Fabrication and Characterization of a Self-Powered n-Bi2Se3/p-Si Nanowire Bulk Heterojunction Broadband Photodetector.

In the present study, vacuum evaporation method is used to deposit Bi2Se3 film onto Si nanowires (NWs) to form bulk heterojunction for the first time. Its photodetector is self-powered, its detection wavelength ranges from 390 nm to 1700 nm and its responsivity reaches its highest value of 84.3 mA/W at 390 nm. In comparison to other Bi2Se3/Si photodetectors previously reported, its infrared detection length is the second longest and its response speed is the third fastest. Before the fabrication of the photodetector, we optimized the growth parameter of the Bi2Se3 film and the best Bi2Se3 film with atomic steps could finally be achieved. The electrical property measurement conducted by the physical property measurement system (PPMS) showed that the grown Bi2Se3 film was n-type conductive and had unique topological insulator properties, such as a metallic state, weak anti-localization (WAL) and linear magnetic resistance (LMR). Subsequently, we fabricated Si NWs by the metal-assisted chemical etching (MACE) method. The interspace between Si NWs and the height of Si NWs could be tuned by Ag deposition and chemical etching times, respectively. Finally, Si NWs fabricated with the Ag deposition time of 60 s and the etching time of 10 min was covered by the best Bi2Se3 film to be processed for the photodetector. The primary n-Bi2Se3/p-Si NWs photodetector that we fabricated can work in a self-powered mode and it has a broadband detection range and fast response speed, which indicates that it can serve as a promising silicon-based near- and mid-infrared photodetector.

Delineating the conformational landscape and intrinsic properties of the angiotensin II type 2 receptor using a computational study.

As a key regulator for the renin-angiotensin system, a class A G protein-coupled receptor (GPCR), AngII type 2 receptor (AT2R), plays a pivotal role in the homeostasis of the cardiovascular system. Compared with other GPCRs, AT2R has a unique antagonist-bound conformation and its mechanism is still an enigma. Here, we applied combined dynamic and evolutional approaches to investigate the conformational space and intrinsic properties of AT2R. With molecular dynamic simulations, Markov State Models, and statistics coupled analysis, we captured the conformational landscape of AT2R and identified its uniquity from both dynamical and evolutional viewpoints. A cryptic pocket was also discovered in the intermediate state during conformation transitions. These findings offer a deeper understanding of the AT2R mechanism at an atomic level and provide hints for the design of novel AT2R modulators.

A facile and practical preparation of P-chiral phosphine oxides.

A practical and cost-effective synthetic method of P-chiral diarylalkyl, aryldialkyl, and triaryl phosphine oxides by using readily available chiral diphenyl-2-pyrrolidinemethanol as the auxiliary is developed. The long-standing racemization issue during solvolysis has been addressed and well controlled by employing a suitable solvent, a low reaction temperature, and an appropriate reaction time.

High glucose upregulates osteopontin expression by FoxO1 activation in macrophages.

Hyperglycemia plays a major role in the development of diabetic macrovascular complications, including atherosclerosis and restenosis, which are responsible for the most of disability and mortality in diabetic patients. Osteopontin (OPN) is an important factor involved in atherogenesis, and hyperglycemia enhances the transcriptional activity of FoxO1 which is closely association with insulin resistance and diabetes. Here, we showed that plasma OPN levels were significantly elevated in type 2 diabetic patients and positively correlated with glycated albumin (GA). The more atherosclerotic lesions were observed in the aorta of diabetic ApoE-/- mice analyzed by Sudan IV staining. High glucose increased both the mRNA and protein expression levels of OPN and inhibited the phosphorylation of FoxO1 in RAW 264.7 cells. Overexpression of WT or constitutively active mutant FoxO1 promoted the expression levels of OPN, while the dominant-negative mutant FoxO1 decreased slightly the expression of OPN. Conversely, knockdown of FoxO1 reduced the expression of OPN. Luciferase reporter assay revealed that high glucose and overexpression of FoxO1 enhanced the activities of the OPN promoter region nt -1918 ~ -713. Furthermore, the interactions between FoxO1 and the OPN promoter were confirmed by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation assay (ChIP). Our results suggest that high glucose upregulates OPN expression via FoxO1 activation, which would play a critical role in the development of diabetic atherogenesis.

Circadian locomotor output cycles kaput accelerates atherosclerotic plaque formation by upregulating plasminogen activator inhibitor-1 expression.

