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There is increasing evidence showing that inflammation occurs in atherosclerosis and contributes to the formation of atherosclerotic plaques. As important inflammatory peptides, kinins are increased in inflammation, eliciting vasodilation, increasing vascular permeability and recruiting inflammatory cells to the injury sites by activating specific receptors, B1 and B2. The two receptors have been reported to increase in inflammation, but their expressions remain to be defined in human carotid atherosclerotic plaques (CAP). In order to assess the gene expression of kinin receptors in human CAP, 47 CAP specimens were collected from patients undergoing endarterectomy and classified into stable and unstable plaque groups, respectively, with 10 mesenteric arteries used as controls. Total mRNA of B1R and B2R was extracted from CAPs and their levels were determined using reverse transcription-polymerase chain reaction. The expression of B1R and B2R mRNA was significantly upregulated in human CAPs compared to the control arteries. In the unstable plaques, the ratios of B1R to the β-actin mRNA level were significantly increased relative to the stable plaques. However, no notable differences were observed in the ratios of B2R to β-actin in mRNA expression between the stable and unstable plaques. The present study suggests that kinin-mediated inflammation involves the formation of atherosclerotic plaque and B1R plays an important role in plaque instability, indicating that kinin receptors can be used as potential targets for future therapeutic interventions.

Background Whether patients presenting with mild stroke should or should not be treated with intravenous rtPA is still controversial. This systematic review aims to assess the safety and outcome of thrombolysis in these patients. Material/Methods We systematically searched PubMed and Cochrane Central Register of Controlled Trials for studies evaluating intravenous rtPA in patients with mild or rapidly improving symptoms except case reports. Excellent outcome (author reported, mainly mRS 0-1), symptomatic intracranial hemorrhage (sICH) and mortality were analyzed. Results Fourteen studies were included (n=1906 patients). Of these, 4 studies were comparative (2 randomized and 2 non-randomized). The remaining were single-arm studies. On the basis of 4 comparative studies with a total of 1006 patients, the meta-analysis did not identify a significant difference in the odds of excellent outcome (OR=0.86; 95% CI: 0.64–1.15; I2=0) between IV rtPA-treated minor stroke and those without rtPA treatment. Eleven studies involving 1083 patients showed the pooled rate of excellent outcome was 76.1% (95% CI: 69.8–81.5%, I2=42.5). Seven studies involving 378 patients showed the mortality rate was 4.5% (95% CI: 2.6–7.5%, I2=1.4). Twelve studies involving 831 patients showed the pooled rate of sICH was 2.4% (95% CI: 1.5–3.8, I2=0). Conclusions Although efficacy is not clearly established, this study reveals the adverse event rates related to thrombolysis are low in mild stroke. Intravenous rtPA should be considered in these patients until more RCT evidence is available.

Bithalamic infarctions initially presenting as a convulsive seizure are rarely reported and, to our best knowledge, have never been reported in China. Here, we present a patient with convulsive seizure at the onset of bilateral paramedian thalamic infarction. The diffusion-weighted imaging revealed that the infarct area is supplied by Percheron artery. Associated with the relationship between seizure and centrencephalic system and reticular formation as previously reported, we suggest that seizure could be the onset symptom of paramedian thalamic infarction. Physicians should recognize this condition, because both seizure control and early ischemic stroke management are required.

Ischemic edema can alter the structure and permeability of the blood-brain barrier. Recent studies have reported that progesterone reduces cerebral edema after cerebral ischemia. However, the underlying mechanism of this effect has not yet been elucidated. In the present study, progesterone effectively reduced Evans blue extravasation in the ischemic penumbra, but not in the ischemic core, 48 hours after cerebral ischemia in rats. Progesterone also inhibited the down-regulation of gene and protein levels of occludin and zonula occludens-1 in the penumbra. These results indicate that progesterone may effectively inhibit the down-regulation of tight junctions, thereby maintaining the integrity of the blood-brain barrier and reducing cerebral edema.