Suzaku and BeppoSAX X-ray Spectra of the Persistently Accreting Neutron-Star Binary 4U 1705-44

We present an analysis of the broad-band spectra of 4U~1705--44 obtained with {\it Suzaku} in 2006--2008 and by {\it BeppoSAX} in 2000. The source exhibits two distinct states: the hard state shows emission from 1 to 150 keV, while the soft state is mostly confined to be $<40$ keV. We model soft-state continuum spectra with two thermal components, one of which is a multicolor accretion disk and the other is a single-temperature blackbody to describe the boundary layer, with additional weak Comptonization represented by either a simple power law or the SIMPL model by Steiner et al. The hard-state continuum spectra are modeled by a single-temperature blackbody for the boundary layer plus strong Comptonization, modeled by a cutoff power law. While we are unable to draw firm conclusions about the physical properties of the disk in the hard state, the accretion disk in the soft state appears to approximately follow $L\propto T^{3.2}$. The deviation from $L\propto T^4$, as expected from a constant inner disk radius, might be caused by a luminosity-dependent spectral hardening factor and/or real changes of the inner disk radius in some part of the soft state. The boundary layer apparent emission area is roughly constant from the hard to the soft states, with a value of about 1/11 of the neutron star surface. The magnetic field on the surface of the NS in 4U~1705--44 is estimated to be less than about $1.9\times 10^8$ G, assuming that the disk is truncated by the ISCO or by the neutron star surface. Broad relativistic Fe lines are detected in most spectra and are modeled with the diskline model. The strength of the Fe lines is found to correlate well with the boundary layer emission in the soft state. In the hard state, the Fe lines are probably due to illumination of the accretion disk by the strong Comptonization emission.Comment: Accepted for publication in the Astrophysical Journa

Prevalence of internet addiction disorder in Chinese university students: A comprehensive meta-analysis of observational studies

Background and aims: Internet addiction disorder (IAD) is common in university students. A number of studies have examined the prevalence of IAD in Chinese university students, but the results have been inconsistent. This is a meta-analysis of the prevalence of IAD and its associated factors in Chinese university students. Methods: Both English (PubMed, PsycINFO, and Embase) and Chinese (Wan Fang Database and Chinese National Knowledge Infrastructure) databases were systematically and independently searched from their inception until January 16, 2017. Results: Altogether 70 studies covering 122,454 university students were included in the meta-analysis. Using the random-effects model, the pooled overall prevalence of IAD was 11.3% (95% CI: 10.1%–12.5%). When using the 8-item Young Diagnostic Questionnaire, the 10-item modified Young Diagnostic Questionnaire, the 20-item Internet Addiction Test, and the 26-item Chen Internet Addiction Scale, the pooled prevalence of IAD was 8.4% (95% CI: 6.7%–10.4%), 9.3% (95% CI: 7.6%–11.4%), 11.2% (95% CI: 8.8%–14.3%), and 14.0% (95% CI: 10.6%–18.4%), respectively. Subgroup analyses revealed that the pooled prevalence of IAD was significantly associated with the measurement instrument (Q = 9.41, p = .024). Male gender, higher grade, and urban abode were also significantly associated with IAD. The prevalence of IAD was also higher in eastern and central of China than in its northern and western regions (10.7% vs. 8.1%, Q = 4.90, p = .027). Conclusions: IAD is common among Chinese university students. Appropriate strategies for the prevention and treatment of IAD in this population need greater attention

Ammonium benzene­phospho­nate

In the crystal structure of the title salt, NH4 +.[(C6H5)P(O)2(OH)]− or NH4 +·C6H6O3P−, the N and O atoms inter­act via hydrogen bonds to generate a layer motif. The phenyl rings are stacked above and below this layer, sandwiching the hydrogen-bonded layer

IL-12 Can Target Human Lung Adenocarcinoma Cells and Normal Bronchial Epithelial Cells Surrounding Tumor Lesions

