Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Semax is the first domestic nootropic drug of an unexhausted type from the group of neuropeptides. In experimental studies it showed angioprotective, antihypoxic and neurotrophic activity in the doses 100-150 micrograms/kg. A combined clinical-electrophysiologic study revealed its high efficiency in acute ischemic stroke. A clinical trial was performed of immunobiochemical mechanisms of neuroprotective properties of Semax in acute period of ischemic stroke. A retrospective comparative clinicoimmunobiochemical analysis provided objective data on the molecular level on activating influence of Semax on antiinflammatory postischemic reactions in the brain. Shifting neuromediatory balance toward a prevalence of the antiinflammatory agents (interleukin-10, tumor necrosis factor-alpha) over the factors maintaining the inflammation (interleukin-8, C-reactive protein).
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PMID:[Investigation of mechanisms of neuro-protective effect of semax in acute period of ischemic stroke]. 1035 12

The effects of physical therapy on immunological parameters were evaluated in 12 patients (8 males and 4 females, 69.2 +/- 9.0 years) with cerebrovascular diseases in a stable situation two to three months after the onset of stroke who entered in our hospital between 1994 and 1997. After a two-month physical therapy program, the proportions of helper-inducer T (Thi) cells and suppressor-inducer T (Tsi) cells were increased significantly and that of cytotoxic T (Tc) cells was decreased, although those of HLA-DR+, suppressor T (Ts) and activated T (Tac) cells were not changed. The antibody dependent cellular cytotoxicity (ADCC) was significantly increased, although natural killer (NK) cell activity was not changed. The serum levels of interleukin-2 receptor was significantly increased but those of interleukin-2, interleukin-6 and interleukin-12 were not changed. The serum levels of interleukin-10, interleukin-12 and tumor necrosis factor-alpha were not detectable, while interleukin-1beta was decreased in 2 patients and interleukin-10 was increased in 2 patients. These findings suggest that daily physical exercise may activate the immune system possibly through the cytokine network in patients with cerebrovascular diseases (CVD).
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PMID:Effects of physical therapy on cytokines and two color analysis-lymphocyte subsets in patients with cerebrovascular diseases. 1051 38

The presence of an inflammatory response in the pathophysiology of acute brain ischemia is relatively well established, but less is known about the anti-inflammatory mechanisms. The aim of the present study was to evaluate part of the immune response in acute stroke patients and to analyze a possible correlation with other hematological parameters, clinical outcome, size of infarct and subtypes of strokes. We prospectively studied 42 stroke patients, without signs of infections or inflammatory diseases, at days 0, 1, 3, 7 and 14, and 39 healthy control subjects. We measured serum levels of the anti-inflammatory cytokine interleukin-10 (IL-10) and the pro-inflammatory cytokine interleukin-6 (IL-6) by ELISA method. We observed a highly inverse correlation between these two molecules in control subjects (r=-0.78, p=0.0000001), and this correlation was lost in stroke patients. Patients had significantly lowered IL-10 serum levels soon after the acute event (p=0.00005), with a slight increase at the seventh day. On the other hand, patients had increased IL-6 serum levels compared with controls after day one until day 14 (p<0.04), with a maximum increase at day 3. Interleukin-6 correlated with clinical outcome whereas interleukin-10 did not. Low levels of interleukin-10 indicate that the antiinflammatory response is down-regulated in acute stroke patients. The pro-inflammatory response begins 24 hours after the onset of acute cerebral ischemia, as indicated by the increased serum levels of interleukin-6. The physiological balance between these two molecules is altered in acute stroke patients.
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PMID:Temporal profile of serum anti-inflammatory and pro-inflammatory interleukins in acute ischemic stroke patients. 1180 50

This study was performed to evaluate whether cytokines, adhesion molecules, ghrelin and S-100B are useful markers in predicting the cerebral infarction after cardiac surgery with cardioplumomary bypass (CPB). The patients (n=20) were classified into two groups; group A (n=4) showed postoperative organized cerebral damage, while group B (n=16) consisted of patients without occurrence of postoperative strokes. Before CPB, serum levels of S-100B in both groups A and B were low (<0.5 ng/mL), while ghrelin concentrations in group A (all patients had history of strokes) were much higher than those in group B. After CPB, when serum levels of S-100B in group A at 24h were higher than those in group B, ghrelin in group A at same time point showed high levels in comparison to group B. At 12 and 24h after CPB, levels of tumor necrosis factor (TNF)-alpha, interleukin-10 and soluble TNF-receptor I in group A were significantly higher than those in group B. In conclusion, it is considered that ghrelin as well as S-100B can be a useful marker for the prediction of stoke after CPB. Increase of TNF-alpha, interleukin-10 and soluble TNF-receptor I after CPB may be involved in the pathogenesis of stroke after CPB.
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PMID:Relationship between cerebral injury and inflammatory responses in patients undergoing cardiac surgery with cardiopulmonary bypass. 1561 77

