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Endoplasmic reticulum stress(ERS) can induce inflammation mediated by NLRP3 inflammatory bodies and link inflammation with oxidative stress in myocardial tissue. Ghrelin is an endogenous growth hormone-releasing peptide that has been proven to have multiple effects, such as regulating energy metabolism and inhibiting inflammation. However, the role of ghrelin in myocardial injury in diabetic rats and the mechanism have not been reported. We found that ghrelin could improve endoplasmic reticulum stress and inflammatory pyroptosis in the myocardial tissue of diabetic rats and reduce ERS and NLRP3 inflammasome crosstalk in H9C2 cardiomyocytes. Interestingly, ghrelin could activate the PI3K/AKT signalling pathway, playing a role in inhibiting endoplasmic reticulum stress and reducing the expression of pyroptosis-related proteins. However, these protective effects could be largely eliminated by LY294002. In summary, we demonstrated that ghrelin inhibited myocardial pyroptosis in diabetic cardiomyopathy by regulating ERS and NLRP3 inflammasome crosstalk through the PI3K/AKT pathway. Our results provide new insights into the mechanism of diabetic myocardial injury induced by high glucose and high palmitic acid and ghrelin-mediated anti-inflammatory protection and provide potential therapeutic targets and strategies for diabetic cardiomyopathy. Ghrelin improves lipid metabolism but not glucose metabolism in rats with diabetic cardiomyopathy. Ghrelin improves cardiac dysfunction and structure disorder in diabetic cardiomyopathy. Ghrelin inhibits cardiomyocyte pyroptosis in diabetic cardiomyopathy by regulating myocardial endoplasmic reticulum stress and NLRP3 inflammasome activation. The protective effect mediated by ghrelin may be related to the activation of PI3K/AKT signal pathway. [ABSTRACT FROM AUTHOR]

The surface properties of fused silica (FS) change after H2O2 treatment, but the surface and subsurface damage behaviors and their mechanisms under various physical contact conditions have not been elucidated yet. This work investigated the effect of H2O2 treatment on mechanical and mechanochemical properties of FS surface. The results show that the hydrophilicity and adsorbed water film thickness of the FS surface increase with the concentration of H2O2 solution. The surface damage, nanowear, and subsurface deformation of FS caused by indentation increase with the concentration of H2O2 solution, while the nanohardness and reduced modulus decrease. Further analysis revealed that the water activity on the FS surface plays a critical role in reducing the mechanical and mechanochemical properties. In addition, the treatment with H2O2 solution on the FS surface shows a weakly corrosive effect, which implies the H2O2 treatment can be an alternative method to remove the surface defects on FS optics. [ABSTRACT FROM AUTHOR]

With increasing graphene oxide (GO) applications in industry and biomedicine, effects of GO on microorganisms, animals, and human health have been frequently studied; however, direct and indirect effects of GO on plants are seldom concerned. In this study, effects of GO and/or Cd2+ on seed germination, seedling growth, and uptake to Cd2+ were investigated in solution culture. The results showed that GO could quickly adsorb Cd2+ in solution, and the higher the GO concentration was, the lower the residual Cd2+ concentration was in solution. Rice seed germination, seminal root length, and bud length decreased with increasing GO and Cd2+ concentrations respectively, while the presence of GO could alleviate the inhibitive effects of Cd2+ on seminal root and bud growth compared with the single Cd2+ treatment. In maize seedling, fresh weights of shoot and root showed similar responses to the presence of Cd2+ and/or GO. Compared with the single Cd2+ treatment, root Cd concentrations were generally increased by GO in high Cd2+ solution (20 mg/L), while were slightly affected by GO in low Cd2+ solution (5 mg/L) independent of GO concentrations except for 100 mg/L GO. Shoot Cd concentrations were decreased by low GO (100 mg/L) while were increased by high GO (> 500 mg/L) independent of Cd2+ concentrations in solution. Moreover, significant interactive effects of GO and Cd2+ on root and shoot Cd concentrations were observed. This study indicates that GO can change the effects of Cd2+ on seed germination, seedling growth, and uptake to Cd2+ in solution through its adsorption on Cd2+. [ABSTRACT FROM AUTHOR]

Metastasis remains the primary cause of prostate cancer (CaP)-related death. Using a genome wide shRNA screen, we identified GABARAPL1 as a potential CaP metastasis suppressor. GABARAPL1 mRNA levels inversely correlate with the invasive potential of a panel of human CaP cell lines. Lower mRNA levels correlate with higher Gleason scores in clinical CaP tumor samples. Moreover, Kaplan-Meier curves analysis showed that GABARAPL1 down-regulation in cancer tissues is associated with decreased disease-free survival in CaP patients. Knockdown of GABARAPL1 in human LNCaP cells results in increased invasion in vitro and lymph node metastasis in vivo. Vice versa, ectopic expression of GABARAPL1 decreases the invasiveness of CWR22Rv1 cells. Our previous in vitro shRNA screening identified FOXO4, a PI3K/Akt-inactivating downstream target, as a potential CaP metastasis suppressor. We show here that silencing FOXOs leads to reduced GABARAPL1 expression and enhanced invasion in LNCaP cells. Transfection of constitutively-activated Akt (myr-Akt) increased the invasion of LNCaP cells, which is associated with the inactivation of FOXOs and decreased GABARAPL1 expression. Indeed, forced expression of GABARAPL1 reversed the increased invasiveness of LNCaP/myr-Akt cells. Finally, immunohistochemistry analysis shows that Akt phosphorylation is negatively correlated with GABARAPL1 expression in human CaP tissues. Taken together, our data indicate that the suppression of FOXOs-GABARAPL1 signaling by Akt is an important mechanism for CaP progression and metastasis.