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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transplantation of bone marrow stromal cells (BMSCs) improves animal neurological functional recovery after stroke. To obtain insight into the mechanisms underlying the therapeutic benefit, we directed our attention to the interaction of BMSCs with astrocytes. Astrocytes become reactive (astrogliosis) after a brain injury, such as stroke. Astrogliosis plays both beneficial and detrimental roles in brain recovery. Previously, we have shown that administration of BMSCs to animals with stroke significantly reduces the thickness of the scar wall formed by reactive astrocytes. We tested the influence of mouse bone marrow stromal cell (mBMSC) on astrogliosis under oxygen-glucose deprivation (OGD)/reoxygenation conditions in vitro, employing an anaerobic chamber. Our data indicate that mBMSCs down-regulate glial fibrillary acidic protein (GFAP) expression in astrocytes after 2 h of OGD and an additional 16 h reoxygenation. mBMSCs protected astrocytes from ischemia, maintaining morphological integrity and proliferation. The IL-6/IL-6R/gp130 pathway is associated with astrogliosis in response to CNS (disorders. Therefore, we examined the effects of mBMSC on the IL-6/IL-6R/gp130 pathway as an underlying mechanism of mBMSC-altered astrogliosis. Furthermore, IL-6 siRNA was used to block IL-6 expression in astrocytes to further investigate IL-6 involvement in mBMSC-altered astrogliosis. Our results indicate that the mBMSC-conferred decline of astrogliosis post-ischemia may derive from the down-regulation of the IL-6/IL-6R/gp130 pathway.
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PMID:Bone marrow stromal cells reduce ischemia-induced astrocytic activation in vitro. 1831 31

The aim of this study was to investigate the relationship between aspirin resistance, ischaemic stroke subtype, stroke severity, and inflammatory cytokines. Aspirin resistance was assessed by thrombelastography in 45 people with ischaemic stroke and 25 controls. Plasma interleukin (IL)-6 was measured. Stroke severity was assessed using the modified Rankin scale and National Institute of Health Stroke Score within 72 h of stroke. Aspirin resistance was more common in the stroke than the control group (67% versus 40%, P=0.028), and within the stroke group the aspirin-resistant group had a higher Rankin score (4.0 versus 2.0, P=0.013). Aspirin resistance was greater in lacunar than embolic strokes (platelet activation 79% versus 59%, P=0.020). The stroke aspirin-resistant group had higher levels of IL-6 than the stroke aspirin-sensitive group (2.4+/-1 versus 1.8+/-0.9 ng/mL, P=0.037). Using multivariate analysis, we examined the interrelationships between aspirin resistance, IL-6, and stroke severity. These analyses showed that IL-6 was independently associated with stroke severity as the outcome (B=3.738, P=0.036), and aspirin resistance was independently associated with IL-6 (B=0.765, P=0.005) as the outcome. In conclusion, aspirin resistance is related to stroke severity and aspirin resistance is more common in lacunar strokes than embolic strokes.
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PMID:Aspirin resistance is more common in lacunar strokes than embolic strokes and is related to stroke severity. 1831 29

Patients with diabetes mellitus (DM) are at risk for Helicobacter pylori infection. This infection has been linked to atherosclerosis and its vascular complications. The aim of this study was to evaluate the: (1) prevalence of H pylori infection in patients with DM; (2) association between diabetic vascular complications and H pylori infection; and (3) influence of H pylori infection on atherosclerosis and inflammatory biomarkers. In this study, we evaluated 80 patients with DM for atherosclerosis; cardiac, cerebral, and peripheral vascular diseases; retinopathy; neuropathy; and nephropathy. We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. H pylori infection was detected in 85% of patients versus 76.7% for control subjects. Carotid artery intima-media thickness was significant in H pylori-infected patients. IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. We concluded that H pylori infection is common in DM and seems to be linked to the presence of atherosclerosis and ischemic cerebrovascular stroke. This effect could be mediated by increasing cytokine levels.
J Stroke Cerebrovasc Dis
PMID:Vascular risks and complications in diabetes mellitus: the role of helicobacter pylori infection. 1834 51

