of 38% (range 13-77%) of baseline. Thirty minutes later, either 2 micrograms/kg/min nimodipine (n = 8) or its vehicle, polyethylene glycol 400 (n = 8), was administered by a continuous intravenous infusion. Over 60 minutes of treatment, both the nimodipine-treated and vehicle-treated groups showed a trivial (3%) mean increase in cerebral blood flow. Nimodipine failed to augment cerebral blood flow regardless of whether the cortex was severely, moderately, or mildly ischemic.

  7. Subcortical cerebral blood flow and metabolic changes elicited by cortical spreading depression in rat

    Energy Technology Data Exchange (ETDEWEB)

    Mraovitch, S.; Calando, Y.; Goadsby, P.J.; Seylaz, J. (Laboratoire de Recherches Cerebrovasculaire, Paris (France))

    1992-06-01

    Changes in cerebral cortical perfusion (CBF{sub LDF}), local cerebral blood flow (lCBF) and local cerebral glucose utilization (lCGU) elicited by unilateral cortical spreading depression (SD) were monitored and measured in separate groups of rats anesthetized with {alpha}-chloralose. CBF{sub LDF} was recorded with laser Doppler flowmetry, while lCBF and lCGU were measured by the quantitative autoradiographic ({sup 14}C)iodoantipyrine and ({sup 14}C)-2-deoxyglucose methods, respectively. SD elicited a wave of hyperemia after a latency of 2 to 3 min followed by an oligemic phase. Ninety minutes following the onset of SD cortical lCBF and lCGU were essentially the same as on the contralateral side and in sham-treated rats. However, alteration in the lCBF and lCGU in upper and lower brainstem persisted. The present results demonstrate that long-lasting cerebrovascular and metabolic alterations take place within the subcortical regions following SD. These regions provide an attractive site to integrate observations in man concerning spreading depression and the aura of migraine with the other features of the syndrome. 19 refs., 2 figs., 1 tab.

  8. History of migraine with aura and cortical spreading depression from 1941 and onwards

    DEFF Research Database (Denmark)

    Tfelt-Hansen, P C

    2010-01-01

    visual cortex. Leão described cortical spreading depression (CSD) in rabbits in 1944 and noticed its similarity to the migraine aura. Despite these scattered pieces of evidence, the prevailing theory was that the migraine aura was caused by a vasospasm and cortical ischaemia. The advent of a technique...... borders of supply of major cerebral arteries. These observations refuted the ischaemic hypothesis. The human studies showed initial hyperaemia followed by prolonged hypoperfusion. The relation between aura and CSD was known to cause short-lasting, and therefore not obvious vasodilation...... expressed in mice and lower the threshold for CSD. The seminal papers on rCBF and CSD published in the 1980s caused a dramatic shift in our concepts of migraine aura. They moved attention from ischaemia to CSD and thereby to the brain itself, and paved the way for subsequent discoveries of brainstem...

  9. Changes in Mice Brain Spontaneous Electrical Activity during Cortical Spreading Depression due to Mobile Phone Radiation

    Science.gov (United States)

    Sallam, Samera M.; Mohamed, Ehab I.; Dawood, Abdel-Fattah B.

    2008-01-01

    The objective of the present study was to investigate changes in spontaneous EEG activity during cortical spreading depression (CSD) in mice brain. The cortical region of anaesthetized mice were exposed to the electromagnetic fields (EMFs) emitted from a mobile phone (MP, 935.2-960.2 MHz, 41.8 mW/cm2). The effect of EMFs on EEG was investigated before and after exposure to different stimuli (MP, 2% KCl, and MP & 2% KCl). The records of brain spontaneous EEG activity, slow potential changes (SPC), and spindle shaped firings were obtained through an interfaced computer. The results showed increases in the amplitude of evoked spindles by about 87%, 17%, and 226% for MP, 2% KCl, and MP & 2% KCl; respectively, as compared to values for the control group. These results showed that the evoked spindle is a more sensitive indicator of the effect of exposure to EMFs from MP. PMID:23675079

  10. Cortical spreading depression in traumatic brain injuries: is there a role for astrocytes?

    Science.gov (United States)

    Torrente, Daniel; Cabezas, Ricardo; Avila, Marco Fidel; García-Segura, Luis Miguel; Barreto, George E; Guedes, Rubem Carlos Araújo

    2014-04-17

    Cortical spreading depression (CSD) is a presumably pathophysiological phenomenon that interrupts local cortical function for periods of minutes to hours. This phenomenon is important due to its association with different neurological disorders such as migraine, malignant stroke and traumatic brain injury (TBI). Glial cells, especially astrocytes, play an important role in the regulation of CSD and in the protection of neurons under brain trauma. The correlation of TBI with CSD and the astrocytic function under these conditions remain unclear. This review discusses the possible link of TBI and CSD and its implication for neuronal survival. Additionally, we highlight the importance of astrocytic function for brain protection, and suggest possible therapeutic strategies targeting astrocytes to improve the outcome following TBI-associated CSD.

  11. Optical coherence tomography reveals in vivo cortical structures of adult rats in response to cerebral ischemia injury

    Science.gov (United States)

    Ni, Yi-rong; Guo, Zhou-yi; Shu, So-yun; Bao, Xin-min

    2008-12-01

    Optical coherence tomography(OCT) is a high resolution imaging technique which uses light to directly image living tissue. we investigate the potential use of OCT for structural imaging of the ischemia injury mammalian cerebral cortex. And we examine models of middle cerebral artery occlusion (MCAO) in rats in vivo using OCT. In particular, we show that OCT can perform in vivo detection of cortex and differentiate normal and abnormal cortical anatomy. This OCT system in this study provided an axial resolution of 10~15μ m, the transverse resolution of the system is about 25 μm. OCT can provide cross-sectional images of cortical of adult rats in response to cerebral ischemia injury.We conclude that OCT represents an exciting new approach to visualize, in real-time, pathological changes in the cerebral cortex structures and may offer a new tool for Possible neuroscience clinical applications.

  12. Ultrastructural changes of rat cortical neurons following ligustrazine intervention for cerebral ischemia/reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Hui Zhang; Jianfeng Dong; Qiuzhen Zhao; Wen Song; Aihua Bo

    2008-01-01

    low-dose group and ligustrazine high-dose group received ligustrazine injections, 50 mg/kg and 100 mg/kg, respectively. Samples were collected at the same time as the model group.MAIN OUTCOME MEASURES: Alterations of the neuronal ultrastructure and main organelles were ob-served by electron microscopy.RESULTS: Forty Wistar rats were included in the final analysis. Plentiful ribosome and rough endoplasmic reticulum existed in the cytoplasm of cortical neurons in the normal group. Edema existed in the nucleus and cytoplasm of neurons in the model group. The cell membrane was damaged, resulting in the external erup-tion of certain cellular organelles. In the low-dose ligustrazine group, neuronal swelling was decreased in the cytoplasm, whereas cellular organelles were relatively increased. However, the mitochondria remained swollen. The double layer structure disappeared in parts of the mitochondrial membrane. The caryotheca was still broken, and neuronal damage was significantly decreased in the high-dose ligustrazine group. In ad-dition, cytoplasmic swelling was reduced andmost part of caryotheca was complete. Fragmentation of the cellular membrane was not detected. Mitochondrial cristae and the lysosome could also be detected. The number of rough endoplasmic reticulum and free ribosomes was increased, and the structure of great part of caryotheca was clear. In addition, the number of nuclear pore was increased. However, the nuclear hetero-chromatin was relatively reduced.CONCLUSION: In the rat, the protective effects of ligustrazine were significant on neuronal membrane structures and main organelles after cerebral ischemia/reperfusion. There was a dose-dependent effect be-tween neuronal changes and Ligustrazine.

  13. PSD-95 uncoupling from NMDA receptors by Tat- N-dimer ameliorates neuronal depolarization in cortical spreading depression.

    Science.gov (United States)

    Kucharz, Krzysztof; Søndergaard Rasmussen, Ida; Bach, Anders; Strømgaard, Kristian; Lauritzen, Martin

    2017-05-01

    Cortical spreading depression is associated with activation of NMDA receptors, which interact with the postsynaptic density protein 95 (PSD-95) that binds to nitric oxide synthase (nNOS). Here, we tested whether inhibition of the nNOS/PSD-95/NMDA receptor complex formation by anti-ischemic compound, UCCB01-144 (Tat- N-dimer) ameliorates the persistent effects of cortical spreading depression on cortical function. Using in vivo two-photon microscopy in somatosensory cortex in mice, we show that fluorescently labelled Tat- N-dimer readily crosses blood-brain barrier and accumulates in nerve cells during the first hour after i.v. injection. The Tat- N-dimer suppressed stimulation-evoked synaptic activity by 2-20%, while cortical blood flow and cerebral oxygen metabolic (CMRO2) responses were preserved. During cortical spreading depression, the Tat- N-dimer reduced the average amplitude of the negative shift in direct current potential by 33% (4.1 mV). Furthermore, the compound diminished the average depression of spontaneous electrocorticographic activity by 11% during first 40 min of post-cortical spreading depression recovery, but did not mitigate the suppressing effect of cortical spreading depression on cortical blood flow and CMRO2. We suggest that uncoupling of PSD-95 from NMDA receptors reduces overall neuronal excitability and the amplitude of the spreading depolarization wave. These findings may be of interest for understanding the neuroprotective effects of the nNOS/PSD-95 uncoupling in stroke.

  14. Spatio-temporal cerebral blood flow perfusion patterns in cortical spreading depression

    Science.gov (United States)

    Verisokin, Andrey Yu.; Verveyko, Darya V.; Postnov, Dmitry E.

    2017-04-01

    Cortical spreading depression (CSD) is an example of one of the most common abnormalities in biophysical brain functioning. Despite the fact that there are many mathematical models describing the cortical spreading depression (CSD), most of them do not take into consideration the role of redistribution of cerebral blood flow (CBF), that results in the formation of spatio-temporal patterns. The paper presents a mathematical model, which successfully explains the CBD role in the CSD process. Numerical study of this model has revealed the formation of stationary dissipative structures, visually analogous to Turing structures. However, the mechanism of their formation is not diffusion. We show these structures occur due to another type of spatial coupling, that is related to tissue perfusion rate. The proposed model predicts that at similar state of neurons the distribution of blood flow and oxygenation may by different. Currently, this effect is not taken into account when the Blood oxygen-level dependent (BOLD) contrast imaging used in functional magnetic resonance imaging (fMRI). Thus, the diagnosis on the BOLD signal can be ambiguous. We believe that our results can be used in the future for a more correct interpretation of the data obtained with fMRI, NIRS and other similar methods for research of the brain activity.

  15. Dynamic changes in proprotein convertase 2 activity in cortical neurons after ischemia/reperfusion and oxygen-glucose deprivation

    Institute of Scientific and Technical Information of China (English)

    Shuqin Zhan; An Zhou; Chelsea Piper; Tao Yang

    2013-01-01

    In this study, a rat model of transient focal cerebral ischemia was established by performing 100 minutes of middle cerebral artery occlusion, and an in vitro model of experimental oxygen-glucose deprivation using cultured rat cortical neurons was established. Proprotein convertase 2 activity gradually decreased in the ischemic cortex with increasing duration of reperfusion. In cultured rat cortical neurons, the number of terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling-positive neurons significantly increased and proprotein convertase 2 activity also decreased gradually with increasing duration of oxygen-glucose deprivation. These experimental findings indicate that proprotein convertase 2 activity decreases in ischemic rat cortex after reperfusion, as well as in cultured rat cortical neurons after oxygen-glucose deprivation. These changes in enzyme activity may play an important pathological role in brain injury.

  16. Ischemia

    Science.gov (United States)

    Byeon, Suk Ho; Kim, Min; Kwon, Oh Woong

    "Ischemia" implies a tissue damage derived from perfusion insufficiency, not just an inadequate blood supply. Mild thickening and increased reflectivity of inner retina and prominent inner part of synaptic portion of outer plexiform layer are "acute retinal ischemic changes" visible on OCT. Over time, retina becomes thinner, especially in the inner portion. Choroidal perfusion supplies the outer portion of retina; thus, choroidal ischemia causes predominant change in the corresponding tissue.

  17. Poloxamer-188 and citicoline provide neuronal membrane integrity and protect membrane stability in cortical spreading depression.

    Science.gov (United States)

    Yıldırım, Timur; Eylen, Alpaslan; Lule, Sevda; Erdener, Sefik Evren; Vural, Atay; Karatas, Hulya; Ozveren, Mehmet Faik; Dalkara, Turgay; Gursoy-Ozdemir, Yasemin

    2015-01-01

    Under pathological conditions such as brain trauma, subarachnoid hemorrhage and stroke, cortical spreading depression (CSD) or peri-infarct depolarizations contribute to brain damage in animal models of neurological disorders as well as in human neurological diseases. CSD causes transient megachannel opening on the neuronal membrane, which may compromise neuronal survival under pathological conditions. Poloxamer-188 (P-188) and citicoline are neuroprotectants with membrane sealing properties. The aim of this study is to investigate the effect of P-188 and citicoline on the neuronal megachannel opening induced by CSD in the mouse brain. We have monitored megachannel opening with propidium iodide, a membrane impermeable fluorescent dye and, demonstrate that P-188 and citicoline strikingly decreased CSD-induced neuronal PI influx in cortex and hippocampal dentate gyrus. Therefore, these agents may be providing neuroprotection by blocking megachannel opening, which may be related to their membrane sealing action and warrant further investigation for treatment of traumatic brain injury and ischemic stroke.

  18. The effects of anesthetics on cortical spreading depression elicitation and c-fos expression in rats.

    Science.gov (United States)

    Kitahara, Y; Taga, K; Abe, H; Shimoji, K

    2001-01-01

    The effects of anesthetics on the generation of cortical spreading depression (CSD) were investigated. Volatile anesthetics halothane, isoflurane, sevoflurane (0.5, 1.0, and 2.0 MAC), and the intravenous anesthetic pentobarbital were studied. Cortical spreading depression was induced by 3M-KCl applied to a surface of brain cortex for 30 minutes. Direct current (DC) potential was recorded, and the number, amplitude, and duration of CSDs were observed. With increasing concentrations of each volatile anesthetic, there was a dose-related reduction in CSD frequency but not in CSD amplitude. At 2.0 MAC of sevoflurane the suppression of CSD was less than with the other volatile anesthetics. In addition, the influence of anesthetics on expression of c-fos mRNA was investigated. Additional animals anesthetized by isoflurane or sevoflurane were studied. Five CSDs were elicited by electric stimulation (0.5 mV, 1 second) in each animal. In situ hybridization with 35S-labeled oligonucleotides was used to evaluate the level of c-fos mRNA. The expression of c-fos was observed in the hemisphere in which CSD was elicited, but there was no difference in expression of c-fos among the groups. We conclude that volatile anesthetics can induce suppression of CSD elicitation in a dose dependent manner, but that at high concentrations sevoflurane is significantly less effective than other volatile agents. Pentobarbital has the least effect on KCl-induced CSD. These data suggest that the choice of anesthetics can impact the results of studies examining membrane depolarization and the ionic changes initiated by CSD.

  19. Cortical Spreading Depression Causes Unique Dysregulation of Inflammatory Pathways in a Transgenic Mouse Model of Migraine.

    Science.gov (United States)

    Eising, Else; Shyti, Reinald; 't Hoen, Peter A C; Vijfhuizen, Lisanne S; Huisman, Sjoerd M H; Broos, Ludo A M; Mahfouz, Ahmed; Reinders, Marcel J T; Ferrari, Michel D; Tolner, Else A; de Vries, Boukje; van den Maagdenberg, Arn M J M

    2017-05-01

    Familial hemiplegic migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the α1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation ('FHM1 R192Q mice') exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here, we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 h after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep serial analysis of gene expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine.

  20. Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury

    DEFF Research Database (Denmark)

    Lauritzen, Martin; Dreier, Jens Peter; Fabricius, Martin

    2011-01-01

    Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence...... treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves....

  1. Effects of Cortical Spreading Depression on Synaptic Activity, Blood Flow and Oxygen Consumption in Rat Cerebral Cortex

    DEFF Research Database (Denmark)

    Hansen, Henning Piilgaard

    2010-01-01

    As the title of this thesis indicates I have during my PhD studied the effects of cortical spreading depression (CSD) on synaptic activity, blood flow and oxygen consumption in rat cerebral cortex. This was performed in vivo using an open cranial window approach in anesthetized rats. I applied...... two different sets of interneurons. Our data imply that for a given cortical area the amplitude of vascular signals will depend critically on the type of input and hence on the type of neurons activated. In the second study I investigated the effect of cortical spreading depression (CSD) on the evoked...... of neurovascular coupling after topical pretreatment with either inhibitor of CaN pathway (FK506), inhibitor of mPTP formation (NIM811) and combined inhibition of both pathways (FK506+NIM811 or cyclosporin A). A result indicating a potential new treatment aspect for disease states where CSD is known to be involved...

  2. Physical exercise versus fluoxetine: antagonistic effects on cortical spreading depression in Wistar rats.

    Science.gov (United States)

    Mirelle Costa Monteiro, Heloísa; Lima Barreto-Silva, Nathália; Elizabete Dos Santos, Gracyelle; de Santana Santos, Amanda; Séfora Bezerra Sousa, Mariana; Amâncio-Dos-Santos, Ângela

    2015-09-05

    The antidepressant fluoxetine and physical exercise exert similar effects on the serotoninergic system by increasing brain serotonin availability, and both show antagonistic action on cortical excitability. Here we provide the first assessment of the interaction of the two together on cortical spreading depression (CSD) in young adult rats. Wistar rats (40-60 days of life) received fluoxetine (10mg/kg/d, orogastrically) or an equivalent volume of water. Half of the animals from each condition were assigned to perform physical exercise in a treadmill, and the other half formed the sedentary (non-treadmill) control groups. Body parameters (Lee index and thoracic and abdominal circumferences) and the velocity of CSD propagation were investigated. Fluoxetine+exercise animals had less weight gain (78.68±3.19g) than either the fluoxetine-only (93.34±4.77g) or exercise-only group (97.04±3.48g), but body parameters did not differ among them. The velocity of CSD propagation was reduced in the fluoxetine-only and exercise-only groups compared to sedentary water controls (3.24±0.39mm/min). For the fluoxetine+exercise group, CSD velocity values were significantly lower (2.92±0.22mm/min) than for fluoxetine only (3.03±0.35mm/min); however, they were similar to values for the exercise-only group (2.96±0.23mm/min). These findings confirm the similar effects of fluoxetine and exercise and suggest a greater effect of physical exercise in reducing brain excitability.

  3. Increased susceptibility to cortical spreading depression in the mouse model of familial hemiplegic migraine type 2.

    Directory of Open Access Journals (Sweden)

    Loredana Leo

    2011-06-01

    Full Text Available Familial hemiplegic migraine type 2 (FHM2 is an autosomal dominant form of migraine with aura that is caused by mutations of the α2-subunit of the Na,K-ATPase, an isoform almost exclusively expressed in astrocytes in the adult brain. We generated the first FHM2 knock-in mouse model carrying the human W887R mutation in the Atp1a2 orthologous gene. Homozygous Atp1a2(R887/R887 mutants died just after birth, while heterozygous Atp1a2(+/R887 mice showed no apparent clinical phenotype. The mutant α2 Na,K-ATPase protein was barely detectable in the brain of homozygous mutants and strongly reduced in the brain of heterozygous mutants, likely as a consequence of endoplasmic reticulum retention and subsequent proteasomal degradation, as we demonstrate in transfected cells. In vivo analysis of cortical spreading depression (CSD, the phenomenon underlying migraine aura, revealed a decreased induction threshold and an increased velocity of propagation in the heterozygous FHM2 mouse. Since several lines of evidence involve a specific role of the glial α2 Na,K pump in active reuptake of glutamate from the synaptic cleft, we hypothesize that CSD facilitation in the FHM2 mouse model is sustained by inefficient glutamate clearance by astrocytes and consequent increased cortical excitatory neurotransmission. The demonstration that FHM2 and FHM1 mutations share the ability to facilitate induction and propagation of CSD in mouse models further support the role of CSD as a key migraine trigger.

  4. Minimum conditions for the induction of cortical spreading depression in brain slices

    Science.gov (United States)

    Tang, Yujie T.; Mendez, Jorge M.; Theriot, Jeremy J.; Sawant, Punam M.; López-Valdés, Héctor E.; Ju, Y. Sungtaek

    2014-01-01

    Cortical spreading depression (CSD) occurs during various forms of brain injury such as stroke, subarachnoid hemorrhage, and brain trauma, but it is also thought to be the mechanism of the migraine aura. It is therefore expected to occur over a range of conditions including the awake behaving state. Yet it is unclear how such a massive depolarization could occur under relatively benign conditions. Using a microfluidic device with focal stimulation capability in a mouse brain slice model, we varied extracellular potassium concentration as well as the area exposed to increased extracellular potassium to determine the minimum conditions necessary to elicit CSD. Importantly, we focused on potassium levels that are physiologically plausible (≤145 mM; the intracellular potassium concentration). We found a strong correlation between the threshold concentration and the slice area exposed to increased extracellular potassium: minimum area of exposure was needed with the highest potassium concentration, while larger areas were needed at lower concentrations. We also found that moderate elevations of extracellular potassium were able to elicit CSD in relatively small estimated tissue volumes that might be activated under noninjury conditions. Our results thus show that CSD may be inducible under the conditions that expected in migraine aura as well as those related to brain trauma. PMID:25122714

  5. In vivo imaging reveals that pregabalin inhibits cortical spreading depression and propagation to subcortical brain structures

    Science.gov (United States)

    Cain, Stuart M.; Bohnet, Barry; LeDue, Jeffrey; Yung, Andrew C.; Garcia, Esperanza; Tyson, John R.; Alles, Sascha R. A.; Han, Huili; van den Maagdenberg, Arn M. J. M.; Kozlowski, Piotr; MacVicar, Brian A.; Snutch, Terrance P.

    2017-01-01

    Migraine is characterized by severe headaches that can be preceded by an aura likely caused by cortical spreading depression (SD). The antiepileptic pregabalin (Lyrica) shows clinical promise for migraine therapy, although its efficacy and mechanism of action are unclear. As detected by diffusion-weighted MRI (DW-MRI) in wild-type (WT) mice, the acute systemic administration of pregabalin increased the threshold for SD initiation in vivo. In familial hemiplegic migraine type 1 mutant mice expressing human mutations (R192Q and S218L) in the CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the speed of SD propagation in vivo. Acute systemic administration of pregabalin in vivo also selectively prevented the migration of SD into subcortical striatal and hippocampal regions in the R192Q strain that exhibits a milder phenotype and gain of CaV2.1 channel function. At the cellular level, pregabalin inhibited glutamatergic synaptic transmission differentially in WT, R192Q, and S218L mice. The study describes a DW-MRI analysis method for tracking the progression of SD and provides support and a mechanism of action for pregabalin as a possible effective therapy in the treatment of migraine. PMID:28223480

  6. Computational model of cerebral blood flow redistribution during cortical spreading depression

    Science.gov (United States)

    Verisokin, Andrey Y.; Verveyko, Darya V.; Postnov, Dmitry E.

    2016-04-01

    In recent decades modelling studies on cortical spreading depression (CSD) and migraine waves successfully contributed to formation of modern view on these fundamental phenomena of brain physiology. However, due to the extreme complexity of object under study (brain cortex) and the diversity of involved physiological pathways, the development of new mathematical models of CSD is still a very relevant and challenging research problem. In our study we follow the functional modelling approach aimed to map the action of known physiological pathways to the specific nonlinear mechanisms that govern formation and evolution of CSD wave patterns. Specifically, we address the role of cerebral blood flow (CBF) redistribution that is caused by excessive neuronal activity by means of neurovascular coupling and mediates a spatial pattern of oxygen and glucose delivery. This in turn changes the local metabolic status of neural tissue. To build the model we simplify the web of known cell-to-cell interactions within a neurovascular unit by selecting the most relevant ones, such as local neuron-induced elevation of extracellular potassium concentration and biphasic response of arteriole radius. We propose the lumped description of distance-dependent hemodynamic coupling that fits the most recent experimental findings.

  7. [The Effect of Cortical Spreading Depression Wave on EEG Spectral Power Anaesthesed and Conscious Rats].

    Science.gov (United States)

    Koroleva, V I; Sakharov, D S; Bogdanov, A V

    2016-01-01

    EEG power changes in anaesthetized and conscious rats were studied (under repeated experiments) in wide frequency band (0.1-200 Hz) during cortical spreading depression wave (SD). In anaesthetized rats the decrease of EEG spectral power was shown through all diapasons under consideration. The most pronounced decay of the EEG power was marked in the 30-40 Hz band (27.3 ± 18.5, p = 2.46 x 10-(11)). In other frequency ranges the power decrease was less but its significance remained high. In conscious rats the simultaneous decay of the EEG power from 20 to 100 Hz range was also the most informative index of SD wave. The maximum power loss was found for band 30-40 Hz (11.2 ± 7.8, p = 2.55 x 10(-7)). It was shown that besides of EEG power decay the development of SD wave was characterized by the appearance of high frequency activity in front of SD and at the end of it. The increase of high-frequency activity in front of SD wave appeared in the ipsilateral hemisphere and moved along the cortex with the velocity of the SD wave itself. However the bursts of high frequency activity at the end of unilateral SD occurred simultaneously in both hemispheres and lasted 1.5-2.5 min. Findings contribute to detection of SD wave on basis of EEG spectral analysis.

  8. NR2A contributes to genesis and propagation of cortical spreading depression in rats.

    Science.gov (United States)

    Bu, Fan; Du, Ruoxing; Li, Yi; Quinn, John P; Wang, Minyan

    2016-03-22

    Cortical spreading depression (CSD) is a transient propagating excitation of synaptic activity followed by depression, which is implicated in migraine. Increasing evidence points to an essential role of NR2A-containing NMDA receptors in CSD propagation in vitro; however, whether these receptors mediate CSD genesis in vivo requires clarification and the role of NR2A on CSD propagation is still under debate. Using in vivo CSD in rats with electrophysiology and in vitro CSD in chick retina with intrinsic optical imaging, we addressed the role of NR2A in CSD. We demonstrated that NVP-AAM077, a potent antagonist for NR2A-containing receptors, perfused through microdialysis probes, markedly reduced cortex susceptibility to CSD, but also reduced magnitude of CSD genesis in rats. Additionally, NVP-AAM077 at 0.3 nmol perfused into the contralateral ventricle, considerably suppressed the magnitude of CSD propagation wave and propagation rate in rats. This reduction in CSD propagation was also observed with TCN-201, a negative allosteric modulator selective for NR2A, at 3 μM, in the chick retina. Our data provides strong evidence that NR2A subunit contributes to CSD genesis and propagation, suggesting drugs selectively antagonizing NR2A-containing receptors might constitute a highly specific strategy treating CSD associated migraine with a likely better safety profile.

  9. Propagation of cortical spreading depression into the hippocampus: The role of the entorhinal cortex.

    Science.gov (United States)

    Martens-Mantai, Tanja; Speckmann, Erwin-Josef; Gorji, Ali

    2014-07-22

    Propagation of cortical spreading depression (CSD) to the subcortical structures could be the underlying mechanism of some neurological deficits in migraine with aura. The entorhinal cortex (EC) as a gray matter bridge between the neocortex and subcortical regions plays an important role in this propagation. In vitro combined neocortex-hippocampus brain slices were used to study the propagation pattern of CSD between the neocortex and the hippocampus. The effects of different compounds as well as tetanic electrical stimulations in the EC on propagation of CSD to the hippocampus were investigated. Repetitive induction of CSD by KCl injection in the somatosensory cortex enhanced the probability of CSD entrance to the hippocampus via EC. Local application of AMPA receptor blocker CNQX and cannabinoid receptor agonist WIN 55212-2 in EC facilitated the propagation of CSD to the hippocampus, whereas application of NMDA receptor blocker APV and GABAA receptor blocker bicuculline in this region reduced the probability of CSD penetration to the hippocampus. Application of tetanic stimulation in EC also facilitated the propagation of CSD entrance to the hippocampus. Our data suggest the importance of synaptic plasticity of EC in filtering the propagation of CSD into subcortical structures and possibly the occurrence of concomitant neurological deficits. Synapse, 2014. © 2014 Wiley Periodicals, Inc.

  10. Direct cortical stimulation but not transcranial electrical stimulation motor evoked potentials detect brain ischemia during brain tumor resection.

    Science.gov (United States)

    Li, Fenghua; Deshaies, Eric M; Allott, Geoffrey; Canute, Gregory; Gorji, Reza

    2011-09-01

    Motor evoked potentials (MEPs) elicited by both direct cortical stimulation (DCS) and transcranial electrical stimulation are used during brain tumor resection. Parallel use of direct cortical stimulation motor evoked potentials (DCS-MEPs) and transcranial electrical stimulation motor evoked potentials (TCeMEPs) has been practiced during brain tumor resection. We report that DCS-MEPs elicited by direct subdural grid stimulation, but not TCeMEPs, detected brain ischemia during brain tumor resection. Following resection of a brainstem high-grade glioma in a 21-year-old, the threshold of cortical motor-evoked-potentials (cMEPs) increased from 13 mA to 20 mA while amplitudes decreased. No changes were noted in transcranial motor evoked potentials (TCMEPs), somatosensory evoked potentials (SSEPs), auditory evoked potentials (AEPs), anesthetics, or hemodynamic parameters. Our case showed the loss of cMEPs and SSEPs, but not TCeMEPs. Permanent loss of DCS-MEPs and SSEPs was correlated with permanent left hemiplegia in our patient even when appropriate action was taken. Parallel use of DCS- and TCeMEPs with SSEPs improves sensitivity of intraoperative detection of motor impairment. DCS may be superior to TCeMEPs during brain tumor resection.

  11. Recording, analysis, and interpretation of spreading depolarizations in neurointensive care

    DEFF Research Database (Denmark)

    Dreier, Jens P; Fabricius, Martin; Ayata, Cenk

    2016-01-01

    recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy...... electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can...

  12. Electro-cortical signs of early neuronal damage following transient global cerebral ischemia in rat

    DEFF Research Database (Denmark)

    Moldovan, M; Zagrean, Ana-Maria; Avramescu, S;

    2004-01-01

    During recovery after a transient global cerebral ischemia (TGCI), rat electrocorticogram (ECoG) shows epochs of synchronized activity (SA) alternating with epochs of low amplitude background activity (BA). The aim of this study was to compare the changes in these electrical activities during a 3...

  13. Point application with Angong Niuhuang sticker protects hippocampal and cortical neurons in rats with cerebral ischemia

    Directory of Open Access Journals (Sweden)

    Dong-shu Zhang

    2015-01-01

    Full Text Available Angong Niuhuang pill, a Chinese materia medica preparation, can improve neurological functions after acute ischemic stroke. Because of its inconvenient application and toxic components (Cinnabaris and Realgar, we used transdermal enhancers to deliver Angong Niuhuang pill by modern technology, which expanded the safe dose range and clinical indications. In this study, Angong Niuhuang stickers administered at different point application doses (1.35, 2.7, and 5.4 g/kg were administered to the Dazhui (DU14, Qihai (RN6 and Mingmen (DU4 of rats with chronic cerebral ischemia, for 4 weeks. The Morris water maze was used to determine the learning and memory ability of rats. Hematoxylin-eosin staining and Nissl staining were used to observe neuronal damage of the cortex and hippocampal CA1 region in rats with chronic cerebral ischemia. The middle- and high-dose point application of Angong Niuhuang stickers attenuated neuronal damage in the cortex and hippocampal CA1 region, and improved the memory of rats with chronic cerebral ischemia with an efficacy similar to interventions by electroacupuncture at Dazhui (DU14, Qihai (RN6 and Mingmen (DU4. Our experimental findings indicate that point application with Angong Niuhuang stickers can improve cognitive function after chronic cerebral ischemia in rats and is neuroprotective with an equivalent efficacy to acupuncture.

  14. Normal distribution and medullary-to-cortical shift of Nestin-expressing cells in acute renal ischemia.

    Science.gov (United States)

    Patschan, D; Michurina, T; Shi, H K; Dolff, S; Brodsky, S V; Vasilieva, T; Cohen-Gould, L; Winaver, J; Chander, P N; Enikolopov, G; Goligorsky, M S

    2007-04-01

    Nestin, a marker of multi-lineage stem and progenitor cells, is a member of intermediate filament family, which is expressed in neuroepithelial stem cells, several embryonic cell types, including mesonephric mesenchyme, endothelial cells of developing blood vessels, and in the adult kidney. We used Nestin-green fluorescent protein (GFP) transgenic mice to characterize its expression in normal and post-ischemic kidneys. Nestin-GFP-expressing cells were detected in large clusters within the papilla, along the vasa rectae, and, less prominently, in the glomeruli and juxta-glomerular arterioles. In mice subjected to 30 min bilateral renal ischemia, glomerular, endothelial, and perivascular cells showed increased Nestin expression. In the post-ischemic period, there was an increase in fluorescence intensity with no significant changes in the total number of Nestin-GFP-expressing cells. Time-lapse fluorescence microscopy performed before and after ischemia ruled out the possibility of engraftment by the circulating Nestin-expressing cells, at least within the first 3 h post-ischemia. Incubation of non-perfused kidney sections resulted in a medullary-to-cortical migration of Nestin-GFP-positive cells with the rate of expansion of their front averaging 40 microm/30 min during the first 3 h and was detectable already after 30 min of incubation. Explant matrigel cultures of the kidney and aorta exhibited sprouting angiogenesis with cells co-expressing Nestin and endothelial marker, Tie-2. In conclusion, several lines of circumstantial evidence identify a sub-population of Nestin-expressing cells with the mural cells, which are recruited in the post-ischemic period to migrate from the medulla toward the renal cortex. These migrating Nestin-positive cells may be involved in the process of post-ischemic tissue regeneration.

  15. Methylene blue protects the cortical blood-brain barrier against ischemia/reperfusion-induced disruptions.

    Science.gov (United States)

    Miclescu, Adriana; Sharma, Hari Shanker; Martijn, Cécile; Wiklund, Lars

    2010-11-01

    To investigate the effects of cardiac arrest and the reperfusion syndrome on blood-brain barrier permeability and evaluate whether methylene blue counteracts blood-brain barrier disruption in a pig model of controlled cardiopulmonary resuscitation. Randomized, prospective, laboratory animal study. University-affiliated research laboratory. Forty-five piglets. Forty-five anesthetized piglets were subjected to cardiac arrest alone or 12-min cardiac arrest followed by 8 mins cardiopulmonary resuscitation. The first group (n = 16) was used to evaluate blood-brain barrier disruptions after untreated cerebral ischemia after 0, 15, or 30 mins after untreated cardiac arrest. The other two groups received either an infusion of saline (n = 10) or infusion of saline with methylene blue (n = 12) 1 min after the start of cardiopulmonary resuscitation and continued 50 mins after return of spontaneous circulation. In these groups, brains were removed for immunohistological analyses at 30, 60, and 180 mins after return of spontaneous circulation. An increase of injured neurons and albumin immunoreactivity was demonstrated with increasing duration of ischemia/reperfusion. Less blood-brain barrier disruption was observed in subjects receiving methylene blue as demonstrated by decreased albumin leakage (p blue treatment reduced cerebral tissue nitrite/nitrate content (p blood-brain barrier permeability and neurologic injury were increased early in reperfusion after cardiac arrest. Methylene blue exerted neuroprotective effects against the brain damage associated with the ischemia/reperfusion injury and ameliorated the blood-brain barrier disruption by decreasing nitric oxide metabolites.

  16. Randomized, double-blind, placebo-controlled, proof-of-concept study of the cortical spreading depression inhibiting agent tonabersat in migraine prophylaxis

    DEFF Research Database (Denmark)

    Goadsby, P J; Ferrari, M D; Csanyi, A

    2009-01-01

    Tonabersat is a novel putative migraine prophylactic agent with an unique stereospecific binding site in the brain. Tonabersat has been shown, in animal models, to inhibit experimentally induced cortical spreading depression, the likely underlying mechanism for migraine aura, and cerebrovascular ...

  17. Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors.

    Science.gov (United States)

    Huang, Ming; Cheng, Gen; Tan, Han; Qin, Rui; Zou, Yimin; Wang, Yun; Zhang, Ying

    2017-09-01

    Capsaicin, the ingredient responsible for the pungent taste of hot chili peppers, is widely used in the study and management of pain. Recently, its neuroprotective effect has been described in multiple studies. Herein, we investigated the underlying mechanisms for the neuroprotective effect of capsaicin. Direct injection of capsaicin (1 or 3nmol) into the peri-infarct area reduced the infarct volume and improved neurological behavioral scoring and motor coordination function in the middle cerebral artery occlusion (MCAO)/reperfusion model in rats. The time window of the protective effect of capsaicin was within 1h after reperfusion, when excitotoxicity is the main reason of cell death. In cultured cortical neurons, administration of capsaicin attenuated glutamate-induced excitotoxic injury. With respect to the mechanisms of the neuroprotective effect of capsaicin, reduced calcium influx after glutamate stimulation was observed following capsaicin pretreatment in cortical neurons. Trpv1 knock-out abolished the inhibitory effect of capsaicin on glutamate-induced calcium influx and subsequent neuronal death. Reduced expression of GluN1 and GluN2B, subunits of NMDA receptor, was examined after capsaicin treatment in cortical neurons. In summary, our studies reveal that the neuroprotective effect of capsaicin in cortical neurons is TRPV1-dependent and down-regulation of the expression and function of NMDA receptors contributes to the protection afforded by capsaicin. Copyright © 2017. Published by Elsevier Inc.

  18. Cytoarchitecture-Dependent Decrease in Propagation Velocity of Cortical Spreading Depression in the Rat Insular Cortex Revealed by Optical Imaging.

    Science.gov (United States)

    Fujita, Satoshi; Mizoguchi, Naoko; Aoki, Ryuhei; Cui, Yilong; Koshikawa, Noriaki; Kobayashi, Masayuki

    2016-04-01

    Cortical spreading depression (SD) is a self-propagating wave of depolarization accompanied by a substantial disturbance of the ionic distribution between the intra- and extracellular compartments. Glial cells, including astrocytes, play critical roles in maintenance of the extracellular environment, including ionic distribution. Therefore, SD propagation in the cerebral cortex may depend on the density of astrocytes. The present study aimed to examine the profile of SD propagation in the insular cortex (IC), which is located between the neocortex and paleocortex and is where the density of astrocytes gradually changes. The velocity of SD propagation in the neocortex, including the somatosensory, motor, and granular insular cortices (5.7 mm/min), was higher than that (2.8 mm/min) in the paleocortex (agranular insular and piriform cortices). Around thick vessels, including the middle cerebral artery, SD propagation was frequently delayed and sometimes disappeared. Immunohistological analysis of glial fibrillary acidic protein (GFAP) demonstrated the sparse distribution of astrocytes in the somatosensory cortex and the IC dorsal to the rhinal fissure, whereas the ventral IC showed a higher density of astrocytes. These results suggest that cortical cytoarchitectonic features, which possibly involve the distribution of astrocytes, are crucial for regulating the velocity of SD propagation in the cerebral cortex.

  19. Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage.

    Science.gov (United States)

    Dreier, Jens P; Major, Sebastian; Manning, Andrew; Woitzik, Johannes; Drenckhahn, Chistoph; Steinbrink, Jens; Tolias, Christos; Oliveira-Ferreira, Ana I; Fabricius, Martin; Hartings, Jed A; Vajkoczy, Peter; Lauritzen, Martin; Dirnagl, Ulrich; Bohner, Georg; Strong, Anthony J

    2009-07-01

    The term cortical spreading depolarization (CSD) describes a wave of mass neuronal depolarization associated with net influx of cations and water. Clusters of prolonged CSDs were measured time-locked to progressive ischaemic damage in human cortex. CSD induces tone alterations in resistance vessels, causing either transient hyperperfusion (physiological haemodynamic response) in healthy tissue; or hypoperfusion [inverse haemodynamic response = cortical spreading ischaemia (CSI)] in tissue at risk for progressive damage, which has so far only been shown experimentally. Here, we performed a prospective, multicentre study in 13 patients with aneurysmal subarachnoid haemorrhage, using novel subdural opto-electrode technology for simultaneous laser-Doppler flowmetry (LDF) and direct current-electrocorticography, combined with measurements of tissue partial pressure of oxygen (ptiO(2)). Regional cerebral blood flow and electrocorticography were simultaneously recorded in 417 CSDs. Isolated CSDs occurred in 12 patients and were associated with either physiological, absent or inverse haemodynamic responses. Whereas the physiological haemodynamic response caused tissue hyperoxia, the inverse response led to tissue hypoxia. Clusters of prolonged CSDs were measured in five patients in close proximity to structural brain damage as assessed by neuroimaging. Clusters were associated with CSD-induced spreading hypoperfusions, which were significantly longer in duration (up to 144 min) than those of isolated CSDs. Thus, oxygen depletion caused by the inverse haemodynamic response may contribute to the establishment of clusters of prolonged CSDs and lesion progression. Combined electrocorticography and perfusion monitoring also revealed a characteristic vascular signature that might be used for non-invasive detection of CSD. Low-frequency vascular fluctuations (LF-VF) (f fashion similar to that shown previously for spreading depressions of high

  20. Mathematical Imaging and Modeling of Cortical Spreading Depression and Wound Healing

    Science.gov (United States)

    2015-02-05

    phase diagram that maps out when a retinal detachment is unstable, or is stable and will likely heal . We have begun to generalize this problem in two...Spreading Depression and W mmd Healing Sb. GRANT NUMBER Sc. PROGRAM ELEMENT NUMBER 611102 6. AUTHORS Sd. PROJECT NUMBER Tom Chou Se. TASK NUMBER...Spreading Depression and Wound Healing ." The research conducted under this grant represents advances made in image analysis, front tracking, modeling

  1. Measurement of distinctive features of cortical spreading depolarizations with different MRI contrasts

    NARCIS (Netherlands)

    Umesh Rudrapatna, S.; Hamming, Arend M.; Wermer, Marieke J H; van der Toorn, A; Dijkhuizen, Rick M.

    2015-01-01

    Growing clinical evidence suggests critical involvement of spreading depolarizations (SDs) in the pathophysiology of neurological disorders such as migraine and stroke. MRI provides powerful tools to detect and assess co-occurring cerebral hemodynamic and cellular changes during SDs. This study

  2. Measurement of distinctive features of cortical spreading depolarizations with different MRI contrasts

    NARCIS (Netherlands)

    Umesh Rudrapatna, S.; Hamming, Arend M.; Wermer, Marieke J H; van der Toorn, A; Dijkhuizen, Rick M.

    2015-01-01

    Growing clinical evidence suggests critical involvement of spreading depolarizations (SDs) in the pathophysiology of neurological disorders such as migraine and stroke. MRI provides powerful tools to detect and assess co-occurring cerebral hemodynamic and cellular changes during SDs. This study repo

  3. Age or ischemia uncouples the blood flow response, tissue acidosis, and direct current potential signature of spreading depolarization in the rat brain.

    Science.gov (United States)

    Menyhárt, Ákos; Zölei-Szénási, Dániel; Puskás, Tamás; Makra, Péter; Bari, Ferenc; Farkas, Eszter

    2017-08-01

    Spreading depolarization (SD) events contribute to lesion maturation in the acutely injured human brain. Neurodegeneration related to SD is thought to be caused by the insufficiency of the cerebral blood flow (CBF) response; yet the mediators of the CBF response, or their deficiency in the aged or ischemic cerebral cortex, remain the target of intensive research. Here, we postulated that tissue pH effectively modulates the magnitude of hyperemia in response to SD, the coupling of which is prone to be dysfunctional in the aged or ischemic cerebral cortex. To test this hypothesis, we conducted systematic correlation analysis between the direct current (DC) potential signature of SD, SD-associated tissue acidosis, and hyperemic element of the CBF response in the isoflurane-anesthetized, young or old, and intact or ischemic rat cerebral cortex. The data demonstrate that the amplitude of the SD-related DC potential shift, tissue acidosis, and hyperemia are tightly coupled in the young intact cortex; ischemia and old age uncouples the amplitude of hyperemia from the amplitude of the DC potential shift and acidosis; the duration of the DC potential shift, hyperemia and acidosis positively correlate under ischemia alone; and old age disproportionally elongates the duration of acidosis with respect to the DC potential shift and hyperemia under ischemia. The coincidence of the variables supports the view that local CBF regulation with SD must have an effective metabolic component, which becomes dysfunctional with age or under ischemia. Finally, the known age-related acceleration of ischemic neurodegeneration may be promoted by exaggerated tissue acidosis.NEW & NOTEWORTHY The hyperemic element of the cerebral blood flow response to spreading depolarization is effectively modulated by tissue pH in the young intact rat cerebral cortex. This coupling becomes dysfunctional with age or under ischemia, and tissue acidosis lasts disproportionally longer in the aged cortex, making

  4. Early malnutrition, but not age, modulates in the rat the L-Arginine facilitating effect on cortical spreading depression.

    Science.gov (United States)

    Frazão, Marília Ferreira; Silva de Seixas Maia, Luciana Maria; Guedes, Rubem Carlos Araújo

    2008-12-05

    Nutritional factors acting during brain development can permanently alter brain electrophysiology. L-Arginine is the precursor of nitric oxide synthesis, which can modulate brain function. Here we investigated the effect of early-in-life administration (during postnatal days 7-28) of L-Arginine (300 mg/(kg day)) on cortical spreading depression (CSD), recorded in well-nourished and malnourished (large litters technique) rats aged 30-40 days (young) and 90-110 days (adult). Compared to water-treated controls, well-nourished L-Arginine-treated rats, but not the malnourished ones, displayed higher CSD velocities (Pbrain weights. It is concluded that early L-Arginine treatment long lastingly increased brain CSD-susceptibility and this effect is abolished by early malnutrition.

  5. Nitroglycerin enhances the propagation of cortical spreading depression: comparative studies with sumatriptan and novel kynurenic acid analogues

    Directory of Open Access Journals (Sweden)

    Knapp L

    2016-12-01

    Full Text Available Levente Knapp,1 Bence Szita,1 Kitti Kocsis,1,2 László Vécsei,2,3 József Toldi1,2 1Department of Physiology, Anatomy, and Neuroscience, University of Szeged, 2MTA-SZTE Neuroscience Research Group, 3Department of Neurology, Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary Background: The complex pathophysiology of migraine is not yet clearly understood; therefore, experimental models are essential for the investigation of the processes related to migraine headache, which include cortical spreading depression (CSD and NO donor-induced neurovascular changes. Data on the assessment of drug efficacy in these models are often limited, which prompted us to investigate a novel combined migraine model in which an effective pharmacon could be more easily identified. Materials and methods: In vivo electrophysiological experiments were performed to investigate the effect of nitroglycerin (NTG on CSD induced by KCl application. In addition, sumatriptan and newly synthesized neuroactive substances (analogues of the neuromodulator kynurenic acid [KYNA] were also tested. Results: The basic parameters of CSDs were unchanged following NTG administration; however, propagation failure was decreased compared to the controls. Sumatriptan decreased the number of CSDs, whereas propagation failure was as minimal as in the NTG group. On the other hand, both of the KYNA analogues restored the ratio of propagation to the control level. Discussion: The ratio of propagation appeared to be the indicator of the effect of NTG. This is the first study providing direct evidence that NTG influences CSD; furthermore, we observed different effects of sumatriptan and KYNA analogues. Sumatriptan changed the generation of CSDs, whereas the analogues acted on the propagation of the waves. Our experimental design overlaps with a large spectrum of processes present in migraine pathophysiology, and it can be a useful experimental model

  6. [Cortical spreading depolarization phenomena in patients with traumatic and ischemic brain injuries. Results of a pilot study].

    Science.gov (United States)

    Sueiras, M; Sahuquillo, J; García-López, B; Sánchez-Guerrero, Á; Poca, M A; Santamarina, E; Riveiro, M; Fabricius, M; Strong, A J

    2014-10-01

    To determine the frequency and duration of cortical spreading depolarization (CSD) and CSD-like episodes in patients with traumatic brain injury (TBI) and malignant middle cerebral artery infarction (MMCAI) requiring craniotomy. A descriptive observational study was carried out during 19 months. Neurocritical patients. Sixteen patients were included: 9 with MMCAI and 7 with moderate or severe TBI, requiring surgical treatment. A 6-electrode subdural electrocorticographic (ECoG) strip was placed onto the perilesional cortex. An analysis was made of the time profile and the number and duration of CSD and CSD-like episodes recorded from the ECoGs. Of the 16 patients enrolled, 9 presented episodes of CSD or CSD-like phenomena, of highly variable frequency and duration. Episodes of CSD and CSD-like phenomena are frequently detected in the ischemic penumbra and/or traumatic cortical regions of patients with MMCAI who require decompressive craniectomy or of patients with contusional TBI. Copyright © 2013 Elsevier España, S.L.U. and SEMICYUC. All rights reserved.

  7. Influence of ovarian hormones on cortical spreading depression and its suppression by L-kynurenine in rat.

    Directory of Open Access Journals (Sweden)

    Virginie Chauvel

    Full Text Available Migraine is sexually dimorphic and associated in 20-30% of patients with an aura most likely caused by cortical spreading depression (CSD. We have previously shown that systemic L-kynurenine (L-KYN, the precursor of kynurenic acid, suppresses CSD and that this effect depends on the stage of the estrous cycle in female rats. The objectives here are to determine the influence of ovarian hormones on KCl-induced CSD and its suppression after L-KYN by directly modulating estradiol or progesterone levels in ovariectomized rats. Adult female rats were ovariectomized and subcutaneously implanted with silastic capsules filled with progesterone or 17β-estradiol mixed with cholesterol, with cholesterol only or left empty. Two weeks after the ovariectomy/capsule implantation, the animals received an i.p. injection of L-KYN (300 mg/kg or NaCl as control. Thirty minutes later CSDs were elicited by applying KCl over the occipital cortex and recorded by DC electrocorticogram for 1 hour. The results show that both estradiol and progesterone increase CSD frequency after ovariectomy. The suppressive effect of L-KYN on CSD frequency, previously reported in normal cycling females, is not found anymore after ovariectomy, but reappears after progesterone replacement therapy. Taken together, these results emphasize the complex role of sex hormones on cortical excitability. The CSD increase by estradiol and, more surprisingly, progesterone may explain why clinically migraine with aura appears or worsens during pregnancy or with combined hormonal treatments.

  8. Unexpected effects of peripherally administered kynurenic acid on cortical spreading depression and related blood–brain barrier permeability

    Directory of Open Access Journals (Sweden)

    Oláh G

    2013-09-01

    Full Text Available Gáspár Oláh,1 Judit Herédi,1 Ákos Menyhárt,1 Zsolt Czinege,2 Dávid Nagy,1 János Fuzik,1 Kitti Kocsis,1 Levente Knapp,1 Erika Krucsó,1 Levente Gellért,1 Zsolt Kis,1 Tamás Farkas,1 Ferenc Fülöp,3 Árpád Párdutz,4 János Tajti,4 László Vécsei,4 József Toldi1 1Department of Physiology, Anatomy and Neuroscience, 2Department of Software Engineering, 3Institute of Pharmaceutical Chemistry and MTA-SZTE Research Group for Stereochemistry, 4Department of Neurology and MTA-SZTE Neuroscience Research Group, University of Szeged, Szeged, Hungary Abstract: Cortical spreading depression (CSD involves a slowly-propagating depolarization wave in the cortex, which can appear in numerous pathophysiological conditions, such as migraine with aura, stroke, and traumatic brain injury. Neurons and glial cells are also depolarized transiently during the phenomena. CSD is followed by a massive increase in glutamate release and by changes in the brain microcirculation. The aim of this study was to investigate the effects of two N-methyl-D-aspartate receptor antagonists, endogenous kynurenic acid (KYNA and dizocilpine, on CSD and the related blood–brain barrier (BBB permeability in rats. In intact animals, KYNA hardly crosses the BBB but has some positive features as compared with its precursor L-Kynurenine, which is frequently used in animal studies (KYNA cannot be metabolized to excitotoxic agents such as 3-hydroxy-L-kynurenine and quinolinic acid. We therefore investigated the possible effects of peripherally administered KYNA. Repetitive CSD waves were elicited by the application of 1 M KCl solution to the cortex. Direct current-electrocorticograms were measured for 1 hour. Four parameters of the waves were compared. Evans blue dye and fluorescent microscopy were used to study the possible changes in the permeability of the BBB. The results demonstrated that N-methyl-D-aspartate receptor antagonists can reduce the number of CSD waves and decrease

  9. Cortical spreading depression and involvement of the motor cortex, auditory cortex, and cerebellum in eyeblink classical conditioning of the rabbit.

    Science.gov (United States)

    Case, Gilbert R; Lavond, David G; Thompson, Richard F

    2002-09-01

    The interrelationships of cerebellar and cerebral neural circuits in the eyeblink paradigm were explored with the controlled application of cortical spreading depression (CSD) and lidocaine in the New Zealand albino rabbit. The initial research focus was directed toward the involvement of the motor cortex in the conditioned eyeblink response. However, CSD timing and triangulation results indicate that other areas in the cerebral cortex, particularly the auditory cortex (acoustic conditioned stimulus), appear to be critical for the CSD effect on the eyeblink response. In summary: (1) CSD can be elicited, monitored, and timed and its side effects controlled in 97% of awake rabbits in the right and/or left cerebral hemisphere(s) during eyeblink conditioning. (2) The motor cortex appears to play little or no part in classical conditioning of the eyeblink in the rabbit in the delay paradigm. (3) Inactivating the auditory cortex with CSD or lidocaine temporarily impairs the conditioned response during the first 5 to 15 days of training, but has little effect past that point.

  10. Large-Scale Mass Spectrometry Imaging Investigation of Consequences of Cortical Spreading Depression in a Transgenic Mouse Model of Migraine

    Science.gov (United States)

    Carreira, Ricardo J.; Shyti, Reinald; Balluff, Benjamin; Abdelmoula, Walid M.; van Heiningen, Sandra H.; van Zeijl, Rene J.; Dijkstra, Jouke; Ferrari, Michel D.; Tolner, Else A.; McDonnell, Liam A.; van den Maagdenberg, Arn M. J. M.

    2015-06-01

    Cortical spreading depression (CSD) is the electrophysiological correlate of migraine aura. Transgenic mice carrying the R192Q missense mutation in the Cacna1a gene, which in patients causes familial hemiplegic migraine type 1 (FHM1), exhibit increased propensity to CSD. Herein, mass spectrometry imaging (MSI) was applied for the first time to an animal cohort of transgenic and wild type mice to study the biomolecular changes following CSD in the brain. Ninety-six coronal brain sections from 32 mice were analyzed by MALDI-MSI. All MSI datasets were registered to the Allen Brain Atlas reference atlas of the mouse brain so that the molecular signatures of distinct brain regions could be compared. A number of metabolites and peptides showed substantial changes in the brain associated with CSD. Among those, different mass spectral features showed significant ( t-test, P migraine pathophysiology. The results also demonstrate the utility of aligning MSI datasets to a common reference atlas for large-scale MSI investigations.

  11. Nitroglycerin enhances the propagation of cortical spreading depression: comparative studies with sumatriptan and novel kynurenic acid analogues

    Science.gov (United States)

    Knapp, Levente; Szita, Bence; Kocsis, Kitti; Vécsei, László; Toldi, József

    2017-01-01

    Background The complex pathophysiology of migraine is not yet clearly understood; therefore, experimental models are essential for the investigation of the processes related to migraine headache, which include cortical spreading depression (CSD) and NO donor-induced neurovascular changes. Data on the assessment of drug efficacy in these models are often limited, which prompted us to investigate a novel combined migraine model in which an effective pharmacon could be more easily identified. Materials and methods In vivo electrophysiological experiments were performed to investigate the effect of nitroglycerin (NTG) on CSD induced by KCl application. In addition, sumatriptan and newly synthesized neuroactive substances (analogues of the neuromodulator kynurenic acid [KYNA]) were also tested. Results The basic parameters of CSDs were unchanged following NTG administration; however, propagation failure was decreased compared to the controls. Sumatriptan decreased the number of CSDs, whereas propagation failure was as minimal as in the NTG group. On the other hand, both of the KYNA analogues restored the ratio of propagation to the control level. Discussion The ratio of propagation appeared to be the indicator of the effect of NTG. This is the first study providing direct evidence that NTG influences CSD; furthermore, we observed different effects of sumatriptan and KYNA analogues. Sumatriptan changed the generation of CSDs, whereas the analogues acted on the propagation of the waves. Our experimental design overlaps with a large spectrum of processes present in migraine pathophysiology, and it can be a useful experimental model for drug screening. PMID:28053504

  12. Ignition's glow: Ultra-fast spread of global cortical activity accompanying local "ignitions" in visual cortex during conscious visual perception.

    Science.gov (United States)

    Noy, N; Bickel, S; Zion-Golumbic, E; Harel, M; Golan, T; Davidesco, I; Schevon, C A; McKhann, G M; Goodman, R R; Schroeder, C E; Mehta, A D; Malach, R

    2015-09-01

    ) with an ultra-fast spread of signals of lower magnitude that invaded selected sites throughout fronto-parietal cortical areas. Our results are compatible with local models in demonstrating a clear task-dependence of the 300 ms fronto-parietal activation. However, they also reveal a more global component of low-magnitude and poor content selectivity that rapidly spreads into fronto-parietal sites. The precise functional role of this global "glow" remains to be elucidated.

  13. Increased 20-HETE synthesis explains reduced cerebral blood flow but not impaired neurovascular coupling after cortical spreading depression in rat cerebral cortex

    DEFF Research Database (Denmark)

    Fordsmann, Jonas Christoffer; ko, Rebecca; Choi, Hyun B

    2013-01-01

    Cortical spreading depression (CSD) is associated with release of arachidonic acid (AA), impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstriction. We tested the hypothesis that the released AA is metabolized by the cytochrome P450 enzyme to produce...... neurovascular coupling after CSD. These findings suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD, and that the attenuation of stimulation-induced CBF responses after CSD has a different mechanism. We suggest that blockade of 20-HETE synthesis may be clinically relevant...

  14. Decreased chronic-stage cortical C-11-flumazenil binding after focal ischemia-reperfusion in baboons - A marker of selective neuronal loss?

    Energy Technology Data Exchange (ETDEWEB)

    Giffard, C.; Landeau, B.; Kerrouche, N.; Young, A.R. [Univ Caen, INSERM Avenir, INSERM U320, INSERM E 0218, F-14032 Caen (France); Giffard, C.; Landeau, B.; Kerrouche, N.; Young, A.R. [Univ Caen, CYCERON, F-14032 Caen (France); Giffard, C.; Landeau, B. [Univ Caen, CYCERON, CEA LRV 10, F-14032 Caen (France); Baron, J.C. [Univ Cambridge, Dept Clin Neurosci, Cambridge CB2 2QQ (United Kingdom)

    2008-07-01

    Background and Purpose - Although the penumbra can be saved by early reperfusion, in the rat it is consistently affected by selective neuronal loss. Mapping selective neuronal loss in the living primate would be desirable. Methods - Five young adult baboons underwent {sup 15}O positron emission tomography for cerebral blood flow, cerebral oxygen consumption, and oxygen extraction fraction mapping at baseline and serially during and after 20-hours temporary middle cerebral artery occlusion. At approximately day 30, {sup 11}C-flumazenil (FMZ), a potential positron emission tomography marker of selective neuronal loss, and structural magnetic resonance-based infarct mapping were obtained, and the brain was perfused-fixed. Reduced FMZ binding in non-infarcted cortical middle cerebral artery areas was searched voxel-wise, and specific binding was assessed using compartmental modeling of FMZ time-activity curves. Results - Visual inspection revealed reduced late FMZ uptake in the affected cortical territory, extending well beyond the infarct. Accordingly, the incidence of selected voxels was greater than chance, documenting mildly but significantly reduced FMZ uptake and specific binding. Serial {sup 15}O positron emission tomography revealed moderately severe acute ischemia followed by reperfusion. Histopathology documented only mild neuronal changes in or near the affected areas. Conclusions - We document moderate but definite late FMZ binding decrements in non-infarcted cortical areas in the baboon, consistent with previous rat and human studies. These were acutely characterized by moderate ischemia followed by reperfusion, consistent with neuronal damage from ischemic or reperfusion injury in the salvaged at-risk tissue. Only mild histopathological changes subtended these FMZ alterations suggesting subtle processes such as isolated dendrite or synapse loss. Whether these changes impact on clinical outcome deserves studying because they may be targeted by specific

  15. The shh signaling pathway is upregulated in multiple cell types in cortical ischemia and influences the outcome of stroke in an animal model.

    Science.gov (United States)

    Jin, Yongmin; Raviv, Nataly; Barnett, Austin; Bambakidis, Nicholas C; Filichia, Emily; Luo, Yu

    2015-01-01

    Recently the sonic hedgehog (shh) signaling pathway has been shown to play an important role in regulating repair and regenerative responses after brain injury, including ischemia. However, the precise cellular components that express and upregulate the shh gene and the cellular components that respond to shh signaling remain to be identified. In this study, using a distal MCA occlusion model, our data show that the shh signal is upregulated both at the cortical area near the injury site and in the adjacent striatum. Multiple cell types upregulate shh signaling in ischemic brain, including neurons, reactive astrocytes and nestin-expressing cells. The shh signaling pathway genes are also expressed in the neural stem cells (NSCs) niche in the subventricular zone (SVZ). Conditional deletion of the shh gene in nestin-expressing cells both at the SVZ niche and at the ischemic site lead to significantly more severe behavioral deficits in these shh iKO mice after cortical stroke, measured using an automated open field locomotion apparatus (Student's t-test, pshh signaling agonist (SAG) demonstrated less deficits in behavioral function, compared to vehicle-treated mice. At 7 days after stroke, SAG-treated mice showed higher values in multiple horizontal movement parameters compared to vehicle treated mice (Student's t-test, p0.05). In summary, our data demonstrate that shh signaling plays critical and ongoing roles in response to ischemic injury and modulation of shh signaling in vivo alters the functional outcome after cortical ischemic injury.

  16. Effects of acupoint versus non-acupoint electroacupuncture on cerebral cortical neuronal Bcl-2,Bax and caspase-3 expression in a rat model of focal cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Jun Wang; Junming Fan; Yongshu Dong; Xia Huang; Hongxia Zhang

    2008-01-01

    BACKGROUND: Several studies have demonstrated that electroacupuncture by acupoint selection can inhibit cerebral cortical neuronal apoptosis following cerebral ischemia/reperfusion.OBJECTIVE: To validate the effects of electroacupuncture by acupoint selection on the expression level of cortical neuronal anti-apoptotic Bcl-2 protein and the apoptotic executive protein, caspase-3, in rat models of focal cerebral ischemia/reperfusion.DESIGN, TIME AND SETTING: This randomized grouping, neural cell and molecular biology animal experiment was performed at the Laboratory of Pharmacology of Traditional Chinese Medicine and the Laboratory Animal Center of Henan Institute of Traditional Chinese Medicine between November 2006 and May 2007.MATERIALS: Atotal of 40 healthy male adult Sprague-Dawley rats were randomly and evenly divided into four groups: sham-operated, model, electroacupuncture and non-acupoint control. G6895 electro-acupuncture instruments were purchased from Shanghai Huayi Instrument Factory, China. Caspase-3, Bcl-2 and Bax kits were provided by Wuhan Boster Bioengineering Co., Ltd., China.METHODS: Middle cerebral artery occlusion was induced in the model, electroacupuncture and non-acupoint groups. In the electroacupuncture group, the acupoints Jianyu (LI15), Waiguan (SJ5), Biguan (ST31), and Zusanli (ST36) were given electroacupuncture. In the non-acupoint control group, at each time point (immediately after ischemia and after reperfusion, or 2 hours after reperfusion), electroacupuncture was performed at the midpoints of Tianquan (PC2)-Quze (PC 3) line, Quze (PC 3)-Ximen (PC4) line, Zuwuli (LRlO)-Yinbao (LRg) line, and Xiguan (LR7)-Zhongdu (LR6) line. Electroacupuncture parameters were set with a continuous wave with a frequency of 10 Hz, wave width 0.6 ms, voltage 1.5-3.0 V, and a duration of 10 minutes. The sham-operated and model groups received only animal fixation without electroacupuncture procedure.MAIN OUTCOME MEASURES: Five rats were selected from

  17. Point application withAngong Niuhuang sticker protects hippocampal and cortical neurons in rats with cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Dong-shu Zhang; Yuan-liang Liu; Dao-qi Zhu; Xiao-jing Huang; Chao-hua Luo

    2015-01-01

    Angong Niuhuang pill, a Chinese materia medica preparation, can improve neurological func-tions after acute ischemic stroke. Because of its inconvenient application and toxic components (Cinnabaris andRealgar), we used transdermal enhancers to deliverAngong Niuhuang pill by modern technology, which expanded the safe dose range and clinical indications. In this study, Angong Niuhuang stickers administered at different point application doses (1.35, 2.7, and 5.4 g/kg) were administered to theDazhui (DU14), Qihai(RN6) andMingmen (DU4) of rats with chronic cerebral ischemia, for 4 weeks. The Morris water maze was used to determine the learning and memory ability of rats. Hematoxylin-eosin staining and Nissl staining were used to observe neuronal damage of the cortex and hippocampal CA1 region in rats with chronic cerebral ischemia. The middle- and high-dose point application ofAngong Niuhuangstickers attenuated neuronal damage in the cortex and hippocampal CA1 region, and improved the memory of rats with chronic cerebral ischemia with an efifcacy similar to interventions by electroacupuncture at Dazhui (DU14),Qihai (RN6) andMingmen (DU4). Our experimental ifndings indicate that point application withAngong Niuhuang stickers can improve cognitive function after chronic cerebral ischemia in rats and is neuroprotective with an equivalent efifcacy to acupuncture.

