Abstract. Acute ischemic stroke induces systemic inflammation, exhibited as changes in body temperature, white blood cell counts and C-reactive protein (CRP) levels. The aim of the present study was to observe the effects of intravenous thrombolytic therapy on inflammatory indices in order to investigate the hypothesis that post-stroke systemic inflammatory response occurs in response to the necrosis of brain tissues. In this study, 62 patients with acute cerebral infarction and indications for intravenous thrombolysis were divided into three groups on the basis of their treatment and response: Successful thrombolysis (n=36), failed thrombolysis (n=12) and control (n=14) groups. The body temperature, white blood cell counts and highsensitivity (hs)-CRP levels were recorded pre-treatment and on post-stroke days 1, 3, 5 and 7. Spearman's correlation analysis showed that the pre-treatment National Institutes of Health Stroke Scale (NIHSS) score positively correlated with body temperature, white blood cell count and hs-CRP levels. On day 3 of effective intravenous thrombolysis, the body temperature and white blood cell were decreased and on days 3 and 5, the serum levels of hs-CRP were reduced compared with those in the failed thrombolysis and control groups. The results indicate that the systemic inflammatory response following acute cerebral infarction was mainly caused by ischemic injury of local brain tissue; the more serious the stroke, the stronger the inflammatory response. Ultra-early thrombolytic therapy may inhibit the necrosis of brain tissue and thereby reduce the inflammatory response.

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The aim of this study was to investigate the effect and mechanism of chronic intermittent hypoxia (CIH) on cerebral injury using the ischemia-reperfusion rat model. In total, 36 SD rats were divided into three groups: pseudo-surgery group (sham group), ischemia-reperfusion (IR) group (CIR group), and CIH intervention group (CIH group). The IR model was established using the suture-occluded method. CIH intervention was performed starting at 12 weeks prior to the establishment of the IR model for rats in the CIH group. Ultra-microstructure was examined using an electron microscope. Expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular endothelial growth factor (VEGF) in rat brain tissue was evaluated by immunohistochemical methods and western blot assays. The neurological deficit scores of rats in the CIH group were higher than those in the CIR group (p < 0.05). Using electron microscopy, we observed more severe edema around the capillaries of the rat brain that resulted in more pressure on the vascular wall of the capillaries in the CIH group compared to the CIR group. The expression of ICAM-1 and VEGF in rat brain tissue was rare in the sham group, but was significantly elevated in the CIR group (p < 0.05) and even higher in the CIH group, compared to the CIR group. Hence, the brain injury in ischemia-reperfusion rat models following CIH intervention may be related to the increased expression of ICAM-1 and VEGF.

ObjectiveTo explore the possible correlation between uric acid levels and leukoaraiosis (LA).MethodsThis cross-sectional study enrolled patients who presented with some neurological discomfort (e.g. dizziness, headache, mild cognitive impairment). Potential demographic and clinical risk factors associated with LA, including sex, age, hypertension, diabetes mellitus, smoking, alcohol consumption, dyslipidaemia, plasma fibrinogen, D-dimer, uric acid, and homocysteine, were investigated using univariate and multivariate logistic regression analyses.ResultsA total of 268 patients were enrolled in the study and divided into the LA group (n = 164) and the non-LA group (n = 104). Compared with the non-LA group, uric acid was significantly higher in the LA group (mean ± SD: 356.49 ± 121.85 µmol/l versus 289.96 ± 102.98 µmol/l). Multivariate logistic regression analyses showed that uric acid was an independent risk factor for LA (odds ratio 1.285; 95% confidence interval 1.062, 1.556).ConclusionHyperuricaemia was an independent risk factor for leukoaraiosis in Chinese patients.

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