Upregulation of Mitochondrial Uncoupling Protein-2 by the AMP-Activated Protein Kinase in Endothelial Cells Attenuates Oxidative Stress in Diabetes

OBJECTIVE—Recent evidence suggests that the AMP-activated protein kinase (AMPK) is an important therapeutic target for diabetes. The present study was conducted to determine how AMPK activation suppressed tyrosine nitration of prostacyclin synthase in diabetes

PRKAA1/AMPKα1 is required for autophagy-dependent mitochondrial clearance during erythrocyte maturation

AMP-activated protein kinase α1 knockout (prkaa1−/−) mice manifest splenomegaly and anemia. The underlying molecular mechanisms, however, remain to be established. In this study, we tested the hypothesis that defective autophagy-dependent mitochondrial clearance in prkaa1−/− mice exacerbates oxidative stress, thereby enhancing erythrocyte destruction. The levels of ULK1 phosphorylation, autophagical flux, mitochondrial contents, and reactive oxygen species (ROS) were examined in human erythroleukemia cell line, K562 cells, as well as prkaa1−/− mouse embryonic fibroblasts and erythrocytes. Deletion of Prkaa1 resulted in the inhibition of ULK1 phosphorylation at Ser555, prevented the formation of ULK1 and BECN1- PtdIns3K complexes, and reduced autophagy capacity. The suppression of autophagy was associated with enhanced damaged mitochondrial accumulation and ROS production. Compared with wild-type (WT) mice, prkaa1−/− mice exhibited a shortened erythrocyte life span, hemolytic destruction of erythrocytes, splenomegaly, and anemia, all of which were alleviated by the administration of either rapamycin to activate autophagy or Mito-tempol, a mitochondria-targeted antioxidant, to scavenge mitochondrial ROS. Furthermore, transplantation of WT bone marrow into prkaa1−/− mice restored mitochondrial removal, reduced intracellular ROS levels, and normalized hematologic parameters and spleen size. Conversely, transplantation of prkaa1 −/− bone marrow into WT mice recapitulated the prkaa1−/− mouse phenotypes. We conclude that PRKAA1-dependent autophagy-mediated clearance of damaged mitochondria is required for erythrocyte maturation and homeostasis

Design and Application of Highly Efficient Flame Retardants for Polycarbonate Combining the Advantages of Cyclotriphosphazene and Silicone Oil

A novel flame retardant (HSPCTP) was successfully designed and incorporated into a polycarbonate (PC) matrix. Combining the advantages of cyclotriphosphazene and silicone oil, PC/HSPCTP composites passed UL-94 V-0 rating testing with only 3 wt% HSPCTP, and their LOI value increased from 25.0% to 28.4%. The findings showed that HSPCTP exhibits both gas-phase and solid-phase flame-retardant effects. Furthermore, the incorporation of HSPCTP into PC could suppress the release of smoke. Finally, the flame-retardant mechanism is discussed in depth

Tyrosine nitration of prostacyclin synthase is associated with enhanced retinal cell apoptosis in diabetes

The risk of diabetic retinopathy is associated with the presence of both oxidative stress and toxic eicosanoids. Whether oxidative stress actually causes diabetic retinopathy via the generation of toxic eicosanoids, however, remains unknown. The aim of the present study was to determine whether tyrosine nitration of prostacyclin synthase (PGIS) contributes to retinal cell death in vitro and in vivo. Exposure of human retinal pericytes to heavily oxidized and glycated LDL (HOG-LDL), but not native forms of LDL (N-LDL), for 24 hours significantly increased pericyte apoptosis, accompanied by increased tyrosine nitration of PGIS and decreased PGIS activity. Inhibition of the thromboxane receptor or cyclooxygenase-2 dramatically attenuated HOG-LDL–induced apoptosis without restoring PGIS activity. Administration of superoxide dismutase (to scavenge superoxide anions) or l-N(G)-nitroarginine methyl ester (l-NAME, a nonselective nitric oxide synthase inhibitor) restored PGIS activity and attenuated pericyte apoptosis. In Akita mouse retinas, diabetes increased intraretinal levels of oxidized LDL and glycated LDL, induced PGIS nitration, enhanced apoptotic cell death, and impaired blood–retinal barrier function. Chronic administration of tempol, a superoxide scavenger, reduced intraretinal oxidized LDL and glycated LDL levels, PGIS nitration, and retina cell apoptosis, thereby preserving the integrity of blood–retinal barriers. In conclusion, oxidized LDL-mediated PGIS nitration and associated thromboxane receptor stimulation might be important in the initiation and progression of diabetic retinopathy

Promoting the efficiency of quantum dots-based solar cells via the Cu:ZnSeS intermediate passivation layer

Constructing the interface passivation layer is of importance to accelerate the charge transfer and thus enhance the efficiency of quantum dots-sensitized solar cells (QDSCs). Here, an effective Cu:ZnSeS intermediate passivation layer (IPL), aiming at improving the charge transfer process, is fabricated on the surface of photoanodes via the facile successive ionic layer adsorption and reaction (SILAR) process. Electrical chemical analysis results exhibit that the Cu:ZnSeS IPL can efficiently hinder the charge recombination and accelerate the charge transport process due to the synergistic effect of ZnSeS alloy layer and Cu ions dopant. Meanwhile, the time-resolved photoluminescence (TRPL) spectroscopy demonstrates the Cu:ZnSeS IPL can not only reduce the surface traps but also accelerate hole capture. Importantly, the laser confocal Kelvin probe force microscopy (KPFM) measurement is first used to investigate the charge transport process via the change of surface potential in dark and under laser irradiation. In terms of the merits of Cu:ZnSeS IPL, the power conversion efficiency (PCE) of the resultant CdSeTe-based QDSCs reaches up to 9.46%, with an enhancement of 14%, compared to the traditional single ZnS passivation layer (∼8.32%). Besides, employing the Cu:ZnSeS intermediate passivation layer, the PCE of 11.64% was achieved, which is considered the highest reported in the reported CdSeTe QDSCs so far. This work demonstrates a facile and effective approach to modulating the charge transport process, thus enhancing the device performance