  18. In Vivo Voltage-Sensitive Dye Study of Lateral Spreading of Cortical Activity in Mouse Primary Visual Cortex Induced by a Current Impulse.

    Directory of Open Access Journals (Sweden)

    Tamás Dávid Fehérvári

    Full Text Available In the mammalian primary visual cortex (V1, lateral spreading of excitatory potentials is believed to be involved in spatial integrative functions, but the underlying cortical mechanism is not well understood. Visually-evoked population-level responses have been shown to propagate beyond the V1 initial activation site in mouse, similar to higher mammals. Visually-evoked responses are, however, affected by neuronal circuits prior to V1 (retina, LGN, making the separate analysis of V1 difficult. Intracortical stimulation eliminates these initial processing steps. We used in vivo RH1691 voltage-sensitive dye (VSD imaging and intracortical microstimulation in adult C57BL/6 mice to elucidate the spatiotemporal properties of population-level signal spreading in V1 cortical circuits. The evoked response was qualitatively similar to that measured in single-cell electrophysiological experiments in rodents: a fast transient fluorescence peak followed by a fast and a slow decrease or hyperpolarization, similar to EPSP and fast and slow IPSPs in single cells. The early cortical response expanded at speeds commensurate with long horizontal projections (at 5% of the peak maximum, 0.08-0.15 m/s however, the bulk of the VSD signal propagated slowly (at half-peak maximum, 0.05-0.08 m/s suggesting an important role of regenerative multisynaptic transmission through short horizontal connections in V1 spatial integrative functions. We also found a tendency for a widespread and fast cortical response suppression in V1, which was eliminated by GABAA-antagonists gabazine and bicuculline methiodide. Our results help understand the neuronal circuitry involved in lateral spreading in V1.

  19. Involvement of mitogen-activated protein kinase pathways in expression of the water channel protein aquaporin-4 after ischemia in rat cortical astrocytes.

    Science.gov (United States)

    Nito, Chikako; Kamada, Hiroshi; Endo, Hidenori; Narasimhan, Purnima; Lee, Yong-Sun; Chan, Pak H

    2012-09-20

    Brain edema after ischemic brain injury is a key determinant of morbidity and mortality. Aquaporin-4 (AQP4) plays an important role in water transport in the central nervous system and is highly expressed in brain astrocytes. However, the AQP4 regulatory mechanisms are poorly understood. In this study, we investigated whether mitogen-activated protein kinases (MAPKs), which are involved in changes in osmolality, might mediate AQP4 expression in models of rat cortical astrocytes after ischemia. Increased levels of AQP4 in primary cultured astrocytes subjected to oxygen-glucose deprivation (OGD) and 2 h of reoxygenation were observed, after which they immediately decreased at 0 h of reoxygenation. Astrocytes exposed to OGD injury had significantly increased phosphorylation of three kinds of MAPKs. Treatment with SB203580, a selective p38 MAPK inhibitor, or SP600125, a selective c-Jun N-terminal kinase inhibitor, significantly attenuated the return of AQP4 to its normal level, and SB203580, but not SP600125, significantly decreased cell death. In an in vivo study, AQP4 expression was upregulated 1-3 days after reperfusion, which was consistent with the time course of p38 phosphorylation and activation, and decreased by the p38 inhibition after transient middle cerebral artery occlusion (MCAO). These results suggest that p38 MAPK may regulate AQP4 expression in cortical astrocytes after ischemic injury.

  20. Forced arm use is superior to voluntary training for motor recovery and brain plasticity after cortical ischemia in rats.

    Science.gov (United States)

    Schneider, Armin; Rogalewski, Andreas; Wafzig, Oliver; Kirsch, Friederike; Gretz, Norbert; Krüger, Carola; Diederich, Kai; Pitzer, Claudia; Laage, Rico; Plaas, Christian; Vogt, Gerhard; Minnerup, Jens; Schäbitz, Wolf-Rüdiger

    2014-02-14

    Both the immobilization of the unaffected arm combined with physical therapy (forced arm use, FAU) and voluntary exercise (VE) as model for enriched environment are promising approaches to enhance recovery after stroke. The genomic mechanisms involved in long-term plasticity changes after different means of rehabilitative training post-stroke are largely unexplored. The present investigation explored the effects of these physical therapies on behavioral recovery and molecular markers of regeneration after experimental ischemia. 42 Wistar rats were randomly treated with either forced arm use (FAU, 1-sleeve plaster cast onto unaffected limb at 8/10 days), voluntary exercise (VE, connection of a freely accessible running wheel to cage), or controls with no access to a running wheel for 10 days starting at 48 hours after photothrombotic stroke of the sensorimotor cortex. Functional outcome was measured using sensorimotor test before ischemia, after ischemia, after the training period of 10 days, at 3 and 4 weeks after ischemia. Global gene expression changes were assessed from the ipsi- and contralateral cortex and the hippocampus. FAU-treated animals demonstrated significantly improved functional recovery compared to the VE-treated group. Both were superior to cage control. A large number of genes are altered by both training paradigms in the ipsi- and contralateral cortex and the hippocampus. Overall, the extent of changes observed correlated well with the functional recovery obtained. One category of genes overrepresented in the gene set is linked to neuronal plasticity processes, containing marker genes such as the NMDA 2a receptor, PKC ζ, NTRK2, or MAP 1b. We show that physical training after photothrombotic stroke significantly and permanently improves functional recovery after stroke, and that forced arm training is clearly superior to voluntary running training. The behavioral outcomes seen correlate with patterns and extent of gene expression changes in all

  1. Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage

    DEFF Research Database (Denmark)

    Dreier, Jens P; Major, Sebastian; Manning, Andrew

    2009-01-01

    -invasive detection of CSD. Low-frequency vascular fluctuations (LF-VF) (f imaging methods, are determined by the brain's resting neuronal activity. CSD provides a depolarization block of the resting activity, recorded electrophysiologically as spreading depression of high...... the differentiation of progressive ischaemia and repair phases in a fashion similar to that shown previously for spreading depressions of high-frequency-electrocorticography activity. In conclusion, it is suggested that (i) CSI is a novel human disease mechanism associated with lesion development and a potential...

  2. Spreading depression induces expression of calcium-independent protein kinase C subspecies in ischaemia-sensitive cortical layers: regulation by N-methyl-D-aspartate receptors and glucocorticoids.

    Science.gov (United States)

    Koponen, S; Keinänen, R; Roivainen, R; Hirvonen, T; Närhi, M; Chan, P H; Koistinaho, J

    1999-01-01

    Spreading depression is a wave of sustained depolarization challenging the energy metabolism of the cells without causing irreversible damage. In the ischaemic brain, sreading depression-like depolarization contributes to the evolution of ischaemia to infarction. The depolarization is propagated by activation of N-methyl-D-aspartate receptors, but changes in signal transduction downstream of the receptors are not known. Because protein phosphorylation is a general mechanism whereby most cellular processes are regulated, and inhibition of N-methyl-D-aspartate receptors or protein kinase C is neuroprotective, the expression of protein kinase C subspecies in spreading depression was examined. Cortical treatment with KCl induced an upregulation of protein kinase Cdelta and zeta messenger RNA at 4 and 8 h, whereas protein kinase Calpha, beta, gamma and epsilon did not show significant changes. The gene induction was the strongest in layers 2 and 3, and was followed by an increased number of protein kinase Cdelta-immunoreactive neurons. Protein kinase Cdelta and zeta inductions were inhibited by pretreatment with an N-methyl-D-aspartate receptor antagonist, dizocilpine maleate, which also blocked spreading depression propagation, and with dexamethasone, which acted without blocking the propagation. Quinacrine, a phospholipase A2 inhibitor, reduced only protein kinase C5 induction. In addition, N(G)(-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, did not influence protein kinase Cdelta or zeta induction, whereas 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione, an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate/kainate receptor antagonist, and the cyclo-oxygenase inhibitors indomethacin and diclophenac tended to increase gene expression. The data show that cortical spreading depression induces Ca2(+)-independent protein kinase C subspecies delta and zeta, but not Ca(2+)-dependent subspecies, through activation of N-methyl-D-aspartate receptors and

  3. Inhibition of Histone Deacetylase 3 (HDAC3) Mediates Ischemic Preconditioning and Protects Cortical Neurons against Ischemia in Rats

    Science.gov (United States)

    Wu, Qimei; Zhang, Lei; Feng, Linyin

    2016-01-01

    Brain ischemic preconditioning (PC) provides vital insights into the endogenous protection against stroke. Genomic and epigenetic responses to PC condition the brain into a state of ischemic tolerance. Notably, PC induces the elevation of histone acetylation, consistent with evidence that histone deacetylase (HDAC) inhibitors protect the brain from ischemic injury. However, less is known about the specific roles of HDACs in this process. HDAC3 has been implicated in several neurodegenerative conditions. Deletion of HDAC3 confers protection against neurotoxicity and neuronal injury. Here, we hypothesized that inhibition of HDAC3 may contribute to the neuronal survival elicited by PC. To address this notion, PC and transient middle cerebral artery occlusion (MCAO) were conducted in Sprague-Dawley rats. Additionally, primary cultured cortical neurons were used to identify the modulators and effectors of HDAC3 involved in PC. We found that nuclear localization of HDAC3 was significantly reduced following PC in vivo and in vitro. Treatment with the HDAC3-specific inhibitor, RGFP966, mimicked the neuroprotective effects of PC 24 h and 7 days after MCAO, causing a reduced infarct volume and less Fluoro-Jade C staining. Improved functional outcomes were observed in the neurological score and rotarod test. We further showed that attenuated recruitment of HDAC3 to promoter regions following PC potentiates transcriptional initiation of genes including Hspa1a, Bcl2l1, and Prdx2, which may underlie the mechanism of protection. In addition, PC-activated calpains were implicated in the cleavage of HDAC3. Pretreatment with calpeptin blockaded the attenuated nuclear distribution of HDAC3 and the protective effect of PC in vivo. Collectively, these results demonstrate that the inhibition of HDAC3 preconditions the brain against ischemic insults, indicating a new approach to evoke endogenous protection against stroke. PMID:27965534

  4. Inhibition of Histone Deacetylase 3 (HDAC3 Mediates Ischemic Preconditioning and Protects Cortical Neurons against Ischemia in Rats

    Directory of Open Access Journals (Sweden)

    Xiaoyu Yang

    2016-11-01

    Full Text Available Brain ischemic preconditioning (PC provides vital insights into the endogenous protection against stroke. Genomic and epigenetic responses to PC condition the brain into a state of ischemic tolerance. Notably, PC induces the elevation of histone acetylation, consistent with evidence that histone deacetylase (HDAC inhibitors protect the brain from ischemic injury. However, less is known about the specific roles of HDACs in this process. HDAC3 has been implicated in several neurodegenerative conditions. Deletion of HDAC3 confers protection against neurotoxicity and neuronal injury. Here, we hypothesized that inhibition of HDAC3 may contribute to the neuronal survival elicited by PC. To address this notion, PC and transient middle cerebral artery occlusion (MCAO were conducted in Sprague-Dawley rats. Additionally, primary cultured cortical neurons were used to identify the modulators and effectors of HDAC3 involved in PC. We found that nuclear localization of HDAC3 was significantly reduced following PC in vivo and in vitro. Treatment with the HDAC3-specific inhibitor, RGFP966, mimicked the neuroprotective effects of PC 24 h and 7 d after MCAO, causing a reduced infarct volume and less Fluoro-Jade C staining. Improved functional outcomes were observed in the neurological score and rotarod test. We further showed that attenuated recruitment of HDAC3 to promoter regions following PC potentiates transcriptional initiation of genes including Hspa1a, Bcl2l1, and Prdx2, which may underlie the mechanism of protection. In addition, PC-activated calpains were implicated in the cleavage of HDAC3. Pretreatment with calpeptin blockaded the attenuated nuclear distribution of HDAC3 and the protective effect of PC in vivo. Collectively, these results demonstrate that the inhibition of HDAC3 preconditions the brain against ischemic insults, indicating a new approach to evoke endogenous protection against stroke.

  5. Enhanced excitatory transmission at cortical synapses as the basis for facilitated spreading depression in Ca(v)2.1 knockin migraine mice.

    Science.gov (United States)

    Tottene, Angelita; Conti, Rossella; Fabbro, Alessandra; Vecchia, Dania; Shapovalova, Maryna; Santello, Mirko; van den Maagdenberg, Arn M J M; Ferrari, Michel D; Pietrobon, Daniela

    2009-03-12

    Migraine is a common disabling brain disorder. A subtype of migraine with aura (familial hemiplegic migraine type 1: FHM1) is caused by mutations in Ca(V)2.1 (P/Q-type) Ca(2+) channels. Knockin mice carrying a FHM1 mutation show increased neuronal P/Q-type current and facilitation of induction and propagation of cortical spreading depression (CSD), the phenomenon that underlies migraine aura and may activate migraine headache mechanisms. We studied cortical neurotransmission in neuronal microcultures and brain slices of FHM1 mice. We show gain of function of excitatory neurotransmission due to increased action-potential-evoked Ca(2+) influx and increased probability of glutamate release at pyramidal cell synapses but unaltered inhibitory neurotransmission at fast-spiking interneuron synapses. Using an in vitro model of CSD, we show a causative link between enhanced glutamate release and CSD facilitation. The synapse-specific effect of FHM1 mutations points to disruption of excitation-inhibition balance and neuronal hyperactivity as the basis for episodic vulnerability to CSD ignition in migraine.

  6. Prooxidant versus antioxidant brain action of ascorbic acid in well-nourished and malnourished rats as a function of dose: a cortical spreading depression and malondialdehyde analysis.

    Science.gov (United States)

    Mendes-da-Silva, Rosângela Figueiredo; Lopes-de-Morais, Andréia Albuquerque Cunha; Bandim-da-Silva, Maria Eduarda; Cavalcanti, Gabriela de Araujo; Rodrigues, Ana Rafaela Oliveira; Andrade-da-Costa, Belmira Lara da Silveira; Guedes, Rubem Carlos Araújo

    2014-11-01

    Although ascorbic acid (AA) is an antioxidant, under certain conditions it can facilitate oxidation, which may underlie the opposite actions of AA on brain excitability in distinct seizure models. Here, we investigated whether chronic AA administration during brain development alters cortical excitability as a function of AA dose, as indexed by cortical spreading depression (CSD) and by the levels of lipid peroxidation-induced malondialdehyde. Well-nourished and early-malnourished rats received per gavage 30, 60, or 120 mg/kg/d of AA, saline, or no gavage treatment (naïve group) at postnatal days 7-28. CSD propagation and malondialdehyde levels were analyzed at 30-40 days. Confirming previous observations, CSD velocities were significantly higher in the early-malnourished groups than in the well-nourished groups. AA dose was important: 30 mg/kg/d AA decelerated CSD and reduced malondialdehyde levels, whereas 60 mg/kg/d and 120 mg/kg/d accelerated CSD and augmented malondialdehyde levels compared with the corresponding saline and naïve groups. Our findings reinforce previous suggestion that AA acts as an antioxidant in the brain when administered at low doses, but as a prooxidant at high doses, as indicated by CSD propagation and malondialdehyde levels. Copyright © 2014 Elsevier Ltd. All rights reserved.

  7. Intestinal Ischemia

    Science.gov (United States)

    ... some generally recognized patterns. Symptoms of acute intestinal ischemia Signs and symptoms of acute intestinal ischemia typically ... confusion in older adults Symptoms of chronic intestinal ischemia Signs and symptoms of chronic intestinal ischemia can ...

  8. Estrogen-dependent effects of 5-hydroxytryptophan on cortical spreading depression in rat: Modelling the serotonin-ovarian hormone interaction in migraine aura.

    Science.gov (United States)

    Chauvel, Virginie; Multon, Sylvie; Schoenen, Jean

    2017-01-01

    Background Cortical spreading depression (CSD) is the likely culprit of the migraine aura. Migraine is sexually dimorphic and thought to be a "low 5-HT" condition. We sought to decipher the interrelation between serotonin, ovarian hormones and cortical excitability in a model of migraine aura. Methods Occipital KCl-induced CSDs were recorded for one hour at parieto-occipital and frontal levels in adult male (n = 16) and female rats (n = 64) one hour after intraperitoneal (i.p.) injection of 5-hydroxytryptophan (5-HTP) or NaCl. Sixty-five oophorectomized females were treated with estradiol- (E2) or cholesterol- (Chol) filled capsules. Two weeks later we recorded CSDs after 5-HTP/NaCl injections before or 20 hours after capsule removal. Results 5-HTP had no effect in males, but decreased CSD frequency in cycling females, significantly so during estrus, at parieto-occipital (-3.5CSD/h, p HTP was significant only in E2-treated rats (-3.4CSD/h, p = 0.006 and -1.8CSD/h, p = 0.029). Neither the estrous cycle phase, nor E2 or 5-HTP treatments significantly modified CSD propagation velocity. Conclusion 5-HTP decreases CSD occurrence in the presence of ovarian hormones, suggesting its potential efficacy in migraine with aura prophylaxis in females. Elevated E2 levels increase CSD susceptibility, while estrogen withdrawal decreases CSD. In a translational perspective, these findings may explain why migraine auras can appear during pregnancy and why menstrual-related migraine attacks are rarely associated with an aura.

  9. Neonatal taurine and alanine modulate anxiety-like behavior and decelerate cortical spreading depression in rats previously suckled under different litter sizes.

    Science.gov (United States)

    Francisco, Elian da Silva; Guedes, Rubem Carlos Araújo

    2015-11-01

    The amino acids taurine and alanine play a role in several physiological processes, including behavior and the electrical activity of the brain. In this study, we investigated the effect of treatment with taurine or alanine on anxiety-like behavior and the excitability-dependent phenomenon known as cortical spreading depression (CSD), using rats suckled in litters with 9 and 15 pups (groups L9 and L15). From postnatal days 7 to 27, the animals received per gavage 300 mg/kg/day of taurine or alanine or both. At 28 days, we tested the animals in the elevated plus maze, and at 33-35 days, we recorded CSD and analyzed its velocity of propagation, amplitude, and duration. Compared with water-treated controls, the L9 groups treated with taurine or alanine displayed anxiolytic behavior (higher number of entries in the open arms; p taurine, alanine, or both) treated at adulthood (90-110 days). The L15 condition resulted in smaller durations and higher CSD velocities compared with the L9 condition. Besides reinforcing previous evidence of behavioral modulation by taurine and alanine, our data are the first confirmation that treatment with these amino acids decelerates CSD regardless of lactation conditions (normal versus unfavorable lactation) or age at amino acid administration (young versus adult). The results suggest a modulating role for both amino acids on anxiety behavior and neuronal electrical activity.

  10. Endogenous mechanisms underlying the activation and sensitization of meningeal nociceptors: the role of immuno-vascular interactions and cortical spreading depression.

    Science.gov (United States)

    Levy, Dan

    2012-06-01

    Migraine is considered one of the most prevalent neurological disorders but its underlying pathophysiology is poorly understood. Over the past two decades, it became widely accepted that activation of primary afferent nociceptive neurons that innervate the intracranial meninges serves as a key process that mediates the throbbing head pain of migraine. Knowledge about the endogenous factors that play a role in promoting this neural process during a migraine attack slowly begins to increase, and a better understanding remains one of the holy grails in migraine research. One endogenous process, which has been invoked as a major player in the genesis of migraine pain, is cortical spreading depression (CSD). Until recently, however, this notion was only supported by indirect evidence. Recently, electrophysiological data provided the first direct evidence that CSD is indeed a powerful endogenous process that can lead to persistent activation of meningeal nociceptors and the migraine pain pathway. CSD has been suggested to promote persistent sensitization and ensuing activation of meningeal nociceptors through a mechanism involving local neurogenic inflammation including the activation of mast cells and macrophages and subsequent release of inflammatory mediators. Local action of such nociceptive mediators can increase the responsiveness of meningeal nociceptors. Recent studies provided key experimental data implicating complex meningeal immuno-vascular interactions, in particular, the interplay between proinflammatory cytokines, the meningeal vasculature and immune cells, in enhancing the responses of meningeal nociceptors.

  11. l-Citrulline ameliorates cerebral blood flow during cortical spreading depression in rats: Involvement of nitric oxide- and prostanoids-mediated pathway.

    Science.gov (United States)

    Kurauchi, Yuki; Mokudai, Koichi; Mori, Asami; Sakamoto, Kenji; Nakahara, Tsutomu; Morita, Masahiko; Kamimura, Ayako; Ishii, Kunio

    2017-02-17

    l-Citrulline is a potent precursor of l-arginine, and exerts beneficial effect on cardiovascular system via nitric oxide (NO) production. Migraine is one of the most popular neurovascular disorder, and imbalance of cerebral blood flow (CBF) observed in cortical spreading depression (CSD) contributes to the mechanism of migraine aura. Here, we investigated the effect of l-citrulline on cardiovascular changes to KCl-induced CSD. in rats. Intravenous injection of l-citrulline prevented the decrease in CBF, monitored by laser Doppler flowmetry, without affecting mean arterial pressure and heart rate during CSD. Moreover, l-citrulline attenuated propagation velocity of CSD induced by KCl. The effect of l-citrulline on CBF change was prevented by l-NAME, an inhibitor of NO synthase, but not by indomethacin, an inhibitor of cyclooxygenase. On the other hand, attenuation effect of l-citrulline on CSD propagation velocity was prevented not only by l-NAME but also by indomethacin. In addition, propagation velocity of CSD was attenuated by intravenous injection of NOR3, a NO donor, which was diminished by ODQ, an inhibitor of soluble guanylyl cyclase. These results suggest that NO/cyclic GMP- and prostanoids-mediated pathway differently contribute to the effect of l-citrulline on the maintenance of CBF.

  12. Electro-acupuncture exerts beneficial effects against cerebral ischemia and promotes the proliferation of neural progenitor cells in the cortical peri-infarct area through the Wnt/β-catenin signaling pathway.

    Science.gov (United States)

    Chen, Bin; Tao, Jing; Lin, Yukun; Lin, Ruhui; Liu, Weilin; Chen, Lidian

    2015-11-01

    Electro-acupuncture (EA) is a novel therapy based on combining traditional acupuncture with modern electrotherapy, and it is currently being investigated as a treatment for ischemic stroke. In the present study, we aimed to investigate the mechanisms through which EA regulates the proliferation of neural progenitor cells (NPCs) in the cortical peri‑infarct area after stroke. The neuroprotective effects of EA on ischemic rats were evaluated by determining the neurological deficit scores and cerebral infarct volumes. The proliferation of the NPCs and the activation of the Wnt/β‑catenin signaling pathway in the cortical peri‑infarct area were examined. Our results revealed that EA significantly alleviated neurological deficits, reduced the infarct volume and enhanced NPC proliferation [nestin/glial fibrillary acidic protein (GFAP)‑double positive] in the cortex of rats subjected to middle cerebral artery occlusion (MCAO). Moreover, the Wnt1 and β‑catenin mRNA and protein levels were increased, while glycogen synthase kinase‑3 (GSK3) transcription was suppressed by EA. These results suggest that the upregulatory effects of EA on the Wnt/β‑catenin signaling pathway may promote NPC proliferation in the cortical peri-infarct area after stroke, consequently providing a therapeutic effect against cerebral ischemia.

  13. EGFR mediates astragaloside IV-induced Nrf2 activation to protect cortical neurons against in vitro ischemia/reperfusion damages

    Energy Technology Data Exchange (ETDEWEB)

    Gu, Da-min [Department of Anesthesiology, Affiliated Yixing People' s Hospital, Jiangsu University, Yixing (China); Lu, Pei-Hua, E-mail: lphty1_1@163.com [Department of Medical Oncology, Wuxi People' s Hospital Affiliated to Nanjing Medical University, Wuxi (China); Zhang, Ke; Wang, Xiang [Department of Anesthesiology, Affiliated Yixing People' s Hospital, Jiangsu University, Yixing (China); Sun, Min [Department of General Surgery, Affiliated Yixing People' s Hospital, Jiangsu University, Yixing (China); Chen, Guo-Qian [Department of Clinical Laboratory, Wuxi People' s Hospital Affiliated to Nanjing Medical University, Wuxi (China); Wang, Qiong, E-mail: WangQiongprof1@126.com [Department of Clinical Laboratory, Wuxi People' s Hospital Affiliated to Nanjing Medical University, Wuxi (China)

    2015-02-13

    In this study, we tested the potential role of astragaloside IV (AS-IV) against oxygen and glucose deprivation/re-oxygenation (OGD/R)-induced damages in murine cortical neurons, and studied the associated signaling mechanisms. AS-IV exerted significant neuroprotective effects against OGD/R by reducing reactive oxygen species (ROS) accumulation, thereby attenuating oxidative stress and neuronal cell death. We found that AS-IV treatment in cortical neurons resulted in NF-E2-related factor 2 (Nrf2) signaling activation, evidenced by Nrf2 Ser-40 phosphorylation, and its nuclear localization, as well as transcription of antioxidant-responsive element (ARE)-regulated genes: heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO-1) and sulphiredoxin 1 (SRXN-1). Knockdown of Nrf2 through lentiviral shRNAs prevented AS-IV-induced ARE genes transcription, and abolished its anti-oxidant and neuroprotective activities. Further, we discovered that AS-IV stimulated heparin-binding-epidermal growth factor (HB-EGF) release to trans-activate epidermal growth factor receptor (EGFR) in cortical neurons. Blockage or silencing EGFR prevented Nrf2 activation by AS-IV, thus inhibiting AS-IV-mediated anti-oxidant and neuroprotective activities against OGD/R. In summary, AS-IV protects cortical neurons against OGD/R damages through activating of EGFR-Nrf2 signaling. - Highlights: • Pre-treatment of astragaloside IV (AS-IV) protects murine cortical neurons from OGD/R. • AS-IV activates Nrf2-ARE signaling in murine cortical neurons. • Nrf2 is required for AS-IV-mediated anti-oxidant and neuroprotective activities. • AS-IV stimulates HB-EGF release to trans-activate EGFR in murine cortical neurons. • EGFR mediates AS-IV-induced Nrf2 activation and neuroprotection against OGD/R.

  14. Neuroprotective effects of a novel single compound 1-methoxyoctadecan-1-ol isolated from Uncaria sinensis in primary cortical neurons and a photothrombotic ischemia model.

    Directory of Open Access Journals (Sweden)

    Ji Yeon Jang

    Full Text Available We identified a novel neuroprotective compound, 1-methoxyoctadecan-1-ol, from Uncaria sinensis (Oliv. Havil and investigated its effects and mechanisms in primary cortical neurons and in a photothrombotic ischemic model. In primary rat cortical neurons against glutamate-induced neurotoxicity, pretreatment with 1-methoxyoctadecan-1-ol resulted in significantly reduced neuronal death in a dose-dependent manner. In addition, treatment with 1-methoxyoctadecan-1-ol resulted in decreased neuronal apoptotic death, as assessed by nuclear morphological approaches. To clarify the neuroprotective mechanism of 1-methoxyoctadecan-1-ol, we explored the downstream signaling pathways of N-methyl-D-aspartate receptor (NMDAR with calpain activation. Treatment with glutamate leads to early activation of NMDAR, which in turn leads to calpain-mediated cleavage of striatal-enriched protein tyrosine phosphatase (STEP and subsequent activation of p38 mitogen activated protein kinase (MAPK. However, pretreatment with 1-methoxyoctadecan-1-ol resulted in significantly attenuated activation of GluN2B-NMDAR and a decrease in calpain-mediated STEP cleavage, leading to subsequent attenuation of p38 MAPK activation. We confirmed the critical role of p38 MAPK in neuroprotective effects of 1-methoxyoctadecan-1-ol using specific inhibitor SB203580. In the photothrombotic ischemic injury in mice, treatment with 1-methoxyoctadecan-1-ol resulted in significantly reduced infarct volume, edema size, and improved neurological function. 1-methoxyoctadecan-1-ol effectively prevents cerebral ischemic damage through down-regulation of calpain-mediated STEP cleavage and activation of p38 MAPK. These results suggest that 1-methoxyoctadecan-1-ol showed neuroprotective effects through down-regulation of calpain-mediated STEP cleavage with activation of GluN2B-NMDAR, and subsequent alleviation of p38 MAPK activation. In addition, 1-methoxyoctadecan-1-ol might be a useful therapeutic agent for

  15. The neuroprotective efficacy of cell-penetrating peptides TAT, penetratin, Arg-9, and Pep-1 in glutamic acid, kainic acid, and in vitro ischemia injury models using primary cortical neuronal cultures.

    Science.gov (United States)

    Meloni, Bruno P; Craig, Amanda J; Milech, Nadia; Hopkins, Richard M; Watt, Paul M; Knuckey, Neville W

    2014-03-01

    Cell-penetrating peptides (CPPs) are small peptides (typically 5-25 amino acids), which are used to facilitate the delivery of normally non-permeable cargos such as other peptides, proteins, nucleic acids, or drugs into cells. However, several recent studies have demonstrated that the TAT CPP has neuroprotective properties. Therefore, in this study, we assessed the TAT and three other CPPs (penetratin, Arg-9, Pep-1) for their neuroprotective properties in cortical neuronal cultures following exposure to glutamic acid, kainic acid, or in vitro ischemia (oxygen-glucose deprivation). Arg-9, penetratin, and TAT-D displayed consistent and high level neuroprotective activity in both the glutamic acid (IC50: 0.78, 3.4, 13.9 μM) and kainic acid (IC50: 0.81, 2.0, 6.2 μM) injury models, while Pep-1 was ineffective. The TAT-D isoform displayed similar efficacy to the TAT-L isoform in the glutamic acid model. Interestingly, Arg-9 was the only CPP that displayed efficacy when washed-out prior to glutamic acid exposure. Neuroprotection following in vitro ischemia was more variable with all peptides providing some level of neuroprotection (IC50; Arg-9: 6.0 μM, TAT-D: 7.1 μM, penetratin/Pep-1: >10 μM). The positive control peptides JNKI-1D-TAT (JNK inhibitory peptide) and/or PYC36L-TAT (AP-1 inhibitory peptide) were neuroprotective in all models. Finally, in a post-glutamic acid treatment experiment, Arg-9 was highly effective when added immediately after, and mildly effective when added 15 min post-insult, while the JNKI-1D-TAT control peptide was ineffective when added post-insult. These findings demonstrate that different CPPs have the ability to inhibit neurodamaging events/pathways associated with excitotoxic and ischemic injuries. More importantly, they highlight the need to interpret neuroprotection studies when using CPPs as delivery agents with caution. On a positive note, the cytoprotective properties of CPPs suggests they are ideal carrier molecules to

  16. Nrdp1 Increases Ischemia Induced Primary Rat Cerebral Cortical Neurons and Pheochromocytoma Cells Apoptosis Via Downregulation of HIF-1α Protein

    Directory of Open Access Journals (Sweden)

    Yuan Zhang

    2017-09-01

    Full Text Available Neuregulin receptor degradation protein-1 (Nrdp1 is an E3 ubiquitin ligase that targets proteins for degradation and regulates cell growth, apoptosis and oxidative stress in various cell types. We have previously shown that Nrdp1 is implicated in ischemic cardiomyocyte death. In this study, we investigated the change of Nrdp1 expression in ischemic neurons and its role in ischemic neuronal injury. Primary rat cerebral cortical neurons and pheochromocytoma (PC12 cells were infected with adenoviral constructs expressing Nrdp1 gene or its siRNA before exposing to oxygen-glucose deprivation (OGD treatment. Our data showed that Nrdp1 was upregulated in ischemic brain tissue 3 h after middle cerebral artery occlusion (MCAO and in OGD-treated neurons. Of note, Nrdp1 overexpression by Ad-Nrdp1 enhanced OGD-induced neuron apoptosis, while knockdown of Nrdp1 with siRNA attenuated this effect, implicating a role of Nrdp1 in ischemic neuron injury. Moreover, Nrdp1 upregulation is accompanied by increased protein ubiquitylation and decreased protein levels of ubiquitin-specific protease 8 (USP8 in OGD-treated neurons, which led to a suppressed interaction between USP8 and HIF-1α and subsequently a reduction in HIF-1α protein accumulation in neurons under OGD conditions. In conclusion, our data support an important role of Nrdp1 upregulation in ischemic neuronal death, and suppressing the interaction between USP8 and HIF-1α and consequently the hypoxic adaptive response of neurons may account for this detrimental effect.

  17. Silent Ischemia

    Science.gov (United States)

    ... silent ischemia: An exercise stress test can show blood flow through your coronary arteries in response to exercise. Holter monitoring records your heart rate and rhythm over a 24-hour period (or ...

  18. 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 ...

  19. Spreading effect of tDCS in individuals with attention-deficit/hyperactivity disorder as shown by functional cortical networks: a randomized, double-blind, sham-controlled trial

    Directory of Open Access Journals (Sweden)

    Camila eCosmo

    2015-08-01

    Full Text Available Transcranial direct current stimulation (tDCS is known to modulate spontaneous neural network excitability. The cognitive improvement observed in previous trials raises the potential of this technique as a possible therapeutic tool for use in attention-deficit/hyperactivity disorder (ADHD population. However, to explore the potential of this technique as a treatment approach the functional parameters of brain connectivity and the extent of its effects need to be more fully investigated.The aim of this study was to investigate a functional cortical network model based on electroencephalographic activity for studying the dynamic patterns of brain connectivity modulated by tDCS and the distribution of its effects in individuals with attention-deficit/hyperactivity disorder (ADHD.Sixty ADHD patients participated in a parallel, randomized, double-blind, sham-controlled trial. Individuals underwent a single session of sham or anodal tDCS at 1 mA of current intensity over the left dorsolateral prefrontal cortex for 20 minutes. The acute effects of stimulation on brain connectivity were assessed using the functional cortical network model based on electroencephalography (EEG activity.Comparing the weighted node degree within groups prior to and following the intervention, a statistically significant difference was found in the electrodes located on the target and correlated areas in the active group (p<0.05, while no statistically significant results were found in the sham group (p ≥0.05; paired-sample Wilcoxon signed rank test. Anodal tDCS increased functional brain connectivity in individuals with ADHD compared to data recorded in the baseline resting state. In addition, although some studies have suggested that the effects of tDCS are selective, the present findings show that its modulatory activity spreads. Further studies need to be performed to investigate the dynamic patterns and physiological mechanisms underlying the modulatory effects of tDCS.

  20. Effects of ketamine,midazolam,thiopental,and propofol on brain ischemia injury in rat cerebral cortical slices%氯胺酮,咪唑安定,硫喷妥钠和异丙酚对大鼠皮层脑片缺血性损伤的作用

    Institute of Scientific and Technical Information of China (English)

    薛庆生; 于布为; 王泽剑; 陈红专

    2004-01-01

    AIM: To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices. METHODS: Cerebral cortical slices were incubated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine,midazolam, thiopental, and propofol were quantitativlye evaluated by ELISA reader of absorbance (A) at 490 nm,which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured. RESULTS: Progressive prolongation of OGD resulted in decreases of TTC staining.The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P<0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD (P<0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited the decrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 μmol/L) and thiopental (400 μmol/L)partly attenuated this decrease. Propofol at high concentration (100 μmol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P<0.01). CONCLUSION: Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.

  1. Spreading depolarization monitoring in neurocritical care of acute brain injury.

    Science.gov (United States)

    Hartings, Jed A

    2017-04-01

    Spreading depolarizations are unique in being discrete pathologic entities that are well characterized experimentally and also occur commonly in patients with substantial acute brain injury. Here, we review essential concepts in depolarization monitoring, highlighting its clinical significance, interpretation, and future potential. Cortical lesion development in diverse animal models is mediated by tissue waves of mass spreading depolarization that cause the toxic loss of ion homeostasis and limit energy substrate supply through associated vasoconstriction. The signatures of such deterioration are observed in electrocorticographic recordings from perilesional cortex of patients with acute stroke or brain trauma. Experimental work suggests that depolarizations are triggered by energy supply-demand mismatch in focal hotspots of the injury penumbra, and depolarizations are usually observed clinically when other monitoring variables are within recommended ranges. These results suggest that depolarizations are a sensitive measure of relative ischemia and ongoing secondary injury, and may serve as a clinical guide for personalized, mechanistically targeted therapy. Both existing and future candidate therapies offer hope to limit depolarization recurrence. Electrocorticographic monitoring of spreading depolarizations in patients with acute brain injury provides a sensitive measure of relative energy shortage in focal, vulnerable brains regions and indicates ongoing secondary damage. Depolarization monitoring holds potential for targeted clinical trial design and implementation of precision medicine approaches to acute brain injury therapy.

  2. 格列本脲对大鼠皮层扩散性抑制中脑血管的调节作用%Regulation of Pial Artery by Glibenclamide During Cortical Spreading Depression in Rats

    Institute of Scientific and Technical Information of China (English)

    杨媛媛; 李鹏程; 曾绍群; 骆清铭

    2006-01-01

    皮层扩散性抑制(cortical spreading depression,CSD)是研究偏头痛、脑梗塞等疾病的重要病理模型.已有研究表明,在普遍被观察到的CSD过程中软脑膜动脉血管大幅度舒张之前,还存在一个较小幅度的软脑膜动脉扩张和收缩.但其中的脑血管调节机制尚不清楚.采用550 nm的内源信号光学成像(opticalintrinsic signalimaging,OISI)监测ATP敏感钾离子通道(ATP-sensitive potassium channels,KATP)的阻断剂格列本脲(glibenclamide,glyb),对针刺诱导的大鼠CSD过程中软脑膜动脉血管舒缩过程的影响.实验中观测到软脑膜血管的初始小收缩(initial slightconstriction,ISC)相对于对照组显著减弱,其中应用10μmol/L glyb时,74.5%的ISC被完全抑制,100μmol/L glyb时则有96.2%的ISC完全消失.相对于CSD发生前,软脑膜动脉血管大幅舒张(large dilation,LD)的峰值也分别显著增强了(53.8±19.3)%和(59.8±19.6)%.结果表明,可能是神经元上的KATP在CSD过程中被glyb阻断从而抑制了软脑膜动脉血管的收缩.

  3. Spreading depolarizations increase delayed brain injury in a rat model of subarachnoid hemorrhage

    NARCIS (Netherlands)

    Hamming, Arend M.; Wermer, Marieke J H; Umesh Rudrapatna, S.; Lanier, Christian; Van Os, Hine J A; Van Den Bergh, Walter M.; Ferrari, Michel D.; van der Toorn, A; Van Den Maagdenberg, Arn M J M; Stowe, Ann M.; Dijkhuizen, Rick M.

    2016-01-01

    Spreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that

  4. Spreading depolarizations increase delayed brain injury in a rat model of subarachnoid hemorrhage

    NARCIS (Netherlands)

    Hamming, Arend M.; Wermer, Marieke J. H.; Rudrapatna, S. Umesh; Lanier, Christian; van Os, Hine J. A.; van den Bergh, Walter M.; Ferrari, Michel D.; van der Toorn, Annette; van den Maagdenberg, Arn M. J. M.; Stowe, Ann M.; Dijkhuizen, Rick M.

    Spreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that

  5. 大鼠皮层扩散性抑制过程的在体内源光信号成像%In vivo Optical Imaging of Intrinsic Signal During Cortical Spreading Depression in Rats

    Institute of Scientific and Technical Information of China (English)

    李鹏程; 陈尚宾; 骆卫华; 骆清铭

    2003-01-01

    皮层扩散性抑制(cortical spreading depression,CSD)是研究偏头痛、脑梗塞等疾病的一种重要病理模型.而CSD过程中伴随发生的皮层血液动力学变化目前尚不完全清楚.利用高分辨的内源光信号成像技术,在体观测了大鼠CSD产生和发展过程中540 nm及660 nm波长皮层反射内源光信号变化的时空动力学特征,分析讨论了引起这一内源光信号变化可能的内在生理机制.实验结果显示,CSD诱发的内源光信号变化呈现多时相的特点,其传播由刺激中心以同心圆的样式向周围扩散,速度约为(3.7±0.4) mm/min.对于540 nm,CSD引起了皮层反射光强的降低[幅度(-2.1±1.2)%, 持续时程(16.2±3.8)s],升高 [幅度(2.9±1.6)%, 持续时程(13.8±2.2)s],再降低 [幅度(-14.2±4.5)%, 持续时程(40.6±8.4)s]和再升高持续时程[(146.2±40.3)s],同时观测到软脑膜动脉的大幅度舒张,血管管径变化峰值增大了(69.2±26.1)%.而对于660 nm, 内源光信号变化的时间特性在皮质区主要表现为反射光强的增大[幅度(3.8±0.6)%, 持续时程(17.9±5.1)s],减小[幅度(-3.0±1.7)%, 持续时程(43.3±6.4)s]和稍后持续缓慢的光强增加.

  6. [Cortical blindness].

    Science.gov (United States)

    Chokron, S

    2014-02-01

    Cortical blindness refers to a visual loss induced by a bilateral occipital lesion. The very strong cooperation between psychophysics, cognitive psychology, neurophysiology and neuropsychology these latter twenty years as well as recent progress in cerebral imagery have led to a better understanding of neurovisual deficits, such as cortical blindness. It thus becomes possible now to propose an earlier diagnosis of cortical blindness as well as new perspectives for rehabilitation in children as well as in adults. On the other hand, studying complex neurovisual deficits, such as cortical blindness is a way to infer normal functioning of the visual system.

  7. EDT,a tetrahydroacridine derivative inhibits cerebral ischemia and protects rat cortical neurons against glutamate-induced cytotoxicity%四氢吖啶类衍生物EDT抑制脑缺血及保护大鼠皮层神经元抗谷氨酸诱发的细胞毒性

    Institute of Scientific and Technical Information of China (English)

    盛瑞; 刘国卿

    2003-01-01

    目的:考察9-(4-乙氧羰基苯氧基)-6,7-二甲氧基-1,2,3,4-四氢吖啶盐酸盐(EDT)对大鼠局灶性脑缺血及谷氨酸(Glu)和硝普钠(SNP)致鼠皮层神经元损伤的作用.方法:灼断小鼠一侧大脑中动脉形成局灶性脑缺血模型,用氯化三苯基四氮唑(TTC)染色法测定脑梗塞率同时对神经症状进行评分.在原代培养的大鼠皮层神经细胞,采用MTT比色法,测定培养质内LDH及NO释放量.结果:EDT 2.5、5和10mg/kg及尼莫地平2 mg/kg灌胃5 d显著改善局灶性脑缺血小鼠的神经运动功能,缩小脑梗塞范围.在原代培养的鼠皮层神经细胞,EDT 0.01-3 μmol/L浓度依赖地对抗Glu诱发的NO过量形成,并提高MTT微量比色值,同时,减少SNP引起的LDH过量释放,提高细胞存活率.结论:EDT能有效对抗脑缺血损伤,其神经保护作用可能是通过阻断Glu受体及抑制N0生成而实现的.%AIM: To study the effects of 9-(4-ethoxycarbonylyphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydroacridine (EDT) on cerebral ischemia and glutamic acid (Glu) and sodium nitroprusside (SNP)-induced neurocytotoxicity in primary cortical culture. METHODS: Focal cerebral ischemia was produced by permanent occlusion of left middle cerebral artery (MCA) in mice. The infarct tissue was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining technique. The extent of neurological deficits was evaluated. In primary cortical culture, colorimetric MTT assay was used to determine cell survival rate, and leakage of LDH and NO release assay were measured. RESULTS: In focal cerebral ischemia, pretreatment with EDT 2.5, 5, and 10 mg/kg and nimodipine 2 mg/kg for 5 d effectively improved the abnormal neurological symptoms and reduced the infarct rate. In primary cortical culture, EDT 0.01-3 μmol/L concentration-dependently attenuated NO release induced by Glu 500 μmol/L and increased the cell survival. It also remarkably reduced the LDH excessive efflux. CONCLUSION: EDT possessed

  8. Cortico-cortical communication dynamics

    Directory of Open Access Journals (Sweden)

    Per E Roland

    2014-05-01

    Full Text Available IIn principle, cortico-cortical communication dynamics is simple: neurons in one cortical area communicate by sending action potentials that release glutamate and excite their target neurons in other cortical areas. In practice, knowledge about cortico-cortical communication dynamics is minute. One reason is that no current technique can capture the fast spatio-temporal cortico-cortical evolution of action potential transmission and membrane conductances with sufficient spatial resolution. A combination of optogenetics and monosynaptic tracing with virus can reveal the spatio-temporal cortico-cortical dynamics of specific neurons and their targets, but does not reveal how the dynamics evolves under natural conditions. Spontaneous ongoing action potentials also spread across cortical areas and are difficult to separate from structured evoked and intrinsic brain activity such as thinking. At a certain state of evolution, the dynamics may engage larger populations of neurons to drive the brain to decisions, percepts and behaviors. For example, successfully evolving dynamics to sensory transients can appear at the mesoscopic scale revealing how the transient is perceived. As a consequence of these methodological and conceptual difficulties, studies in this field comprise a wide range of computational models, large-scale measurements (e.g., by MEG, EEG, and a combination of invasive measurements in animal experiments. Further obstacles and challenges of studying cortico-cortical communication dynamics are outlined in this critical review.

  9. Acute Mesenteric Ischemia

    Science.gov (United States)

    ... Side Effects Additional Content Medical News Acute Mesenteric Ischemia By Parswa Ansari, MD, Department of Surgery, Lenox ... Abscesses Abdominal Wall Hernias Inguinal Hernia Acute Mesenteric Ischemia Appendicitis Ileus Intestinal Obstruction Ischemic Colitis Perforation of ...

  10. Mesenteric artery ischemia

    Science.gov (United States)

    ... medlineplus.gov/ency/article/001156.htm Mesenteric artery ischemia To use the sharing features on this page, please enable JavaScript. Mesenteric artery ischemia occurs when there is a narrowing or blockage ...

  11. Intestinal ischemia and infarction

    Science.gov (United States)

    ... medlineplus.gov/ency/article/001151.htm Small intestinal ischemia and infarction To use the sharing features on this page, please enable JavaScript. Intestinal ischemia and infarction occurs when there is a narrowing ...

  12. Microglia protect neurons against ischemia by synthesis of tumor necrosis factor

    DEFF Research Database (Denmark)

    Lambertsen, Kate Lykke; Clausen, Bettina Hjelm; Babcock, Alicia Anne

    2009-01-01

    Microglia and infiltrating leukocytes are considered major producers of tumor necrosis factor (TNF), which is a crucial player in cerebral ischemia and brain inflammation. We have identified a neuroprotective role for microglial-derived TNF in cerebral ischemia in mice. We show that cortical infa...

  13. Poly-IC preconditioning protects against cerebral and renal ischemia-reperfusion injury.

    Science.gov (United States)

    Packard, Amy E B; Hedges, Jason C; Bahjat, Frances R; Stevens, Susan L; Conlin, Michael J; Salazar, Andres M; Stenzel-Poore, Mary P

    2012-02-01

    Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is a new powerful prophylactic treatment that offers promise as a clinical therapeutic strategy to minimize damage in patient populations at risk of ischemic injury.

  14. Migraine and ischemia

    NARCIS (Netherlands)

    van der Wammes-van der Heijden, E.A.

    2009-01-01

    An association between migraine and ischemic events, especially ischemic stroke, has been debated for many years. Whether migraine is a risk factor for ischemic events or ischemia triggers migraine, or both, is still unclear. This thesis explores different relationships between migraine and ischemia

  15. 吡格列酮对缺血-再灌注损伤大鼠皮质神经元的保护作用%Protective effect of pioglitazone and the role on the cultured cortical neuron after ischemia-reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    黄昭; 王思荣; 刘继云

    2009-01-01

    Objective To explore the protective effect of proliferator activated receptor-γ (PPAR-γ)activator pioglitazone on the expression of inflammatory cytokines in cultured cortical neurons after ischemia-reperfusion injury and its mechanism. Method The ischemie-reperfusion model was established by deprivating both glucose an oxygen in medium and then gave them back. Medium or that with pioglitazone was added at the beginning of reperfusion. The MTT values of neurons were determined in control or treatment groups, ANOVA was used to detect the expression of PPAR-γ. The expression of tumor necrosis factors-α(TNF-α) and interleukin-lβ(IL-lβ) were detected by Western Blotting. Results Compared to control group, the markedly reduction of MTT values and enhanced expression of PPAR-γ, TNF-a and IL-1β was observed in the ischemia-reperfusion neurons (P < 0.05). After they were treated by pioglitazone, the reduction of MTT values and enhanced expression of TNF-a and IL-1β were prominently reversed by the further activation of PPAR-γ ( P < 0.05). Conclusions Treatment of PPAR-γ activator pioglitazone has protective effect on neurons after ischemia-reperfusion injury. Its mechanism may be associated with the inhibition of inflammation after injury.%目的 探讨过氧化物酶增值物激活受体-γ(PPAR-γ)及其激活剂噻唑烷二酮类药物-吡格列酮(pioglitazone)对缺血.再灌注损伤大鼠皮质神经元肿瘤坏死因子(TNF-α)、白介素(IL-1β)表达的影响.方法 采用原代培养的皮质神经元,通过去除培养液中的糖和氧,模拟缺血缺氧,恢复糖氧供给模拟再灌注.再灌注时分别加用普通培养或含吡格列酮20 μmol/L培养基分别再培养6 h后,以上各组及正常细胞组均采用RT-PCR检测PPAR-γ mRNA表达,MTT法检测细胞活性,同时免疫蛋白印记法检测TNF-α,IL-β蛋白表达.统计学采用单因素方差分析进行统计处理.结果 与正常细胞对照组相比,缺血-再灌注组细

  16. Transient cortical blindness as a complication of posterior spinal surgery in a pediatric patient.

    Science.gov (United States)

    Nathan, Senthil T; Jain, Viral; Lykissas, Marios G; Crawford, Alvin H; West, Constance E

    2013-09-01

    Postoperative vision loss after spinal surgery is a well-known but devastating complication that may result from direct ocular ischemia, embolism to the central retinal artery, ischemic optic neuropathy, or occipital cortical ischemia. The occipital cortex is situated in the posterior border zone of the middle and posterior cerebral arteries and is susceptible to ischemic damage. Transient cortical blindness as a cause of postoperative vision loss has never been reported after spine surgery in a child. We report an 11-year-old female patient with muscular dystrophy who underwent posterior spinal fusion and instrumentation under hypotensive anesthesia for scoliosis who developed transient cortical blindness.

  17. Silent myocardial ischemia.

    Science.gov (United States)

    Gutterman, David D

    2009-05-01

    Although much progress has been made in reducing mortality from ischemic cardiovascular disease, this condition remains the leading cause of death throughout the world. This might in part be due to the fact that over half of patients have a catastrophic event (heart attack or sudden death) as their initial manifestation of coronary disease. Contributing to this statistic is the observation that the majority of myocardial ischemic episodes are silent, indicating an inability or failure to sense ischemic damage or stress on the heart. This review examines the clinical characteristics of silent myocardial ischemia, and explores mechanisms involved in the generation of angina pectoris. Possible mechanisms for the more common manifestation of injurious reductions in coronary flow; namely, silent ischemia, are also explored. A new theory for the mechanism of silent ischemia is proposed. Finally, the prognostic importance of silent ischemia and potential future directions for research are discussed.

  18. Critical Limb Ischemia (CLI)

    Science.gov (United States)

    ... Buerger’s Disease Carotid Artery Disease Chronic Venous Insufficiency Congenital Vascular Malformation Critical Limb Ischemia (CLI) Deep Vein Thrombosis (DVT) Diabetes and Vascular Disease Fibromuscular Dysplasia High Blood Pressure and Vascular Disease Kidney Failure ...

  19. Cerebral ischemia produces laddered DNA fragments distinct from cardiac ischemia and archetypal apoptosis.

    Science.gov (United States)

    MacManus, J P; Fliss, H; Preston, E; Rasquinha, I; Tuor, U

    1999-05-01

    The electrophoretic pattern of laddered DNA fragments which has been observed after cerebral ischemia is considered to indicate that neurons are dying by apoptosis. Herein the authors directly demonstrate using ligation-mediated polymerase chain reaction methods that 99% of the DNA fragments produced after either global or focal ischemia in adult rats, or produced after hypoxia-ischemia in neonatal rats, have staggered ends with a 3' recess of approximately 8 to 10 nucleotides. This is in contrast to archetypal apoptosis in which the DNA fragments are blunt ended as seen during developmental programmed cell death in dying cortical neurons, neuroblastoma, or thymic lymphocytes. It is not simply ischemia that results in staggered ends in DNA fragments because ischemic myocardium is similar to archetypal apoptosis with a vast majority of blunt-ended fragments. It is concluded that the endonucleases that produce this staggered fragmentation of the DNA backbone in ischemic brain must be different than those of classic or type I apoptosis.

  20. Cortical Visual Impairment

    Science.gov (United States)

    ... Frequently Asked Questions Español Condiciones Chinese Conditions Cortical Visual Impairment En Español Read in Chinese What is cortical visual impairment? Cortical visual impairment (CVI) is a decreased visual ...

  1. Effect of Salvianolic Acid B on Mitochondrial Function of Cerebral Ischemia in Mice

    Institute of Scientific and Technical Information of China (English)

    JIANG Yufeng; LUO Xuechun; WANG Ximei; FANG Lei; HUANG Qifu

    2009-01-01

    The effects of salvianolic acid B (SalB) on the mitochondrial membrane potential (MMP), calcium, and apoptosis of neurons with cerebral ischemia in mice were investigated using an acute cerebral ischemia model established by ligating the bilateral common carotid arteries in mica. The MMP, the intracellular cal-cium concentration, and the apoptosis rate of cortical neurons were measured at 6 min, 12 min, 18 min, 24 min, and 30 min after cerebral ischemia by a flow cytometer. The experiments show that SalB increases the MMP and reduces the intracellular calcium and the apoptosis rate at different stages of the cerebral ischemia in mice. The results show that the protective mechanism of SalB on cerebral ischemia enhances the MMP and maintains intracellular calcium homeostasis.

  2. [Cerebral ischemia and histamine].

    Science.gov (United States)

    Adachi, Naoto

    2002-10-01

    Cerebral ischemia induces excess release of glutamate and an increase in the intracellular Ca2+ concentration, which provoke catastrophic enzymatic processes leading to irreversible neuronal injury. Histamine plays the role of neurotransmitter in the central nervous system, and histaminergic fibers are widely distributed in the brain. In cerebral ischemia, release of histamine from nerve endings has been shown to be enhanced by facilitation of its activity. An inhibition of the histaminergic activity in ischemia aggravates the histologic outcome. In contrast, intracerebroventricular administration of histamine improves the aggravation, whereas blockade of histamine H2 receptors aggravates ischemic injury. Furthermore, H2 blockade enhances ischemic release of glutamate and dopamine. These findings suggest that central histamine provides beneficial effects against ischemic neuronal damage by suppressing release of excitatory neurotransmitters. However, histaminergic H2 action facilitates the permeability of the blood-brain barrier and shows deleterious effects on cerebral edema.

  3. Effects of rizatriptan on cortical spreading depression and c-Fos expression within periaqueductal grey%苯甲酸利扎曲普坦对皮质扩布性抑制及中脑导水管周围灰质c-Fos表达的影响

    Institute of Scientific and Technical Information of China (English)

    李凤鹏; 刘若卓; 姜磊; 于生元; 管维平; 石宏; 陈淑莉; 晋志高; 吴士文; 董钊; 邱恩超

    2008-01-01

    Objective To determine whether rizatriptan has an effect on cortical spreading depression (CSD) and c-Fos expression within periaqueductal grey (PAG) induced by CSD in rats. Methods The experimental SD rats were randomly divided into group A injected with KCl, group B KCl plus rizatriptan and group C NaCL The number and amplitude of CSD were recorded after KCl or NaCl injection. C-Fos positive neurons of different layer were identified by the immunohistochemical technique 2 hours after the first injection of KCl or NaCl. Results There was no CSD in group C. The number of CSD in group A ( 10.70±3.23 ) was significantly more than that in group B (6.10±2.56, t = - 3.528, P < 0.01 ). The amplitude of CSD in group A ( 17.33 (95% CI 11.45--23.11 ) mV) was significantly greater than that in group B (11.82 (95%CI 9.24--14.70) mV, Z= -4.360, P< 0.01). There were more cFos-like immnoreactive neurons in every layer in group A than in group C (P < 0.01 ) and in group B (P < 0.05 ). Conclusion Rizatriptan has an inhibitory effect on CSD, which might induce the headache through exciting the neurons in PAG.%目的 观察苯甲酸利扎曲普坦对大鼠皮质扩布性抑制(cortical spreading depression,CSD)和CSD引起中脑导水管周围灰质(periaqueduetal grey,PAG)内c-Fos表达的影响.方法 实验选用的SD大鼠随机分为3组,A组:氯化钾刺激组;B组:氯化钾刺激+苯甲酸利扎曲普坦组;C组:氯化钠刺激组.对各组大鼠使用氯化钾(或氯化钠)刺激,以观察CSD出现的个数和波幅;第1次刺激2 h后使用免疫组织化学法检测各组PAG内不同层面c-Fos阳性神经元.结果 C组未记录到CSI).A组CSD个数(10.70±3.23)较B组(6.10±2.56)显著增多(t=-3.528,P<0.01);A组CSD波幅[17.33(95%CI 11.45~23.11)mV]较B组[11.82(95%CI 9.24~14.70)mV]显著增加(Z=-4.360,P<0.01).A组各层面c-Fos阳性细胞数较B、C组显著增多(P<0.05).结论 苯甲酸利扎曲普坦对CSD有抑制作用,可使CSD引起PAG内神经元兴奋作用减弱.

  4. Ischemia-driven angiogenesis.

    Science.gov (United States)

    Dor, Y; Keshet, E

    1997-11-01

    New blood vessels usually develop in places where they are most needed. A prime example of neovascularization representing a positive feedback response to insufficient perfusion is the development of collateral blood vessels in the ischemic myocardium and leg. The recent discoveries of hypoxia-inducible transcription and angiogenic factors have provided important mechanistic links between the metabolic consequences of ischemia and compensatory angiogenesis. Vascular endothelial growth factor (VEGF) has emerged as the key mediator of ischemia-driven angiogenesis. Environmental stresses, including hypoxia, hypoglycemia, and hypoferremia, upregulate VEGF expression at both the transcriptional and posttranscriptional levels. VEGF acts in turn on adjacent vascular beds expressing cognate receptors and induces sprouting and capillary growth toward the ischemic tissue. In addition to expanding the vasculature at sites where existing vessels have been occluded or obliterated, VEGF also functions to match the vascular density according to development and physiologic increases in oxygen consumption. Fine adjustment of the vasculature includes a step of oxygen-regulated vascular pruning mediated by VEGF in its capacity as a survival factor for newly formed vessels. Pathologic settings of ischemia-driven angiogenesis include a major component of stress-induced angiogenesis during tumor neovascularization and abnormal vessel growth associated with retinopathies. The latter represents an excessive angiogenic response to conditions of severe retinal ischemia. Further insights into the mechanism of stress-induced angiogenesis are likely to suggest new ways to augment growth of collateral vessels and to restrain unwarranted neovascularization in tumors and retinopathies. (Trends Cardiovasc Med 1997;7:289-294). © 1997, Elsevier Science Inc.

  5. Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia.

    Science.gov (United States)

    Käsmann, B; Ruprecht, K W

    1995-07-01

    Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.

  6. Spreading depolarization may link migraine and stroke.

    Science.gov (United States)

    Eikermann-Haerter, Katharina

    2014-01-01

    Migraine increases the risk of stroke, particularly in young and otherwise healthy adults. Being the most frequent neurological condition, migraine prevalence is on a par with that of other common stroke risk factors, such as diabetes or hypertension. Several patterns of association have emerged: (1) migraine and stroke share a common association (eg, vasculopathies, patent foramen ovale, or pulmonary A-V malformations); (2) injury to the arterial wall such as acute arterial dissections can present as migraine aura attacks or stroke; (3) strokes rarely develop during a migraine attack, as described for "migrainous stroke." Increasing experimental evidence suggests that cerebral hyperexcitability and enhanced susceptibility to spreading depolarization, the electrophysiologic event underlying migraine, may serve as a mechanism underlying the migraine-stroke association. Mice carrying human vascular or neuronal migraine mutations exhibit an enhanced susceptibility to spreading depolarization while being particularly vulnerable to cerebral ischemia. The severe stroke phenotype in migraine mutant mice can be prevented by suppressing spreading depolarization. If confirmed in the clinical setting, inhibiting spreading depolarization might protect migraineurs at stroke risk as well as decrease attacks of migraine. © 2014 American Headache Society.

  7. Recombinant human erythropoietin increases cerebral cortical width index and neurogenesis following ischemic stroke

    Institute of Scientific and Technical Information of China (English)

    Zhongmin Wen; Peiji Wang

    2012-01-01

    The cerebral cortical expansion index refers to the ratio between left and right cortex width and is recognized as an indicator for cortical hyperplasia. Cerebral ischemia was established in CB-17 mice in the present study, and the mice were subsequently treated with recombinant human erythropoietin via subcutaneous injection. Results demonstrated that cerebral cortical width index significantly increased. Immunofluorescence detection showed that the number of nuclear antigen antibody/5-bromodeoxyuridine-positive cells at the infarction edge significantly increased. Correlation analysis revealed a negative correlation between neurological scores and cortical width indices in rats following ischemic stroke. These experimental findings suggested that recombinant human erythropoietin promoted cerebral cortical hyperplasia, increased cortical neurogenesis, and enhanced functional recovery following ischemic stroke.

  8. Ischemia causes muscle fatigue

    Science.gov (United States)

    Murthy, G.; Hargens, A. R.; Lehman, S.; Rempel, D. M.

    2001-01-01

    The purpose of this investigation was to determine whether ischemia, which reduces oxygenation in the extensor carpi radialis (ECR) muscle, causes a reduction in muscle force production. In eight subjects, muscle oxygenation (TO2) of the right ECR was measured noninvasively and continuously using near infrared spectroscopy (NIRS) while muscle twitch force was elicited by transcutaneous electrical stimulation (1 Hz, 0.1 ms). Baseline measurements of blood volume, muscle oxygenation and twitch force were recorded continuously, then a tourniquet on the upper arm was inflated to one of five different pressure levels: 20, 40, 60 mm Hg (randomized order) and diastolic (69 +/- 9.8 mm Hg) and systolic (106 +/- 12.8 mm Hg) blood pressures. Each pressure level was maintained for 3-5 min, and was followed by a recovery period sufficient to allow measurements to return to baseline. For each respective tourniquet pressure level, mean TO2 decreased from resting baseline (100% TO2) to 99 +/- 1.2% (SEM), 96 +/- 1.9%, 93 +/- 2.8%, 90 +/- 2.5%, and 86 +/- 2.7%, and mean twitch force decreased from resting baseline (100% force) to 99 +/- 0.7% (SEM), 96 +/- 2.7%, 93 +/- 3.1%, 88 +/- 3.2%, and 86 +/- 2.6%. Muscle oxygenation and twitch force at 60 mm Hg tourniquet compression and above were significantly lower (P ischemia leading to a 7% or greater reduction in muscle oxygenation causes decreased muscle force production in the forearm extensor muscle. Thus, ischemia associated with a modest decline in TO2 causes muscle fatigue.

  9. Ischemia causes muscle fatigue

    Science.gov (United States)

    Murthy, G.; Hargens, A. R.; Lehman, S.; Rempel, D. M.

    2001-01-01

    The purpose of this investigation was to determine whether ischemia, which reduces oxygenation in the extensor carpi radialis (ECR) muscle, causes a reduction in muscle force production. In eight subjects, muscle oxygenation (TO2) of the right ECR was measured noninvasively and continuously using near infrared spectroscopy (NIRS) while muscle twitch force was elicited by transcutaneous electrical stimulation (1 Hz, 0.1 ms). Baseline measurements of blood volume, muscle oxygenation and twitch force were recorded continuously, then a tourniquet on the upper arm was inflated to one of five different pressure levels: 20, 40, 60 mm Hg (randomized order) and diastolic (69 +/- 9.8 mm Hg) and systolic (106 +/- 12.8 mm Hg) blood pressures. Each pressure level was maintained for 3-5 min, and was followed by a recovery period sufficient to allow measurements to return to baseline. For each respective tourniquet pressure level, mean TO2 decreased from resting baseline (100% TO2) to 99 +/- 1.2% (SEM), 96 +/- 1.9%, 93 +/- 2.8%, 90 +/- 2.5%, and 86 +/- 2.7%, and mean twitch force decreased from resting baseline (100% force) to 99 +/- 0.7% (SEM), 96 +/- 2.7%, 93 +/- 3.1%, 88 +/- 3.2%, and 86 +/- 2.6%. Muscle oxygenation and twitch force at 60 mm Hg tourniquet compression and above were significantly lower (P < 0.05) than baseline value. Reduced twitch force was correlated in a dose-dependent manner with reduced muscle oxygenation (r = 0.78, P < 0.001). Although the correlation does not prove causation, the results indicate that ischemia leading to a 7% or greater reduction in muscle oxygenation causes decreased muscle force production in the forearm extensor muscle. Thus, ischemia associated with a modest decline in TO2 causes muscle fatigue.

