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Many individual studies on oat β-glucan (OBG) confirmed its functionality in improving type 2 diabetes mellitus (T2DM), but disagreements were identified among those results. To derive a pooled estimate of these results, relevant articles, published before 5 September 2015, were collected from four electronic databases (Pubmed, Cochrane Library, Scopus, and Web of Science) and subjected to meta-analysis in the present work. In total, four articles, dealing with 350 T2DM patients combined, met the inclusion criteria. Compared to control, T2DM patients administrated OBG from 2.5 to 3.5 g/day for 3 to 8 weeks presented significantly lowered concentrations in fasting plasma glucose (FPG) by −0.52 (95% CI: −0.94, −0.10) mmol/L (p = 0.01) and glycosylated hemoglobin (HbA1c) by −0.21% (95% CI: −0.40, −0.02) (p = 0.03). However, OBG intake did not significantly lower the fasting plasma insulin (FPI) concentration. In conclusion, mediate-term OBG intake (3–8 weeks) favored the glycaemic control of T2DM patients but did not improve their insulin sensitivity. Regrettably, data upon the effects of long-term OBG intake on glycaemic control and insulin sensitivity were scarce, which is of much importance and should be addressed in future research.

Apoptosis of neurons in the maturing neocortex has been recorded in a wide variety of mammals, but very little is known about its effects on cortical differentiation. Recent research has implicated the RhoA GTPase subfamily in the control of apoptosis in the developing nervous system and in other tissue types. Rho GTPases are important components of the signaling pathways linking extracellular signals to the cytoskeleton. To investigate the role of the RhoA GTPase subfamily in neocortical apoptosis and differentiation, we have engineered a mouse line in which a dominant-negative RhoA mutant (N19 -RhoA) is expressed from the Mapt locus, such that all neurons of the developing nervous system are expressing the N19 -RhoA inhibitor. Postnatal expression of N19 -RhoA led to no major changes in neocortical anatomy. Six layers of the neocortex developed and barrels (whisker-related neural modules) formed in layer IV. However, the density and absolute number of neurons in the somatosensory cortex increased by 12-26% compared with wild-type littermates. This was not explained by a change in the migration of neurons during the formation of cortical layers but rather by a large decrease in the amount of neuronal apoptosis at postnatal day 5, the developmental maximum of cortical apoptosis. In addition, overexpression of RhoA in cortical neurons was seen to cause high levels of apoptosis. These results demonstrate that RhoA-subfamily members play a major role in developmental apoptosis in postnatal neocortex of the mouse but that decreased apoptosis does not alter cortical cytoarchitecture and patterning.

Ochratoxin A (OTA) is a toxic secondary fungal metabolite that widely takes place in various kinds of foodstuffs and feeds. Human beings and animals are inevitably threatened by OTA as a result. Therefore, it is necessary to adopt various measures to detoxify OTA-contaminated foods and feeds. Biological detoxification methods, with better safety, flavor, nutritional quality, organoleptic properties, availability, and cost-effectiveness, are more promising than physical and chemical detoxification methods. The state-of-the-art research advances of OTA biodetoxification by degradation, adsorption, or enzymes are reviewed in the present paper. Researchers have discovered a good deal of microorganisms that could degrade and/or adsorb OTA, including actinobacteria, bacteria, filamentous fungi, and yeast. The degradation of OTA to non-toxic or less toxic OTα via the hydrolysis of the amide bond is the most important OTA biodegradation mechanism. The most important influence factor of OTA adsorption capacity of microorganisms is cell wall components. A large number of microorganisms with good OTA degradation and/or adsorption ability, as well as some OTA degradation enzymes isolated or cloned from microorganisms and animal pancreas, have great application prospects in food and feed industries.

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Oxidative stress and apoptosis are involved in Ochratoxin A (OTA)-induced renal cytotoxicity. Apoptosis signal-regulating kinase 1 (ASK1) is a Mitogen-Activated Protein Kinase Kinase Kinase (MAPKKK, MAP3K) family member that plays an important role in oxidative stress-induced cell apoptosis. In this study, we performed RNA interference of ASK1 in HEK293 cells and employed an iTRAQ-based quantitative proteomics approach to globally investigate the regulatory mechanism of ASK1 in OTA-induced renal cytotoxicity. Our results showed that ASK1 knockdown alleviated OTA-induced ROS generation and Δψm loss and thus desensitized the cells to OTA-induced apoptosis. We identified 33 and 24 differentially expressed proteins upon OTA treatment in scrambled and ASK1 knockdown cells, respectively. Pathway classification and analysis revealed that ASK1 participated in OTA-induced inhibition of mRNA splicing, nucleotide metabolism, the cell cycle, DNA repair, and the activation of lipid metabolism. We concluded that ASK1 plays an essential role in promoting OTA-induced renal cytotoxicity.