Superconducting Gap of UCoGe probed by Thermal Transport

Thermal conductivity measurements in the superconducting state of the ferromagnet UCoGe were performed at very low temperatures and under magnetic field on samples of different qualities and with the heat current along the three crystallographic axis. This allows to disentangle intrinsic and extrinsic effects, confirm the situation of multigap superconductivity and shed new light on the situation expected or claimed for the gap in these ferromagnetic superconductors, like evidences of absence of "partially gapped" Fermi surfaces.Comment: 6 pages, 5 figures. To be appeared in Physical Review Rapid Communicatio

Takagi-Taupin Description of X-ray Dynamical Diffraction from Diffractive Optics with Large Numerical Aperture

We present a formalism of x-ray dynamical diffraction from volume diffractive optics with large numerical aperture and high aspect ratio, in an analogy to the Takagi-Taupin equations for strained single crystals. We derive a set of basic equations for dynamical diffraction from volume diffractive optics, which enable us to study the focusing property of these optics with various grating profiles. We study volume diffractive optics that satisfy the Bragg condition to various degrees, namely flat, tilted and wedged geometries, and derive the curved geometries required for ultimate focusing. We show that the curved geometries satisfy the Bragg condition everywhere and phase requirement for point focusing, and effectively focus hard x-rays to a scale close to the wavelength.Comment: 18 pages, 12 figure

Transient x-ray diffraction used to diagnose shock compressed Si crystals on the Nova laser

Transient x-ray diffraction is used to record time-resolved information about the shock compression of materials. This technique has been applied on Nova shock experiments driven using a hohlraum x-ray drive. Data were recorded from the shock release at the free surface of a Si crystal, as well as from Si at an embedded ablator/Si interface. Modeling has been done to simulate the diffraction data incorporating the strained crystal rocking curves and Bragg diffraction efficiencies. Examples of the data and post-processed simulations are presented

Extracellular DNA release, quorum sensing, and PrrF1/F2 small RNAs are key players in Pseudomonas aeruginosa tobramycin-enhanced biofilm formation

Biofilms are structured microbial communities that are the leading cause of numerous chronic infections which are difficult to eradicate. Within the lungs of individuals with cystic fibrosis (CF), Pseudomonas aeruginosa causes persistent biofilm infection that is commonly treated with aminoglycoside antibiotics such as tobramycin. However, sublethal concentrations of this aminoglycoside were previously shown to increase biofilm formation by P. aeruginosa, but the underlying adaptive mechanisms still remain elusive. Herein, we combined confocal laser scanning microscope analyses, proteomics profiling, gene expression assays and phenotypic studies to unravel P. aeruginosa potential adaptive mechanisms in response to tobramycin exposure during biofilm growth. Under this condition, we show that the modified biofilm architecture is related at least in part to increased extracellular DNA (eDNA) release, most likely as a result of biofilm cell death. Furthermore, the activity of quorum sensing (QS) systems was increased, leading to higher production of QS signaling molecules. We also demonstrate upon tobramycin exposure an increase in expression of the PrrF small regulatory RNAs, as well as expression of iron uptake systems. Remarkably, biofilm biovolumes and eDNA relative abundances in pqs and prrF mutant strains decrease in the presence of tobramycin. Overall, our findings offer experimental evidences for a potential adaptive mechanism linking PrrF sRNAs, QS signaling, biofilm cell death, eDNA release, and tobramycin-enhanced biofilm formation in P. aeruginosa. These specific adaptive mechanisms should be considered to improve treatment strategies against P. aeruginosa biofilm establishment in CF patients’ lungs

Colonoscopic screening for colorectal cancer improves quality of life measures: a population-based screening study

