bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diet quality and its relationship with central obesity among Mexican Americans: findings from National Health and Nutrition Examination Survey (NHANES) 1999–2012
Authors: Yoshida Yilin , Scribner Richard , Chen Liwei , Broyles Stephanie , Phillippi Stephen , Tseng Tung-Sung 
Published: December 2016

AbstractObjectiveUsing the Healthy Eating Index-2010 (HEI-2010), the present study aimed to examine diet quality and the impact of overall diet quality and its components on central obesity among Mexican-American men and women.DesignCross-sectional data from NHANES 1999–2012 were used. The HEI-2010 data, including twelve components for a total score of 100, were collected with a 24 h recall interview. Central obesity was defined as a waist circumference of ≥88 cm for women and ≥102 cm for men. Weighted logistic regressions were performed to assess associations between HEI-2010 scores and central obesity.SettingNational Health and Nutrition Examination Survey (NHANES) 1999–2012.SubjectsA total of 6847 Mexican Americans aged ≥20 years with reliable dietary recall status and non-pregnancy status.ResultsHigher HEI-2010 total score was associated with lower odds of central obesity in Mexican-American men (OR; 95 % CI=0·98; 0·98, 1·00). Among all Mexican Americans, one-unit higher score of total fruit and sodium (i.e. lower level of intake) was associated with 4 % (0·96; 0·93, 0·99) and 2 % (0·98; 0·96, 0·99) lower odds of central obesity, respectively. However, a higher total proteins score was associated with higher odds of central obesity (1·08; 1·00, 1·16). In gender-specific analyses, a higher whole fruit or sodium score was inversely associated with central obesity in men but not in women.ConclusionsHEI-2010 scores of total fruit and sodium were inversely associated with central obesity among all Mexican Americans. However, total proteins score and central obesity was positively associated. In Mexican-American men, HEI-2010 total and whole fruit scores were inversely associated with central obesity.
Insight, self-stigma and psychosocial outcomes in Schizophrenia: a structural equation modelling approach
Authors: Lien Y.-J. , Chang H.-A. , Kao Y.-C. , Tzeng N.-S. , Lu C.-W. , Loh C.-H. 
Published: December 2016

Aims.Poor insight is prevalent in patients with schizophrenia and has been associated with acute illness severity, medication non-adherence and poor treatment outcomes. Paradoxically, high insight has been associated with various undesirable outcomes, including low self-esteem, depression and low subjective quality of life (QoL) in patients with schizophrenia. Despite the growing body of studies conducted in Western countries supporting the pernicious effects of improved insight in psychosis, which bases on the level of self-stigma, the effects are unclear in non-Western societies. The current study examined the role of self-stigma in the relationship between insight and psychosocial outcomes in a Chinese population.Methods.A total of 170 outpatients with schizophrenia spectrum disorders were recruited from two general university hospitals. Sociodemographic data and clinical variables were recorded and self-report scales were employed to measure self-stigma, depression, insight, self-esteem and subjective QoL. Structural equation modelling (SEM) was used to analyse the cross-sectional data.Results.High levels of self-stigma were reported by 39% of the participants (n = 67). The influences of insight, self-stigma, self-esteem and depression on subjective QoL were confirmed by the SEM results. Our model with the closest fit to the data (χ2 = 33.28; df = 20; p = 0.03; χ2/df = 1.66; CFI = 0.98; TLI = 0.97; RMSEA = 0.06) demonstrated that self-stigma might fully mediate the association of insight with low self-esteem, depression and poor subjective QoL. High insight into illness contributed to self-stigma, which caused low self-esteem and depression and, consequently, low QoL. Notably, insight did not directly affect self-esteem, depression or QoL. Furthermore, the association of insight with poor psychosocial outcomes was not moderated by self-stigma.Conclusions.Our findings support the mediating model of insight relevant to the poor psychosocial outcomes of individuals diagnosed with schizophrenia in non-Western societies, in which self-stigma plays a pivotal role. These findings elucidate the direct and indirect effects of insight on psychosocial outcomes and imply that identifying and correcting self-stigma in people with schizophrenia could be beneficial. Additional studies are required to identify whether several other neurocognitive or psychosocial variables mediate or moderate the association of insight with self-esteem, depression and QoL in patients with schizophrenia. Studies with detailed longitudinal assessments are necessary to confirm our findings.
Downregulated expression of microRNA-124 in pediatric intestinal failure patients modulates macrophages activation by inhibiting STAT3 and AChE
Authors: Xiao Yong-Tao , Wang Jun , Lu Wei , Cao Yi , Cai Wei 
Published: December 2016

