scholarly journals Cerebral Ischemic Stroke: is Gender Important?

2013 ◽  
Vol 33 (9) ◽  
pp. 1355-1361 ◽  
Author(s):  
Claire L Gibson
Keyword(s):  
Ischemic Stroke ◽  
Developed Countries ◽  
Cerebral Stroke ◽  
Clinical Investigations ◽  
Neuroprotective Strategies ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Gender Influences ◽  
Gender Specific

Cerebral stroke continues to be a major cause of death and the leading cause of long-term disability in developed countries. Evidence reviewed here suggests that gender influences various aspects of the clinical spectrum of ischemic stroke, in terms of influencing how a patients present with ischemic stroke through to how they respond to treatment. In addition, this review focuses on discussing the various pathologic mechanisms of ischemic stroke that may differ according to gender and compares how intrinsic and hormonal mechanisms may account for such gender differences. All clinical trials to date investigating putative neuroprotective treatments for ischemic stroke have failed, and it may be that our understanding of the injury cascade initiated after ischemic injury is incomplete. Revealing aspects of the pathophysiological consequences of ischemic stroke that are gender specific may enable gender relevant and effective neuroprotective strategies to be identified. Thus, it is possible to conclude that gender does, in fact, have an important role in ischemic stroke and must be factored into experimental and clinical investigations of ischemic stroke.

scholarly journals COMPARISON OF THE DYNAMIC CHANGES OF AMINO ACID BLOOD PLASMA SPECTRUM IN PATIENTS WITH THE PRIMARY CEREBRAL ISCHEMIC STROKE DEPENDING ON THE POSTAPOPLECTIC SPASTICITY DEVELOPMENT IN THE RECOVERY PERIOD

2016 ◽  
Vol 3 ◽  
pp. 17-23
Author(s):  
Anzhelika Payenok ◽  
Maria Bilobryn ◽  
Iryna Mitelman
Keyword(s):  
Ischemic Stroke ◽  
Blood Plasma ◽  
Recovery Period ◽  
Control Group ◽  
Cerebral Stroke ◽  
Early Recovery ◽  
Dynamic Changes ◽  
Acute Period ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

The aim of research was to reveal the dynamic changes of the level of excitatory and inhibitory neuroamino acids in patients with the primary cerebral ischemic stroke depending on postapoplectic spasticity presence at the end of the early recovery period. For this aim was studied the concentration of excitatory and inhibitory neuroamino acids in the blood plasma in first 72 hours in 97 patients with the primary ischemic cerebral stroke depending on postapoplectic spasticity on the sixth month after ischemic event. The control group included 15 patients with diagnosed chronic cerebral ischemia. In the result of research we revealed that the common sign for the two groups (with spasticity on the sixth month and without it) was the reliable rise of the level of excitatory amino acids comparing with the control. In patients without spasticity the heightened level of excitatory neurotransmitters in the most acute period of ischemic cerebral stroke was attended with the heightened level of inhibitory neuroamino acids. The distinctive feature of patients with postapoplectic spasticity was the decreased or stable level of transmitters of inhibitory action. During 6th moth after ischemic stroke was detected the rise of all studied neuroamino acids in patients with spasticity unlike to the ones without spasticity who were characterized only with the rise of taurine level and decrease of glycine and aspartate levels. So, the received results allow assume the insufficient activation of the inhibitory neuroamino acids system in the most acute period of the ischemic stroke in certain category of patients that in future are inclined to the spasticity development after stroke.

Abstract P806: Sirtuin1 Plays a Critical Role in Reversing Skeletal Muscle Atrophy in Cerebral Ischemic Stroke

