bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gender differences in the prevalence of household food insecurity: a systematic review and meta-analysis
Authors: Jung Natália Miranda , de Bairros Fernanda Souza , Pattussi Marcos Pascoal , Pauli Sílvia , Neutzling Marilda Borges 
Published: November 2016

AbstractObjectiveThe present review aimed to identify and synthesize literature on household food insecurity with respect to whether the respondent was male or female.DesignA systematic review of prevalence studies followed by a meta-analysis was conducted between 28 August 2014 and 19 October 2014 in seven electronic databases. The search was updated in April 2016. The included studies used experience-based measures to assess household food insecurity. Dichotomous measures of food insecurity were used. Pooled odds ratios of household food insecurity prevalence in women v. men were obtained through random-effect modelling. Quality assessment, publication bias diagnostics and subgroup analysis were also performed.SettingPopulation-based studies (i.e. non-clinical populations).SubjectsParticipants aged 18 years or over.ResultsOut of the 5145 articles initially identified, forty-two studies with a total population of 233 153 were included. In general, results showed that the odds for household food insecurity was 40 % higher in studies where women were the respondent (95 % CI 1·27, 1·54; P<0·001). Besides, subgroup analysis revealed that female-headed households were 75% (95 % CI 49–96%) more likely to be food insecure than male-headed households.ConclusionsOur results confirm the existence of gender differences in reporting household food insecurity. Furthermore, they indicate that households headed by women constitute a segment of the population that is particularly vulnerable to food insecurity.
Reed-Sternberg cells in Hodgkin’s lymphoma present features of cellular senescence
Authors: Gopas J , Stern E , Zurgil U , Ozer J , Ben-Ari A , Shubinsky G , Braiman A , Sinay R , Ezratty J , Dronov V , Balachandran S , Benharroch D , Livneh E 
Published: November 2016

AbstractHodgkin’s Lymphoma (HL) is one of the most prevailing malignancies in young adults. Reed–Sternberg (RS) cells in HL have distinctive large cell morphology, are characteristic of the disease and their presence is essential for diagnosis. Enlarged cells are one of the hallmarks of senescence, but whether RS cells are senescent has not been previously investigated. Here we show that RS cells have characteristics of senescent cells; RS cells in HL biopsies specifically express the senescence markers and cell cycle inhibitors p21Cip1 and p16INK4a and are negative for the proliferation marker Ki-67, suggesting that these cells have ceased to proliferate. Moreover, the RS-like cells in HL lines, stained specifically for senescence-associated β-galactosidase (SA-β-gal). Oxidative stress promoted senescence in these cells as demonstrated by their staining for p21Cip1, p16INK4a, p53 and γH2AX. Senescent cells produce copious amounts of inflammatory cytokines termed ‘senescence-associated secretory phenotype’ (SASP), primarily regulated by Nuclear Factor κB (NF-κB). Indeed, we show that NF-κB activity and NF-κB-dependent cytokines production (e.g., IL-6, TNF-α, GM-CSF) were elevated in RS-like cells. Furthermore, NF-κB inhibitors, JSH-23 and curcumin reduced IL-6 secretion from RS-like cells. Thus, defining RS cells as senescent offers new insights on the origin of the proinflammatory microenvironment in HL.
Tissue-type plasminogen activator controls neuronal death by raising surface dynamics of extrasynaptic NMDA receptors
Authors: Lesept Flavie , Chevilley Arnaud , Jezequel Julie , Ladépêche Laurent , Macrez Richard , Aimable Margaux , Lenoir Sophie , Bertrand Thomas , Rubrecht Laëtitia , Galea Pascale , Lebouvier Laurent , Petersen Karl-Uwe , Hommet Yannick , Maubert Eric , Ali Carine , Groc Laurent , Vivien Denis 
Published: November 2016