  10. Oligodendrogenesis after Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Ruilan eZhang

    2013-10-01

    Full Text Available AbstractNeural stem cells in the subventricular zone (SVZ of the lateral ventricle of adult rodent brain generate oligodendrocyte progenitor cells (OPCs that disperse throughout the corpus callosum and striatum where some of OPCs differentiate into mature oligodendrocytes. Studies in animal models of stroke demonstrate that cerebral ischemia induces oligodendrogenesis during brain repair processes. This article will review evidence of stroke-induced proliferation and differentiation of OPCs that are either resident in white matter or are derived from SVZ neural progenitor cells and of therapies that amplify endogenous oligodendrogenesis in ischemic brain.

  11. Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex

    DEFF Research Database (Denmark)

    Hansen, Henning Piilgaard; Lauritzen, Martin

    2009-01-01

    trauma. Here we tested the hypothesis that single episodes of CSD induced acute hypoxia, and prolonged impairment of neurovascular and neurometabolic coupling. Cortical spreading depression was induced in rat frontal cortex, whereas cortical electrical activity and local field potentials (LFPs) were...... neurovascular coupling was explained by both reduced vascular reactivity and suppressed function of cortical inhibitory interneurons. The protracted effects of CSD on basal CMRO(2) and neurovascular coupling may contribute to cellular dysfunction in patients with migraine and acutely injured cerebral cortex....

  12. Spreading Depolarizations Have Prolonged Direct Current Shifts and Are Associated with Poor Outcome in Brain Trauma

    Science.gov (United States)

    2011-01-01

    prognosis . Keywords: cortical spreading depression; electroencephalography; craniotomy; signal processing; acute brain injury Introduction Cortical...GCS =Glasgow coma scale. differed from normality and Kruskai-Wallis tests were used for non-parametric analysis of variance. Data are reported as...graded prognosis corresponding to 100% (isoelectric depolarizations), 60% (depolarizations with de- pression periods) and 23% (no depolarizations) of

  13. Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia.

    Science.gov (United States)

    Kaplan, B; Brint, S; Tanabe, J; Jacewicz, M; Wang, X J; Pulsinelli, W

    1991-08-01

    We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.

  14. Information in CDS Spreads

    NARCIS (Netherlands)

    L. Norden (Lars)

    2014-01-01

    textabstractWe investigate how public and private information drives corporate CDS spreads before rating announcements. We find that CDS spreads of firms with higher news intensity move significantly earlier and stronger before rating announcements, which can be explained with public information fro

  15. The spreading of disorder.

    Science.gov (United States)

    Keizer, Kees; Lindenberg, Siegwart; Steg, Linda

    2008-12-12

    Imagine that the neighborhood you are living in is covered with graffiti, litter, and unreturned shopping carts. Would this reality cause you to litter more, trespass, or even steal? A thesis known as the broken windows theory suggests that signs of disorderly and petty criminal behavior trigger more disorderly and petty criminal behavior, thus causing the behavior to spread. This may cause neighborhoods to decay and the quality of life of its inhabitants to deteriorate. For a city government, this may be a vital policy issue. But does disorder really spread in neighborhoods? So far there has not been strong empirical support, and it is not clear what constitutes disorder and what may make it spread. We generated hypotheses about the spread of disorder and tested them in six field experiments. We found that, when people observe that others violated a certain social norm or legitimate rule, they are more likely to violate other norms or rules, which causes disorder to spread.

  16. The effect of hypothermia therapy on cortical laminar disruption following ischemic injury in neonatal mice.

    Directory of Open Access Journals (Sweden)

    Hiroyuki Kida

    Full Text Available Hypothermia has been proposed as a treatment for reducing neuronal damage in the brain induced by hypoxic ischemia. In the developing brain, hypoxic ischemia-induced injury may give rise to cerebral palsy (CP. However, it is unknown whether hypothermia might affect the development of CP. The purpose of this study was to investigate whether hypothermia would have a protective effect on the brains of immature, 3-day old (P3 mice after a challenge of cerebral ischemia. Cerebral ischemia was induced in P3 mice with a right common carotid artery ligation followed by hypoxia (6% O2, 37°C for 30 min. Immediately after hypoxic ischemia, mice were exposed to hypothermia (32°C or normothermia (37°C for 24 h. At 4 weeks of age, mouse motor development was tested in a behavioral test. Mice were sacrificed at P4, P7, and 5 weeks to examine brain morphology. The laminar structure of the cortex was examined with immunohistochemistry (Cux1/Ctip2; the number of neurons was counted; and the expression of myelin basic protein (MBP was determined. The hypothermia treatment was associated with improved neurological outcomes in the behavioral test. In the normothermia group, histological analyses indicated reduced numbers of neurons, reduced cortical laminar thickness in the deep, ischemic cortical layers, and significant reduction in MBP expression in the ischemic cortex compared to the contralateral cortex. In the hypothermia group, no reductions were noted in deep cortical layer thickness and in MBP expression in the ischemic cortex compared to the contralateral cortex. At 24 h after the hypothermia treatment prevented the neuronal cell death that had predominantly occurred in the ischemic cortical deep layers with normothermia treatment. Our findings may provide a preclinical basis for testing hypothermal therapies in patients with CP induced by hypoxic ischemia in the preterm period.

  17. Higher Order Spreading Models

    CERN Document Server

    Argyros, S A; Tyros, K

    2012-01-01

    We introduce the higher order spreading models associated to a Banach space $X$. Their definition is based on $\\ff$-sequences $(x_s)_{s\\in\\ff}$ with $\\ff$ a regular thin family and the plegma families. We show that the higher order spreading models of a Banach space $X$ form an increasing transfinite hierarchy $(\\mathcal{SM}_\\xi(X))_{\\xi<\\omega_1}$. Each $\\mathcal{SM}_\\xi (X)$ contains all spreading models generated by $\\ff$-sequences $(x_s)_{s\\in\\ff}$ with order of $\\ff$ equal to $\\xi$. We also provide a study of the fundamental properties of the hierarchy.

  18. Motor cortical organization in an adult with hemimegalencephaly and late onset epilepsy.

    Science.gov (United States)

    Civardi, Carlo; Vicentini, Roberta; Collini, Alessandra; Boccagni, Cristina; Cantello, Roberto; Monaco, Francesco

    2009-08-28

    Hemimegalencephaly is a rare brain malformation whose physiology is largely obscure. In a single patient, we studied motor cortex using several transcranial magnetic stimulation variables testing cortical excitability, and mapping motor area. The megalencephalic hemisphere showed an enlargement of cortical motor map with abnormal axonal orientation and an excess spread of corticospinal excitation, associated with multiple defects of cortical inhibition. TMS gave new information on the anatomic/functional features and epileptogenesis in this complex and physiologically obscure syndrome.

  19. Evolution of cortical neurogenesis.

    Science.gov (United States)

    Abdel-Mannan, Omar; Cheung, Amanda F P; Molnár, Zoltán

    2008-03-18

    The neurons of the mammalian neocortex are organised into six layers. By contrast, the reptilian and avian dorsal cortices only have three layers which are thought to be equivalent to layers I, V and VI of mammals. Increased repertoire of mammalian higher cognitive functions is likely a result of an expanded cortical surface area. The majority of cortical cell proliferation in mammals occurs in the ventricular zone (VZ) and subventricular zone (SVZ), with a small number of scattered divisions outside the germinal zone. Comparative developmental studies suggest that the appearance of SVZ coincides with the laminar expansion of the cortex to six layers, as well as the tangential expansion of the cortical sheet seen within mammals. In spite of great variation and further compartmentalisation in the mitotic compartments, the number of neurons in an arbitrary cortical column appears to be remarkably constant within mammals. The current challenge is to understand how the emergence and elaboration of the SVZ has contributed to increased cortical cell diversity, tangential expansion and gyrus formation of the mammalian neocortex. This review discusses neurogenic processes that are believed to underlie these major changes in cortical dimensions in vertebrates.

  20. Cortical Lewy Body Dementia

    Directory of Open Access Journals (Sweden)

    W. R. G. Gibb

    1990-01-01

    Full Text Available In cortical Lewy body dementia the distribution of Lewy bodies in the nervous system follows that of Parkinson's disease, except for their greater profusion in the cerebral cortex. The cortical tangles and plaques of Alzheimer pathology are often present, the likely explanation being that Alzheimer pathology provokes dementia in many patients. Pure cortical Lewy body dementia without Alzheimer pathology is uncommon. The age of onset reflects that of Parkinson's disease, and clinical features, though not diagnostic, include aphasias, apraxias, agnosias, paranoid delusions and visual hallucinations. Parkinsonism may present before or after the dementia, and survival duration is approximately half that seen in Parkinson's disease without dementia.

  1. Neuronal networks provide rapid neuroprotection against spreading toxicity.

    Science.gov (United States)

    Samson, Andrew J; Robertson, Graham; Zagnoni, Michele; Connolly, Christopher N

    2016-09-21

    Acute secondary neuronal cell death, as seen in neurodegenerative disease, cerebral ischemia (stroke) and traumatic brain injury (TBI), drives spreading neurotoxicity into surrounding, undamaged, brain areas. This spreading toxicity occurs via two mechanisms, synaptic toxicity through hyperactivity, and excitotoxicity following the accumulation of extracellular glutamate. To date, there are no fast-acting therapeutic tools capable of terminating secondary spreading toxicity within a time frame relevant to the emergency treatment of stroke or TBI patients. Here, using hippocampal neurons (DIV 15-20) cultured in microfluidic devices in order to deliver a localized excitotoxic insult, we replicate secondary spreading toxicity and demonstrate that this process is driven by GluN2B receptors. In addition to the modeling of spreading toxicity, this approach has uncovered a previously unknown, fast acting, GluN2A-dependent neuroprotective signaling mechanism. This mechanism utilizes the innate capacity of surrounding neuronal networks to provide protection against both forms of spreading neuronal toxicity, synaptic hyperactivity and direct glutamate excitotoxicity. Importantly, network neuroprotection against spreading toxicity can be effectively stimulated after an excitotoxic insult has been delivered, and may identify a new therapeutic window to limit brain damage.

  2. US Features of Experimentally-induced Transient Ischemia and Infarct of Renal Segmental Artery of Rabbits

    Energy Technology Data Exchange (ETDEWEB)

    Park, Byung Kwan [Seoul National University College of Medicine, Seoul (Korea, Republic of); Kim, Seung Hyup; Moon, Min Hoan [Samsung Medical Center, Sungkyunkwan University College of Medicine, Seoul (Korea, Republic of)

    2004-09-15

    The goal of this study was to analyze and compare the changes in renal parenchymal morphology and cortical perfusion following transient arterial ischemia and infarct in rabbits using ultrasonography (US). Six rabbits were divided into the ischemia (n=3) and infarct groups (n=3). In the ischemia group, a lower polar branch of the left renal artery was surgically ligated for a duration of 60 minutes and then released, in order to induce transient renal ischemia and reperfusion. In the infarct group, a lower polar branch of the left renal artery was permanently ligated without release, in order to induce renal infarction. Gray-scale and contrast-enhanced color/power Doppler US were performed in the two groups at specific times, namely before ligation, immediately after release or ligation (for the ischemia and infarct groups, respectively?), and on the 1st, 3rd, 7th, 14th and 28th postoperative days. The left kidneys of all rabbits were harvested after the last US, for the purpose of evaluating the pathologic correlations. In the US images, swelling, hypo- or hyperechoic areas of the involved parenchyma, tissue loss and perfusion defects were more predominant in the infarct group than in the ischemia group. In successive images, hyperechoic renal parenchyma with no reperfusion changed into renal infarct, while that with reperfusion became normal tissue. In the pathologic analysis, the specimens obtained from the ischemia group revealed mild parenchymal infarct with interstitial fibrosis, whereas those from the infarct group revealed extensive tissue loss and scarring in the involved area of the lower pole. Gray-scale and contrast-enhanced color/power Doppler US can demonstrate the morphological and hemodynamic changes in cases of renal ischemia and infarct

  3. Retrograde Renal Cooling to Minimize Ischemia

    Directory of Open Access Journals (Sweden)

    Janet L. Colli

    2013-01-01

    Full Text Available Objective: During partial nephrectomy, renal hypothermia has been shown to decrease ischemia induced renal damage which occurs from renal hilar clamping. In this study we investigate the infusion rate required to safely cool the entire renal unit in a porcine model using retrograde irrigation of iced saline via dual-lumen ureteral catheter. Materials and Methods: Renal cortical, renal medullary, bowel and rectal temperatures during retrograde cooling in a laparoscopic porcine model were monitored in six renal units. Iced normal saline was infused at 300 cc/hour, 600 cc/hour, 1000 cc/hour and gravity (800 cc/hour for 600 seconds with and without hilar clamping. Results: Retrograde cooling with hilar clamping provided rapid medullary renal cooling and significant hypothermia of the medulla and cortex at infusion rates ≥ 600 cc/hour. With hilar clamping, cortical temperatures decreased at -0.9° C/min. reaching a threshold temperature of 26.9° C, and medullary temperatures decreased at -0.90 C/min. reaching a temperature of 26.1° C over 600 seconds on average for combined data at infusion rates ≥ 600 cc/hour. The lowest renal temperatures were achieved with gravity infusion. Without renal hilum clamping, retrograde cooling was minimal at all infusion rates. Conclusions: Significant renal cooling by gravity infusion of iced cold saline via a duel lumen catheter with a clamped renal hilum was achieved in a porcine model. Continuous retrograde irrigation with iced saline via a two way ureteral catheter may be an effective method to induce renal hypothermia in patients undergoing robotic assisted and/or laparoscopic partial nephrectomy.

  4. Focal cortical dysplasia - review.

    Science.gov (United States)

    Kabat, Joanna; Król, Przemysław

    2012-04-01

    Focal cortical dysplasia is a malformation of cortical development, which is the most common cause of medically refractory epilepsy in the pediatric population and the second/third most common etiology of medically intractable seizures in adults.Both genetic and acquired factors are involved in the pathogenesis of cortical dysplasia. Numerous classifications of the complex structural abnormalities of focal cortical dysplasia have been proposed - from Taylor et al. in 1971 to the last modification of Palmini classification made by Blumcke in 2011. In general, three types of cortical dysplasia are recognized.Type I focal cortical dysplasia with mild symptomatic expression and late onset, is more often seen in adults, with changes present in the temporal lobe.Clinical symptoms are more severe in type II of cortical dysplasia usually seen in children. In this type, more extensive changes occur outside the temporal lobe with predilection for the frontal lobes.New type III is one of the above dysplasias with associated another principal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early life.Brain MRI imaging shows abnormalities in the majority of type II dysplasias and in only some of type I cortical dysplasias.THE MOST COMMON FINDINGS ON MRI IMAGING INCLUDE: focal cortical thickening or thinning, areas of focal brain atrophy, blurring of the gray-white junction, increased signal on T2- and FLAIR-weighted images in the gray and subcortical white matter often tapering toward the ventricle. On the basis of the MRI findings, it is possible to differentiate between type I and type II cortical dysplasia. A complete resection of the epileptogenic zone is required for seizure-free life. MRI imaging is very helpful to identify those patients who are likely to benefit from surgical treatment in a group of patients with drug-resistant epilepsy.However, in type I cortical dysplasia, MR imaging is often normal, and also in both types

  5. Postpartum cortical blindness.

    Science.gov (United States)

    Faiz, Shakeel Ahmed

    2008-09-01

    A 30-years-old third gravida with previous normal pregnancies and an unremarkable prenatal course had an emergency lower segment caesarean section at a periphery hospital for failure of labour to progress. She developed bilateral cortical blindness immediately after recovery from anesthesia due to cerebral angiopathy shown by CT and MR scan as cortical infarct cerebral angiopathy, which is a rare complication of a normal pregnancy.

  6. Neuroprotective effects of the immunomodulatory drug Setarud on cerebral ischemia in male rats

    Institute of Scientific and Technical Information of China (English)

    Farzaneh Vafaee; Nasser Zangiabadi; Fatemeh Mehdi Pour; Farzaneh Dehghanian; Majid Asadi-Shekaari; Hossein Karimi Afshar

    2012-01-01

    Anti-inflammatory and anti-oxidant agents can alleviate ischemic cerebral injury. The immunomodulary drug Setarud, which is composed of herbal extracts including Rosa canina, Urtica dioica and Tanacetum vulgare, supplemented with selenium exhibits anti-inflammatory and anti-oxidant properties. Therefore, we hypothesized that Setarud will have a neuroprotective effect against ischemic cerebral injury. To validate this hypothesis, rats were intraperitoneally administered with 0.66 mL/kg Setarud for 30 minutes after middle cerebral artery occlusion. Triphenyltetrazolium chloride staining showed that Setarud could reduce cerebral infarct volume of rats subjected to cerebral ischemia. Transmission electron microscopy and hematoxylin-eosin staining results showed that Setarud could alleviate the degenerative changes in cortical neurons of rats with cerebral ischemia. The inclined plate test and prehensile test showed that Setarud could significantly improve the motor function of rats with cerebral ischemia. These findings suggest that Setarud shows neuroprotective effects against ischemic brain injury.

  7. Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Wang-shu Xu; Xuan Sun; Cheng-guang Song; Xiao-peng Mu; Wen-ping Ma; Xing-hu Zhang; Chuan-sheng Zhao

    2016-01-01

    Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumeta-nide 200 µg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These ifndings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.

  8. Cofilin Inhibition Restores Neuronal Cell Death in Oxygen-Glucose Deprivation Model of Ischemia.

    Science.gov (United States)

    Madineni, Anusha; Alhadidi, Qasim; Shah, Zahoor A

    2016-03-01

    Ischemia is a condition associated with decreased blood supply to the brain, eventually leading to death of neurons. It is associated with a diverse cascade of responses involving both degenerative and regenerative mechanisms. At the cellular level, the changes are initiated prominently in the neuronal cytoskeleton. Cofilin, a cytoskeletal actin severing protein, is known to be involved in the early stages of apoptotic cell death. Evidence supports its intervention in the progression of disease states like Alzheimer's and ischemic kidney disease. In the present study, we have hypothesized the possible involvement of cofilin in ischemia. Using PC12 cells and mouse primary cultures of cortical neurons, we investigated the potential role of cofilin in ischemia in two different in vitro ischemic models: chemical induced oxidative stress and oxygen-glucose deprivation/reperfusion (OGD/R). The expression profile studies demonstrated a decrease in phosphocofilin levels in all models of ischemia, implying stress-induced cofilin activation. Furthermore, calcineurin and slingshot 1L (SSH) phosphatases were found to be the signaling mediators of the cofilin activation. In primary cultures of cortical neurons, cofilin was found to be significantly activated after 1 h of OGD. To delineate the role of activated cofilin in ischemia, we knocked down cofilin by small interfering RNA (siRNA) technique and tested the impact of cofilin silencing on neuronal viability. Cofilin siRNA-treated neurons showed a significant reduction of cofilin levels in all treatment groups (control, OGD, and OGD/R). Additionally, cofilin siRNA-reduced cofilin mitochondrial translocation and caspase 3 cleavage, with a concomitant increase in neuronal viability. These results strongly support the active role of cofilin in ischemia-induced neuronal degeneration and apoptosis. We believe that targeting this protein mediator has a potential for therapeutic intervention in ischemic brain injury and stroke.

  9. The learning curve and factors affecting warm ischemia time during robot-assisted partial nephrectomy

    Directory of Open Access Journals (Sweden)

    Hitesh Dube

    2015-01-01

    Full Text Available Introduction: The learning curve for robotic partial nephrectomy was investigated for an experienced laparoscopic surgeon and factors associated with warm ischemia time (WIT were assessed. Materials and Methods: Between 2007 and 2014, one surgeon completed 171 procedures. Operative time, blood loss, complications and ischemia time were examined to determine the learning curve. The learning curve was defined as the number of procedures needed to reach the targeted goal for WIT, which most recently was 20 min. Statistical analyses including multivariable regression analysis and matching were performed. Results: Comparing the first 30 to the last 30 patients, mean ischemia time (23.0-15.2 min, P < 0.01 decreased while tumor size (2.4-3.4 cm, P = 0.02 and nephrometry score (5.9-7.0, P = 0.02 increased. Body mass index (P = 0.87, age (P = 0.38, complication rate (P = 0.16, operating time (P = 0.78 and estimated blood loss (P = 0.98 did not change. Decreases in ischemia time corresponded with revised goals in 2011 and early vascular unclamping with the omission of cortical renorrhaphy in selected patients. A multivariable analysis found nephrometry score, tumor diameter, cortical renorrhaphy and year of surgery to be significant predictors of WIT. Conclusions: Adoption of robotic assistance for a surgeon experienced with laparoscopic surgery was associated with low complication rates even during the initial cases of robot-assisted partial nephrectomy. Ischemia time decreased while no significant changes in blood loss, operating time or complications were seen. The largest decrease in ischemia time was associated with adopting evidence-based goals and new techniques, and was not felt to be related to a learning curve.

  10. Spread codes and spread decoding in network coding

    OpenAIRE

    Manganiello, F; Gorla, E.; Rosenthal, J.

    2008-01-01

    In this paper we introduce the class of spread codes for the use in random network coding. Spread codes are based on the construction of spreads in finite projective geometry. The major contribution of the paper is an efficient decoding algorithm of spread codes up to half the minimum distance.

  11. Spreading depression transiently disrupts myelin via interferon-gamma signaling.

    Science.gov (United States)

    Pusic, Aya D; Mitchell, Heidi M; Kunkler, Phillip E; Klauer, Neal; Kraig, Richard P

    2015-02-01

    Multiple sclerosis and migraine with aura are clinically correlated and both show imaging changes suggestive of myelin disruption. Furthermore, cortical myelin loss in the cuprizone animal model of multiple sclerosis enhances susceptibility to spreading depression, the likely underlying cause of migraine with aura. Since multiple sclerosis pathology involves inflammatory T cell lymphocyte production of interferon-gamma and a resulting increase in oxidative stress, we tested the hypothesis that spreading depression disrupts myelin through similar signaling pathways. Rat hippocampal slice cultures were initially used to explore myelin loss in spreading depression, since they contain T cells, and allow for controlled tissue microenvironment. These experiments were then translated to the in vivo condition in neocortex. Spreading depression in slice cultures induced significant loss of myelin integrity and myelin basic protein one day later, with gradual recovery by seven days. Myelin basic protein loss was abrogated by T cell depletion, neutralization of interferon-gamma, and pharmacological inhibition of neutral sphingomyelinase-2. Conversely, one day after exposure to interferon-gamma, significant reductions in spreading depression threshold, increases in oxidative stress, and reduced levels of glutathione, an endogenous neutral sphingomyelinase-2 inhibitor, emerged. Similarly, spreading depression triggered significant T cell accumulation, sphingomyelinase activation, increased oxidative stress, and reduction of gray and white matter myelin in vivo. Myelin disruption is involved in spreading depression, thereby providing pathophysiological links between multiple sclerosis and migraine with aura. Myelin disruption may promote spreading depression by enhancing aberrant excitability. Thus, preservation of myelin integrity may provide novel therapeutic targets for migraine with aura.

  12. ENDOMETRIOSIS WITH LYMPHATIC SPREAD

    Directory of Open Access Journals (Sweden)

    Narmadha

    2014-10-01

    Full Text Available Pelvic endometriosis is a common gynaecologic problem. But the histogenesis of endometriosis was not so clear. Various theories have been proposed by Pathologist in the past. Here we present a case of endometriosis of fallopian tube by lymphatic spread which has been proved histopathologically

  13. Spreading of miscible liquids

    Science.gov (United States)

    Walls, Daniel J.; Haward, Simon J.; Shen, Amy Q.; Fuller, Gerald G.

    2016-05-01

    Miscible liquids commonly contact one another in natural and technological situations, often in the proximity of a solid substrate. In the scenario where a drop of one liquid finds itself on a solid surface and immersed within a second, miscible liquid, it will spread spontaneously across the surface. We show experimental findings of the spreading of sessile drops in miscible environments that have distinctly different shape evolution and power-law dynamics from sessile drops that spread in immiscible environments, which have been reported previously. We develop a characteristic time to scale radial data of the spreading sessile drops based on a drainage flow due to gravity. This time scale is effective for a homologous subset of the liquids studied. However, it has limitations when applied to significantly chemically different, yet miscible, liquid pairings; we postulate that the surface energies between each liquid and the solid surface becomes important for this other subset of the liquids studied. Initial experiments performed with pendant drops in miscible environments support the drainage flow observed in the sessile drop systems.

  14. Virus spread in networks

    NARCIS (Netherlands)

    Mieghem, P. van; Omic, J.; Kooij, R.E.

    2009-01-01

    The influence of the network characteristics on the virus spread is analyzed in a new-the N-intertwined Markov chain-model, whose only approximation lies in the application of mean field theory. The mean field approximation is quantified in detail. The N-intertwined model has been compared with the

  15. Neuronal autophagy in cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Feng Xu; Jin-Hua Gu; Zheng-Hong Qin

    2012-01-01

    Autophagy has evolved as a conserved process for the bulk degradation and recycling of cytosolic components,such as long-lived proteins and organelles.In neurons,autophagy is important for homeostasis and protein quality control and is maintained at relatively low levels under normal conditions,while it is upregulated in response to pathophysiological conditions,such as cerebral ischemic injury.However,the role of autophagy is more complex.It depends on age or brain maturity,region,severity of insult,and the stage of ischemia.Whether autophagy plays a beneficial or a detrimental role in cerebral ischemia depends on various pathological conditions.In this review,we elucidate the role of neuronal autophagy in cerebral ischemia.

  16. Animal models of cerebral ischemia

    Science.gov (United States)

    Khodanovich, M. Yu.; Kisel, A. A.

    2015-11-01

    Cerebral ischemia remains one of the most frequent causes of death and disability worldwide. Animal models are necessary to understand complex molecular mechanisms of brain damage as well as for the development of new therapies for stroke. This review considers a certain range of animal models of cerebral ischemia, including several types of focal and global ischemia. Since animal models vary in specificity for the human disease which they reproduce, the complexity of surgery, infarct size, reliability of reproduction for statistical analysis, and adequate models need to be chosen according to the aim of a study. The reproduction of a particular animal model needs to be evaluated using appropriate tools, including the behavioral assessment of injury and non-invasive and post-mortem control of brain damage. These problems also have been summarized in the review.

  17. Optimizing Hybrid Spreading in Metapopulations

    CERN Document Server

    Zhang, Changwang; Cox, Ingemar J; Chain, Benjamin M

    2014-01-01

    Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by \\textit{local spreading}, where infected nodes can only infect a limited set of direct target nodes and \\textit{global spreading}, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemics, and examine the optimum balance between spreading mechanisms in terms of achieving the maximum outbreak size. In a metapopulation, made up of many weakly connected subpopulations, we show that one can calculate an optimal tradeoff between local and global spreading which will maximise the extent of the epidemic. As an example we analyse the 2008 outbreak of the Internet worm Conficker, which uses hybrid spreading to propagate through the internet. Our results suggests that the worm would have been eve...

  18. Combinatorics of spreads and parallelisms

    CERN Document Server

    Johnson, Norman

    2010-01-01

    Partitions of Vector Spaces Quasi-Subgeometry Partitions Finite Focal-SpreadsGeneralizing André SpreadsThe Going Up Construction for Focal-SpreadsSubgeometry Partitions Subgeometry and Quasi-Subgeometry Partitions Subgeometries from Focal-SpreadsExtended André SubgeometriesKantor's Flag-Transitive DesignsMaximal Additive Partial SpreadsSubplane Covered Nets and Baer Groups Partial Desarguesian t-Parallelisms Direct Products of Affine PlanesJha-Johnson SL(2,

  19. Susceptibility of Primary Sensory Cortex to Spreading Depolarizations

    OpenAIRE

    Bogdanov, VB; Middleton, NA; Theriot, JJ; Parker, PD; Abdullah, OM; Ju, YS; Hartings, JA; Brennan, KC

    2016-01-01

    Spreading depolarizations (SDs) are recognized as actors in neurological disorders as diverse as migraine and traumatic brain injury (TBI). Migraine aura involves sensory percepts, suggesting that sensory cortices might be intrinsically susceptible to SDs. We used optical imaging, MRI, and field potential and potassium electrode recordings in mice and electrocorticographic recordings in humans to determine the susceptibility of different brain regions to SDs. Optical imaging experiments in mi...

  20. Quasirandom Rumor Spreading

    CERN Document Server

    Doerr, Benjamin; Sauerwald, Thomas

    2010-01-01

    We propose and analyse a quasirandom analogue of the classical push model for disseminating information in networks ("randomized rumor spreading"). In the classical model, in each round each informed vertex chooses a neighbor at random and informs it, if it was not before. It is known that this simple protocol succeeds in spreading a rumor from one vertex to all others within O(log n) rounds on complete graphs, hypercubes, random regular graphs, Erdos-Renyi random graph and Ramanujan graphs with high probability. In the quasirandom model, we assume that each vertex has a (cyclic) list of its neighbors. Once informed, it starts at a random position of the list, but from then on informs its neighbors in the order of the list. Surprisingly, irrespective of the orders of the lists, the above mentioned bounds still hold. In some cases even better bounds than for the classical model can be shown.

  1. Spread spectrum image steganography.

    Science.gov (United States)

    Marvel, L M; Boncelet, C R; Retter, C T

    1999-01-01

    In this paper, we present a new method of digital steganography, entitled spread spectrum image steganography (SSIS). Steganography, which means "covered writing" in Greek, is the science of communicating in a hidden manner. Following a discussion of steganographic communication theory and review of existing techniques, the new method, SSIS, is introduced. This system hides and recovers a message of substantial length within digital imagery while maintaining the original image size and dynamic range. The hidden message can be recovered using appropriate keys without any knowledge of the original image. Image restoration, error-control coding, and techniques similar to spread spectrum are described, and the performance of the system is illustrated. A message embedded by this method can be in the form of text, imagery, or any other digital signal. Applications for such a data-hiding scheme include in-band captioning, covert communication, image tamperproofing, authentication, embedded control, and revision tracking.

  2. Controversies in cardiovascular care: silent myocardial ischemia

    Science.gov (United States)

    Hollenberg, N. K.

    1987-01-01

    The objective evidence of silent myocardial ischemia--ischemia in the absence of classical chest pain--includes ST-segment shifts (usually depression), momentary left ventricular failure, and perfusion defects on scintigraphic studies. Assessment of angina patients with 24-hour ambulatory monitoring may uncover episodes of silent ischemia, the existence of which may give important information regarding prognosis and may help structure a more effective therapeutic regimen. The emerging recognition of silent ischemia as a significant clinical entity may eventually result in an expansion of current therapy--not only to ameliorate chest pain, but to minimize or eliminate ischemia in the absence of chest pain.

  3. 皮层电刺激联合康复锻炼对大鼠局灶性脑缺血模型前肢运动功能及运动区突触可塑性相关蛋白表达的影响%Cortical electrical Stimulation Combined with Rehabilitative Training Enhance Forelimb Motor Function and Synaptic Plasticity Following Focal Cortical Ischemia in Rats

    Institute of Scientific and Technical Information of China (English)

    郑建; 杨力军; 谢瑞禄; 赵兰峰; 薛晓伟; 王硕; 赵继宗; 曹勇

    2011-01-01

    Objective To assess the behavioral and synaptic plasticity effects of combining epidural cortical electrical stimulation with motor skills training following unilateral sensorimotor cortex (SMC)lesions in adult male rats.Methods Prior to lesion/electrode implantation surgeries, rats were pre-trained on the 'single pellet retrieval task' to a minimum criterion of 30% success rate for two consecutive days. Then these rats received partial unilateral SMC lesions and implantation of electrodes over the remaining SMC. Fourteen days later, rats received daily reach training concurrent with anodal or cathodal 100 Hz or no stimulation for 14 days. Performance was measured as the percent of successes out of the total number of reach attempts [(total successes/total reach attempts)*100]. Conventional avidin biotinylated enzyme complex (ABC) immunohistochemical method was used quantify the expression and distribution of microtubule-associated protein 2 (MAP-2) and growth associated protein 43 (GAP-43) in motor cortical area underlying the electrode.Results There was no statistical significance between the two groups on the 14th day of preoperative training (P=0.546). The stimulation group had significantly greater rates of improvement with the impaired forelimb in comparison to control group (49.12% vs 21.67%, P=0.004). The expression and distribution of MAP-2 and GAP-43 in the stimulating group were better than those in control group (GAP-43 : 0.3338 vs 0.3056. P=0.008; MAP-2: 0.4825 vs 0.4327. P=0.027).Conclusion These data indicate that cortical stimulation greatly improves the efficacy of rehabilitative reach training following SMC damage and raise the possibility that CS-induced functional improvements may be mediated by promoting the expression of MAP-2 and GAP-43 in perilesion cortex. and thus improve synaptic plasticity in cerebral ischemic rats.%目的 探讨皮层电刺激联合康复锻炼对大鼠局灶性脑缺血模型前肢运动功能恢复和运动区

  4. Sequential development of reversible and irreversible neuronal damage following cerebral ischemia.

    Science.gov (United States)

    Petito, C K; Pulsinelli, W A

    1984-03-01

    The ultrastructure of reversibly injured cortical neurons and irreversibly injured striatal neurons was studied at 3, 15, 30, and 120 minutes (min) and 24 hours (h) following severe cerebral ischemia produced in rats by permanent occlusion of the vertebral arteries and 30 min occlusion of the carotid arteries. Animals meeting the established criterion of unresponsiveness had widespread neuronal death in the dorsolateral striatum, but no permanent damage in the paramedian cortex. Reversible mitochondrial swelling at three min was followed by dissociation of polyribosomes, decrease in rough endoplasmic reticulum (RER) profiles, and transformation of Golgi apparatus into large clusters of small vesicles without cisterns in both cortical and striatal neurons. Reaccumulation of RER was seen in cortical neurons by 30-120 min and all cortical neurons appeared normal at 24 h. In contrast, most striatal neurons developed dilatation of the Golgi vesicles by 120 min after reperfusion, followed by progressive cell shrinkage and ischemic cell change. Approximately 10-15% of striatal neurons contained cytoplasmic membranous whorls, some continuous with the plasma membrane. The results suggest that structural abnormalities in the Golgi apparatus and in plasma membranes may participate in functional changes critical to irreversible neuronal injury following cerebral ischemia.

  5. Sirt1 in cerebral ischemia

    Directory of Open Access Journals (Sweden)

    Kevin B Koronowski

    2015-01-01

    Full Text Available Cerebral ischemia is among the leading causes of death worldwide. It is characterized by a lack of blood flow to the brain that results in cell death and damage, ultimately causing motor, sensory, and cognitive impairments. Today, clinical treatment of cerebral ischemia, mostly stroke and cardiac arrest, is limited and new neuroprotective therapies are desperately needed. The Sirtuin family of oxidized nicotinamide adenine dinucleotide (NAD +-dependent deacylases has been shown to govern several processes within the central nervous system as well as to possess neuroprotective properties in a variety of pathological conditions such as Alzheimer′s Disease, Parkinson′s Disease, and Huntington′s Disease, among others. Recently, Sirt1 in particular has been identified as a mediator of cerebral ischemia, with potential as a possible therapeutic target. To gather studies relevant to this topic, we used PubMed and previous reviews to locate, select, and resynthesize the lines of evidence presented here. In this review, we will first describe some functions of Sirt1 in the brain, mainly neurodevelopment, learning and memory, and metabolic regulation. Second, we will discuss the experimental evidence that has implicated Sirt1 as a key protein in the regulation of cerebral ischemia as well as a potential target for the induction of ischemic tolerance.

  6. Sirt1 in cerebral ischemia

    Science.gov (United States)

    Koronowski, Kevin B.; Perez-Pinzon, Miguel A.

    2015-01-01

    Cerebral ischemia is among the leading causes of death worldwide. It is characterized by a lack of blood flow to the brain that results in cell death and damage, ultimately causing motor, sensory, and cognitive impairments. Today, clinical treatment of cerebral ischemia, mostly stroke and cardiac arrest, is limited and new neuroprotective therapies are desperately needed. The Sirtuin family of oxidized nicotinamide adenine dinucleotide (NAD+)-dependent deacylases has been shown to govern several processes within the central nervous system as well as to possess neuroprotective properties in a variety of pathological conditions such as Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease, among others. Recently, Sirt1 in particular has been identified as a mediator of cerebral ischemia, with potential as a possible therapeutic target. To gather studies relevant to this topic, we used PubMed and previous reviews to locate, select, and resynthesize the lines of evidence presented here. In this review, we will first describe some functions of Sirt1 in the brain, mainly neurodevelopment, learning and memory, and metabolic regulation. Second, we will discuss the experimental evidence that has implicated Sirt1 as a key protein in the regulation of cerebral ischemia as well as a potential target for the induction of ischemic tolerance. PMID:26819971

  7. Effects of crocin on reperfusion-induced oxidative/nitrative injury to cerebral microvessels after global cerebral ischemia.

    Science.gov (United States)

    Zheng, Yong-Qiu; Liu, Jian-Xun; Wang, Jan-Nong; Xu, Li

    2007-03-23

    This paper studied the effects of crocin, a pharmacologically active component of Crocus sativus L., on ischemia/reperfusion (I/R) injury in mice cerebral microvessels. Transient global cerebral ischemia (20 min), followed by 24 h of reperfusion, significantly promoted the generation of nitric oxide (NO) and malondialdehyde (MDA) in cortical microvascular homogenates, as well as markedly reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and promoted the activity of nitric oxide synthase (NOs). Reperfusion for 24 h led to serous edema with substantial microvilli loss, vacuolation, membrane damage and mitochondrial injuries in cortical microvascular endothelial cells (CMEC). Furthermore, enhanced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and decreased expression of matrix metalloproteinase-9 (MMP-9) were detected in cortical microvessels after I (20 min)/R (24 h). Reperfusion for 24 h also induced membrane (functional) G protein-coupled receptor kinase 2 (GRK2) expression, while it reduced cytosol GRK2 expression. Pretreatment with crocin markedly inhibited oxidizing reactions and modulated the ultrastructure of CMEC in mice with 20 min of bilateral common carotid artery occlusion (BCCAO) followed by 24 h of reperfusion in vivo. Furthermore, crocin inhibited GRK2 translocation from the cytosol to the membrane and reduced ERK1/2 phosphorylation and MMP-9 expression in cortical microvessels. We propose that crocin protects the brain against excessive oxidative stress and constitutes a potential therapeutic candidate in transient global cerebral ischemia.

  8. Cortical myoclonus and cerebellar pathology

    NARCIS (Netherlands)

    Tijssen, MAJ; Thom, M; Ellison, DW; Wilkins, P; Barnes, D; Thompson, PD; Brown, P

    2000-01-01

    Objective To study the electrophysiologic and pathologic findings in three patients with cortical myoclonus. In two patients the myoclonic ataxic syndrome was associated with proven celiac disease. Background: The pathologic findings in conditions associated with cortical myoclonus commonly involve

  9. Cortical Abnormalities in ADHD

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2003-12-01

    Full Text Available Grey-matter abnormalities at the cortical surface and regional brain size were mapped by high-resolution MRI and surface-based, computational image analytical techniques in a group of 27 children and adolescents with attention deficit hyperactivity disorder (ADHD and 46 controls, matched by age and sex, at the University of California at Los Angeles.

  10. Transient cortical blindness after coronary artery angiography.

    Science.gov (United States)

    Terlecki, Michał; Wojciechowska, Wiktoria; Rajzer, Marek; Jurczyszyn, Artur; Bazan-Socha, Stanisława; Bryniarski, Leszek; Czarnecka, Danuta

    2013-01-01

    Coronary angiography is the current gold standard for the diagnosis of ischemic heart disease and therefore the prevalence of percutaneous coronary procedures such as angiography and angioplasty is high. The occurrence of cerebral complications after coronary angiography and coronary angioplasty is low and it mainly includes transient ischemic attack and stroke. The prevalence of transient cortical blindness after X-ray contrast media is low and it is usually seen after cerebral angiography. Until now only a few cases of transient cortical blindness have been described after coronary artery angiography. Regarding the spread of coronary angiography worldwide and in Poland this complication is uniquely rare. A 32-year-old man with multiple extrasystolic ventricular arrhythmia suggesting Brugada syndrome diagnosis according to morphology of the left bundle branch block and with decreased left ventricular ejection fraction was admitted to the First Department of Cardiology and Hypertension, Medical College of the Jagiellonian University in Krakow. Coronary angiography was performed in order to exclude ischemic etiology of the observed abnormalities. No arteriosclerotic lesions were found in coronary arteries. Transient cortical blindness was observed directly after angiography which may have been caused by the neurotoxic effect of the used X-ray contrast medium. In ophthalmologic and neurologic examination as well as in the cerebral computed tomography scan no pathologies were found. Visual impairment disappeared totally within several hours.

  11. Functional rehabilitation of partial cortical blindness?

    Science.gov (United States)

    Stoerig, Petra

    2008-01-01

    The current doctrine regards fields of partial cortical blindness as permanent once a temporally restricted window for spontaneous recovery has passed. Accordingly, neuropsychological rehabilitation mainly applies compensatory procedures that train patients to make better use of their sighted field. The more ambitious goal of functional recovery depends on the survival of pathways that continue to transmit retinal information from the blind field. Although wide-spread antero- and retrograde degeneration follows lesions that destroy or denervate the primary visual cortex and cause partial cortical blindness, several retinofugal pathways survive in cats, monkeys, and humans. In all three species, they subserve a variety of visual functions which develop and improve with practice. Post lesion plasticity is greater when the lesion occurs early in life, but changes in behavioural performance and brain responses have also been demonstrated in late lesion subjects. Although the extent of functional improvement is variable, and the most effective approaches still need to be established across cohorts, the evidence for perceptual learning in fields of cortical blindness indicates that the visual processes mediated by the surviving parts of the visual system can be harnessed to improve functional outcome.

  12. Temperature modulation of cerebral depolarization during focal cerebral ischemia in rats: correlation with ischemic injury.

    Science.gov (United States)

    Chen, Q; Chopp, M; Bodzin, G; Chen, H

    1993-05-01

    The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30 degrees C, n = 4), normothermic (37 degrees C, n = 4), and hyperthermic (40 degrees C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes were measured using two active Ag-AgCl electrodes placed in the cortical lesion. Animals were killed 1 week after ischemia. The brains were sectioned and stained with hematoxylin and eosin, for evaluation of neuronal damage, and calculation of infarct volume. All animals exhibited an initial depolarization within 30 min of ischemia, followed by a single depolarization event in hypothermic animals, and multiple periodic depolarization events in both normothermic and hyperthermic animals. Hyperthermic animals exhibited significantly more (p < 0.05) DC potential deflections (n = 6.17 +/- 0.67) than normothermic animals (n = 2.75 +/- 0.96). The ischemic infarct volume (% of hemisphere) was significantly different for the various groups; hypothermic animals exhibited no measurable infarct volume, while the ischemic infarct volume was 10.2 +/- 12.3% in normothermic animals and 36.5 +/- 3.4% in hyperthermic animals (p < 0.05). A significant correlation was detected between the volume of infarct and number of depolarization events (r = 0.90, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

  13. Estimation of wave directional spreading

    Digital Repository Service at National Institute of Oceanography (India)

    Deo, M.C.; Gondane, D.S.; SanilKumar, V.

    One of the useful measures of waves directional spreading at a given location is the directional spreading parameter. This paper presents a new approach to arrive at its characteristic value using the computational technique of Artificial Neural...

  14. Ischemia Induces Release of Endogenous Amino Acids from the Cerebral Cortex and Cerebellum of Developing and Adult Mice

    Directory of Open Access Journals (Sweden)

    Simo S. Oja

    2013-01-01

    Full Text Available Ischemia enhanced release of endogenous neuroactive amino acids from cerebellar and cerebral cortical slices. More glutamate was released in adult than developing mice. Taurine release enhanced by K+ stimulation and ischemia was more than one magnitude greater than that of GABA or glutamate in the developing cerebral cortex and cerebellum, while in adults the releases were almost comparable. Aspartate release was prominently enhanced by both ischemia and K+ stimulation in the adult cerebral cortex. In the cerebellum K+ stimulation and ischemia evoked almost 10-fold greater GABA release in 3-month olds than in 7-day olds. The release of taurine increased severalfold in the cerebellum of 7-day-old mice in high-K+ media, whereas the K+-evoked effect was rather small in adults. In 3-month-old mice no effects of K+ stimulation or ischemia were seen in the release of aspartate, glycine, glutamine, alanine, serine, or threonine. The releases from the cerebral cortex and cerebellum were markedly different and also differed between developing and adult mice. In developing mice only the release of inhibitory taurine may be large enough to counteract the harmful effects of excitatory amino acids in ischemia in both cerebral cortex and cerebellum, in particular since at that age the release of glutamate and aspartate cannot be described as massive.

  15. COMMUNICATION: Electrophysiological response dynamics during focal cortical infarction

    Science.gov (United States)

    Chiganos, Terry C., Jr.; Jensen, Winnie; Rousche, Patrick J.

    2006-12-01

    While the intracellular processes of hypoxia-induced necrosis and the intercellular mechanisms of post-ischemic neurotoxicity associated with stroke are well documented, the dynamic electrophysiological (EP) response of neurons within the core or periinfarct zone remains unclear. The present study validates a method for continuous measurement of the local EP responses during focal cortical infarction induced via photothrombosis. Single microwire electrodes were acutely implanted into the primary auditory cortex of eight rats. Multi-unit neural activity, evoked via a continuous 2 Hz click stimulus, was recorded before, during and after infarction to assess neuronal function in response to local, permanent ischemia. During sham infarction, the average stimulus-evoked peak firing rate over 20 min remained stable at 495.5 ± 14.5 spikes s-1, indicating temporal stability of neural function under normal conditions. Stimulus-evoked peak firing was reliably reduced to background levels (firing frequency in the absence of stimulus) following initiation of photothrombosis over a period of 439 ± 92 s. The post-infarction firing patterns exhibited unique temporal degradation of the peak firing rate, suggesting a variable response to ischemic challenge. Despite the inherent complexity of cerebral ischemia secondary to microvascular occlusion, complete loss of EP function consistently occurred 300-600 s after photothrombosis. The results suggest that microwire recording during photothrombosis provides a simple and highly efficacious strategy for assessing the electrophysiological dynamics of cortical infarction.

  16. Hybrid spread spectrum radio system

    Science.gov (United States)

    Smith, Stephen F [London, TN; Dress, William B [Camas, WA

    2010-02-09

    Systems and methods are described for hybrid spread spectrum radio systems. A method, includes receiving a hybrid spread spectrum signal including: fast frequency hopping demodulating and direct sequence demodulating a direct sequence spread spectrum signal, wherein multiple frequency hops occur within a single data-bit time and each bit is represented by chip transmissions at multiple frequencies.

  17. Enhanced subcortical spreading depression in familial hemiplegic migraine type 1 mutant mice.

    Science.gov (United States)

    Eikermann-Haerter, Katharina; Yuzawa, Izumi; Qin, Tao; Wang, Yumei; Baek, Kwangyeol; Kim, Young Ro; Hoffmann, Ulrike; Dilekoz, Ergin; Waeber, Christian; Ferrari, Michel D; van den Maagdenberg, Arn M J M; Moskowitz, Michael A; Ayata, Cenk

    2011-04-13

    Familial hemiplegic migraine type 1, a monogenic migraine variant with aura, is linked to gain-of-function mutations in the CACNA1A gene encoding Ca(V)2.1 channels. The S218L mutation causes severe channel dysfunction, and paroxysmal migraine attacks can be accompanied by seizures, coma, and hemiplegia; patients expressing the R192Q mutation exhibit hemiplegia only. Familial hemiplegic migraine knock-in mice expressing the S218L or R192Q mutation are highly susceptible to cortical spreading depression, the electrophysiological surrogate for migraine aura, and develop severe and prolonged motor deficits after spreading depression. The S218L mutants also develop coma and seizures and sometimes die. To investigate underlying mechanisms for these symptoms, we used multielectrode electrophysiological recordings, diffusion-weighted magnetic resonance imaging, and c-fos immunohistochemistry to trace spreading depression propagation into subcortical structures. We showed that unlike the wild type, cortical spreading depression readily propagated into subcortical structures in both familial hemiplegic migraine type 1 mutants. Whereas the facilitated subcortical spread appeared limited to the striatum in R192Q, hippocampal and thalamic spread was detected in the S218L mutants with an allele-dosage effect. Both strains exhibited increased susceptibility to subcortical spreading depression and reverberating spreading depression waves. Altogether, these data show that spreading depression propagates between cortex, basal ganglia, diencephalon, and hippocampus in genetically susceptible brains, which could explain the prolonged hemiplegia, coma, and seizure phenotype in this variant of migraine with aura.

  18. Purely Cortical Anaplastic Ependymoma

    Directory of Open Access Journals (Sweden)

    Flávio Ramalho Romero

    2012-01-01

    Full Text Available Ependymomas are glial tumors derived from ependymal cells lining the ventricles and the central canal of the spinal cord. It may occur outside the ventricular structures, representing the extraventicular form, or without any relationship of ventricular system, called ectopic ependymona. Less than fifteen cases of ectopic ependymomas were reported and less than five were anaplastic. We report a rare case of pure cortical ectopic anaplastic ependymoma.

  19. Fundamentals of spread spectrum modulation

    CERN Document Server

    Ziemer, Rodger E

    2007-01-01

    This lecture covers the fundamentals of spread spectrum modulation, which can be defined as any modulation technique that requires a transmission bandwidth much greater than the modulating signal bandwidth, independently of the bandwidth of the modulating signal. After reviewing basic digital modulation techniques, the principal forms of spread spectrum modulation are described. One of the most important components of a spread spectrum system is the spreading code, and several types and their characteristics are described. The most essential operation required at the receiver in a spread spect

  20. [Posterior cortical atrophy].

    Science.gov (United States)

    Solyga, Volker Moræus; Western, Elin; Solheim, Hanne; Hassel, Bjørnar; Kerty, Emilia

    2015-06-02

    Posterior cortical atrophy is a neurodegenerative condition with atrophy of posterior parts of the cerebral cortex, including the visual cortex and parts of the parietal and temporal cortices. It presents early, in the 50s or 60s, with nonspecific visual disturbances that are often misinterpreted as ophthalmological, which can delay the diagnosis. The purpose of this article is to present current knowledge about symptoms, diagnostics and treatment of this condition. The review is based on a selection of relevant articles in PubMed and on the authors' own experience with the patient group. Posterior cortical atrophy causes gradually increasing impairment in reading, distance judgement, and the ability to perceive complex images. Examination of higher visual functions, neuropsychological testing, and neuroimaging contribute to diagnosis. In the early stages, patients do not have problems with memory or insight, but cognitive impairment and dementia can develop. It is unclear whether the condition is a variant of Alzheimer's disease, or whether it is a separate disease entity. There is no established treatment, but practical measures such as the aid of social care workers, telephones with large keypads, computers with voice recognition software and audiobooks can be useful. Currently available treatment has very limited effect on the disease itself. Nevertheless it is important to identify and diagnose the condition in its early stages in order to be able to offer patients practical assistance in their daily lives.

  1. Rifts in spreading wax layers

    CERN Document Server

    Ragnarsson, R; Santangelo, C D; Bodenschatz, E; Ragnarsson, Rolf; Ford, J Lewis; Santangelo, Christian D; Bodenschatz, Eberhard

    1995-01-01

    We report experimental results on the rift formation between two freezing wax plates. The plates were pulled apart with constant velocity, while floating on the melt, in a way akin to the tectonic plates of the earth's crust. At slow spreading rates, a rift, initially perpendicular to the spreading direction, was found to be stable, while above a critical spreading rate a "spiky" rift with fracture zones almost parallel to the spreading direction developed. At yet higher spreading rates a second transition from the spiky rift to a zig-zag pattern occurred. In this regime the rift can be characterized by a single angle which was found to be dependent on the spreading rate. We show that the oblique spreading angles agree with a simple geometrical model. The coarsening of the zig-zag pattern over time and the three-dimensional structure of the solidified crust are also discussed.

  2. Clinical Neuroimaging of cerebral ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Nakagawara, Jyoji [Nakamura Memorial Hospital, Sapporo (Japan)

    1999-06-01

    Notice points in clinical imaging of cerebral ischemia are reviewed. When cerebral blood flow is determined in acute stage of cerebral embolism (cerebral blood flow SPECT), it is important to find area of ischemic core and ischemic penumbra. When large cortex area is assigned to ischemic penumbra, thrombolytic therapy is positively adapted, but cautious correspondence is necessary when ischemic core is recognized. DWI is superior in the detection of area equivalent to ischemic core of early stage, but, in imaging of area equivalent to ischemic penumbra, perfusion image or distribution image of cerebral blood volume (CBV) by MRI need to be combined. Luxury perfusion detected by cerebral blood flow SPECT in the cases of acute cerebral embolism suggests vascular recanalization, but a comparison with CT/MRI and continuous assessment of cerebral circulation dynamics were necessary in order to predict brain tissue disease (metabolic abnormality). In hemodynamic cerebral ischemia, it is important to find stage 2 equivalent to misery perfusion by quantification of cerebral blood flow SPECT. Degree of diaschisis can indicate seriousness of brain dysfunction for lacuna infarct. Because cerebral circulation reserve ability (perfusion pressure) is normal in all areas of the low cerebral blood flow by diaschisis mechanism, their areas are easily distinguished from those of hemodynamic cerebral ischemia. (K.H.)

  3. Predictive Modeling of Cardiac Ischemia

    Science.gov (United States)

    Anderson, Gary T.

    1996-01-01

    The goal of the Contextual Alarms Management System (CALMS) project is to develop sophisticated models to predict the onset of clinical cardiac ischemia before it occurs. The system will continuously monitor cardiac patients and set off an alarm when they appear about to suffer an ischemic episode. The models take as inputs information from patient history and combine it with continuously updated information extracted from blood pressure, oxygen saturation and ECG lines. Expert system, statistical, neural network and rough set methodologies are then used to forecast the onset of clinical ischemia before it transpires, thus allowing early intervention aimed at preventing morbid complications from occurring. The models will differ from previous attempts by including combinations of continuous and discrete inputs. A commercial medical instrumentation and software company has invested funds in the project with a goal of commercialization of the technology. The end product will be a system that analyzes physiologic parameters and produces an alarm when myocardial ischemia is present. If proven feasible, a CALMS-based system will be added to existing heart monitoring hardware.

  4. Familial Hemiplegic Migraine and Spreading Depression

    Directory of Open Access Journals (Sweden)

    Hadi KAZEMI

    2014-07-01

    mutations. Neurology 2009 31;72(13:1178-83.Thomsen LL, Ostergaard E, Olesen J, Russell MB. Evidence for a separate type of migraine with aura: sporadic hemiplegic migraine. Neurology 2003;60(4:595-601.van den Maagdenberg AM, Haan J, Terwindt GM, Ferrari MD. Migraine: gene mutations and functional consequences. Curr Opin Neurol 2007; 20:299–305.Gritz SM, Radcliffe RA. Genetic effects of ATP1A2 in familial hemiplegic migraine type II and animal models. Hum Genomics 2013;5;7:8.Ophoff RA, Terwindt GM, Vergouwe MN, et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNL1A4. Cell 1996;87:543–552.Gargus JJ, Tournay A. Novel Mutation Confirms Seizure Locus SCN1A is Also Familial Hemiplegic Migraine Locus FHM3.PediatrNeurol 2007;37:407-410.Tottene A, Conti R, Fabbro A, Vecchia D, Shapovalova M, Santello M, et al.Enhanced excitatory transmission at cortical synapses as the basis for facilitated spreading depression in Ca(v2.1 knockin migraine mice. Neuron 2009;61(5:762-73.Terwindt GM, Ophoff RA, Haan J, Sandkuijl LA, Frants RR, Ferrari MD. Migraine, ataxia and epilepsy: a challenging spectrum of genetically determined calcium channelopathies. Dutch Migraine Genetics Research Group. Eur J Hum Genet 1998;6(4:297-307.Terwindt GM, Ophoff RA, van Eijk R, Vergouwe MN, Haan J, Frants RR, et al. Dutch Migraine Genetics Research Group. Involvement of the CACNA1A gene containing region on 19p13 in migraine with and without aura. Neurology 2001;56(8:1028-32.Franceschini A, Vilotti S, Ferrari MD, van den Maagdenberg AM, Nistri A, Fabbretti E. TNFα levels and macrophages expression reflect an inflammatory potential of trigeminal ganglia in a mouse model of familial hemiplegic migraine. PLoS One 2013;8:e52394.Kodangattil JN, Möddel G, Müller, M, Weber W, Gorji A.The inflammatory chemokine CXCL10 modulates synaptic plasticity and neuronal activity in the hippocampus. European Journal of Inflammation 2012;10(3:311-328Leao AAP

  5. Microtubule-associated protein 2 (MAP2)--a promising approach to diagnosis of forensic types of hypoxia-ischemia.

    Science.gov (United States)

    Kühn, Johanna; Meissner, Christoph; Oehmichen, Manfred

    2005-12-01

    The loss of neuronal immunoreactivity of the cytoskeletal microtubule-associated protein 2 (MAP2) is known to be a marker of--at least--transient functional failure of neurons following ischemia. Because there are no specific neuropathological findings in forensic types of acute hypoxia-ischemia, detection of this relevant cause of death is often complicated and a reliable ischemic biomarker would be of great importance. We therefore investigated the neuronal immunoreactivity of MAP2 in human cases of forensic significance. A control group (n=27) was compared to a group of cases of hypoxia-ischemia (n=45), comprising death due to hanging (n=19), drowning (n=14) and carbon monoxide (CO) poisoning (n=12). Using immunohistochemical staining, the percentage of MAP2-positive neurons in the hippocampus (areas CA1-CA4) and frontal cortex (layers II-VI) was evaluated and compared. The hypoxia-ischemia group showed decreased MAP2 immunostaining in the hippocampal areas CA2-CA4 (P<0.05) and in cortical layers II-VI (P<0.001) compared to controls. Most vulnerable regions seem to be the hippocampal CA4 area and cortical layers III-V. Within the hypoxia-ischemia group, death due to CO poisoning was characterized by the lowest MAP2 immunoreactivity. The hypoxic-ischemic groups differ from controls by a distinct decrease of MAP2 immunostaining. Thus, the loss of MAP2 immunoreactivity may support the diagnosis of neuronal injury in forensic types of hypoxia-ischemia, although investigations on postmortem tissue must be interpreted cautiously.

  6. Effects of rapamycin on cerebral oxygen supply and consumption during reperfusion after cerebral ischemia.

    Science.gov (United States)

    Chi, O Z; Barsoum, S; Vega-Cotto, N M; Jacinto, E; Liu, X; Mellender, S J; Weiss, H R

    2016-03-01

    Activation of the mammalian target of rapamycin (mTOR) leads to cell growth and survival. We tested the hypothesis that inhibition of mTOR would increase infarct size and decrease microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. This was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1h and reperfusion for 2h with and without rapamycin (20mg/kg once daily for two days prior to ischemia). Regional cerebral blood flow was determined using a C(14)-iodoantipyrine autoradiographic technique. Regional small-vessel arterial and venous oxygen saturations were determined microspectrophotometrically. The control ischemic-reperfused cortex had a similar blood flow and O2 consumption to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex. Rapamycin significantly increased cerebral O2 consumption and further reduced O2 supply/consumption balance in the reperfused area. This was associated with an increased cortical infarct size (13.5±0.8% control vs. 21.5±0.9% rapamycin). We also found that ischemia-reperfusion increased AKT and S6K1 phosphorylation, while rapamycin decreased this phosphorylation in both the control and ischemic-reperfused cortex. This suggests that mTOR is important for not only cell survival, but also for the control of oxygen balance after cerebral ischemia-reperfusion.

  7. How long is sufficient for optimal neuroprotection with cerebral cooling after ischemia in fetal sheep?

    Science.gov (United States)

    Davidson, Joanne O; Draghi, Vittoria; Whitham, Sean; Dhillon, Simerdeep K; Wassink, Guido; Bennet, Laura; Gunn, Alistair J

    2017-01-01

    The optimal duration of mild "therapeutic" hypothermia for neonates with hypoxic-ischemic encephalopathy is surprisingly unclear. This study assessed the relative efficacy of cooling for 48 h versus 72 h. Fetal sheep (0.85 gestation) received sham ischemia (n = 9) or 30 min global cerebral ischemia followed by normothermia (n = 8) or delayed hypothermia from 3 h to 48 h (n = 8) or 72 h (n = 8). Ischemia was associated with profound loss of electroencephalogram (EEG) power, neurons in the cortex and hippocampus, and oligodendrocytes and myelin basic protein expression in the white matter, with increased Iba-1-positive microglia and proliferation. Hypothermia for 48 h was associated with improved outcomes compared to normothermia, but a progressive deterioration of EEG power after rewarming compared to 72 h of hypothermia, with impaired neuronal survival and myelin basic protein, and more microglia in the white matter and cortex. These findings show that head cooling for 48 h is partially neuroprotective, but is inferior to cooling for 72 h after cerebral ischemia in fetal sheep. The close association between rewarming at 48 h, subsequent deterioration in EEG power and increased cortical inflammation strongly suggests that deleterious inflammation can be reactivated by premature rewarming.

  8. Aerobic exercise combined with huwentoxin-I mitigates chronic cerebral ischemia injury

    Institute of Scientific and Technical Information of China (English)

    Hai-feng Mao; Jun Xie; Jia-qin Chen; Chang-fa Tang; Wei Chen; Bo-cun Zhou; Rui Chen; Hong-lin Qu; Chu-zu Wu

    2017-01-01

    Ca2+ channel blockers have been shown to protect neurons from ischemia, and aerobic exercise has significant protective effects on a variety of chronic diseases. The present study injected huwentoxin-I (HWTX-I), a spider peptide toxin that blocks Ca2+ channels, into the caudal vein of a chronic cerebral ischemia mouse model, once every 2 days, for a total of 15 injections. During this time, a subgroup of mice was subjected to treadmill exercise for 5 weeks. Results showed amelioration of cortical injury and improved neurological function in mice with chronic cerebral ischemia in the HWTX-I + aerobic exercise group. The combined effects of HWTX I and exercise were superior to HWTX-I or aerobic exercise alone. HWTX-I effectively activated the Notch signal transduction pathway in brain tissue. Aerobic exercise up-regulated synaptophysin mRNA expression. These results demonstrated that aerobic exercise, in combination with HWTX-I, effectively relieved neuronal injury induced by chronic cerebral ischemia via the Notch signaling pathway and promoting synaptic regeneration.

  9. Expression profiles of microRNAs after focal cerebral ischemia/reperfusion injury in rats

    Institute of Scientific and Technical Information of China (English)

    Fengguo Zhai; Xiuping Zhang; Yue Guan; Xudong Yang; Yang Li; Gaochen Song; Lixin Guan

    2012-01-01

    Rat models of focal cerebral ischemia/reperfusion injury were established by occlusion of the middle cerebral artery. Microarray analysis showed that 24 hours after cerebral ischemia, there were nine up-regulated and 27 down-regulated microRNA genes in cortical tissue. Bioinformatic analysis showed that bcl-2 was the target gene of microRNA-384-5p and microRNA-494, and caspase-3 was the target gene of microRNA-129, microRNA-320 and microRNA-326. Real-time PCR and western blot analyses showed that 24 hours after cerebral ischemia, bcl-2 mRNA and protein levels in brain tissue were significantly decreased, while caspase-3 mRNA and protein levels were significantly increased. This suggests that following cerebral ischemia, differentially expressed microRNA-384-5p, microRNA-494, microRNA-320, microRNA-129 and microRNA-326 can regulate bcl-2 and caspase-3 expression in brain tissue.

  10. Expression of nerve growth factor precursor, mature nerve growth factor and their receptors during cerebral ischemia-reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Guoqian He; Jian Guo; Jiachuan Duan; Wenming Xu; Ning Chen; Hongxia Li; Li He

    2011-01-01

    We investigated nerve growth factor precursor (proNGF) and mature NGF expression in ischemic and non-ischemic cortices after cerebral ischemia-reperfusion injury.In both ischemic and non-ischemic cortices, proNGF was found to be present in the extracellular space and cytoplasm.In addition, mature NGF was expressed in extracellular space, but with a very low signal.In ischemic cortex only, proNGF was significantly decreased, reaching a minimal level at 1 day.Mature NGF was increased at 4 hours, then reached a minimal level at 3 days.The p75 neurotrophin receptor (p75NTR) was significantly decreased after ischemia, and increased at 3 days after ischemia.These results confirmed that proNGF was the predominant form of NGF during the pathological process of cerebral ischemia-reperfusion injury.In addition, our findings suggest that ischemic injury may influence the conversion of proNGF to mature NGF, and that proNGF/p75NTR may be involved in reperfusion injury.