To explore the association between clock circadian regulator circadian locomotor output cycles kaput gene (CLOCK) and the forming of atherosclerotic plaques and its underlying mechanisms, mouse aortic endothelial cells (MAECs) and atherosclerosis (AS) mouse model were recruited for our study. The apoE gene knockout mouse was used as the model of AS and we accelerated the formation of unstable plaques through the combination of carotid artery ligation and high-fat (HF) diet administration (0.2% cholesterol, 20% fat). The mRNA and protein expressions of CLOCK in peripheral blood monouclear cells of acute coronary syndrome (ACS) patients or mouse AS model were detected by qPCR, western blot analysis and immunohistochemical staining. The number of adherent cells and atherosclerotic plaques was counted to assess the effects of CLOCK on the progression of ACS, and adherence-associated genes, such as vascular cell adhesion molecule (VCAM)-1, C-C motif chemokine ligand 2 (CCL-2), and CCL-5. The results showed that CLOCK expression was significantly increased in both ACS patients and AS mouse model. The levels of CLOCK, leukemia inhibitory factor (LIF), intercellular adhesion molecule 1 (ICAM-1), perilipin 2 (ADFP), nuclear factor kappa B (NF-κB), and plasminogen activator inhibitor-1 (PAI-1), as well as the number of atherosclerotic plaques were elevated in the AS mouse model, as compared with the control group. Chromatin immunoprecipitation assay showed that CLOCK bound directly to the promoter of PAI-1 gene and CLOCK could positively regulate the expressions of LIF, ICAM-1, ADFP, NF-κB, and PAI-1. Reduction of CLOCK expression would decrease the expressions of VCAM-1, CCL-2, and CCL-5, and the number of adherent cells and atherosclerotic plaques, but these effects were neutralized when PAI-1 was simultaneously overexpressed in either mouse model or MAECs. Our results demonstrate that CLOCK overexpression triggers the formation of atherosclerotic plaques by directly upregulating PAI-1 expression.

Passivation mechanism of thermal atomic layer-deposited Al2O3 films on silicon at different annealing temperatures.

Thermal atomic layer-deposited (ALD) aluminum oxide (Al2O3) acquires high negative fixed charge density (Qf) and sufficiently low interface trap density after annealing, which enables excellent surface passivation for crystalline silicon. Qf can be controlled by varying the annealing temperatures. In this study, the effect of the annealing temperature of thermal ALD Al2O3 films on p-type Czochralski silicon wafers was investigated. Corona charging measurements revealed that the Qf obtained at 300°C did not significantly affect passivation. The interface-trapping density markedly increased at high annealing temperature (>600°C) and degraded the surface passivation even at a high Qf. Negatively charged or neutral vacancies were found in the samples annealed at 300°C, 500°C, and 750°C using positron annihilation techniques. The Al defect density in the bulk film and the vacancy density near the SiOx/Si interface region decreased with increased temperature. Measurement results of Qf proved that the Al vacancy of the bulk film may not be related to Qf. The defect density in the SiOx region affected the chemical passivation, but other factors may dominantly influence chemical passivation at 750°C.

Effects of telmisartan on insulin resistance and visceral fat distribution in Chinese hypertensive patients with obesity.

OBJECTIVE: To investigate the effects of telmisartan on body fat distribution and insulin sensitivity in patients with hypertension and obesity. METHODS: In this prospective, randomized study, outpatients from the Sixth People's Hospital affiliated to Shanghai Jiaotong University, Shanghai, China were treated with telmisartan (n=23), or losartan (n=22) for 16 weeks between December 2009 to January 2011. Parameters such as waist and hip circumference, body mass index, fasting blood glucose, insulin, lipids, serum adiponectin, and tumor necrosis factor-alpha (TNF-alpha) were measured before and after treatment. The abdominal visceral fat area (VFA) and subcutaneous fat area (SFA) were determined by magnetic resonance imaging. Insulin sensitivity was estimated by homeostasis model assessment (HOMA-IR). RESULTS: Compared with baseline, the systolic and diastolic blood pressure decreased significantly in both groups. However, the levels of HOMA-IR, serum adiponectin, and TNF-alpha only improved in the telmisartan group. Similarly, the VFA was reduced in the telmisartan group, while the SFA did not change in either group. CONCLUSION: Telmisartan improves both hemodynamic and metabolic abnormalities found in hypertensive patients with obesity. The additional benefits may be partly due to visceral fat remodeling.

MicroRNA-1 regulates cardiomyocyte apoptosis by targeting Bcl-2.

MicroRNA-1 (miR-1) is preferentially expressed in cardiac muscles, and the expression has been demonstrated to be involved in cardiac development and cardiovascular diseases. Here we report that miR-1 is closely related with ischemia/reperfusion injury in a rat model. The level of miR-1 is inversely correlated with Bcl-2 protein expression in cardiomyocytes of the I/R rat model. In vitro, the level of miR-1 was dramatically increased in response to H(2)O(2). Overexpression of miR-1 facilitated H(2)O(2)-induced apoptosis in cardiomyocytes. Inhibition of miR-1 by antisense inhibitory oligonucleotides caused marked resistance to H(2)O(2). Through bioinformatics, we identified the potential target sites for miR-1 on the 3' UTR of Bcl-2. miR-1 significantly reduced the expression of Bcl-2 in the levels of mRNA and protein. The post-transcriptional repression of Bcl-2 was further confirmed by luciferase reporter experiments. These data demonstrated that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which is involved in post-transcriptional repression of Bcl-2.