bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hetero-oligomerization between the TNF receptor superfamily members CD40, Fas and TRAILR2 modulate CD40 signalling
Authors: Smulski Cristian R , Decossas Marion , Chekkat Neila , Beyrath Julien , Willen Laure , Guichard Gilles , Lorenzetti Raquel , Rizzi Marta , Eibel Hermann , Schneider Pascal , Fournel Sylvie 
Published: February 2017

AbstractTNF receptor superfamily members (TNFRSF) such as CD40, Fas and TRAIL receptor 2 (TRAILR2) participate to the adaptive immune response by eliciting survival, proliferation, differentiation and/or cell death signals. The balance between these signals determines the fate of the immune response. It was previously reported that these receptors are able to self-assemble in the absence of ligand through their extracellular regions. However, the role of this oligomerization is not well understood, and none of the proposed hypotheses take into account potential hetero-association of receptors. Using CD40 as bait in a flow cytometry Förster resonance energy transfer assay, TNFRSF members with known functions in B cells were probed for interactions. Both Fas and TRAILR2 associated with CD40. Immunoprecipitation experiments confirmed the interaction of CD40 with Fas at the endogenous levels in a BJAB B-cell lymphoma cell line deficient for TRAILR2. TRAILR2-expressing BJAB cells displayed a robust CD40–TRAILR2 interaction at the expense of the CD40–Fas interaction. The same results were obtained by proximity ligation assay, using TRAILR2-positive and -negative BJAB cells and primary human B cells. Expression of the extracellular domains of Fas or TRAILR2 with a glycolipid membrane anchor specifically reduced the intrinsic signalling pathway of CD40 in 293T cells. Conversely, BJAB cells lacking endogenous Fas or TRAILR2 showed an increased NF-κB response to CD40L. Finally, upregulation of TRAILR2 in primary human B cells correlated with reduced NF-κB activation and reduced proliferation in response to CD40L. Altogether, these data reveal that selective interactions between different TNFRSF members may modulate ligand-induced responses upstream signalling events.
MicroRNA-144 is regulated by CP2 and decreases COX-2 expression and PGE2 production in mouse ovarian granulosa cells
Authors: Zhou Jiawei , Lei Bin , Li Huanan , Zhu Lihua , Wang Lei , Tao Hu , Mei Shuqi , Li Fenge 
Published: February 2017

AbstractMammalian folliculogenesis is a complex process in which primordial follicles develop into pre-ovulatory follicles, followed by ovulation to release mature oocytes. In this study, we explored the role of miR-144 in ovulation. miR-144 was one of the differentially expressed microRNAs, which showed 5.59-fold changes, in pre-ovulatory ovarian follicles between Large White and Chinese Taihu sows detected by Solexa deep sequencing. We demonstrated that overexpression of miR-144 significantly decreased the luciferase reporter activity under the control of the cyclooxygenase-2 (COX-2) or mothers against decapentaplegic homologue 4 (Smad4) 3'-untranslated region (3'-UTR) and suppressed COX-2 and Smad4 expression. In contrast, a miR-144 inhibitor increased COX-2 and Smad4 expression in mouse granulosa cells (mGCs). Meanwhile, Smad4 upregulated COX-2 expression, but this effect was abolished when the mGCs were treated with the transforming growth factor beta signalling pathway inhibitor SB431542. Moreover, luciferase reporter, chromatin immunoprecipitation and electrophoretic mobility shift assay results showed that the transcription factor CP2 upregulated miR-144 expression, which partially contributed to the suppression of COX-2 in mGCs. Both CP2 and miR-144 alter prostaglandin E2 (PGE2) production by regulating COX-2 expression. In addition, miR-144 regulated mGC apoptosis and affected follicular atresia, but these activities did not appear to be through COX-2 and Smad4. Taken together, we revealed an important CP2/miR-144/COX-2/PGE2/ovulation pathway in mGCs.
Prenatal alcohol exposure impairs autophagy in neonatal brain cortical microvessels
Authors: Girault Virginie , Gilard Vianney , Marguet Florent , Lesueur Céline , Hauchecorne Michelle , Ramdani Yasmina , Laquerrière Annie , Marret Stéphane , Jégou Sylvie , Gonzalez Bruno Jose , Brasse-Lagnel Carole , Bekri Soumeya 
Published: February 2017