  11. Osteocyte lacunar properties in rat cortical bone

    DEFF Research Database (Denmark)

    Bach-Gansmo, Fiona Linnea; Weaver, James C.; Jensen, Mads Hartmann

    2015-01-01

    to osteocyte function, osteocyte lacunar properties such as volume, shape, orientation, and density are now frequently reported in studies investigating osteocyte activity. Despite this increasing interest in lacunar morphometrics, many studies show a large spread in such values, suggesting a large inter......-species but also inter-site variation in lacunar properties. Here, osteocyte lacunae in rat cortical bone have been studied using synchrotron radiation micro computed tomography (SR μCT) and backscattered electron (BE) microscopy. Quantitative lacunar geometric characteristics are reported based on the synchrotron...... radiation data, differentiating between circumferential lamellar bone and a central, more disordered bone type. From these studies, no significant differences were found in lacunar volumes between lamellar and central bone, whereas significant differences in lacunar orientation, shape and density values...

  12. Recipient twin limb ischemia with postnatal onset.

    Science.gov (United States)

    Broadbent, Roland Spencer

    2007-02-01

    After the occurrence of 3 local cases of limb ischemia in newborn twins, we reviewed the literature to investigate this combination systematically. This review reveals a distinct condition: postnatal onset limb ischemia affecting recipient twins in twin-twin transfusion syndrome.

  13. Retinal ischemia and embolism. Causes and outcomes

    NARCIS (Netherlands)

    Wijman, C.A.C.

    2007-01-01

    The ocular fundus allows direct visualization of the retinal vasculature, blood vessels that are part of the cerebral circulation. Unraveling the causes of retinal ischemia may provide further insight in the pathophysiological processes that underlie cerebral ischemia. The primary aim of the studies

  14. Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex

    DEFF Research Database (Denmark)

    Hansen, Henning Piilgaard; Lauritzen, Martin

    2009-01-01

    Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head t...

  15. Transient myocardial ischemia after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction...... the prevalence of ambulatory or transient myocardial ischemia is lower than in patients with chronic, stable coronary artery disease. A greater proportion of ischemic episodes, however, are silent than in other subgroups with ischemic heart disease. Early after the infarction, transient myocardial ischemia...... exhibits a circadian variation with a peak activity occurring in the late evening hours. Patients with non-Q wave infarction have more transient myocardial ischemia, whereas thrombolytic therapy seems to result in less residual ischemia. Exercise testing is more sensitive than ambulatory monitoring...

  16. Transient myocardial ischemia after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction...... the prevalence of ambulatory or transient myocardial ischemia is lower than in patients with chronic, stable coronary artery disease. A greater proportion of ischemic episodes, however, are silent than in other subgroups with ischemic heart disease. Early after the infarction, transient myocardial ischemia...... exhibits a circadian variation with a peak activity occurring in the late evening hours. Patients with non-Q wave infarction have more transient myocardial ischemia, whereas thrombolytic therapy seems to result in less residual ischemia. Exercise testing is more sensitive than ambulatory monitoring...

  17. Heat transfer and fire spread

    Science.gov (United States)

    Hal E. Anderson

    1969-01-01

    Experimental testing of a mathematical model showed that radiant heat transfer accounted for no more than 40% of total heat flux required to maintain rate of spread. A reasonable prediction of spread was possible by assuming a horizontal convective heat transfer coefficient when certain fuel and flame characteristics were known. Fuel particle size had a linear relation...

  18. Drop spreading with random viscosity

    CERN Document Server

    Xu, Feng

    2016-01-01

    We examine theoretically the spreading of a viscous liquid drop over a thin film of uniform thickness, assuming the liquid's viscosity is regulated by the concentration of a solute that is carried passively by the spreading flow. The solute is assumed to be initially heterogeneous, having a spatial distribution with prescribed statistical features. To examine how this variability influences the drop's motion, we investigate spreading in a planar geometry using lubrication theory, combining numerical simulations with asymptotic analysis. We assume diffusion is sufficient to suppress solute concentration gradients across but not along the film. The solute field beneath the bulk of the drop is stretched by the spreading flow, such that the initial solute concentration immediately behind the drop's effective contact lines has a long-lived influence on the spreading rate. Over long periods, solute swept up from the precursor film accumulates in a short region behind the contact line, allowing patches of elevated v...

  19. Sinking, wedging, spreading - viscous spreading on a layer of fluid

    Science.gov (United States)

    Bergemann, Nico; Juel, Anne; Heil, Matthias

    2016-11-01

    We study the axisymmetric spreading of a sessile drop on a pre-existing layer of the same fluid in a regime where the drop is sufficiently large so that the spreading is driven by gravity while capillary and inertial effects are negligible. Experiments performed with 5 ml drops and layer thicknesses in the range 0.1 mm drop evolves as R tn , where the spreading exponent n increases with the layer thickness h. Numerical simulations, based on the axisymmetric free-surface Navier-Stokes equations, reveal three distinct spreading regimes depending on the layer thickness. For thick layers the drop sinks into the layer, accompanied by significant flow in the layer. By contrast, for thin layers the layer ahead of the propagating front is at rest and the spreading behaviour resembles that of a gravity-driven drop spreading on a dry substrate. In the intermediate regime the spreading is characterised by an advancing wedge, which is sustained by fluid flow from the drop into the layer.

  20. Evaluating mandibular cortical index quantitatively.

    Science.gov (United States)

    Yasar, Fusun; Akgunlu, Faruk

    2008-10-01

    The aim was to assess whether Fractal Dimension and Lacunarity analysis can discriminate patients having different mandibular cortical shape. Panoramic radiographs of 52 patients were evaluated for mandibular cortical index. Weighted Kappa between the observations were varying between 0.718-0.805. These radiographs were scanned and converted to binary images. Fractal Dimension and Lacunarity were calculated from the regions where best represents the cortical morphology. It was found that there were statistically significant difference between the Fractal Dimension and Lacunarity of radiographs which were classified as having Cl 1 and Cl 2 (Fractal Dimension P:0.000; Lacunarity P:0.003); and Cl 1 and Cl 3 cortical morphology (Fractal Dimension P:0.008; Lacunarity P:0.001); but there was no statistically significant difference between Fractal Dimension and Lacunarity of radiographs which were classified as having Cl 2 and Cl 3 cortical morphology (Fractal Dimension P:1.000; Lacunarity P:0.758). FD and L can differentiate Cl 1 mandibular cortical shape from both Cl 2 and Cl 3 mandibular cortical shape but cannot differentiate Cl 2 from Cl 3 mandibular cortical shape on panoramic radiographs.

  1. [Tonic pupil caused by ischemia].

    Science.gov (United States)

    Wilhelm, H

    1989-01-01

    Tonic pupil is usually an idiopathic condition. In some cases, the cause of the ciliary ganglion lesion leading to tonic pupils is obvious. Rarely ischemia causes a lesion of the ciliary ganglion or the short ciliary nerves due to the good blood supply of the ciliary ganglion. Only two cases of tonic pupils in the course of giant cell arteritis are mentioned in the literature, but tonic pupils are probably much more common with this disease. Five cases are demonstrated here. All had associated ischemic optic neuropathy, and stagnation of the blood flow in the supratrochlear artery could be demonstrated in two cases by Doppler sonography. Tonic pupils may also occur when an oclusion of the internal carotid artery resolves, probably because of transient stasis of the orbital blood flow. In another case, tonic pupils were associated with choroidal ischemia (proved by video fluorescent angiography) of unknown origin. The diagnosis of tonic pupils was made by pharmacological testing for cholinergic hypersensitivity with 0.1% pilocarpine.

  2. Metabolic Adaptation to Muscle Ischemia

    Science.gov (United States)

    Cabrera, Marco E.; Coon, Jennifer E.; Kalhan, Satish C.; Radhakrishnan, Krishnan; Saidel, Gerald M.; Stanley, William C.

    2000-01-01

    Although all tissues in the body can adapt to varying physiological/pathological conditions, muscle is the most adaptable. To understand the significance of cellular events and their role in controlling metabolic adaptations in complex physiological systems, it is necessary to link cellular and system levels by means of mechanistic computational models. The main objective of this work is to improve understanding of the regulation of energy metabolism during skeletal/cardiac muscle ischemia by combining in vivo experiments and quantitative models of metabolism. Our main focus is to investigate factors affecting lactate metabolism (e.g., NADH/NAD) and the inter-regulation between carbohydrate and fatty acid metabolism during a reduction in regional blood flow. A mechanistic mathematical model of energy metabolism has been developed to link cellular metabolic processes and their control mechanisms to tissue (skeletal muscle) and organ (heart) physiological responses. We applied this model to simulate the relationship between tissue oxygenation, redox state, and lactate metabolism in skeletal muscle. The model was validated using human data from published occlusion studies. Currently, we are investigating the difference in the responses to sudden vs. gradual onset ischemia in swine by combining in vivo experimental studies with computational models of myocardial energy metabolism during normal and ischemic conditions.

  3. Effect of propofol pretreatment on apoptosis in rat brain cortex after focal cerebral ischemia and reperfusion

    Institute of Scientific and Technical Information of China (English)

    Haiyan Xu; Chengwei Zhang; Chunxiao Zhang

    2011-01-01

    The present study aimed to observe cortical expression of Bcl-2 and Bax, cysteine-dependent aspartate directed proteases-3 activity and apoptotic cell death in a rat model of middle cerebral artery occlusion pretreated with propofol. Results showed that, propofol pretreatment significantly reduced oxidative stress levels and attenuated neuronal apoptosis in the cortex of rats. Propofol pretreatment upregulated Bcl-2 expression, and downregulated Bax expression and cysteine-dependent aspartate directed proteases-3 activity. These findings indicate that propofol pretreatment inhibits cell apoptosis during focal cerebral ischemia/reperfusion injury. This neuroprotective effect is most likely achieved through the Bcl-2/Bax/cysteine-dependent aspartate directed proteases-3 pathway.

  4. Modeling cortical circuits.

    Energy Technology Data Exchange (ETDEWEB)

    Rohrer, Brandon Robinson; Rothganger, Fredrick H.; Verzi, Stephen J.; Xavier, Patrick Gordon

    2010-09-01

    The neocortex is perhaps the highest region of the human brain, where audio and visual perception takes place along with many important cognitive functions. An important research goal is to describe the mechanisms implemented by the neocortex. There is an apparent regularity in the structure of the neocortex [Brodmann 1909, Mountcastle 1957] which may help simplify this task. The work reported here addresses the problem of how to describe the putative repeated units ('cortical circuits') in a manner that is easily understood and manipulated, with the long-term goal of developing a mathematical and algorithmic description of their function. The approach is to reduce each algorithm to an enhanced perceptron-like structure and describe its computation using difference equations. We organize this algorithmic processing into larger structures based on physiological observations, and implement key modeling concepts in software which runs on parallel computing hardware.

  5. Cortical and spinal assessment

    DEFF Research Database (Denmark)

    Fischer, I W; Gram, Mikkel; Hansen, T M

    2017-01-01

    BACKGROUND: Standardized objective methods to assess the analgesic effects of opioids, enable identification of underlying mechanisms of drug actions in the central nervous system. Opioids may exert their effect on both cortical and spinal levels. In this study actions of morphine at both levels...... subjects was included in the data analysis. There was no change in the activity in resting EEG (P>0.05) after morphine administration as compared to placebo. During cold pressor stimulation, morphine significantly lowered the relative activity in the delta (1-4Hz) band (P=0.03) and increased the activity...... morphine administration (P>0.05). CONCLUSIONS: Cold pressor EEG and the nociceptive reflex were more sensitive to morphine analgesia than resting EEG and can be used as standardized objective methods to assess opioid effects. However, no correlation between the analgesic effect of morphine on the spinal...

  6. Hiperostosis cortical infantil

    OpenAIRE

    Salvador Javier Santos Medina; Orelvis Pérez Duerto

    2015-01-01

    La enfermedad de Caffey, o hiperostosis cortical infantil, es una rara enfermedad ósea autolimitada, que aparece de preferencia en lactantes con signos inespecíficos sistémicos; el más relevante es la reacción subperióstica e hiperostosis en varios huesos del cuerpo, con predilección en el 75-80 % de los casos por la mandíbula. Su pronóstico es bueno, la mayoría no deja secuelas. El propósito del presente trabajo es describir las características clínicas, presentes en un lactante de cinco mes...

  7. Progressive posterior cortical dysfunction

    Directory of Open Access Journals (Sweden)

    Fábio Henrique de Gobbi Porto

    Full Text Available Abstract Progressive posterior cortical dysfunction (PPCD is an insidious syndrome characterized by prominent disorders of higher visual processing. It affects both dorsal (occipito-parietal and ventral (occipito-temporal pathways, disturbing visuospatial processing and visual recognition, respectively. We report a case of a 67-year-old woman presenting with progressive impairment of visual functions. Neurologic examination showed agraphia, alexia, hemispatial neglect (left side visual extinction, complete Balint's syndrome and visual agnosia. Magnetic resonance imaging showed circumscribed atrophy involving the bilateral parieto-occipital regions, slightly more predominant to the right . Our aim was to describe a case of this syndrome, to present a video showing the main abnormalities, and to discuss this unusual presentation of dementia. We believe this article can contribute by improving the recognition of PPCD.

  8. Cortical plasticity and rehabilitation.

    Science.gov (United States)

    Moucha, Raluca; Kilgard, Michael P

    2006-01-01

    The brain is constantly adapting to environmental and endogenous changes (including injury) that occur at every stage of life. The mechanisms that regulate neural plasticity have been refined over millions of years. Motivation and sensory experience directly shape the rewiring that makes learning and neurological recovery possible. Guiding neural reorganization in a manner that facilitates recovery of function is a primary goal of neurological rehabilitation. As the rules that govern neural plasticity become better understood, it will be possible to manipulate the sensory and motor experience of patients to induce specific forms of plasticity. This review summarizes our current knowledge regarding factors that regulate cortical plasticity, illustrates specific forms of reorganization induced by control of each factor, and suggests how to exploit these factors for clinical benefit.

  9. Moringa Oleifera Lam Mitigates Oxidative Damage and Brain Infarct Volume in Focal Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Woranan Kirisattayakul

    2012-01-01

    Full Text Available Problem statement: At present, the therapeutic outcome of cerebral ischemia is still not in the satisfaction level. Therefore, the preventive strategy is considered. Based on the protective effect against oxidative damage of Moringa oleifera Lam. Leaves extract, we hypothesized that this plant extract might protect against cerebral ischemia, one of the challenge problems nowadays. In order to test this hypothesis, we aimed to determine the protective effect of M.oleifera leaves extract in animal model of focal cerebral ischemia induced by permanent occlusion of right middle cerebral artery. Approach: Male Wistar rats, weighing 300-350 g, were orally given the extract once daily at doses of 100, 200 and 400 mg kg-1 BW at a period of 2 weeks, then, they were permanently occluded the right Middle Cerebral Artery (MCAO. The animals were assessed the cerebral infarction volume and oxidative damage markers including MDA level and the activities of SOD, CAT and GSHPx enzymes at 24 h after occlusion. Results: Rats subjected to M.oleifera extract at all doses used in this study significantly decreased brain infarct volume both at cortical and subcortical structures in accompany with the elevation of SOD activity in both hippocampus and striatum while only the rats exposed to the extract at doses of 100 and 400 mg kg-1 BW showed the increased GSHPx activity in hippocampus. No the changes were observed. Therefore, our results demonstrates the potential benefit of M.oleifera leaves to decrease oxidative stress damage and brain infarct volume. Conclusion: This study is the first study to demonstrate the neuroprotective effect against focal cerebral ischemia of M.oleifera leaves. It suggests that M.oleifera may be served as natural resource for developing neuroprotectant against focal cerebral ischemia. However, the precise underlying mechanism and possible active ingredient are still required further study.

  10. Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

    DEFF Research Database (Denmark)

    Dreier, Jens P; Major, Sebastian; Pannek, Heinz-Wolfgang

    2012-01-01

    Spreading depolarization of cells in cerebral grey matter is characterized by massive ion translocation, neuronal swelling and large changes in direct current-coupled voltage recording. The near-complete sustained depolarization above the inactivation threshold for action potential generating...

  11. Acute mesenteric ischemia in young adults.

    Science.gov (United States)

    Ozturk, Gurkan; Aydinli, Bulent; Atamanalp, S Selcuk; Yildirgan, M Ilhan; Ozoğul, Bünyami; Kısaoğlu, Abdullah

    2012-08-01

    Acute mesenteric ischemia is commonly seen in old patients. This study was undertaken to show that mesenteric ischemia might be seen in individuals under 40 years of age and that its diagnosis is challenging. Twenty-six patients with acute mesenteric ischemia under the age of 40 were studied. The main symptom on admission was abdominal pain. Symptom duration varied between 12 h and 5 days. The medical history of the patients revealed that 9 had no previous diseases. Other 17 had predisposing factors in the first evaluation. None of the patients had any history of narcotic or drug abuse. Ten patients presented with signs and symptoms of sepsis and septic shock. Preoperative diagnosis was acute intestinal ischemia only in 6 patients. Preoperatively, all the patients had intestinal or colonic ischemia and necrosis; one had additional ischemia of the liver, stomach, duodenum, and pancreas. Six patients had massive intestinal necrosis. The overall postoperative complication and overall mortality rates were 61.5 and 26.9 %, respectively. Complications and mortality were determined to be associated with previous pulmonary disease, acidosis, presence of septic shock, acute renal failure, extent of the ischemia and extent of resection, second look operations, previous cardiac events, and the kind of affected bowel (colon involvement).

  12. Myocardial Ischemia Caused by Subepicardial Hematoma

    Science.gov (United States)

    Grieshaber, Philippe; Nef, Holger; Böning, Andreas; Niemann, Bernd

    2017-01-01

    Background Bleeding from bypass anastomosis leakage occurs early after coronary artery bypass grafting. Later, once the anastomosis is covered by intima, spontaneous bleeding is unlikely. Case Description A 63-year-old male patient developed a pseudoaneurysm-like, subepicardial late-term bleeding resulting in a hematoma that compromised coronary artery flow by increasing extracoronary pressure. This resulted in severe angina pectoris (Canadian Cardiovascular Society IV) and myocardial ischemia within the affected area. After surgical removal of the hematoma and repair of the anastomosis, the patient's symptoms disappeared and no signs of myocardial ischemia were present. Conclusion Surgical removal is an efficient therapy for subepicardial hematoma inducing myocardial ischemia.

  13. Filtrate of Phellinus linteus Broth Culture Reduces Infarct Size Significantly in a Rat Model of Permanent Focal Cerebral Ischemia.

    Science.gov (United States)

    Suzuki, Sakiko; Kawamata, Takakazu; Okada, Yoshikazu; Kobayashi, Tomonori; Nakamura, Tomoyuki; Hori, Tomokatsu

    2011-01-01

    Phellinus linteus, a natural growing mushroom, has been known to exhibit anti-tumor, anti-inflammatory, anti-allergic and anti-oxidant effects. Aiming to exploit the neuroprotective effects of P. linteus, we evaluated its effects on infarct volume reduction in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to right middle cerebral artery occlusion. Filtrate of P. linteus broth culture (various doses), fractionated filtrate (based on molecular weight) or control medium was administered intraperitoneally to rats before or after ischemia induction. Rats were killed at 24 h after the stroke surgery. Cortical and caudoputaminal infarct volumes were determined separately using an image analysis program following staining with 2,3,5-triphenyltetrazolium chloride. Significant cortical infarct volume reductions were found in the pre-treatment groups (30 and 60 minutes before onset of cerebral ischemia) compared with the control group, showing dose dependence. Posttreatment (30 minutes after ischemic onset) also significantly reduced cortical infarct volume. Furthermore, the higher molecular weight (≥12 000) fraction of the culture filtrate was more effective compared with the lower molecular weight fraction. The present findings suggest that P. linteus may be a new promising approach for the treatment of focal cerebral ischemia, with the additional benefit of a wide therapeutic time window since significant infarct volume reduction is obtained by administration even after the ischemic event. Our finding that the higher molecular weight fraction of the P. linteus culture filtrate demonstrated more prominent effect may provide a clue to identify the neuroprotective substances and mechanisms.

  14. Filtrate of Phellinus linteus Broth Culture Reduces Infarct Size Significantly in a Rat Model of Permanent Focal Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Sakiko Suzuki

    2011-01-01

    Full Text Available Phellinus linteus, a natural growing mushroom, has been known to exhibit anti-tumor, anti-inflammatory, anti-allergic and anti-oxidant effects. Aiming to exploit the neuroprotective effects of P. linteus, we evaluated its effects on infarct volume reduction in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to right middle cerebral artery occlusion. Filtrate of P. linteus broth culture (various doses, fractionated filtrate (based on molecular weight or control medium was administered intraperitoneally to rats before or after ischemia induction. Rats were killed at 24 h after the stroke surgery. Cortical and caudoputaminal infarct volumes were determined separately using an image analysis program following staining with 2,3,5-triphenyltetrazolium chloride. Significant cortical infarct volume reductions were found in the pre-treatment groups (30 and 60 minutes before onset of cerebral ischemia compared with the control group, showing dose dependence. Posttreatment (30 minutes after ischemic onset also significantly reduced cortical infarct volume. Furthermore, the higher molecular weight (≥12 000 fraction of the culture filtrate was more effective compared with the lower molecular weight fraction. The present findings suggest that P. linteus may be a new promising approach for the treatment of focal cerebral ischemia, with the additional benefit of a wide therapeutic time window since significant infarct volume reduction is obtained by administration even after the ischemic event. Our finding that the higher molecular weight fraction of the P. linteus culture filtrate demonstrated more prominent effect may provide a clue to identify the neuroprotective substances and mechanisms.

  15. Models of cortical malformation--Chemical and physical.

    Science.gov (United States)

    Luhmann, Heiko J

    2016-02-15

    Pharmaco-resistant epilepsies, and also some neuropsychiatric disorders, are often associated with malformations in hippocampal and neocortical structures. The mechanisms leading to these cortical malformations causing an imbalance between the excitatory and inhibitory system are largely unknown. Animal models using chemical or physical manipulations reproduce different human pathologies by interfering with cell generation and neuronal migration. The model of in utero injection of methylazoxymethanol (MAM) acetate mimics periventricular nodular heterotopia. The freeze lesion model reproduces (poly)microgyria, focal heterotopia and schizencephaly. The in utero irradiation model causes microgyria and heterotopia. Intraperitoneal injections of carmustine 1-3-bis-chloroethyl-nitrosurea (BCNU) to pregnant rats produces laminar disorganization, heterotopias and cytomegalic neurons. The ibotenic acid model induces focal cortical malformations, which resemble human microgyria and ulegyria. Cortical dysplasia can be also observed following prenatal exposure to ethanol, cocaine or antiepileptic drugs. All these models of cortical malformations are characterized by a pronounced hyperexcitability, few of them also produce spontaneous epileptic seizures. This dysfunction results from an impairment in GABAergic inhibition and/or an increase in glutamatergic synaptic transmission. The cortical region initiating or contributing to this hyperexcitability may not necessarily correspond to the site of the focal malformation. In some models wide-spread molecular and functional changes can be observed in remote regions of the brain, where they cause pathophysiological activities. This paper gives an overview on different animal models of cortical malformations, which are mostly used in rodents and which mimic the pathology and to some extent the pathophysiology of neuronal migration disorders associated with epilepsy in humans.

  16. Spreading the Bible in China

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    According to records of the Bible Society in China, more than 300 million copies of the Bible in Chinese have been published and distributed since 1823. The spread of the Bible in China has gone through five stages.

  17. Spread effects - methodology; Spredningseffekter - metodegrunnlag

    Energy Technology Data Exchange (ETDEWEB)

    NONE

    2004-07-01

    Diffusion of technology, environmental effects and rebound effects are the principal effects from the funding of renewable energy and energy economising. It is difficult to estimate the impact of the spread effects both prior to the measures are implemented and after the measures are carried out. Statistical methods can be used to estimate the spread effects, but they are insecure and always need to be complemented with qualitative and subjective evaluations. It is more adequate to evaluate potential spread effects from market and market data surveillance for a selection of technologies and parties. Based on this information qualitative indicators for spread effects can be constructed and used both ex ante and ex post (ml)

  18. Roles of Ties in Spreading

    CERN Document Server

    Cui, Ai-Xiang; Zhou, Tao

    2012-01-01

    Background: Controlling global epidemics in the real world and accelerating information propagation in the artificial world are of great significance, which have activated an upsurge in the studies on networked spreading dynamics. Lots of efforts have been made to understand the impacts of macroscopic statistics (e.g., degree distribution and average distance) and mesoscopic structures (e.g., communities and rich clubs) on spreading processes while the microscopic elements are less concerned. In particular, roles of ties are not yet clear to the academic community. Methodology/Principle Findings: Every edges is stamped by its strength that is defined solely based on the local topology. According to a weighted susceptible-infected-susceptible model, the steady-state infected density and spreading speed are respectively optimized by adjusting the relationship between edge's strength and spreading ability. Experiments on six real networks show that the infected density is increased when strong ties are favored i...

  19. Epidemic spreading in complex networks

    Institute of Scientific and Technical Information of China (English)

    Jie ZHOU; Zong-hua LIU

    2008-01-01

    The study of epidemic spreading in complex networks is currently a hot topic and a large body of results have been achieved.In this paper,we briefly review our contributions to this field,which includes the underlying mechanism of rumor propagation,the epidemic spreading in community networks,the influence of varying topology,and the influence of mobility of agents.Also,some future directions are pointed out.

  20. Fluoxetine Enhances Neurogenesis in Aged Rats with Cortical Infarcts, but This is not Reflected in a Behavioral Recovery.

    Science.gov (United States)

    Sun, Xiaoyu; Zhou, Zhike; Liu, Tingting; Zhao, Mei; Zhao, Shanshan; Xiao, Ting; Jolkkonen, Jukka; Zhao, Chuansheng

    2016-02-01

    Age is associated with poor outcome and impaired functional recovery after stroke. Fluoxetine, which is widely used in clinical practice, can regulate hippocampal neurogenesis in young rodents. As the rate of neurogenesis is dramatically reduced during aging, we studied the effect of post-stroke fluoxetine treatment on neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of dentate gyrus (DG) and whether this would be associated with any behavioral recovery after the cortical infarct in aged rats. Aged rats were randomly assigned to four groups: sham-operated rats, sham-operated rats treated with fluoxetine, rats subjected to cerebral ischemia, and rats with ischemia treated with fluoxetine. Focal cortical ischemia was induced by intracranial injection of vasoconstrictive peptide, endothelin-1 (ET-1). Fluoxetine was administered in the drinking water for 3 weeks starting 1 week after ischemia at a dose of 18 mg/kg/day. Behavioral recovery was evaluated on post-stroke days 29 to 31 after which the survival rate and fate of proliferating cells in the SVZ and DG were assessed by immunohistochemistry. Apoptosis was measured with the TUNEL assay. The results indicated that chronic fluoxetine treatment after stroke enhanced the proliferation of newborn neurons in the SVZ, but not in SGZ, and it suppressed perilesional apoptosis. Fluoxetine treatment did not affect the survival or differentiation of newly generated cells in the SVZ i.e., the enhanced neurogenesis was not translated into a behavioral outcome.

  1. Mitochondrial Targeted Antioxidant in Cerebral Ischemia.

    Science.gov (United States)

    Ahmed, Ejaz; Donovan, Tucker; Yujiao, Lu; Zhang, Quanguang

    There has been much evidence suggesting that reactive oxygen species (ROS) generated in mitochondria during cerebral ischemia play a major role in programming the senescence of organism. Antioxidants dealing with mitochondria slow down the appearance and progression of symptoms in cerebral ischemia and increase the life span of organisms. The mechanisms of mitochondrial targeted antioxidants, such as SKQ1, Coenzyme Q10, MitoQ, and Methylene blue, include increasing adenosine triphosphate (ATP) production, decreasing production of ROS and increasing antioxidant defenses, providing benefits in neuroprotection following cerebral ischemia. A number of studies have shown the neuroprotective role of these mitochondrial targeted antioxidants in cerebral ischemia. Here in this short review we have compiled the literature supporting consequences of mitochondrial dysfunction, and the protective role of mitochondrial targeted antioxidants.

  2. Lateral spread of orientation selectivity in V1 is controlled by intracortical cooperativity

    Directory of Open Access Journals (Sweden)

    Frédéric eChavane

    2011-02-01

    Full Text Available Neurons in the primary visual cortex receive subliminal information originating from the periphery of their receptive fields through a variety of cortical connections. In the cat primary visual cortex, long-range horizontal axons have been reported to preferentially bind to distant columns of similar orientation preferences, whereas feedback connections from higher visual areas provide a more diverse functional input. To understand the role of these lateral interactions, it is crucial to characterize their effective functional connectivity and tuning properties. However, the overall functional impact of cortical lateral connections, whatever their anatomical origin, is unknown since it has never been directly characterized. Using direct measurements of postsynaptic integration in cat areas 17/18, we performed multi-scale assessments of the functional impact of visually driven lateral networks. Voltage-sensitive dye imaging showed that local oriented stimuli evoke an orientation-selective activity that remains confined to the cortical feedforward imprint of the stimulus. Beyond a distance of one hypercolumn, the lateral spread of cortical activity gradually lost its orientation preference approximated as an exponential with a space constant of about 1mm. Intracellular recordings showed that this loss of orientation selectivity arises from the diversity of converging synaptic input patterns originating from outside the classical receptive field. In contrast, when the stimulus size was increased, we observed orientation-selective spread of activation beyond the feedforward imprint. We conclude that stimulus-induced cooperativity enhances the long-range orientation-selective spread.

  3. Focal cortical dysplasia – review

    Science.gov (United States)

    Kabat, Joanna; Król, Przemysław

    2012-01-01

    Summary Focal cortical dysplasia is a malformation of cortical development, which is the most common cause of medically refractory epilepsy in the pediatric population and the second/third most common etiology of medically intractable seizures in adults. Both genetic and acquired factors are involved in the pathogenesis of cortical dysplasia. Numerous classifications of the complex structural abnormalities of focal cortical dysplasia have been proposed – from Taylor et al. in 1971 to the last modification of Palmini classification made by Blumcke in 2011. In general, three types of cortical dysplasia are recognized. Type I focal cortical dysplasia with mild symptomatic expression and late onset, is more often seen in adults, with changes present in the temporal lobe. Clinical symptoms are more severe in type II of cortical dysplasia usually seen in children. In this type, more extensive changes occur outside the temporal lobe with predilection for the frontal lobes. New type III is one of the above dysplasias with associated another principal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early life. Brain MRI imaging shows abnormalities in the majority of type II dysplasias and in only some of type I cortical dysplasias. The most common findings on MRI imaging include: focal cortical thickening or thinning, areas of focal brain atrophy, blurring of the gray-white junction, increased signal on T2- and FLAIR-weighted images in the gray and subcortical white matter often tapering toward the ventricle. On the basis of the MRI findings, it is possible to differentiate between type I and type II cortical dysplasia. A complete resection of the epileptogenic zone is required for seizure-free life. MRI imaging is very helpful to identify those patients who are likely to benefit from surgical treatment in a group of patients with drug-resistant epilepsy. However, in type I cortical dysplasia, MR imaging is often normal, and also

  4. Analysis of Cortical Flow Models In Vivo

    Science.gov (United States)

    Benink, Hélène A.; Mandato, Craig A.; Bement, William M.

    2000-01-01

    Cortical flow, the directed movement of cortical F-actin and cortical organelles, is a basic cellular motility process. Microtubules are thought to somehow direct cortical flow, but whether they do so by stimulating or inhibiting contraction of the cortical actin cytoskeleton is the subject of debate. Treatment of Xenopus oocytes with phorbol 12-myristate 13-acetate (PMA) triggers cortical flow toward the animal pole of the oocyte; this flow is suppressed by microtubules. To determine how this suppression occurs and whether it can control the direction of cortical flow, oocytes were subjected to localized manipulation of either the contractile stimulus (PMA) or microtubules. Localized PMA application resulted in redirection of cortical flow toward the site of application, as judged by movement of cortical pigment granules, cortical F-actin, and cortical myosin-2A. Such redirected flow was accelerated by microtubule depolymerization, showing that the suppression of cortical flow by microtubules is independent of the direction of flow. Direct observation of cortical F-actin by time-lapse confocal analysis in combination with photobleaching showed that cortical flow is driven by contraction of the cortical F-actin network and that microtubules suppress this contraction. The oocyte germinal vesicle serves as a microtubule organizing center in Xenopus oocytes; experimental displacement of the germinal vesicle toward the animal pole resulted in localized flow away from the animal pole. The results show that 1) cortical flow is directed toward areas of localized contraction of the cortical F-actin cytoskeleton; 2) microtubules suppress cortical flow by inhibiting contraction of the cortical F-actin cytoskeleton; and 3) localized, microtubule-dependent suppression of actomyosin-based contraction can control the direction of cortical flow. We discuss these findings in light of current models of cortical flow. PMID:10930453

  5. Spreading depression and the clinical correlates of migraine.

    Science.gov (United States)

    Eikermann-Haerter, Katharina; Negro, Andrea; Ayata, Cenk

    2013-01-01

    Migraine is the most common neurologic condition. One-third of migraineurs experience transient neurologic symptoms, the so-called aura. There is strong evidence that spreading depression (SD) is the electrophysiologic substrate of migraine aura. SD is an intense pan-depolarization wave that slowly propagates in gray matter by way of contiguity and transiently disrupts neuronal function. When induced subcortically, striatal SD causes hemiparesis, hippocampal SD can trigger seizures and impact cognition, and bilateral thalamic SD can diminish consciousness. Recent data show that transgenic mice expressing familial hemiplegic migraine (FHM) type 1 mutations in voltage-gated Ca2+ channels (Cav2.1) develop mutation-specific aura-like signs after a cortical SD similar to patients with the respective mutation. These signs are associated with facilitated subcortical SD propagation. As in FHM, mice with the R192Q mutation develop pure hemiplegia associated with cortical SDs propagating into caudoputamen. S218L mice display additional signs such as seizures and coma when SD propagates into hippocampus and thalamus. In hyperexcitable FHM brains, SD may propagate between cortex and subcortical structures via permissive gray matter bridges, or originate de novo in subcortical structures, to explain unusual and severe aura signs and symptoms. Reciprocal spread and reverberating waves can explain protracted attacks.

  6. Are bone marrow regenerative cells ideal seed cells for the treatment of cerebral ischemia?

    Institute of Scientific and Technical Information of China (English)

    Yi Li; Xuming Hua; Fang Hua; Wenwei Mao; Liang Wan; Shiting Li

    2013-01-01

    Bone marrow cells for the treatment of ischemic brain injury may depend on the secretion of a large number of neurotrophic factors. Bone marrow regenerative cells are capable of increasing the secretion of neurotrophic factors. In this study, after tail vein injection of 5-fluorouracil for 7 days, bone marrow cells and bone marrow regenerative cells were isolated from the tibias and femurs of rats, and then administered intravenously via the tail vein after focal cerebral ischemia. Immunohistological staining and reverse transcription-PCR detection showed that transplanted bone marrow cells and bone marrow regenerative cells could migrate and survive in the ischemic regions, such as the cortical and striatal infarction zone. These cells promote vascular endothelial cell growth factor mRNA expression in the ischemic marginal zone surrounding the ischemic penumbra of the cortical and striatal infarction zone, and have great advantages in promoting the recovery of neurological function, reducing infarct size and promoting angiogenesis. Bone marrow regenerative cells exhibited stronger neuroprotective effects than bone marrow cells. Our experimental findings indicate that bone marrow regenerative cells are preferable over bone marrow cells for cell therapy for neural regeneration after cerebral ischemia. Their neuroprotective effect is largely due to their ability to induce the secretion of factors that promote vascular regeneration, such as vascular endothelial growth factor.

  7. Hiperostosis cortical infantil

    Directory of Open Access Journals (Sweden)

    Salvador Javier Santos Medina

    2015-04-01

    Full Text Available La enfermedad de Caffey, o hiperostosis cortical infantil, es una rara enfermedad ósea autolimitada, que aparece de preferencia en lactantes con signos inespecíficos sistémicos; el más relevante es la reacción subperióstica e hiperostosis en varios huesos del cuerpo, con predilección en el 75-80 % de los casos por la mandíbula. Su pronóstico es bueno, la mayoría no deja secuelas. El propósito del presente trabajo es describir las características clínicas, presentes en un lactante de cinco meses de edad, atendido en el Hospital Pediátrico Provincial “Mártires de Las Tunas” con este diagnóstico, quien ingresó en el servicio de miscelánea B por una celulitis facial. Presentaba aumento de volumen en la región geniana izquierda, febrícola e inapetencia. Se impuso tratamiento con cefazolina y se egresó a los siete días. Acudió nuevamente con tumefacción blanda y difusa de ambas hemicaras, irritabilidad y fiebre. Se interconsultó con cirugía maxilofacial, se indicaron estudios sanguíneos y radiológicos. Se diagnosticó como enfermedad de Caffey, basado en la edad del niño, tumefacción facial sin signos inflamatorios agudos e hiperostosis en ambas corticales mandibulares a la radiografía AP mandíbula; unido a anemia ligera, leucocitosis y eritrosedimentación acelerada. El paciente se trató sintomáticamente y con antinflamatorios no esteroideos. Esta rara entidad se debe tener presente en casos de niños y lactantes con irritabilidad y fiebre inespecífica

  8. Early protective effects of iloprost after experimental spinal cord ischemia in rabbits.

    Science.gov (United States)

    Coskun, K; Attar, A; Tuna, H; Sargon, M F; Yüceer, N; Türker, R K; Egemen, N

    2000-01-01

    The potential role of Iloprost, a stable analogue of prostocyclin, in treating spinal cord ischemia was investigated in rabbits subjected to aortic occlusion for 15 minutes. Ten adult rabbits weighing 2-2.5 kg received an intravenous infusion of saline (SF) as a control group and 14 rabbits received an intravenous infusion of Iloprost, 25 microg/kg/h. Iloprost infusion was started immediately after clamping of the aorta and continued 60 minutes thereafter. Cortical somatosensorial evoked potentials (CSEP) were recorded during the pre-ischemic period as a baseline and post-ischemic readings were taken at 15, 30 and 60 minutes. There was no statistically significant difference between CSEP of the saline and Iloprost treated groups (p < 0.05). All animals were examined neurologically by using a modification of Tarlov scale and all subjects were then deeply anesthetized and their spinal cords were removed for light and electron microscopic examinations at 24 h after spinal cord ischemia. In order to obtain an accurate comparison of ultrastructural changes between saline treated and Iloprost treated groups, a grading scale was performed. The light microscopic and ultrastructural analysis of the Iloprost treated group revealed that there was moderate protection of the myelin and axons and edema was attenuated. Findings of this study suggest that Iloprost exerts a protective effect on spinal cord ischemia. However, further studies are needed to reveal possible mechanisms of protection provided by Iloprost.

  9. Spreading dynamics in complex networks

    CERN Document Server

    Pei, Sen

    2013-01-01

    Searching for influential spreaders in complex networks is an issue of great significance for applications across various domains, ranging from the epidemic control, innovation diffusion, viral marketing, social movement to idea propagation. In this paper, we first display some of the most important theoretical models that describe spreading processes, and then discuss the problem of locating both the individual and multiple influential spreaders respectively. Recent approaches in these two topics are presented. For the identification of privileged single spreaders, we summarize several widely used centralities, such as degree, betweenness centrality, PageRank, k-shell, etc. We investigate the empirical diffusion data in a large scale online social community -- LiveJournal. With this extensive dataset, we find that various measures can convey very distinct information of nodes. Of all the users in LiveJournal social network, only a small fraction of them involve in spreading. For the spreading processes in Li...

  10. 9 CFR 319.762 - Ham spread, tongue spread, and similar products.

    Science.gov (United States)

    2010-01-01

    ... 9 Animals and Animal Products 2 2010-01-01 2010-01-01 false Ham spread, tongue spread, and similar products. 319.762 Section 319.762 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... Salads and Meat Spreads § 319.762 Ham spread, tongue spread, and similar products. “Ham Spread,” “Tongue...

  11. Expression of somatostatin mRNA and peptide in rat hippocampus after cerebral ischemia

    DEFF Research Database (Denmark)

    Bering, Robert; Johansen, Flemming Fryd

    1993-01-01

    Somatostatin, ischemia, hippocampus, rat, in situ hybridisation, immunocytochemistry, neuropathology......Somatostatin, ischemia, hippocampus, rat, in situ hybridisation, immunocytochemistry, neuropathology...

  12. [Critical limb ischemia--update].

    Science.gov (United States)

    Melamed, Eitan; Kotyba, Baydousi; Galili, Offer; Karmeli, Ron

    2010-12-01

    Critical limb ischemia (CLI) is the most severe manifestation of peripheral artery occlusive disease. Without timely diagnosis and revascularization, patients with CLI are at risk of devastating complications including loss of limb and life. Therapeutic goals in treating patients with CLI include reducing cardiovascular risk factors, relieving ischemic pain, heating ulcers, preventing major amputation, improving quality of life and increasing survival. These aims may be achieved through medical therapy, revascularization or amputation. The past decade has seen substantial growth in endovascular therapies and options now exist for treating long segment occlusive disease, but surgical bypass may still yield more durable results. Patients who are younger, more active, and at low risk for surgery, may have better outcomes undergoing an operation. This is also indicated for endovascular failures, which may include technical failures or late occlusions after stents or other procedures. In contrast, frail patients with a limited life expectancy may experience better outcomes with endovascular therapy. For patients who are non-ambulatory, demented, or unfit to undergo revascularization, an amputation should be considered.

  13. Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia: a molecular docking study exploring possible neuroprotection

    Directory of Open Access Journals (Sweden)

    Anand Kumar Pandey

    2015-01-01

    Full Text Available The main pathophysiology of cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Resveratrol has been reported to be one of the most potent chemopreventive agents that can inhibit cellular processes associated with ischemic stroke. Matrix metalloproteinases (MMPs has been considered as a potential drug target for the treatment of cerebral ischemia. To explore this, we tried to investigate the interaction of resveratrol with MMPs through molecular docking studies. At 30 minutes before and 2 hours after cerebral ischemia/reperfusion induced by occlusion of the middle cerebral artery, 40 mg/kg resveratrol was intraperitoneally administered. After resveratrol administration, neurological function and brain edema were significantly alleviated, cerebral infarct volume was significantly reduced, and nitrite and malondialdehyde levels in the cortical and striatal regions were significantly decreased. The molecular docking study of resveratrol and MMPs revealed that resveratrol occupied the active site of MMP-2 and MMP-9. The binding energy of the complexes was -37.848672 kJ/mol and -36.6345 kJ/mol for MMP-2 and MMP-9, respectively. In case of MMP-2, Leu 164, Ala 165 and Thr 227 were engaged in H-Bonding with resveratrol and in case of MMP-9, H-bonding was found with Glu 402, Ala 417 and Arg 424 residues. These findings collectively reveal that resveratrol exhibits neuroprotective effects on cerebral ischemia through inhibiting MMP-2 and MMP-9 activity.

  14. Cortical Correlates of Fitts’ Law

    Directory of Open Access Journals (Sweden)

    Peter eIfft

    2011-12-01

    Full Text Available Fitts' law describes the fundamental trade-off between movement accuracy and speed: It states that the duration of reaching movements is a function of target size and distance. While Fitts' law has been extensively studied in ergonomics and has guided the design of human-computer interfaces, there have been few studies on its neuronal correlates. To elucidate sensorimotor cortical activity underlying Fitts’ law, we implanted two monkeys with multielectrode arrays in the primary motor (M1 and primary somatosensory (S1 cortices. The monkeys performed reaches with a joystick-controlled cursor towards targets of different size. The reaction time, movement time and movement velocity changed with target size, and M1 and S1 activity reflected these changes. Moreover, modifications of cortical activity could not be explained by changes of movement parameters alone, but required target size as an additional parameter. Neuronal representation of target size was especially prominent during the early reaction time period where it influenced the slope of the firing rate rise preceding movement initiation. During the movement period, cortical activity was mostly correlated with movement velocity. Neural decoders were applied to simultaneously decode target size and motor parameters from cortical modulations. We suggest using such classifiers to improve neuroprosthetic control.

  15. Phenolic alkaloids from Menispermum dauricum rhizome protect against brain ischemia injury via regulation of GLT-1, EAAC1 and ROS generation.

    Science.gov (United States)

    Zhao, Bo; Chen, Yang; Sun, Xi; Zhou, Mei; Ding, Jie; Zhan, Jin-Jin; Guo, Lian-Jun

    2012-03-06

    Menispermum dauricum rhizome has been widely used in China to treat various cardiovascular and thrombosis disorders. Some studies have reported that the phenolic alkaloids of Menispermum dauricum rhizome (PAM) have protective effects against brain ischemia injury, but the mechanism of this action remains to be clarified. In the present study, we investigated the possible mechanisms of action of PAM on experimental brain ischemia injury. Oxygen and glucose deprivation (OGD) in rat primary cortical cultures and middle cerebral artery occlusion in rats were used to mimic ischemia-reperfusion injury, respectively. The results suggested that PAM protected rat primary cortical cultures against OGD-reoxygenation induced cytotoxicity. PAM decreased extracellular glutamate content and markedly prevented the effects induced by OGD on protein level of GLT-1 and EAAC1 glutamate transporters. In addition, it reduced intracellular ROS generation. In vivo, PAM significantly reduced cerebral infarct area and ameliorated neurological functional deficits at different time points. Our findings revealed that the possible mechanism of action of PAM protected against brain ischemia injury involves regulation of GLT-1, EAAC1 and ROS generation.

  16. Phenolic Alkaloids from Menispermum dauricum Rhizome Protect against Brain Ischemia Injury via Regulation of GLT-1, EAAC1 and ROS Generation

    Directory of Open Access Journals (Sweden)

    Lian-Jun Guo

    2012-03-01

    Full Text Available Menispermum dauricum rhizome has been widely used in China to treat various cardiovascular and thrombosis disorders. Some studies have reported that the phenolic alkaloids of Menispermum dauricum rhizome (PAM have protective effects against brain ischemia injury, but the mechanism of this action remains to be clarified. In the present study, we investigated the possible mechanisms of action of PAM on experimental brain ischemia injury. Oxygen and glucose deprivation (OGD in rat primary cortical cultures and middle cerebral artery occlusion in rats were used to mimic ischemia-reperfusion injury, respectively. The results suggested that PAM protected rat primary cortical cultures against OGD-reoxygenation induced cytotoxicity. PAM decreased extracellular glutamate content and markedly prevented the effects induced by OGD on protein level of GLT-1 and EAAC1 glutamate transporters. In addition, it reduced intracellular ROS generation. In vivo, PAM significantly reduced cerebral infarct area and ameliorated neurological functional deficits at different time points. Our findings revealed that the possible mechanism of action of PAM protected against brain ischemia injury involves regulation of GLT-1, EAAC1 and ROS generation.

  17. Olive oil in food spreads

    National Research Council Canada - National Science Library

    Blanco Muñoz, Miguel A

    2004-01-01

    .... The use of olive oil to prepare fat spread opens new insights into the commercial development of healthy novel foods with a positive image in terms of consumer appeal.La hidrogenación química de los...

  18. Worldwide spreading of economic crisis

    CERN Document Server

    Garas, Antonios; Rozenblat, Celine; Tomassini, Marco; Havlin, Shlomo

    2010-01-01

    We model the spreading of a crisis by constructing a global economic network and applying the Susceptible-Infected-Recovered (SIR) epidemic model with a variable probability of infection. The probability of infection depends on the strength of economic relations between the pair of countries, and the strength of the target country. It is expected that a crisis which originates in a large country, such as the USA, has the potential to spread globally, like the recent crisis. Surprisingly we show that also countries with much lower GDP, such as Belgium, are able to initiate a global crisis. Using the {\\it k}-shell decomposition method to quantify the spreading power (of a node), we obtain a measure of ``centrality'' as a spreader of each country in the economic network. We thus rank the different countries according to the shell they belong to, and find the 12 most central countries. These countries are the most likely to spread a crisis globally. Of these 12 only six are large economies, while the other six ar...

  19. Spreading dynamics in complex networks

    Science.gov (United States)

    Pei, Sen; Makse, Hernán A.

    2013-12-01

    Searching for influential spreaders in complex networks is an issue of great significance for applications across various domains, ranging from epidemic control, innovation diffusion, viral marketing, and social movement to idea propagation. In this paper, we first display some of the most important theoretical models that describe spreading processes, and then discuss the problem of locating both the individual and multiple influential spreaders respectively. Recent approaches in these two topics are presented. For the identification of privileged single spreaders, we summarize several widely used centralities, such as degree, betweenness centrality, PageRank, k-shell, etc. We investigate the empirical diffusion data in a large scale online social community—LiveJournal. With this extensive dataset, we find that various measures can convey very distinct information of nodes. Of all the users in the LiveJournal social network, only a small fraction of them are involved in spreading. For the spreading processes in LiveJournal, while degree can locate nodes participating in information diffusion with higher probability, k-shell is more effective in finding nodes with a large influence. Our results should provide useful information for designing efficient spreading strategies in reality.

  20. Assessment of Renal Ischemia By Optical Spectroscopy

    Energy Technology Data Exchange (ETDEWEB)

    Fitzgerald, J T; Demos, S; Michalopoulou, A; Pierce, J L; Troppmann, C

    2004-01-07

    Introduction: No reliable method currently exists for quantifying the degree of warm ischemia in kidney grafts prior to transplantation. We describe a method for evaluating pretransplant warm ischemia time using optical spectroscopic methods. Methods: Lewis rat kidney vascular pedicles were clamped unilaterally in vivo for 0, 5, 10, 20, 30, 60, 90 or 120 minutes; 8 animals were studied at each time point. Injured and contra-lateral control kidneys were then flushed with Euro-Collins solution, resected and placed on ice. 335 nm excitation autofluorescence as well as cross polarized light scattering images were taken of each injured and control kidney using filters of various wavelengths. The intensity ratio of the injured to normal kidneys was compared to ischemia time. Results: Autofluorescence intensity ratios through a 450 nm filter and light scattering intensity ratios through an 800 nm filter both decreased significantly with increasing ischemia time (p < 0.0001 for each method, one-way ANOVA). All adjacent and non-adjacent time points between 0 and 90 minutes were distinguishable using one of these two modalities by Fisher's PLSD. Conclusions: Optical spectroscopic methods can accurately quantify warm ischemia time in kidneys that have been subsequently hypothermically preserved. Further studies are needed to correlate results with physiological damage and posttransplant performance.

  1. Proper Treatment of Acute Mesenteric Ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Sung Kwan; Han, Young Min [Dept. of Radiology, Chonbuk National University Hospital and School of Medicine, Jeonju (Korea, Republic of); Kwak, Hyo Sung [Research Institue of Clinical Medicine, Chonbuk National University Hospital and School of Medicine, Jeonju (Korea, Republic of); Yu, Hee Chul [Dept. of Radiology, Chonbuk National University Hospital and School of Medicine, Jeonju (Korea, Republic of)

    2011-10-15

    To evaluate the effectiveness of treatment options for Acute Mesenteric Ischemia and establish proper treatment guidelines. From January 2007 to May 2010, 14 patients (13 men and 1 woman, mean age: 52.1 years) with acute mesenteric ischemia were enrolled in this study. All of the lesions were detected by CT scan and angiography. Initially, 4 patients underwent conservative treatment. Eleven patients were managed by endovascular treatment. We evaluated the therapeutic success and survival rate of each patient. The causes of ischemia included thromboembolism in 6 patients and dissection in 8 patients. Nine patients showed bowel ischemia on CT scans, 4 dissection patients underwent conservative treatment, 3 patients had recurring symptoms, and 5 dissection patients underwent endovascular treatment. Overall success and survival rate was 100%. However, overall success was 83% and survival rate was 40% in the 6 thromboembolism patients. The choice of 20 hours as the critical time in which the procedure is ideally performed was statistically significant (p = 0.0476). A percutaneous endovascular procedure is an effective treatment for acute mesenteric ischemia, especially in patients who underwent treatment within 20 hours. However, further study and a long term follow-up are needed.

  2. Protective effects of icariin on neurons injured by cerebral ischemia/reperfusion

    Institute of Scientific and Technical Information of China (English)

    LI Li; ZHOU Qi-xin; SHI Jing-shan

    2005-01-01

    Background It is very important to search for novel anti-ischemia/reperfusion neuroprotective drugs for prevention or treatment of cerebrovascular diseases. Icariin, the major active component of traditional Chinese herb Yinyanghuo, may have a beneficial role for neurons in cerebral ischemia/reperfusion caused by accident. However, it was not clear yet. In this study, we observed the protective effects of icariin on neurons injured by ischemia/reperfusion in vitro and in vivo and investigated its protective mechanism.Methods Cerebral cortical neurons of Wistar rats in primary culture were studied during the different periods of oxygen-glucose deprivation and reperfusion with oxygen and glucose. Cell viability was determined by methyl thiazoleterazolium (MTT) assay. The activity of lactate dehydrogenase (LDH) leaked from neurons, cell apoptosis and the concentration of intracellular free calcium were measured respectively. On the other hand, the mice model of transient cerebral ischemia/reperfusion was made by bilateral occlusion of common carotid arteries and ischemic hypotension/reperfusion. The mice were divided into several groups at random: sham operated group, model group and icariin preventive treatment group. The changes of mice behavioral, activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured, respectively. Results Treatment with icariin (final concentration 0.25, 0.5, and 1 mg/L) during ischemia/reperfusion-mimetic incubation in vitro concentration-dependently attenuated neuronal damage with characteristics of increasing injured neuronal absorbance of MTT, decreasing LDH release, decreasing cell apoptosis, and blunting elevation of intracellular calcium concentration. And in vivo the learning and memory abilities significantly decreased,activities of SOD were diminished and MDA level increased obviously in model group,compared with that in sham operated group. But pre-treatment of model mice with icariin (10, 30

  3. Cortical myoclonus in Huntington's disease.

    Science.gov (United States)

    Thompson, P D; Bhatia, K P; Brown, P; Davis, M B; Pires, M; Quinn, N P; Luthert, P; Honovar, M; O'Brien, M D; Marsden, C D

    1994-11-01

    We describe three patients with Huntington's disease, from two families, in whom myoclonus was the predominant clinical feature. The diagnosis was confirmed at autopsy in two cases and by DNA analysis in all three. These patients all presented before the age of 30 years and were the offspring of affected fathers. Neurophysiological studies documented generalised and multifocal action myoclonus of cortical origin that was strikingly stimulus sensitive, without enlargement of the cortical somatosensory evoked potential. The myoclonus improved with piracetam therapy in one patient and a combination of sodium valproate and clonazepam in the other two. Cortical reflex myoclonus is a rare but disabling component of the complex movement disorder of Huntington's disease, which may lead to substantial diagnostic difficulties.

  4. Grid cells and cortical representation.

    Science.gov (United States)

    Moser, Edvard I; Roudi, Yasser; Witter, Menno P; Kentros, Clifford; Bonhoeffer, Tobias; Moser, May-Britt

    2014-07-01

    One of the grand challenges in neuroscience is to comprehend neural computation in the association cortices, the parts of the cortex that have shown the largest expansion and differentiation during mammalian evolution and that are thought to contribute profoundly to the emergence of advanced cognition in humans. In this Review, we use grid cells in the medial entorhinal cortex as a gateway to understand network computation at a stage of cortical processing in which firing patterns are shaped not primarily by incoming sensory signals but to a large extent by the intrinsic properties of the local circuit.

  5. Paroxysmal kinesigenic dyskinesia : Cortical or non-cortical origin

    NARCIS (Netherlands)

    van Strien, Teun W.; van Rootselaar, Anne-Fleur; Hilgevoord, Anthony A. J.; Linssen, Wim H. J. P.; Groffen, Alexander J. A.; Tijssen, Marina A. J.

    2012-01-01

    Paroxysmal kinesigenic dyskinesia (PKD) is characterized by involuntary dystonia and/or chorea triggered by a sudden movement. Cases are usually familial with an autosomal dominant inheritance. Hypotheses regarding the pathogenesis of PKD focus on the controversy whether PKD has a cortical or non-co

  6. Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia

    DEFF Research Database (Denmark)

    Astrup, J; Symon, L; Branston, N M;

    1977-01-01

    As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory...

  7. [Chronic cerebral ischemia associated with Raynaud's syndrome].

    Science.gov (United States)

    Putilina, M V

    2015-01-01

    Over the last years, a number of patients with chronic cerebral ischemia has been increased significantly. Compensatory possibilities of the brain and cerebral circulatory system are so great that even serious disturbances of blood circulation could not cause clinical signs of brain dysfunction for a long time. At the same time, long-term ischemia can lead to peripheral local disturbances of microcirculation that is appears to be a first signal of the problems with homeostasis. Therefore, Raynaud's syndrome may be one of the predictors of standard symptoms of chronic cerebral ischemia (CCI). This phenomenon is explicitly considered as a sign of blood circulation impairment while the pathogenetic mechanism of vascular arterial bed instability is completely ignored. Detailed study of clinical correlations of Raynaud's syndrome in CCI would help to develop a common pharmacotherapeutic approach to its treatment.

  8. CSF transthyretin neuroprotection in a mouse model of brain ischemia

    DEFF Research Database (Denmark)

    Santos, Sofia Duque; Lambertsen, Kate Lykke; Clausen, Bettina Hjelm

    2010-01-01

    Brain injury caused by ischemia is a major cause of human mortality and physical/cognitive disability worldwide. Experimentally, brain ischemia can be induced surgically by permanent middle cerebral artery occlusion. Using this model, we studied the influence of transthyretin in ischemic stroke...... neuronal cell death, edema and inflammation, thereby influencing the survival of endangered neurons in cerebral ischemia....

  9. Pyruvate-Enhanced Resuscitation for Hemorrhagic Shock and Hindlimb Ischemia

    Science.gov (United States)

    2015-06-06

    Pyruvate-Enhanced Resuscitation for Hemorrhagic Shock and Hindlimb Ischemia The overall goals of this investigation were to test the ability of...Final Report: Pyruvate-Enhanced Resuscitation for Hemorrhagic Shock and Hindlimb Ischemia Report Title The overall goals of this investigation were to...during ischemia -reperfusion injury and cause cellular damage which likely contributes to myocardial contractile dysfunction. ROS oxidize and

  10. Modulation of cerebral RAGE expression following nitric oxide synthase inhibition in rats subjected to focal cerebral ischemia.

    Science.gov (United States)

    Greco, Rosaria; Demartini, Chiara; Zanaboni, Anna Maria; Blandini, Fabio; Amantea, Diana; Tassorelli, Cristina

    2017-04-05

    The receptor for advanced glycation endproducts (RAGE) is a key mediator of neuroinflammation following cerebral ischemia. Nitric oxide (NO) plays a dualistic role in cerebral ischemia, depending on whether it originates from neuronal, inducible or endothelial synthase. Although a dynamic interplay between RAGE and NO pathways exists, its relevance in ischemic stroke has not been investigated. The aim of this study is to evaluate the effect of the NO synthase (NOS) inhibition on RAGE expression in rats subjected to transient middle cerebral artery occlusion (tMCAo). Full-length (fl-RAGE) gene expression was elevated in the striatum and, to a lesser extent, in the cortex of rats undergone tMCAo. The exacerbation of cortical damage caused by systemic administration of L-N-(1-iminoethyl)ornithine (L-NIO), a relatively selective inhibitor of endothelial NOS (eNOS), was associated with elevated mRNA levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α and fl-RAGE in both the cortex and the striatum. Conversely, NG-nitro-l-arginine methyl ester (L-NAME), a non-selective NOS inhibitor, decreased cortical damage, did not affect cerebral cytokine mRNA levels, while it increased fl-RAGE mRNA expression only in the striatum. Fl-RAGE striatal protein levels varied accordingly with observed mRNA changes in the striatum, while in the cortex, RAGE protein levels were reduced by tMCAo and further decreased following L-NIO treatment. Modulation of RAGE expression by different inhibitors of NOS may have opposite effects on transient cortical ischemia: the non selective inhibition of NOS activity is protective, while the selective inhibition of eNOS is harmful, probably via the activation of inflammatory pathways. Copyright © 2017 Elsevier B.V. All rights reserved.

  11. Recurrent Spontaneous Spreading Depolarizations Facilitate Acute Dendritic Injury in the Ischemic Penumbra

    OpenAIRE

    Risher, W Christopher; Ard, Deborah; Yuan, Jianghe; Kirov, Sergei A.

    2010-01-01

    Spontaneous spreading depolarizations (SDs) occur in the penumbra surrounding ischemic core. These SDs, often referred to as peri-infarct depolarizations, cause vasoconstriction and recruitment of the penumbra into the ischemic core in the critical first hours after focal ischemic stroke; however, the real-time spatiotemporal dynamics of SD-induced injury to synaptic circuitry in the penumbra remain unknown. A modified cortical photothrombosis model was used to produce a square-shaped lesion ...

  12. Spreading lengths of Hermite polynomials

    CERN Document Server

    Sánchez-Moreno, P; Manzano, D; Yáñez, R; 10.1016/j.cam.2009.09.043

    2009-01-01

    The Renyi, Shannon and Fisher spreading lengths of the classical or hypergeometric orthogonal polynomials, which are quantifiers of their distribution all over the orthogonality interval, are defined and investigated. These information-theoretic measures of the associated Rakhmanov probability density, which are direct measures of the polynomial spreading in the sense of having the same units as the variable, share interesting properties: invariance under translations and reflections, linear scaling and vanishing in the limit that the variable tends towards a given definite value. The expressions of the Renyi and Fisher lengths for the Hermite polynomials are computed in terms of the polynomial degree. The combinatorial multivariable Bell polynomials, which are shown to characterize the finite power of an arbitrary polynomial, play a relevant role for the computation of these information-theoretic lengths. Indeed these polynomials allow us to design an error-free computing approach for the entropic moments (w...

  13. Epidemic spreading by objective traveling

    Science.gov (United States)

    Tang, Ming; Liu, Zonghua; Li, Baowen

    2009-07-01

    A fundamental feature of agent traveling in social networks is that traveling is usually not a random walk but with a specific destination and goes through the shortest path from starting to destination. A serious consequence of the objective traveling is that it may result in a fast epidemic spreading, such as SARS etc. In this letter we present a reaction-traveling model to study how the objective traveling influences the epidemic spreading. We consider a random scale-free meta-population network with sub-population at each node. Through a SIS model we theoretically prove that near the threshold of epidemic outbreak, the objective traveling can significantly enhance the final infected population and the infected fraction at a node is proportional to its betweenness for the traveling agents and approximately proportional to its degree for the non-traveling agents. Numerical simulations have confirmed the theoretical predictions.

  14. Region-specific effects on brain metabolites of hypoxia and hyperoxia overlaid on cerebral ischemia in young and old rats: a quantitative proton magnetic resonance spectroscopy study

    Directory of Open Access Journals (Sweden)

    Giuliani Patricia

    2010-02-01

    Full Text Available Abstract Background Both hypoxia and hyperoxia, deregulating the oxidative balance, may play a role in the pathology of neurodegenerative disorders underlain by cerebral ischemia. In the present study, quantitative proton magnetic resonance spectroscopy was used to evaluate regional metabolic alterations, following a 24-hour hypoxic or hyperoxic exposure on the background of ischemic brain insult, in two contrasting age-groups of rats: young - 3 months old and aged - 24 months old. Methods Cerebral ischemia was induced by ligation of the right common carotid artery. Concentrations of eight metabolites (alanine, choline-containing compounds, total creatine, γ-aminobutyric acid, glutamate, lactate, myo-inositol and N-acetylaspartate were quantified from extracts in three different brain regions (fronto-parietal and occipital cortices and the hippocampus from both hemispheres. Results In the control normoxic condition, there were significant increases in lactate and myo-inositol concentrations in the hippocampus of the aged rats, compared with the respective values in the young ones. In the ischemia-hypoxia condition, the most prevalent changes in the brain metabolites were found in the hippocampal regions of both young and aged rats; but the effects were more evident in the aged animals. The ischemia-hyperoxia procedure caused less dedicated changes in the brain metabolites, which may reflect more limited tissue damage. Conclusions We conclude that the hippocampus turns out to be particularly susceptible to hypoxia overlaid on cerebral ischemia and that old age further increases this susceptibility.

  15. Equatorial Spread F Fossil Plumes

    Science.gov (United States)

    2010-11-01

    Satyanarayana , P., and Ossakow, S. L.: The morphology of a multi-bubble system in the ionosphere, J. Geophys. Res., 88, 5528–5536, 1983. de La Beaujardiere...Haerendel, G.: Theory of equatorial spread F , preprint, Max Planck Inst. Extraterr. Phys., Munich, Germany, 1974. Haerendel, G., Eccles, J. V ., and...weather issues, J. Atmos. Terr. Phys., 58, 1527–1574, 1996. Sekar, R., Chakrabarty, D., Sarkhel, S., Patra, A. K., Devasia, C. V ., and Kelley, M. C

  16. Technique of green mulch spreading

    OpenAIRE

    Schäfer, Winfried; Väisänen, Jaana; Pihala, Marjo

    2001-01-01

    Finland’s policy of subsidising the conversion to organic production precipitated the rapid growth of organic farming in the 1990’s. As a consequence, many stockless farms encountered the problems of nitrogen deficit, poor grain quality, and weed control. Since the spreading of green mulch on cash crops is very common especially in tropical agriculture, organic fertilisers like green mulch may be an alternative that would compensate for the prohibition on the use of mineral N-fertilisers. How...