AbstractN-methyl-d-aspartate receptors (NMDARs) are ion channels whose synapticversusextrasynaptic localization critically influences their functions. This distribution of NMDARs is highly dependent on their lateral diffusion at the cell membrane. Each obligatory subunit of NMDARs (GluN1 and GluN2) contains two extracellular clamshell-like domains with an agonist-binding domain and a distal N-terminal domain (NTD). To date, the roles and dynamics of the NTD of the GluN1 subunit in NMDAR allosteric signaling remain poorly understood. Using single nanoparticle tracking in mouse neurons, we demonstrate that the extracellular neuronal protease tissue-type plasminogen activator (tPA), well known to have a role in the synaptic plasticity and neuronal survival, leads to a selective increase of the surface dynamics and subsequent diffusion of extrasynaptic NMDARs. This process explains the previously reported ability of tPA to promote NMDAR-mediated calcium influx. In parallel, we developed a monoclonal antibody capable of specifically blocking the interaction of tPA with the NTD of the GluN1 subunit of NMDAR. Using this original approach, we demonstrate that the tPA binds the NTD of the GluN1 subunit at a lysine in position 178. Accordingly, when applied to mouse neurons, our selected antibody (named Glunomab) leads to a selective reduction of the tPA-mediated surface dynamics of extrasynaptic NMDARs, subsequent signaling and neurotoxicity, bothin vitroandin vivo. Altogether, we demonstrate that the tPA is a ligand of the NTD of the obligatory GluN1 subunit of NMDAR acting as a modulator of their dynamic distribution at the neuronal surface and subsequent signaling.
Epidermal-specific deletion of CD44 reveals a function in keratinocytes in response to mechanical stress
Authors: Shatirishvili M , Burk A S , Franz C M , Pace G , Kastilan T , Breuhahn K , Hinterseer E , Dierich A , Bakiri L , Wagner E F , Ponta H , Hartmann T N , Tanaka M , Orian-Rousseau V 
Published: November 2016

AbstractCD44, a large family of transmembrane glycoproteins, plays decisive roles in physiological and pathological conditions. CD44 isoforms are involved in several signaling pathways essential for life such as growth factor-induced signaling by EGF, HGF or VEGF. CD44 is also the main hyaluronan (HA) receptor and as such is involved in HA-dependent processes. To allow a genetic dissection of CD44 functions in homeostasis and disease, we generated a Cd44 floxed allele allowing tissue- and time-specific inactivation of all CD44 isoforms in vivo. As a proof of principle, we inactivated Cd44 in the skin epidermis using the K14Cre allele. Although the skin of such Cd44Δker mutants appeared morphologically normal, epidermal stiffness was reduced, wound healing delayed and TPA induced epidermal thickening decreased. These phenotypes might be caused by cell autonomous defects in differentiation and HA production as well as impaired adhesion and migration on HA by Cd44Δker keratinocytes. These findings support the usefulness of the conditional Cd44 allele in unraveling essential physiological and pathological functions of CD44 isoforms.
Knockout of Ccr2 alleviates photoreceptor cell death in rodent retina exposed to chronic blue light
Authors: Hu Zizhong , Zhang Yi , Wang Junling , Mao Pingan , Lv Xuehua , Yuan Songtao , Huang Zhengru , Ding Yuzhi , Xie Ping , Liu Qinghuai 
Published: November 2016

AbstractAge-related macular degeneration (AMD), the leading cause of visual loss after the age of 60 years, is a degenerative retinal disease involving a variety of environmental and hereditary factors. Although it has been implicated that immune system is involved in the disease progression, the exact role that microglia has is still unclear. Here we demonstrated that knockout of Ccr2 gene could alleviate photoreceptor cell death in mice retinas exposed to chronic blue light. In Ccr2−/− mice, a damaged microglia recruitment was shown in retina and this could protect the visual function in electroretinogram and alleviate the photoreceptor apoptosis, which thus helped attenuate the blue light-induced retinopathy. We further found an increased co-location of NLRP3, Iba-1, and IL-1β in fluorescence and a concomitant increased protein expression of NLRP3, caspase-1, and IL-1β in western blotting in chronic blue light-induced retinopathy. Moreover, the activation of microglia and their cellular NLRP3 inflammasomes occurred as an earlier step before the structural and functional damage of the mice retinas, which collectively supported that microglial NLRP3 inflammasome might be the key to the chronic blue light-induced retinopathy.
Skin-derived stem cells as a source of primordial germ cell- and oocyte-like cells
Authors: Ge Wei , Cheng Shun-Feng , Dyce Paul W , De Felici Massimo , Shen Wei 
Published: November 2016