BACKGROUND: Non small cell lung cancer (NSCLC) is a leading cause of cancer death. We have shown previously that IL-12rb2 KO mice develop spontaneously lung adenocarcinomas or bronchioalveolar carcinomas. Aim of the study was to investigate i) IL-12Rbeta2 expression in human primary lung adenocarcinomas and in their counterparts, i.e. normal bronchial epithelial cells (NBEC), ii) the direct anti-tumor activity of IL-12 on lung adenocarcinoma cells in vitro and vivo, and the mechanisms involved, and iii) IL-12 activity on NBEC. METHODOLOGY/PRINCIPAL FINDINGS: Stage I lung adenocarcinomas showed significantly (P = 0.012) higher frequency of IL-12Rbeta2 expressing samples than stage II/III tumors. IL-12 treatment of IL-12R(+) neoplastic cells isolated from primary adenocarcinoma (n = 6) inhibited angiogenesis in vitro through down-regulation of different pro-angiogenic genes (e.g. IL-6, VEGF-C, VEGF-D, and laminin-5), as assessed by chorioallantoic membrane (CAM) assay and PCR array. In order to perform in vivo studies, the Calu6 NSCLC cell line was transfected with the IL-12RB2 containing plasmid (Calu6/beta2). Similar to that observed in primary tumors, IL-12 treatment of Calu6/beta2(+) cells inhibited angiogenesis in vitro. Tumors formed by Calu6/beta2 cells in SCID/NOD mice, inoculated subcutaneously or orthotopically, were significantly smaller following IL-12 vs PBS treatment due to inhibition of angiogenesis, and of IL-6 and VEGF-C production. Explanted tumors were studied by histology, immuno-histochemistry and PCR array. NBEC cells were isolated and cultured from lung specimens of non neoplastic origin. NBEC expressed IL-12R and released constitutively tumor promoting cytokines (e.g. IL-6 and CCL2). Treatment of NBEC with IL-12 down-regulated production of these cytokines. CONCLUSIONS: This study demonstrates that IL-12 inhibits directly the growth of human lung adenocarcinoma and targets the adjacent NBEC. These novel anti-tumor activities of IL-12 add to the well known immune-modulatory properties of the cytokine and may provide a rational basis for the development of a clinical trial

High Density Lipoprotein Protects Mesenchymal Stem Cells from Oxidative Stress-Induced Apoptosis via Activation of the PI3K/Akt Pathway and Suppression of Reactive Oxygen Species

The therapeutic effect of transplantation of mesenchymal stem cells (MSCs) in myocardial infarction (MI) appears to be limited by poor cell viability in the injured tissue, which is a consequence of oxidative stress and pro-apoptotic factors. High density lipoprotein (HDL) reverses cholesterol transport and has anti-oxidative and anti-apoptotic properties. We, therefore, investigated whether HDL could protect MSCs from oxidative stress-induced apoptosis. MSCs derived from the bone marrow of rats were pre-incubated with or without HDL, and then were exposed to hydrogen peroxide (H2O2) in vitro, or were transplanted into experimentally infarcted hearts of rats in vivo. Pre-incubation of MSCs with HDL increased cell viability, reduced apoptotic indices and resulted in parallel decreases in reactive oxygen species (ROS) in comparison with control MSCs. Each of the beneficial effects of HDL on MSCs was attenuated by inhibiting the PI3K/Akt pathway. Preconditioning with HDL resulted in higher MSC survival rates, improved cardiac remodeling and better myocardial function than in the MSC control group. Collectively, these results suggest that HDL may protect against H2O2-induced apoptosis in MSCs through activation of a PI3K/Akt pathway, and by suppressing the production of ROS

Rapamycin pre-treatment abrogates Tumour Necrosis Factor-\u3b1 down-regulatory effects on LXR-\u3b1 and PXR mRNA expression via inhibition of c-Jun N-terminal kinase 1 activation in HepG2 cells

The Liver X Receptor (LXR) and Pregnane X Receptor (PXR) are members of the nuclear receptor superfamily. Previously, they have been classified as important regulators of lipid homeostasis. However, recent studies have shown that they may be implicated in anti-inflammatory responses as well. This study shows that Tumour Necrosis Factor-\u3b1 (TNF-\u3b1) treatment reduces both LXR-\u3b1 and PXR mRNA expression. However, pre-treatment with rapamycin, an mTOR inhibitor, followed by TNF-\u3b1 stimulation, significantly induces LXR-\u3b1 and PXR mRNA expression to ~17- and ~2-fold, respectively. This suggests that mTORC1, a multi-molecular complex of which mTOR is a member, may act as a negative regulator that inhibits the induction of LXR-\u3b1 and PXR as anti-inflammatory genes. It is also shown here that inhibition of JNK1 via the mTOR/Akt pathway coincides with the up-regulation of LXR-\u3b1 and PXR mRNA, after TNF-\u3b1 treatment. Together, these observations suggest that JNK1 possibly act downstream of mTORC1 as an LXR-\u3b1 and PXR inhibitor. From the results gleaned in this study, rapamycin (and its analogues) may be used to reduce acute inflammation by promoting the induction of LXR-\u3b1 and PXR as anti-inflammatory genes

Transcriptomic analyses of regenerating adult feathers in chicken

Transcriptome Expression Data. Table of mapped reads to Galgal4 transcripts for all 15 data sets. FPKM (Fragments per kilobase of exon per million fragments mapped): normalized transcript abundance values for each gene in the indicated tissues. (CSV 1314 kb

Magnetotransport in an aluminum thin film on a GaAs substrate grown by molecular beam epitaxy

Magnetotransport measurements are performed on an aluminum thin film grown on a GaAs substrate. A crossover from electron- to hole-dominant transport can be inferred from both longitudinal resistivity and Hall resistivity with increasing the perpendicular magnetic field B. Also, phenomena of localization effects can be seen at low B. By analyzing the zero-field resistivity as a function of temperature T, we show the importance of surface scattering in such a nanoscale film