ObjectivesObesity is suggested to be a risk factor for knee osteoarthritis (OA). This meta-analysis aimed to examine the relationship between body mass index (BMI) and the risk of knee OA in published prospective studies.DesignMeta-analysis.Studies reviewedAn extensive literature review was performed, and relevant studies published in English were retrieved from the computerised databases MEDLINE, EMBASE and Cochrane.MethodsThe effect estimate (RR or HR) and its 95% CI are investigated on the basis of the evaluation of differences of knee OR risk in overweight or obesity versus those with normal weight. Category-specific risk estimates were further transformed into estimates of the RR in terms of per increase of 5 in BMI by using the generalised least-squares method for trend estimation. Studies were independently reviewed by two investigators. Subgroup analysis was performed. Heterogeneity and publication bias were assessed. Data from eligible studies were extracted, and the meta-analysis was performed by using the STATA software V.12.0.Results14 studies were finally included in the analysis. The results showed that overweight and obesity were significantly associated with higher knee OA risks of 2.45 (95% CI 1.88 to 3.20, p<0.001) and 4.55 (95% CI 2.90 to 7.13, p<0.001), respectively. The risk of knee OA increases by 35% (95% CI 1.18 to 1.53, p<0.001) with a 5 kg/m2 increase in BMI. Subgroup analysis showed that obesity was an independent predictor of knee OA risk regardless of the study country, sample size, gender proportion of participants, duration of follow-up, presence of adjusted knee injury and assessed study quality above or below an NOS score of 8. No publication bias was detected.ConclusionsObesity was a robust risk factor for knee OA. Professionals should take a possible weight reduction into account for the treatment of knee OA whenever a patient is significantly overweight.
Our aim was to clarify whether substitution of cytosine for adenine at position 1166 (A1166C) polymorphism of the angiotensin II type 1 receptor (AT1R) gene is associated with susceptibility to essential hypertension in Han, Tibetan and Yi populations in China. This study involved 302 normotensive and 446 hypertensive subjects. The polymorphism was detected by polymelase chain reaction of genomic DNA and restriction fragment length polymorphism (PCR-RFLP) in genomic DNA. The data were analyzed by analysis of covariance (ANCOVA), X2 test, and multiple logistic regression. In normotensive controls, the A1166 allele frequencies were 0.979, 0.939 and 0.965 in Han, Tibetan and Yi participants, respectively. There was no significant intergroup variation in frequency of the allele in normotensives (X2=4.166, p=0.125). The frequency of the A1166 allele was significantly higher in Tibetan male hypertensives than that in normotensives (X2=11.46, p=0.001). There was no significant difference in A1166C genotype distribution and allele frequency between normotensives and hypertensives either in the Han (p=0.465) or Yi (p=0.357) populations. Body mass index in the Han and Yi populations (p=0.0001), age in the Tibetan and Yi populations (p=0.0001), and AA genotype in the Tibetan male population (p=0.0034) all were independent risk factors for hypertension. Diastolic blood pressure levels were significantly higher in Tibetan male subjects with the AA genotype than in those with the AC+CC genotype (p=0.0040). We concluded that the A1166 allele is very common in Han, Tibetan and Yi populations, approximately 1.35-fold more common than in Caucasians. The A1166 allele of the AT1R gene may be a predisposing factor for essential hypertension in Tibetan males. A1166C polymorphism of the AT1R gene is probably not involved in the pathogenesis of essential hypertension in Han or Yi populations.
Hypotonic challenge evoked vascular cell proliferation through activation of volume-regulated ·H 2 0), which caused significantly increase in WNK1 phosphorylation without altering WNK1 protein expression. WNK1 overexpression significantly increased hypotonic-induced A10 cell proliferation, whereas silencing of WNK1 caused an opposite action. WNK1 mutation did not affect hypotonic-induced WNK1 phosphorylation and cell proliferation. Silencing of WNK1 caused cell cycle arrest at G 0 /G 1 phase and prevented transition from G 1 to S phase, whereas the WNK1 overexpression accelerated cell cycle transition from G 1 to S phase. Silencing of WNK1 significantly inhibited cyclin D1/cyclin E1 expression and increased p27KIP/p21CIP expression. WNK1 overexpression significantly increased cyclin D1/cyclin E1 expression and reduced p27 KIP /p21 CIP expression. In addition, WNK1 knockdown or overexpression significantly attenuated or increased the hypotonic-induced phosphorylation of Akt and PI3K respectively. In conclusion, the reduction in [Cl -] i caused by hypotonic challenge-induced VRCC opening evokes WNK1 phosphorylation in A10 VSMCs, which mediates cell cycle transition from G 0 /G 1 to S phase and proliferation through the PI3K-Akt signaling pathway.
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