Aim: Human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) have been shown to ameliorate cerebral ischemia in animal models. In this study we investigated the effects of hUCB-MSCs on inflammatory responses and neuronal apoptosis during the early stage of focal cerebral ischemia in rabbits. Methods: Focal cerebral ischemia was induced in male New Zealand rabbits by occlusion of MCA for 2 h. The blood samples were collected at different time points prior and during MCAO-reperfusion. The animals were euthanized 3 d after MCAO, and the protein levels of IL-1β, IL-6, IL-10, and TNF-α in the serum and peri-ischemic brain tissues were detected using Western blot and ELISA, respectively. Inflammatory cell infiltration, neuronal apoptosis and neuronal density were measured morphologically. hUCB-MSCs (5×10 6 ) were iv injected a few minutes after MCAO. Results: The serum levels of IL-1β, IL-6, and TNF-α were rapidly increased, and peaked at 2 h after the start of MCAO. hUCB-MSC transplantation markedly and progressively suppressed the ischemia-induced increases of serum IL-1β, IL-6, and TNF-α levels within 6 h MCAO-reperfusion. Focal cerebral ischemia decreased the serum level of IL-10, which was prevented by hUCB-MSC transplantation. The expression of IL-1β, IL-6, IL-10, and TNF-α in the peri-ischemic brain tissues showed similar changes as in the serum. hUCB-MSC transplantation markedly suppressed the infiltration of inflammatory cells, and increased the neuronal density around the ischemic region. Furthermore, hUCB-MSC transplantation significantly decreased the percentage of apoptosis around the ischemic region. Conclusion: hUCB-MSCs transplantation suppresses inflammatory responses and neuronal apoptosis during the early stage focal cerebral ischemia in rabbits.
It was more reliable to study the associated factors on TMD with the exclusion of the possible confounding factors, and only unilateral chewing preference and psychological stress had a significant association with TMD. In addition, the salivary cortisol levels might assist to assess psychological stress in epidemiological research.
BackgroundAccumulating evidence indicates that stroke risk may be increased following herpes zoster. The aim of this study is to perform a meta-analysis of current literature to systematically analyze and quantitatively estimate the short and long-term effects of herpes zoster on the risk of stroke.MethodsEmbase, PubMed and Cochrane library databases were searched for relevant studies up to March 2016. Studies were selected for analysis based on certain inclusion and exclusion criteria. Relative risks with 95% confidence interval (CI) were extracted to assess the association between herpes zoster and stroke.ResultsA total of 8 articles were included in our analysis. The present meta-analysis showed that the risks of stroke after herpes zoster were 2.36 (95% CI: 2.17–2.56) for first 2 weeks, 1.56 (95% CI: 1.46–1.66) for first month, 1.17 (95% CI: 1.13–1.22) for first year, and 1.09 (95% CI: 1.02–1.16) for more than 1 year, respectively.ConclusionThe results of our study demonstrated that herpes zoster was associated with a higher risk of stroke, but the risks decreased along with the time after herpes zoster.
In order to explore multiple risk factors of hepatocellular carcinoma (HCC), a total of 13 737 male adult residents in 12 townships were studied for an average follow‐up period of 5.2 years. Sociodemographic characteristics, history of cigarette smoking and alcohol drinking, dietary habits, as well as personal and familial history of chronic liver diseases were obtained through standardized interviews based on structured questionnaires at the recruitment. Blood samples were also collected from 9688 (71%) study subjects and examined for the hepatitis B surface antigen (HBsAg). A total of 60 new HCC cases occurred giving an incidence rate of 83.3 per 100 000 person‐years. Cox's proportional hazards models were used to analyse multiple risk factors of HCC. In addition the HBsAg carrier status which showed a multivariate‐adjusted relative risk of 17.0, cumulative cigarette smoking, alcohol drinking quantity, vegetarian habit and low vegetable consumption were associated with the development of HCC. The multivariate‐adjusted relative risk was 1.8 for those who smoked 26 or more pack‐years of cigarettes compared with non‐smokers, 3.1 for those who drank alcohol 50 mL or more per day compared with those who were non‐drinkers or drank less than 50 mL per day, 2.5 for vegetarians compared with non‐vegetarians, as well as 4.6 and 2.6, respectively, for those who had a weekly vegetable consumption frequency of less than two meals and two to five meals compared with those who had a frequency of six or more meals.
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