A summary of the BARREL campaigns: Technique for studying electron precipitation.

BARREL observed electron precipitation over wide range of energy and timescalesPrecipitating electron distribution is determined using spectroscopy for 19 January 2013 eventBARREL timing data has accuracy within sampling interval of 0.05 s

Induction of resistance in cucumber against seedling damping-off by plant growth-promoting rhizobacteria (PGPR) Bacillus megaterium strain L8

Bacillus megaterium L8, a plant growth-promoting rhizobacterium (PGPR), was isolated and evaluated for its ability to induce resistance in cucumber against seedling damping-off caused by Pythium aphanidermatum. Root-splitting challenge experiments showed that L8 treatment of cucumber roots more effectively suppressed seedling damping-off than did the control as judged by seedling survival rate (83.45 versus 31.68% at 28 days), indicating that strain L8 is capable of inducing systemic disease resistance in cucumber. To explore the potential mechanism underlying the induced systemic resistance (ISR) mediated by L8, the expression profile of several plant defense-related enzymes: superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), polyphenol oxidase (PPO) and phenylalanine ammonia-lyase (PAL) were monitored in the roots treated with L8 or P. aphanidermatum and untreated leaves in a time course of 13 days. Levels of SOD, POD, CAT, PPO and PAL activities in the treated roots and untreated leaves of cucumber seedlings were all significantly higher as compared with the control and respectively peaked in the roots at 3, 3, 5, 5 and 5 days and correspondingly in the leaves at 5, 3, 5, 5 and 5 days post-inoculation. The enhanced expression patterns of the above enzymes following L8 or P. aphanidermatum treatment suggested that systemic induction of plant defense enzymes by L8 might account for its ability to provide effective protection for cucumber from seedling damping-off caused by the soil-borne fungal pathogen P. aphanidermatum.Key words: Plant growth-promoting rhizobacteria (PGPR), defense enzymes, damping-off of cucumber seedlings, induced resistance

A Full Pharmacological Analysis of the Three Turkey β-Adrenoceptors and Comparison with the Human β-Adrenoceptors

There are three turkey β-adrenoceptors: the original turkey β-adrenoceptor from erythrocytes (tβtrunc, for which the X-ray crystal structure has recently been determined), tβ3C and tβ4C-receptors. This study examined the similarities and differences between these avian receptors and mammalian receptors with regards to binding characteristics and functional high and low affinity agonist conformations.Stable cell lines were constructed with each of the turkey β-adrenoceptors and 3H-CGP12177 whole cell binding, CRE-SPAP production and (3)H-cAMP accumulation assays performed. It was confirmed that the three turkey β-adrenoceptors are distinct from each other in terms of amino acid sequence and binding characteristics. The greatest similarity of any of the turkey β-adrenoceptors to human β-adrenoceptors is between the turkey β3C-receptor and the human β2-adrenoceptor. There are pharmacologically distinct differences between the binding of ligands for the tβtrunc and tβ4C and the human β-adrenoceptors (e.g. with CGP20712A and ICI118551). The tβtrunc and tβ4C-adrenoceptors appear to exist in at least two different agonist conformations in a similar manner to that seen at both the human and rat β1-adrenoceptor and human β3-adrenoceptors. The tβ3C-receptor, similar to the human β2-adrenoceptor, does not, at least so far, appear to exist in more than one agonist conformation.There are several similarities, but also several important differences, between the recently crystallised turkey β-adrenoceptor and the human β-adrenoceptors. These findings are important for those the field of drug discovery using the recently structural information from crystallised receptors to aid drug design. Furthermore, comparison of the amino-acid sequence for the turkey and human adrenoceptors may therefore shed more light on the residues involved in the existence of the secondary β-adrenoceptor conformation

Co3O4 Nanocrystals on Graphene as a Synergistic Catalyst for Oxygen Reduction Reaction

Catalysts for oxygen reduction and evolution reactions are at the heart of key renewable energy technologies including fuel cells and water splitting. Despite tremendous efforts, developing oxygen electrode catalysts with high activity at low costs remains a grand challenge. Here, we report a hybrid material of Co3O4 nanocrystals grown on reduced graphene oxide (GO) as a high-performance bi-functional catalyst for oxygen reduction reaction (ORR) and oxygen evolution reaction (OER). While Co3O4 or graphene oxide alone has little catalytic activity, their hybrid exhibits an unexpected, surprisingly high ORR activity that is further enhanced by nitrogen-doping of graphene. The Co3O4/N-doped graphene hybrid exhibits similar catalytic activity but superior stability to Pt in alkaline solutions. The same hybrid is also highly active for OER, making it a high performance non-precious metal based bi-catalyst for both ORR and OER. The unusual catalytic activity arises from synergetic chemical coupling effects between Co3O4 and graphene.Comment: published in Nature Material

Characterization of High-Fat, Diet-Induced, Non-alcoholic Steatohepatitis with Fibrosis in Rats

An ideal animal model is necessary for a clear understanding of the etiology, pathogenesis, and mechanisms of human non-alcoholic steatohepatitis (NASH) and for facilitating the design of effective therapy for this condition. We aimed to establish a rat model of NASH with fibrosis by using a high-fat diet (HFD). Male Sprague–Dawley (SD) rats were fed a HFD consisting of 88 g normal diet, 10 g lard oil, and 2 g cholesterol. Control rats were fed normal diet. Rats were killed at 4, 8, 12, 16, 24, 36, and 48 weeks after HFD exposure. Body weight, liver weight, and epididymal fat weight were measured. Serum levels of fasting glucose, triglyceride, cholesterol, alanine aminotransferase (ALT), free fatty acids (FFA), insulin, and tumor necrosis factor-alpha (TNF-α) were determined. Hepatic histology was examined by H&E stain. Hepatic fibrosis was assessed by VG stain and immunohistochemical staining for transforming growth factor beta 1 (TGF-β1), and alpha-smooth-muscle actin (α-SMA). The liver weight and liver index increased from week 4, when hepatic steatosis was also observed. By week 8, the body weight and epididymal fat weight started increasing, which was associated with increased serum levels of FFA, cholesterol, and TNF-α, as well as development of simple fatty liver. The serum ALT level increased from week 12. Steatohepatitis occurred from weeks 12 through 48. Apparent hepatic perisinosodial fibrosis did not occur until week 24, and progressed from week 36 to 48 with insulin resistance. Therefore, this novel model may be potentially useful in NASH study