BACKGROUND: Screening asymptomatic individuals for neoplasia can have adverse consequences on quality of life. Colon cancer screening is widespread but the quality of life (QOL) consequences are unknown. This study determined the impact of screening colonoscopy on QOL measures in asymptomatic average-risk participants. METHODS: Asymptomatic male and female participants aged 55–74 years were randomly selected from the Australian Electoral Roll or six primary care physicians' databases. Participants completed the Short-Form (SF-36) Quality of Life Assessment at baseline and at a mean of 39 days after colonoscopy. Outcome measures were (i) significant changes in raw scores in any of the eight SF-36 domains assessed following colonoscopic screening and (ii) improvements or declines in previously validated categories, representing clinically significant changes, within any of the eight SF-36 domains. RESULTS: Baseline QOL measures were similar to those of a matched general population sample. Role Limitations due to Emotions, Mental Health and Vitality raw scores significantly improved following colonoscopy (P < 0.05, 2-tailed t-test). Health ratings according to Category were similar (same clinical status) in the majority of participants. However, 30% participants recorded clinically significant improvement in the Mental Health and Vitality domains (P < 0.05, Wilcoxon Signed-Ranks test). This improvement was not offset by declines in other domains or in other participants. Improvement in QOL was not related to colonoscopy results. CONCLUSION: Average-risk persons benefit significantly from colon cancer screening with colonoscopy, improving in Mental Health and Vitality domains of Quality of Life. This improvement is not offset by declines in other domains

iCLIP Predicts the Dual Splicing Effects of TIA-RNA Interactions

Transcriptome-wide analysis of protein-RNA interactions predicts the dual splicing effects of TIA proteins, showing that their local enhancing function is associated with diverse distal splicing silencing effects

HIV-1-Infected and Immune-Activated Macrophages Induce Astrocytic Differentiation of Human Cortical Neural Progenitor Cells via the STAT3 Pathway

Diminished adult neurogenesis is considered a potential mechanism in the pathogenesis of HIV-1-associated dementia (HAD). In HAD, HIV-1-infected and immune-activated brain mononuclear phagocytes (MP; perivascular macrophages and microglia) drive central nervous system (CNS) inflammation and may alter normal neurogenesis. We previously demonstrated HIV-1-infected and lipopolysaccharide (LPS) activated monocyte-derived macrophages (MDM) inhibit human neural progenitor cell (NPC) neurogenesis, while enhancing astrogliogenesis through the secretion of the inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), in vitro and in vivo. Here we further test the hypothesis that HIV-1-infected/activated MDM promote NPC astrogliogenesis via activation of the transcription factor signal transducer and activator of transcription 3 (STAT3), a critical factor for astrogliogenesis. Our results show that LPS-activated MDM-conditioned medium (LPS-MCM) and HIV-infected/LPS-activated MDM-conditioned medium (LPS+HIV-MCM) induced Janus kinase 1 (Jak1) and STAT3 activation. Induction of the Jak-STAT3 activation correlated with increased glia fibrillary acidic protein (GFAP) expression, demonstrating an induction of astrogliogenesis. Moreover, STAT3-targeting siRNA (siSTAT3) decreased MCM-induced STAT3 activation and NPC astrogliogenesis. Furthermore, inflammatory cytokines (including IL-6, IL-1β and TNF-α) produced by LPS-activated and/or HIV-1-infected MDM may contribute to MCM-induced STAT3 activation and astrocytic differentiation. These observations were confirmed in severe combined immunodeficient (SCID) mice with HIV-1 encephalitis (HIVE). In HIVE mice, siRNA control (without target sequence, sicon) pre-transfected NPCs injected with HIV-1-infected MDM showed more astrocytic differentiation and less neuronal differentiation of NPCs as compared to NPC injection alone. siSTAT3 abrogated HIV-1-infected MDM-induced astrogliogenesis of injected NPCs. Collectively, these observations demonstrate that HIV-1-infected/activated MDM induces NPC astrogliogenesis through the STAT3 pathway. This study generates important data elucidating the role of brain inflammation in neurogenesis and may provide insight into new therapeutic strategies for HAD