AbstractBrain developmental lesions are a devastating consequence of prenatal alcohol exposure (PAE). We recently showed that PAE affects cortical vascular development with major effects on angiogenesis and endothelial cell survival. The underlying molecular mechanisms of these effects remain poorly understood. This study aimed at characterizing the ethanol exposure impact on the autophagic process in brain microvessels in human fetuses with fetal alcohol syndrome (FAS) and in a PAE mouse model. Our results indicate that PAE induces an increase of autophagic vacuole number in human fetal and neonatal mouse brain cortical microvessels. Subsequently, ex vivo studies using green fluorescent protein (GFP)-LC3 mouse microvessel preparations revealed that ethanol treatment alters autophagy in endothelial cells. Primary cultures of mouse brain microvascular endothelial cells were used to characterize the underlying molecular mechanisms. LC3 and p62 protein levels were significantly increased in endothelial cells treated with 50 mM ethanol. The increase of autophagic vacuole number may be due to excessive autophagosome formation associated with the partial inhibition of the mammalian target of rapamycin pathway upon ethanol exposure. In addition, the progression from autophagosomes to autolysosomes, which was monitored using autophagic flux inhibitors and mRFP–EGFP vector, showed a decrease in the autolysosome number. Besides, a decrease in the Rab7 protein level was observed that may underlie the impairment of autophagosome–lysosome fusion. In addition, our results showed that ethanol-induced cell death is likely to be mediated by decreased mitochondrial integrity and release of apoptosis-inducing factor. Interestingly, incubation of cultured cells with rapamycin prevented ethanol effects on autophagic flux, ethanol-induced cell death and vascular plasticity. Taken together, these results are consistent with autophagy dysregulation in cortical microvessels upon ethanol exposure, which could contribute to the defects in angiogenesis observed in patients with FAS. Moreover, our results suggest that rapamycin represents a potential therapeutic strategy to reduce PAE-related brain developmental disorders.
Wave-based liquid-interface metamaterials
Authors: Francois N , Xia H , Punzmann H , Fontana P W , Shats M 
Published: February 2017

AbstractThe control of matter motion at liquid–gas interfaces opens an opportunity to create two-dimensional materials with remotely tunable properties. In analogy with optical lattices used in ultra-cold atom physics, such materials can be created by a wave field capable of dynamically guiding matter into periodic spatial structures. Here we show experimentally that such structures can be realized at the macroscopic scale on a liquid surface by using rotating waves. The wave angular momentum is transferred to floating micro-particles, guiding them along closed trajectories. These orbits form stable spatially periodic patterns, the unit cells of a two-dimensional wave-based material. Such dynamic patterns, a mirror image of the concept of metamaterials, are scalable and biocompatible. They can be used in assembly applications, conversion of wave energy into mean two-dimensional flows and for organising motion of active swimmers.
Strong coupling and high-contrast all-optical modulation in atomic cladding waveguides
Authors: Stern Liron , Desiatov Boris , Mazurski Noa , Levy Uriel 
Published: February 2017

AbstractIn recent years, there has been marked increase in research aimed to introduce alkali vapours into guided-wave configurations. Owing to the significant reduction in device dimensions, the increase in density of states, the interaction with surfaces and primarily the high intensities carried along the structure, a plethora of light–vapour interactions can be studied. Moreover, such platform may exhibit new functionalities such as low-power nonlinear light–matter interactions. One immense challenge is to study the effects of quantum coherence and shifts in nanoscale waveguides, characterized by ultra-small mode areas and fast dynamics. Here, we construct a highly compact 17 mm long serpentine silicon-nitride atomic vapour cladding waveguide. Fascinating and important phenomena such as van-der-Waals shifts, dynamical stark shifts and coherent effects such as strong coupling (in the form of Autler–Townes splitting) are observed. Some of these effects may play an important role in applications such as all-optical switching, frequency referencing and magnetometry.
Sleep habits, academic performance, and the adolescent brain structure
Authors: Urrila Anna S. , Artiges Eric , Massicotte Jessica , Miranda Ruben , Vulser Hélène , Bézivin-Frere Pauline , Lapidaire Winok , Lemaître Hervé , Penttilä Jani , Conrod Patricia J. , Garavan Hugh , Paillère Martinot Marie-Laure , Martinot Jean-Luc ,   The IMAGEN consortium, Banaschewski Tobias , Flor Herta , Fauth-Bühler Mira , Poutska Louise , Nees Frauke , Grimmer Yvonne , Struve Maren , Heinz Andeas , Ströhle Andreas , Kappel Viola , van Noort Betteke Maria , Poline Jean-Baptiste , Schwartz Yanick , Thyreau Benjamin , Ireland James , Rogers John , Bordas Nadège , Bricaud Zuleima , Filippi Irina , Galinowski André , Gollier-Briant Fanny , Ménard Vincent , Schumann Gunter , Desrivières Sylvane , Cattrell Anna , Goodman Robert , Stringaris Argyris , Nymberg Charlotte , Reed Laurence , Barker Gareth J , Ittermann Berndt , Brühl Ruediger , Smolka Michael , Hübner Thomas , Müller Kathrin , Bokde Arun L. W. , Büchel Christian , Bromberg Uli , Gallinat Jurgen , Fadai Tahmine , Gowland Pennylaire , Lawrence C , Paus Tomas 
Published: February 2017

