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Subsequently to the publication of this paper, while performing a careful reexamination of the scientific integrity of the data included in their publications, the authors have realized that they inadvertently used the incorrect western blotting images in Fig. 2B of this article, However, still having access to their original data, the authors were able to reassemble Fig. 2 correctly, and the corrected version of this figure is shown below. Note that this error did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors thank the Editor of Molecular Medicine Reports for granting them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published on Molecular Medicine Reports 14: 17091713, 2016; DOI: 10.3892/mmr.2016.5411].
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BACKGROUND: A systematic review assessing the association between overweight and obesity in young adulthood and stroke risk is lacking. Therefore, we conducted a meta-analysis to evaluate the association between overweight and obesity in young adulthood and stroke risk. METHODS: We systematically searched PubMed and Embase databases for related studies of human subjects in the English language. Two investigators independently selected original studies in a 2-step process. Fixed- and random-effects models were used to calculate pooled relative risks (RRs) and 95% confidence intervals (CIs). Subgroup analyses were also performed. RESULTS: Eight studies met the inclusion criteria. The pooled adjusted RR of stroke was 1.36 (95% CI: 1.28-1.44) for overweight in young adulthood and 1.81 (95% CI: 1.45-2.25) for obesity in young adulthood. In subgroup analyses, overweight and obesity in young adulthood increased the risk of stroke in most groups, except for the group of stroke subtype. For ischemic stroke, the adjusted RR was 1.40 (95% CI: 1.24-1.58) for overweight in young adulthood and 1.78 (95% CI: 1.003-3.16) for obesity in young adulthood, whereas adjusted RR for hemorrhagic stroke was 1.25 (95% CI: .83-1.90) for overweight in young adulthood and 1.80 (95% CI: .97-3.35) for obesity in young adulthood. CONCLUSIONS: Overweight and obesity in young adulthood are associated with an increased risk of stroke, probably, independent of other cardiovascular risk factors. The risk effect gradually increases with increasing body weight.
Asunto(s)
Obesidad Infantil/epidemiología , Accidente Cerebrovascular/epidemiología , Edad de Inicio , Índice de Masa Corporal , Humanos , Oportunidad Relativa , Obesidad Infantil/diagnóstico , Medición de Riesgo , Factores de Riesgo , Accidente Cerebrovascular/diagnóstico , Aumento de PesoRESUMEN
Leptomeningeal fibrosis is important in the pathogenesis of communicating hydrocephalus following subarachnoid hemorrhage; however, the underlying mechanisms of leptomeningeal fibrosis remain largely unclear. In the present study, primary meningeal mesothelial cells (MMCs) were used as a cell model to investigate the effect of transforming growth factorß1 (TGFß1) on leptomeningeal fibrosis. Firstly, primary MMCs were isolated from rat brains and characterized by immunofluorescene, staining positive for keratin and vimentin, but negative for factor VIII. Upon TGFß1 treatment, MMCs were induced to express connective tissue growth factor (CTGF), an indicator of fibrosis, in a dosedependent manner. Furthermore, p38 mitogenactivated protein kinase (MAPK) signaling was significantly activated by TGFß1. However, in the presence of a p38 MAPK inhibitor, TGFß1induced CTGF expression was markedly suppressed. Together, these data suggest that TGFß1 could induce fibrosis of MMCs via the p38 MAPK signaling pathway, providing a novel potential target for intervention in TGFß1induced leptomeningeal fibrosis.