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Junaith S Mohamed ◽  
Peter J Ferrandi ◽  
Paez G Hector ◽  
Christopher R Pitzer ◽  
Stephen E Alway
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Stroke ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Rna Seq ◽  
Stroke Patients ◽  
Post Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Stroke is a leading cause of mortality and long-term disability in patients worldwide. Skeletal muscle is the primary systemic target organ of stroke that severely induces muscle wasting and weakness, which contributes more to the long-term functional disability in stroke patients than any other disease. Currently, no approved pharmacological drug is available to treat stroke-induced muscle loss. Rehabilitative therapy is the only available option to improve muscle function in stroke patients. However, higher muscle fatigability and lower muscle strength from extensive muscle wasting in post-stroke patients provide poor rehabilitative outcomes. As a result, about two-thirds of stroke survivors persist in a state of insufficient recovery and experience physical disability that drastically reduces their health and quality of life. The major challenge in the drug discovery effort for treating post-stroke muscle wasting is the lack of our understanding of the molecular and/or cellular mechanisms that underlie the muscle wasting in stroke. To understand the molecular origin of stroke-induced muscle atrophy, gene expression profiling and associated biological pathway enrichment studies were performed in a mouse model of cerebral ischemic stroke using high-throughput RNA sequencing and extensive bioinformatic analyses. RNA-seq data revealed that the elevated atrophy in skeletal muscle observed in response to stroke was primairly associated with the altered expression of genes involved in the muscle protein degradation pathway. Further analysis of RNA-seq data identified Sirtuin1 (SirT1) as a critical protein that plays a significant role in regulating post-stroke muscle mass. SirT1 gain-of-function in skeletal muscle significantly reversed stroke-induced muscle atrophy via inhibiting the activation of the ubiquitin proteasomal pathway and restoring autophagy function. Collectively, this study identified suppression of SirT1as a novel mechanism by which stroke induces muscle atrophy.

scholarly journals Intra-Arterial Tirofiban Infusion for Partial Recanalization with Stagnant Flow in Hyperacute Cerebral Ischemic Stroke

2011 ◽  
Vol 17 (4) ◽  
pp. 442-451 ◽  
Author(s):  
S.K. Baik ◽  
S.J. Oh ◽  
K-P. Park ◽  
J-H. Lee
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Clinical Status ◽  
Cerebral Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Antegrade Flow ◽  
Stagnant Flow ◽  
Iv Tpa

Early reocclusion is a major concern associated with poor clinical outcomes in patients with an ischemic cerebral stroke. This occurs most frequently in patients with partial initial recanalization. This study focuses on partial recanalization with stagnant antegrade flow after intravenous (IV) tPA or spontaneously, treated with the administration of intra-arterial (IA) tirofiban. Three patients with initial M1 occlusion on diagnostic studies had an occluded segment that was recanalized with stagnant flow after IV tPA or spontaneously. In all cases, IA tirofiban was administrated. We evaluated the distal blood flow and the degree of vascular narrowing in the pre and post-procedure angiography and at follow-up in addition to the clinical status. In all patients, severe vascular narrowing with stagnation of blood flow was detected in the initial M1. After infusion of IA tirofiban, improvement of the distal blood flow was achieved rapidly within 40 minutes in all patients. The severe vascular narrowing resolved rapidly in two patients without residual stenosis. In one patient, moderate vascular narrowing was still present. The median baseline National Institutes of Health Stroke Scale (NIHSS) scores were 18 and the median post-procedural NIHSS scores were 2 at two weeks. No intracerebral hemorrhage occurred in any of the patients. Treatment with IA tirofiban was safe and effective in patients with partial initial recanalization. It can be suggested that detection of any partial recanalization is time for administration of glycoprotein IIb-IIIa receptor inhibitor in hyperacute ischemic stroke.

scholarly journals Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke

2021 ◽  
Vol 8 ◽  
Author(s):  
Amanda Moya Gómez ◽  
Lena Pérez Font ◽  
Bert Brône ◽  
Annelies Bronckaers
Keyword(s):  
Ischemic Stroke ◽  
Treatment Options ◽  
Cell Types ◽  
Cerebral Stroke ◽  
Signal Pathways ◽  
Extensive Literature ◽  
New Therapeutic Approaches ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Cerebral stroke is a leading cause of death and adult-acquired disability worldwide. To this date, treatment options are limited; hence, the search for new therapeutic approaches continues. Electromagnetic fields (EMFs) affect a wide variety of biological processes and accumulating evidence shows their potential as a treatment for ischemic stroke. Based on their characteristics, they can be divided into stationary, pulsed, and sinusoidal EMF. The aim of this review is to provide an extensive literature overview ranging from in vitro to even clinical studies within the field of ischemic stroke of all EMF types. A thorough comparison between EMF types and their effects is provided, as well as an overview of the signal pathways activated in cell types relevant for ischemic stroke such as neurons, microglia, astrocytes, and endothelial cells. We also discuss which steps have to be taken to improve their therapeutic efficacy in the frame of the clinical translation of this promising therapy.

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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