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To evaluate the hemodynamics of maxillary artery (MA), superficial temporal artery (STA) and ophthalmic artery (OA), and evaluate the hemodynamics prediction capability of these arteries formed compensatory arteries into intracranial using Doppler ultrasonography.The evaluation of MA, STA, and OA with transcranial doppler ultrasonography and with cerebral angiography was made in 106 MMD patients (total of 212 hemispheres of the brain), 58 male and 48 female, aged 39.3±12.0 years old. Doppler ultrasonography measured the following blood flow parameters: peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistance index (RI). DSA evaluate whether MA, STA, OA formed compensatory arteries into intracranial. Based on the compensation situation, the patients were divided into two groups: compensatory group and non-compensatory group. The differences of patient's hemodynamic parameters between compensatory and non-compensatory groups were performed using independent two-sample t-tests with equal or non-equal variance as appropriate. Categorical variables were summarized using frequency and percentage and compared using Chi-square tests. We evaluated the prediction ability of each hemodynamic parameters for each artery (combining left and right side) using Receiver Operating Curve. All the analyses were performed using SAS 9.4 (Cary, NC).Comparing the hemodynamic parameters between the compensatory group and non-compensatory group, all hemodynamic parameters of MA, STA and OA have statistically significant differences between the two groups. Depending on the ROC Curve, EDV (AUC=0.6933±0.0463) for MA, RI (AUC=0.8910±0.0569) for STA, EDV (AUC=0.7863± 0.0330) for OA are better predictors of compensatory growth.Color duplex ultrasonography is a reliable, noninvasive and economic tool to assess hemodynamic changes of MA, STA and OA, and has prediction capability of these arteries formed compensatory arteries into intracranial.

Genome-wide association studies have shown that variants near the melanocortin 4 receptor gene (MC4R) (rs17782313 and rs12970134) are associated with risk of obesity in Europeans. As obesity is associated with an increased risk of type 2 diabetes, many studies have investigated the association between polymorphisms near the MC4R gene and type 2 diabetes risk across different ethnic populations, with inconsistent results. In this study, we performed a meta-analysis to clarify the association of variants near MC4R with type 2 diabetes risk. Published literature from PubMed and Embase was retrieved. All studies that evaluated the association of at least one of the two MC4R polymorphism(s) with type 2 diabetes were included in the study. Pooled ORs with 95% CIs were calculated using the fixed-effects model. A total of 19 studies (comprising 34,195 cases and 89,178 controls) of the rs17782313 polymorphism (or its proxy rs12970134) were included in the meta-analysis. The results indicated that the rs17782313 polymorphism was significantly associated with type 2 diabetes risk among the overall study population (OR 1.10, 95% CI 1.07, 1.13, p = 2.83 × 10−12 [Z test], I 2 = 9.1%, p = 0.345 [heterogeneity]). The association remained significant even after adjustment for body mass index (BMI) (OR 1.06, 95% CI 1.03, 1.09, p = 2.14 × 10–5 [Z test], I 2 = 4.9%, p = 0.397 [heterogeneity]). Further sensitivity analysis confirmed the statistically significant association of rs17782313 polymorphism with type 2 diabetes, and no publication bias was detected. The present meta-analysis confirmed the significant association of the rs17782313 polymorphism near the MC4R gene with type 2 diabetes risk, which was independent of BMI.

Mesenchymal stem cells (MSC) have recently been shown to possess immunomodulatory properties in vitro and in vivo. The present study aimed to investigate the regulatory effect of MSC transplantation on the immuno-inflammatory response in myocardial infarction (MI). Methods MI was induced in SpragueDawley rats by left anterior descending coronary artery ligation, and the animals were randomly assigned into the following three groups: sham ( n8); phosphate-buffered saline (PBS) injected (MIPBS, n8); and MSC transplantation (MI MSC, n8). BrdU-labeled MSC or PBS was transplanted into periinfarct myocardium by direct myocardial injection. At 1 and 28 days post-transplantation, cardiac function was evaluated by echocardiography. Transplanted cells were investigated through immunohistochemistry. Lymphocyte cytotoxic activity was evaluated with the crystal violet method. The activity of NF-kB and protein expression of tumor necrosis factor-a (TNF-a), interleukin (IL)-6 and IL-10 in myocardium were assessed by immunohistochemistry and Western blot. Results Echocardiographic examination revealed that the MSC transplantation prevented left ventricular dilation and dysfunction at 28 days after the operation. BrdU-stained cells were found living in host heart 4 weeks after transplantation. MSC transplantation attenuated the cytotoxic activity of spleen lymphocytes. Transplantation of MSC inhibited the activity of NF-kB, attenuated the protein production of TNF-a and IL-6, and increased the expression of IL-10 in periinfarct myocardium. Discussion MSC transplantation modulated the immuno-inflammatory response in MI. The immuno-inflammatory regulatory effect of MSC transplantation might partly account for the cardiac protection in myocardial infarction.

Stathmin, a major microtubule-depolymerizing protein, is involved in cell cycle progression and cell motility. This study aimed to elucidate its role in the progression, early tumour recurrence (ETR), and prognosis of hepatocellular carcinoma (HCC). Stathmin mRNA was overexpressed in 88/156 (56%) resected, unifocal, primary HCCs, while p53 mutation was present in 72 (46%) and osteopontin mRNA overexpression in 79 (51%). Stathmin mRNA expression exhibited high concordance (93%) with protein expression in 107 cases examined by immunohistochemistry. Stathmin overexpression correlated with high alpha-fetoprotein (200 ng/ml, p = 0.02), larger tumour size (5 cm, p = 0.012), high tumour grade (p0.0002), high tumour stage (stage IIIA-IV) with vascular invasion and various degrees of intrahepatic metastasis (p1 x 10(-8)), ETR (p = 0.003), and lower 5-year survival (p = 0.0007). Stathmin protein expression was often more intense in the peripheral regions of tumour trabeculae, tumour borders, and portal vein tumour thrombi. Stathmin overexpression correlated with p53 mutation (p = 0.017) and osteopontin overexpression (p = 1 x 10(-8)), both of which were associated with vascular invasion (both p0.0001) and poorer prognosis (p0.0004 and p = 0.0004, respectively). Regardless of the status of p53 mutation or osteopontin expression, stathmin overexpression was associated with higher vascular invasion (all p0.0001). Approximately 90% of HCCs harbouring stathmin overexpression with concomitant p53 mutation or osteopontin overexpression exhibited vascular invasion, and hence the lowest 5-year survival, p = 0.00018 and p = 0.0009, respectively. However, we did not find that stathmin overexpression exerted prognostic impact independent of tumour stage. In conclusion, stathmin expression correlates with metastatic potential, is an important prognostic factor for HCC, and may serve as a useful marker to predict ETR.