Stroke causes neuronal necrosis and generates inflammation. Pro-inflammatory molecules intervene in this process by triggering glial cell activation and leucocyte infiltration to the injured tissue. Cytokines are major mediators of the inflammatory response. Pro-inflammatory and anti-inflammatory cytokines are released in the ischaemic brain. Anti-inflammatory cytokines, such as interleukin-10, promote cell survival, whereas pro-inflammatory cytokines, such as TNFalpha (tumour necrosis factor alpha), can induce cell death. However, deleterious effects of certain cytokines can turn to beneficial actions, depending on particular features such as the concentration, time point and the very intricate network of intracellular signals that become activated and interact. A key player in the intracellular response to cytokines is the JAK (Janus kinase)/STAT (signal transducer and activator of transcription) pathway that induces alterations in the pattern of gene transcription. These changes are associated either with cell death or survival depending, among other things, on the specific proteins involved. STAT1 activation is related to cell death, whereas STAT3 activation is often associated with survival. Yet, it is clear that STAT activation must be tightly controlled, and for this reason the function of JAK/STAT modulators, such as SOCS (suppressors of cytokine signalling) and PIAS (protein inhibitor of activated STAT), and phosphatases is most relevant. Besides local effects in the ischaemic brain, cytokines are released to the circulation and affect the immune system. Unbalanced pro-inflammatory and anti-inflammatory plasma cytokine concentrations favouring an 'anti-inflammatory' state can decrease the immune response. Robust evidence now supports that stroke can induce an immunodepression syndrome, increasing the risk of infection. The contribution of individual cytokines and their intracellular signalling pathways to this response needs to be further investigated.
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PMID:Signalling pathways mediating inflammatory responses in brain ischaemia. 1707 99

This current review summarized animal models of heatstroke experimentation that promote our current knowledge of therapeutic effects on cerebrovascular dysfunction, coagulopathy, and/or systemic inflammation with human umbilical cord blood cells (HUCBCs) or estrogen in the setting of heatstroke. Accumulating evidences have demonstrated that HUCBCs provide a promising new therapeutic method against neurodegenerative diseases, such as stroke, traumatic brain injury, and spinal cord injury as well as blood disease. More recently, we have also demonstrated that post- or pretreatment by HUCBCs may resuscitate heatstroke rats with by reducing circulatory shock, and cerebral nitric oxide overload and ischemic injury. Moreover, CD34+ cells sorted from HUCBCs may improve survival by attenuating inflammatory, coagulopathy, and multiorgan dysfunction during experimental heatstroke. Many researchers indicated pro- (e.g. tumor necrosis factor-alpha [TNF-alpha]) and anti-inflammatory (e.g. interleukin-10 [IL-10]) cytokines in the peripheral blood stream correlate with severity of circulatory shock, cerebral ischemia and hypoxia, and neuronal damage occurring in heatstroke. It has been shown that intravenous administration of CD34+ cells can secrete therapeutic molecules, such as neurotrophic factors, and attenuate systemic inflammatory reactions by decreasing serum TNF-alpha but increasing IL-10 during heatstroke. Another line of evidence has suggested that estrogen influences the severity of injury associated with cerebrovascular shock. Recently, we also successfully demonstrated estrogen resuscitated heatstroke rats by ameliorating systemic inflammation. Conclusively, HUCBCs or estrogen may be employed as a beneficial therapeutic strategy in prevention and repair of cerebrovascular dysfunction, coagulopathy, and/or systemic inflammation during heatstroke.
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PMID:Human umbilical cord blood cells or estrogen may be beneficial in treating heatstroke. 1738 84

Cerebrovascular disease is a significant cause of morbidity and mortality in the world. Inflammatory processes induce several pathological responses such as atherosclerosis, which have fundamental roles in stroke in the etiology of ischemic cerebrovascular disease and the pathophysiology of cerebral ischemia. Viral interleukin-10 (vIL-10), a potential anti-inflammatory cytokine, has been studied extensively. However, the efficacy of vIL-10 on cerebrovascular dysfunction is not well known. Our goal in this study was to explore the effect of gene transfer of vIL-10 mediated by adenovirus (Ad/vIL-10) on cerebrovascular function using a model of vasocontraction of isolated basilar artery from mongrel dogs induced by lysophosphatidylcholine (lysoPC), a proinflammatory and atherogenic serum lysophospholipid. To clarify the relation between contraction of basilar aorta and cell adhesion and adhesion molecules, our further study explored effects of Ad/vIL-10 on monocyte-cerebrovascular endothelial cells adhesion and expression of cell adhesion molecule by cultured cerebromicrovascular endothelial cells, bEnd.3, after incubation by lysoPC. Our results showed that Ad/vIL-10 significantly decreased contractive response of basilar aorta produced by lysoPC and augmented vasorelaxation to acetylcholine. Further studies showed the Ad/vIL-10 significantly depressed adherence of monocytes to cerebrovascular endothelial cells and inhibited up-regulation of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) which are bio-markers in inflammatory progress. These data demonstrated the protective effects of Ad/vIL-10 on cerebrovascular dysfunction induced by inflammation, and proved that inhibition of expression of cell adhesion molecules should be one of ways of vIL-10 to protect vascular function during inflammation.
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PMID:Adenoviral gene transfer of viral interleukin-10 protects cerebrovascular impairment induced by lysophosphatidylcholine. 1815 52