AbstractHere we report the first and most robust evidence about how sleep habits are associated with regional brain grey matter volumes and school grade average in early adolescence. Shorter time in bed during weekdays, and later weekend sleeping hours correlate with smaller brain grey matter volumes in frontal, anterior cingulate, and precuneus cortex regions. Poor school grade average associates with later weekend bedtime and smaller grey matter volumes in medial brain regions. The medial prefrontal - anterior cingulate cortex appears most tightly related to the adolescents’ variations in sleep habits, as its volume correlates inversely with both weekend bedtime and wake up time, and also with poor school performance. These findings suggest that sleep habits, notably during the weekends, have an alarming link with both the structure of the adolescent brain and school performance, and thus highlight the need for informed interventions.
Determining the nature of the gap in semiconducting graphene
Authors: Prestigiacomo J. C. , Nath A. , Osofsky M. S. , Hernández S. C. , Wheeler V. D. , Walton S. G. , Gaskill D. K. 
Published: February 2017

AbstractSince its discovery, graphene has held great promise as a two-dimensional (2D) metal with massless carriers and, thus, extremely high-mobility that is due to the character of the band structure that results in the so-called Dirac cone for the ideal, perfectly ordered crystal structure. This promise has led to only limited electronic device applications due to the lack of an energy gap which prevents the formation of conventional device geometries. Thus, several schemes for inducing a semiconductor band gap in graphene have been explored. These methods do result in samples whose resistivity increases with decreasing temperature, similar to the temperature dependence of a semiconductor. However, this temperature dependence can also be caused by highly diffusive transport that, in highly disordered materials, is caused by Anderson-Mott localization and which is not desirable for conventional device applications. In this letter, we demonstrate that in the diffusive case, the conventional description of the insulating state is inadequate and demonstrate a method for determining whether such transport behavior is due to a conventional semiconductor band gap.
PARP-1/PARP-2 double deficiency in mouse T cells results in faulty immune responses and T lymphomas
Authors: Navarro Judith , Gozalbo-López Beatriz , Méndez Andrea C. , Dantzer Françoise , Schreiber Valérie , Martínez Carlos , Arana David M. , Farrés Jordi , Revilla-Nuin Beatriz , Bueno María F. , Ampurdanés Coral , Galindo-Campos Miguel A. , Knobel Philip A. , Segura-Bayona Sandra , Martin-Caballero Juan , Stracker Travis H. , Aparicio Pedro , Del Val Margarita , Yélamos José 
Published: February 2017

AbstractThe maintenance of T-cell homeostasis must be tightly regulated. Here, we have identified a coordinated role of Poly(ADP-ribose) polymerase-1 (PARP-1) and PARP-2 in maintaining T-lymphocyte number and function. Mice bearing a T-cell specific deficiency of PARP-2 in a PARP-1-deficient background showed defective thymocyte maturation and diminished numbers of peripheral CD4+ and CD8+ T-cells. Meanwhile, peripheral T-cell number was not affected in single PARP-1 or PARP-2-deficient mice. T-cell lymphopenia was associated with dampened in vivo immune responses to synthetic T-dependent antigens and virus, increased DNA damage and T-cell death. Moreover, double-deficiency in PARP-1/PARP-2 in T-cells led to highly aggressive T-cell lymphomas with long latency. Our findings establish a coordinated role of PARP-1 and PARP-2 in T-cell homeostasis that might impact on the development of PARP-centred therapies.
Lack of phylogenetic signals within environmental niches of tropical tree species across life stages
Authors: Zhang Caicai , Yang Jie , Sha Liqing , Ci Xiuqin , Li Jie , Cao Min , Brown Calum , Swenson Nathan G. , Lin Luxiang 
Published: February 2017