  17. Quality Improvement of Cheese Spread

    Science.gov (United States)

    2008-02-25

    Annatto (2% bixin) 3.5 mL Use as needed to conform color Vitamin A 0.14 0.003 Not less than 800 retinol units Added to comply with product...for samples with citrates (CIT) and altered levels of phosphates (LP) (Table 7). Although the citrates and phosphates have similar ionic components...Effect of vitamins The guidelines for cheese spread fortification include the addition of retinol (vitamin A), thiamine (vitamin B1), pyridoxine

  18. Physically Protected Spread Spectrum Communications

    Science.gov (United States)

    2016-04-14

    for the FH system in those days was because of implementation issues, such as a frequency -ringing problem , which occurred whenever a frequency was...PS-TR-2016-0046 HAS BEEN REVIEWED AND IS APPROVED FOR PUBLICATION IN ACCORDANCE WITH ASSIGNED DISTRIBUTION STATEMENT. KHANH PHAM PAUL D. LEVAN...keying (MPSK) and M-ary quadrature amplitude-shift keying (MQAM) for a slow frequency hopping (FH) spread spectrum (SS) system because, recently

  19. Face activated neurodynamic cortical networks.

    Science.gov (United States)

    Susac, Ana; Ilmoniemi, Risto J; Ranken, Doug; Supek, Selma

    2011-05-01

    Previous neuroimaging studies have shown that complex visual stimuli, such as faces, activate multiple brain regions, yet little is known on the dynamics and complexity of the activated cortical networks during the entire measurable evoked response. In this study, we used simulated and face-evoked empirical MEG data from an oddball study to investigate the feasibility of accurate, efficient, and reliable spatio-temporal tracking of cortical pathways over prolonged time intervals. We applied a data-driven, semiautomated approach to spatio-temporal source localization with no prior assumptions on active cortical regions to explore non-invasively face-processing dynamics and their modulation by task. Simulations demonstrated that the use of multi-start downhill simplex and data-driven selections of time intervals submitted to the Calibrated Start Spatio-Temporal (CSST) algorithm resulted in improved accuracy of the source localization and the estimation of the onset of their activity. Locations and dynamics of the identified sources indicated a distributed cortical network involved in face processing whose complexity was task dependent. This MEG study provided the first non-invasive demonstration, agreeing with intracranial recordings, of an early onset of the activity in the fusiform face gyrus (FFG), and that frontal activation preceded parietal for responses elicited by target faces.

  20. Different effects of thiopental in severe hypoxia, total ischemia and low-flow ischemia in rat heart muscle

    NARCIS (Netherlands)

    Ruigrok, T.J.C.; Slade, A.M.; Meer, P. van der; Moes, D. de; Sinclair, D.M.; Poole-Wilson, P.A.; Meijler, F.L.

    1985-01-01

    The effect of thiopental (100 mg .1-1) during total ischemia, low-flow ischemia, and severe hypoxia with maintained flow was investigated in the isolated perfused rat heart. During total ischemia the rate of decline of tissue creatine phosphate and adenosine triphosphate was no different in thiopent

  1. Drop Spreading with Random Viscosity

    Science.gov (United States)

    Xu, Feng; Jensen, Oliver

    2016-11-01

    Airway mucus acts as a barrier to protect the lung. However as a biological material, its physical properties are known imperfectly and can be spatially heterogeneous. In this study we assess the impact of these uncertainties on the rate of spreading of a drop (representing an inhaled aerosol) over a mucus film. We model the film as Newtonian, having a viscosity that depends linearly on the concentration of a passive solute (a crude proxy for mucin proteins). Given an initial random solute (and hence viscosity) distribution, described as a Gaussian random field with a given correlation structure, we seek to quantify the uncertainties in outcomes as the drop spreads. Using lubrication theory, we describe the spreading of the drop in terms of a system of coupled nonlinear PDEs governing the evolution of film height and the vertically-averaged solute concentration. We perform Monte Carlo simulations to predict the variability in the drop centre location and width (1D) or area (2D). We show how simulation results are well described (at much lower computational cost) by a low-order model using a weak disorder expansion. Our results show for example how variability in the drop location is a non-monotonic function of the solute correlation length increases. Engineering and Physical Sciences Research Council.

  2. Epidemic Spread in Human Networks

    CERN Document Server

    Sahneh, Faryad Darabi

    2011-01-01

    One of the popular dynamics on complex networks is the epidemic spreading. An epidemic model describes how infections spread throughout a network. Among the compartmental models used to describe epidemics, the Susceptible-Infected-Susceptible (SIS) model has been widely used. In the SIS model, each node can be susceptible, become infected with a given infection rate, and become again susceptible with a given curing rate. In this paper, we add a new compartment to the classic SIS model to account for human response to epidemic spread. Each individual can be infected, susceptible, or alert. Susceptible individuals can become alert with an alerting rate if infected individuals exist in their neighborhood. An individual in the alert state is less probable to become infected than an individual in the susceptible state; due to a newly adopted cautious behavior. The problem is formulated as a continuous-time Markov process on a general static graph and then modeled into a set of ordinary differential equations using...

  3. Spread of entanglement and causality

    CERN Document Server

    Casini, Horacio; Mezei, Márk

    2015-01-01

    We investigate causality constraints on the time evolution of entanglement entropy after a global quench in relativistic theories. We first provide a general proof that the so-called tsunami velocity is bounded by the speed of light. We then generalize the free particle streaming model of arXiv:cond-mat/0503393 to general dimensions and to an arbitrary entanglement pattern of the initial state. In more than two spacetime dimensions the spread of entanglement in these models is highly sensitive to the initial entanglement pattern, but we are able to prove an upper bound on the normalized rate of growth of entanglement entropy, and hence the tsunami velocity. The bound is smaller than what one gets for quenches in holographic theories, which highlights the importance of interactions in the spread of entanglement in many-body systems. We propose an interacting model which we believe provides an upper bound on the spread of entanglement for interacting relativistic theories. In two spacetime dimensions with multi...

  4. Spread of entanglement and causality

    Science.gov (United States)

    Casini, Horacio; Liu, Hong; Mezei, Márk

    2016-07-01

    We investigate causality constraints on the time evolution of entanglement entropy after a global quench in relativistic theories. We first provide a general proof that the so-called tsunami velocity is bounded by the speed of light. We then generalize the free particle streaming model of [1] to general dimensions and to an arbitrary entanglement pattern of the initial state. In more than two spacetime dimensions the spread of entanglement in these models is highly sensitive to the initial entanglement pattern, but we are able to prove an upper bound on the normalized rate of growth of entanglement entropy, and hence the tsunami velocity. The bound is smaller than what one gets for quenches in holographic theories, which highlights the importance of interactions in the spread of entanglement in many-body systems. We propose an interacting model which we believe provides an upper bound on the spread of entanglement for interacting relativistic theories. In two spacetime dimensions with multiple intervals, this model and its variations are able to reproduce intricate results exhibited by holographic theories for a significant part of the parameter space. For higher dimensions, the model bounds the tsunami velocity at the speed of light. Finally, we construct a geometric model for entanglement propagation based on a tensor network construction for global quenches.

  5. Cortical factor feedback model for cellular locomotion and cytofission.

    Directory of Open Access Journals (Sweden)

    Shin I Nishimura

    2009-03-01

    Full Text Available Eukaryotic cells can move spontaneously without being guided by external cues. For such spontaneous movements, a variety of different modes have been observed, including the amoeboid-like locomotion with protrusion of multiple pseudopods, the keratocyte-like locomotion with a widely spread lamellipodium, cell division with two daughter cells crawling in opposite directions, and fragmentations of a cell to multiple pieces. Mutagenesis studies have revealed that cells exhibit these modes depending on which genes are deficient, suggesting that seemingly different modes are the manifestation of a common mechanism to regulate cell motion. In this paper, we propose a hypothesis that the positive feedback mechanism working through the inhomogeneous distribution of regulatory proteins underlies this variety of cell locomotion and cytofission. In this hypothesis, a set of regulatory proteins, which we call cortical factors, suppress actin polymerization. These suppressing factors are diluted at the extending front and accumulated at the retracting rear of cell, which establishes a cellular polarity and enhances the cell motility, leading to the further accumulation of cortical factors at the rear. Stochastic simulation of cell movement shows that the positive feedback mechanism of cortical factors stabilizes or destabilizes modes of movement and determines the cell migration pattern. The model predicts that the pattern is selected by changing the rate of formation of the actin-filament network or the threshold to initiate the network formation.

  6. Active Chemical Thermodynamics promoted by activity of cortical actin

    Science.gov (United States)

    Bhattacharya, Bhaswati; Chaudhuri, Abhishek; Gowrishankar, Kripa; Rao, Madan

    2011-03-01

    The spatial distribution and dynamics of formation and breakup of the nanoclusters of cell surface proteins is controlled by the active remodeling dynamics of the underlying cortical actin. To explain these observations, we have proposed a novel mechanism of nanoclustering, involving the transient binding to and advection along constitutively occuring ``asters'' of cortical actin. We study the consequences of such active actin-based clustering, in the context of chemical reactions involving conformational changes of cell surface proteins. We find that the active remodeling of cortical actin, can give rise to a dramatic increase in efficiency and extent of conformational spread, even at low levels of expression at the cell surface. We define a activity temperature (τa) arising due to actin activities which can be used to describe chemical thermodynamics of the system. We plot TTT (time-temparature-transformation) curves and compute the Arrhenius factors which depend on τa . With this, the active asters can be treated as enzymes whose enzymatic reaction rate can be related to the activity.

  7. Cultured networks of excitatory projection neurons and inhibitory interneurons for studying human cortical neurotoxicity.

    Science.gov (United States)

    Xu, Jin-Chong; Fan, Jing; Wang, Xueqing; Eacker, Stephen M; Kam, Tae-In; Chen, Li; Yin, Xiling; Zhu, Juehua; Chi, Zhikai; Jiang, Haisong; Chen, Rong; Dawson, Ted M; Dawson, Valina L

    2016-04-06

    Translating neuroprotective treatments from discovery in cell and animal models to the clinic has proven challenging. To reduce the gap between basic studies of neurotoxicity and neuroprotection and clinically relevant therapies, we developed a human cortical neuron culture system from human embryonic stem cells or human inducible pluripotent stem cells that generated both excitatory and inhibitory neuronal networks resembling the composition of the human cortex. This methodology used timed administration of retinoic acid to FOXG1(+) neural precursor cells leading to differentiation of neuronal populations representative of the six cortical layers with both excitatory and inhibitory neuronal networks that were functional and homeostatically stable. In human cortical neuronal cultures, excitotoxicity or ischemia due to oxygen and glucose deprivation led to cell death that was dependent on N-methyl-D-aspartate (NMDA) receptors, nitric oxide (NO), and poly(ADP-ribose) polymerase (PARP) (a cell death pathway called parthanatos that is distinct from apoptosis, necroptosis, and other forms of cell death). Neuronal cell death was attenuated by PARP inhibitors that are currently in clinical trials for cancer treatment. This culture system provides a new platform for the study of human cortical neurotoxicity and suggests that PARP inhibitors may be useful for ameliorating excitotoxic and ischemic cell death in human neurons.

  8. Reverse preferential spread in complex networks

    Science.gov (United States)

    Toyoizumi, Hiroshi; Tani, Seiichi; Miyoshi, Naoto; Okamoto, Yoshio

    2012-08-01

    Large-degree nodes may have a larger influence on the network, but they can be bottlenecks for spreading information since spreading attempts tend to concentrate on these nodes and become redundant. We discuss that the reverse preferential spread (distributing information inversely proportional to the degree of the receiving node) has an advantage over other spread mechanisms. In large uncorrelated networks, we show that the mean number of nodes that receive information under the reverse preferential spread is an upper bound among any other weight-based spread mechanisms, and this upper bound is indeed a logistic growth independent of the degree distribution.

  9. Tenoxicam exerts a neuroprotective action after cerebral ischemia in rats.

    Science.gov (United States)

    Galvão, Rita I M; Diógenes, João P L; Maia, Graziela C L; Filho, Emídio A S; Vasconcelos, Silvânia M M; de Menezes, Dalgimar B; Cunha, Geanne M A; Viana, Glauce S B

    2005-01-01

    In this study we investigated the effects of Tenoxicam, a type 2 cyclooxygenase (COX-2) inhibitor, on brain damage induced by ischemia-reperfusion. Male Wistar rats (18-month old average) were anesthetized and submitted to ischemia occlusion of both common carotid arteries (BCAO) for 45 min. After 24 h of reperfusion, rats were decapitated and hippocampi removed for further assays. Animals were divided into sham-operated, ischemia, ischemia + Tenoxicam 2.5 mg/kg, and ischemia + Tenoxicam 10 mg/kg groups. Tenoxicam was administered intraperitoneally immediately after BCAO. Histological analyses show that ischemia produced significant striatal as well as hippocampal lesions which were reversed by the Tenoxicam treatment. Tenoxicam also significantly reduced, to control levels, the increased myeloperoxidase activity in hippocampus homogenates observed after ischemia. However, nitrite concentrations showed only a tendency to decrease in the ischemia + Tenoxicam groups, as compared to that of ischemia alone. On the other hand, hippocampal glutamate and aspartate levels were not altered by Tenoxicam. In conclusion, we showed that ischemia is certainly related to inflammation and to increased free radical production, and selective COX-2 inhibitors might be neuroprotective agents of potential benefit in the treatment of cerebral brain ischemia.

  10. Recent progress in migraine pathophysiology: role of cortical spreading depression and magnetic resonance imaging

    NARCIS (Netherlands)

    Bhaskar, S.; Saeidi, K.; Borhani, P.; Amiri, H.

    2013-01-01

    Migraine is characterised by debilitating pain, which affects the quality of life in affected patients in both the western and the eastern worlds. The purpose of this article is to give a detailed outline of the pathophysiology of migraine pain, which is one of the most confounding pathologies among

  11. Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer's pathology

    OpenAIRE

    Schmitz, Taylor W.; Nathan Spreng, R.; Weiner, Michael W.; Aisen, Paul; Petersen, Ronald; Jack, Clifford R; Jagust, William; Trojanowki, John Q.; Toga, Arthur W; Beckett, Laurel; Green, Robert C.; Saykin, Andrew J.; Morris, John; Leslie M Shaw; Khachaturian, Zaven

    2016-01-01

    There is considerable debate whether Alzheimer's disease (AD) originates in basal forebrain or entorhinal cortex. Here we examined whether longitudinal decreases in basal forebrain and entorhinal cortex grey matter volume were interdependent and sequential. In a large cohort of age-matched older adults ranging from cognitively normal to AD, we demonstrate that basal forebrain volume predicts longitudinal entorhinal degeneration. Models of parallel degeneration or entorhinal origin received ne...

  12. [Epidemiology of critical ischemia of the limbs].

    Science.gov (United States)

    Estevan, J M; Valle, A; Pacho, J

    1993-01-01

    Authors report their results from a study made during 1991. The study was made in order to analyze the clinical complications (morbidity and mortality) and the socioeconomic consequences that are related to the cure of patients with highly developed ischemic diseases (critical ischemia). Economic expenses mean a 1.5% from the total budget of the Public Sanity into the Asturian Autonomic Community.

  13. Innate immune signaling in cardiac ischemia

    NARCIS (Netherlands)

    Arslan, F.; de Kleijn, D.P.V.; Pasterkamp, G.

    2011-01-01

    Despite advances in treatment of patients who suffer from ischemic heart disease, morbidity related to myocardial infarction is increasing in Western societies. Acute and chronic immune responses elicited by myocardial ischemia have an important role in the functional deterioration of the heart. Res

  14. Geodynamic environments of ultra-slow spreading

    Science.gov (United States)

    Kokhan, Andrey; Dubinin, Evgeny

    2015-04-01

    Ultra-slow spreading is clearly distinguished as an outstanding type of crustal accretion by recent studies. Spreading ridges with ultra-slow velocities of extension are studied rather well. But ultra-slow spreading is characteristic feature of not only spreading ridges, it can be observed also on convergent and transform plate boundaries. Ultra-slow spreading is observed now or could have been observed in the past in the following geodynamic environments on divergent plate boundaries: 1. On spreading ridges with ultra-slow spreading, both modern (f.e. Gakkel, South-West Indian, Aden spreading center) and ceased (Labrador spreading center, Aegir ridge); 2. During transition from continental rifting to early stages of oceanic spreading (all spreading ridges during incipient stages of their formation); 3. During incipient stages of formation of spreading ridges on oceanic crust as a result of ridge jumps and reorganization of plate boundaries (f.e. Mathematicians rise and East Pacific rise); 4. During propagation of spreading ridge into the continental crust under influence of hotspot (Aden spreading center and Afar triple junction), under presence of strike-slip faults preceding propagation (possibly, rift zone of California Bay). Ultra-slow spreading is observed now or could have been observed in the past in the following geodynamic environments on transform plate boundaries: 1. In transit zones between two "typical" spreading ridges (f.e. Knipovich ridge); 2. In semi strike-slip/extension zones on the oceanic crust (f.e. American-Antarctic ridge); 3. In the zones of local extension in regional strike-slip areas in pull-apart basins along transform boundaries (Cayman trough, pull-apart basins of the southern border of Scotia plate). Ultra-slow spreading is observed now or could have been observed in the past in the following geodynamic environments on convergent plate boundaries: 1. During back-arc rifting on the stage of transition into back-arc spreading (central

  15. Motor cortical thresholds and cortical silent periods in epilepsy.

    Science.gov (United States)

    Tataroglu, Cengiz; Ozkiziltan, Safa; Baklan, Baris

    2004-10-01

    We studied motor cortical thresholds (TIs) and cortical silent periods (SPs) evoked by transcranial magnetic stimulation (TMS) in 110 epileptic patients. Sixty-two had primary generalised, 48 had partial type seizures. Fifteen out 110 patients were analysed both before and after anticonvulsant medication. Our aims were to evaluate the TI levels and the duration of SPs in patients with epilepsy and to determine the reliability of TMS in patients with epilepsy. There was no negative effect of TMS on the clinical status and EEG findings in patients with epilepsy. TIs obtained from patients with partial epilepsy were higher than those obtained from both controls and primary epileptics. The duration of SP in patients with primary epileptics was more prolonged than those obtained from controls. There was no correlation between EEG lateralisation and both SP duration and TI values. In de novo patient group, SP duration was significantly prolonged after anticonvulsant medication. We concluded that TMS is a reliable electrophysiological investigation in patients with epilepsy. The analysis of SP duration may be an appropriate investigation in monitoring the effect of anticonvulsant medication on the cortical inhibitory activity.

  16. Diagnosis and management of splanchnic ischemia

    Institute of Scientific and Technical Information of China (English)

    Jeroen J Kolkman; Marloes Bargeman; Ad B Huisman; Robert H Geelkerken

    2008-01-01

    Splanchnic or gastrointestinal ischemia is rare and randomized studies are absent.This review focuses on new developments in clinical presentation,diagnostic approaches,and treatments.Splanchnic ischemia can be caused by occlusions of arteries or veins and by physiological vasoconstriction during low-flow states.The prevalence of significant splanchnic arterial stenoses is high,but it remains mostly asymptomatic due to abundant collateral circulation.This is known as chronic splanchnic disease (CSD).Chronic splanchnic syndrome (CSS) occurs when ischemic symptoms develop.Ischemic symptoms are characterized by postprandial pain,fear of eating and weight loss.CSS is diagnosed by a test for actual ischemia.Recently,gastro-intestinal tonometry has been validated as a diagnostic test to detect splanchnic ischemia and to guide treatment.In singlevessel CSD,the complication rate is very low,but some patients have ischemic complaints,and can be treated successfully.In multi-vessel stenoses,the complication rate is considerable,while most have CSS and treatment should be strongly considered.CT and MR-based angiographic reconstruction techniques have emerged as alternatives for digital subtraction angiography for imaging of splanchnic vessels.Duplex ultrasound is still the first choice for screening purposes.The strengths and weaknesses of each modality will be discussed.CSS may be treated by minimally invasive endoscopic treatment of the celiac axis compression syndrome,endovascular antegrade stenting,or laparotomy-assisted retrograde endovascular recanalization and stenting.The treatment plan is highly individualized and is mainly based on precise vessel anatomy,body weight,comorbidity and severity of ischemia.

  17. TDCS increases cortical excitability: direct evidence from TMS-EEG.

    Science.gov (United States)

    Romero Lauro, Leonor J; Rosanova, Mario; Mattavelli, Giulia; Convento, Silvia; Pisoni, Alberto; Opitz, Alexander; Bolognini, Nadia; Vallar, Giuseppe

    2014-09-01

    Despite transcranial direct current stimulation (tDCS) is increasingly used in experimental and clinical settings, its precise mechanisms of action remain largely unknown. At a neuronal level, tDCS modulates the resting membrane potential in a polarity-dependent fashion: anodal stimulation increases cortical excitability in the stimulated region, while cathodal decreases it. So far, the neurophysiological underpinnings of the immediate and delayed effects of tDCS, and to what extent the stimulation of a given cerebral region may affect the activity of anatomically connected regions, remain unclear. In the present study, we used a combination of Transcranial Magnetic Stimulation (TMS) and Electroencephalography (EEG) in order to explore local and global cortical excitability modulation during and after active and sham tDCS. Single pulse TMS was delivered over the left posterior parietal cortex (PPC), before, during, and after 15 min of tDCS over the right PPC, while EEG was recorded from 60 channels. For each session, indexes of global and local cerebral excitability were obtained, computed as global and local mean field power (Global Mean Field Power, GMFP and Local Mean Field Power, LMFP) on mean TMS-evoked potentials (TEPs) for three temporal windows: 0-50, 50-100, and 100-150 msec. The global index was computed on all 60 channels. The local indexes were computed in six clusters of electrodes: left and right in frontal, parietal and temporal regions. GMFP increased, compared to baseline, both during and after active tDCS in the 0-100 msec temporal window. LMFP increased after the end of stimulation in parietal and frontal clusters bilaterally, while no difference was found in the temporal clusters. In sum, a diffuse rise of cortical excitability occurred, both during and after active tDCS. This evidence highlights the spreading of the effects of anodal tDCS over remote cortical regions of stimulated and contralateral hemispheres.

  18. Plume spread and atmospheric stability

    Energy Technology Data Exchange (ETDEWEB)

    Weber, R.O. [Paul Scherrer Inst. (PSI), Villigen (Switzerland)

    1999-08-01

    The horizontal spread of a plume in atmospheric dispersion can be described by the standard deviation of horizontal direction. The widely used Pasquill-Gifford classes of atmospheric stability have assigned typical values of the standard deviation of horizontal wind direction and of the lapse rate. A measured lapse rate can thus be used to estimate the standard deviation of wind direction. It is examined by means of a large dataset of fast wind measurements how good these estimates are. (author) 1 fig., 2 refs.

  19. Liquid Spreading under Nanoscale Confinement

    Science.gov (United States)

    Checco, Antonio

    2009-03-01

    Dynamic atomic force microscopy in the noncontact regime is used to study the morphology of a nonvolatile liquid (squalane) as it spreads along wettable nanostripes embedded in a nonwettable surface. Results show that the liquid profile depends on the amount of lateral confinement imposed by the nanostripes, and it is truncated at the microscopic contact line in good qualitative agreement with classical mesoscale hydrodynamics. However, the width of the contact line is found to be significantly larger than expected theoretically. This behavior may originate from small chemical inhomogeneity of the patterned stripes as well as from thermal fluctuations of the contact line.

  20. Spreading widths of doorway states

    Energy Technology Data Exchange (ETDEWEB)

    De Pace, A., E-mail: depace@to.infn.i [Istituto Nazionale di Fisica Nucleare, Sezione di Torino, via P. Giuria 1, I-10125 Torino (Italy); Molinari, A. [Dipartimento di Fisica Teorica dell' Universita di Torino, via P. Giuria 1, I-10125 Torino (Italy); Istituto Nazionale di Fisica Nucleare, Sezione di Torino, via P. Giuria 1, I-10125 Torino (Italy); Weidenmueller, H.A. [Max-Planck-Institut fuer Kernphysik, D-69029 Heidelberg (Germany)

    2011-01-01

    As a function of energy E, the average doorway strength function S(E)-bar of a doorway state is commonly assumed to be Lorentzian in shape and characterized by two parameters, the peak energy E{sub 0} and the spreading width {Gamma}{sup {down_arrow}}. The simple picture is modified when the density of background states that couple to the doorway state changes significantly in an energy interval of size {Gamma}{sup {down_arrow}}. For that case we derive an approximate analytical expression for S(E)-bar. We test our result successfully against numerical simulations. Our result may have important implications for shell-model calculations.

  1. Migration Helps Spread Bird Flu Worldwide

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_161473.html Migration Helps Spread Bird Flu Worldwide Scientists recommend keeping ... birds can spread bird flu worldwide and monitoring migration routes could provide early warning of outbreaks, researchers ...

  2. Lexical Ambiguity: Making a Case against Spread

    Science.gov (United States)

    Kaplan, Jennifer J.; Rogness, Neal T.; Fisher, Diane G.

    2012-01-01

    We argue for decreasing the use of the word "spread" when describing the statistical idea of dispersion or variability in introductory statistics courses. In addition, we argue for increasing the use of the word "variability" as a replacement for "spread."

  3. Unimodal primary sensory cortices are directly connected by long-range horizontal projections in the rat sensory cortex

    Directory of Open Access Journals (Sweden)

    Jimmy eStehberg

    2014-09-01

    Full Text Available Research based on functional imaging and neuronal recordings in the barrel cortex subdivision of primary somatosensory cortex (SI of the adult rat has revealed novel aspects of structure-function relationships in this cortex. Specifically, it has demonstrated that single whisker stimulation evokes subthreshold neuronal activity that spreads symmetrically within gray matter from the appropriate barrel area, crosses cytoarchitectural borders of SI and reaches deeply into other unimodal primary cortices such as primary auditory (AI and primary visual (VI. It was further demonstrated that this spread is supported by a spatially matching underlying diffuse network of border-crossing, long-range projections that could also reach deeply into AI and VI. Here we seek to determine whether such a network of border-crossing, long-range projections is unique to barrel cortex or characterizes also other primary, unimodal sensory cortices and therefore could directly connect them. Using anterograde (BDA and retrograde (CTb tract-tracing techniques, we demonstrate that such diffuse horizontal networks directly and mutually connect VI, AI and SI. These findings suggest that diffuse, border-crossing axonal projections connecting directly primary cortices are an important organizational motif common to all major primary sensory cortices in the rat. Potential implications of these findings for topics including cortical structure-function relationships, multisensory integration, functional imaging and cortical parcellation are discussed.

  4. Imprinting and recalling cortical ensembles.

    Science.gov (United States)

    Carrillo-Reid, Luis; Yang, Weijian; Bando, Yuki; Peterka, Darcy S; Yuste, Rafael

    2016-08-12

    Neuronal ensembles are coactive groups of neurons that may represent building blocks of cortical circuits. These ensembles could be formed by Hebbian plasticity, whereby synapses between coactive neurons are strengthened. Here we report that repetitive activation with two-photon optogenetics of neuronal populations from ensembles in the visual cortex of awake mice builds neuronal ensembles that recur spontaneously after being imprinted and do not disrupt preexisting ones. Moreover, imprinted ensembles can be recalled by single- cell stimulation and remain coactive on consecutive days. Our results demonstrate the persistent reconfiguration of cortical circuits by two-photon optogenetics into neuronal ensembles that can perform pattern completion. Copyright © 2016, American Association for the Advancement of Science.

  5. Cortical sensorimotor integration: a hypothesis.

    Science.gov (United States)

    Batuev, A S

    1989-01-01

    A hypothesis is proposed that neocortex is constructed from structural neuronal modules (columns and rings). Each module is considered as unit for cortical sensorimotor integration. Complex functional relationships between modules can be arranged by intracortical inhibition participation. High pronounced neocortical plasticity ensures the process of continuous formation of various dominating operative constellations comprising stable neuronal modules whose component structure and distributive characteristic are determined by the dominant motivation and the central motor program.

  6. The spreading of misinformation online.

    Science.gov (United States)

    Del Vicario, Michela; Bessi, Alessandro; Zollo, Fabiana; Petroni, Fabio; Scala, Antonio; Caldarelli, Guido; Stanley, H Eugene; Quattrociocchi, Walter

    2016-01-19

    The wide availability of user-provided content in online social media facilitates the aggregation of people around common interests, worldviews, and narratives. However, the World Wide Web (WWW) also allows for the rapid dissemination of unsubstantiated rumors and conspiracy theories that often elicit rapid, large, but naive social responses such as the recent case of Jade Helm 15--where a simple military exercise turned out to be perceived as the beginning of a new civil war in the United States. In this work, we address the determinants governing misinformation spreading through a thorough quantitative analysis. In particular, we focus on how Facebook users consume information related to two distinct narratives: scientific and conspiracy news. We find that, although consumers of scientific and conspiracy stories present similar consumption patterns with respect to content, cascade dynamics differ. Selective exposure to content is the primary driver of content diffusion and generates the formation of homogeneous clusters, i.e., "echo chambers." Indeed, homogeneity appears to be the primary driver for the diffusion of contents and each echo chamber has its own cascade dynamics. Finally, we introduce a data-driven percolation model mimicking rumor spreading and we show that homogeneity and polarization are the main determinants for predicting cascades' size.

  7. [Parietal Cortices and Body Information].

    Science.gov (United States)

    Naito, Eiichi; Amemiya, Kaoru; Morita, Tomoyo

    2016-11-01

    Proprioceptive signals originating from skeletal muscles and joints contribute to the formation of both the human body schema and the body image. In this chapter, we introduce various types of bodily illusions that are elicited by proprioceptive inputs, and we discuss distinct functions implemented by different parietal cortices. First, we illustrate the primary importance of the motor network in the processing of proprioceptive (kinesthetic) signals originating from muscle spindles. Next, we argue that the right inferior parietal cortex, in concert with the inferior frontal cortex (both regions connected by the inferior branch of the superior longitudinal fasciculus-SLF III), may be involved in the conscious experience of body image. Further, we hypothesize other functions of distinct parietal regions: the association between internal hand motor representation with external object representation in the left inferior parietal cortex, visuo-kinesthetic processing in the bilateral posterior parietal cortices, and the integration of somatic signals from different body parts in the higher-order somatosensory parietal cortices. Our results indicate that a distinct parietal region, in concert with its anatomically and functionally connected frontal regions, probably plays specialized roles in the processing of body-related information.

  8. Monitored extended secondary arterial ischemia in a free muscle transfer.

    Science.gov (United States)

    Sværdborg, Mille; Birke-Sørensen, Hanne

    2012-02-01

    In reconstructive microsurgery, flap failure can be catastrophic to the patient. Different monitoring methods have been implemented in an attempt to recognize secondary ischemia during its early stages. However, the exact onset of secondary ischemia can be difficult to determine because there are no well-documented and reliable monitoring techniques that offer true continuous monitoring in a clinical setting. Because of the uncertain time in terms of the onset of secondary ischemia, the exact length of ischemia before revascularization, the secondary ischemia time, cannot be obtained. This is probably part of the reason why not much has been published regarding the effect of secondary ischemia time in reference to flap survival. We present a case of a free gracilis muscle flap that was salvaged despite more than 11 hours of arterial ischemia. The flap was monitored using microdialysis and at no time was the ischemia clearly demonstrated by clinical inspection. We conclude that clinical monitoring in some cases can be an unreliable method for monitoring free muscle transfers suffering from arterial ischemia and that further studies are needed for more specific guidelines regarding the critical secondary ischemia time in muscle flaps.

  9. Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Bo Zhao; Wenwei Gao; Jiabao Hou; Yang Wu; Zhongyuan Xia

    2012-01-01

    The present study established global brain ischemia using the four-vessel occlusion method.Following three rounds of reperfusion for 30 seconds,and occlusion for 10 seconds,followed by reperfusion for 48 hours,infarct area,the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced.However,glycogen synthase kinase-3β activity,cortical Bax and caspase-3 expression significantly increased,similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity,a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway,which reduces caspase-3 expression to protect the brain against ischemic injury.

  10. The electrophysiological time course of the interaction of stimulus conflict and the multisensory spread of attention.

    Science.gov (United States)

    Zimmer, U; Itthipanyanan, S; Grent-'t-Jong, T; Woldorff, M G

    2010-05-01

    Previously, we have shown that spatial attention to a visual stimulus can spread across both space and modality to a synchronously presented but task-irrelevant sound arising from a different location, reflected by a late-onsetting, sustained, negative-polarity event-related potential (ERP) wave over frontal-central scalp sites, probably originating in part from the auditory cortices. Here we explore the influence of cross-modal conflict on the amplitude and temporal dynamics of this multisensory spreading-of-attention activity. Subjects attended selectively to one of two concurrently presented lateral visually-presented letter streams to perform a sequential comparison task, while ignoring task-irrelevant, centrally presented spoken letters that could occur synchronously with either the attended or unattended lateral visual letters and could be either congruent or incongruent with them. Extracted auditory ERPs revealed that, collapsed across congruency conditions, attentional spreading across modalities started at approximately 220 ms, replicating our earlier findings. The interaction between attentional spreading and conflict occurred beginning at approximately 300 ms, with attentional-spreading activity being larger for incongruent trials. Thus, the increased processing of an incongruent, task-irrelevant sound in a multisensory stimulation appeared to occur some time after attention has spread from the attended visual part to the ignored auditory part, presumably reflecting the conflict detection and associated attentional capture requiring accrual of some multisensory interaction processes at a higher-level semantic processing stage.

  11. Rumor spreading in gaming social networks

    CERN Document Server

    Zhang, Yichao; Guan, Jihong; Zhou, Shuigeng

    2011-01-01

    So far, the focus on rumor spreading are mainly on some simple backgrounds, in other words, only taking consideration of the overall topological influences on its dynamical behavior. However, in the prospect of the individuality, personal strategies in the social networks play a more non-trivial role in the real social networks. To fill this gap, we will investigate the rumor spreading in gaming social networks. Our analysis is supported by the results of numerical simulations. We observe that the original rumor is still the most well known edition in case that the content is modified by the defectors. However, the portion decays with the stimulus generally. For the case that defectors keep silence in the spreading process, the scale of spreading decays with stimulus generally, suggesting the rumor can hardly spread in a community of defectors. This highlights the key role that stimulus plays in rumor spreading and the necessity to study information spreading in competitive circumstances.

  12. Random Information Spread in Networks

    CERN Document Server

    Lapus, Raymond; Tittmann, Peter

    2010-01-01

    Let G=(V,E) be an undirected loopless graph with possible parallel edges and s and t be two vertices of G. Assume that vertex s is labelled at the initial time step and that every labelled vertex copies its labelling to neighbouring vertices along edges with one labelled endpoint independently with probability p in one time step. In this paper, we establish the equivalence between the expected s-t first arrival time of the above spread process and the notion of the stochastic shortest s-t path. Moreover, we give a short discussion of analytical results on special graphs including the complete graph and s-t series-parallel graphs. Finally, we propose some lower bounds for the expected s-t first arrival time.

  13. Bank Lending, Housing and Spreads

    DEFF Research Database (Denmark)

    Aslam, Aqib; Santoro, Emiliano

    The framework presented in this paper takes its cue from recent financial events and attempts to develop a tractable framework for policy analysis of macro-linkages, in particular a first attempt at the integration of an independent profit-maximising banking sector that lends to and borrows from...... agents in the economy, and through which changes in the monetary policy rate by the central bank are transmitted. The inter-linkages between housing and the role of the banking sector in the transmission of monetary policy is emphasized. Two competing effects are highlighted: (i) a financial accelerator...... channel, due to the presence of collateralized borrowers, and (ii) a banking attenuator effect, which crucially arises from the spread in interest rates caused by the introduction of monopolistically competitive financial intermediaries. We show how the classical amplification mechanism explored in models...

  14. Interpolating point spread function anisotropy

    CERN Document Server

    Gentile, M; Meylan, G

    2012-01-01

    Planned wide-field weak lensing surveys are expected to reduce the statistical errors on the shear field to unprecedented levels. In contrast, systematic errors like those induced by the convolution with the point spread function (PSF) will not benefit from that scaling effect and will require very accurate modeling and correction. While numerous methods have been devised to carry out the PSF correction itself, modeling of the PSF shape and its spatial variations across the instrument field of view has, so far, attracted much less attention. This step is nevertheless crucial because the PSF is only known at star positions while the correction has to be performed at any position on the sky. A reliable interpolation scheme is therefore mandatory and a popular approach has been to use low-order bivariate polynomials. In the present paper, we evaluate four other classical spatial interpolation methods based on splines (B-splines), inverse distance weighting (IDW), radial basis functions (RBF) and ordinary Kriging...

  15. Bank Lending, Housing and Spreads

    DEFF Research Database (Denmark)

    Aslam, Aqib; Santoro, Emiliano

    of private borrowing between collaterally-constrained 'impatient' households and unconstrained 'patient' households, such as those put forward by Kiyotaki and Moore (1997) and Iacoviello (2005), is counteracted by the banking attenuator effect, given an endogenous steady state spread between loan and savings......The framework presented in this paper takes its cue from recent financial events and attempts to develop a tractable framework for policy analysis of macro-linkages, in particular a first attempt at the integration of an independent profit-maximising banking sector that lends to and borrows from...... agents in the economy, and through which changes in the monetary policy rate by the central bank are transmitted. The inter-linkages between housing and the role of the banking sector in the transmission of monetary policy is emphasized. Two competing effects are highlighted: (i) a financial accelerator...

  16. Collateral blood flow in different cerebrovascular hierarchy provides endogenous protection in cerebral ischemia.

    Science.gov (United States)

    Luo, Chuanming; Liang, Fengyin; Ren, Huixia; Yao, Xiaoli; Liu, Qiang; Li, Mingyue; Qin, Dajiang; Yuan, Ti-Fei; Pei, Zhong; Su, Huanxing

    2016-11-15

    Collateral blood flow as vascular adaptions to focal cerebral ischemia is well recognized. However, few studies directly investigate the dynamics of collateral vessel recruitment in vivo and little is known about the effect of collateral blood flow in different cerebrovascular hierarchy on the neuropathology after focal ischemic stroke. Here, we report that collateral blood flow is critically involved in blood vessel compensations following regional ischemia. We occluded a pial arteriole using femtosecond laser ablating under the intact thinned skull and documented the changes of collateral flow around the surface communication network and between the surface communication network and subsurface microcirculation network using in vivo two photon microscopy imaging. Occlusion of the pial arteriole apparently increased the diameter and collateral blood flow of its leptomeningeal anastomoses, which significantly reduced the cortical infarction size. This result suggests that the collateral flow via surface communicating network connected with leptomeningeal anastomoses could greatly impact on the extent of infarction. We then further occluded the target pial arteriole and all of its leptomeningeal anastomoses. Notably, this type of occlusion led to reversals of blood flow in the penetrating arterioles mainly proximal to the occluded pial arteriole in a direction from the subsurface microcirculation network to surface arterioles. Interesting, the cell death in the area of ischemic penumbra was accelerated when we performed occlusion to cease the reversed blood flow in those penetrating arterioles, suggesting that the collateral blood flow from subsurface microcirculation network exerts protective roles in delaying cell death in the ischemic penumbra. In conclusion, we provide the first experimental evidence that collateral blood vessels at different cerebrovascular hierarchy are endogenously compensatory mechanisms in brain ischemia. This article is protected by

  17. Endovascular management of acute limb ischemia.

    Science.gov (United States)

    Peeters, P; Verbist, J; Keirse, K; Deloose, K; Bosiers, M

    2010-06-01

    Acute limb ischemia (ALI) refers to a rapid worsening of limb perfusion resulting in rest pain, ischemic ulcers or gangrene. With an estimated incidence of 140 million/year, ALI is serious limb-threatening and life-threatening medical emergency demanding prompt action. Three prospective, randomized clinical trials provide data on trombolytic therapy versus surgical intervention in patients with acute lower extremity ischemia. Although they did not give us the final answer, satisfactory results are reported for percutaneous thrombolysis compared with surgery. Moreover, they suggest an important advantage of thrombolysis in acute bypass graft occlusions. Therefore, we believe thrombolytic therapy should be a part of the vascular surgeon's armamentarium to safely and successfully treat ALI patients.

  18. Spinal cord ischemia secondary to hypovolemic shock.

    Science.gov (United States)

    Oh, Jacob Yl; Kapoor, Siddhant; Koh, Roy Km; Yang, Eugene Wr; Hee, Hwan-Tak

    2014-12-01

    A 44-year-old male presented with symptoms of spinal cord compression secondary to metastatic prostate cancer. An urgent decompression at the cervical-thoracic region was performed, and there were no complications intraoperatively. Three hours postoperatively, the patient developed acute bilateral lower-limb paralysis (motor grade 0). Clinically, he was in class 3 hypovolemic shock. An urgent magnetic resonance imaging (MRI) was performed, showing no epidural hematoma. He was managed aggressively with medical therapy to improve his spinal cord perfusion. The patient improved significantly, and after one week, he was able to regain most of his motor functions. Although not commonly reported, spinal cord ischemia post-surgery should be recognized early, especially in the presence of hypovolemic shock. MRI should be performed to exclude other potential causes of compression. Spinal cord ischemia needs to be managed aggressively with medical treatment to improve spinal cord perfusion. The prognosis depends on the severity of deficits, and is usually favorable.

  19. Update in management of mesenteric ischemia

    Institute of Scientific and Technical Information of China (English)

    Robert W Chang; John B Chang; Walter E Longo

    2006-01-01

    Mesenteric ischemia disorders are precipitated by a circulation insufficiency event that deprives one or several abdominal organs of adequate respiration to meet metabolic demands. Although mesenteric ischemia occurs infrequently, the mortality rate is from 60% to 100%, depending on the source of obstruction. The successful outcome is dependent upon a high index of suspicion and prompt management. We briefly review the pathophysiology and presentation of the various ischemic entities and review the current state of the art in diagnosis and treatment. Despite advances in both diagnosis and treatment, prompt diagnosis and supportive care remain critical for successful outcome.New imaging techniques, endovascular therapy and emerging research may improve our approach to this deadly condition.

  20. Intracerebral adenosine infusion improves neurological outcome after transient focal ischemia in rats.

    Science.gov (United States)

    Kitagawa, Hisashi; Mori, Atsushi; Shimada, Jun; Mitsumoto, Yasuhide; Kikuchi, Tetsuro

    2002-04-01

    Second Institute of New Drug Research, Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan In order to elucidate the role of adenosine in brain ischemia, the possible protective effects of adenosine on ischemic brain injury were investigated in a rat model of brain ischemia both in vitro and in vivo. Exogenous adenosine dose-dependently rescued cortical neuronal cells from injury after glucose deprivation in vitro. Adenosine (1 mM) also significantly reduced hypoglycemia/hypoxia-induced glutamate release from the hippocampal slice. In a rat model of transient middle cerebral artery occlusion (MCAO), extracellular adenosine concentration was increased immediately after occlusion, and then returned to the baseline by 30 min after reperfusion. Adenosine infusion through a microdialysis probe into the ipsilateral striatum (1 mM adenosine, 2 microl min(-1), total 4.5 h from the occlusion to 3 h after reperfusion) showed a significant improvement in the neurological outcome, and about 25% reduction of infarct volume, although the effect did not reach statistical significance, compared with the vehicle-treated group at 20 h after 90 min of MCAO. These results demonstrated the neuroprotective effect of adenosine against ischemic brain injury both in vitro and in vivo, suggesting the possible therapeutic application of adenosine regulating agents, which inhibit adenosine uptake or metabolism to enhance or maintain extracellular endogenous adenosine levels, for stroke treatment.

  1. Dibucaine mitigates spreading depolarization in human neocortical slices and prevents acute dendritic injury in the ischemic rodent neocortex.

    Directory of Open Access Journals (Sweden)

    W Christopher Risher

    Full Text Available Spreading depolarizations that occur in patients with malignant stroke, subarachnoid/intracranial hemorrhage, and traumatic brain injury are known to facilitate neuronal damage in metabolically compromised brain tissue. The dramatic failure of brain ion homeostasis caused by propagating spreading depolarizations results in neuronal and astroglial swelling. In essence, swelling is the initial response and a sign of the acute neuronal injury that follows if energy deprivation is maintained. Choosing spreading depolarizations as a target for therapeutic intervention, we have used human brain slices and in vivo real-time two-photon laser scanning microscopy in the mouse neocortex to study potentially useful therapeutics against spreading depolarization-induced injury.We have shown that anoxic or terminal depolarization, a spreading depolarization wave ignited in the ischemic core where neurons cannot repolarize, can be evoked in human slices from pediatric brains during simulated ischemia induced by oxygen/glucose deprivation or by exposure to ouabain. Changes in light transmittance (LT tracked terminal depolarization in time and space. Though spreading depolarizations are notoriously difficult to block, terminal depolarization onset was delayed by dibucaine, a local amide anesthetic and sodium channel blocker. Remarkably, the occurrence of ouabain-induced terminal depolarization was delayed at a concentration of 1 µM that preserves synaptic function. Moreover, in vivo two-photon imaging in the penumbra revealed that, though spreading depolarizations did still occur, spreading depolarization-induced dendritic injury was inhibited by dibucaine administered intravenously at 2.5 mg/kg in a mouse stroke model.Dibucaine mitigated the effects of spreading depolarization at a concentration that could be well-tolerated therapeutically. Hence, dibucaine is a promising candidate to protect the brain from ischemic injury with an approach that does not rely on

  2. Selective gene expression in focal cerebral ischemia.

    Science.gov (United States)

    Jacewicz, M; Kiessling, M; Pulsinelli, W A

    1986-06-01

    Regional patterns of protein synthesis were examined in rat cortex made ischemic by the occlusion of the right common carotid and middle cerebral arteries. At 2 h of ischemia, proteins were pulse labeled with intracortical injections of a mixture of [3H]leucine, [3H]isoleucine, and [3H]proline. Newly synthesized proteins were analyzed by two-dimensional gel fluorography, and the results correlated with local CBF, measured with [14C]iodoantipyrine as tracer. Small blood flow reductions (CBF = 50-80 ml 100 g-1 min-1) were accompanied by a modest inhibition in synthesis of many proteins and a marked increase in one protein (Mr 27,000). With further reduction in blood flow (CBF = 40 ml 100 g-1 min-1), synthesis became limited to a small group of proteins (Mr 27,000, 34,000, 73,000, 79,000, and actin) including two new polypeptides (Mr 55,000 and 70,000). Severe ischemia (CBF = 15-25 ml 100 g-1 min-1) caused the isoelectric modification of several proteins (Mr 44,000, 55,000, and 70,000) and induced synthesis of another protein (Mr 40,000). Two polypeptides (Mr 27,000 and 70,000) dominated residual protein synthesis in severe ischemia. The changes in protein synthesis induced by different grades of ischemia most likely comprise a variation of the so-called "heat shock" or "stress" response found in all eukaryotic cells subjected to adverse conditions. Since heat shock genes are known to confer partial protection against anoxia and a variety of other noxious insults, their induction may be a factor in limiting the extent of ischemic tissue damage.

  3. Urticarial Vasculitis-Associated Intestinal Ischemia

    Directory of Open Access Journals (Sweden)

    Uni Wong

    2016-01-01

    Full Text Available Urticarial vasculitis (UV is a rare small vessel vasculitis. UV is often idiopathic but can also present in the context of autoimmune disorders such as systemic lupus erythematosus, drug reactions, infections, or a paraneoplastic syndrome. Extracutaneous complications include intestinal ischemic injuries, in UV patients with nonspecific gastrointestinal symptoms such as abdominal pain and nausea. Prompt recognition and treatment can minimize morbidity and mortality. This paper describes a case of urticarial vasculitis-associated intestinal ischemia.

  4. Endovascular Management of Acute Limb Ischemia.

    LENUS (Irish Health Repository)

    Hynes, Brian G

    2011-09-14

    Despite major advances in pharmacologic and endovascular therapies, acute limb ischemia (ALI) continues to result in significant morbidity and mortality. The incidence of ALI may be as high as 13-17 cases per 100,000 people per year, with mortality rates approaching 18% in some series. This review will address the contemporary endovascular management of ALI encompassing pharmacologic and percutaneous interventional treatment strategies.

  5. Colonic urticaria pattern due to early ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Greenberg, H.M.; Goldberg, H.I.; Axel, L.

    1981-05-15

    The unusual radiographic pattern of bleb-like mounds on the surface of the colon mucosa, previously described as colonic urticaria, was seen in 3 patients in whom no allergic state was present. This urticaria-like pattern was due to colonic distention in all 3, and represented only submucosal edema on the gross and microscopic specimens. We hypothesize that this pattern is due to early changes of ischemia caused by colon distention.

  6. Is longer sevoflurane preconditioning neuroprotective in permanent focal cerebral ischemia?

    Institute of Scientific and Technical Information of China (English)

    Caiwei Qiu; Bo Sheng; Shurong Wang; Jin Liu

    2013-01-01

    Sevoflurane preconditioning has neuroprotective effects in the cerebral ischemia/reperfusion model. However, its influence on permanent cerebral ischemia remains unclear. In the present study, the rats were exposed to sevoflurane for 15, 30, 60, and 120 minutes, fol owed by induction of perma-nent cerebral ischemia. Results demonstrated that 30-and 60-minute sevoflurane preconditioning significantly reduced the infarct volume at 24 hours after cerebral ischemia, and 60-minute lurane preconditioning additional y reduced the number of TUNEL-and caspase-3-positive cel s in the ischemic penumbra. However, 120-minute sevoflurane preconditioning did not show evident neuroprotective effects. Moreover, 60-minute sevoflurane preconditioning significantly attenuated neurological deficits and infarct volume in rats at 4 days after cerebral ischemia. These findings in-dicated that 60-minute sevoflurane preconditioning can induce the best neuroprotective effects in rats with permanent cerebral ischemia through the inhibition of apoptosis.

  7. Detection and quantification of regional cortical gray matter damage in multiple sclerosis utilizing gradient echo MRI

    Directory of Open Access Journals (Sweden)

    Jie Wen

    2015-01-01

    Full Text Available Cortical gray matter (GM damage is now widely recognized in multiple sclerosis (MS. The standard MRI does not reliably detect cortical GM lesions, although cortical volume loss can be measured. In this study, we demonstrate that the gradient echo MRI can reliably and quantitatively assess cortical GM damage in MS patients using standard clinical scanners. High resolution multi-gradient echo MRI was used for regional mapping of tissue-specific MRI signal transverse relaxation rate values (R2* in 10 each relapsing–remitting, primary-progressive and secondary-progressive MS subjects. A voxel spread function method was used to correct artifacts induced by background field gradients. R2* values from healthy controls (HCs of varying ages were obtained to establish baseline data and calculate ΔR2* values – age-adjusted differences between MS patients and HC. Thickness of cortical regions was also measured in all subjects. In cortical regions, ΔR2* values of MS patients were also adjusted for changes in cortical thickness. Symbol digit modalities (SDMT and paced auditory serial addition (PASAT neurocognitive tests, as well as Expanded Disability Status Score, 25-foot timed walk and nine-hole peg test results were also obtained on all MS subjects. We found that ΔR2* values were lower in multiple cortical GM and normal appearing white matter (NAWM regions in MS compared with HC. ΔR2* values of global cortical GM and several specific cortical regions showed significant (p < 0.05 correlations with SDMT and PASAT scores, and showed better correlations than volumetric measures of the same regions. Neurological tests not focused on cognition (Expanded Disability Status Score, 25-foot timed walk and nine-hole peg tests showed no correlation with cortical GM ΔR2* values. The technique presented here is robust and reproducible. It requires less than 10 min and can be implemented on any MRI scanner. Our results show that quantitative tissue-specific R2

  8. Pranlukast reduces neutrophil but not macrophage/microglial accumulation in brain after focal cerebral ischemia in mice

    Institute of Scientific and Technical Information of China (English)

    Li-sheng CHU; Er-qing WEI; Guo-liang YU; San-hua FANG; Yu ZHOU; Meng-ling WANG; Wei-ping ZHANG

    2006-01-01

    Aim:To determine whether pranlukast.a cysteinyl leukotriene receptor-1 antagonist,exerts an anti-inflammatory effect on focal cerebral ischemia in mice.Methods:Focal cerebral ischemia in mice was induced by permanent middle cerebral artery occlusion(MCAO).In addition to neurological deficits,infarct volume,degenerated neurons and endogenous IgG exudation,we detected accumulation of neutrophils and macrophage/microglia in the ischemic brain tissue 72 h after MCAO.Pranlukast was iP injected 30 min before and after MCAO.Results:Pranlukast significantly attenuated neurological deficits,infarct volume,neuron degeneration and IgG exudation.Importantly,pranlukast(0.01 and 0.1 mg/kg) inhibited myeloperoxidase-positive neutrophil,but not CDllb-positive macrophage/microglial accumulation in the ischemic cortical tissue.Conclusion:Pranlukast exerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phase that is limited to neutrophil recruitment through the disrupted blood-brain barrier.

  9. Nimodipine pretreatment improves cerebral blood flow and reduces brain edema in conscious rats subjected to focal cerebral ischemia.

    Science.gov (United States)

    Jacewicz, M; Brint, S; Tanabe, J; Wang, X J; Pulsinelli, W A

    1990-11-01

    The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 micrograms/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a "vascular steal" and reduced the volume of the ischemic core (cortex with CBF of less than 25 ml/100 g/min) and accompanying edema by approximately 50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50-75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20-30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.

  10. Relative Contribution of Prolyl Hydroxylase-Dependent and -Independent Degradation of HIF-1alpha by Proteasomal Pathways in Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Yomna Badawi

    2017-05-01

    Full Text Available Hypoxia inducible factor-1 (HIF-1 is a key regulator in hypoxia and can determine the fate of brain cells during ischemia. However, the mechanism of HIF-1 regulation is still not fully understood in ischemic brains. We tested a hypothesis that both the 26S and the 20S proteasomal pathways were involved in HIF-1α degradation under ischemic conditions. Using in vitro ischemic model (oxygen and glucose deprivation and a mouse model of middle cerebral artery occlusion, we tested effects of inhibitors of proteasomes and prolyl hydroxylase (PHD on HIF-1α stability and brain injury in cerebral ischemia. We observed that 30 and 60 min of oxygen-glucose deprivation significantly increased the 20S proteasomal activity. We demonstrated that proteasome inhibitors increased HIF-1α stabilization and cell viability and were more effective than PHD inhibitors in primary cultured cortical neurons exposed to oxygen and glucose deprivation. Furthermore, the administration of the proteasome inhibitor, epoxomicin, to mice resulted in smaller infarct size and brain edema than a PHD inhibitor. Our results indicate that 20S proteasomes are involved in HIF-1α degradation in ischemic neurons and that proteasomal inhibition provides more HIF-1α stabilization and neuroprotection than PHD inhibition in cerebral ischemia.

  11. Astrocytic exportin-7 responds to ischemia through mediating LKB1 translocation from the nucleus to the cytoplasm.

    Science.gov (United States)

    Liang, Hai Jie; Chai, Rui Chao; Li, Xi; Kong, Jin Ge; Jiang, Jiao Hua; Ma, Ju; Vatcher, Greg; Yu, Albert Cheung Hoi

    2015-02-01

    The superfamily of importin-β-related proteins is the largest class of nuclear transport receptors and can be generally divided into importins and exportins according to their transport directions. Eleven importins and seven exportins have been identified, and the expression patterns of both classes are important for their functions in nucleocytoplasmic transport activities. This study demonstrates that all of the importins (importin-β; transportin-1, -2, and -3; and importin-4, -5, -7, -8, -9, -11, and -13) and all the exportins (exportin-1, -2, -4, -5, -6, -7, and -t) are differentially expressed in the cerebral cortex, cerebellum, hippocampus, and brainstem and in primary cultures of cerebral cortical astrocytes and neurons. For astrocytes, we observed that different importins and exportins displayed different expression changes during 0-6 hr of ischemia treatment, especially an increase of both the mRNA and the protein of exportin-7. Immunostaining showed that exportin-7 accumulated inside the nucleus and around the nuclear envelope. In addition, we noticed an increased cytoplasmic distribution of one of the cargo proteins of exportin-7, LKB1, an important element in maintaining energy homeostasis. This increased cytoplasmic distribution was accompanied by an increased expression of exportin-7 under ischemia in astrocytes. We demonstrate that exportin-7 responds to ischemia in astrocytes and that this response involves translocation of LKB1, a protein that plays important roles during metabolic stress, from the nucleus to the cytoplasm.

  12. Oxaliplatin Induced Digital Ischemia and Necrosis

    Directory of Open Access Journals (Sweden)

    Kubilay Karabacak

    2015-01-01

    Full Text Available Introduction. Digital ischemia is a rare complication of several chemotherapeutic medications. We aimed to present a patient with digital ischemia, secondary to a new generation chemotherapeutic drug, oxaliplatin. Case Report. 62-year-old woman presented to our department with severe pain, paresthesia, and distal acrocyanosis on her right hand fingertips. Her complaints started five days after the third cycle of a chemotherapy protocol consisting of 5-fluorourasil (5-FU, folinic acid, and oxaliplatin due to advanced colon carcinoma. On physical examination, hemorrhagic and partly ulcerative lesions were detected at her right hand fingertips. Radial and ulnar pulses were absent at affected side. Digital subtraction angiography revealed severe vascular resistance in the affected extremity. Iloprost trometamol treatment was started with the dosage of 1 ng/kg/min. In addition, low-molecule-weight heparin was used for preventing possible microemboli. Symptomatic relief was provided after five days, and patient was discharged on 7th day of treatment. Discussion. The pathogenesis of oxaliplatin induced vascular toxicity remains unclear. Endothelial damage, increased adherence of platelets, deposition of immune complexes as an immunologic effect of oxaliplatin, and hypercoagulable state may be the reason for arterial thrombosis, digital microemboli, possible digital ischemia, and their several consequences.

  13. Post-Traumatic Late Onset Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Gencer Genc

    2014-03-01

    Full Text Available Artery-to-artery emboli or occlusion of craniocervical arteries mostly due to dissection are the most common causes of ischemia after trauma. A 29 year-old male had been admitted to another hospital with loss of consciousness lasting for about 45 minutes after a hard parachute landing without head trauma three days ago. As his neurological examination and brain CT were normal, he had been discharged after 24 hours of observation. Two days after his discharge, he was admitted to our department with epileptic seizure. His neurological examination revealed left hemianopia. After observing occipital subacute ischemia at right side in brain magnetic resonance imaging (MRI, we performed cerebral angiography and no dissection was observed. Excluding the rheumatologic, cardiologic and vascular events, our final diagnosis was late onset cerebral ischemia. Anti-edema and antiepileptic treatment was initiated. He was discharged with left hemianopia and mild cognitive deficit. We suggest that it will be wise to hospitalize patients for at least 72 hours who has a history of unconsciousness following trauma.

  14. Purine Metabolism in Acute Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Ye. V. Oreshnikov

    2008-01-01

    Full Text Available Objective: to study the specific features of purine metabolism in clinically significant acute cerebral ischemia. Subjects and materials. Three hundred and fifty patients with the acutest cerebral ischemic stroke were examined. The parameters of gas and electrolyte composition, acid-base balance, the levels of malonic dialdehyde, adenine, guanine, hypox-anthine, xanthine, and uric acid, and the activity of xanthine oxidase were determined in arterial and venous bloods and spinal fluid. Results. In ischemic stroke, hyperuricemia reflects the severity of cerebral metabolic disturbances, hemodynamic instability, hypercoagulation susceptiility, and the extent of neurological deficit. In ischemic stroke, hyperuri-corachia is accompanied by the higher spinal fluid levels of adenine, guanine, hypoxanthine, and xanthine and it is an indirect indicator of respiratory disorders of central genesis, systemic acidosis, hypercoagulation susceptibility, free radical oxidation activation, the intensity of a stressor response to cerebral ischemia, cerebral metabolic disturbances, the depth of reduced consciousness, and the severity of neurological deficit. Conclusion. The high venous blood activity of xanthine oxidase in ischemic stroke is associated with the better neurological parameters in all follow-up periods, the better early functional outcome, and lower mortality rates. Key words: hyperuricemia, stroke, xanthine oxidase, uric acid, cerebral ischemia.

  15. Myocardic extended ischemia after scombroid syndrome

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    Maria Serena Bassoni

    2006-08-01

    Full Text Available We describe a case of a healthy woman, presenting to the emergency department because of sudden onset of diffuse pruriginous erythema, profound arterial hypotension and anginal chest pain, just after consuing a meal with cooked fresh tuna fish. She developed progressive ECG signs of myocardial ischemia suggesting subendocardial infarction and increased serum level of troponin I. After vigourous fluid resuscitation with iv fluids and treatment with anti-hystamine drugs, corticosteroids, beta-blockers and calcium-channell blockers she progressively recovered. A clinical diagnosis of sgombroid syndrome was established: it is a syndrome which may follow the ingestion of some spoiled fish, characterized by urticara, headhache, gastrointestinal upset and rarely bronchospasm, shock, coronary ischemia and arrythmias. A sample of the consumed fish could be analysed, finding a very high level of hystamine concentration, conferming the diagnosis of sgombroid syndrome. A coronary angiography was performed and confermed the patient had a normal coronary tree, devoid of atherosclerotic lesions. Her anginal symptoms and ECG signs were probably due to functional ischemia determined by hystamine mediated vasoconstriction and hypotension. This not so rare but not well known syndrome is further discussed and addressed to the emergency physicians’ attention, because of its importance in the differential diagnoses of suspected food allergies

  16. Hamilton-Jacobi skeleton on cortical surfaces.

    Science.gov (United States)

    Shi, Y; Thompson, P M; Dinov, I; Toga, A W

    2008-05-01

    In this paper, we propose a new method to construct graphical representations of cortical folding patterns by computing skeletons on triangulated cortical surfaces. In our approach, a cortical surface is first partitioned into sulcal and gyral regions via the solution of a variational problem using graph cuts, which can guarantee global optimality. After that, we extend the method of Hamilton-Jacobi skeleton [1] to subsets of triangulated surfaces, together with a geometrically intuitive pruning process that can trade off between skeleton complexity and the completeness of representing folding patterns. Compared with previous work that uses skeletons of 3-D volumes to represent sulcal patterns, the skeletons on cortical surfaces can be easily decomposed into branches and provide a simpler way to construct graphical representations of cortical morphometry. In our experiments, we demonstrate our method on two different cortical surface models, its ability of capturing major sulcal patterns and its application to compute skeletons of gyral regions.

  17. Disorders of cortical formation: MR imaging features.

    Science.gov (United States)

    Abdel Razek, A A K; Kandell, A Y; Elsorogy, L G; Elmongy, A; Basett, A A

    2009-01-01

    The purpose of this article was to review the embryologic stages of the cerebral cortex, illustrate the classification of disorders of cortical formation, and finally describe the main MR imaging features of these disorders. Disorders of cortical formation are classified according to the embryologic stage of the cerebral cortex at which the abnormality occurred. MR imaging shows diminished cortical thickness and sulcation in microcephaly, enlarged dysplastic cortex in hemimegalencephaly, and ipsilateral focal cortical thickening with radial hyperintense bands in focal cortical dysplasia. MR imaging detects smooth brain in classic lissencephaly, the nodular cortex with cobblestone cortex with congenital muscular dystrophy, and the ectopic position of the gray matter with heterotopias. MR imaging can detect polymicrogyria and related syndromes as well as the types of schizencephaly. We concluded that MR imaging is essential to demonstrate the morphology, distribution, and extent of different disorders of cortical formation as well as the associated anomalies and related syndromes.

  18. Effect of heat shock protein 70 on cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Wen Yan; Xiulian Chen; Rui Chen; Shiming Xu; Lijuan Zhang; Hongjuan Wang; Chunyue Huo

    2006-01-01

    OBJECTIVE: To summarize the relationship between heat shock protein 70 (HSP70) and cerebral ischemia.DATA SOURCES: An online search of Medline database was undertaken to identify relevant articles published in English from January 1980 to December 2005 by using the keywords of "heat shock protein 70, ischemia". Meanwhile, Chinese relevant articles published from January 2000 to December 2005 were searched in China National Knowledge Infrastructure (CNKI) database and Chinese Journal of Clinical Rehabilitation with the keywords of "heat shock protein 70, cerebral ischemia" in Chinese.STUDY SELECTION: More than 100 related articles were screened, and 29 references mainly about HSP70and cerebral ischemia were selected, including basic and clinical researches. As to the articles with similar content, those published in the authoritative journals in recent 3 years were preferential.DATA EXTRACTION : A total of 29 articles were collected and classified according to the structure, function and clinical application of HSP70. Among them, 1 article is about the structure of HSP70, 27 about the relationship between HSP70 and cerebral ischemia, and 2 about the clinical application of HSP70.DATA SYNTHESTS: HSP70 is one of the most conservative proteins during biological evolution. Experiments in cerebral ischemia revealed that HSP70 expression was time-dependent, also correlated with the injured site and severity. The cerebral ischemia induced HSP70 gene expression in hippocampus of gerbil had protection to tolerance of fatal ischemic injury for neurons. The increase of HSP70 expression may be one of the endogenous protective mechanisms during cerebral ischemia, and can effectively alleviate cerebral ischemia. Thus HSP70 protein and HSP70 mRNA have been taken as important indexes extensively applied in the basic study of cerebral ischemia by some scholars abroad.CONCLUSTON: HSP70 plays a protective role in cerebral ischemia, and a deeper research into the biological function of

  19. A Rare Hydrocephalus Complication: Cortical Blindness.

    Science.gov (United States)

    Ünal, Emre; Göçmen, Rahşan; Işıkay, Ayşe İlksen; Tekşam, Özlem

    2015-01-01

    Cortical blindness related to bilateral occipital lobe infarction is an extremely rare complication of hydrocephalus. Compression of the posterior cerebral artery, secondary to tentorial herniation, is the cause of occipital infarction. Particularly in children and mentally ill patients, cortical blindness may be missed. Therefore, early diagnosis and treatment of hydrocephalus is important. We present herein a child of ventricular shunt malfunction complicated by cortical blindness.