Stabilization of carotid artery plaques by pharmacologic intervention is a promising strategy for the prevention of ischemic stroke. In this study, we examined the effect of 12 months of statin therapy on carotid plaque echogenicity. This study included 81 hypercholesterolemic patients with carotid atherosclerotic plaques. Echogenicity of the largest plaque in each patient was evaluated by ultrasound with integrated backscatter analysis. All patients underwent dietary modification. Forty patients were treated with simvastatin (10 mg/day, n = 24) or atorvastatin (5 mg/day, n = 16) according to the choice by each attending physician. Carotid plaques were monitored by measuring plaque thickness and echogenicity during a 12-month follow-up period. Levels of serum high-sensitivity CRP (hs-CRP), interleukin (IL)-6 and IL-18 were determined in all patients. Total cholesterol, triglyceride, hs-CRP and IL-18 were significantly decreased after 12 months of statin therapy. The change in IL-6 level was not significant. Significant increases in echogenicity of carotid plaques and decreases in plaque thickness were noted after statin therapy. In the 41 patients without statin therapy, carotid plaque echogenicity, plaque thickness and serum levels of inflammatory markers were not significantly altered. Our results suggest that statin therapy in hypercholesterolemic patients for 12 months increases carotid plaque echogenicity and decreases plaque thickness, in addition to lowering serum levels of lipids and inflammatory markers.
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PMID:Statin therapy increases carotid plaque echogenicity in hypercholesterolemic patients. 1837 81

Combined 2-MHz ultrasound (US) and second-generation, sulfur hexafluoride microbubbles (MB) treatment (US+MB) was performed in a permanent middle cerebral artery (MCA) occlusion model in rats to evaluate possible effects on the ischemic cascade. We used 16 Wistar rats and the MCA occlusion model for stroke induction. Glutamate, pyruvate, lactate and glycerol levels were measured by intracerebral microdialysis before and after stroke induction and after US+MB application (n = 8) for 20 h. After 24 h, brain infarct volume, apoptosis and IL-6 and TNF-alpha levels were evaluated. The infarct volume was significantly reduced (p < 0.05) in the US+MB-treated group compared with control animals. In additional, glutamate levels were significantly lower in US+MB-treated animals, and these animals showed a higher rate of apoptotic cell death in the infarcted area. The levels of IL-6 and TNF-alpha concentrations were not different in both groups, and there was no apoptotic cell death outside the infarction in animals treated with US+MB. The results demonstrate that US+MB with second generation microbubbles does not have a harmful effect on ischemic stroke in an MCA occlusion model of the rat.
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PMID:Effect of combined ultrasound and microbubbles treatment in an experimental model of cerebral ischemia. 1843 68

The authors reported recently that endotoxaemia mediated elevated levels of tumour necrosis factor (TNF-alpha) and interleukin-1alpha (IL-1alpha) were involved in the pathophysiology of acute heat stroke patients. Pentoxifylline (PTX) is known to modulate neutrophil functions. In the present study the effects of PTX on lipopolysaccharide (LPS) and cytokine induced T-cell and macrophage (PhiM) activation, and on natural killer (NK) cell and lymphokine activated killer (LAK) cell mediated cytotoxicity were examined. Finally, the effect of PTX on the expression of adhesion molecules (LFA-1, Mac-1 and ICAM-1), and cytokine (IL-1alpha, IL-2, TNF-alpha, IL-6 and IFN-gamma) production and their surface receptor expression in response to LPS activation was investigated. PTX free cultures served as a control. Results revealed that PTX can down-regulate all the above-mentioned immunological parameters in a dosedependent manner. These findings might have far reaching clinical implications.
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PMID:Mechanism of pentoxifylline mediated down-regulation of killer lineage cell functions. 1847 49

The inflammation plays a critical role in the stroke onset and even in the worsening of the lesions. Therefore, the investigation of inflammatory response in the acute stage may contribute to improve the treatment of ischemic stroke. High-sensitive CRP (hsCRP), IL-6 and TNFalpha were measured as inflammatory markers on admission and in the 28th day after the onset. Oxidized LDL was measured simultaneously, since it can be a marker of reactive oxygen species which reflect the activity of inflammation. Ischemic stroke patients within 24 h after the onset (n=105) were included in this study. All patients were classified into cardioembolism, large-artery atherosclerosis, lacunar infarction, branch atheromatous disease and arterial dissection groups based on the findings of MRI and MRA and clinical records. Oxidized LDL was significantly increased in the acute phase of all cases. The amplified level of IL-6 was related to the worse outcome. The increase of TNFalpha in lacunar infarction was statistically correlated to the neurological severity on admission. In conclusion, IL-6 may predict not only the severity of the stroke lesions but also the outcome of patients. TNFalpha may suggest the small arterial lesions.
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PMID:The impact of inflammation on the pathogenesis and prognosis of ischemic stroke. 1847 10