X-ray Time Lags in TeV Blazars

We use Monte Carlo/Fokker-Planck simulations to study the X-ray time lags. Our results show that soft lags will be observed as long as the decay of the flare is dominated by radiative cooling, even when acceleration and cooling timescales are similar. Hard lags can be produced in presence of a competitive achromatic particle energy loss mechanism if the acceleration process operates on a timescale such that particles are slowly moved towards higher energy while the flare evolves. In this type of scenario, the {\gamma} -ray/X-ray quadratic relation is also reproduced.Comment: 4 pages, 6 figures, Proceeding of `Multiwavelength Variability of Blazars', Guangzhou, Chin

Evaluation of the Osteogenic Potential of Growth Factorâ Rich Demineralized Bone Matrix In Vivo

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141502/1/jper0036.pd

Atomically dispersed Pt-N-4 sites as efficient and selective electrocatalysts for the chlorine evolution reaction

Chlorine evolution reaction (CER) is a critical anode reaction in chlor-alkali electrolysis. Although precious metal-based mixed metal oxides (MMOs) have been widely used as CER catalysts, they suffer from the concomitant generation of oxygen during the CER. Herein, we demonstrate that atomically dispersed Pt-N-4 sites doped on a carbon nanotube (Pt-1/CNT) can catalyse the CER with excellent activity and selectivity. The Pt-1/CNT catalyst shows superior CER activity to a Pt nanoparticle-based catalyst and a commercial Ru/Ir-based MMO catalyst. Notably, Pt-1/CNT exhibits near 100% CER selectivity even in acidic media, with low Cl- concentrations (0.1M), as well as in neutral media, whereas the MMO catalyst shows substantially lower CER selectivity. In situ electrochemical X-ray absorption spectroscopy reveals the direct adsorption of Cl- on Pt-N-4 sites during the CER. Density functional theory calculations suggest the PtN4C12 site as the most plausible active site structure for the CER

Universal scaling relation in high-temperature superconductors

Scaling laws express a systematic and universal simplicity among complex systems in nature. For example, such laws are of enormous significance in biology. Scaling relations are also important in the physical sciences. The seminal 1986 discovery of high transition-temperature (high-T_c) superconductivity in cuprate materials has sparked an intensive investigation of these and related complex oxides, yet the mechanism for superconductivity is still not agreed upon. In addition, no universal scaling law involving such fundamental properties as T_c and the superfluid density \rho_s, a quantity indicative of the number of charge carriers in the superconducting state, has been discovered. Here we demonstrate that the scaling relation \rho_s \propto \sigma_{dc} T_c, where the conductivity \sigma_{dc} characterizes the unidirectional, constant flow of electric charge carriers just above T_c, universally holds for a wide variety of materials and doping levels. This surprising unifying observation is likely to have important consequences for theories of high-T_c superconductivity.Comment: 11 pages, 2 figures, 2 table

Genetic and epigenetic silencing of the beclin 1 gene in sporadic breast tumors

<p>Abstract</p> <p>Background</p> <p>Beclin 1, an important autophagy-related protein in human cells, is involved in cell death and cell survival. <it>Beclin 1 </it>mapped to human chromosome 17q21. It is widely expressed in normal mammary epithelial cells. Although down-regulated expression with mono-allelic deletions of <it>beclin 1 </it>gene was frequently observed in breast tumors, whether there was other regulatory mechanism of <it>beclin 1 </it>was to be investigated. We studied the expression of beclin 1 and explored the possible regulatory mechanisms on its expression in breast tumors.</p> <p>Methods</p> <p>20 pairs of tumors and adjacent normal tissues from patients with sporadic breast invasive ductal cancer (IDCs) were collected. The mRNA expression of <it>beclin 1 </it>was detected by real-time quantitative RT-PCR. Loss of heterozygosity (LOH) was determined by real-time quantitative PCR and microsatellite methods. The protein expression of beclin 1, p53, BRCA1 and BRCA2 was assessed by immunohistochemistry. CpG islands in 5' genomic region of beclin 1 gene were identified using MethylPrimer Program. Sodium bisulfite sequencing was used in examining the methylation status of each CpG island.</p> <p>Results</p> <p>Decreased <it>beclin 1 </it>mRNA expression was detected in 70% of the breast tumors, and the protein levels were co-related to the mRNA levels. Expression of <it>beclin 1 </it>mRNA was demonstrated to be much higher in the BRCA1 positive tumors than that in the BRCA1 negative ones. Loss of heterozygosity was detected in more than 45% of the breast tumors, and a dense cluster of CpG islands was found from the 5' end to the intron 2 of the <it>beclin 1 </it>gene. Methylation analysis showed that the promoter and the intron 2 of beclin 1 were aberrantly methylated in the tumors with decreased expression.</p> <p>Conclusions</p> <p>These data indicated that LOH and aberrant DNA methylation might be the possible reasons of the decreased expression of <it>beclin 1 </it>in the breast tumors. The findings here shed some new light on the regulatory mechanisms of beclin 1 in breast cancer.</p