  20. Acute hepatic encephalopathy with diffuse cortical lesions

    Energy Technology Data Exchange (ETDEWEB)

    Arnold, S.M.; Spreer, J.; Schumacher, M. [Section of Neuroradiology, Univ. of Freiburg (Germany); Els, T. [Dept. of Neurology, University of Freiburg (Germany)

    2001-07-01

    Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

  1. Post-anesthetic cortical blindness in cats: twenty cases.

    Science.gov (United States)

    Stiles, J; Weil, A B; Packer, R A; Lantz, G C

    2012-08-01

    The medical records of 20 cats with post-anesthetic cortical blindness were reviewed. Information collected included signalment and health status, reason for anesthesia, anesthetic protocols and adverse events, post-anesthetic visual and neurological abnormalities, clinical outcome, and risk factors. The vascular anatomy of the cat brain was reviewed by cadaver dissections. Thirteen cats were anaesthetised for dentistry, four for endoscopy, two for neutering procedures and one for urethral obstruction. A mouth gag was used in 16/20 cats. Three cats had had cardiac arrest, whereas in the remaining 17 cases, no specific cause of blindness was identified. Seventeen cats (85%) had neurological deficits in addition to blindness. Fourteen of 20 cats (70%) had documented recovery of vision, whereas four (20%) remained blind. Two cats (10%) were lost to follow up while still blind. Ten of 17 cats (59%) with neurological deficits had full recovery from neurological disease, two (12%) had mild persistent deficits and one (6%) was euthanased as it failed to recover. Four cats (23%) without documented resolution of neurological signs were lost to follow up. Mouth gags were identified as a potential risk factor for cerebral ischemia and blindness in cats.

  2. Adult midgut malrotation presented with acute bowel obstruction and ischemia

    Directory of Open Access Journals (Sweden)

    Akile Zengin

    2016-01-01

    Conclusion: Malrotation should be considered in differential diagnosis in patients presented with acute abdomen and intestinal ischemia. Surgical intervention should be prompt to limit morbidity and mortality.

  3. Decreased cortical inhibition and yet cerebellar pathology in 'familial cortical myoclonic tremor with epilepsy'

    NARCIS (Netherlands)

    van Rootselaar, Anne-Fleur; van der Salm, Sandra M. A.; Bour, Lo J.; Edwards, Mark J.; Brown, Peter; Aronica, Eleonora; Rozemuller-Kwakkel, Johanna M.; Koehler, Peter J.; Koelman, Johannes H. T. M.; Rothwell, John C.; Tijssen, Marina A. J.

    2007-01-01

    Cortical hyperexcitability is a feature of "familial cortical myoclonic tremor with epilepsy" (FCMTE). However, neuropathological investigations in a single FCMTE patient showed isolated cerebellar pathology. Pathological investigations in a second FCMTE patient, reported here, confirmed cerebellar

  4. Negative Correlations in Visual Cortical Networks

    National Research Council Canada - National Science Library

    Chelaru, Mircea I; Dragoi, Valentin

    2016-01-01

    .... Whereas positive noise correlations have been extensively studied using experimental and theoretical tools, the functional role of negative correlations in cortical circuits has remained elusive...

  5. Spread spectrum time domain reflectometry

    Science.gov (United States)

    Smith, Paul Samuel

    For many years, wiring has been treated as a system that could be installed and expected to work for the life of the aircraft. As aircraft age far beyond their original expected life span, this attitude is rapidly changing. Wiring problems have recently been identified as the cause of several tragic mishaps and hundreds of thousands of lost mission hours. Intermittent wiring faults have been and continue to be difficult to resolve. Test methods that pinpoint faults on the ground can miss intermittent failures. New test methods involving spread spectrum signals are investigated that could be used in flight to locate intermittent failures, including open circuits, short circuits, and arcs. Spread spectrum time domain reflectometry (SSTDR) and sequence time domain reflectometry (STDR) are analyzed in light of the signals commonly present on aircraft wiring. Pseudo noise codes used for the generation of STDR and SSTDR signals are analyzed for application in a STDR/SSTDR test system in the presence of noise. The effects of Mil-Std 1553 and white noise on the STDR and SSTDR signals are discussed analytically, through simulations, and with the use of test hardware. A test system using STDR and SSTDR is designed, built, and used to collect STDR and SSTDR test data. The data collected with the STDR/SSTDR test hardware is analyzed and compared to the theoretical results. Experimental data for open and short circuits collected using SSTDR and a curve fitting algorithm shows a maximum range estimation error of +/-0.2 ft for 75O coaxial cable up to 100ft, and +/-0.6ft for a sample 32.5ft non-controlled impedance aircraft cable. Mil-Std 1553 is specified to operate reliably with a signal-to-noise ratio of 17.5dB, and the SSTDR test system was able to locate an open circuit on a cable also carrying simulated Mil-Std 1553 data where the SSTDR signal was 50dB below the Mil-Std 1553 signal. STDR and SSTDR are shown to be effective in detecting and locating dry and wet arcs on wires.

  6. Hot spots and labyrinths: Why cortical neuromodulation for episodic migraine with aura should be personalized

    Directory of Open Access Journals (Sweden)

    Markus A Dahlem

    2015-03-01

    Full Text Available Stimulation protocols for medical devices should be rationally designed. For episodic migraine with aura we outline model-based design strategies towards preventive and acute therapies using stereotactic cortical neuromodulation. To this end, we regard a localized spreading depression (SD wave segment as a central element in migraine pathophysiology. To describe nucleation and propagation features of the SD wave segment, we define the new concepts of cortical hot spots and labyrinths, respectively. In particular, we firstly focus exclusively on curvature-induced dynamical properties by studying a generic reaction-diffusion model of SD on the folded cortical surface. This surface is described with increasing level of details, including finally personalized simulations using patient's magnetic resonance imaging (MRI scanner readings. At this stage, the only relevant factor that can modulate nucleation and propagation paths is the Gaussian curvature, which has the advantage of being rather readily accessible by MRI. We conclude with discussing further anatomical factors, such as areal, laminar, and cellular heterogeneity, that in addition to and in relation to Gaussian curvature determine the generalized concept of cortical hot spots and labyrinths as target structures for neuromodulation. Our numerical simulations suggest that these target structures are like fingerprints, they are individual features of each migraine sufferer. The goal in the future will be to provide individualized neural tissue simulations. These simulations should predict the clinical data and therefore can also serve as a test bed for exploring stereotactic cortical neuromodulation.

  7. Impacts of suppressing guide on information spreading

    CERN Document Server

    Xu, Jinghong; Ma, Baojun; Wu, Ye

    2015-01-01

    It is quite common that guides are introduced to suppress the information spreading in modern society for different purposes. In this paper, an agent-based model is established to quantitatively analyze the impacts of suppressing guides on information spreading. We find that the spreading threshold depends on the attractiveness of the information and the topology of the social network with no suppressing guides at all. Usually, one would expect that the existence of suppressing guides in the spreading procedure may result in less diffusion of information within the overall network. However, we find that sometimes the opposite is true: the manipulating nodes of suppressing guides may lead to more extensive information spreading when there are audiences with the reversal mind. These results can provide valuable theoretical references to public opinion guidance on various information, e.g., rumor or news spreading.

  8. Impacts of suppressing guide on information spreading

    Science.gov (United States)

    Xu, Jinghong; Zhang, Lin; Ma, Baojun; Wu, Ye

    2016-02-01

    It is quite common that guides are introduced to suppress the information spreading in modern society for different purposes. In this paper, an agent-based model is established to quantitatively analyze the impacts of suppressing guides on information spreading. We find that the spreading threshold depends on the attractiveness of the information and the topology of the social network with no suppressing guides at all. Usually, one would expect that the existence of suppressing guides in the spreading procedure may result in less diffusion of information within the overall network. However, we find that sometimes the opposite is true: the manipulating nodes of suppressing guides may lead to more extensive information spreading when there are audiences with the reversal mind. These results can provide valuable theoretical references to public opinion guidance on various information, e.g., rumor or news spreading.

  9. CT and MRI findings of cerebral ischemic lesions in the cortical and perforating arterial system

    Energy Technology Data Exchange (ETDEWEB)

    Kameyama, Masakuni; Udaka, Fukashi; Nishinaka, Kazuto; Kodama, Mitsuo; Urushidani, Makoto; Kawamura, Kazuyuki; Inoue, Haruhisa; Kageyama, Taku [Sumitomo Hospital, Osaka (Japan)

    1995-07-01

    It is clinically useful to divide the location of infarction into the cortical and perforating arterial system. Computerized tomography (CT) and magnetic resonance imaging (MRI) now make the point of infarction a simple and useful task in daily practice. The diagnostic modality has also demonstrated that risk factors and clinical manifestations are different for infarction in the cortical as opposed to the perforating system. In this paper, we present various aspects of images of cerebral ischemia according to CT and/or MRI findings. With the advance of imaging mechanics, diagnostic capability of CT or/and MRI for cerebral infarction has markedly been improved. We must consider these points on evaluating the previously reported results. In addition, we always consider the pathological background of these image-findings for the precise interpretation of their clinical significance. In some instances, dynamic study such as PET or SPECT is needed for real interpretations of CT and/or MRI images. We paid special reference to lacunar stroke and striatocapsular infarct. In addition, `branch atheromatous disease (Caplan)` was considered, in particular, for their specific clinical significances. Large striatocapsular infarcts frequently show cortical signs and symptoms such as aphasia or agnosia in spite of their subcortical localization. These facts, although have previously been known, should be re-considered for their pathoanatomical mechanism. (author).

  10. Antioxidant and Protective Mechanisms against Hypoxia and Hypoglycaemia in Cortical Neurons in Vitro

    Directory of Open Access Journals (Sweden)

    José Joaquín Merino

    2014-02-01

    Full Text Available In the present work, we have studied whether cell death could be induced in cortical neurons from rats subjected to different period of O2 deprivation and low glucose (ODLG. This “in vitro” model is designed to emulate the penumbra area under ischemia. In these conditions, cortical neurons displayed loss of mitochondrial respiratory ability however, nor necrosis neither apoptosis occurred despite ROS production. The absence of cellular death could be a consequence of increased antioxidant responses such as superoxide dismutase-1 (SOD1 and GPX3. In addition, the levels of reduced glutathione were augmented and HIF-1/3α overexpressed. After long periods of ODLG (12–24 h cortical neurons showed cellular and mitochondrial membrane alterations and did not recuperate cellular viability during reperfusion. This could mean that therapies directed toward prevention of cellular and mitochondrial membrane imbalance or cell death through mechanisms other than necrosis or apoptosis, like authophagy, may be a way to prevent ODLG damage.

  11. Gyrification from constrained cortical expansion

    CERN Document Server

    Tallinen, Tuomas; Biggins, John S; Mahadevan, L

    2015-01-01

    The exterior of the mammalian brain - the cerebral cortex - has a conserved layered structure whose thickness varies little across species. However, selection pressures over evolutionary time scales have led to cortices that have a large surface area to volume ratio in some organisms, with the result that the brain is strongly convoluted into sulci and gyri. Here we show that the gyrification can arise as a nonlinear consequence of a simple mechanical instability driven by tangential expansion of the gray matter constrained by the white matter. A physical mimic of the process using a layered swelling gel captures the essence of the mechanism, and numerical simulations of the brain treated as a soft solid lead to the formation of cusped sulci and smooth gyri similar to those in the brain. The resulting gyrification patterns are a function of relative cortical expansion and relative thickness (compared with brain size), and are consistent with observations of a wide range of brains, ranging from smooth to highl...

  12. Cortical control of facial expression.

    Science.gov (United States)

    Müri, René M

    2016-06-01

    The present Review deals with the motor control of facial expressions in humans. Facial expressions are a central part of human communication. Emotional face expressions have a crucial role in human nonverbal behavior, allowing a rapid transfer of information between individuals. Facial expressions can be either voluntarily or emotionally controlled. Recent studies in nonhuman primates and humans have revealed that the motor control of facial expressions has a distributed neural representation. At least five cortical regions on the medial and lateral aspects of each hemisphere are involved: the primary motor cortex, the ventral lateral premotor cortex, the supplementary motor area on the medial wall, and the rostral and caudal cingulate cortex. The results of studies in humans and nonhuman primates suggest that the innervation of the face is bilaterally controlled for the upper part and mainly contralaterally controlled for the lower part. Furthermore, the primary motor cortex, the ventral lateral premotor cortex, and the supplementary motor area are essential for the voluntary control of facial expressions. In contrast, the cingulate cortical areas are important for emotional expression, because they receive input from different structures of the limbic system.

  13. SLEEP AND OLFACTORY CORTICAL PLASTICITY

    Directory of Open Access Journals (Sweden)

    Dylan eBarnes

    2014-04-01

    Full Text Available In many systems, sleep plays a vital role in memory consolidation and synaptic homeostasis. These processes together help store information of biological significance and reset synaptic circuits to facilitate acquisition of information in the future. In this review, we describe recent evidence of sleep-dependent changes in olfactory system structure and function which contribute to odor memory and perception. During slow-wave sleep, the piriform cortex becomes hypo-responsive to odor stimulation and instead displays sharp-wave activity similar to that observed within the hippocampal formation. Furthermore, the functional connectivity between the piriform cortex and other cortical and limbic regions is enhanced during slow-wave sleep compared to waking. This combination of conditions may allow odor memory consolidation to occur during a state of reduced external interference and facilitate association of odor memories with stored hedonic and contextual cues. Evidence consistent with sleep-dependent odor replay within olfactory cortical circuits is presented. These data suggest that both the strength and precision of odor memories is sleep-dependent. The work further emphasizes the critical role of synaptic plasticity and memory in not only odor memory but also basic odor perception. The work also suggests a possible link between sleep disturbances that are frequently co-morbid with a wide range of pathologies including Alzheimer’s disease, schizophrenia and depression and the known olfactory impairments associated with those disorders.

  14. A general method for identifying node spreading influence via the adjacent matrix and spreading rate

    CERN Document Server

    Lin, Jian-Hong; Guo, Qiang

    2014-01-01

    With great theoretical and practical significance, identifying the node spreading influence of complex network is one of the most promising domains. So far, various topology-based centrality measures have been proposed to identify the node spreading influence in a network. However, the node spreading influence is a result of the interplay between the network topology structure and spreading dynamics. In this paper, we build up the systematic method by combining the network structure and spreading dynamics to identify the node spreading influence. By combining the adjacent matrix $A$ and spreading parameter $\\beta$, we theoretical give the node spreading influence with the eigenvector of the largest eigenvalue. Comparing with the Susceptible-Infected-Recovered (SIR) model epidemic results for four real networks, our method could identify the node spreading influence more accurately than the ones generated by the degree, K-shell and eigenvector centrality. This work may provide a systematic method for identifyi...

  15. Equatorial spread F fossil plumes

    Directory of Open Access Journals (Sweden)

    S. L. Ossakow

    2010-11-01

    Full Text Available Behaviour of equatorial spread F (ESF fossil plumes, i.e., ESF plumes that have stopped rising, is examined using the NRL SAMI3/ESF three-dimensional simulation code. We find that fossil bubbles, plasma density depletions associated with fossil plumes, can persist as high-altitude equatorial depletions even while being "blown" by zonal winds. Corresponding airglow-proxy images of fossil plumes, plots of electron density versus longitude and latitude at a constant altitude of 288 km, are shown to partially "fill in" in most cases, beginning with the highest altitude field lines within the plume. Specifically, field lines upon which the E field has fallen entirely to zero are affected and only the low altitude (≤600 km portion if each field line fills in. This suggests that it should be possible to observe a bubble at high altitude on a field line for which the corresponding airglow image no longer shows a depletion. In all cases ESF plumes stop rising when the flux-tube-integrated ion mass density inside the upper edge of the bubble is equal to that of the nearby background, further supporting the result of Krall et al. (2010b.

  16. Drops spreading on flexible fibers

    Science.gov (United States)

    Somszor, Katarzyna; Boulogne, François; Sauret, Alban; Dressaire, Emilie; Stone, Howard

    2015-11-01

    Fibrous media are encountered in many engineered systems such as textile, paper and insulating materials. In most of these materials, fibers are randomly oriented and form a complex network in which drops of wetting liquid tend to accumulate at the nodes of the network. Here we investigate the role of the fiber flexibility on the spreading of a small volume of liquid on a pair of crossed flexible fibers. A drop of silicone oil is dispensed at the point of contact of the fibers and we characterize the liquid morphologies as we vary the volume of liquid, the angle between the fibers, and the length and bending modulus of the fibers. Drop morphologies previously reported for rigid fibers, i.e. a drop, a column and a mixed morphology, are also observed on flexible fibers with modified domains of existence. Moreover, at small inclination angles of the fibers, a new behavior is observed: the fibers bend and collapse. Depending on the volume, the liquid can adopt a column or a mixed morphology on the collapsed fibers. We rationalize our observations with a model based on energetic considerations. Our study suggests that the fiber flexibility adds a rich variety of behaviors that can be crucial for industrial applications.

  17. Information Spreading in Dynamic Graphs

    CERN Document Server

    Clementi, Andrea; Trevisan, Luca

    2011-01-01

    We present a general approach to study the flooding time (a measure of how fast information spreads) in dynamic graphs (graphs whose topology changes with time according to a random process). We consider arbitrary converging Markovian dynamic graph process, that is, processes in which the topology of the graph at time $t$ depends only on its topology at time $t-1$ and which have a unique stationary distribution. The most well studied models of dynamic graphs are all Markovian and converging. Under general conditions, we bound the flooding time in terms of the mixing time of the dynamic graph process. We recover, as special cases of our result, bounds on the flooding time for the \\emph{random trip} model and the \\emph{random path} models; previous analysis techniques provided bounds only in restricted settings for such models. Our result also provides the first bound for the \\emph{random waypoint} model (which is tight for certain ranges of parameters) whose analysis had been an important open question.

  18. Dynamical model for virus spread

    CERN Document Server

    Camelo-Neto, G

    1995-01-01

    The steady state properties of the mean density population of infected cells in a viral spread is simulated by a general forest fire like cellular automaton model with two distinct populations of cells ( permissive and resistant ones) and studied in the framework of the mean field approximation. Stochastic dynamical ingredients are introduced in this model to mimic cells regeneration (with probability {\\it p}) and to consider infection processes by other means than contiguity (with probability {\\it f}). Simulations are carried on a L \\times L square lattice considering the eight first neighbors. The mean density population of infected cells (D_i) is measured as function of the regeneration probability {\\it p}, and analyzed for small values of the ratio {\\it f/p } and for distinct degrees of the cell resistance. The results obtained by a mean field like approach recovers the simulations results. The role of the resistant parameter R (R \\geq 2) on the steady state properties is investigated and discussed in com...

  19. What Drives the POLONIA Spread in Poland?

    OpenAIRE

    Yinqiu Lu

    2012-01-01

    Since the start of the 2008 - 09 financial crisis, the Polish Overnight Index Average (POLONIA) has persistently been below the policy rate, suggesting a limited influence of the NBP’s open market operations on the short-term interbank rate. In this regard, this paper analyzes the behavior of the POLONIA spread and explore several potential factors that could influence the spread. An empirical analysis confirms that the negative POLONIA spread is related to a few factors, which include the ...

  20. The AMPA antagonist, NBQX, protects against ischemia-induced loss of cerebellar Purkinje cells

    DEFF Research Database (Denmark)

    Balchen, T.; Diemer, Nils Henrik

    1992-01-01

    Neuropathology, NBQX, AMPA antagonist, cerebellar cells, ischemia, rats, Purkinje, neuronal death......Neuropathology, NBQX, AMPA antagonist, cerebellar cells, ischemia, rats, Purkinje, neuronal death...

  1. Is Spreading Depolarization Characterized by an Abrupt, Massive Release of Gibbs Free Energy from the Human Brain Cortex?

    Science.gov (United States)

    Dreier, Jens P.; Isele, Thomas; Reiffurth, Clemens; Offenhauser, Nikolas; Kirov, Sergei A.; Dahlem, Markus A.; Herreras, Oscar

    2012-01-01

    In the evolution of the cerebral cortex, the sophisticated organization in a steady state far away from thermodynamic equilibrium has produced the side effect of two fundamental pathological network events: ictal epileptic activity and spreading depolarization. Ictal epileptic activity describes the partial disruption, and spreading depolarization describes the near-complete disruption of the physiological double Gibbs–Donnan steady state. The occurrence of ictal epileptic activity in patients has been known for decades. Recently, unequivocal electrophysiological evidence has been found in patients that spreading depolarizations occur abundantly in stroke and brain trauma. The authors propose that the ion changes can be taken to estimate relative changes in Gibbs free energy from state to state. The calculations suggest that in transitions from the physiological state to ictal epileptic activity to spreading depolarization to death, the cortex releases Gibbs free energy in a stepwise fashion. Spreading depolarization thus appears as a twilight state close to death. Consistently, electrocorticographic recordings in the core of focal ischemia or after cardiac arrest display a smooth transition from the initial spreading depolarization component to the later ultraslow negative potential, which is assumed to reflect processes in cellular death. PMID:22829393

  2. Information spreading and development of cultural centers

    CERN Document Server

    Dybiec, Bartlomiej; Sneppen, Kim

    2012-01-01

    The historical interplay between societies are governed by many factors, including in particular spreading of languages, religion and other symbolic traits. Cultural development, in turn, is coupled to emergence and maintenance of information spreading. Strong centralized cultures exist thanks to attention from their members, which faithfulness in turn relies on supply of information. Here, we discuss a culture evolution model on a planar geometry that takes into account aspects of the feedback between information spreading and its maintenance. Features of model are highlighted by comparing it to cultural spreading in ancient and medieval Europe, where it in particular suggests that long lived centers should be located in geographically remote regions.

  3. Credit Spreads Across the Business Cycle

    DEFF Research Database (Denmark)

    Nielsen, Mads Stenbo

    This paper studies how corporate bond spreads vary with the business cycle. I show that both level and slope of empirical credit spread curves are correlated with the state of the economy, and I link this to variation in idiosyncratic jump risk. I develop a structural credit risk model that accou......This paper studies how corporate bond spreads vary with the business cycle. I show that both level and slope of empirical credit spread curves are correlated with the state of the economy, and I link this to variation in idiosyncratic jump risk. I develop a structural credit risk model...... to firm fundamentals....

  4. CT perfusion during delayed cerebral ischemia after subarachnoid hemorrhage: distinction between reversible ischemia and ischemia progressing to infarction

    Energy Technology Data Exchange (ETDEWEB)

    Cremers, Charlotte H.P. [University Medical Center Utrecht, Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, PO Box 85500, Utrecht, Utrecht (Netherlands); University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Vos, Pieter C. [University Medical Center Utrecht, Image Sciences Institute, Utrecht (Netherlands); Schaaf, Irene C. van der; Velthuis, Birgitta K.; Dankbaar, Jan Willem [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Vergouwen, Mervyn D.I.; Rinkel, Gabriel J.E. [University Medical Center Utrecht, Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, PO Box 85500, Utrecht, Utrecht (Netherlands)

    2015-09-15

    Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) can be reversible or progress to cerebral infarction. In patients with a deterioration clinically diagnosed as DCI, we investigated whether CT perfusion (CTP) can distinguish between reversible ischemia and ischemia progressing to cerebral infarction. From a prospectively collected series of aSAH patients, we included those with DCI, CTP on the day of clinical deterioration, and follow-up imaging. In qualitative CTP analyses (visual assessment), we calculated positive and negative predictive value (PPV and NPV) with 95 % confidence intervals (95%CI) of a perfusion deficit for infarction on follow-up imaging. In quantitative analyses, we compared perfusion values of the least perfused brain tissue between patients with and without infarction by using receiver-operator characteristic curves and calculated a threshold value with PPV and NPV for the perfusion parameter with the highest area under the curve. In qualitative analyses of 33 included patients, 15 of 17 patients (88 %) with and 6 of 16 patients (38 %) without infarction on follow-up imaging had a perfusion deficit during clinical deterioration (p = 0.002). Presence of a perfusion deficit had a PPV of 71 % (95%CI: 48-89 %) and NPV of 83 % (95%CI: 52-98 %) for infarction on follow-up. Quantitative analyses showed that an absolute minimal cerebral blood flow (CBF) threshold of 17.7 mL/100 g/min had a PPV of 63 % (95%CI: 41-81 %) and a NPV of 78 % (95%CI: 40-97 %) for infarction. CTP may differ between patients with DCI who develop infarction and those who do not. For this purpose, qualitative evaluation may perform marginally better than quantitative evaluation. (orig.)

  5. Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: a target of uric acid treatment.

    Science.gov (United States)

    Onetti, Yara; Dantas, Ana P; Pérez, Belén; Cugota, Roger; Chamorro, Angel; Planas, Anna M; Vila, Elisabet; Jiménez-Altayó, Francesc

    2015-04-15

    Ischemia impairs blood supply to the brain, and reperfusion is important to restore cerebral blood flow (CBF) and rescue neurons from cell death. However, reperfusion can induce CBF values exceeding the basal values before ischemia. This hyperemic effect has been associated with a worse ischemic brain damage, albeit the mechanisms that contribute to infarct expansion are not clear. In this study, we investigated the influence of early postischemic hyperemia on brain damage and middle cerebral artery (MCA) properties and the effect of treatment with the endogenous antioxidant uric acid (UA). The MCA was occluded for 90 min followed by 24 h reperfusion in adult male Sprague-Dawley rats. Cortical CBF increases at reperfusion beyond 20% of basal values were taken as indicative of hyperemia. UA (16 mg/kg) or vehicle (Locke's buffer) was administered intravenously 135 min after MCA occlusion. Hyperemic compared with nonhyperemic rats showed MCA wall thickening (sham: 22.4 ± 0.8 μm; nonhyperemic: 23.1 ± 1.2 μm; hyperemic: 27.8 ± 0.9 at 60 mmHg; P < 0.001, hyperemic vs. sham) involving adventitial cell proliferation, increased oxidative stress, and interleukin-18, and more severe brain damage. Thus MCA remodeling after ischemia-reperfusion takes place under vascular oxidative and inflammatory stress conditions linked to hyperemia. UA administration attenuated MCA wall thickening, induced passive lumen expansion, and reduced brain damage in hyperemic rats, although it did not increase brain UA concentration. We conclude that hyperemia at reperfusion following brain ischemia induces vascular damage that can be attenuated by administration of the endogenous antioxidant UA. Copyright © 2015 the American Physiological Society.

  6. Response of Quiescent Cerebral Cortical Astrocytes to Nanofibrillar Scaffold Properties

    Science.gov (United States)

    Ayres, Virginia; Mujdat Tiryaki, Volkan; Xie, Kan; Ahmed, Ijaz; Shreiber, David I.

    2013-03-01

    We present results of an investigation to examine the hypothesis that the extracellular environment can trigger specific signaling cascades with morphological consequences. Differences in the morphological responses of quiescent cerebral cortical astrocytes cultured on the nanofibrillar matrices versus poly-L-lysine functionalized glass and Aclar, and unfunctionalized Aclar surfaces were demonstrated using atomic force microscopy (AFM) and phalloidin staining of F-actin. The differences and similarities of the morphological responses were consistent with differences and similarities of the surface polarity and surface roughness of the four surfaces investigated in this work, characterized using contact angle and AFM measurements. The three-dimensional capability of AFM was also used to identify differences in cell spreading. An initial quantitative immunolabeling study further identified significant differences in the activation of the Rho GTPases: Cdc42, Rac1, and RhoA, which are upstream regulators of the observed morphological responses: filopodia, lamellipodia, and stress fiber formation. The results support the hypothesis that the extracellular environment can trigger preferential activation of members of the Rho GTPase family with demonstrable morphological consequences for cerebral cortical astrocytes. The support of NSF PHY-095776 is acknowledged.

  7. Olive oil in food spreads

    Directory of Open Access Journals (Sweden)

    Blanco Muñoz, Miguel A.

    2004-03-01

    Full Text Available Chemical hydrogenation of unsaturated fatty acids is a commonly applied reaction to food industries. The process may imply the movement of double bonds in their positions on the fatty acid carbon chain, producing positional and geometrical isomers ( trans fatty acids. Through hydrogenation, unsaturated oils are converted to margarines and vegetable shortenings. The presence of trans fatty acids in foods is undesirable, as trans fatty acids raise the plasma levels of total and low-density lipoproteins (LDL, while decrease the plasma level of high-density lipoproteins (HDL, among other effects. The use of olive oil to prepare fat spread opens new insights into the commercial development of healthy novel foods with a positive image in terms of consumer appeal.La hidrogenación química de los ácidos grasos insaturados es una reacción que se utiliza con frecuencia en la industria alimentaria. El proceso implica el movimiento de los dobles enlaces en la cadena hidrocarbonada de los ácidos grasos, y la aparición de isómeros posicionales y geométricos (ácidos grasos trans . La ingesta inadecuada de alimentos que pueden contener cantidades significativas de ácidos grasos trans se asocia con el aumento en sangre de colesterol total y LDL, y la disminución de HDL, entre otros efectos. Por lo tanto, el uso de aceite de oliva en la preparación de grasas para untar constituye un importante avance en el desarrollo comercial de nuevos alimentos saludables con una imagen positiva para el consumidor.

  8. Prognosis of critical limb ischemia: Major vs. minor amputation comparison.

    Science.gov (United States)

    Matsuzaki, Kyoichi; Hayashi, Ruka; Okabe, Keisuke; Aramaki-Hattori, Noriko; Kishi, Kazuo

    2015-09-01

    Healthcare providers treating wounds have difficulties assessing the prognosis of patients with critical limb ischemia who had been discharged after complete healing of major amputation wounds. The word "major" in "major amputation" gives the impression of "being more severe" than "minor amputation." Therefore, even if wounds are healed after major amputation, they imagine that prognosis after major amputation would be poorer than that after minor amputation. We investigated the prognosis of diabetic nephropathy patients 2 years after amputations. Those patients underwent dialysis as well as amputation following percutaneous transluminal angioplasty for their foot wounds. They were ambulatory prior to these surgeries. Among 56 cases of minor amputation, 45 were males and 11 were females, and mortality was 41.1%. The mortality of cases with and without a coronary intervention history was 53.1% and 25.0%, respectively (p = 0.034). Among 10 cases of major amputation, 9 were males and 1 was female, and mortality was 60%. The mortality of cases with and without a coronary intervention history was 75.0% and 0%, respectively. Although we predicted poor prognosis in cases with major amputation, there was no significant difference in mortality 2 years after amputations (p = 0.267). Thus far poor prognosis has been reported for major amputation. It might be due to inclusion of the following patients: patients with wounds proximal to ankle joints, patients with extensive gangrene spreading to the lower legs, patients with septicemia from wound infection and who died around the time of operation, and patients with malnutrition. The results of our present study showed that the outcomes at 2 years postoperatively were similar between patients with major amputations and those with minor amputations, if surgical wounds were able to heal. We should not estimate the prognosis by the level of amputation, rather we should consider the effect of coronary intervention history on

  9. EEG Monitoring in Cerebral Ischemia: Basic Concepts and Clinical Applications

    NARCIS (Netherlands)

    van Putten, Michel Johannes Antonius Maria; Hofmeijer, Jeannette

    2016-01-01

    EEG is very sensitive to changes in neuronal function resulting from ischemia. The authors briefly review essentials of EEG generation and the effects of ischemia on the underlying neuronal processes. They discuss the differential sensitivity of various neuronal processes to energy limitations, incl

  10. Serum Markers and Intestinal Mucosal Injury in Chronic Gastrointestinal Ischemia

    NARCIS (Netherlands)

    D. van Noord (Désirée); P.B.F. Mensink (Peter); R.J. de Knegt (Robert); M. Ouwendijk (Martine); J. Francke (Jan Paul); A.J. van Vuuren (Hanneke); B.E. Hansen (Bettina); E.J. Kuipers (Ernst)

    2010-01-01

    textabstractBackground: Diagnosing chronic gastrointestinal ischemia (CGI) is a challenging problem in clinical practice. Serum markers for CGI would be of great diagnostic value as a non-invasive test method. Aims: This study investigated serum markers in patients with well-defined ischemia. Furthe

  11. Review on herbal medicine on brain ischemia and reperfusion简

    Institute of Scientific and Technical Information of China (English)

    Nahid; Jivad; Zahra; Rabiei

    2015-01-01

    Brain ischemia and reperfusion is the leading cause of serious and long-range disability in the world. Clinically significant changes in central nervous system function are observed following brain ischemia and reperfusion. Stroke patients exhibit behavioral, cognitive,emotional, affective and electrophysiological changes during recovery phase. Brain injury by transient complete global brain ischemia or by transient incomplete brain ischemia afflicts a very large number of patients in the world with death or permanent disability. In order to reduce this damage, we must sufficiently understand the mechanisms involved in brain ischemia and reperfusion and repair to design clinically effective therapy.Cerebral ischemia and reperfusion is known to induce the generation of reactive oxygen species that can lead to oxidative damage of proteins, membrane lipids and nucleic acids.A decrease in tissue antioxidant capacity, an increase in lipid peroxidation as well as an increase in lipid peroxidation inhibitors have been demonstrated in several models of brain ischemia. This paper reviews the number of commonly used types of herbal medicines effective for the treatment of stroke. The aim of this paper was to review evidences from controlled studies in order to discuss whether herbal medicine can be helpful in the treatment of brain ischemia and reperfusion.

  12. Ergotamine-induced upper extremity ischemia: a case report

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Man Deuk; Lee, Gun [Bundang CHA General Hospital, Pochon (China); Shin, Sung Wook [Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul (Korea, Republic of)

    2005-06-15

    Ergotamine-induced limb ischemia is an extremely rare case. We present a case of a 64-year-old man, who developed ischemia on the right upper extremity due to long-term use of Ergot for migraine headache. Angiography revealed diffused, smooth, and tapered narrowing of the brachial artery. The patient was successfully treated with intravenous nitroprusside.

  13. Review on herbal medicine on brain ischemia and reperfusion

    Institute of Scientific and Technical Information of China (English)

    Nahid Jivad; Zahra Rabiei

    2015-01-01

    Brain ischemia and reperfusion is the leading cause of serious and long-range disability in the world. Clinically significant changes in central nervous system function are observed following brain ischemia and reperfusion. Stroke patients exhibit behavioral, cognitive, emotional, affective and electrophysiological changes during recovery phase. Brain injury by transient complete global brain ischemia or by transient incomplete brain ischemia afflicts a very large number of patients in the world with death or permanent disability. In order to reduce this damage, we must sufficiently understand the mechanisms involved in brain ischemia and reperfusion and repair to design clinically effective therapy. Cerebral ischemia and reperfusion is known to induce the generation of reactive oxygen species that can lead to oxidative damage of proteins, membrane lipids and nucleic acids. A decrease in tissue antioxidant capacity, an increase in lipid peroxidation as well as an increase in lipid peroxidation inhibitors have been demonstrated in several models of brain ischemia. This paper reviews the number of commonly used types of herbal medicines effective for the treatment of stroke. The aim of this paper was to review evidences from controlled studies in order to discuss whether herbal medicine can be helpful in the treatment of brain ischemia and reperfusion.

  14. Retino-choroidal ischemia in central retinal vein occlusion

    OpenAIRE

    Hussain, Nazimul; Hussain, Anjli

    2014-01-01

    A 41-year-old gentleman with insulin dependent diabetes had decreased vision in the right eye due to non-ischemic central retinal vein occlusion with macular edema. One month following intravitreal ranibizumab, he developed retino-choroidal ischemia with further loss of vision. Authors show the fluorescein angiographic transition from non-ischemic central retinal vein occlusion to retino-choroidal ischemia.

  15. Mesenteric ischemia after abdominal aortic aneurysm repair : a systemic review

    NARCIS (Netherlands)

    Bruggink, J. L. M.; Tielliu, I. F. J.; Zeebregts, C. J.; Pol, R. A.

    2014-01-01

    Mesenteric ischemia after abdominal aneurysm repair is a devastating complication with mortality rates up to 70%. Incidence however is relatively low. The aim of this review was to provide an overview on current insights, diagnostic modalities and on mesenteric ischemia after abdominal aortic aneury

  16. Anterior Segment Ischemia after Strabismus Surgery

    Science.gov (United States)

    Göçmen, Emine Seyhan; Atalay, Yonca; Evren Kemer, Özlem; Sarıkatipoğlu, Hikmet Yavuz

    2017-01-01

    A 46-year-old male patient was referred to our clinic with complaints of diplopia and esotropia in his right eye that developed after a car accident. The patient had right esotropia in primary position and abduction of the right eye was totally limited. Primary deviation was over 40 prism diopters at near and distance. The patient was diagnosed with sixth nerve palsy and 18 months after trauma, he underwent right medial rectus muscle recession. Ten months after the first operation, full-thickness tendon transposition of the superior and inferior rectus muscles (with Foster suture) was performed. On the first postoperative day, slit-lamp examination revealed corneal edema, 3+ cells in the anterior chamber and an irregular pupil. According to these findings, the diagnosis was anterior segment ischemia. Treatment with 0.1/5 mL topical dexamethasone drops (16 times/day), cyclopentolate hydrochloride drops (3 times/day) and 20 mg oral fluocortolone (3 times/day) was initiated. After 1 week of treatment, corneal edema regressed and the anterior chamber was clean. Topical and systemic steroid treatment was gradually discontinued. At postoperative 1 month, the patient was orthophoric and there were no pathologic symptoms besides the irregular pupil. Anterior segment ischemia is one of the most serious complications of strabismus surgery. Despite the fact that in most cases the only remaining sequel is an irregular pupil, serious circulation deficits could lead to phthisis bulbi. Clinical properties of anterior segment ischemia should be well recognized and in especially risky cases, preventative measures should be taken. PMID:28182149

  17. Cortical control of whisker movement.

    Science.gov (United States)

    Petersen, Carl C H

    2014-01-01

    Facial muscles drive whisker movements, which are important for active tactile sensory perception in mice and rats. These whisker muscles are innervated by cholinergic motor neurons located in the lateral facial nucleus. The whisker motor neurons receive synaptic inputs from premotor neurons, which are located within the brain stem, the midbrain, and the neocortex. Complex, distributed neural circuits therefore regulate whisker movement during behavior. This review focuses specifically on cortical whisker motor control. The whisker primary motor cortex (M1) strongly innervates brain stem reticular nuclei containing whisker premotor neurons, which might form a central pattern generator for rhythmic whisker protraction. In a parallel analogous pathway, the whisker primary somatosensory cortex (S1) strongly projects to the brain stem spinal trigeminal interpolaris nucleus, which contains whisker premotor neurons innervating muscles for whisker retraction. These anatomical pathways may play important functional roles, since stimulation of M1 drives exploratory rhythmic whisking, whereas stimulation of S1 drives whisker retraction.

  18. The origin of cortical neurons

    Directory of Open Access Journals (Sweden)

    J.G. Parnavelas

    2002-12-01

    Full Text Available Neurons of the mammalian cerebral cortex comprise two broad classes: pyramidal neurons, which project to distant targets, and the inhibitory nonpyramidal cells, the cortical interneurons. Pyramidal neurons are generated in the germinal ventricular zone, which lines the lateral ventricles, and migrate along the processes of radial glial cells to their positions in the developing cortex in an `inside-out' sequence. The GABA-containing nonpyramidal cells originate for the most part in the ganglionic eminence, the primordium of the basal ganglia in the ventral telencephalon. These cells follow tangential migratory routes to enter the cortex and are in close association with the corticofugal axonal system. Once they enter the cortex, they move towards the ventricular zone, possibly to obtain positional information, before they migrate radially in the direction of the pial surface to take up their positions in the developing cortex. The mechanisms that guide interneurons throughout these long and complex migratory routes are currently under investigation.

  19. Cortical cartography and Caret software.

    Science.gov (United States)

    Van Essen, David C

    2012-08-15

    Caret software is widely used for analyzing and visualizing many types of fMRI data, often in conjunction with experimental data from other modalities. This article places Caret's development in a historical context that spans three decades of brain mapping--from the early days of manually generated flat maps to the nascent field of human connectomics. It also highlights some of Caret's distinctive capabilities. This includes the ease of visualizing data on surfaces and/or volumes and on atlases as well as individual subjects. Caret can display many types of experimental data using various combinations of overlays (e.g., fMRI activation maps, cortical parcellations, areal boundaries), and it has other features that facilitate the analysis and visualization of complex neuroimaging datasets. Copyright © 2011 Elsevier Inc. All rights reserved.

  20. Digital Ischemia in Scleroderma Spectrum of Diseases

    Directory of Open Access Journals (Sweden)

    Elena Schiopu

    2010-01-01

    Full Text Available Systemic Sclerosis (Scleroderma, SSc is a disease of unknown etiology characterized by widespread vasculopathy and extracellular matrix deposition leading to fibrosis and autoimmune processes. Digital ischemia (digital ulcers (DUs is the hallmark of SSc-related vasculopathy and is characterized by endothelial dysfunction leading to intimal proliferation and thrombosis. It happens frequently (30% of the patients each year and it is associated with significant morbidity. This paper summarizes the current information regarding pathogenesis, definitions, management, and exploratory therapies in DUs associated with SSc.

  1. Silent ischemia and beta-blockade

    DEFF Research Database (Denmark)

    Egstrup, K

    1991-01-01

    and should also be directed at the other coronary artery risk factors of the patients. The effects of beta-blockers, which reduce the duration and frequency of silent ischemic episodes, is well described. The effect is most pronounced in the morning, when the frequency of ischemia is highest......, and the mechanism of action seems mainly mediated through a reduction in myocardial oxygen demand. beta-Blockers have shown effectiveness in both effort-induced angina and mixed angina, and increased anti-ischemic potency may be achieved by combination therapy with a calcium antagonist. Abrupt withdrawal of beta-blockers...

  2. Intracoronary levosimendan during ischemia prevents myocardial apoptosis.

    Directory of Open Access Journals (Sweden)

    Markus eMalmberg

    2012-02-01

    Full Text Available Background. Levosimendan is a calcium-sensitizing inotropic agent that prevents myocardial contractile depression following cardiac surgery. Levosimendan has also anti-apoptotic properties, but the role of this mechanism is not clear. We studied whether levosimendan prevents cardiomyocyte apoptosis and post-operative stunning after either intracoronary administration or intravenous infusion in an experimental model. Methods. Pigs (n=24 were subjected to 40 minutes of global, cardioplegic ischemia under cardiopulmonary bypass and 240 minutes of reperfusion. L-IV group received intravenous infusion of levosimendan (65 μg/kg 40 minutes before ischemia and L-IC group received levosimendan (65 μg/kg during ischemia administered intracoronary. Control group was operated without levosimendan. Echocardiography was performed to all animals. Apoptosis was determined from transmyocardial biopsies taken from left ventricle using TUNEL assay and immunohistochemistry of active caspace-3. Results. Apoptosis was induced after ischemia-reperfusion in all groups (pre L-IV 0.002±0.004 % vs. post L-IV 0.020±0.017 % p=0.02, pre L-IC 0.001±0.004 % vs. post L-IC 0.020±0.017 % p<0.001, pre control 0.007±0.013 % vs. post control 0.062±0.044 % p=0.01. The amount of apoptosis was higher in the controls, compared with the L-IV (p=0.03 and the L-IC (p=0.03 groups. Longitudinal left ventricular contraction was significantly reduced in the L-IC and the control groups when compared to the L-IV group (L-IV 0.75±0.12 mm vs. L-IC 0.53±0.11 mm p=0.003, L-IV vs. control 0.54±0.11 p=0.01. Conclusions. Both intracoronary administration and pre-ischemic intravenous infusion of levosimendan equally prevented apoptosis, but intravenous administration was required for optimal preservation of the post-operative systolic left ventricle function.

  3. Hydrogen Ion Buffering During Complete Brain Ischemia

    OpenAIRE

    Kraig, Richard P.; PULSINELLI, WILLIAM A.; Plum, Fred

    1985-01-01

    As a first step to quantify [H+] changes in brain during ischemia we used H+-selective microelectrodes and enzyme fluorometric techniques to describe the relationship between interstitial [H+] ([H+]o) and peak tissue lactate after cardiac arrest. We found a step function relationship between [H+]o and tissue lactate rather than the linear titration expected in a homogeneous protein solution. Within a blood glucose range from 3–7 mM, brain lactate rose from 8–13 mmol/kg along with a rise in [H...

  4. Cocaine-associated lower limb ischemia.

    LENUS (Irish Health Repository)

    Collins, Chris G

    2011-07-25

    Cocaine-associated thrombosis has been reported in the literature with reports of vascular injuries to cardiac, pulmonary, intestinal, placental, and musculoskeletal vessels; however, injury of the pedal vessels is rare. We report on a 31-year-old man who presented 2 months following a cocaine binge with limb-threatening ischemia without an otherwise identifiable embolic source. Angiography confirmed extensive occlusive disease of the tibioperoneal vessels. The patient improved following therapy with heparin and a prostacyclin analogue. Cocaine-induced thrombosis should be considered in patients presenting with acute arterial insufficiency in the lower limb without any other identifiable cause.

  5. Age, spreading rates, and spreading asymmetry of the world's ocean crust

    Data.gov (United States)

    National Oceanic and Atmospheric Administration, Department of Commerce — The authors present four companion digital models of the age, age uncertainty, spreading rates and spreading asymmetries of the world's ocean basins as geographic...

  6. Unsupervised fetal cortical surface parcellation

    Science.gov (United States)

    Dahdouh, Sonia; Limperopoulos, Catherine

    2016-03-01

    At the core of many neuro-imaging studies, atlas-based brain parcellations are used for example to study normal brain evolution across the lifespan. These atlases rely on the assumption that the same anatomical features are present on all subjects to be studied and that these features are stable enough to allow meaningful comparisons between different brain surfaces and structures These methods, however, often fail when applied to fetal MRI data, due to the lack of consistent anatomical features present across gestation. This paper presents a novel surface-based fetal cortical parcellation framework which attempts to circumvent the lack of consistent anatomical features by proposing a brain parcellation scheme that is based solely on learned geometrical features. A mesh signature incorporating both extrinsic and intrinsic geometrical features is proposed and used in a clustering scheme to define a parcellation of the fetal brain. This parcellation is then learned using a Random Forest (RF) based learning approach and then further refined in an alpha-expansion graph-cut scheme. Based on the votes obtained by the RF inference procedure, a probability map is computed and used as a data term in the graph-cut procedure. The smoothness term is defined by learning a transition matrix based on the dihedral angles of the faces. Qualitative and quantitative results on a cohort of both healthy and high-risk fetuses are presented. Both visual and quantitative assessments show good results demonstrating a reliable method for fetal brain data and the possibility of obtaining a parcellation of the fetal cortical surfaces using only geometrical features.

  7. Modelling unidirectional liquid spreading on slanted microposts

    DEFF Research Database (Denmark)

    Cavalli, Andrea; Blow, Matthew L.; Yeomans, Julia M.

    2013-01-01

    A lattice Boltzmann algorithm is used to simulate the slow spreading of drops on a surface patterned with slanted micro-posts. Gibb's pinning of the interface on the sides or top of the posts leads to unidirectional spreading over a wide range of contact angles and inclination angles of the posts...

  8. Spreading to localized targets in complex networks

    Science.gov (United States)

    Sun, Ye; Ma, Long; Zeng, An; Wang, Wen-Xu

    2016-12-01

    As an important type of dynamics on complex networks, spreading is widely used to model many real processes such as the epidemic contagion and information propagation. One of the most significant research questions in spreading is to rank the spreading ability of nodes in the network. To this end, substantial effort has been made and a variety of effective methods have been proposed. These methods usually define the spreading ability of a node as the number of finally infected nodes given that the spreading is initialized from the node. However, in many real cases such as advertising and news propagation, the spreading only aims to cover a specific group of nodes. Therefore, it is necessary to study the spreading ability of nodes towards localized targets in complex networks. In this paper, we propose a reversed local path algorithm for this problem. Simulation results show that our method outperforms the existing methods in identifying the influential nodes with respect to these localized targets. Moreover, the influential spreaders identified by our method can effectively avoid infecting the non-target nodes in the spreading process.

  9. The Imaging of Large Nerve Perineural Spread.

    Science.gov (United States)

    Gandhi, Mitesh; Sommerville, Jennifer

    2016-04-01

    We present a review of the imaging findings of large nerve perineural spread within the skull base. The MRI techniques and reasons for performing different sequences are discussed. A series of imaging examples illustrates the appearance of perineural tumor spread with an emphasis on the zonal staging system.

  10. Fire spread characteristics determined in the laboratory

    Science.gov (United States)

    Richard C. Rothermel; Hal E. Anderson

    1966-01-01

    Fuel beds of ponderosa pine needles and white pine needles were burned under controlled environmental conditions to determine the effects of fuel moisture and windspeed upon the rate of fire spread. Empirical formulas are presented to show the effect of these parameters. A discussion of rate of spread and some simple experiments show how fuel may be preheated before...

  11. A distinct boundary between the higher brain's susceptibility to ischemia and the lower brain's resistance.

    Directory of Open Access Journals (Sweden)

    C Devin Brisson

    Full Text Available Higher brain regions are more susceptible to global ischemia than the brainstem, but is there a gradual increase in vulnerability in the caudal-rostral direction or is there a discrete boundary? We examined the interface between `higher` thalamus and the hypothalamus the using live brain slices where variation in blood flow is not a factor. Whole-cell current clamp recording of 18 thalamic neurons in response to 10 min O2/glucose deprivation (OGD revealed a rapid anoxic depolarization (AD from which thalamic neurons do not recover. Newly acquired neurons could not be patched following AD, confirming significant regional thalamic injury. Coinciding with AD, light transmittance (LT imaging during whole-cell recording showed an elevated LT front that initiated in midline thalamus and that propagated into adjacent hypothalamus. However, hypothalamic neurons patched in paraventricular nucleus (PVN, n= 8 magnocellular and 12 parvocellular neurons and suprachiasmatic nucleus (SCN, n= 18 only slowly depolarized as AD passed through these regions. And with return to control aCSF, hypothalamic neurons repolarized and recovered their input resistance and action potential amplitude. Moreover, newly acquired hypothalamic neurons could be readily patched following exposure to OGD, with resting parameters similar to neurons not previously exposed to OGD. Thalamic susceptibility and hypothalamic resilience were also observed following ouabain exposure which blocks the Na(+/K(+ pump, evoking depolarization similar to OGD in all neuronal types tested. Finally, brief exposure to elevated [K(+]o caused spreading depression (SD, a milder, AD-like event only in thalamic neurons so SD generation is regionally correlated with strong AD. Therefore the thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus. In contrast hypothalamic neurons are

  12. Towards a 'canonical' agranular cortical microcircuit

    Directory of Open Access Journals (Sweden)

    Sarah F. Beul

    2015-01-01

    Full Text Available Based on regularities in the intrinsic microcircuitry of cortical areas, variants of a 'canonical' cortical microcircuit have been proposed and widely adopted, particularly in computational neuroscience and neuroinformatics. However, this circuit is founded on striate cortex, which manifests perhaps the most extreme instance of cortical organization, in terms of a very high density of cells in highly differentiated cortical layers. Most other cortical regions have a less well differentiated architecture, stretching in gradients from the very dense eulaminate primary cortical areas to the other extreme of dysgranular and agranular areas of low density and poor laminar differentiation. It is unlikely for the patterns of inter- and intra-laminar connections to be uniform in spite of strong variations of their structural substrate. This assumption is corroborated by reports of divergence in intrinsic circuitry across the cortex. Consequently, it remains an important goal to define local microcircuits for a variety of cortical types, in particular, agranular cortical regions. As a counterpoint to the striate microcircuit, which may be anchored in an exceptional cytoarchitecture, we here outline a tentative microcircuit for agranular cortex. The circuit is based on a synthesis of the available literature on the local microcircuitry in agranular cortical areas of the rodent brain, investigated by anatomical and electrophysiological approaches. A central observation of these investigations is a weakening of interlaminar inhibition as cortical cytoarchitecture becomes less distinctive. Thus, our study of agranular microcircuitry revealed deviations from the well-known 'canonical' microcircuit established for striate cortex, suggesting variations in the intrinsic circuitry across the cortex that may be functionally relevant.

  13. Ischemia reperfusion injury, ischemic conditioning and diabetes mellitus.

    Science.gov (United States)

    Lejay, Anne; Fang, Fei; John, Rohan; Van, Julie A D; Barr, Meredith; Thaveau, Fabien; Chakfe, Nabil; Geny, Bernard; Scholey, James W

    2016-02-01

    Ischemia/reperfusion, which is characterized by deficient oxygen supply and subsequent restoration of blood flow, can cause irreversible damages to tissue. Mechanisms contributing to the pathogenesis of ischemia reperfusion injury are complex, multifactorial and highly integrated. Extensive research has focused on increasing organ tolerance to ischemia reperfusion injury, especially through the use of ischemic conditioning strategies. Of morbidities that potentially compromise the protective mechanisms of the heart, diabetes mellitus appears primarily important to study. Diabetes mellitus increases myocardial susceptibility to ischemia reperfusion injury and also modifies myocardial responses to ischemic conditioning strategies by disruption of intracellular signaling responsible for enhancement of resistance to cell death. The purpose of this review is twofold: first, to summarize mechanisms underlying ischemia reperfusion injury and the signal transduction pathways underlying ischemic conditioning cardioprotection; and second, to focus on diabetes mellitus and mechanisms that may be responsible for the lack of effect of ischemic conditioning strategies in diabetes.

  14. Spreading Modes on Copper and Steel Surfaces

    Directory of Open Access Journals (Sweden)

    Feoktistov Dmitry

    2016-01-01

    Full Text Available This work presents the experimental results of the studying the effect of surface roughness, microstructure and liquid flow rate on the dynamic contact angle during spreading of distilled nondeaerated water drop on a solid horizontal substrate. Copper and steel substrates with different roughness have been investigated. Three spreading modes were conventionally indicated. It was found that the spreading of drops on substrates made of different materials occurs in similar modes. However, the duration of each mode for substrates made of copper and steel are different. Spreading of a liquid above the asperities of a surface micro relief was observed to be dominant for large volumetric flow rates of drops (0.01 ml/s. Liquid was spreading inside the grooves of a rough substrate at low rates (0.005 ml/s.

  15. Information spreading on dynamic social networks

    CERN Document Server

    Liu, Chuang

    2012-01-01

    Nowadays, information spreading on social networks has triggered an explosive attention in various disciplines. Most of previous related works in this area mainly focus on discussing the effects of spreading probability or immunization strategy on static networks. However, in real systems, the peer-to-peer network structure changes constantly according to frequently social activities of users. In order to capture this dynamical property and study its impact on information spreading, in this Letter, a link rewiring strategy based on the Fermi function is introduced. In the present model, the informed individuals tend to break old links and reconnect to ones with more uninformed neighbors. Simulation results on the susceptible-infected (\\textit{SI}) model with non-redundancy contacts indicate that the information spread more faster and broader with the rewiring strategy. Extensive analyses of the information cascading show that the spreading process of the initial steps plays a very important role, that is to s...

  16. Enhanced droplet spreading due to thermal fluctuations

    Energy Technology Data Exchange (ETDEWEB)

    Willis, A M; Freund, J B, E-mail: jbfreund@illinois.ed [Department of Mechanical Science and Engineering, College of Engineering, University of Illinois at Urbana-Champaign, 1206 West Green Street, Urbana, IL 61801 (United States)

    2009-11-18

    The lubrication equation that governs the dynamics of thin liquid films can be augmented to account for stochastic stresses associated with the thermal fluctuations of the fluid. It has been suggested that under certain conditions the spreading rate of a liquid drop on a surface will be increased by these stochastic stresses. Here, an atomistic simulation of a spreading drop is designed to examine such a regime and provide a quantitative assessment of the stochastic lubrication equation for spreading. It is found that the atomistic drop does indeed spread faster than the standard lubrication equations would suggest and that the stochastic lubrication equation of Gruen et al (2006 J. Stat. Phys. 122 1261-91) predicts the spread rate.

  17. Interpolating point spread function anisotropy

    Science.gov (United States)

    Gentile, M.; Courbin, F.; Meylan, G.

    2013-01-01

    Planned wide-field weak lensing surveys are expected to reduce the statistical errors on the shear field to unprecedented levels. In contrast, systematic errors like those induced by the convolution with the point spread function (PSF) will not benefit from that scaling effect and will require very accurate modeling and correction. While numerous methods have been devised to carry out the PSF correction itself, modeling of the PSF shape and its spatial variations across the instrument field of view has, so far, attracted much less attention. This step is nevertheless crucial because the PSF is only known at star positions while the correction has to be performed at any position on the sky. A reliable interpolation scheme is therefore mandatory and a popular approach has been to use low-order bivariate polynomials. In the present paper, we evaluate four other classical spatial interpolation methods based on splines (B-splines), inverse distance weighting (IDW), radial basis functions (RBF) and ordinary Kriging (OK). These methods are tested on the Star-challenge part of the GRavitational lEnsing Accuracy Testing 2010 (GREAT10) simulated data and are compared with the classical polynomial fitting (Polyfit). In all our methods we model the PSF using a single Moffat profile and we interpolate the fitted parameters at a set of required positions. This allowed us to win the Star-challenge of GREAT10, with the B-splines method. However, we also test all our interpolation methods independently of the way the PSF is modeled, by interpolating the GREAT10 star fields themselves (i.e., the PSF parameters are known exactly at star positions). We find in that case RBF to be the clear winner, closely followed by the other local methods, IDW and OK. The global methods, Polyfit and B-splines, are largely behind, especially in fields with (ground-based) turbulent PSFs. In fields with non-turbulent PSFs, all interpolators reach a variance on PSF systematics σ2sys better than the 1

  18. Mangafodipir protects against hepatic ischemia-reperfusion injury in mice.

    Directory of Open Access Journals (Sweden)

    Romain Coriat

    Full Text Available INTRODUCTION AND AIM: Mangafodipir is a contrast agent used in magnetic resonance imaging that concentrates in the liver and displays pleiotropic antioxidant properties. Since reactive oxygen species are involved in ischemia-reperfusion damages, we hypothesized that the use of mangafodipir could prevent liver lesions in a mouse model of hepatic ischemia reperfusion injury. Mangafodipir (MnDPDP was compared to ischemic preconditioning and intermittent inflow occlusion for the prevention of hepatic ischemia-reperfusion injury in the mouse. METHODS: Mice were subjected to 70% hepatic ischemia (continuous ischemia for 90 min. Thirty minutes before the ischemic period, either mangafodipir (10 mg/kg or saline was injected intraperitoneally. Those experimental groups were compared with one group of mice preconditioned by 10 minutes' ischemia followed by 15 minutes' reperfusion, and one group with intermittent inflow occlusion. Hepatic ischemia-reperfusion injury was evaluated by measurement of serum levels of aspartate aminotransferase (ASAT activity, histologic analysis of the livers, and determination of hepatocyte apoptosis (cytochrome c release, caspase 3 activity. The effect of mangafodipir on the survival rate of mice was studied in a model of total hepatic ischemia. RESULTS: Mangafodipir prevented experimental hepatic ischemia-reperfusion injuries in the mouse as indicated by a reduction in serum ASAT activity (P<0.01, in liver tissue damages, in markers of apoptosis (P<0.01, and by higher rates of survival in treated than in untreated animals (P<0.001. The level of protection by mangafodipir was similar to that observed following intermittent inflow occlusion and higher than after ischemic preconditioning. CONCLUSIONS: Mangafodipir is a potential new preventive treatment for hepatic ischemia-reperfusion injury.

  19. 14,15-EET promotes mitochondrial biogenesis and protects cortical neurons against oxygen/glucose deprivation-induced apoptosis

    Energy Technology Data Exchange (ETDEWEB)

    Wang, Lai; Chen, Man; Yuan, Lin; Xiang, Yuting [Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing (China); Zheng, Ruimao, E-mail: rmzheng@pku.edu.cn [Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing (China); Zhu, Shigong, E-mail: sgzhu@bjmu.edu.cn [Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing (China)

    2014-07-18

    Highlights: • 14,15-EET inhibits OGD-induced apoptosis in cortical neurons. • Mitochondrial biogenesis of cortical neurons is promoted by 14,15-EET. • 14,15-EET preserves mitochondrial function of cortical neurons under OGD. • CREB mediates effect of 14,15-EET on mitochondrial biogenesis and function. - Abstract: 14,15-Epoxyeicosatrienoic acid (14,15-EET), a metabolite of arachidonic acid, is enriched in the brain cortex and exerts protective effect against neuronal apoptosis induced by ischemia/reperfusion. Although apoptosis has been well recognized to be closely associated with mitochondrial biogenesis and function, it is still unclear whether the neuroprotective effect of 14,15-EET is mediated by promotion of mitochondrial biogenesis and function in cortical neurons under the condition of oxygen–glucose deprivation (OGD). In this study, we found that 14,15-EET improved cell viability and inhibited apoptosis of cortical neurons. 14,15-EET significantly increased the mitochondrial mass and the ratio of mitochondrial DNA to nuclear DNA. Key makers of mitochondrial biogenesis, peroxisome proliferator activator receptor gamma-coactivator 1 alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM), were elevated at both mRNA and protein levels in the cortical neurons treated with 14,15-EET. Moreover, 14,15-EET markedly attenuated the decline of mitochondrial membrane potential, reduced ROS, while increased ATP synthesis. Knockdown of cAMP-response element binding protein (CREB) by siRNA blunted the up-regulation of PGC-1α and NRF-1 stimulated by 14,15-EET, and consequently abolished the neuroprotective effect of 14,15-EET. Our results indicate that 14,15-EET protects neurons from OGD-induced apoptosis by promoting mitochondrial biogenesis and function through CREB mediated activation of PGC-1α and NRF-1.

  20. Matrix metalloproteinase-9: A deleterious link between hepatic ischemia-reperfusion and colorectal cancer

    Institute of Scientific and Technical Information of China (English)

    Sébastien Lenglet; Fran(c)ois Mach; Fabrizio Montecucco

    2012-01-01

    Despite the advent of improved surgical techniques and the development of cytotoxic chemotherapeutic agents useful for the treatment of colorectal cancer,the primary clinical challenge remains that of preventing and combating metastatic spread.Surgical resection is the best treatment for colorectal metastases isolated to the liver.However,in rodent models,the hepatic ischemia-reperfusion (I/R) applied during the surgery accelerates the outgrowth of implanted tumors.Among the adverse effects of I/R on cellular function,several studies have demonstrated an over expression of the matrix metalloproteinase-9 (MMP-9) in the ischemic liver.Since several studies showed high local levels of expression and activity of this proteolytic enzyme in the primary colorectal adenocarcinoma,the role of MMP-9 might be considered as a potential common mediator,favoring both growth of local tumor and the dissemination of colorectal carcinoma metastases.

  1. Hydrogen ion buffering during complete brain ischemia.

    Science.gov (United States)

    Kraig, R P; Pulsinelli, W A; Plum, F

    1985-09-09

    As a first step to quantify [H+] changes in brain during ischemia we used H+-selective microelectrodes and enzyme fluorometric techniques to describe the relationship between interstitial [H+] ([H+]o) and peak tissue lactate after cardiac arrest. We found a step function relationship between [H+]o and tissue lactate rather than the linear titration expected in a homogeneous protein solution. Within a blood glucose range from 3-7 mM, brain lactate rose from 8-13 mmol/kg along with a rise in [H+]o of 99 +/- 6 nM(0.44 +/- 0.02 pH). At higher blood glucose levels (17-80 mM), brain lactate accumulated to levels of 16-31 mmol/kg; concurrently [H+]o rose by 608 +/- 16 nM (1.07 +/- 0.02 pH). The unchanging level of [H+]o between 8-13 and 16-31 mmol/kg lactate implies that [H+]o is at a steady-state, but not equilibrium with respect to [H+] in other brain compartments. We propose that ion-transport characteristics of astroglia account for the observed relationship of [H+]o to tissue lactate during complete ischemia and suggest that brain infarction develops after plasma membranes in brain cells can no longer transport ions to regulate [H+].