This study examined endotoxin-mediated cytokinemia during exertional heat stress (EHS). Subjects were divided into trained [TR; n=12, peak aerobic power (VO2peak)=70+/-2 ml.kg lean body mass(-1).min(-1)] and untrained (UT; n=11, VO2peak=50+/-1 ml.kg lean body mass(-1).min(-1)) groups before walking at 4.5 km/h with 2% elevation in a climatic chamber (40 degrees C, 30% relative humidity) wearing protective clothing until exhaustion (Exh). Venous blood samples at baseline and 0.5 degrees C rectal temperature increments (38.0, 38.5, 39.0, 39.5, and 40.0 degrees C/Exh) were analyzed for endotoxin, lipopolysaccharide binding protein, circulating cytokines, and intranuclear NF-kappaB translocation. Baseline and Exh samples were also stimulated with LPS (100 ng/ml) and cultured in vitro in a 37 degrees C water bath for 30 min. Phenotypic determination of natural killer cell frequency was also determined. Enhanced blood (104+/-6 vs. 84+/-3 ml/kg) and plasma volumes (64+/-4 vs. 51+/-2 ml/kg) were observed in TR compared with UT subjects. EHS produced an increased concentration of circulating endotoxin in both TR (8+/-2 pg/ml) and UT subjects (15+/-3 pg/ml) (range: not detected to 32 pg/ml), corresponding with NF-kappaB translocation and cytokine increases in both groups. In addition, circulating levels of tumor necrosis factor-alpha and IL-6 were also elevated combined with concomitant increases in IL-1 receptor antagonist in both groups and IL-10 in TR subjects only. Findings suggest that the threshold for endotoxin leakage and inflammatory activation during EHS occurs at a lower temperature in UT compared with TR subjects and support the endotoxin translocation hypothesis of exertional heat stroke, linking endotoxin tolerance and heat tolerance.
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PMID:Mild endotoxemia, NF-kappaB translocation, and cytokine increase during exertional heat stress in trained and untrained individuals. 1856 34

The aim of the authors is to examine the relationship between the cytokine levels that are thought to be involved in stroke etiopathogenesis (tumor necrosis factor [TNF]-alpha, interleukin [IL]-2, IL-6, IL-8, IL-11), soluble protein C receptor (sEPCR), and factor VIII (FVIII) levels. The study included 27 patients with stroke and 30 healthy controls, aged 0 to 18. In the comparison of the sEPCR, cytokine, and FVIII levels between patient and control groups, median levels of TNF-alpha, IL-2, IL-6, and IL-8 are found to be high in the patient group when compared with controls, whereas there is no difference in sEPCR, IL-11, and FVIII levels. In the patient group, a positive correlation is seen between TNF-alpha levels and IL-2 and IL-6 levels, between IL-2 and IL-6 levels, and between IL-6 and IL-8 levels, whereas a negative relationship is seen between sEPCR and FVIII. In the control group apart from the patient group, a negative relationship is seen between TNF-alpha and FVIII, whereas there is a positive relationship between IL-11 and sEPCR levels. Median sEPCR levels in patients who have normal or low FVIII levels are significantly high when compared with those with high FVIII levels. In conclusion, in the pediatric population, an increase in TNF-alpha, IL-2, IL-6, and IL-8 levels is seen. Also, an inverse relationship of sEPCR and FVIII levels is shown for the first time. This study provides a basis for ongoing studies that aim to clarify stroke etiopathogenesis. Studies with larger series of patients are warranted to confirm this hypothesis.
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PMID:The relation between cytokines, soluble endothelial protein C receptor, and factor VIII levels in Turkish pediatric stroke patients. 1859 Nov 80

Investigations aimed at studying of peripheral blood levels of free nitric oxide (NO) and proinflammatory cytokines IL-1beta, IL- 6 and TNF-alpha in correlation with initial ischemic lesion size and neurological dynamics during a month of acute brain ischemia. Forty two patients aged 60-75 (26 male) have been investigated. Initial neurological status, later deterioration and functional outcome were evaluated using Glasgow Coma Scale (GCS), National institutes of Health Stroke Scale (NIHSS) and Barthel Index (BI). Patients were divided into two groups: severe stroke (GCS<or=10, NIHSS >15, BI<16, n=25) and a moderate/mild stroke (GCS>10, NIHSS<or=15, BI>or=18, n=17). The NO concentration was detected by spectrophotometric and Electron Paramagnetic Resonance (EPR) methods. Cytokine plasma levels were determined applying the Enzyme-Linked Immuno Sorbent Assay (ELISA). Statistical evaluation was performed by SPSS. Mean values calculated using the t-paired test. Pearson correlation ad multivariate logistic regression have been applied. In the first days of stroke onset the plasma levels of IL-1beta and TNF-alpha revealed the slight negative correlation toward the functional outcome, while the elderly patients found to have the significant negative correlation of IL-6 plasma levels toward the functional outcome (p<0.01). The NO plasma concentration within 48 hours after stroke onset more profoundly was reduced in aged patients, while in less severe cases and in relatively young patients it was significantly elevated (p<0.01). The high plasma level of IL-6 in the acute phase of stroke seems to be the strong predictor of poor outcome rather for aged, than for younger patients.
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PMID:Proinflammatory reactants as determinants of stroke severity in elderly. 1883 25


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