Hyperbaric oxygen preconditioning improves postoperative cognitive dysfunction by reducing oxidant stress and inflammation

Postoperative cognitive dysfunction is a crucial public health issue that has been increasingly studied in efforts to reduce symptoms or prevent its occurrence. However, effective advances remain lacking. Hyperbaric oxygen preconditioning has proved to protect vital organs, such as the heart, liver, and brain. Recently, it has been introduced and widely studied in the prevention of postoperative cognitive dysfunction, with promising results. However, the neuroprotective mechanisms underlying this phenomenon remain controversial. This review summarizes and highlights the definition and application of hyperbaric oxygen preconditioning, the perniciousness and pathogenetic mechanism underlying postoperative cognitive dysfunction, and the effects that hyperbaric oxygen preconditioning has on postoperative cognitive dysfunction. Finally, we conclude that hyperbaric oxygen preconditioning is an effective and feasible method to prevent, alleviate, and improve postoperative cognitive dysfunction, and that its mechanism of action is very complex, involving the stimulation of endogenous antioxidant and anti-inflammation defense systems.

Deformation effect of lateral roof roadway in close coal seams after repeated mining

This paper analyzed the deformation mechanism in lateral roof roadway of the Ding Wu-3 roadway which was disturbed by repeated mining of close coal seams Wu-8 and Wu-10 in Pingdingshan No. 1 Mine. To determine the strata disturbance scope, the strata displacement angle was used to calculate the protection pillar width. A numerical model was built considering the field geological conditions. In simulation, the mining stress borderline was defined as the contour where the induced stress is 1.5 times of the original stress. Simulation results show the mining stress borderline of the lateral roadway extended 91.7 m outward after repeated mining. Then the original stress increased, deforming the road- way of interest. This deformation agreed with the in situ observations. Moreover, the strata displacement angle changed due to repeated mining. Therefore, reselection of the displacement angle was required to design the protective pillar width. Since a constant strata displacement angle was used in traditional design, the orooosed method was beneficial in field cases.

Effect of Tetrahydroberberine on improving vascular endothelial cell injury

Objective:To investigate the effects and mechanisms of tetrahydroberberine(THB)on vascular endothelial cell injury induced by oxygen glucose deprivation(OGD)and LPS-induced cell injury model.Methods:MTT assay was used to detect the effects of THB final concentration on the survival rate of EA.hy926 cells,which were 0μg/mL,2.5μg/mL,5μg/mL,10μg/mL,20μg/mL and 40μg/mL,respectively.Group I of the experiment:normal control group,OGD group,OGD+THB-10μg/mL group,OGD+THB-20μg/mL group,OGD+THB-40μg/mL group;Experimental group II group:normal Control group,LPS group,OGD+LPS group and OGD+LPS+THB-20μg/mL group.The relative expression of inflammation-related factors such as Caspase-1,ASC,IL-1βand IL-6 was detected by fluorescence quantitative PCR,and the expression of IL-1βand HO-1 was detected by Western Blot analysis.Results:The results of MTT assay showed that THB had no effect on the survival of EA.hy926 cells.The qPCR results of the experimental group I and II showed that the OGD model could play an anti-inflammatory protective role by down-regulating the expression of Caspase-1,ASC,IL-1βand IL-6 genes.The anti-inflammatory effect of THB on the OGD model was general,but it was found that THB also exerted an anti-inflammatory effect by down-regulating the expression of inflammatory genes by OGD+LPS group compared with OGD+LPS+THB-20μg/mL group.Western Blot analysis showed that the expression of IL-1βprotein was consistent with the results of qPCR.The expression of HO-1 protein as a protective factor was contrary to that of inflammatory factor fluorescence quantitative analysis.Conclusion:OGD model can improve the protective effect of cell stress.THB plays an anti-inflammatory role by down-regulating the expression of Caspase-1,ASC,IL-1βand IL-6 genes,up-regulating the expression of HO-1 protein and inhibiting the activation of NLRP3 inflammatory bodies.

Overproduction of Alkaloid Phytoalexins in California Poppy Cells Is Associated with the Co-Expression of Biosynthetic and Stress-Protective Enzymes

Many plant cells respond to pathogens by the induction of phytoalexin biosynthesis, but the underlying changes of gene expression are often obscured by their close linkage to the complex rearrangements during pathogen defense, especially the hypersensitive cell death. In root-derived cell cultures of Eschscholzia californica, the overproduction of cytotoxic benzophenanthridine alkaloids can be triggered by a minimum of pathogen pressure that does not evoke hypersensitive reactions. Such conditions activate a signal chain that is initiated by a short contact to low concentrations of yeast glycoprotein elicitor and includes a transient acidification of the cytoplasm. In contrast, high elicitor concentrations signal via an increase of jasmonate and trigger hypersensitive cell death, preceded by a drastic decay of translatable mRNAs. The main changes in protein and mRNA patterns caused by either signal path were compared by 2D proteomic separation, MS/MS sequencing and mRNA-in vitro translation. The four proteins showing the highest overexpression were identical between cells that received low or high-elicitor treatment and overlapped with the three proteins most upregulated by artificial pH shifts. They comprised one biosynthetic enzyme （norcoclaurine：SAM 4＇ O-methyl-transferase） plus a unique combination of stress-protective proteins： a heat shock protein （hsp 70）; a peptidyl-prolyl-cis/trans isomerase （cyclophilin）; and a glyceraldehyde-3-phosphate dehydrogenase. It appears that overproduction of the benzophenanthri- dine phytoalexins requires the up-regulation of a rate-limiting biosynthetic enzyme plus the coordinated expression of a specific set of protective enzymes and thus is managed like an oxidative stress.