AbstractThe skin is a unique organ that contains a variety of stem cells for the maintenance of skin homeostasis and the repair of skin tissues following injury and disease. Skin-derived stem cells (SDSCs) constitute a heterogeneous population of stem cells generated in vitro from dermis, which can be cultured as spherical aggregates of cells in suspension culture. Under certain in vitro or in vivo conditions, SDSCs show multipotency and can generate a variety of neural, mesodermal, and endodermal cell types such as neurons, glia, fibroblasts, adipocytes, muscle cells, chondroblasts, osteoblats, and islet β-cell-like cells. SDSCs are likely derived from multipotent stem cells located in the hair follicles that are, in turn, derived from embryonic migratory neural crest or mesoderm cells. During the past decade, a wave of reports have shown that germ cells can be generated from various types of stem cells. It has been shown that SDSCs are able to produce primordial germ cell-like cells in vitro, and even oocyte-like cells (OLCs). Whether these germ cell-like cells (GCLCs) can give rise to viable progeny remains, however, unknown. In this review, we will discuss the origin and characteristics of SDSCs from which the GCLC are derived, the possible mechanisms of this differentiation process, and finally the prospective biomedical applications of the SDSC-derived GCLCs.
Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3
Authors: Ao Xiang , Nie Peipei , Wu Baoyan , Xu Wei , Zhang Tao , Wang Songmao , Chang Haocai , Zou Zhengzhi 
Published: November 2016

AbstractChemoresistance is a major obstacle to effective breast cancer chemotherapy. However, the underlying molecular mechanisms remain unclear. In this study, nuclear receptor coactivator 3 (NCOA3) was found to be significantly increased in taxol-resistant breast cancer tissues and cells. Moreover, overexpression of NCOA3 enhanced breast cancer cell resistance to taxol, whereas depletion of NCOA3 decreased taxol resistance. Subsequently, we investigated whether NCOA3 expression was regulated by miRNAs in breast cancer. By bioinformatics prediction in combination with the data of previous report, miR-17 and miR-20b were selected as the potential miRNAs targeting NCOA3. By real-time PCR analysis, we found that miR-17 and miR-20b were significantly reduced in taxol-resistant breast cancer tissues and cells. In addition, we provided some experimental evidences that miR-17 and miR-20b attenuated breast cancer resistance to taxolin vitroandin vivomodels. Furthermore, by luciferase reporter assays, we further validated that both miR-17 and miR-20b directly binded the 3′-untranslated region ofNCOA3mRNA and inhibited its expression in breast cancer cells. Finally, both miR-17 and miR-20b levels were found to be significantly negatively correlated withNCOA3mRNA levels in breast cancer tissues. Together, our results indicated that loss of miR-17 and miR-20b enhanced breast cancer resistance to taxol by upregulating NCOA3 levels. Our study suggested miR-17, miR-20b and NCOA3 may serve as some predictive biomarkers and potential therapeutic targets in taxol-resistant breast cancer treatment.
ERK/Drp1-dependent mitochondrial fission is involved in the MSC-induced drug resistance of T-cell acute lymphoblastic leukemia cells
Authors: Cai Jianye , Wang Jiancheng , Huang Yinong , Wu Haoxiang , Xia Ting , Xiao Jiaqi , Chen Xiaoyong , Li Hongyu , Qiu Yuan , Wang Yingnan , Wang Tao , Xia Huimin , Zhang Qi , Xiang Andy Peng 
Published: November 2016

AbstractThe bone marrow microenvironment facilitates the proliferation and survival of leukemia cells, contributing to disease relapse. Bone marrow-derived mesenchymal stem cells (MSCs) are well known to promote cancer chemoresistance via soluble factors and cell adhesion. However, little is known about the effects of MSCs on the mitochondrial dynamics of T-cell acute lymphoblastic leukemia (T-ALL) cells, or how this may influence the chemoresistance of these cells. Here, we tested both indirect (Transwell) and direct coculture strategies, and found that MSCs protected T-ALL cells from chemotherapeutic cell death and cytotoxicity under both culture conditions. In addition, cell viability was higher in the direct contact system compared with the Transwell system. We further showed that exposure of T-ALL cells to MSCs decreased mitochondrial reactive oxygen species (ROS) levels and promoted a pro-glycolytic shift that was characterized by increased glucose uptake and lactate production with concomitant reductions in adenosine triphosphate production and mitochondrial membrane potential. In T-ALL cells cocultured with MSCs, the mitochondrial morphology of T-ALL cells were altered from elongation to fragmentation because of the extracellular signal-regulated kinase activation-mediated phosphorylation of the pro-fission factor, dynamin-related protein 1 (Drp1), at residue S616. Consistent with this, the expression of S616-phosphorylated Drp1 recapitulated the mitochondrial dynamics, mitochondrial ROS levels, metabolic switching and chemoresistance seen in T-ALL cells cocultured with MSCs. These findings suggest that the ability of MSCs to trigger Drp1 activation-induced changes in mitochondrial dynamics is crucial to their ability to protect cells against chemotherapeutic agents.
High-energy electron emission from metallic nano-tips driven by intense single-cycle terahertz pulses
Authors: Li Sha , Jones R. R. 
Published: November 2016