  2. Autophagy and Liver Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Raffaele Cursio

    2015-01-01

    Full Text Available Liver ischemia-reperfusion (I-R injury occurs during liver resection, liver transplantation, and hemorrhagic shock. The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved. Autophagy is an intracellular self-digesting pathway responsible for removal of long-lived proteins, damaged organelles, and malformed proteins during biosynthesis by lysosomes. Autophagy is found in normal and diseased liver. Although depending on the type of ischemia, warm and/or cold, the dynamic process of liver I-R results mainly in adenosine triphosphate depletion and in production of reactive oxygen species (ROS, leads to both, a local ischemic insult and an acute inflammatory-mediated reperfusion injury, and results finally in cell death. This process can induce liver dysfunction and can increase patient morbidity and mortality after liver surgery and hemorrhagic shock. Whether autophagy protects from or promotes liver injury following warm and/or cold I-R remains to be elucidated. The present review aims to summarize the current knowledge in liver I-R injury focusing on both the beneficial and the detrimental effects of liver autophagy following warm and/or cold liver I-R.

  3. Mixed models in cerebral ischemia study

    Directory of Open Access Journals (Sweden)

    Matheus Henrique Dal Molin Ribeiro

    2016-06-01

    Full Text Available The data modeling from longitudinal studies stands out in the current scientific scenario, especially in the areas of health and biological sciences, which induces a correlation between measurements for the same observed unit. Thus, the modeling of the intra-individual dependency is required through the choice of a covariance structure that is able to receive and accommodate the sample variability. However, the lack of methodology for correlated data analysis may result in an increased occurrence of type I or type II errors and underestimate/overestimate the standard errors of the model estimates. In the present study, a Gaussian mixed model was adopted for the variable response latency of an experiment investigating the memory deficits in animals subjected to cerebral ischemia when treated with fish oil (FO. The model parameters estimation was based on maximum likelihood methods. Based on the restricted likelihood ratio test and information criteria, the autoregressive covariance matrix was adopted for errors. The diagnostic analyses for the model were satisfactory, since basic assumptions and results obtained corroborate with biological evidence; that is, the effectiveness of the FO treatment to alleviate the cognitive effects caused by cerebral ischemia was found.

  4. Organisation of Xenopus oocyte and egg cortices.

    Science.gov (United States)

    Chang, P; Pérez-Mongiovi, D; Houliston, E

    1999-03-15

    The division of the Xenopus oocyte cortex into structurally and functionally distinct "animal" and "vegetal" regions during oogenesis provides the basis of the organisation of the early embryo. The vegetal region of the cortex accumulates specific maternal mRNAs that specify the development of the endoderm and mesoderm, as well as functionally-defined "determinants" of dorso-anterior development, and recognisable "germ plasm" determinants that segregate into primary germ cells. These localised elements on the vegetal cortex underlie both the primary animal-vegetal polarity of the egg and the organisation of the developing embryo. The animal cortex meanwhile becomes specialised for the events associated with fertilisation: sperm entry, calcium release into the cytoplasm, cortical granule exocytosis, and polarised cortical contraction. Cortical and subcortical reorganisations associated with meiotic maturation, fertilisation, cortical rotation, and the first mitotic cleavage divisions redistribute the vegetal cortical determinants, contributing to the specification of dorso-anterior axis and segregation of the germ line. In this article we consider what is known about the changing organisation of the oocyte and egg cortex in relation to the mechanisms of determinant localisation, anchorage, and redistribution, and show novel ultrastructural views of cortices isolated at different stages and processed by the rapid-freeze deep-etch method. Cortical organisation involves interactions between the different cytoskeletal filament systems and internal membranes. Associated proteins and cytoplasmic signals probably modulate these interactions in stage-specific ways, leaving much to be understood.

  5. Somatosensory Misrepresentation Associated with Chronic Pain: Spatiotemporal Correlates of Sensory Perception in a Patient following a Complex Regional Pain Syndrome Spread.

    Science.gov (United States)

    Büntjen, Lars; Hopf, Jens-Max; Merkel, Christian; Voges, Jürgen; Knape, Stefan; Heinze, Hans-Jochen; Schoenfeld, Mircea Ariel

    2017-01-01

    Chronic pain is suggested to be linked to reorganization processes in the sensorimotor cortex. In the current study, the somatosensory representation of the extremities was investigated in a patient with a complex regional pain syndrome (CRPS) that initially occurred in the right hand and arm and spread later into the left hand and right leg. After the spread, magnetoencephalographic recordings in conjunction with somatosensory stimulation revealed that the clinical symptoms were associated with major changes in the primary somatosensory representation. Tactile stimulation of body parts triggering CRPS-related pain elicited activity located in the left primary somatosensory region corresponding to the right hand representation, where the CRPS initially appeared. Solely the unaffected left foot was observed to have a regular S1 representation. The pain distribution pattern was matching the cortical somatosensory misrepresentation suggesting that cortical reorganization processes might contribute and possibly underlie the development and spread of the CRPS.

  6. Development of Pistachio (Pistacia vera L.) spread.

    Science.gov (United States)

    Shakerardekani, Ahmad; Karim, Roselina; Ghazali, Hasanah Mohd; Chin, Nyuk Ling

    2013-03-01

    Pistachio nut (Pistacia vera L.) is one of the most delicious and nutritious nuts in the world. Pistachio spreads were developed using pistachio paste as the main component, icing sugar, soy protein isolate (SPI), and red palm oil (RPO), at different ratios. The highest mean scores of all the sensory attributes were depicted by spreads that were made without addition of SPI. It was found that the work of shear was 0 to 11.0 kg s for an acceptable spread. Sensory spreadability, overall texture, spreadability, and overall acceptability were negatively correlated (R > 0.83) with the work of shear of spreads. The findings indicated that the presence of RPO had a direct effect on the viscoelastic behavior of the pistachio spreads. The a values, which are related to the green color of the pistachio product ranged from 1.7 to 3.9 for spread without addition of RPO, and 4.0 to 5.3 in the presence of RPO. The development of pistachio spread would potentially increase the food uses of pistachio and introduce consumers with a healthier snack food. © 2013 Institute of Food Technologists®

  7. Neuroprotective effect of an angiotensin receptor type 2 agonist following cerebral ischemia in vitro and in vivo

    Directory of Open Access Journals (Sweden)

    Lee Seyoung

    2012-08-01

    Full Text Available Abstract Background Intracerebral administration of the angiotensin II type 2 receptor (AT2R agonist, CGP42112, is neuroprotective in a rat model of ischemic stroke. To explore further its possible cellular target(s and therapeutic utility, we firstly examined whether CGP42112 may exert direct protective effects on primary neurons following glucose deprivation in vitro. Secondly, we tested whether CGP42112 is effective when administered systemically in a mouse model of cerebral ischemia. Methods Primary cortical neurons were cultured from E17 C57Bl6 mouse embryos for 9 d, exposed to glucose deprivation for 24 h alone or with drug treatments, and percent cell survival assessed using trypan blue exclusion. Ischemic stroke was induced in adult male C57Bl6 mice by middle cerebral artery occlusion for 30 min, followed by reperfusion for 23.5 h. Neurological assessment was performed and then mice were euthanized and infarct and edema volume were analysed. Results During glucose deprivation, CGP42112 (1x10-8 M and 1x10-7 M reduced cell death by ~30%, an effect that was prevented by the AT2R antagonist, PD123319 (1x10-6 M. Neuroprotection by CGP42112 was lost at a higher concentration (1x10-6 M but was unmasked by co-application with the AT1R antagonist, candesartan (1x10-7 M. By contrast, Compound 21 (1x10-8 M to 1x10-6 M, a second AT2R agonist, had no effect on neuronal survival. Mice treated with CGP42112 (1 mg/kg i.p. after cerebral ischemia had improved functional outcomes over vehicle-treated mice as well as reduced total and cortical infarct volumes. Conclusions These results indicate that CGP42112 can directly protect neurons from ischemia-like injury in vitro via activation of AT2Rs, an effect opposed by AT1R activation at high concentrations. Furthermore, systemic administration of CGP42112 can reduce functional deficits and infarct volume following cerebral ischemia in vivo.

  8. Contrast-induced transient cortical blindness.

    Science.gov (United States)

    Shah, Parth R; Yohendran, Jayshan; Parker, Geoffrey D; McCluskey, Peter J

    2013-05-01

    We present a case of transient cortical blindness secondary to contrast medium toxicity. A 58-year-old man had successful endovascular coiling of a right posterior inferior cerebellar artery aneurysm but became confused and unable to see after the procedure. His visual acuity was no light perception bilaterally. Clinically, there was no new intra-ocular pathology. An urgent non-contrast computed tomography scan of the brain showed cortical hyperdensity in both parieto-occipital cortices, consistent with contrast medium leakage through the blood-brain barrier from the coiling procedure. The man remained completely blind for 72 hours, after which his visual acuity improved gradually back to his baseline level.

  9. Reversible cortical blindness: posterior reversible encephalopathy syndrome.

    Science.gov (United States)

    Bandyopadhyay, Sabyasachi; Mondal, Kanchan Kumar; Das, Somnath; Gupta, Anindya; Biswas, Jaya; Bhattacharyya, Subir Kumar; Biswas, Gautam

    2010-11-01

    Cortical blindness is defined as visual failure with preserved pupillary reflexes in structurally intact eyes due to bilateral lesions affecting occipital cortex. Bilateral oedema and infarction of the posterior and middle cerebral arterial territory, trauma, glioma and meningioma of the occipital cortex are the main causes of cortical blindness. Posterior reversible encephalopathy syndrome (PRES) refers to the reversible subtype of cortical blindness and is usually associated with hypertension, diabetes, immunosuppression, puerperium with or without eclampsia. Here, 3 cases of PRES with complete or partial visual recovery following treatment in 6-month follow-up are reported.

  10. Tibial cortical lesions: A multimodality pictorial review

    Energy Technology Data Exchange (ETDEWEB)

    Tyler, P.A., E-mail: philippa.tyler@rnoh.nhs.uk [Department of Radiology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP (United Kingdom); Mohaghegh, P., E-mail: pegah1000@gmail.com [Department of Radiology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP (United Kingdom); Foley, J., E-mail: jfoley1@nhs.net [Department of Radiology, Glasgow Royal Infirmary, 16 Alexandra Parade, Glasgow G31 2ES (United Kingdom); Isaac, A., E-mail: amandaisaac@doctors.org.uk [Department of Radiology, King' s College Hospital, Denmark Hill, London SE5 9RS (United Kingdom); Zavareh, A., E-mail: ali.zavareh@gmail.com [Department of Radiology, North Bristol NHS Trust, Frenchay, Bristol BS16 1LE (United Kingdom); Thorning, C., E-mail: cthorning@doctors.org.uk [Department of Radiology, East Surrey Hospital, Canada Avenue, Redhill, Surrey RH1 5RH (United Kingdom); Kirwadi, A., E-mail: anandkirwadi@gmail.com [Department of Radiology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL (United Kingdom); Pressney, I., E-mail: ipressney@hotmail.com [Department of Radiology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP (United Kingdom); Amary, F., E-mail: fernanda.amary@rnoh.nhs.uk [Department of Histopathology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP (United Kingdom); Rajeswaran, G., E-mail: grajeswaran@gmail.com [Department of Radiology, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH (United Kingdom)

    2015-01-15

    Highlights: • Multimodality imaging plays an important role in the investigation and diagnosis of shin pain. • We review the multimodality imaging findings of common cortically based tibial lesions. • We also describe the rarer pathologies of tibial cortical lesions. - Abstract: Shin pain is a common complaint, particularly in young and active patients, with a wide range of potential diagnoses and resulting implications. We review the natural history and multimodality imaging findings of the more common causes of cortically-based tibial lesions, as well as the rarer pathologies less frequently encountered in a general radiology department.

  11. Spread polynomials, rotations and the butterfly effect

    CERN Document Server

    Goh, Shuxiang

    2009-01-01

    The spread between two lines in rational trigonometry replaces the concept of angle, allowing the complete specification of many geometrical and dynamical situations which have traditionally been viewed approximately. This paper investigates the case of powers of a rational spread rotation, and in particular, a curious periodicity in the prime power decomposition of the associated values of the spread polynomials, which are the analogs in rational trigonometry of the Chebyshev polynomials of the first kind. Rational trigonometry over finite fields plays a role, together with non-Euclidean geometries.

  12. Pulsations, interpulsations, and sea-floor spreading.

    Science.gov (United States)

    Pessagno, E. A., Jr.

    1973-01-01

    It is postulated that worldwide transgressions (pulsations) and regressions (interpulsations) through the course of geologic time are related to the elevation and subsidence of oceanic ridge systems and to sea-floor spreading. Two multiple working hypotheses are advanced to explain major transgressions and regressions and the elevation and subsidence of oceanic ridge systems. One hypothesis interrelates the sea-floor spreading hypothesis to the hypothesis of sub-Mohorovicic serpentinization. The second hypothesis relates the sea-floor spreading hypothesis to a hypothesis involving thermal expansion and contraction.

  13. Stochastic dynamic model of SARS spreading

    Institute of Scientific and Technical Information of China (English)

    SHI Yaolin

    2003-01-01

    Based upon the simulation of the stochastic process of infection, onset and spreading of each SARS patient, a system dynamic model of SRAS spreading is constructed. Data from Vietnam is taken as an example for Monte Carlo test. The preliminary results indicate that the time-dependent infection rate is the most important control factor for SARS spreading. The model can be applied to prediction of the course with fluctuations of the epidemics, if the previous history of the epidemics and the future infection rate under control measures are known.

  14. Detection of spreading depolarization with intraparenchymal electrodes in the injured human brain

    DEFF Research Database (Denmark)

    Jeffcote, Toby; Hinzman, Jason M; Jewell, Sharon L

    2014-01-01

    BACKGROUND: Spreading depolarization events following ischemic and traumatic brain injury are associated with poor patient outcome. Currently, monitoring these events is limited to patients in whom subdural electrodes can be placed at open craniotomy. This study examined whether these events can ...... for craniotomy. The method provides a new investigative tool for the evaluation of the contribution of these events to secondary brain injury in human patients.......BACKGROUND: Spreading depolarization events following ischemic and traumatic brain injury are associated with poor patient outcome. Currently, monitoring these events is limited to patients in whom subdural electrodes can be placed at open craniotomy. This study examined whether these events can...... for traumatic brain injury or aneurysmal subarachnoid hemorrhage were monitored for depolarization events in an intensive care setting with concurrent strip (subdural) and depth (intra-parenchymal) electrode recordings. RESULTS: (1) Depolarization events can be reliably detected from intra-cortically placed...

  15. Spreading depolarizations have prolonged direct current shifts and are associated with poor outcome in brain trauma

    DEFF Research Database (Denmark)

    Hartings, Jed A; Watanabe, Tomas; Bullock, M Ross

    2011-01-01

    Cortical spreading depolarizations occur spontaneously after ischaemic, haemorrhagic and traumatic brain injury. Their effects vary spatially and temporally as graded phenomena, from infarction to complete recovery, and are reflected in the duration of depolarization measured by the negative direct...... current shift of electrocorticographic recordings. In the focal ischaemic penumbra, peri-infarct depolarizations have prolonged direct current shifts and cause progressive recruitment of the penumbra into the core infarct. In traumatic brain injury, the effects of spreading depolarizations are unknown......, although prolonged events have not been observed in animal models. To determine whether detrimental penumbral-type depolarizations occur in human brain trauma, we analysed electrocorticographic recordings obtained by subdural electrode-strip monitoring during intensive care. Of 53 patients studied, 10...

  16. Post-operative monitoring of cortical taurine in patients with subarachnoid hemorrhage: a microdialysis study.

    Science.gov (United States)

    De Micheli, E; Pinna, G; Alfieri, A; Caramia, G; Bianchi, L; Colivicchi, M A; Della Corte, L; Bricolo, A

    2000-01-01

    Intracerebral MD enables the retrieval of endogenous substances from the extracellular fluid (ECF) of the brain and has been demonstrated to be a sensitive technique for early detection of subtle vasospasm-induced neurometabolic abnormalities in patients with subarachnoid hemorrhage (SAH). The aim of this study was to monitor cortical extracellular concentrations of energy metabolism markers, such as glucose and lactate, neurotransmitter amino acids, such as glutamate, aspartate, GABA and taurine to identify any neurochemical patterns of cerebral ischemia. A prospective clinical study was conducted on a group of 16 patients with non-severe SAH operated on within 72 hours after initial bleeding. Following aneurysm clipping, an MD catheter was inserted in the cortical region where vasospasm could be expected to develop, and perfused with artificial CSF at 0.3 microl/min flow rate. Dialysate was collected every 6 hours and then analyzed on High Performance Liquid Cromatography (HPLC) for glucose, lactate, pyruvate, glutamate, aspartate, GABA and taurine. Mean ECF taurine concentrations ranged from 1.4 + 0.7 to 12.3 + 7.8 micromol/l in single patients: global mean value was 5.8 + 3.8 micromol/l. In this series, the highest absolute taurine value was 25.7 micromol/l, observed in a patient who developed clinical and radiological signs of cerebral ischemia. Nine patients presented clinical disturbances related to cerebral vasospasm. In this setting, representing a mild-to-moderate hypoxic condition, MD data demonstrated that lactate is the most sensitive marker of cellular energy imbalance. Increased lactate levels positively correlated with glutamate (P<0.0001), aspartate (P<0.0001), GABA (P<0.0001) and taurine (P<0.0001) concentrations. These results suggest that also in humans increased taurine levels reflect a condition of cellular stress. This study confirms that MD is a sensitive technique to reveal subtle metabolic abnormalities possibly resulting in cell damage.

  17. Quercetin protects rat skeletal muscle from ischemia reperfusion injury.

    Science.gov (United States)

    Ekinci Akdemir, Fazile Nur; Gülçin, İlhami; Karagöz, Berna; Soslu, Recep

    2016-01-01

    In this study, we investigated the potential beneficial effects of quercetin on skeletal muscle ischemia reperfusion injury. Twenty-four Sprague-Dawley type rats were randomly divided into four groups. In the sham group, only gastrocnemius muscle were removed and given no quercetin. In ischemia group, all the femoral artery, vein and collaterals were occluded in the left hindlimb by applying tourniquate under general anaesthesia for three hours but reperfusion was not done. In the Quercetin + Ischemia reperfusion group, quercetin (200 mg kg(-1) dose orally) was given during one-week reoperation and later ischemia reperfusion model was done. Finally, gastrocnemius muscle samples were removed to measure biochemical parameters. The biomarkers, MDA levels, SOD, CAT and GPx activities, were evaluated related to skeletal muscle ischemia reperfusion injury. MDA levels reduced and SOD, CAT and GPx activities increased significantly in Quercetin + Ischemia reperfusion group. Results clearly showed that Quercetin have a protective role against oxidative damage induced by ischemia reperfusion in rats.

  18. Hyperphosphorylation of tau protein in the ipsilateral thalamus after focal cortical infarction in rats.

    Science.gov (United States)

    Dong, Da-Wei; Zhang, Yu-Sheng; Yang, Wan-Yong; Wang-Qin, Run-Qi; Xu, An-Ding; Ruan, Yi-Wen

    2014-01-16

    Hyperphosphorylation of tau has been considered as an important risk factor for neurodegenerative diseases. It has been found also in the cortex after focal cerebral ischemia. The present study is aimed at investigating changes of tau protein expression in the ipsilateral thalamus remote from the primary ischemic lesion site after distal middle cerebral artery occlusion (MCAO). The number of neurons in the ventroposterior thalamic nucleus (VPN) was evaluated using Nissl staining and neuronal nuclei (NeuN) immunostaining. Total tau and phosphorylated tau at threonine 231 (p-T231-tau) and serine 199 (p-S199-tau) levels, respectively, in the thalamus were measured using immunostaining and immunoblotting. Moreover, apoptosis was detected with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling (TUNEL) assay. It was found that the numbers of intact neurons and NeuN(+) cells within the ipsilateral VPN were reduced significantly compared with the sham-operated group, but the levels of p-T231-tau and p-S199-tau in the ipsilateral thalamus were increased significantly in rats subjected to ischemia for 3 days, 7 days and 28 days. Furthermore, the number of TUNEL-positive cells was increased in the ipsilateral VPN at 7 days and 28 days after MCAO. Thus, hyperphosphorylated tau protein is observed in ipsilateral thalamus after focal cerebral infarction in this study. Our findings suggest that the expression of hyperphosphorylated tau protein induced by ischemia may be associated with the secondary thalamic damage after focal cortical infarction via an apoptotic pathway.

  19. Persistent Aura with Small Occipital Cortical Infarction: Implications for Migraine Pathophysiology

    Directory of Open Access Journals (Sweden)

    Sam Thissen

    2014-08-01

    Full Text Available Objective: The pathophysiology of migraine with aura is thought to be related to cortical spreading depression and cortical hypersensitivity, in which inhibitory interneurons may play a role. Persistent migraine aura (PMA without infarction is defined as auras that last longer than 1 week in the absence of infarction. We describe a case of persistent aura with a small occipital cortical infarction and discuss implications of this case and PMA for pathophysiological concepts of migrainous auras. Methods: We present a case and discuss the implications for pathophysiological concepts. Results: The case presented cannot be diagnosed as PMA as the patient was found to have an occipital cortical infarction with hypoactivity on fluorodeoxyglucose-positron emission tomography. Nevertheless, the patient suffered from persistent aura (with infarction. We argue that the infarction may have been responsible for an increased imbalance in one of the primary visual cortex networks that was already hyperexcitable due to the migraine aura condition. Conclusion: PMA with occipital infarction has not been reported previously. We believe the findings of the present case and PMA cases reported in the past may support the intracortical disinhibition hypothesis in migraine.

  20. Zika Probably Not Spread Through Saliva: Study

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_167531.html Zika Probably Not Spread Through Saliva: Study Research with ... HealthDay News) -- Scientists have some interesting news about Zika: You're unlikely to get the virus from ...

  1. Spreading paths in partially observed social networks

    CERN Document Server

    Onnela, Jukka-Pekka

    2011-01-01

    Understanding how far information, behaviors, or pathogens spread in social networks is an important problem, having implications for both predicting the size of epidemics, as well as for planning effective interventions. There are, however, two main challenges for inferring spreading path lengths in real-world networks. One is the practical difficulty of observing a dynamic process on a network, and the other is the typical constraint of only partially observing a network. Using a static, structurally realistic social network as a platform for simulations, we juxtapose three distinct paths: (1) the stochastic path taken by a simulated spreading process from source to target; (2) the topologically shortest path in the fully observed network, and hence the single most likely stochastic path, between the two nodes; and (3) the topologically shortest path in a partially observed network. In a sampled network, how closely does the partially observed shortest path (3) emulate the unobserved spreading path (1)? Alt...

  2. Reactive spreading: Adsorption, ridging and compound formation

    Energy Technology Data Exchange (ETDEWEB)

    Saiz, E.; Cannon, R.M.; Tomsia, A.P.

    2000-09-11

    Reactive spreading, in which a chemically active element is added to promote wetting of noble metals on nonmetallic materials, is evaluated. Theories for the energetics and kinetics of the necessary steps involved in spreading are outlined and compared to the steps in compound formation that typically accompany reactive wetting. These include: fluid flow, active metal adsorption, including nonequilibrium effects, and triple line ridging. All of these can be faster than compound nucleation under certain conditions. Analysis and assessment of recently reported experiments on metal/ceramic systems lead to a focus on those conditions under which spreading proceeds ahead of the actual formation of a new phase at the interface. This scenario may be more typical than believed, and perhaps the most effective situation leading to enhanced spreading. A rationale for the pervasive variability and hysteresis observed during high temperature wetting also emerges.

  3. Emergence of Blind Areas in Information Spreading

    CERN Document Server

    Zhang, Zi-Ke; Han, Xiao-Pu; Liu, Chuang

    2013-01-01

    Recently, contagion-based (disease, information, etc.) spreading on social networks has been extensively studied. In this paper, other than traditional full interaction, we propose a partial interaction based spreading model, considering that the informed individuals would transmit information to only a certain fraction of their neighbors due to the transmission ability in real-world social networks. Simulation results on three representative networks (BA, ER, WS) indicate that the spreading efficiency is highly correlated with the network heterogeneity. In addition, a special phenomenon, namely \\emph{Information Blind Areas} where the network is separated by several information-unreachable clusters, will emerge from the spreading process. Furthermore, we also find that the size distribution of such information blind areas obeys power-law-like distribution, which has very similar exponent with that of site percolation. Detailed analyses show that the critical value is decreasing along with the network heterog...

  4. Silent ischemia and severity of pain in acute myocardial infarction

    DEFF Research Database (Denmark)

    Nielsen, F E; Nielsen, S L; Knudsen, F

    1991-01-01

    An overall low tendency to complain of pain, due to a low perception of pain, has been suggested in the pathogenesis of silent ischemia, independent of the extent of the diseased coronaries and a history of previous acute myocardial infarction. This hypothesis has been tested indirectly...... in this retrospective study by comparison of the use of analgesics during admission for a first acute myocardial infarction with the occurrence of silent ischemia at exertion tests four weeks after discharge from hospital. The study did not show a lower use of analgesics in patients with silent ischemia, but this may...

  5. Superresolution improves MRI cortical segmentation with FACE

    DEFF Research Database (Denmark)

    Eskildsen, Simon Fristed; Manjón, José V.; Coupé, Pierrick

    Brain cortical surface extraction from MRI has applications for measurement of gray matter (GM) atrophy, functional mapping, source localization and preoperative neurosurgical planning. Accurate cortex segmentation requires high resolution morphological images and several methods for extracting...

  6. Perceptual incongruence influences bistability and cortical activation

    NARCIS (Netherlands)

    Brouwer, G.J.; Tong, F.; Hagoort, P.; van Ee, R.

    2009-01-01

    We employed a parametric psychophysical design in combination with functional imaging to examine the influence of metric changes in perceptual incongruence on perceptual alternation rates and cortical responses. Subjects viewed a bistable stimulus defined by incongruent depth cues; bistability

  7. Transient cortical blindness after coronary angiography.

    Science.gov (United States)

    Alp, B N; Bozbuğa, N; Tuncer, M A; Yakut, C

    2009-01-01

    Transient cortical blindness is rarely encountered after angiography of native coronary arteries or bypass grafts. This paper reports a case of transient cortical blindness that occurred 72 h after coronary angiography in a 56-year old patient. This was the patient's fourth exposure to contrast medium. Neurological examination demonstrated cortical blindness and the absence of any focal neurological deficit. A non-contrast-enhanced computed tomographic scan of the brain revealed bilateral contrast enhancement in the occipital lobes and no evidence of cerebral haemorrhage, and magnetic resonance imaging of the brain showed no pathology. Sight returned spontaneously within 4 days and his vision gradually improved. A search of the current literature for reported cases of transient cortical blindness suggested that this is a rarely encountered complication of coronary angiography.

  8. Reversible cortical blindness after lung transplantation.

    Science.gov (United States)

    Knower, Mark T; Pethke, Scott D; Valentine, Vincent G

    2003-06-01

    Cyclosporine (CYA) is a calcineurin inhibitor widely used in immunosuppressive regimens after organ transplantation. Several neurologic side effects are frequently associated with CYA use; however, reversible cortical blindness is a rare manifestation of CYA toxicity traditionally seen after liver and bone marrow transplantation. This report presents a case of reversible cortical blindness after lung transplantation, then details the risk factors and clinical course of 28 previously well-documented cases of CYA-induced cortical blindness after transplantation. Identification of known risk factors, clinical clues, and typical radiographic findings may aid in the diagnosis of CYA-induced cortical blindness, since reduction in CYA dose or cessation of CYA therapy usually permits resolution of the neurologic effects.

  9. Cortical areas involved in Arabic number reading.

    Science.gov (United States)

    Roux, F-E; Lubrano, V; Lauwers-Cances, V; Giussani, C; Démonet, J-F

    2008-01-15

    Distinct functional pathways for processing words and numbers have been hypothesized from the observation of dissociated impairments of these categories in brain-damaged patients. We aimed to identify the cortical areas involved in Arabic number reading process in patients operated on for various brain lesions. Direct cortical electrostimulation was prospectively used in 60 brain mappings. We used object naming and two reading tasks: alphabetic script (sentences and number words) and Arabic number reading. Cortical areas involved in Arabic number reading were identified according to location, type of interference, and distinctness from areas associated with other language tasks. Arabic number reading was sustained by small cortical areas, often extremely well localized (area (Brodmann area 45), the anterior part of the dominant supramarginal gyrus (Brodmann area 40; p area (Brodmann area 37; p areas.

  10. The Diversity of Cortical Inhibitory Synapses

    Directory of Open Access Journals (Sweden)

    Yoshiyuki eKubota

    2016-04-01

    Full Text Available The most typical and well known inhibitory action in the cortical microcircuit is a strong inhibition on the target neuron by axo-somatic synapses. However, it has become clear that synaptic inhibition in the cortex is much more diverse and complicated. Firstly, at least ten or more inhibitory non-pyramidal cell subtypes engage in diverse inhibitory functions to produce the elaborate activity characteristic of the different cortical states. Each distinct non-pyramidal cell subtype has its own independent inhibitory function. Secondly, the inhibitory synapses innervate different neuronal domains, such as axons, spines, dendrites and soma, and their IPSP size is not uniform. Thus cortical inhibition is highly complex, with a wide variety of anatomical and physiological modes. Moreover, the functional significance of the various inhibitory synapse innervation styles and their unique structural dynamic behaviors differ from those of excitatory synapses. In this review, we summarize our current understanding of the inhibitory mechanisms of the cortical microcircuit.

  11. Stress preconditioning of spreading depression in the locust CNS.

    Directory of Open Access Journals (Sweden)

    Corinne I Rodgers

    Full Text Available Cortical spreading depression (CSD is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG of locusts. Using K(+ -sensitive microelectrodes, we measured extracellular K(+ concentration ([K(+](o in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K(+ in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na(+/K(+ ATPase impairment, K(+ injection was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45 degrees C and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K(+ that was not linked to changes in ATP levels or total Na(+/K(+ ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin.

  12. Spreading of charged micro-droplets

    Directory of Open Access Journals (Sweden)

    Joseph Iaia

    2013-09-01

    Full Text Available We consider the spreading of a charged microdroplet on a flat dielectric surface whose spreading is driven by surface tension and electrostatic repulsion. This leads to a third order nonlinear partial differential equation that gives the evolution of the height profile. Assuming the droplets are circular we are able to prove existence of solutions with infinite contact angle and in many cases we are able to prove nonexistence of solutions with finite contact angle.

  13. Mapping the Spread of Mounted Warfare

    Directory of Open Access Journals (Sweden)

    Peter Turchin

    2016-12-01

    Full Text Available Military technology is one of the most important factors affecting the evolution of complex societies. In particular, mounted warfare, the use of horse-riders in military operations, revolutionized war as it spread to different parts of Eurasia and Africa during the Ancient and Medieval eras, and to the Americas during the Early Modern period. Here we use a variety of sources to map this spread.

  14. Cortical Source Localization of Infant Cognition

    OpenAIRE

    Reynolds, GD; Richards, JE

    2009-01-01

    Neuroimaging techniques such as positron emission topography (PET) and functional magnetic resonance imaging (fMRI) have been utilized with older children and adults to identify cortical sources of perceptual and cognitive processes. However, due to practical and ethical concerns, these techniques cannot be routinely applied to infant participants. An alternative to such neuroimaging techniques appropriate for use with infant participants is high-density EEG recording and cortical source loca...

  15. CLADA: cortical longitudinal atrophy detection algorithm.

    Science.gov (United States)

    Nakamura, Kunio; Fox, Robert; Fisher, Elizabeth

    2011-01-01

    Measurement of changes in brain cortical thickness is useful for the assessment of regional gray matter atrophy in neurodegenerative conditions. A new longitudinal method, called CLADA (cortical longitudinal atrophy detection algorithm), has been developed for the measurement of changes in cortical thickness in magnetic resonance images (MRI) acquired over time. CLADA creates a subject-specific cortical model which is longitudinally deformed to match images from individual time points. The algorithm was designed to work reliably for lower resolution images, such as the MRIs with 1×1×5 mm(3) voxels previously acquired for many clinical trials in multiple sclerosis (MS). CLADA was evaluated to determine reproducibility, accuracy, and sensitivity. Scan-rescan variability was 0.45% for images with 1mm(3) isotropic voxels and 0.77% for images with 1×1×5 mm(3) voxels. The mean absolute accuracy error was 0.43 mm, as determined by comparison of CLADA measurements to cortical thickness measured directly in post-mortem tissue. CLADA's sensitivity for correctly detecting at least 0.1mm change was 86% in a simulation study. A comparison to FreeSurfer showed good agreement (Pearson correlation=0.73 for global mean thickness). CLADA was also applied to MRIs acquired over 18 months in secondary progressive MS patients who were imaged at two different resolutions. Cortical thinning was detected in this group in both the lower and higher resolution images. CLADA detected a higher rate of cortical thinning in MS patients compared to healthy controls over 2 years. These results show that CLADA can be used for reliable measurement of cortical atrophy in longitudinal studies, even in lower resolution images.

  16. Cortical Neural Computation by Discrete Results Hypothesis

    Science.gov (United States)

    Castejon, Carlos; Nuñez, Angel

    2016-01-01

    One of the most challenging problems we face in neuroscience is to understand how the cortex performs computations. There is increasing evidence that the power of the cortical processing is produced by populations of neurons forming dynamic neuronal ensembles. Theoretical proposals and multineuronal experimental studies have revealed that ensembles of neurons can form emergent functional units. However, how these ensembles are implicated in cortical computations is still a mystery. Although cell ensembles have been associated with brain rhythms, the functional interaction remains largely unclear. It is still unknown how spatially distributed neuronal activity can be temporally integrated to contribute to cortical computations. A theoretical explanation integrating spatial and temporal aspects of cortical processing is still lacking. In this Hypothesis and Theory article, we propose a new functional theoretical framework to explain the computational roles of these ensembles in cortical processing. We suggest that complex neural computations underlying cortical processing could be temporally discrete and that sensory information would need to be quantized to be computed by the cerebral cortex. Accordingly, we propose that cortical processing is produced by the computation of discrete spatio-temporal functional units that we have called “Discrete Results” (Discrete Results Hypothesis). This hypothesis represents a novel functional mechanism by which information processing is computed in the cortex. Furthermore, we propose that precise dynamic sequences of “Discrete Results” is the mechanism used by the cortex to extract, code, memorize and transmit neural information. The novel “Discrete Results” concept has the ability to match the spatial and temporal aspects of cortical processing. We discuss the possible neural underpinnings of these functional computational units and describe the empirical evidence supporting our hypothesis. We propose that fast

  17. Mean field methods for cortical network dynamics

    DEFF Research Database (Denmark)

    Hertz, J.; Lerchner, Alexander; Ahmadi, M.

    2004-01-01

    We review the use of mean field theory for describing the dynamics of dense, randomly connected cortical circuits. For a simple network of excitatory and inhibitory leaky integrate- and-fire neurons, we can show how the firing irregularity, as measured by the Fano factor, increases with the stren...... cortex. Finally, an extension of the model to describe an orientation hypercolumn provides understanding of how cortical interactions sharpen orientation tuning, in a way that is consistent with observed firing statistics...

  18. Cortical depth dependence of the diffusion anisotropy in the human cortical gray matter in vivo.

    Directory of Open Access Journals (Sweden)

    Trong-Kha Truong

    Full Text Available Diffusion tensor imaging (DTI is typically used to study white matter fiber pathways, but may also be valuable to assess the microstructure of cortical gray matter. Although cortical diffusion anisotropy has previously been observed in vivo, its cortical depth dependence has mostly been examined in high-resolution ex vivo studies. This study thus aims to investigate the cortical depth dependence of the diffusion anisotropy in the human cortex in vivo on a clinical 3 T scanner. Specifically, a novel multishot constant-density spiral DTI technique with inherent correction of motion-induced phase errors was used to achieve a high spatial resolution (0.625 × 0.625 × 3 mm and high spatial fidelity with no scan time penalty. The results show: (i a diffusion anisotropy in the cortical gray matter, with a primarily radial diffusion orientation, as observed in previous ex vivo and in vivo studies, and (ii a cortical depth dependence of the fractional anisotropy, with consistently higher values in the middle cortical lamina than in the deep and superficial cortical laminae, as observed in previous ex vivo studies. These results, which are consistent across subjects, demonstrate the feasibility of this technique for investigating the cortical depth dependence of the diffusion anisotropy in the human cortex in vivo.

  19. Cortical depth dependence of the diffusion anisotropy in the human cortical gray matter in vivo.

    Science.gov (United States)

    Truong, Trong-Kha; Guidon, Arnaud; Song, Allen W

    2014-01-01

    Diffusion tensor imaging (DTI) is typically used to study white matter fiber pathways, but may also be valuable to assess the microstructure of cortical gray matter. Although cortical diffusion anisotropy has previously been observed in vivo, its cortical depth dependence has mostly been examined in high-resolution ex vivo studies. This study thus aims to investigate the cortical depth dependence of the diffusion anisotropy in the human cortex in vivo on a clinical 3 T scanner. Specifically, a novel multishot constant-density spiral DTI technique with inherent correction of motion-induced phase errors was used to achieve a high spatial resolution (0.625 × 0.625 × 3 mm) and high spatial fidelity with no scan time penalty. The results show: (i) a diffusion anisotropy in the cortical gray matter, with a primarily radial diffusion orientation, as observed in previous ex vivo and in vivo studies, and (ii) a cortical depth dependence of the fractional anisotropy, with consistently higher values in the middle cortical lamina than in the deep and superficial cortical laminae, as observed in previous ex vivo studies. These results, which are consistent across subjects, demonstrate the feasibility of this technique for investigating the cortical depth dependence of the diffusion anisotropy in the human cortex in vivo.

  20. The cortical and sub-cortical network of sensory evoked response in healthy subjects.

    Science.gov (United States)

    Muthuraman, M; Hellriegel, H; Groppa, S; Deuschl, G; Raethjen, J

    2013-01-01

    The aim of this study was to find the cortical and sub-cortical network responsible for the sensory evoked coherence in healthy subjects during electrical stimulation of right median nerve at wrist. The multitaper method was used to estimate the power and coherence spectrum followed by the source analysis method dynamic imaging of coherent sources (DICS) to find the highest coherent source for the basic frequency 3 Hz and the complete cortical and sub-cortical network responsible for the sensory evoked coherence in healthy subjects. The highest coherent source for the basic frequency was in the posterior parietal cortex for all the subjects. The cortical and sub-cortical network comprised of the primary sensory motor cortex (SI), secondary sensory motor cortex (SII), frontal cortex and medial pulvinar nucleus in the thalamus. The cortical and sub-cortical network responsible for the sensory evoked coherence was found successfully with a 64-channel EEG system. The sensory evoked coherence is involved with a thalamo-cortical network in healthy subjects.

  1. Gossip spread in social network Models

    Science.gov (United States)

    Johansson, Tobias

    2017-04-01

    Gossip almost inevitably arises in real social networks. In this article we investigate the relationship between the number of friends of a person and limits on how far gossip about that person can spread in the network. How far gossip travels in a network depends on two sets of factors: (a) factors determining gossip transmission from one person to the next and (b) factors determining network topology. For a simple model where gossip is spread among people who know the victim it is known that a standard scale-free network model produces a non-monotonic relationship between number of friends and expected relative spread of gossip, a pattern that is also observed in real networks (Lind et al., 2007). Here, we study gossip spread in two social network models (Toivonen et al., 2006; Vázquez, 2003) by exploring the parameter space of both models and fitting them to a real Facebook data set. Both models can produce the non-monotonic relationship of real networks more accurately than a standard scale-free model while also exhibiting more realistic variability in gossip spread. Of the two models, the one given in Vázquez (2003) best captures both the expected values and variability of gossip spread.

  2. Wave directional spreading from point field measurements

    Science.gov (United States)

    McAllister, M. L.; Venugopal, V.; Borthwick, A. G. L.

    2017-04-01

    Ocean waves have multidirectional components. Most wave measurements are taken at a single point, and so fail to capture information about the relative directions of the wave components directly. Conventional means of directional estimation require a minimum of three concurrent time series of measurements at different spatial locations in order to derive information on local directional wave spreading. Here, the relationship between wave nonlinearity and directionality is utilized to estimate local spreading without the need for multiple concurrent measurements, following Adcock & Taylor (Adcock & Taylor 2009 Proc. R. Soc. A 465, 3361-3381. (doi:10.1098/rspa.2009.0031)), with the assumption that directional spreading is frequency independent. The method is applied to measurements recorded at the North Alwyn platform in the northern North Sea, and the results compared against estimates of wave spreading by conventional measurement methods and hindcast data. Records containing freak waves were excluded. It is found that the method provides accurate estimates of wave spreading over a range of conditions experienced at North Alwyn, despite the noisy chaotic signals that characterize such ocean wave data. The results provide further confirmation that Adcock and Taylor's method is applicable to metocean data and has considerable future promise as a technique to recover estimates of wave spreading from single point wave measurement devices.

  3. Does machine perfusion decrease ischemia reperfusion injury?

    Science.gov (United States)

    Bon, D; Delpech, P-O; Chatauret, N; Hauet, T; Badet, L; Barrou, B

    2014-06-01

    In 1990's, use of machine perfusion for organ preservation has been abandoned because of improvement of preservation solutions, efficient without perfusion, easy to use and cheaper. Since the last 15 years, a renewed interest for machine perfusion emerged based on studies performed on preclinical model and seems to make consensus in case of expanded criteria donors or deceased after cardiac death donations. We present relevant studies highlighted the efficiency of preservation with hypothermic machine perfusion compared to static cold storage. Machines for organ preservation being in constant evolution, we also summarized recent developments included direct oxygenation of the perfusat. Machine perfusion technology also enables organ reconditioning during the last hours of preservation through a short period of perfusion on hypothermia, subnormothermia or normothermia. We present significant or low advantages for machine perfusion against ischemia reperfusion injuries regarding at least one primary parameter: risk of DFG, organ function or graft survival. Copyright © 2014 Elsevier Masson SAS. All rights reserved.

  4. Management of Raynaud's phenomenon and digital ischemia.

    Science.gov (United States)

    Herrick, Ariane L

    2013-01-01

    This review focuses on new findings and developments relevant to the clinician caring for patients with primary and secondary [especially systemic sclerosis (SSc)-related] Raynaud phenomenon (RP). In the last 18 months, several clinical trials and observational studies of RP and of SSc-related digital ulceration have been published, reflecting increased awareness of disease burden and increased interest by pharmaceutical companies: new insights into pathophysiology are driving new approaches to treatment. Key developments are the increased use of phosphodiesterase type V inhibitors in severe RP, and of bosentan (an endothelin-1 receptor antagonist) for prevention of recurrent SSc-related digital ulcers. Other treatments being researched include topical glyceryl trinitrate (applied locally to the digits), botulinum toxin (for severe digital ischemia/ulceration), and several other drugs including oral prostanoids. Increased availability and interest in nailfold capillaroscopy, by facilitating early diagnosis of SSc, should pave the way for studies of early intervention and vascular protection.

  5. Real-Time Visualization of Tissue Ischemia

    Science.gov (United States)

    Bearman, Gregory H. (Inventor); Chrien, Thomas D. (Inventor); Eastwood, Michael L. (Inventor)

    2000-01-01

    A real-time display of tissue ischemia which comprises three CCD video cameras, each with a narrow bandwidth filter at the correct wavelength is discussed. The cameras simultaneously view an area of tissue suspected of having ischemic areas through beamsplitters. The output from each camera is adjusted to give the correct signal intensity for combining with, the others into an image for display. If necessary a digital signal processor (DSP) can implement algorithms for image enhancement prior to display. Current DSP engines are fast enough to give real-time display. Measurement at three, wavelengths, combined into a real-time Red-Green-Blue (RGB) video display with a digital signal processing (DSP) board to implement image algorithms, provides direct visualization of ischemic areas.

  6. Modeling the mechanics of cells in the cell-spreading process driven by traction forces

    Science.gov (United States)

    Fang, Yuqiang; Lai, King W. C.

    2016-04-01

    Mechanical properties of cells and their mechanical interaction with the extracellular environments are main factors influencing cellular function, thus indicating the progression of cells in different disease states. By considering the mechanical interactions between cell adhesion molecules and the extracellular environment, we developed a cell mechanical model that can characterize the mechanical changes in cells during cell spreading. A cell model was established that consisted of various main subcellular components, including cortical cytoskeleton, nuclear envelope, actin filaments, intermediate filaments, and microtubules. We demonstrated the structural changes in subcellular components and the changes in spreading areas during cell spreading driven by traction forces. The simulation of nanoindentation tests was conducted by integrating the indenting force to the cell model. The force-indentation curve of the cells at different spreading states was simulated, and the results showed that cell stiffness increased with increasing traction forces, which were consistent with the experimental results. The proposed cell mechanical model provides a strategy to investigate the mechanical interactions of cells with the extracellular environments through the adhesion molecules and to reveal the cell mechanical properties at the subcellular level as cells shift from the suspended state to the adherent state.

  7. Cortical thinning in former professional soccer players.

    Science.gov (United States)

    Koerte, Inga K; Mayinger, Michael; Muehlmann, Marc; Kaufmann, David; Lin, Alexander P; Steffinger, Denise; Fisch, Barbara; Rauchmann, Boris-Stephan; Immler, Stefanie; Karch, Susanne; Heinen, Florian R; Ertl-Wagner, Birgit; Reiser, Maximilian; Stern, Robert A; Zafonte, Ross; Shenton, Martha E

    2016-09-01

    Soccer is the most popular sport in the world. Soccer players are at high risk for repetitive subconcussive head impact when heading the ball. Whether this leads to long-term alterations of the brain's structure associated with cognitive decline remains unknown. The aim of this study was to evaluate cortical thickness in former professional soccer players using high-resolution structural MR imaging. Fifteen former male professional soccer players (mean age 49.3 [SD 5.1] years) underwent high-resolution structural 3 T MR imaging, as well as cognitive testing. Fifteen male, age-matched former professional non-contact sport athletes (mean age 49.6 [SD 6.4] years) served as controls. Group analyses of cortical thickness were performed using voxel-based statistics. Soccer players demonstrated greater cortical thinning with increasing age compared to controls in the right inferolateral-parietal, temporal, and occipital cortex. Cortical thinning was associated with lower cognitive performance as well as with estimated exposure to repetitive subconcussive head impact. Neurocognitive evaluation revealed decreased memory performance in the soccer players compared to controls. The association of cortical thinning and decreased cognitive performance, as well as exposure to repetitive subconcussive head impact, further supports the hypothesis that repetitive subconcussive head impact may play a role in early cognitive decline in soccer players. Future studies are needed to elucidate the time course of changes in cortical thickness as well as their association with impaired cognitive function and possible underlying neurodegenerative process.

  8. Cortical swallowing processing in early subacute stroke

    Directory of Open Access Journals (Sweden)

    Fischer Maren

    2011-03-01

    Full Text Available Abstract Background Dysphagia is a major complication in hemispheric as well as brainstem stroke patients causing aspiration pneumonia and increased mortality. Little is known about the recovery from dysphagia after stroke. The aim of the present study was to determine the different patterns of cortical swallowing processing in patients with hemispheric and brainstem stroke with and without dysphagia in the early subacute phase. Methods We measured brain activity by mean of whole-head MEG in 37 patients with different stroke localisation 8.2 +/- 4.8 days after stroke to study changes in cortical activation during self-paced swallowing. An age matched group of healthy subjects served as controls. Data were analyzed by means of synthetic aperture magnetometry and group analyses were performed using a permutation test. Results Our results demonstrate strong bilateral reduction of cortical swallowing activation in dysphagic patients with hemispheric stroke. In hemispheric stroke without dysphagia, bilateral activation was found. In the small group of patients with brainstem stroke we observed a reduction of cortical activation and a right hemispheric lateralization. Conclusion Bulbar central pattern generators coordinate the pharyngeal swallowing phase. The observed right hemispheric lateralization in brainstem stroke can therefore be interpreted as acute cortical compensation of subcortically caused dysphagia. The reduction of activation in brainstem stroke patients and dysphagic patients with cortical stroke could be explained in terms of diaschisis.

  9. Thoracic sympathectomy for upper extremity ischemia.

    Science.gov (United States)

    Hoexum, Frank; Coveliers, Hans M; Lu, Joyce J; Jongkind, Vincent; Yeung, Kakkhee K; Wisselink, Willem

    2016-12-01

    Thoracic sympathectomy is performed in the management of a variety of disorders of the upper extremity. To evaluate the contemporary results of thoracic sympathectomy for upper extremity ischemia a systematic review of the literature was conducted. We performed a PubMed, EMBASE and Cochrane search of the literature written in the English language from January 1975 to December 2015. All articles presenting original patient data regarding the effect of treatment on symptoms or on the healing of ulcers were eligible for inclusion. Individual analyses for Primary Raynaud's Disease (PRD) and Secondary Raynaud's Phenomenon (SRP) were performed. We included 6 prospective and 23 retrospective series with a total of 753 patients and 1026 affected limbs. Early beneficial effects of thoracic sympathectomy were noticed in 63-100% (median 94%) of all patients, in 73-100% (median 98%) of PRD patients and in 63-100% (median 94%) of SRP patients. The beneficial effect was noted to lessen over time. Long-term beneficial effects were reported in 13-100% (median 75%) of all patients, in 22-100% (median 58%) of PRD patients, and in 13-100% (median 79%) of SRD patients. Complete or improved ulcer healing was achieved in 33-100% and 25-67% respectively, of all patients. Thoracic sympathectomy can be beneficial in the treatment of upper extremity ischemia in select patients. Although the effect in patients with PRD will lessen over time, it may still reduce the severity of symptoms. In SRD, effects are more often long-lasting. In addition, thoracic sympathectomy may maximize tissue preservation or prevent amputation in cases of digital ulceration.

  10. The treatment of chronic intestinal ischemia.

    Science.gov (United States)

    Illuminati, G; Caliò, F G; D'Urso, A; Papaspyropoulos, V; Mancini, P; Ceccanei, G; Vietri, F

    2004-01-01

    Due to the rarity of the condition, large and prospective series defining the optimal method of digestive arteries revascularization, for the treatment of chronic intestinal ischemia, are lacking. The aim of this consecutive sample clinical study was to test the hypothesis that flexible application of different revascularization methods, according to individual cases, will yield the best results in the management of chronic intestinal ischemia. Eleven patients, of a mean age of 57 years, underwent revascularization of 11 digestive arteries for symptomatic chronic mesenteric occlusive disease. Eleven superior mesenteric arteries and one celiac axis were revascularized. The revascularization techniques included retrograde bypass grafting in 7 cases, antegrade bypass grafting in 2, percutaneous arterial angioplasty in 1, and arterial reimplantation in one case. The donor axis for either reimplantation or bypass grafting was the infrarenal aorta in 4 cases, an infrarenal Dacron graft in 4, and the celiac aorta in one case. Grafting materials included 5 polytetrafluoroethylene (PTFE) and 3 Dacron grafts. Concomitant procedures included 3 aorto-ilio-femoral grafts and one renal artery revascularization. Mean follow-up length was 31 months. There was no operative mortality. Cumulative survival rate was 88.9% at 36 months (SE 12.1%). Primary patency rate was 90% at 36 months (SE 11.6%). The symptom free rate was 90% at 36 months (SE 11.6%). Direct reimplantation, antegrade and retrograde bypass grafting, all allow good mid-term results: the choice of the optimal method depends on the anatomic and general patients status. Associated infrarenal and renal arterial lesions can be safely treated in the same time of digestive revascularization. Angioplasty alone yields poor results and should be limited to patients at poor risk for surgery.

  11. Microglial involvement in neuroplastic changes following focal brain ischemia in rats.

    Directory of Open Access Journals (Sweden)

    Alexandre Madinier

    Full Text Available The pathogenesis of ischemic stroke is a complex sequence of events including inflammatory reaction, for which the microglia appears to be a major cellular contributor. However, whether post-ischemic activation of microglial cells has beneficial or detrimental effects remains to be elucidated, in particular on long term brain plasticity events. The objective of our study was to determine, through modulation of post-stroke inflammatory response, to what extent microglial cells are involved in some specific events of neuronal plasticity, neurite outgrowth and synaptogenesis. Since microglia is a source of neurotrophic factors, the identification of the brain-derived neurophic factor (BDNF as possible molecular actor involved in these events was also attempted. As a means of down-regulating the microglial response induced by ischemia, 3-aminobenzamide (3-AB, 90 mg/kg, i.p. was used to inhibit the poly(ADP-ribose polymerase-1 (PARP-1. Indeed, PARP-1 contributes to the activation of the transcription factor NF-kB, which is essential to the upregulation of proinflammatory genes, in particular responsible for microglial activation/proliferation. Experiments were conducted in rats subjected to photothrombotic ischemia which leads to a strong and early microglial cells activation/proliferation followed by an infiltration of macrophages within the cortical lesion, events evaluated at serial time points up to 1 month post-ictus by immunostaining for OX-42 and ED-1. Our most striking finding was that the decrease in acute microglial activation induced by 3-AB was associated with a long term down-regulation of two neuronal plasticity proteins expression, synaptophysin (marker of synaptogenesis and GAP-43 (marker of neuritogenesis as well as to a significant decrease in tissue BDNF production. Thus, our data argue in favour of a supportive role for microglia in brain neuroplasticity stimulation possibly through BDNF production, suggesting that a targeted

  12. Isolation and Characterization of Ischemia-Derived Astrocytes (IDAs) with Ability to Transactivate Quiescent Astrocytes

    Science.gov (United States)

    Villarreal, Alejandro; Rosciszewski, Gerardo; Murta, Veronica; Cadena, Vanesa; Usach, Vanina; Dodes-Traian, Martin M.; Setton-Avruj, Patricia; Barbeito, Luis H.; Ramos, Alberto J.

    2016-01-01

    Reactive gliosis involving activation and proliferation of astrocytes and microglia, is a widespread but largely complex and graded glial response to brain injury. Astroglial population has a previously underestimated high heterogeneity with cells differing in their morphology, gene expression profile, and response to injury. Here, we identified a subset of reactive astrocytes isolated from brain focal ischemic lesions that show several atypical characteristics. Ischemia-derived astrocytes (IDAs) were isolated from early ischemic penumbra and core. IDA did not originate from myeloid precursors, but rather from pre-existing local progenitors. Isolated IDA markedly differ from primary astrocytes, as they proliferate in vitro with high cell division rate, show increased migratory ability, have reduced replicative senescence and grow in the presence of macrophages within the limits imposed by the glial scar. Remarkably, IDA produce a conditioned medium that strongly induced activation on quiescent primary astrocytes and potentiated the neuronal death triggered by oxygen-glucose deprivation. When re-implanted into normal rat brains, eGFP-IDA migrated around the injection site and induced focal reactive gliosis. Inhibition of gamma secretases or culture on quiescent primary astrocytes monolayers facilitated IDA differentiation to astrocytes. We propose that IDA represent an undifferentiated, pro-inflammatory, highly replicative and migratory astroglial subtype emerging from the ischemic microenvironment that may contribute to the expansion of reactive gliosis. Main Points: Ischemia-derived astrocytes (IDA) were isolated from brain ischemic tissue IDA show reduced replicative senescence, increased cell division and spontaneous migration IDA potentiate death of oxygen-glucose deprived cortical neurons IDA propagate reactive gliosis on quiescent astrocytes in vitro and in vivo Inhibition of gamma secretases facilitates IDA differentiation to astrocytes PMID:27313509

  13. Astrocytic gap junctional networks suppress cellular damage in an in vitro model of ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Shinotsuka, Takanori; Yasui, Masato; Nuriya, Mutsuo, E-mail: mnuriya@z2.keio.jp

    2014-02-07

    Highlights: • Astrocytes exhibit characteristic changes in [Ca{sup 2+}]{sub i} under OGD. • Astrocytic [Ca{sup 2+}]{sub i} increase is synchronized with a neuronal anoxic depolarization. • Gap junctional couplings protect neurons as well as astrocytes during OGD. - Abstract: Astrocytes play pivotal roles in both the physiology and the pathophysiology of the brain. They communicate with each other via extracellular messengers as well as through gap junctions, which may exacerbate or protect against pathological processes in the brain. However, their roles during the acute phase of ischemia and the underlying cellular mechanisms remain largely unknown. To address this issue, we imaged changes in the intracellular calcium concentration ([Ca{sup 2+}]{sub i}) in astrocytes in mouse cortical slices under oxygen/glucose deprivation (OGD) condition using two-photon microscopy. Under OGD, astrocytes showed [Ca{sup 2+}]{sub i} oscillations followed by larger and sustained [Ca{sup 2+}]{sub i} increases. While the pharmacological blockades of astrocytic receptors for glutamate and ATP had no effect, the inhibitions of gap junctional intercellular coupling between astrocytes significantly advanced the onset of the sustained [Ca{sup 2+}]{sub i} increase after OGD exposure. Interestingly, the simultaneous recording of the neuronal membrane potential revealed that the onset of the sustained [Ca{sup 2+}]{sub i} increase in astrocytes was synchronized with the appearance of neuronal anoxic depolarization. Furthermore, the blockade of gap junctional coupling resulted in a concurrent faster appearance of neuronal depolarizations, which remain synchronized with the sustained [Ca{sup 2+}]{sub i} increase in astrocytes. These results indicate that astrocytes delay the appearance of the pathological responses of astrocytes and neurons through their gap junction-mediated intercellular network under OGD. Thus, astrocytic gap junctional networks provide protection against tissue damage

  14. Oxygen and glucose deprivation (OGD)-induced spreading depression in the Substantia Nigra.

    Science.gov (United States)

    Karunasinghe, Rashika N; Lipski, Janusz

    2013-08-21

    Spreading depression (SD) is a profound depolarization of neurons and glia that propagates in a wave-like manner across susceptible brain regions, and can develop during periods of compromised cellular energy such as ischemia, when it influences the severity of acute neuronal damage. Although SD has been well characterized in the cerebral cortex and hippocampus, little is known of this event in the Substantia Nigra (SN), a brainstem nucleus engaged in motor control and reward-related behavior. Transverse brain slices (250 μm; P21-23 rats) containing the SN were subject to oxygen and glucose deprivation (OGD) tests, modeling brain ischemia. SD developed in lateral aspects of the SN within 3.3±0.2 min of OGD onset, and spread through the Substantia Nigra pars reticulata (SNr), as indicated by fast-occurring and propagating increased tissue light transmittance and negative shift of extracellular DC potential. These events were associated with profound mitochondrial membrane depolarization (ΔΨm) throughout the SN, as demonstrated by increased Rhodamine 123 fluorescence. Extracellular recordings from individual SNr neurons indicated rapid depolarization followed by depolarizing block, while dopaminergic neurons in the Substantia Nigra pars compacta (SNc) showed inhibition of firing associated with hyperpolarization. SD evoked in the SNr was similar to OGD-induced SD in the CA1 region in hippocampal slices. In the hippocampus, SD also developed during anoxia or aglycemia alone (associated with less profound ΔΨm than OGD), while these conditions rarely led to SD in the SNr. Our results demonstrate that OGD consistently evokes SD in the SN, and that this phenomenon only involves the SNr. It remains to be established whether nigral SD contributes to neuronal damage associated with a sudden-onset form of Parkinson's disease known as 'vascular parkinsonism'.

  15. Spreading of liquid drops over porous substrates.

    Science.gov (United States)

    Starov, V M; Zhdanov, S A; Kosvintsev, S R; Sobolev, V D; Velarde, M G

    2003-07-01

    The spreading of small liquid drops over thin and thick porous layers (dry or saturated with the same liquid) has been investigated in the case of both complete wetting (silicone oils of different viscosities) and partial wetting (aqueous SDS solutions of different concentrations). Nitrocellulose membranes of different porosity and different average pore size have been used as a model of thin porous layers, glass and metal filters have been used as a model of thick porous substrates. The first problem under investigation has been the spreading of small liquid drops over thin porous layers saturated with the same liquid. An evolution equation describing the drop spreading has been deduced, which showed that both an effective lubrication and the liquid exchange between the drop and the porous substrates are equally important. Spreading of silicone oils over different nitrocellulose microfiltration membranes was carried out. The experimental laws of the radius of spreading on time confirmed the theory predictions. The spreading of small liquid drops over thin dry porous layers has also been investigated from both theoretical and experimental points of view. The drop motion over a dry porous layer appears caused by the interplay of two processes: (a). the spreading of the drop over already saturated parts of the porous layer, which results in a growth of the drop base, and (b). the imbibition of the liquid from the drop into the porous substrate, which results in a shrinkage of the drop base and a growth of the wetted region inside the porous layer. As a result of these two competing processes the radius of the drop base goes through a maximum as time proceeds. A system of two differential equations has been derived to describe the time evolution of the radii of both the drop base and the wetted region inside the porous layer. This system includes two parameters, one accounts for the effective lubrication coefficient of the liquid over the wetted porous substrate, and

  16. Hippocampal neurogenesis in the new model of global cerebral ischemia

    Science.gov (United States)

    Kisel, A. A.; Chernysheva, G. A.; Smol'yakova, V. I.; Savchenko, R. R.; Plotnikov, M. B.; Khodanovich, M. Yu.

    2015-11-01

    The study aimed to evaluate the changes of hippocampal neurogenesis in a new model of global transient cerebral ischemia which was performed by the occlusion of the three main vessels (tr. brachiocephalicus, a. subclavia sinistra, and a. carotis communis sinistra) branching from the aortic arch and supplying the brain. Global transitory cerebral ischemia was modeled on male rats (weight = 250-300 g) under chloral hydrate with artificial lung ventilation. Animals after the same surgical operation without vessel occlusion served as sham-operated controls. The number of DCX-positive (doublecortin, the marker of immature neurons) cells in dentate gyrus (DG) and CA1-CA3 fields of hippocampus was counted at the 31st day after ischemia modeling. It was revealed that global cerebral ischemia decreased neurogenesis in dentate gyrus in comparison with the sham-operated group (Pneurogenesis in CA1-CA3 fields was increased as compared to the control (P<0.05).

  17. Reactive astrocytes express NADPH diaphorase in vivo after transient ischemia.

    Science.gov (United States)

    Endoh, M; Maiese, K; Pulsinelli, W A; Wagner, J A

    1993-05-14

    In the hippocampus, ten minutes of transient global ischemia results in the death of CA1 pyramidal cells after a period of one to three days. The neurons in the CA1 region constitutively express NADPH-D (NADPH diaphorase activity). In contrast, astrocytes in the hippocampus do not normally express NADPH-D; but a population of reactive astrocytes (GFAP+ cells) begin to express of NADPH-D one day after transient global ischemia. NADPH-D is thought to be a histological marker for Nitric Oxide Synthase (NOS), the enzyme that is responsible for the synthesis of NO, a potent neurotoxin. We suggest that this increase in NADPH-D/NOS expression is an important element in the sequence of changes that occurs after ischemia, and that NO derived from reactive astrocytes or from neurons may play a causal role in neural cell death after ischemia in the hippocampus.

  18. Mechanisms of symptomatic spinal cord ischemia after TEVAR

    DEFF Research Database (Denmark)

    Czerny, Martin; Eggebrecht, Holger; Sodeck, Gottfried;

    2012-01-01

    To test the hypothesis that simultaneous closure of at least 2 independent vascular territories supplying the spinal cord and/or prolonged hypotension may be associated with symptomatic spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR)....

  19. Preclinical models to investigate retinal ischemia: Advances and drawbacks

    Directory of Open Access Journals (Sweden)

    Gillipsie eMinhas

    2012-05-01

    Full Text Available Retinal ischemia is a frequent source of irreparable visual impairment affecting over a hundred million individuals in the world. It is associated with a wide range of retinal disorders like ischemic optic neuropathies, obstructive retinopathies, carotid occlusive disorders, diabetic retinopathy and glaucoma. Compared to other tissues retina has a higher metabolic rate; any disruption in blood supply can have an effect on the supply of oxygen leading to retinal ischemia. If occlusion is not rescued the outcome is irreversible with ischemic and apoptotic cascades resulting in cell death. In addition to in-vitro models, animal models are necessary to further our understanding of the etiology, pathology, and evolution of retinal ischemia besides the evaluation, development, and improvement of therapeutic strategies. The various existing animal models of retinal ischemia are characterised by obstruction of retinal circulation that allows the study of neurovascular changes. In this review we provide an overview of major models and emerging preclinical therapeutic strategies.

  20. Exercise Tonometry for the Diagnosis of Chronic Gastrointestinal Ischemia

    NARCIS (Netherlands)

    J.A. Otte

    2006-01-01

    textabstractThis thesis investigates the role of gastrointestinal exercise tonometry as a functional diagnostic test in patients suspected of chronic gastrointestinal ischemia. In contrast with all other diagnostic modalities (angiography, duplex sonography, CT- and MRangiography) that only provi

  1. Myocardial ischemia in hypertrophic cardiomyopathy; Isquemia miocardica na cardiomiopatia hipertrofica

    Energy Technology Data Exchange (ETDEWEB)

    Lima Filho, Moyses de Oliveira; Figueiredo, Geraldo L.; Simoes, Marcus V.; Pyntia, Antonio O.; Marin Neto, Jose Antonio [Sao Paulo Univ., Ribeirao Preto, SP (Brazil). Faculdade de Medicina. Div. de Cardiologia

    2000-08-01

    Myocardial ischemia in hypertrophic cardiomyopathy is multifactorial and explains the occurrence of angina, in about 50% of patients. The pathophysiology of myocardial ischemia may be explained by the increase of the ventricular mass and relative paucity of the coronary microcirculation; the elevated ventricular filling pressures and myocardial stiffness causing a compression of the coronary microvessels; the impaired coronary vasodilator flow reserve caused by anatomic and functional abnormalities; and the systolic compression of epicardial vessel (myocardial bridges). Myocardial ischemia must be investigated by perfusion scintigraphic methods since its presence influences the prognosis and has relevant clinical implications for management of patients. Patients with hypertrophic cardiomyopathy and documented myocardial ischemia usually need to undergo invasive coronary angiography to exclude the presence of concomitant atherosclerotic coronary disease. (author)

  2. Multiple coronary arterial loops as a cause of myocardial ischemia

    Science.gov (United States)

    Bashour, Tali T.; Mansour, Nagi N.; Lee, Damon

    1993-01-01

    A case of long-standing angina with ischemia documented by exercise testing and thallium scintigraphy in a patient who had multiple proximal loops in all three major coronary arteries in the absence of luminal stenosis, is reported.

