Objective To explore the correlations between serum soluble growth stimulation gene 2 protein (sST2), brain natriuretic peptide (BNP) and the degree of carotid atherosclerosis in patients with acute ischemic stroke. Methods A total of 205 patients with acute ischemic stroke were selected as study group, and were divided into mild group with 100 cases, moderate group with 70 cases, and severe group with 35 cases according to the severity of carotid atherosclerosis. Another 150 healthy people who received physical examination during the same period were selected as control group. Serum levels of sST2 and BNP were compared among all groups. The correlations of sST2 and BNP levels with the degree of carotid atherosclerosis were analyzed. The influencing factors of different degree of carotid atherosclerosis in patients with acute ischemic stroke were analyzed. The predictive value of sST2 combined with BNP on the degree of carotid atherosclerosis in patients with acute ischemic stroke was analyzed. Results The serum sST2 level of the study group was significantly lower than that of the control group, and the serum BNP level was significantly higher than that of the control group (P < 0.05). The sST2 levels in moderate and severe groups were significantly lower, BNP levels were significantly higher than that in the mild group (P < 0.05). BNP level in the severe group was significantly higher, sST2 level was significantly lower than that in the moderate group (P < 0.05). The degree of carotid atherosclerosis in patients with acute ischemic stroke was correlated with age, history of hypertension, history of smoking, history of diabetes, levels of total cholesterol (TC), C-reactive protein (CRP), homocysteine (Hcy) and low density lipoprotein (LDL) (P < 0.05). Age, hypertension history, smoking history, diabetes history, TC, CRP, Hcy, LDL, BNP and sST2 were the influencing factors for degree of carotid atherosclerosis (P < 0.05). Serum BNP level was positively correlated with the degree of carotid atherosclerosis, while sST2 level was negatively correlated with the degree of carotid atherosclerosis (P < 0.001). The area under the curve (AUC) for the combined prediction of sST2 and BNP was significantly greater than that for the individual prediction of sST2 and BNP (P < 0.001). Conclusion Clinical observation of the changes in serum levels of sST2 and BNP in patients with acute ischemic stroke can effectively assess the progression of the disease, which is beneficial for improving the severity of carotid atherosclerosis in patients. The combined assessment of sST2 and BNP shows good diagnostic performance for evaluating the severity of carotid atherosclerosis in patients with acute ischemic stroke.

Bilateral middle pontine brachium and cerebral peduncula infarction is an extremely rare posterior circulation infarction.This article analyzed a patient with bilateral middle pontine brachium and cerebral peduncula infarction, reviewed the literature, and determined the cause through detailed medical history and imaging examinations.

CD146 is a newly identified endothelial biomarker that has been implicated in angiogenesis. Though in vitro angiogenic function of CD146 has been extensively reported, in vivo evidence is still lacking. To address this issue, we generated endothelial-specific CD146 knockout (CD146(EC-KO)) mice using the Tg(Tek-cre) system. Surprisingly, these mice did not exhibit any apparent morphological defects in the development of normal retinal vasculature. To evaluate the role of CD146 in pathological angiogenesis, a xenograft tumor model was used. We found that both tumor volume and vascular density were significantly lower in CD146(EC-KO) mice when compared to WT littermates. Additionally, the ability for sprouting, migration and tube formation in response to VEGF treatment was impaired in endothelial cells (ECs) of CD146(EC-KO) mice. Mechanistic studies further confirmed that VEGF-induced VEGFR-2 phosphorylation and AKT/p38 MAPKs/NF-κB activation were inhibited in these CD146-null ECs, which might present the underlying cause for the observed inhibition of tumor angiogenesis in CD146(EC-KO) mice. These results suggest that CD146 plays a redundant role in physiological angiogenic processes, but becomes essential during pathological angiogenesis as observed in tumorigenesis.
Animals ; CD146 Antigen ; genetics ; metabolism ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Female ; Fibrosarcoma ; metabolism ; pathology ; Male ; Melanoma, Experimental ; metabolism ; pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B ; metabolism ; Neovascularization, Physiologic ; drug effects ; Phosphorylation ; drug effects ; Proto-Oncogene Proteins c-akt ; metabolism ; Retinal Vein ; growth & development ; pathology ; Signal Transduction ; drug effects ; Transplantation, Homologous ; Vascular Endothelial Growth Factor A ; pharmacology ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism