No effect of energy intake overall on risk of endometrial cancers: a meta-analysis.

BACKGROUND: Previous epidemiologic studies on the association between energy intake and endometrial cancer risk have only generated contradictory results. The role of energy intake in endometrial carcinogenesis thus remains unclear. To quantitatively assess the potential association between energy intake and endometrial cancer, a meta-analysis of case-control and cohort studies was here conducted. MATERIALS AND METHODS: Eligible studies were retrieved via both computerized searches and review of references. Fixed-or random-effect models were used to summarize the estimates of OR with 95%CIs. Stratified analyses on study design, region and macronutrients' calorie were performed. RESULTS: Sixteen studies met the inclusion criteria of the meta-analysis. No association between total energy intake and endometrial cancer was observed in either overall group (OR=1.11, 95%CI 0.92-1.30) or subgroups stratified by study design and region. In the specific macronutrients' calorie analysis, higher fat energy intake was found to be associated with increased endometrial risk (OR=1.72, 95%CI 1.12- 2.32) while energy from carbohydrate and protein was not related to endometrial cancer risk. CONCLUSIONS: Our analysis did not support that total energy intake is related to endometrial cancer risk, in contrast to fat energy.

A systematic review and meta-analysis of buyang huanwu decoction in animal model of focal cerebral ischemia.

Buyang Huanwu Decoction (BHD) is a well-known Chinese herbal prescription for ischemic stroke. The objective of this systematic review and meta-analysis is to provide the current evidence for neuroprotective effects of BHD and its possible mechanisms in animal models of focal ischemia. A systematic literature search, through October 2012, was performed using six databases. The outcome measures assessed were infarct size and/or neurological score. Fifty-six studies with 1270 animals that met the inclusion criteria were identified. The median score for methodological quality was 3 with a range of 2 to 6. Compared with vehicle or no treatment controls, BHD gave a 37% improvement in outcome for all doses ranging from 1.0 g/kg to 60 g/kg at each time point that BHD was administered (P < 0.01). Efficacy was higher in mouse models that utilized suture occlusion and temporary ischemia. The neuroprotective effects of BHD are involved in multiple mechanisms and act upon multiple cell types. In conclusion, BHD possesses substantial neuroprotective effects in experimental stroke probably as a result of the multitarget therapy strategy typically utilized in traditional Chinese medicine. Future research should examine the presence of possible experimental bias and an in-depth study of herbal compound preparations.

Severe global cerebral ischemia-induced programmed necrosis of hippocampal CA1 neurons in rat is prevented by 3-methyladenine: a widely used inhibitor of autophagy.

The true programmed mechanisms of delayed neuronal death induced by global cerebral ischemia/reperfusion injury remain incompletely characterized. Autophagic cell death and programmed necrosis are 2 kinds of programmed cell death distinct from apoptosis. Here, we studied the death mechanisms of hippocampal cornu ammonis 1 neuronal death after a 20-minute severe global ischemia/reperfusion injury in young adult rats and the effects of 3-methyladenine (3-MA), a widely used inhibitor of autophagy. The morphological changes detected by electron microscopy, together with the activation of autophagy, transferase-mediated UTP nick end-labeling-positive neurons, and delayed death, demonstrated that cornu ammonis 1 neuronal death induced in this paradigm was programmed necrosis. No significant activation of caspase-3 after injury was detected by Western blot and immunohistochemistry. Treatment with 3-MA provided time-dependent protection against cornu ammonis 1 neuronal death at 7 days of reperfusion when it was administered before ischemia; administration 60 minutes after reperfusion was not beneficial. The redistribution of the lysosomal enzyme cathepsin B after injury was inhibited by 3-MA administered before ischemia, suggesting that this might be another important mechanism for the protective effect of 3-MA in ischemic neuronal injury.