AbstractThe lasting imprint of phylogenetic history on current day ecological patterns has long intrigued biologists. Over the past decade ecologists have increasingly sought to quantify phylogenetic signals in environmental niche preferences and, especially, traits to help uncover the mechanisms driving plant community assembly. However, relatively little is known about how phylogenetic patterns in environmental niches and traits compare, leaving significant uncertainty about the ecological implications of trait-based analyses. We examined phylogenetic signals within known environmental niches of 64 species, at seedling and adult life stages, in a Chinese tropical forest, to test whether local environmental niches had consistent relationships with phylogenies. Our analyses show that local environmental niches are highly phylogenetically labile for both seedlings and adult trees, with closely related species occupying niches that are no more similar than expected by random chance. These findings contrast with previous trait-based studies in the same forest, suggesting that phylogenetic signals in traits might not a reliable guide to niche preferences or, therefore, to community assembly processes in some ecosystems, like the tropical seasonal rainforest in this study.
HIV-related proteins prolong macrophage survival through induction of Triggering receptor expressed on myeloid cells-1
Authors: Yuan Zhihong , Fan Xian , Staitieh Bashar , Bedi Chetna , Spearman Paul , Guidot David M , Sadikot Ruxana T 
Published: February 2017

AbstractTriggering receptor expressed on myeloid cells-1(TREM-1) is a member of the superimmunoglobulin receptor family. We have previously shown that TREM-1 prolongs survival of macrophages treated with lipoolysaccharide through Egr2-Bcl2 signaling. Recent studies suggest a role for TREM-1 in viral immunity. Human immunodeficiency virus-1 (HIV) targets the monocyte/macrophage lineage at varying stages of infection. Emerging data suggest that macrophages are key reservoirs for latent HIV even in individuals on antiretroviral therapy. Here, we investigated the potential role of TREM-1 in HIV latency in macrophages. Our data show that human macrophages infected with HIV show an increased expression of TREM-1. In parallel, direct exposure to the HIV-related proteins Tat or gp120 induces TREM-1 expression in macrophages and confers anti-apoptotic attributes.NF-κB p65 silencing identified that these proteins induce TREM-1 in p65-dependent manner. TREM-1 silencing in macrophages exposed to HIV-related proteins led to increased caspase 3 activation and reduced Bcl-2 expression, rendering them susceptible to apotosis. These novel data reveal that TREM-1 may play a critical role in establishing HIV reservoir in macrophages by inhibiting apoptosis. Therefore, targeting TREM-1 could be a novel therapeutic approach to enhance clearance of the HIV reservoir, at least within the macrophage pools.
Dissecting the brown adipogenic regulatory network using integrative genomics
Authors: Pradhan Rachana N. , Bues Johannes J. , Gardeux Vincent , Schwalie Petra C. , Alpern Daniel , Chen Wanze , Russeil Julie , Raghav Sunil K. , Deplancke Bart 
Published: February 2017

AbstractBrown adipocytes regulate energy expenditure via mitochondrial uncoupling, which makes them attractive therapeutic targets to tackle obesity. However, the regulatory mechanisms underlying brown adipogenesis are still poorly understood. To address this, we profiled the transcriptome and chromatin state during mouse brown fat cell differentiation, revealing extensive gene expression changes and chromatin remodeling, especially during the first day post-differentiation. To identify putatively causal regulators, we performed transcription factor binding site overrepresentation analyses in active chromatin regions and prioritized factors based on their expression correlation with thebona-fidebrown adipogenic markerUcp1across multiple mouse and human datasets. Using loss-of-function assays, we evaluated both the phenotypic effect as well as the transcriptomic impact of several putative regulators on the differentiation process, uncovering ZFP467, HOXA4 and Nuclear Factor I A (NFIA) as novel transcriptional regulators. Of these, NFIA emerged as the regulator yielding the strongest molecular and cellular phenotypes. To examine its regulatory function, we profiled the genomic localization of NFIA, identifying it as a key early regulator of terminal brown fat cell differentiation.
Genetic susceptibility variants for lung cancer: replication study and assessment as expression quantitative trait loci
Authors: Pintarelli Giulia , Cotroneo Chiara Elisabetta , Noci Sara , Dugo Matteo , Galvan Antonella , Delli Carpini Simona , Citterio Lorena , Manunta Paolo , Incarbone Matteo , Tosi Davide , Santambrogio Luigi , Dragani Tommaso A. , Colombo Francesca 
Published: February 2017