Essential hypertension is a common disease with fatal clinical complications. Epidemiological and family studies have confirmed the role of genetic predisposition in its development. Hypertensive patients have been shown to have an altered profile of pro- and anti-inflammatory cytokines. The aim of our investigation was to reveal the association of interleukin-6, interleukin-12, and interleukin-10 gene polymorphisms with essential hypertension and its clinical complications in a Tatar ethnic group from Bashkortostan, Russia. The study involved 362 hypertensive patients and 244 healthy subjects from this Tatar ethnic group (Bashkortostan, Russia). DNA was isolated from whole venous blood using phenol-chloroform extraction by the standard method. IL6 -572 G/C, IL12B 1159 C/A, and IL10 -627 C/A genotypes were typed using polymerase chain reaction followed by restriction enzyme digestion. We found that the IL10 -627 *C/*C genotype was associated with decreased risk of hypertension (OR = 0.64, P = 0.035). IL6 genotypes and allele distribution did not differ significantly between subjects with and without hypertension, but the IL6 -572 *G/*G genotype frequency was found to be significantly higher among those patients who had stroke, compared with normotensive control subjects (P = 0.036). Carriers of the IL12B 1159 *A/*A genotype had a lower risk of stroke (OR = 0.38, P = 0.028). Our study has shown the association between IL10 -627 C/A polymorphism and essential hypertension in the Tatar ethnic group from Bashkortostan, Russia. The IL10 -627*C/*C genotype was found to be protective against hypertension. We also demonstrated that hypertensive patients with the IL12B *A/*A and IL6 *G/*G genotypes had increased risk of stroke. Our results suggest a role for cytokines in cardiovascular disease development in the Tatar ethnic group, but further investigation is needed.
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PMID:Association of interleukin-6, interleukin-12, and interleukin-10 gene polymorphisms with essential hypertension in Tatars from Russia. 1816 9

Stroke is accompanied by a strong inflammatory reaction in the brain. Periodontal disease is a chronic local infection which causes a systemic low grade inflammation. We hypothesized that a mild systemic inflammatory reaction as caused by periodontal disease prior to stroke onset, may exert a neuroprotective effect in a rat model of focal ischemia. To test this hypothesis, marginal periodontitis was induced by ligatures on the second maxillary molars in BB/LL Wistar rats for 3 weeks. Two weeks after periodontitis initiation, focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery. After a survival time of 7 days after ischemia, rats were killed and bone loss was determined on the buccal and palatinal surfaces of the defleshed jaw. In addition, markers of systemic inflammation were determined in a different group of laboratory animals at 14 days after the onset of periodontitis. The infarct size and markers of the inflammatory reaction in the brain were determined by immunohistochemistry. We found: (i) rats with ligatures exhibited significantly more periodontal bone loss than the control rats; (ii) the development of periodontitis was associated with an elevated gene expression for several markers of systemic inflammation (interleukin-10, transforming growth factor beta 1, tumor necrosis factor alpha, interleukin-1beta and interferon gamma; (iii) rats with periodontitis and a mild systemic inflammation had a significantly reduced infarct volume and a significant reduction in the number of brain macrophages in the infarcted area. In conclusion we found that mild systemic inflammation elicited prior to stroke onset may have a neuroprotective effect in rats by reducing the infarct volume and tissue destruction by brain macrophages.
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PMID:Mild systemic inflammation has a neuroprotective effect after stroke in rats. 1899 56

Systemic and local inflammatory processes have a key, mainly detrimental role in the pathophysiology of ischemic stroke. Currently, little is known about endogenous counterregulatory immune mechanisms. We examined the role of the key immunomodulators CD4(+)CD25(+) forkhead box P3 (Foxp3)(+) regulatory T lymphocytes (T(reg) cells), after experimental brain ischemia. Depletion of T(reg) cells profoundly increased delayed brain damage and deteriorated functional outcome. Absence of T(reg) cells augmented postischemic activation of resident and invading inflammatory cells including microglia and T cells, the main sources of deleterious cerebral tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), respectively. Early antagonization of TNF-alpha and delayed neutralization of IFN-gamma prevented infarct growth in T(reg) cell-depleted mice. Intracerebral interleukin-10 (IL-10) substitution abrogated the cytokine overexpression after T(reg) cell depletion and prevented secondary infarct growth, whereas transfer of IL-10-deficient T(reg) cells in an adoptive transfer model was ineffective. In conclusion, T(reg) cells are major cerebroprotective modulators of postischemic inflammatory brain damage targeting multiple inflammatory pathways. IL-10 signaling is essential for their immunomodulatory effect.
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PMID:Regulatory T cells are key cerebroprotective immunomodulators in acute experimental stroke. 1919 85


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