A crack-free AlN film with 4.5 μm thickness was grown on a 2-inch hole-type nano-patterned sapphire substrates(NPSSs) by hydride vapor phase epitaxy(HVPE). The coalescence, stress evolution, and dislocation annihilat...A crack-free AlN film with 4.5 μm thickness was grown on a 2-inch hole-type nano-patterned sapphire substrates(NPSSs) by hydride vapor phase epitaxy(HVPE). The coalescence, stress evolution, and dislocation annihilation mechanisms in the AlN layer have been investigated. The large voids located on the pattern region were caused by the undesirable parasitic crystallites grown on the sidewalls of the nano-pattern in the early growth stage. The coalescence of the c-plane AlN was hindered by these three-fold crystallites and the special triangle void appeared. The cross-sectional Raman line scan was used to characterize the change of stress with film thickness, which corresponds to the characteristics of different growth stages of AlN. Threading dislocations(TDs) mainly originate from the boundary between misaligned crystallites and the c-plane AlN and the coalescence of two adjacent c-plane AlN crystals, rather than the interface between sapphire and AlN.展开更多
AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal...AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal,and assessed by histological,serum transaminases,and mortality analyses. Hepatocellular apoptosis was quantified by transferase d UTP nick end labeling assay and Westernblot analysis of cleaved caspase-3. Liver inflammatory chemokine and cytochrome P450 expression was analyzed by quantitative reverse transcription-PCR. Neutrophil infiltration was evaluated by myeloperoxidase activity. Expression and phosphorylation of ERK,JNK,p65,and H2 A.X was determined by Western blot. Oxidative stress was evaluated by measuring malondialdehyde production and nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity.RESULTS: following LPS/D-Gal exposure,Recql5-deficient mice exhibited enhanced liver injury,as evidenced by more severe hepatic hemorrhage,higher serum aspartate transaminase and alanine transaminase levels,and lower survival rate. As compared to WT mice,Recql5-deficient mice showed an increased number of apoptotic hepatocytes and higher cleaved caspase-3 levels. Recql5-deficient mice exhibited increased DNA damage,as evidenced by increased γ-H2 A.X levels. Inflammatory cytokine levels,neutrophil infiltration,and ERK phosphorylation were also significantly increased in the knockout mice. Additionally,Recql5-deficicent mice exhibited increased malondialdehyde production and elevated inducible nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity,indicative of enhanced oxidative stress. Moreover,CYP450 expression was significantly downregulated in Recql5-deficient mice after LPS/D-Gal treatment.CONCLUSION: Recql5 protects the liver against LPS/D-Gal-induced injury through suppression of hepatocyte apoptosis and oxidative stress and modulation of CYP450 expression.展开更多
基金supported by the National Natural Science Foundation of China (Grant No. 61974158)the Natural Science Fund of Jiangsu Province, China (Grant No. BK20191456)。
文摘A crack-free AlN film with 4.5 μm thickness was grown on a 2-inch hole-type nano-patterned sapphire substrates(NPSSs) by hydride vapor phase epitaxy(HVPE). The coalescence, stress evolution, and dislocation annihilation mechanisms in the AlN layer have been investigated. The large voids located on the pattern region were caused by the undesirable parasitic crystallites grown on the sidewalls of the nano-pattern in the early growth stage. The coalescence of the c-plane AlN was hindered by these three-fold crystallites and the special triangle void appeared. The cross-sectional Raman line scan was used to characterize the change of stress with film thickness, which corresponds to the characteristics of different growth stages of AlN. Threading dislocations(TDs) mainly originate from the boundary between misaligned crystallites and the c-plane AlN and the coalescence of two adjacent c-plane AlN crystals, rather than the interface between sapphire and AlN.
基金Project(51431008)supported by the National Natural Science Foundation of ChinaProjects(2017YFB0703001,2017YFB0305100)supported by the National Key Research and Development Program of China
基金Supported by National Natural Science Foundation of China,No.81101472 and No.81472556(to Liao W),and No.81372490(to Lu X)Zhejiang Provincial Natural Science Foundation,No.LZ14H160003(to Lu X)+2 种基金Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents(to Lu X)National Basic Research Program of China(973 Project),No.2011CB504603Wenzhou Municipal Science and Technology Bureau Foundation,No.Y20110090(to Li H)
文摘AIM: To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine(LPS/D-Gal).METHODS: Liver injury was induced in wild type(WT) or Recql5-deficient mice using LPS/D-Gal,and assessed by histological,serum transaminases,and mortality analyses. Hepatocellular apoptosis was quantified by transferase d UTP nick end labeling assay and Westernblot analysis of cleaved caspase-3. Liver inflammatory chemokine and cytochrome P450 expression was analyzed by quantitative reverse transcription-PCR. Neutrophil infiltration was evaluated by myeloperoxidase activity. Expression and phosphorylation of ERK,JNK,p65,and H2 A.X was determined by Western blot. Oxidative stress was evaluated by measuring malondialdehyde production and nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity.RESULTS: following LPS/D-Gal exposure,Recql5-deficient mice exhibited enhanced liver injury,as evidenced by more severe hepatic hemorrhage,higher serum aspartate transaminase and alanine transaminase levels,and lower survival rate. As compared to WT mice,Recql5-deficient mice showed an increased number of apoptotic hepatocytes and higher cleaved caspase-3 levels. Recql5-deficient mice exhibited increased DNA damage,as evidenced by increased γ-H2 A.X levels. Inflammatory cytokine levels,neutrophil infiltration,and ERK phosphorylation were also significantly increased in the knockout mice. Additionally,Recql5-deficicent mice exhibited increased malondialdehyde production and elevated inducible nitric oxide synthase,superoxide dismutase,glutathione peroxidase,catalase,and glutathione reductase activity,indicative of enhanced oxidative stress. Moreover,CYP450 expression was significantly downregulated in Recql5-deficient mice after LPS/D-Gal treatment.CONCLUSION: Recql5 protects the liver against LPS/D-Gal-induced injury through suppression of hepatocyte apoptosis and oxidative stress and modulation of CYP450 expression.
