First Principles Study on the Electronic Structure and Interface Stability of Hybrid Silicene/Fluorosilicene Nanoribbons

© 2015 Macmillan Publishers Limited. The interface stability of hybrid silicene/fluorosilicene nanoribbons (SFNRs) has been investigated by using density functional theory calculations, where fluorosilicene is the fully fluorinated silicene. It is found that the diffusion of F atoms at the zigzag and armchair interfaces of SFNRs is endothermic, and the corresponding minimum energy barriers are respectively 1.66 and 1.56 eV, which are remarkably higher than the minimum diffusion energy barrier of one F atom and two F atoms on pristine silicene 1.00 and 1.29 eV, respectively. Therefore, the thermal stability of SFNRs can be significantly enhanced by increasing the F diffusion barriers through silicene/fluorosilicene interface engineering. In addition, the electronic and magnetic properties of SFNRs are also investigated. It is found that the armchair SFNRs are nonmagnetic semiconductors, and the band gap of armchair SFNRs presents oscillatory behavior when the width of silicene part changing. For the zigzag SFNRs, the antiferromagnetic semiconducting state is the most stable one. This work provides fundamental insights for the applications of SFNRs in electronic devices

Density functional theory study on the electronic properties and stability of silicene/silicane nanoribbons

© The Royal Society of Chemistry 2015. The thermal stability of silicene/silicane nanoribbons (SSNRs) has been investigated by using density functional theory calculations, where silicane is the fully hydrogenated silicene. It was found that the minimum energy barriers for the diffusion of hydrogen atoms at the zigzag and armchair interfaces of SSNRs are 1.54 and 1.47 eV, respectively, while the diffusion of H atoms at both interfaces is always endothermic. Meanwhile, the minimum diffusion energy barriers of one H atom and two H atoms on pristine silicene are 0.73 and 0.87 eV, respectively. Therefore, the thermal stability of SSNRs can be significantly enhanced by increasing the hydrogen diffusion barriers through silicene/silicane interface engineering. In addition, the zigzag SSNR remains metallic, whereas the armchair SSNR is semiconducting. However, the silicene nanoribbons part-determine the metallic or semiconducting behaviour in the SSNRs. This work provides fundamental insights for the applications of SSNRs in electronic devices. This journal i

Antagonistic bioactivity of an endophytic bacterium H-6

An endophytic bacterium, H-6, was isolated from leaves of Huperzia serrata grown in the Lushan Mountain, China. The strain was identified as Burkholderia sp. H-6 based on morphological, physiological and biochemical methods as well as on 16S rDNA analysis. This strain inhibited mycelium growth in vitro of 6 plant pathogenic fungi, especially of Phytophthora capsici, Fusarium graminearumt and Sclerotinia libertiana. In greenhouse pot experiments, soil drenches with cell densities of 106, 108 and 1010 CFU ml-1 H-6 reduced significantly P. capsici, in pepper seedling by 51.7, 58.7 and 60.2%, respectively, compared to the inoculated control, 3 weeks after sowing. Growth parameters such as lengths and fresh weights of roots and shoots of P. capsici-inoculated control plants were significantly lower compared to P. capsici-inoculated and H-6-treated plants, which is an added advantage of the strain used as potential biocontrol agent in future.Key words: Endophytic bacterium, 16S rDNA gene, antagonistic activity, Huperzia serrata

Simple and efficient methods for isolation and activity measurement of the recombinant hirudin variant 3 from Bacillus subtilis

A simple purification approach of the recombinant hirudin variant 3 from the Bacillus subtilis was established, by which the hirudin could be purified to the purity of 95% through one-step chromatography with the total recovery rate of 83.9%. A modified Markwardt thrombin titration method for measuring hirudin activity was also set up. Briefly, a series of concentrations of thrombin was prepared and titrated to hirudin sample, respectively and the anti-thrombin activity-range of hirudin was narrowed down by several thrombin solutions at high or low concentration and the optimum group of thrombin concentrations was determined for titration of the hirudin sample. In this modified method, the hirudin activity was determined more accurately, concisely and promptly than the classic Markwardt method.Key words: Hirudin, thrombin titration method, chromatography, purification

Unique Carboniferous-Permian tectonic-metallogenic framework of Northern Xinjiang (NW China): Constraints for the tectonics of the southern Paleoasian Domain