  3. The complement system in ischemia-reperfusion injuries.

    Science.gov (United States)

    Gorsuch, William B; Chrysanthou, Elvina; Schwaeble, Wilhelm J; Stahl, Gregory L

    2012-11-01

    Tissue injury and inflammation following ischemia and reperfusion of various organs have been recognized for many years. Many reviews have been written over the last several decades outlining the role of complement in ischemia/reperfusion injury. This short review provides a current state of the art knowledge on the complement pathways activated, complement components involved and a review of the clinical biologics/inhibitors used in the clinical setting of ischemia/reperfusion. This is not a complete review of the complement system in ischemia and reperfusion injury but will give the reader an updated view point of the field, potential clinical use of complement inhibitors, and the future studies needed to advance the field.

  4. Parallel Impurity Spreading During Massive Gas Injection

    Science.gov (United States)

    Izzo, V. A.

    2016-10-01

    Extended-MHD simulations of disruption mitigation in DIII-D demonstrate that both pre-existing islands (locked-modes) and plasma rotation can significantly influence toroidal spreading of impurities following massive gas injection (MGI). Given the importance of successful disruption mitigation in ITER and the large disparity in device parameters, empirical demonstrations of disruption mitigation strategies in present tokamaks are insufficient to inspire unreserved confidence for ITER. Here, MHD simulations elucidate how impurities injected as a localized jet spread toroidally and poloidally. Simulations with large pre-existing islands at the q = 2 surface reveal that the magnetic topology strongly influences the rate of impurity spreading parallel to the field lines. Parallel spreading is largely driven by rapid parallel heat conduction, and is much faster at low order rational surfaces, where a short parallel connection length leads to faster thermal equilibration. Consequently, the presence of large islands, which alter the connection length, can slow impurity transport; but the simulations also show that the appearance of a 4/2 harmonic of the 2/1 mode, which breaks up the large islands, can increase the rate of spreading. This effect is seen both for simulations with spontaneously growing and directly imposed 4/2 modes. Given the prevalence of locked-modes as a cause of disruptions, understanding the effect of large islands is of particular importance. Simulations with and without islands also show that rotation can alter impurity spreading, even reversing the predominant direction of spreading, which is toward the high-field-side in the absence of rotation. Given expected differences in rotation for ITER vs. DIII-D, rotation effects are another important consideration when extrapolating experimental results. Work supported by US DOE under DE-FG02-95ER54309.

  5. A network model for Ebola spreading.

    Science.gov (United States)

    Rizzo, Alessandro; Pedalino, Biagio; Porfiri, Maurizio

    2016-04-01

    The availability of accurate models for the spreading of infectious diseases has opened a new era in management and containment of epidemics. Models are extensively used to plan for and execute vaccination campaigns, to evaluate the risk of international spreadings and the feasibility of travel bans, and to inform prophylaxis campaigns. Even when no specific therapeutical protocol is available, as for the Ebola Virus Disease (EVD), models of epidemic spreading can provide useful insight to steer interventions in the field and to forecast the trend of the epidemic. Here, we propose a novel mathematical model to describe EVD spreading based on activity driven networks (ADNs). Our approach overcomes the simplifying assumption of homogeneous mixing, which is central to most of the mathematically tractable models of EVD spreading. In our ADN-based model, each individual is not bound to contact every other, and its network of contacts varies in time as a function of an activity potential. Our model contemplates the possibility of non-ideal and time-varying intervention policies, which are critical to accurately describe EVD spreading in afflicted countries. The model is calibrated from field data of the 2014 April-to-December spreading in Liberia. We use the model as a predictive tool, to emulate the dynamics of EVD in Liberia and offer a one-year projection, until December 2015. Our predictions agree with the current vision expressed by professionals in the field, who consider EVD in Liberia at its final stage. The model is also used to perform a what-if analysis to assess the efficacy of timely intervention policies. In particular, we show that an earlier application of the same intervention policy would have greatly reduced the number of EVD cases, the duration of the outbreak, and the infrastructures needed for the implementation of the intervention.

  6. High-temperature spreading kinetics of metals

    Energy Technology Data Exchange (ETDEWEB)

    Rauch, N.

    2005-05-15

    In this PhD work a drop transfer setup combined with high speed photography has been used to analyze the spreading of Ag on polished polycrystalline Mo and single crystalline Mo (110) and (100) substrates. The objective of this work was to unveil the basic phenomena controlling spreading in metal-metal systems. The observed spreading kinetics were compared with current theories of low and high temperature spreading such as a molecular kinetic model and a fluid flow model. Analyses of the data reveal that the molecular model does describe the fastest velocity data well for all the investigated systems. Therefore, the energy which is dissipated during the spreading process is a dissipation at the triple line rather than dissipation due to the viscosity in the liquid. A comparison of the determined free activation energy for wetting of {delta}G95{approx}145kJ/mol with literature values allows the statement that the rate determining step seems to be a surface diffusion of the Ag atoms along the triple line. In order to investigate possible ridge formation, due to local atomic diffusion of atoms of the substrate at the triple during the spreading process, grooving experiments of the polycrystalline Mo were performed to calculate the surface diffusities that will control ridge evolution. The analyses of this work showed that a ridge formation at the fastest reported wetting velocities was not possible if there is no initial perturbation for a ridge. If there was an initial perturbation for a ridge the ridge had to be much smaller than 1 nm in order to be able to move with the liquid font. Therefore ridge formation does not influence the spreading kinetics for the studied system and the chosen conditions. SEM, AFM and TEM investigations of the triple line showed that ridge formation does also not occur at the end of the wetting experiment when the drop is close to equilibrium and the wetting velocity is slow. (orig.)

  7. Pylephlebitis secondary to strangulated umbilical hernia with small bowel ischemia

    Directory of Open Access Journals (Sweden)

    Ennio Bruschi

    2013-08-01

    Full Text Available Pylephlebitis is a septic thrombophlebitis of the portal venous system that infrequently complicates small bowel infarction. We present a case of pylephlebitis with portomesenteric vein gas bubbles secondary to small bowel ischemia caused by a strangulated umbilical hernia, diagnosed on computed tomography (CT and confirmed in the operating theater. This case is an example of the usefulness of CT in early recognition of suggestive radiologic findings of pylephlebitis associated with intestinal ischemia for prompt treatment of the patient.

  8. Effect of thrombolytic therapy on postinfarction myocardial ischemia

    DEFF Research Database (Denmark)

    Mickley, H; Junker, A; Møller, M

    1994-01-01

    be responsible for the reduction in cardiac death. So far it has not been clearly established how thrombolytic therapy affects postinfarction myocardial ischemia. From studies evaluating ST segment changes on exercise testing or ambulatory monitoring it is concluded that thrombolysis probably results...... in a reduction of residual ischemia. The reduced ischemic burden is proposed to be one important pathophysiological mechanism underlying the frequently observed improvement in hemodynamic stress test variables following thrombolytic treatment....

  9. Quantitative Ischemia Detection During Cardiac MR Stress Testing

    Science.gov (United States)

    2007-11-02

    of Health, Bethesda, MD, USA 4 Cardiology Division of the School of Medicine, Johns Hopkins University, Baltimore, MD, USA Abstract- Because ECG...independent detection of the onset of ischemia during acute coronary occlusion. Six mongrel dogs underwent acute coronary artery ischemia of 2 minutes...revised 1985). Six mongrel dogs (20-25 kgs) were preanesthetized with 10 mg/kg ketamine, 2.4 mg/kg xylazine, and 0.02 mg/kg atropine intramuscularly

  10. Spinal cord ischemia following thoracotomy without epidural anesthesia.

    Science.gov (United States)

    Raz, Aeyal; Avramovich, Aharon; Saraf-Lavi, Efrat; Saute, Milton; Eidelman, Leonid A

    2006-06-01

    Paraplegia is an uncommon yet devastating complication following thoracotomy, usually caused by compression or ischemia of the spinal cord. Ischemia without compression may be a result of global ischemia, vascular injury and other causes. Epidural anesthesia has been implicated as a major cause. This report highlights the fact that perioperative cord ischemia and paraplegia may be unrelated to epidural intervention. A 71-yr-old woman was admitted for a left upper lobectomy for resection of a non-small cell carcinoma of the lung. The patient refused epidural catheter placement and underwent a left T5-6 thoracotomy under general anesthesia. During surgery, she was hemodynamically stable and good oxygen saturation was maintained. Several hours following surgery the patient complained of loss of sensation in her legs. Neurological examination disclosed a complete motor and sensory block at the T5-6 level. Magnetic resonance imaging (MRI) revealed spinal cord ischemia. The patient received iv steroid treatment, but remained paraplegic. Five months following the surgery there was only partial improvement in her motor symptoms. A follow-up MRI study was consistent with a diagnosis of spinal cord ischemia. In this case of paraplegia following thoracic surgery for lung resection, epidural anesthesia/analgesia was not used. The MRI demonstrated evidence of spinal cord ischemia, and no evidence of cord compression. This case highlights that etiologies other than epidural intervention, such as injury to the spinal segmental arteries during thoracotomy, should be considered as potential causes of cord ischemia and resultant paraplegia in this surgical population.

  11. Cerebral Ischemia Due to Traumatic Carotid Artery Dissection: Case Report

    Directory of Open Access Journals (Sweden)

    Deniz Kamacı Şener

    2012-12-01

    Full Text Available Blunt injury to the neck region may lead to carotid artery dissection and cerebral ischemia. Blunt injury to carotid artery is not frequent but determination of the presence of trauma in the history of stroke patients will provide early diagnosis and treatment of them. In this article, a case with cerebral ischemia resulting from traumatic carotid artery dissection is presented and clinical findings, diagnostic procedures and choice of treatment are discussed in the light of the literature.

  12. MICROCIRCULATORY ISCHEMIA AND STATINS: LESSONS OF INTERVENTION CARDIOLOGY

    Directory of Open Access Journals (Sweden)

    An. A. Alexandrov

    2015-12-01

    Full Text Available Review is devoted to the pathogenesis of microcirculatory ischemia. Microcirculatory dysfunction has been identified in different groups of patients including syndrome X, diabetes mellitus 2 type, coronary heart disease. In coronary patients after transluminal angioplasty microcirculatory dysfunction is the reason of phenomenon of “non-reflow”. In result the procedure of revascularization is less effective. Therapy by statins can be beneficial for patients with microcirculatory ischemia.

  13. [Antioxidant effects of antihypoxic drugs in cerebral ischemia].

    Science.gov (United States)

    Plotnikov, M B; Kobzeva, E A; Plotnikova, T M

    1992-05-01

    Cerebral ischemia in rats (both carotid arteries occlusion) during 30 min, 3 hours and recirculation (1 hour) after ischemia (30 min) stimulated diene conjugates and fluorescent products accumulation in brain tissue. Intraperitoneal injection of sodium hydroxybutyrate (100 mg/kg), bemitil (50 mg/kg), ethomersol (50 mg/kg) reduced brain lipid peroxidation and did not yield in this respect to emoxypin (5 mg/kg). In contrast to emoxypin, sodium hydroxybutyrate, bemitil and ethomersol had no antiradical activity.

  14. Intermittent Ischemia but Not Ischemic Preconditioning Is Effective in Restoring Bile Flow After Ischemia Reperfusion Injury in the Livers of Aged Rats

    NARCIS (Netherlands)

    Schiesser, Marc; Wittert, Anna; Nieuwenhuijs, Vincent B.; Morphett, Arthur; Padbury, Robert T. A.; Barritt, Greg J.

    2009-01-01

    BackgroundlAims. Ischemic preconditioning (IPC) and intermittent ischemia (INT) reduce liver injury following ischemia reperfusion in liver resections. Aged livers are at higher risk for ischemia reperfusion injury, but little is known of the effectiveness of IPC and INT in aged livers. The aim of t

  15. Variation of wave directional spread parameters along the Indian coast

    Digital Repository Service at National Institute of Oceanography (India)

    SanilKumar, V.

    Directional spreading of wave energy is popularly modeled with the help of the Cosine Power model and it mainly depends on the spreading parameter. This paper describes the variation of the spreading parameter estimated based on the wave data...

  16. Reperfusion of specific cortical areas is associated with improvement in distinct forms of hemispatial neglect.

    Science.gov (United States)

    Khurshid, Shaan; Trupe, Lydia A; Newhart, Melissa; Davis, Cameron; Molitoris, John J; Medina, Jared; Leigh, Richard; Hillis, Argye E

    2012-05-01

    To test the hypothesis that restoring blood flow to specific right cortical regions in acute stroke results in improvement in distinct forms of hemispatial neglect distinguished by reference frame: viewer-centered versus stimulus-centered neglect. Twenty five patients with acute right stroke were evaluated at Day 1 and Day 3-5 with a battery of neglect tests and Diffusion- and Perfusion-Weighted MR Imaging. Multivariate linear regression analysis revealed Brodmann areas (BAs) where reperfusion predicted degree of improvement in scores on each type of neglect, independently of reperfusion of other areas, total change in the volume of infarct or hypoperfusion, and age. Reperfusion of dorsal frontoparietal cortex (including BAs 40, 46, and 4) independently predicted improvement in viewer-centered neglect, such as detecting stimuli on left in line cancellation and scene copying (r=.951; p<.0001). Reperfusion of a more ventral temporo-occipital cortex, including right BAs 37, 38, 21 and 18, independently contributed to improvement in stimulus-centered neglect, such as detecting left gaps in circles (r=.926; p<.0001). Reperfusion of right midfusiform gyrus (temporal occipital cortex), change in total volume of ischemia, change in volume of hypoperfusion and age predicted degree of improvement in reading (reduction in "neglect dyslexic" errors; r=.915; p<.0001). Results demonstrate that reperfusing specific cortical regions yields improvement in different types of neglect. Copyright © 2011 Elsevier Srl. All rights reserved.

  17. Small-World Characteristics of Cortical Connectivity Changes in Acute Stroke.

    Science.gov (United States)

    Caliandro, Pietro; Vecchio, Fabrizio; Miraglia, Francesca; Reale, Giuseppe; Della Marca, Giacomo; La Torre, Giuseppe; Lacidogna, Giordano; Iacovelli, Chiara; Padua, Luca; Bramanti, Placido; Rossini, Paolo Maria

    2017-01-01

    Background After cerebral ischemia, disruption and subsequent reorganization of functional connections occur both locally and remote to the lesion. Recently, complexity of brain connectivity has been described using graph theory, a mathematical approach that depicts important properties of complex systems by quantifying topologies of network representations. Functional and dynamic changes of brain connectivity can be reliably analyzed via electroencephalography (EEG) recordings even when they are not yet reflected in structural changes of connections. Objective We tested whether and how ischemic stroke in the acute stage may determine changes in small-worldness of cortical networks as measured by cortical sources of EEG. Methods Graph characteristics of EEG of 30 consecutive stroke patients in acute stage (no more than 5 days after the event) were examined. Connectivity analysis was performed using eLORETA in both hemispheres. Results Network rearrangements were mainly detected in delta, theta, and alpha bands when patients were compared with healthy subjects. In delta and alpha bands similar findings were observed in both hemispheres regardless of the side of ischemic lesion: bilaterally decreased small-worldness in the delta band and bilaterally increased small-worldness in the alpha2 band. In the theta band, bilaterally decreased small-worldness was observed only in patients with stroke in the left hemisphere. Conclusions After an acute stroke, brain cortex rearranges its network connections diffusely, in a frequency-dependent modality probably in order to face the new anatomical and functional frame.

  18. Contribution of constitutively proliferating precursor cell subtypes to dentate neurogenesis after cortical infarcts

    Directory of Open Access Journals (Sweden)

    Oberland Julia

    2010-11-01

    Full Text Available Abstract Background It is well known that focal ischemia increases neurogenesis in the adult dentate gyrus of the hippocampal formation but the cellular mechanisms underlying this proliferative response are only poorly understood. We here investigated whether precursor cells which constitutively proliferate before the ischemic infarct contribute to post-ischemic neurogenesis. To this purpose, transgenic mice expressing green fluorescent protein (GFP under the control of the nestin promoter received repetitive injections of the proliferation marker bromodeoxyuridine (BrdU prior to induction of cortical infarcts. We then immunocytochemically analyzed the fate of these BrdU-positive precursor cell subtypes from day 4 to day 28 after the lesion. Results Quantification of BrdU-expressing precursor cell populations revealed no alteration in number of radial glia-like type 1 cells but a sequential increase of later precursor cell subtypes in lesioned animals (type 2a cells at day 7, type 3 cells/immature neurons at day 14. These alterations result in an enhanced survival of mature neurons 4 weeks postinfarct. Conclusions Focal cortical infarcts recruit dentate precursor cells generated already before the infarct and significantly contribute to an enhanced neurogenesis. Our findings thereby increase our understanding of the complex cellular mechanisms of postlesional neurogenesis.

  19. Autoregulation of cerebral blood flow in experimental focal brain ischemia.

    Science.gov (United States)

    Dirnagl, U; Pulsinelli, W

    1990-05-01

    The relationship between systemic arterial pressure (SAP) and neocortical microcirculatory blood-flow (CBF) in areas of focal cerebral ischemia was studied in 15 spontaneously hypertensive rats (SHRs) anesthetized with halothane (0.5%). Ischemia was induced by ipsilateral middle cerebral artery/common carotid artery occlusion and CBF was monitored continuously in the ischemic territory using laser-Doppler flowmetry during manipulation of SAP with I-norepinephrine (hypertension) or nitroprusside (hypotension). In eight SHRs not subjected to focal ischemia, we demonstrated that 0.5% halothane and the surgical manipulations did not impair autoregulation. Autoregulation was partly preserved in ischemic brain tissue with a CBF of greater than 30% of preocclusion values. In areas where ischemic CBF was less than 30% of preocclusion values, autoregulation was completely lost. Changes in SAP had a greater influence on CBF in tissue areas where CBF ranged from 15 to 30% of baseline (9% change in CBF with each 10% change in SAP) than in areas where CBF was less than 15% of baseline (6% change in CBF with each 10% change in SAP). These findings demonstrate that the relationship between CBF and SAP in areas of focal ischemia is highly dependent on the severity of ischemia. Autoregulation is lost in a gradual manner until CBF falls below 30% of normal. In areas without autoregulation, the slope of the CBF/SAP relationship is inversely related to the degree of ischemia.

  20. Neuroprotective effects of rutaecarpine on cerebral ischemia reperfusion injury**

    Institute of Scientific and Technical Information of China (English)

    Chunlin Yan; Ji Zhang; Shu Wang; Guiping Xue; Yong Hou

    2013-01-01

    Rutaecarpine, an active component of the traditional Chinese medicine Tetradium ruticarpum, has been shown to improve myocardial ischemia reperfusion injury. Because both cardiovascular and cerebrovascular diseases are forms of ischemic vascular disease, they are closely related. We hypothesized that rutaecarpine also has neuroprotective effects on cerebral ischemia reperfusion injury. A cerebral ischemia reperfusion model was established after 84, 252 and 504 µg/kg carpine were given to mice via intraperitoneal injection, daily for 7 days. Results of the step through test, 2,3,5-triphenyl tetrazolium chloride dyeing and oxidative stress indicators showed that rutae-carpine could improve learning and memory ability, neurological symptoms and reduce infarction volume and cerebral water content in mice with cerebral ischemia reperfusion injury. Rutaecarpine could significantly decrease the malondialdehyde content and increase the activities of superoxide dismutase and glutathione peroxidase in mouse brain. Therefore, rutaecarpine could improve neu-rological function fol owing injury induced by cerebral ischemia reperfusion, and the mechanism of this improvement may be associated with oxidative stress. These results verify that rutaecarpine has neuroprotective effects on cerebral ischemia reperfusion in mice.

  1. Renal Cortical Lactate Dehydrogenase: A Useful, Accurate, Quantitative Marker of In Vivo Tubular Injury and Acute Renal Failure.

    Directory of Open Access Journals (Sweden)

    Richard A Zager

    Full Text Available Studies of experimental acute kidney injury (AKI are critically dependent on having precise methods for assessing the extent of tubular cell death. However, the most widely used techniques either provide indirect assessments (e.g., BUN, creatinine, suffer from the need for semi-quantitative grading (renal histology, or reflect the status of residual viable, not the number of lost, renal tubular cells (e.g., NGAL content. Lactate dehydrogenase (LDH release is a highly reliable test for assessing degrees of in vitro cell death. However, its utility as an in vivo AKI marker has not been defined. Towards this end, CD-1 mice were subjected to graded renal ischemia (0, 15, 22, 30, 40, or 60 min or to nephrotoxic (glycerol; maleate AKI. Sham operated mice, or mice with AKI in the absence of acute tubular necrosis (ureteral obstruction; endotoxemia, served as negative controls. Renal cortical LDH or NGAL levels were assayed 2 or 24 hrs later. Ischemic, glycerol, and maleate-induced AKI were each associated with striking, steep, inverse correlations (r, -0.89 between renal injury severity and renal LDH content. With severe AKI, >65% LDH declines were observed. Corresponding prompt plasma and urinary LDH increases were observed. These observations, coupled with the maintenance of normal cortical LDH mRNA levels, indicated the renal LDH efflux, not decreased LDH synthesis, caused the falling cortical LDH levels. Renal LDH content was well maintained with sham surgery, ureteral obstruction or endotoxemic AKI. In contrast to LDH, renal cortical NGAL levels did not correlate with AKI severity. In sum, the above results indicate that renal cortical LDH assay is a highly accurate quantitative technique for gauging the extent of experimental acute ischemic and toxic renal injury. That it avoids the limitations of more traditional AKI markers implies great potential utility in experimental studies that require precise quantitation of tubule cell death.

  2. Spreading of Cholera through Surface Water

    Science.gov (United States)

    Bertuzzo, E.; Casagrandi, R.; Gatto, M.; Rodriguez-Iturbe, I.; Rinaldo, A.

    2009-12-01

    Cholera epidemics are still a major public health concern to date in many areas of the world. In order to understand and forecast cholera outbreaks, one of the most important factors is the role played by the environmental matrix in which the disease spreads. We study how river networks, acting as environmental corridors for pathogens, affect the spreading of cholera epidemics. The environmental matrix in which the disease spreads is constituted by different human communities and their hydrologic interconnections. Each community is characterized by its spatial position, population size, water resources availability and hygiene conditions. By implementing a spatially explicit cholera model we seek the effects on epidemic dynamics of: i) the topology and metrics of the pathogens pathways that connect different communities; ii) the spatial distribution of the population size; and iii) the spatial distributions and quality of surface water resources and public health conditions, and how they vary with population size. The model has been applied to study the space-time evolution of a well documented cholera epidemic occurred in the KwaZulu-Natal province of South Africa. The epidemic lasted for two years and involved about 140,000 confirmed cholera cases. The model does well in reproducing the distribution of the cholera cases during the two outbreaks as well as their spatial spreading. We further extend the model by deriving the speed of propagation of traveling fronts in the case of uniformly distributed systems for different topologies: one and two dimensional lattices and river networks. The derivation of the spreading celerity proves instrumental in establishing the overall conditions for the relevance of spatially explicit models. The conditions are sought by comparison between spreading and disease timescales. Consider a cholera epidemic that starts from a point and spreads throughout a finite size system, it is possible to identify two different timescales: i

  3. Free energy analysis of cell spreading.

    Science.gov (United States)

    McEvoy, Eóin; Deshpande, Vikram S; McGarry, Patrick

    2017-10-01

    In this study we present a steady-state adaptation of the thermodynamically motivated stress fiber (SF) model of Vigliotti et al. (2015). We implement this steady-state formulation in a non-local finite element setting where we also consider global conservation of the total number of cytoskeletal proteins within the cell, global conservation of the number of binding integrins on the cell membrane, and adhesion limiting ligand density on the substrate surface. We present a number of simulations of cell spreading in which we consider a limited subset of the possible deformed spread-states assumed by the cell in order to examine the hypothesis that free energy minimization drives the process of cell spreading. Simulations suggest that cell spreading can be viewed as a competition between (i) decreasing cytoskeletal free energy due to strain induced assembly of cytoskeletal proteins into contractile SFs, and (ii) increasing elastic free energy due to stretching of the mechanically passive components of the cell. The computed minimum free energy spread area is shown to be lower for a cell on a compliant substrate than on a rigid substrate. Furthermore, a low substrate ligand density is found to limit cell spreading. The predicted dependence of cell spread area on substrate stiffness and ligand density is in agreement with the experiments of Engler et al. (2003). We also simulate the experiments of Théry et al. (2006), whereby initially circular cells deform and adhere to "V-shaped" and "Y-shaped" ligand patches. Analysis of a number of different spread states reveals that deformed configurations with the lowest free energy exhibit a SF distribution that corresponds to experimental observations, i.e. a high concentration of highly aligned SFs occurs along free edges, with lower SF concentrations in the interior of the cell. In summary, the results of this study suggest that cell spreading is driven by free energy minimization based on a competition between decreasing

  4. Soluble epoxide hydrolase gene deletion improves blood flow and reduces infarct size after cerebral ischemia in reproductively senescent female mice

    Directory of Open Access Journals (Sweden)

    Kristen L Zuloaga

    2015-01-01

    Full Text Available Soluble epoxide hydrolase (sEH, a key enzyme in the metabolism of vasodilatory epoxyeicosatrienoic acids (EETs, is sexually dimorphic, suppressed by estrogen, and contributes to underlying sex differences in cerebral blood flow and injury after cerebral ischemia. We tested the hypothesis that sEH inhibition or gene deletion in reproductively senescent (RS female mice would increase cerebral perfusion and decrease infarct size following stroke. RS (15-18 month old and young (3-4 month old female sEH knockout (sEHKO mice and wild type (WT mice were subjected to 45 min middle cerebral artery occlusion (MCAO with laser Doppler perfusion monitoring. WT mice were treated with vehicle or a sEH inhibitor t-AUCB at the time of reperfusion and every 24hrs thereafter for 3 days. Differences in regional cerebral blood flow were measured in vivo using optical microangiography. Infarct size was measured 3 days after reperfusion. Infarct size and cerebral perfusion 24h after MCAO were not altered by age. Both sEH gene deletion and sEH inhibition increased cortical perfusion 24h after MCAO. Neither sEH gene deletion nor sEH inhibition reduced infarct size in young mice. However, sEH gene deletion, but not sEH inhibition of the hydrolase domain of the enzyme, decreased infarct size in RS mice. Results of these studies show that sEH gene deletion and sEH inhibition enhance cortical perfusion following MCAO and sEH gene deletion reduces damage after ischemia in RS female mice; however this neuroprotection in absent is young mice.

  5. Post-Tanner spreading of nematic droplets

    Energy Technology Data Exchange (ETDEWEB)

    Mechkov, S; Oshanin, G [Laboratoire de Physique Theorique de la Matiere Condensee, Universite Pierre et Marie Curie, 4 place Jussieu, 75252 Paris Cedex 5 (France); Cazabat, A M, E-mail: mechkov@lptmc.jussieu.f, E-mail: anne-marie.cazabat@lps.ens.f, E-mail: oshanin@lptmc.jussieu.f [Laboratoire de Physique Statistique, Ecole Normale Superieure, 75252 Paris Cedex 5 (France)

    2009-11-18

    The quasistationary spreading of a circular liquid drop on a solid substrate typically obeys the so-called Tanner law, with the instantaneous base radius R(t) growing with time as Rapproxt{sup 1/10}-an effect of the dominant role of capillary forces for a small-sized droplet. However, for droplets of nematic liquid crystals, a faster spreading law sets in at long times, so that Rapproxt{sup a}lpha with alpha significantly larger than the Tanner exponent 1/10. In the framework of the thin film model (or lubrication approximation), we describe this 'acceleration' as a transition to a qualitatively different spreading regime driven by a strong substrate-liquid interaction specific to nematics (antagonistic anchoring at the interfaces). The numerical solution of the thin film equation agrees well with the available experimental data for nematics, even though the non-Newtonian rheology has yet to be taken into account. Thus we complement the theory of spreading with a post-Tanner stage, noting that the spreading process can be expected to cross over from the usual capillarity-dominated stage to a regime where the whole reservoir becomes a diffusive film in the sense of Derjaguin.

  6. [How to evaluate recirculation effect on brain function after global ischemia--broad spectral EEG analysis by Fourier method].

    Science.gov (United States)

    Nakata, M

    1987-03-01

    EEG alterations after 5 or 10 minutes of global ischemia were investigated for 6 hours of postischemic period in 18 adult cats, together with biophysiological parameters such as cerebral blood flow, intracranial pressure, systemic blood pressure, heart rate, and blood gases. Our EEG analytical system is composed of high fidelity pre-amplifier, AA 6 MK II (Medelec Limited, England) and signal processor 7T 08 (NEC-SanEi, Japan). It is qualified to analyze frequencies up to 20 kHz within 3 dB cut-off. Particular features of our EEG analytical method are focused on Fourier analysis about broad frequency bands, frequency and amplitude spectra to be expressed on bi-logarithmic graph and direct EEG recordings from various structures of the brain. On the basis of fluctuation theory following 3 types were divided; Type f which corresponds to 1/f fluctuation, Type L which corresponds to Lorentzian fluctuation, Type f+L which is the sum of Type f and L. The distribution of these types in the central nervous system corresponds with cortical structures, spinal cord and brain stem respectively. In conclusion, there was a good correlation between EEG and blood flow in the motor cortex. The functional reversibility after ischemia was different according to the types. Type f structures, namely the motor cortex, hippocampus and amygdala were vulnerable and Type f+L structures namely ventrolateral nucleus of the thalamus and midbrain reticular formation tended to recover or stay in preservation.

  7. Opuntia ficus-indica attenuates neuronal injury in in vitro and in vivo models of cerebral ischemia.

    Science.gov (United States)

    Kim, Jung-Hoon; Park, Shin-Mi; Ha, Hyun-Joo; Moon, Chang-Jong; Shin, Tae-Kyun; Kim, Jung-Mi; Lee, Nam-Ho; Kim, Hyoung-Chun; Jang, Kyung-Jin; Wie, Myung-Bok

    2006-03-08

    We examined whether the methanol extract of Opuntia ficus-indica (MEOF) has a neuroprotective action against N-methyl-d-aspartate (NMDA)-, kainate (KA)-, and oxygen-glucose deprivation (OGD)-induced neuronal injury in cultured mouse cortical cells. We also evaluated the protective effect of MEOF in the hippocampal CA1 region against neuronal damage evoked by global ischemia in gerbils. Treatment of neuronal cultures with MEOF (30, 300, and 1000 microg/ml) inhibited NMDA (25 microM)-, KA (30 microM)-, and OGD (50 min)-induced neurotoxicity dose-dependently. The butanol fraction of Opuntia ficus-indica (300 microg/ml) significantly reduced NMDA (20 microM)-induced delayed neurotoxicity by 27%. Gerbils were treated with MEOF every 24h for 3 days (0.1, 1.0, and 4.0 g/kg, p.o.) or for 4 weeks (0.1 and 1.0 g/kg, p.o.), and ischemic injury was induced after the last dose. Neuronal cell damage in the hippocampal CA1 region was evaluated quantitatively at 5 days after the ischemic injury. When gerbils were given doses of 4.0 g/kg (3 days) and 1.0 g/kg (4 weeks), the neuronal damage in the hippocampal region was reduced by 32 and 36%, respectively. These results suggest that the preventive administration of Opuntia ficus-indica extracts may be helpful in alleviating the excitotoxic neuronal damage induced by global ischemia.

  8. CART attenuates endoplasmic reticulum stress response induced by cerebral ischemia and reperfusion through upregulating BDNF synthesis and secretion.

    Science.gov (United States)

    Qiu, Bin; Hu, Shengdi; Liu, Libing; Chen, Man; Wang, Lai; Zeng, Xianwei; Zhu, Shigong

    2013-07-12

    Cocaine and amphetamine regulated transcript (CART), a neuropeptide, has shown strong neuroprotective effects against cerebral ischemia and reperfusion (I/R) injury in vivo and in vitro. Here, we report a new effect of CART on ER stress which is induced by cerebral I/R in a rat model of middle cerebral artery occlusion (MCAO) or by oxygen and glucose deprivation (OGD) in cultured cortical neurons, as well as a new functionality of BDNF in the neuroprotection by CART against the ER stress in cerebral I/R. The results showed that CART was effective in reducing the neuronal apoptosis and expression of ER stress markers (GRP78, CHOP and cleaved caspase12), and increasing the BDNF expression in I/R injury rat cortex both in vivo and in vitro. In addition, the effects of CART on ischemia-induced neuronal apoptosis and ER stress were suppressed by tyrosine receptor kinase B (TrkB) IgG, whereas the effects of CART on BDNF transcription, synthesis and secretion were abolished by CREB siRNA. This work suggests that CART is functional in inhibiting the cerebral I/R-induced ER stress and neuronal apoptosis by facilitating the transcription, synthesis and secretion of BDNF in a CREB-dependent way.

  9. Quantitative radiology: radiogrammetry of cortical bone.

    Science.gov (United States)

    Dequeker, J

    1976-11-01

    Based on personal experience and data in the literature, an overview is given of radiogrammetry of cortical bone of the second metacarpal. There is a within- and between-observer error which amounts respectively to 1.2 and 1.5% for the outer diameter and 4.8 and 6.4% for the inner diameter. The systematic + or-- trend between observers indicates that one observer working according to certain defined rules obtains the most reliable results. There is a large variability in amount of bone within one age and sex group which is partly due to skeletal size differences, are insufficient since skeletal size differences still exist. The variability is reduced when the data are divided into strata of skeletal size. Since cortical area shows the best correlation with outer diameter within each age group and since cortical area represents best the ash content of the bones the values of this index are most suited to be grouped according to outer diameter. In differentiating pathological from physiological bone loss this procedure is an improvement on the previously published indices of amount of bone. When comparing different populations this method has advantages since skeletal size differences are eliminated. Comparing seven populations it was found that populations living in the United States of America have more bone for a given skeletal size than populations in Europe or Nigeria. Bone loss with age is a general phenomenon but differences in rate of loss are observed between the sexes and between ethnic different populations. The decrease of bone mass is faster after the age of 50 years in woman than in men. Blacks living in the United States loose less bone with age than whites. Radiogrammetry of cortical bone in groups gives useful information on bond remodelling during ageing and in pathological conditions. At an individual level, however, it is difficult to evaluate changes on a short term basis with radiogrammetry. Radiogrammetry of cortical bone is a simple and

  10. Social distancing strategies against disease spreading

    CERN Document Server

    Valdez, L D; Macri, P A; Braunstein, L A

    2013-01-01

    The recurrent infectious diseases and their increasing impact on the society has promoted the study of strategies to slow down the epidemic spreading. In this review we outline the applications of percolation theory to describe strategies against epidemic spreading on complex networks. We give a general outlook of the relation between link percolation and the susceptible-infected-recovered model, and introduce the node void percolation process to describe the dilution of the network composed by healthy individual, $i.e$, the network that sustain the functionality of a society. Then, we survey two strategies: the quenched disorder strategy where an heterogeneous distribution of contact intensities is induced in society, and the intermittent social distancing strategy where health individuals are persuaded to avoid contact with their neighbors for intermittent periods of time. Using percolation tools, we show that both strategies may halt the epidemic spreading. Finally, we discuss the role of the transmissibil...

  11. Epidemic spreading on evolving signed networks

    CERN Document Server

    Saeedian, M; Jafari, G R; Kertesz, J

    2016-01-01

    Most studies of disease spreading consider the underlying social network as obtained without the contagion, though epidemic influences peoples willingness to contact others: A friendly contact may be turned to unfriendly to avoid infection. We study the susceptible-infected (SI) disease spreading model on signed networks, in which each edge is associated with a positive or negative sign representing the friendly or unfriendly relation between its end nodes. In a signed network, according to Heiders theory, edge signs evolve such that finally a state of structural balance is achieved, corresponding to no frustration in physics terms. However, the danger of infection affects the evolution of its edge signs. To describe the coupled problem of the sign evolution and disease spreading, we generalize the notion of structural balance by taking into account the state of the nodes. We introduce an energy function and carry out Monte-Carlo simulations on complete networks to test the energy landscape, where we find loc...

  12. Temporal network structures controlling disease spreading

    Science.gov (United States)

    Holme, Petter

    2016-08-01

    We investigate disease spreading on eight empirical data sets of human contacts (mostly proximity networks recording who is close to whom, at what time). We compare three levels of representations of these data sets: temporal networks, static networks, and a fully connected topology. We notice that the difference between the static and fully connected networks—with respect to time to extinction and average outbreak size—is smaller than between the temporal and static topologies. This suggests that, for these data sets, temporal structures influence disease spreading more than static-network structures. To explain the details in the differences between the representations, we use 32 network measures. This study concurs that long-time temporal structures, like the turnover of nodes and links, are the most important for the spreading dynamics.

  13. Substrate stress relaxation regulates cell spreading

    Science.gov (United States)

    Chaudhuri, Ovijit; Gu, Luo; Darnell, Max; Klumpers, Darinka; Bencherif, Sidi A.; Weaver, James C.; Huebsch, Nathaniel; Mooney, David J.

    2015-02-01

    Studies of cellular mechanotransduction have converged upon the idea that cells sense extracellular matrix (ECM) elasticity by gauging resistance to the traction forces they exert on the ECM. However, these studies typically utilize purely elastic materials as substrates, whereas physiological ECMs are viscoelastic, and exhibit stress relaxation, so that cellular traction forces exerted by cells remodel the ECM. Here we investigate the influence of ECM stress relaxation on cell behaviour through computational modelling and cellular experiments. Surprisingly, both our computational model and experiments find that spreading for cells cultured on soft substrates that exhibit stress relaxation is greater than cells spreading on elastic substrates of the same modulus, but similar to that of cells spreading on stiffer elastic substrates. These findings challenge the current view of how cells sense and respond to the ECM.

  14. Disordered contact process with asymmetric spreading.

    Science.gov (United States)

    Juhász, Róbert

    2013-02-01

    An asymmetric variant of the contact process where the activity spreads with different and independent random rates to the left and to the right is introduced. A real space renormalization scheme is formulated for the model by means of which it is shown that the local asymmetry of spreading is irrelevant on large scales if the model is globally (statistically) symmetric. Otherwise, in the presence of a global bias in either direction, the renormalization method predicts two distinct phase transitions, which are related to the spreading of activity in and against the direction of the bias. The latter is found to be described by an infinite randomness fixed point while the former is not.

  15. Extended oil spill spreading with Langmuir circulation.

    Science.gov (United States)

    Simecek-Beatty, Debra; Lehr, William J

    2017-09-15

    When spilled in the ocean, most crude oils quickly spread into a thin film that ruptures into smaller slicks distributed over a larger area. Observers have also reported the film tearing apart into streaks that eventually merge forming fewer but longer bands of floating oil. Understanding this process is important to model oil spill transport. First, slick area is calculated using a spreading model. Next, Langmuir circulation models are used to approximate the merging of oiled bands. Calculations are performed on Troll blended and Alaska North Slope crude oils and results compared with measurements from the 1990s North Sea field experiments. Langmuir circulation increases the oil area but decreases the surface coverage of oil. This work modifies existing oil spreading formulas by providing a surface area correction due to the effects of Langmuir circulation. The model's simplicity is advantageous in situations with limited data, such as emergency oil spill response. Published by Elsevier Ltd.

  16. Temporal network structures controlling disease spreading

    CERN Document Server

    Holme, Petter

    2016-01-01

    We investigate disease spreading on eight empirical data sets of human contacts (mostly proximity networks recording who is close to whom, at what time). We compare three levels of representations of these data sets: temporal networks, static networks and a fully connected topology. We notice that the difference between the static and fully-connected networks -- with respect to time to extinction and average outbreak size -- is smaller than between the temporal and static topologies. This suggests that, for these data sets, temporal structures influence disease spreading more than static network structures. To explain the details in the differences between the representations, we use 32 network measures. This study concur that long-time temporal structures, like the turnover of nodes and links, are the most important for the spreading dynamics.

  17. Cortical hierarchy governs rat claustrocortical circuit organization.

    Science.gov (United States)

    White, Michael G; Cody, Patrick A; Bubser, Michael; Wang, Hui-Dong; Deutch, Ariel Y; Mathur, Brian N

    2017-04-15

    The claustrum is a telencephalic gray matter structure with various proposed functions, including sensory integration and attentional allocation. Underlying these concepts is the reciprocal connectivity of the claustrum with most, if not all, areas of the cortex. What remains to be elucidated to inform functional hypotheses further is whether a pattern exists in the strength of connectivity between a given cortical area and the claustrum. To this end, we performed a series of retrograde neuronal tract tracer injections into rat cortical areas along the cortical processing hierarchy, from primary sensory and motor to frontal cortices. We observed that the number of claustrocortical projections increased as a function of processing hierarchy; claustrum neurons projecting to primary sensory cortices were scant and restricted in distribution across the claustrum, whereas neurons projecting to the cingulate cortex were densely packed and more evenly distributed throughout the claustrum. This connectivity pattern suggests that the claustrum may preferentially subserve executive functions orchestrated by the cingulate cortex. J. Comp. Neurol. 525:1347-1362, 2017. © 2016 Wiley Periodicals, Inc. © 2016 Wiley Periodicals, Inc.

  18. Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury

    Directory of Open Access Journals (Sweden)

    Nicolosi Alfred C

    2009-12-01

    Full Text Available Abstract Background The lanthanide cation, gadolinium (GdCl3 protects the myocardium against infarction following ischemia and reperfusion. Neutrophils and macrophages are the main leukocytes responsible for infarct expansion after reperfusion. GdCl3 interferes with macrophage and neutrophil function in the liver by decreasing macrophage secretion of inflammatory cytokines and neutrophil infiltration. We hypothesized that GdCl3 protects against ischemia and reperfusion injury by decreasing inflammation. We determined the impact of GdCl3 treatment for reperfusion injury on 1 circulating monoctye and neutrophil counts, 2 secretion of inflammatory cytokines, and 3 influx of monocytes and neutrophils into the myocardium. Methods Rats (n = 3-6/gp were treated with saline or GdCl3 (20 μmol/kg 15 min prior to a 30 min period of regional ischemia and 120 min reperfusion. Sham rats were not subject to ischemia. Blood was collected either after 30 min ischemia or 120 min reperfusion and hearts were harvested at 120 min reperfusion for tissue analysis. Blood was analyzed for leukocytes counts and cytokines. Tissue was analyzed for cytokines and markers of neutrophil and monocyte infiltration by measuring myeloperoxidase (MPO and α-naphthyl acetate esterase (ANAE. Results GdCl3 did not affect the number of circulating neutrophils prior to ischemia. Two hours reperfusion resulted in a 2- and 3- fold increase in circulating monocytes and neutrophils, respectively. GdCl3 decreased the number of circulating monocytes and neutrophils during reperfusion to levels below those present prior to ischemia. Furthermore, after 120 min of reperfusion, GdCl3 decreased ANAE and MPO activity in the myocardium by 1.9-fold and 6.5-fold respectively. GdCl3 decreased MPO activity to levels below those measured in the Sham group. Serum levels of the major neutrophil chemoattractant cytokine, IL-8 were increased from pre-ischemic levels during ischemia and reperfusion in both

  19. Analysis of BER Performance of the Spread Spectrum Communication System with Constrained Spreading Code

    OpenAIRE

    長谷川, 孝明; 羽渕, 裕真

    1996-01-01

    Copyright notice. c1996 IEICE All rights reserved. "Analysis of BER Performance of the Spread Spectrum Communication System with Constrained Spreading Code"Hiromasa HABUCHI, Toshio TAKEBAYASHI, Takaaki HASEGAWA. IEICE TRANSACTIONS on Fundamentals of Electronics, Communications and Computer Sciences ,1996 Vol.E79-A No.12 pp. 2078-2080 許諾No.07RB0055.

  20. Spreading of Ultrarelativistic Wave Packet and Redshift

    CERN Document Server

    Lev, Felix M

    2012-01-01

    The red shift of light coming to the Earth from distant objects is usually explained as a consequence of the fact that the Universe is expanding. Such an explanation implies that photons emitted by distant objects travel in the interstellar medium practically without interaction with interstellar matter and hence they can survive their long journey to the Earth. We analyze this assumption by considering wave-packet spreading for an ultrarelativistic particle. We derive a formula which shows that spreading in the direction perpendicular to the particle momentum is very important and cannot be neglected. The implications of the results are discussed.

  1. Origin and turbulence spreading of plasma blobs

    Energy Technology Data Exchange (ETDEWEB)

    Manz, P.; Birkenmeier, G.; Stroth, U. [Physik-Department E28, Technische Universität München, James-Franck. Str. 1, Garching (Germany); Max-Planck-Institut für Plasmaphysik, Boltzmannstr. 2, Garching (Germany); Ribeiro, T. T.; Scott, B. D.; Carralero, D.; Müller, S. H.; Müller, H. W.; Wolfrum, E. [Max-Planck-Institut für Plasmaphysik, Boltzmannstr. 2, Garching (Germany); Fuchert, G. [IJL, Université de Lorraine, CNRS (UMR 7198), BP 40239, Vandoeuvre-lès-Nancy (France)

    2015-02-15

    The formation of plasma blobs is studied by analyzing their trajectories in a gyrofluid simulation in the vicinity of the separatrix. Most blobs arise at the maximum radial electric field outside the separatrix. In general, blob generation is not bound to one particular radial position or instability. A simple model of turbulence spreading for the scrape-off layer is derived. The simulations show that the blob dynamics can be represented by turbulence spreading, which constitutes a substantial energy drive for far scrape-off layer turbulence and is a more suitable quantity to study blob generation compared to the skewness.

  2. Technique for Controlling Spread of Limnotic Oncomelania

    Institute of Scientific and Technical Information of China (English)

    Li Damei(李大美); WANG Xiangsan(王祥三); LAI Yonggen

    2003-01-01

    Schistosomiasis is a parasitic disease mostly found in areas along the Changjiang River of China. The disease is spread solely through an intermediary named oncomelania, so its spread of schistosomiasis can be controlled by properly designing water intakes which prevent oncomelania from entering fanning land or residential areas. This paper reports a successful design process and a new oncomelania-free intake device. The design of the new intake is based on a sound research program in which extensive experimental studies were carried out to gain knowledge of oncomelania eco-hydraulic behavior and detailed flow field information through CFD simulation.

  3. Burstiness and spreading on temporal networks

    CERN Document Server

    Lambiotte, Renaud; Delvenne, Jean-Charles

    2013-01-01

    We discuss how spreading processes on temporal networks are impacted by the shape of their inter-event time distributions. Through simple mathematical arguments and toy examples, we find that the key factor is the ordering in which events take place, a property that tends to be affected by the bulk of the distributions and not only by their tail, as usually considered in the literature. We show that a detailed modeling of the temporal patterns observed in complex networks can change dramatically the properties of a spreading process, such as the ergodicity of a random walk process or the persistence of an epidemic.

  4. Effects and Mechanism of Action of Inducible Nitric Oxide Synthase on Apoptosis in a Rat Model of Cerebral Ischemia-Reperfusion Injury.

    Science.gov (United States)

    Zheng, Li; Ding, Junli; Wang, Jianwei; Zhou, Changman; Zhang, Weiguang

    2016-02-01

    Inducible nitric oxide synthase (iNOS) is a key enzyme in regulating nitric oxide (NO) synthesis under stress, and NO has varying ability to regulate apoptosis. The aim of this study was to investigate the effects and possible mechanism of action of iNOS on neuronal apoptosis in a rat model of cerebral focal ischemia and reperfusion injury in rats treated with S-methylisothiourea sulfate (SMT), a high-selective inhibitor of iNOS. Seventy-two male Sprague-Dawley (SD) rats were randomly divided into three groups: the sham, middle cerebral artery occlusion (MCAO) + vehicle, and MCAO + SMT groups. Neurobehavioral deficits, infarct zone size, and cortical neuron morphology were evaluated through the modified Garcia scores, 2,3,5-triphenyltetrazolium chloride (TTC), and Nissl staining, respectively. Brain tissues and serum samples were collected at 72 hr post-reperfusion for immunohistochemical analysis, Western blotting, Terminal deoxynucleotidyl transferase-mediated dUTP-biotin Nick End Labeling assay (TUNEL) staining, and enzyme assays. The study found that inhibition of iNOS significantly attenuated the severity of the pathological changes observed as a result of ischemia-reperfusion injury: SMT reduced NO content as well as total nitric oxide synthase (tNOS) and iNOS activities in both ischemic cerebral hemisphere and serum, improved neurobehavioral scores, reduced mortality, reduced the infarct volume ratio, attenuated morphological changes in cortical neurons, decreased the rate of apoptosis (TUNEL and caspase-3-positive), and increased phospho (p)-AKT expression in ischemic penumbra. These results suggested that inhibition of iNOS might reduce the severity of ischemia-reperfusion injury by inhibiting neuronal apoptosis via maintaining p-AKT activity.

  5. Neurodynamics of somatosensory cortices studied by magnetoencephelography.

    Science.gov (United States)

    Kishida, Kuniharu

    2013-09-01

    From the viewpoint of statistical inverse problems, identification of transfer functions in feedback models is applied for neurodynamics of somatosensory cortices, and brain communication among active regions can be expressed in terms of transfer functions. However, brain activities have been investigated mainly by averaged waveforms in the conventional magnetoencephalography analysis, and thus brain communication among active regions has not yet been identified. It is shown that brain communication among two more than three brain regions is determined, when fluctuations related to concatenate averaged waveforms can be obtained by using a suitable blind source separation method. In blind identification of feedback model, some transfer functions or their impulse responses between output variables of current dipoles corresponding to active regions are identified from reconstructed time series data of fluctuations by the method of inverse problem. Neurodynamics of somatosensory cortices in 5 Hz median nerve stimuli can be shown by cerebral communication among active regions of somatosensory cortices in terms of impulse responses of feedback model.

  6. Endogenous protease nexin-1 protects against cerebral ischemia.

    Science.gov (United States)

    Mirante, Osvaldo; Price, Melanie; Puentes, Wilfredo; Castillo, Ximena; Benakis, Corinne; Thevenet, Jonathan; Monard, Denis; Hirt, Lorenz

    2013-08-14

    The serine protease thrombin plays a role in signalling ischemic neuronal death in the brain. Paradoxically, endogenous neuroprotective mechanisms can be triggered by preconditioning with thrombin (thrombin preconditioning, TPC), leading to tolerance to cerebral ischemia. Here we studied the role of thrombin's endogenous potent inhibitor, protease nexin-1 (PN-1), in ischemia and in tolerance to cerebral ischemia induced by TPC. Cerebral ischemia was modelled in vitro in organotypic hippocampal slice cultures from rats or genetically engineered mice lacking PN-1 or with the reporter gene lacZ knocked into the PN-1 locus PN-1HAPN-1-lacZ/HAPN-1-lacZ (PN-1 KI) exposed to oxygen and glucose deprivation (OGD). We observed increased thrombin enzyme activity in culture homogenates 24 h after OGD. Lack of PN-1 increased neuronal death in the CA1, suggesting that endogenous PN-1 inhibits thrombin-induced neuronal damage after ischemia. OGD enhanced β-galactosidase activity, reflecting PN-1 expression, at one and 24 h, most strikingly in the stratum radiatum, a glial cell layer adjacent to the CA1 layer of ischemia sensitive neurons. TPC, 24 h before OGD, additionally increased PN-1 expression 1 h after OGD, compared to OGD alone. TPC failed to induce tolerance in cultures from PN-1(-/-) mice confirming PN-1 as an important TPC target. PN-1 upregulation after TPC was blocked by the c-Jun N-terminal kinase (JNK) inhibitor, L-JNKI1, known to block TPC. This work suggests that PN-1 is an endogenous neuroprotectant in cerebral ischemia and a potential target for neuroprotection.

  7. Endogenous Protease Nexin-1 Protects against Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Jonathan Thevenet

    2013-08-01

    Full Text Available The serine protease thrombin plays a role in signalling ischemic neuronal death in the brain. Paradoxically, endogenous neuroprotective mechanisms can be triggered by preconditioning with thrombin (thrombin preconditioning, TPC, leading to tolerance to cerebral ischemia. Here we studied the role of thrombin’s endogenous potent inhibitor, protease nexin-1 (PN-1, in ischemia and in tolerance to cerebral ischemia induced by TPC. Cerebral ischemia was modelled in vitro in organotypic hippocampal slice cultures from rats or genetically engineered mice lacking PN-1 or with the reporter gene lacZ knocked into the PN-1 locus PN-1HAPN-1-lacZ/HAPN-1-lacZ (PN-1 KI exposed to oxygen and glucose deprivation (OGD. We observed increased thrombin enzyme activity in culture homogenates 24 h after OGD. Lack of PN-1 increased neuronal death in the CA1, suggesting that endogenous PN-1 inhibits thrombin-induced neuronal damage after ischemia. OGD enhanced β-galactosidase activity, reflecting PN-1 expression, at one and 24 h, most strikingly in the stratum radiatum, a glial cell layer adjacent to the CA1 layer of ischemia sensitive neurons. TPC, 24 h before OGD, additionally increased PN-1 expression 1 h after OGD, compared to OGD alone. TPC failed to induce tolerance in cultures from PN-1−/− mice confirming PN-1 as an important TPC target. PN-1 upregulation after TPC was blocked by the c-Jun N-terminal kinase (JNK inhibitor, L-JNKI1, known to block TPC. This work suggests that PN-1 is an endogenous neuroprotectant in cerebral ischemia and a potential target for neuroprotection.

  8. Novel biomarkers of arterial and venous ischemia in microvascular flaps.

    Directory of Open Access Journals (Sweden)

    Gerard K Nguyen

    Full Text Available The field of reconstructive microsurgery is experiencing tremendous growth, as evidenced by recent advances in face and hand transplantation, lower limb salvage after trauma, and breast reconstruction. Common to all of these procedures is the creation of a nutrient vascular supply by microsurgical anastomosis between a single artery and vein. Complications related to occluded arterial inflow and obstructed venous outflow are not uncommon, and can result in irreversible tissue injury, necrosis, and flap loss. At times, these complications are challenging to clinically determine. Since early intervention with return to the operating room to re-establish arterial inflow or venous outflow is key to flap salvage, the accurate diagnosis of early stage complications is essential. To date, there are no biochemical markers or serum assays that can predict these complications. In this study, we utilized a rat model of flap ischemia in order to identify the transcriptional signatures of venous congestion and arterial ischemia. We found that the critical ischemia time for the superficial inferior epigastric fasciocutaneus flap was four hours and therefore performed detailed analyses at this time point. Histolgical analysis confirmed significant differences between arterial and venous ischemia. The transcriptome of ischemic, congested, and control flap tissues was deciphered by performing Affymetrix microarray analysis and verified by qRT-PCR. Principal component analysis revealed that arterial ischemia and venous congestion were characterized by distinct transcriptomes. Arterial ischemia and venous congestion was characterized by 408 and 1536>2-fold differentially expressed genes, respectively. qRT-PCR was used to identify five candidate genes Prol1, Muc1, Fcnb, Il1b, and Vcsa1 to serve as biomarkers for flap failure in both arterial ischemia and venous congestion. Our data suggests that Prol1 and Vcsa1 may be specific indicators of venous congestion and

  9. Usefulness of percutaneous transluminal coronary angioplasty in silent myocardial ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Hou, Mami [Toho Univ., Tokyo (Japan). School of Medicine

    1996-04-01

    The usefulness of percutaneous transluminal coronary angioplasty (PTCA) was assessed in patients with exercise-induced asymptomatic myocardial ischemia (silent ischemia) and compared with exercise-induced symptomatic myocardial ischemia (symptomatic ischemia). Patients with single vessel coronary artery disease (51 with angina pectoris, 40 with old myocardial infarction) and evidence of stress-induced ischemia on thallium-201 single photon emission computed tomography (SPECT) underwent successful PTCA. Thirty-seven percent of angina patients and 60% of infarction patients showed asymptomatic exercise-induced ischemia. There was no significant difference in population characteristics between silent and symptomatic patients. Patients with silent angina had significantly higher percentage thallium uptake and washout rate than symptomatic patients. After PTCA, both percentage diameter stenosis and percentage thallium uptake were improved in all patients with angina irrespective of the presence or absence of symptoms. There were no significant differences in percentage thallium uptake and washout rate between patients with silent and symptomatic infarction. After PTCA, percentage diameter stenosis, percentage thallium uptake, and washout rate improved in all infarction patients irrespective of the symptoms. Zero percent of silent angina patients, 12% of symptomatic angina patients, 12% of silent infarction patients, 19% of symptomatic infarction patients had cardiac events during about 4.5 years after PTCA. The incidence of cardiac events did not significantly differ in any patient group. PTCA improved myocardial perfusion in all patients, and the incidence of cardiac events did not differ between the silent and symptomatic groups. Revascularization with PTCA is suitable for patients with silent as well as symptomatic ischemia. (author).

  10. Treatment of Digital Ischemia with Liposomal Bupivacaine

    Directory of Open Access Journals (Sweden)

    José Raul Soberón

    2014-01-01

    Full Text Available Objective. This report describes a case in which the off-label use of liposomal bupivacaine (Exparel in a peripheral nerve block resulted in marked improvement of a patient’s vasoocclusive symptoms. The vasodilating and analgesic properties of liposomal bupivacaine in patients with ischemic symptoms are unknown, but our clinical experience suggests a role in the management of patients suffering from vasoocclusive disease. Case Report. A 45-year-old African American female was admitted to the hospital with severe digital ischemic pain. She was not a candidate for any vascular surgical or procedural interventions. Two continuous supraclavicular nerve blocks were placed with modest clinical improvement. These effects were also short-lived, with the benefits resolving after the discontinuation of the peripheral nerve blocks. She continued to report severe pain and was on multiple anticoagulant medications, so a decision was made to perform an axillary nerve block using liposomal bupivacaine (Exparel given the compressibility of the site as well as the superficial nature of the target structures. Conclusions. This case report describes the successful off-label usage of liposomal bupivacaine (Exparel in a patient with digital ischemia. Liposomal bupivacaine (Exparel is currently FDA approved only for wound infiltration use at this time.

  11. The ontogeny of the cortical language network.

    Science.gov (United States)

    Skeide, Michael A; Friederici, Angela D

    2016-05-01

    Language-processing functions follow heterogeneous developmental trajectories. The human embryo can already distinguish vowels in utero, but grammatical complexity is usually not fully mastered until at least 7 years of age. Examining the current literature, we propose that the ontogeny of the cortical language network can be roughly subdivided into two main developmental stages. In the first stage extending over the first 3 years of life, the infant rapidly acquires bottom-up processing capacities, which are primarily implemented bilaterally in the temporal cortices. In the second stage continuing into adolescence, top-down processes emerge gradually with the increasing functional selectivity and structural connectivity of the left inferior frontal cortex.

  12. Rasmussen's encephalitis presenting as focal cortical dysplasia

    Directory of Open Access Journals (Sweden)

    D.J. O'Rourke

    2014-01-01

    Full Text Available Rasmussen's encephalitis is a rare syndrome characterized by intractable seizures, often associated with epilepsia partialis continua and symptoms of progressive hemispheric dysfunction. Seizures are usually the hallmark of presentation, but antiepileptic drug treatment fails in most patients and is ineffective against epilepsia partialis continua, which often requires surgical intervention. Co-occurrence of focal cortical dysplasia has only rarely been described and may have implications regarding pathophysiology and management. We describe a rare case of dual pathology of Rasmussen's encephalitis presenting as a focal cortical dysplasia (FCD and discuss the literature on this topic.

  13. Cortical activation elicited by unrecognized stimuli

    Directory of Open Access Journals (Sweden)

    Badgaiyan Rajendra D

    2006-05-01

    Full Text Available Abstract Background It is unclear whether a stimulus that cannot be recognized consciously, could elicit a well-processed cognitive response. Methods We used functional imaging to examine the pattern of cortical activation elicited by unrecognized stimuli during memory processing. Subjects were given a recognition task using recognizable and non-recognizable subliminal stimuli. Results Unrecognized stimuli activated the cortical areas that are associated with retrieval attempt (left prefrontal, and novelty detection (left hippocampus. This indicates that the stimuli that were not consciously recognized, activated neural network associated with aspects of explicit memory processing. Conclusion Results suggest that conscious recognition of stimuli is not necessary for activation of cognitive processing.

  14. Elemental mercury poisoning probably causes cortical myoclonus.

    Science.gov (United States)

    Ragothaman, Mona; Kulkarni, Girish; Ashraf, Valappil V; Pal, Pramod K; Chickabasavaiah, Yasha; Shankar, Susarla K; Govindappa, Srikanth S; Satishchandra, Parthasarthy; Muthane, Uday B

    2007-10-15

    Mercury toxicity causes postural tremors, commonly referred to as "mercurial tremors," and cerebellar dysfunction. A 23-year woman, 2 years after injecting herself with elemental mercury developed disabling generalized myoclonus and ataxia. Electrophysiological studies confirmed the myoclonus was probably of cortical origin. Her deficits progressed over 2 years and improved after subcutaneous mercury deposits at the injection site were surgically cleared. Myoclonus of cortical origin has never been described in mercury poisoning. It is important to ask patients presenting with jerks about exposure to elemental mercury even if they have a progressive illness, as it is a potentially reversible condition as in our patient.

  15. Posterior cortical atrophy: a brief review.

    Science.gov (United States)

    Kirshner, Howard S; Lavin, Patrick J M

    2006-11-01

    Posterior cortical atrophy is a striking clinical syndrome in which a dementing illness begins with visual symptoms. Initially, the problem may seem to be loss of elementary vision, but over time the patient develops features of visual agnosia, topographical difficulty, optic ataxia, simultanagnosia, ocular apraxia (Balint's syndrome), alexia, acalculia, right-left confusion, and agraphia (Gerstmann's syndrome), and later a more generalized dementia. Occasional patients have visual hallucinations and signs of Parkinson's disease or Lewy body dementia. A number of different neuropathologic disorders are associated with posterior cortical atrophy.

  16. Relativistic suppression of wave packet spreading.

    Science.gov (United States)

    Su, Q; Smetanko, B; Grobe, R

    1998-03-30

    We investigate numerically the solution of Dirac equation and analytically the Klein-Gordon equation and discuss the relativistic motion of an electron wave packet in the presence of an intense static electric field. In contrast to the predictions of the (non-relativistic) Schroedinger theory, the spreading rate in the field's polarization direction as well as in the transverse directions is reduced.

  17. Hiding Single Photons With Spread Spectrum Technology

    CERN Document Server

    Belthangady, Chinmay; Yu, Ite A; Yin, G Y; Kahn, J M; Harris, S E

    2010-01-01

    We describe a proof-of-principal experiment demonstrating the use of spread spectrum technology at the single photon level. We show how single photons with a prescribed temporal shape, in the presence of interfering noise, may be hidden and recovered.

  18. Modeling and simulation of epidemic spread

    DEFF Research Database (Denmark)

    Shatnawi, Maad; Lazarova-Molnar, Sanja; Zaki, Nazar

    2013-01-01

    and control such epidemics. This paper presents an overview of the epidemic spread modeling and simulation, and summarizes the main technical challenges in this field. It further investigates the most relevant recent approaches carried out towards this perspective and provides a comparison and classification...

  19. Restricted spread of tomato spotted wilt virus

    NARCIS (Netherlands)

    Maris, P.C.; Joosten, N.N.; Goldbach, R.W.; Peters, D.

    2003-01-01

    Spread of Tomato spotted wilt virus (TSWV) and population development of its vector Frankliniella occidentalis were studied on the pepper accessions CPRO-1 and Pikante Reuzen, which are resistant and susceptible to thrips, respectively. Viruliferous thrips were released on plants of each accession (

  20. Damage spreading on networks: Clustering effects

    Indian Academy of Sciences (India)

    Z Z Guo; Xiao-Wei Wu; Chun-An Wang

    2007-04-01

    The damage spreading of the Ising model on three kinds of networks is studied with Glauber dynamics. One of the networks is generated by evolving the hexagonal lattice with the star-triangle transformation. Another kind of network is constructed by connecting the midpoints of the edges of the topological hexagonal lattice. With the evolution of these structures, damage spreading transition temperature increases and a general explanation for this phenomenon is presented from the view of the network. The relationship between the transition temperature and the network measure-clustering coefficient is set up and it is shown that the increase of damage spreading transition temperature is the result of more and more clustering of the network. We construct the third kind of network-random graphs with Poisson degree distributions by changing the average degree of the network. We show that the increase in the average degree is equivalent to the clustering of nodes and this leads to the increase in damage spreading transition temperature.