Molecular biology reports
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Molecular biology reports · Oct 2012
Meta AnalysisQuantitative assessment of the associations between four polymorphisms (FokI, ApaI, BsmI, TaqI) of vitamin D receptor gene and risk of diabetes mellitus.
The vitamin D receptor (VDR) gene polymorphisms have been suggested to be involved in the development of diabetes mellitus, including type 1 diabetes (T1DM) and type 2 diabetes (T2DM). However, the results have been inconsistent. In this study, we performed a meta-analysis to investigate the associations. ⋯ F: OR 1.36, 95 % CI: 1.21-1.54, P < 0.001). However, no significant association was observed between ApaI or TaqI polymorphism and diabetes risk with the exception of significant association between ApaI polymorphism and T1DM risk in East Asians. Thus, the authors found BsmI polymorphism in the VDR gene may increase the risk of T1DM in East Asians and the FokI polymorphism may increase the risk of T2DM in East Asians.
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Molecular biology reports · Sep 2012
Meta AnalysisCTLA-4 polymorphisms and susceptibility to Behcet's disease: a meta-analysis.
The aim of this study was to explore whether cytotoxic T lymphocyte antigen-4 (CTLA-4) polymorphisms confer susceptibility to Behcet's disease (BD). A meta-analysis was conducted on the associations between the CTLA-4 +49 A/G, -318 C/T, CT60 A/G polymorphisms and BD using; (1) allele contrast, (2) the recessive model, (3) the dominant model, and (4) the additive model. A total of 8 separate comparison studies on BD were considered in the meta-analysis. ⋯ No association was found between BD and the CTLA-4 +49 A/G polymorphisms using recessive or dominant models or contrast of homozygotes. No association was found between BD and the CTLA-4 -318 C/T or CT60 A/G polymorphisms. This meta-analysis showed that no association was found between CTLA-4 +49 A/G, -318 C/T or CT60 A/G polymorphisms and BD.
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Molecular biology reports · Jun 2012
Meta AnalysisAssociation between the COMT Val158Met polymorphism and breast cancer risk: a meta-analysis of 30,199 cases and 38,922 controls.
Many studies have reported the role of COMT Val158Met with breast cancer risk, but the results remained controversial. In addition, previous meta-analysis on COMT Val158Met showed conflicting results. Hence, we performed a meta-analysis to investigate the association between breast cancer and COMT Val158Met (30,199 cases and 38,922 controls) in different inheritance models. ⋯ In the stratified analysis by ethnicity significantly decreased breast cancer risk was observed in Caucasian population (recessive model: OR = 0.96, 95% CI = 0.92-1.00, P(h) = 0.419, I(2) = 3.1%). In conclusion, this meta-analysis indicates that COMT Val158Met polymorphism may be associated with decreased breast cancer risk in Caucasian population. However, a study with the larger sample size is needed to further evaluated gene-environment interaction on COMT Val158Met polymorphisms and breast cancer risk.
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Molecular biology reports · May 2012
The effect of sevoflurane postconditioning on cardioprotection against ischemia-reperfusion injury in rabbits.
Sevoflurane postconditioning is a potential clinical measure to protect myocardial. This experiment was designed to investigate the efficacy of sevoflurane postconditioning against ischemia-reperfusion injury. A total of 132 Japanese White Rabbits were enrolled into this study. ⋯ The infarct sizes were significantly (P < 0.05) reduced after 15 min ischemia (5.5 ± 3.3%, 5.8 ± 3.6% vs. 20.3 ± 6.9% for 2% sev, 4% sev vs. control, respectively) and 30 min ischemia (23.5 ± 5.0%, 20.7 ± 5.9% vs. 50.9 ± 10.2%, for 2% sev, 4% sev vs. control, respectively; P < 0.05). However, it had no effect on infarct size after 60 min ischemia (64.1 ± 5.9%, 62.3 ± 7.6% vs. 72.7 ± 9.2% for 2% sev, 4% sev vs. control, respectively, P > 0.05). The efficacy of sevoflurane postconditioning gradually weakened with increasing ischemia duration and disappears after 60 min ischemia in rabbits in vivo.
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Molecular biology reports · May 2012
Sevoflurane-induced delayed neuroprotection involves mitoK(ATP) channel opening and PKC ε activation.
There is an increasing body of evidence that a brief exposure to anesthesia induces ischemic tolerance in rat brain (anesthetic preconditioning). However, it is unknown whether preconditioning with sevoflurane, a commonly used volatile anesthetic in current clinical practice, produces a delayed window of neuroprotection against ischemia and what the mechanisms are for this protection. To address these issues, adult male Sprague-Dawley rats were subjected to middle cerebral arterial occlusion (MCAO) for 2 h. ⋯ Application of a selective antagonist for mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel, 5-hydroxydecanoate (5-HD, 40 mg/kg i.p.) 30 min before sevoflurane exposure attenuated this beneficial effect. Moreover, protein kinase C ε (PKC ε) was translocated to the membrane fraction at 6 h, but not 24 h, after brain reperfusion in animals preconditioned with sevoflurane and this effect was also abolished by 5-HD. We concluded that sevoflurane preconditioning induces a delayed neuroprotection and that mitochondrial K(ATP) channels and PKC ε may be involved in this neuroprotection.