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<p><b>BACKGROUND</b>The mortality and disability associated with progressing ischemic stroke are much higher than general ischemic stroke. This study was conducted to determine the risk factors for progressing ischemic stroke in the Han population of northeast China.</p><p><b>METHODS</b>A total of 2511 patients with ischemic stroke within 24 hours admitted to Department of Neurology, First Affiliated Hospital of Harbin Medical University were studied, from November 2007 to May 2009. All of the patients were classified into the progressing or non-progressing group according to the scores of the Scandinavian Neurological Stroke Scale. Fifteen putative risk factors were evaluated. The influence of risk factors for progressing ischemic stroke was analyzed with the simple Logistic analysis, the multiple Logistic analysis, and the stepwise Logistic regression model. All the statistical analysis was performed by SAS 9.1.</p><p><b>RESULTS</b>Totally 359 (14.3%) patients met the criteria for progressing ischemic stroke. The Logistic analysis showed that age, family stroke history, smoking history, hypertension on admission, a drop in blood pressure after admission to the hospital, high serum glucose on admission, and fever were related to progressing ischemic stroke in the Han population of northeast China.</p><p><b>CONCLUSION</b>People of the ischemic stroke with these factors are more likely to develop progressing ischemic stroke.</p>
Assuntos
Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , China , Epidemiologia , Análise de Regressão , Fatores de Risco , Acidente Vascular Cerebral , EpidemiologiaRESUMO
Objective To investigate the expressions of transient receptor potential canonical 1 (TRPC1)and melastatin 7(TRPM7)in rat brains after focal cerebral ischemia-reperfusion injuries,and discuss the molecular mechanisms of brain damage caused by focal cerebral ischemia-reperfusion.Methods Rat models of cerebral artery occlusion(MCAO)were established by suture method.Fifty adult Wistar rats were randomly divided into sham-operated group(n=10)and ischemia-reperfusion group (n=40).The rats were sacrificed 3,12,24 and 72 h after MCAO and the ischemia-reperfusion group was assigned to 4 subgroups(n=10)accordingly.The mRNA expressions of TRPC1 and TRPM7 in the ischemic cortex at different phases after reperfusion were examined by RT-PCR and the protein expressions of them were detected by Western blotting and immunohistochemistry staining.Results Low expression level of TRPC1 and TRPM7 in the rat brain was found in the sham-operated group.The expression of TRPC1 began to increase 3 h after reperfusion and gradually increased with the progress of repcffusion,peaking at 12 h of reperfusion;the expressions of TRPC1 decreased gradually thereafter,but it was still higher 72 h after reperfusion as compared with that in the sham-operated group(P<0.05).Except the peaked expression level of TRPM7 was detected 24 h after repcrfusion,the expression trends of TRPM7 were similar to those of TRPC1.Conclusion TRPC1 and TRPM7 may involve in the pathologic process of focal cerebral ischemia-reperfusion injury.
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Objective To observe the expressions of Kir4.1 and aquaporin-4 (AQP4) in rats with focal brain ischemia-reperfusion (IR) injury and clarify the role of Kir4.1 and AQP4 in IR injury. Methods Male Wistar rats were randomized into 5 groups, including a sham-operated group and 4 IR groups with focal brain IR injury induced by middle cerebral artery occlusion (MCAO). In the 4 IR groups, the rats were subjected to a 2-hour ischemia and sacrificed atter reperfusion for 3, 12, 24 or 72 h. Immunohistochemistry and RT-PCR were used to detect the expressions of Kir4.1 and AQP4 proteins and mRNAs in the brain tissues, respectively. Results Compared with the sham-operated group, the IR groups showed significantly increased expressions of Kir4.1 and AQP4 in the peri-infarct cortex surrounding the primary infarct area (P<0.05), which began at 3 h after the reperfusion and reached the peak level at 24 h, subsiding at 72 h. The mRNA levels of Kir4.1 (represented as the absorbance) were 0.343±0.02, 0.47±0.06, 0.61±0.08, 0.83±0.10 and 0.68±0.09 in the sham-operated group and the 4 IR groups with reperfusion for 3, 12, 24 and 72 h, respectively. The mRNA levels of AQP4 were 0.49±0.05, 0.66±0.09, 0.91±0.09, 1.12±0.11 and 0.94±0.08 in the 5 groups, respectively. Kir4.1 expression was positively correlated to AQP4 expression at the mRNA level (r=0.780, P=0.000). Conclusion Kir4.1 and AQP4 react with each other in the course of focal brain ischemia-reperfusion, both playing roles in the mechanism of brain IR injury.
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<p><b>OBJECTIVE</b>To investigate the role of T cell and its subsets in the induction of insulitis and type 1 diabetes mellitus (T1DM) in BALB/c mice.</p><p><b>METHODS</b>Autoimmune diabetes mellitus was developed by intraperitoneal injection of 40 mg/kg streptozotocin (STZ) daily for 5 consecutive days in BALB/c mice as sources of donor cells. Spleen cells from diabetic mice were then cultured for 7 days in the stimulation of interleukin-2 (IL-2) to harvest diabetogenic T cells, which were subsequently transferred into normal BALB/c mice recipients. MTT, ELISA, and HE staining were used to analyze the lymphocyte proliferation, cytokine (IL-2, interferon-gamma, IL-4, and IL-10) levels, and pathological changes in pancreatic islets.</p><p><b>RESULTS</b>As few as 3 x 10(6) diabetogenic T cells successfully induced diabetes mellitus in recipients pretreated with STZ twice, whereas transfer of equal amount of normal splenocytes, T cell-depleted diabetogenic splenocytes, or diabetogenic CD4+ T cells alone in recipients receiving STZ twice pretreatment was proved not to induce diabetes mellitus either. A markedly increased lymphocyte proliferation, high levels of interferon-gamma and IL-2 in the supernatants of diabetogenic T cells were observed. In addition, a markedly enhanced lymphocyte proliferation, a high level of interferon-gamma secretion in serum, and numerous lymphocytes infiltration in pancreatic islets were detected in the diabetic mice induced by diabetogenic T cells transfer.</p><p><b>CONCLUSIONS</b>A novel T1DM murine model is established in STZ-pretreated BALB/c mice by adoptive transfer of diabetogenic T cells. CD4+ T cells with interferon-gamma may promote the onset of diabetes mellitus.</p>