AbstractElectrons ejected from atoms and subsequently driven to high energies in strong laser fields enable techniques from attosecond pulse generation to imaging with rescattered electrons. Analogous processes govern strong-field electron emission from nanostructures, where long wavelength radiation and large local field enhancements hold the promise for producing electrons with substantially higher energies, allowing for higher resolution time-resolved imaging. Here we report on the use of single-cycle terahertz pulses to drive electron emission from unbiased nano-tips. Energies exceeding 5 keV are observed, substantially greater than previously attained at higher drive frequencies. Despite large differences in the magnitude of the respective local fields, we find that the maximum electron energies are only weakly dependent on the tip radius, for 10 nm<R<1,000 nm. Due to the single-cycle nature of the field, the high-energy electron emission is predicted to be confined to a single burst, potentially enabling a variety of applications.
Structure-conserving spontaneous transformations between nanoparticles
Authors: Krishnadas K. R. , Baksi Ananya , Ghosh Atanu , Natarajan Ganapati , Pradeep Thalappil 
Published: November 2016

AbstractAmbient, structure- and topology-preserving chemical reactions between two archetypal nanoparticles, Ag25(SR)18 and Au25(SR)18, are presented. Despite their geometric robustness and electronic stability, reactions between them in solution produce alloys, AgmAun(SR)18 (m+n=25), keeping their M25(SR)18 composition, structure and topology intact. We demonstrate that a mixture of Ag25(SR)18 and Au25(SR)18 can be transformed to any arbitrary alloy composition, AgmAun(SR)18 (n=1–24), merely by controlling the reactant compositions. We capture one of the earliest events of the process, namely the formation of the dianionic adduct, (Ag25Au25(SR)36)2−, by electrospray ionization mass spectrometry. Molecular docking simulations and density functional theory (DFT) calculations also suggest that metal atom exchanges occur through the formation of an adduct between the two clusters. DFT calculations further confirm that metal atom exchanges are thermodynamically feasible. Such isomorphous transformations between nanoparticles imply that microscopic pieces of matter can be transformed completely to chemically different entities, preserving their structures, at least in the nanometric regime.
Spin exchange broadening of magnetic resonance lines in a high-sensitivity rotating K-Rb-21Ne co-magnetometer
Authors: Chen Yao , Quan Wei , Zou Sheng , Lu Yan , Duan Lihong , Li Yang , Zhang Hong , Ding Ming , Fang Jiancheng 
Published: November 2016

AbstractAtomic co-magnetometers can be utilized for high-precision angular velocity sensing or fundamental physics tests. The sensitivity of a co-magnetometer determines the angle random walk of an angular velocity sensor and the detection limit for a fundamental physics test. A high-sensitivity K-Rb-21Ne co-magnetometer, which is utilized for angular velocity sensing, is presented in this paper. A new type of spin relaxation of Rb atom spins, which can broaden the zero-field magnetic resonance lines of the co-magnetometer, is discovered. Further studies show that the spin relaxation of Rb atoms is caused by a high Rb electron magnetization field. With this discovery, the total relaxation rate of Rb atoms is optimized to improve the sensitivity of the co-magnetometer. Moreover, its sensitivity is optimized by suppressing various noises. Especially, to suppress laser-related noises, the co-magnetometer is designed such that the sensitive axis of the co-magnetometer can be fixed to the direction in which the projection input of the earth’s rotation is 0. This is called a rotating co-magnetometer. A magnetic field sensitivity of 1.0 fT/Hz−1/2@5 Hz, which is equal to an angular velocity sensitivity of 2.1 × 10−8 rad s−1 Hz−1/2@5 Hz, is demonstrated using a spherical vapour cell with a diameter of 14 mm.
Meta-analysis of gene expression studies in endometrial cancer identifies gene expression profiles associated with aggressive disease and patient outcome
Authors: O’Mara Tracy A. , Zhao Min , Spurdle Amanda B. 
Published: November 2016