AbstractMany single nucleotide polymorphisms (SNPs) have been associated with lung cancer but lack confirmation and functional characterization. We retested the association of 56 candidate SNPs with lung adenocarcinoma risk and overall survival in a cohort of 823 Italian patients and 779 healthy controls, and assessed their function as expression quantitative trait loci (eQTLs). In the replication study, eight SNPs (rs401681, rs3019885, rs732765, rs2568494, rs16969968, rs6495309, rs11634351, and rs4105144) associated with lung adenocarcinoma risk and three (rs9557635, rs4105144, and rs735482) associated with survival. Five of these SNPs acted as cis-eQTLs, being associated with the transcription of IREB2 (rs2568494, rs16969968, rs11634351, rs6495309), PSMA4 (rs6495309) and ERCC1 (rs735482), out of 10,821 genes analyzed in lung. For these three genes, we obtained experimental evidence of differential allelic expression in lung tissue, pointing to the existence of in-cis genomic variants that regulate their transcription. These results suggest that these SNPs exert their effects on cancer risk/outcome through the modulation of mRNA levels of their target genes.
mecA-related structure in methicillin-resistant coagulase-negative staphylococci from street food in Taiwan
Authors: Yang Tsung-Ying , Hung Wei-Wen , Lin Lin , Hung Wei-Chun , Tseng Sung-Pin 
Published: February 2017

AbstractAntibiotic-resistant patterns, a mecA homologue complex, and staphylococcal cassette chromosome mec (SCCmec) were analysed in samples of ready-to-eat (RTE) street food in Taiwan. RTE food samples (270) were collected in three densely populated Taiwanese cities between June and November 2014. Among 14 strains being identified as methicillin-resistant coagulase-negative staphylococci (MRCoNS), genetic diversities was determined by PFGE analysis. SCCmec types IV, V, VIII and TXG-24 were detected in 9, and mecASs (a mecA homologue) detected in 8. The mecASs gene complex from S. sciuri subsp. sciuri TXG-24 was found to be closely related to those found in both S. sciuri subsp. sciuri (ATCC29062) and S. sciuri subsp. rodentium (ATCC700061). SCCmecTXG24 carries a class A mec complex, a ccrA5B3-like gene complex, a heavy metal gene complex, and an IS1216 mobile element carrying tet(S). Matching identity to ccrA5 was 84.5% for ccrA in S. pseudintermedius KM241. Matching identify to ccrB3 was 92.1% for ccrB in S. pseudintermedius AI16. Similar ccrA and SCCmec boundary sequences suggest that SCCmec is easily transmitted to coagulase-negative staphylococci (CoNS). Based on MRCoNS strains identified in this research, Taiwanese RTE food products likely carry multiple antibiotic resistance genes that can be transmitted to hospitals and other clinical settings.
Sirtuin1 protects endothelial Caveolin-1 expression and preserves endothelial function via suppressing miR-204 and endoplasmic reticulum stress
Authors: Kassan Modar , Vikram Ajit , Kim Young-Rae , Li Qiuxia , Kassan Adam , Patel Hemal H. , Kumar Santosh , Gabani Mohanad , Liu Jing , Jacobs Julia S. , Irani Kaikobad 
Published: February 2017

AbstractSirtuin1 (Sirt1) is a class III histone deacetylase that regulates a variety of physiological processes, including endothelial function. Caveolin1 (Cav1) is also an important determinant of endothelial function. We asked if Sirt1 governs endothelial Cav1 and endothelial function by regulating miR-204 expression and endoplasmic reticulum (ER) stress. Knockdown of Sirt1 in endothelial cells, and in vivo deletion of endothelial Sirt1, induced endothelial ER stress and miR-204 expression, reduced Cav1, and impaired endothelium-dependent vasorelaxation. All of these effects were reversed by a miR-204 inhibitor (miR-204 I) or with overexpression of Cav1. A miR-204 mimic (miR-204 M) decreased Cav1 in endothelial cells. In addition, high-fat diet (HFD) feeding induced vascular miR-204 and reduced endothelial Cav1. MiR-204-I protected against HFD-induced downregulation of endothelial Cav1. Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1. In conclusion, Sirt1 preserves Cav1-dependent endothelial function by mitigating miR-204-mediated vascular ER stress.