The late Paleozoic tectonic-metallogenic framework of North Xinjiang of the southern Paleoasian Domain was characterized by a serious of Carboniferous-Permian events, including: (1) late Carboniferous-Permian Chinese Altay island arc and its metamorphism, granulite in the Chinese Altay, radiolarian chert and high-pressure/ultra-high-pressure metamorphism; (2) late Carboniferous-early Permian adakites, Alaskan-type mafic-ultramafic complexes, and calc-alkaline magmatism, together with porphyry copper deposits, which occurred in the North Xinjiang; and (3) late Carboniferous ophiolite and island arc volcanic rocks located in the Tian Shan. Combined with the facts that there was no typical foreland basin, no typical collisional-type granitoid, and there were large amount of strike-slip faulting, it is suggested that in the Carboniferous-early Permian North Xinjiang was characterized by the coexistence of compression-extension-strike-slip structures with active magmatism and metallogeny. These phenomena all indicate that there were active margins during the late Carboniferous-early Permian, leading to the notion that the complicated accretionary orogeny along the southern Paleoasian Domain may have lasted to the latest Carboniferous-Permian.新疆北部晚古生代独特的构造一成矿作用以发育大量石炭纪一二叠纪构造一成矿事件为特征, 其中包括: (l) 发育于晚石炭世一二叠世的阿尔泰岛弧及其变质事件、阿尔泰麻粒岩与基性杂岩、西南天山放射虫硅质岩和高压一超高压一低压麻拉岩相变质事件; (2 )北疆发育的石炭纪(一二叠世)埃达克岩一高镁安山岩一富N d 玄武质岩组合、阿拉斯加型基性一超基性杂岩和大量的与俯冲相关的钙碱性岩浆活动与斑岩型铜矿床成矿作用; (3) 天山晚石炭世晚期蛇绿岩与岛弧火山岩等。结合北疆地区相关的前陆盆地发育不明显、碰撞型花岗岩欠发育与大量发育平行造山带大型走滑构造等现象, 可以认为新疆北部在石炭纪一二叠纪挤压一伸展一走滑并存, 岩浆活动与成矿作用活跃。这些新进展表明新疆北部在晚石炭世一二叠纪可能仍存在活动陆缘, 因此, 古亚洲洋构造域南部复杂增生造山作用最后延至晚石炭世晚期一二叠纪。published_or_final_versio

Critical Role of NADPH Oxidase in Neuronal Oxidative Damage and Microglia Activation following Traumatic Brain Injury

BACKGROUND: Oxidative stress is known to play an important role in the pathology of traumatic brain injury. Mitochondria are thought to be the major source of the damaging reactive oxygen species (ROS) following TBI. However, recent work has revealed that the membrane, via the enzyme NADPH oxidase can also generate the superoxide radical (O(2)(-)), and thereby potentially contribute to the oxidative stress following TBI. The current study thus addressed the potential role of NADPH oxidase in TBI. METHODOLOGY/PRINCIPAL FINDINGS: The results revealed that NADPH oxidase activity in the cerebral cortex and hippocampal CA1 region increases rapidly following controlled cortical impact in male mice, with an early peak at 1 h, followed by a secondary peak from 24-96 h after TBI. In situ localization using oxidized hydroethidine and the neuronal marker, NeuN, revealed that the O(2)(-) induction occurred in neurons at 1 h after TBI. Pre- or post-treatment with the NADPH oxidase inhibitor, apocynin markedly inhibited microglial activation and oxidative stress damage. Apocynin also attenuated TBI-induction of the Alzheimer's disease proteins β-amyloid and amyloid precursor protein. Finally, both pre- and post-treatment of apocynin was also shown to induce significant neuroprotection against TBI. In addition, a NOX2-specific inhibitor, gp91ds-tat was also shown to exert neuroprotection against TBI. CONCLUSIONS/SIGNIFICANCE: As a whole, the study demonstrates that NADPH oxidase activity and superoxide production exhibit a biphasic elevation in the hippocampus and cortex following TBI, which contributes significantly to the pathology of TBI via mediation of oxidative stress damage, microglial activation, and AD protein induction in the brain following TBI

Acetylation of the Pro-Apoptotic Factor, p53 in the Hippocampus following Cerebral Ischemia and Modulation by Estrogen

Recent studies demonstrate that acetylation of the transcription factor, p53 on lysine(373) leads to its enhanced stabilization/activity and increased susceptibility of cells to stress. However, it is not known whether acetylation of p53 is altered in the hippocampus following global cerebral ischemia (GCI) or is regulated by the hormone, 17β-estradiol (17β-E(2)), and thus, this study examined these issues.The study revealed that Acetyl p53-Lysine(373) levels were markedly increased in the hippocampal CA1 region after GCI at 3 h, 6 h and 24 h after reperfusion, an effect strongly attenuated by 17β-E(2). 17β-E(2) also enhanced interaction of p53 with the ubiquitin ligase, Mdm2, increased ubiquitination of p53, and induced its down-regulation, as well as attenuated elevation of the p53 transcriptional target, Puma. We also observed enhanced acetylation of p53 at a different lysine (Lys(382)) at 3 h after reperfusion, and 17β-E(2) also markedly attenuated this effect. Furthermore, administration of an inhibitor of CBP/p300 acetyltransferase, which acetylates p53, was strongly neuroprotective of the CA1 region following GCI. In long-term estrogen deprived (LTED) animals, the ability of 17β-E(2) to attenuate p53 acetylation was lost, and intriguingly, Acetyl p53-Lysine(373) levels were markedly elevated in sham (non-ischemic) LTED animals. Finally, intracerebroventricular injections of Gp91ds-Tat, a specific NADPH oxidase (NOX2) inhibitor, but not the scrambled tat peptide control (Sc-Tat), attenuated acetylation of p53 and reduced levels of Puma following GCI.The studies demonstrate that p53 undergoes enhanced acetylation in the hippocampal CA1 region following global cerebral ischemia, and that the neuroprotective agent, 17β-E(2), markedly attenuates the ischemia-induced p53 acetylation. Furthermore, following LTED, the suppressive effect of 17β-E(2) on p53 acetylation is lost, and p53 acetylation increases in the hippocampus, which may explain previous reports of increased sensitivity of the hippocampus to ischemic stress following LTED