AbstractAlthough endometrioid endometrial cancer (EEC; comprising ~80% of all endometrial cancers diagnosed) is typically associated with favourable patient outcome, a significant portion (~20%) of women with this subtype will relapse. We hypothesised that gene expression predictors of the more aggressive non-endometrioid endometrial cancers (NEEC) could be used to predict EEC patients with poor prognosis. To explore this hypothesis, we performed meta-analysis of 12 gene expression microarray studies followed by validation using RNA-Seq data from The Cancer Genome Atlas (TCGA) and identified 1,253 genes differentially expressed between EEC and NEEC. Analysis found 121 genes were associated with poor outcome among EEC patients. Forward selection likelihood-based modelling identified a 9-gene signature associated with EEC outcome in our discovery RNA-Seq dataset which remained significant after adjustment for clinical covariates, but was not significant in a smaller RNA-Seq dataset. Our study demonstrates the value of employing meta-analysis to improve the power of gene expression microarray data, and highlight genes and molecular pathways of importance for endometrial cancer therapy.
Novel Agonist Bioisosteres and Common Structure-Activity Relationships for The Orphan G Protein-Coupled Receptor GPR139
Authors: Shehata Mohamed A. , Nøhr Anne C. , Lissa Delphine , Bisig Christoph , Isberg Vignir , Andersen Kirsten B. , Harpsøe Kasper , Björkling Fredrik , Bräuner-Osborne Hans , Gloriam David E. 
Published: November 2016

AbstractGPR139 is an orphan class A G protein-coupled receptor found mainly in the central nervous system. It has its highest expression levels in the hypothalamus and striatum, regions regulating metabolism and locomotion, respectively, and has therefore been suggested as a potential target for obesity and Parkinson’s disease. The two aromatic amino acids L-Trp and L-Phe have been proposed as putative endogenous agonists, and three structurally related benzohydrazide, glycine benzamide, and benzotriazine surrogate agonist series have been published. Herein, we assayed 158 new analogues selected from a pharmacophore model, and identified 12 new GPR139 agonists, containing previously untested bioisosteres. Furthermore, we present the first combined structure-activity relationships, and a refined pharmacophore model to serve as a rationale for future ligand identification and optimization.
Suilysin-induced Platelet-Neutrophil Complexes Formation is Triggered by Pore Formation-dependent Calcium Influx
Authors: Zhang Shengwei , Zheng Yuling , Chen Shaolong , Huang Shujing , Liu Keke , Lv Qingyu , Jiang Yongqiang , Yuan Yuan 
Published: November 2016

AbstractPlatelet activation and platelet–neutrophil interactions have been found to be involved in inflammation, organ failure and soft-tissue necrosis in bacterial infections. Streptococcus suis, an emerging human pathogen, can cause streptococcal toxic-shock syndrome (STSS) similarly to Streptococcus pyogenes. Currently, S. suis–platelet interactions are poorly understood. Here, we found that suilysin (SLY), the S. suis cholesterol-dependent cytolysin (CDC), was the sole stimulus of S. suis that induced platelet-neutrophil complexes (PNC) formation. Furthermore, P-selectin released in α-granules mediated PNC formation. This process was triggered by the SLY-induced pore forming-dependent Ca2+ influx. Moreover, we demonstrated that the Ca2+ influx triggered an MLCK-dependent pathway playing critical roles in P-selectin activation and PNC formation, however, PLC-β-IP3/DAG-MLCK and Rho-ROCK-MLCK signalling were not involved. Additionally, the “outside-in” signalling had a smaller effect on the SLY-induced P-selectin release and PNC formation. Interestingly, other CDCs including pneumolysin and streptolysin O have also been found to induce PNC formation in a pore forming-dependent Ca2+ influx manner. It is possible that the bacterial CDC-mediated PNC formation is a similar response mechanism used by a wide range of bacteria. These findings may provide useful insight for discovering potential therapeutic targets for S. suis-associated STSS.
Effect of nematic ordering on electronic structure of FeSe
Authors: Fedorov A. , Yaresko A. , Kim T. K. , Kushnirenko Y. , Haubold E. , Wolf T. , Hoesch M. , Grüneis A. , Büchner B. , Borisenko S. V. 
Published: November 2016

AbstractElectronically driven nematic order is often considered as an essential ingredient of high-temperature superconductivity. Its elusive nature in iron-based superconductors resulted in a controversy not only as regards its origin but also as to the degree of its influence on the electronic structure even in the simplest representative material FeSe. Here we utilized angle-resolved photoemission spectroscopy and density functional theory calculations to study the influence of the nematic order on the electronic structure of FeSe and determine its exact energy and momentum scales. Our results strongly suggest that the nematicity in FeSe is electronically driven, we resolve the recent controversy and provide the necessary quantitative experimental basis for a successful theory of superconductivity in iron-based materials which takes into account both, spin-orbit interaction and electronic nematicity.