AbstractIntestinal inflammation plays a critical role in the pathogenesis of intestinal failure (IF). The macrophages are essential to maintain the intestinal homeostasis. However, the underlying mechanisms of intestinal macrophages activation remain poorly understood. Since microRNAs (miRNAs) have pivotal roles in regulation of immune responses, here we aimed to investigate the role of miR-124 in the activation of intestinal macrophages. In this study, we showed that the intestinal macrophages increased in pediatric IF patients and resulted in the induction of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The miRNA fluorescence in situ hybridization analysis showed that the expression of miR-124 significantly reduced in intestinal macrophages in IF patients. Overexpression of miR-124 was sufficient to inhibit intestinal macrophages activation by attenuating production of IL-6 and TNF-α. Further studies showed that miR-124 could directly target the 3′-untranslated region of both signal transducer and activator of transcription 3 (STAT3) and acetylcholinesterase (AChE) mRNAs, and suppress their protein expressions. The AChE potentially negates the cholinergic anti-inflammatory signal by hydrolyzing the acetylcholine. We here showed that intestinal macrophages increasingly expressed the AChE and STAT3 in IF patients when compared with controls. The inhibitors against to STAT3 and AChE significantly suppressed the lipopolysaccharides-induced IL-6 and TNF-α production in macrophages. Taken together, these findings highlight an important role for miR-124 in the regulation of intestinal macrophages activation, and suggest a potential application of miR-124 in pediatric IF treatment regarding as suppressing intestinal inflammation.
Enhancing radiation tolerance by controlling defect mobility and migration pathways in multicomponent single-phase alloys
Authors: Lu Chenyang , Niu Liangliang , Chen Nanjun , Jin Ke , Yang Taini , Xiu Pengyuan , Zhang Yanwen , Gao Fei , Bei Hongbin , Shi Shi , He Mo-Rigen , Robertson Ian M. , Weber William J. , Wang Lumin 
Published: December 2016

AbstractA grand challenge in material science is to understand the correlation between intrinsic properties and defect dynamics. Radiation tolerant materials are in great demand for safe operation and advancement of nuclear and aerospace systems. Unlike traditional approaches that rely on microstructural and nanoscale features to mitigate radiation damage, this study demonstrates enhancement of radiation tolerance with the suppression of void formation by two orders magnitude at elevated temperatures in equiatomic single-phase concentrated solid solution alloys, and more importantly, reveals its controlling mechanism through a detailed analysis of the depth distribution of defect clusters and an atomistic computer simulation. The enhanced swelling resistance is attributed to the tailored interstitial defect cluster motion in the alloys from a long-range one-dimensional mode to a short-range three-dimensional mode, which leads to enhanced point defect recombination. The results suggest design criteria for next generation radiation tolerant structural alloys.
Ageing and brain white matter structure in 3,513 UK Biobank participants
Authors: Cox Simon R. , Ritchie Stuart J. , Tucker-Drob Elliot M. , Liewald David C. , Hagenaars Saskia P. , Davies Gail , Wardlaw Joanna M. , Gale Catharine R. , Bastin Mark E. , Deary Ian J. 
Published: December 2016

AbstractQuantifying the microstructural properties of the human brain’s connections is necessary for understanding normal ageing and disease. Here we examine brain white matter magnetic resonance imaging (MRI) data in 3,513 generally healthy people aged 44.64–77.12 years from the UK Biobank. Using conventional water diffusion measures and newer, rarely studied indices from neurite orientation dispersion and density imaging, we document large age associations with white matter microstructure. Mean diffusivity is the most age-sensitive measure, with negative age associations strongest in the thalamic radiation and association fibres. White matter microstructure across brain tracts becomes increasingly correlated in older age. This may reflect an age-related aggregation of systemic detrimental effects. We report several other novel results, including age associations with hemisphere and sex, and comparative volumetric MRI analyses. Results from this unusually large, single-scanner sample provide one of the most extensive characterizations of age associations with major white matter tracts in the human brain.
The in vivo hydrocarbon formation by vanadium nitrogenase follows a secondary metabolic pathway
Authors: Rebelein Johannes G. , Lee Chi Chung , Hu Yilin , Ribbe Markus W. 
Published: December 2016

AbstractThe vanadium (V)-nitrogenase of Azotobacter vinelandii catalyses the in vitro conversion of carbon monoxide (CO) to hydrocarbons. Here we show that an A. vinelandii strain expressing the V-nitrogenase is capable of in vivo reduction of CO to ethylene (C2H4), ethane (C2H6) and propane (C3H8). Moreover, we demonstrate that CO is not used as a carbon source for cell growth, being instead reduced to hydrocarbons in a secondary metabolic pathway. These findings suggest a possible role of the ancient nitrogenase as an evolutionary link between the carbon and nitrogen cycles on Earth and establish a solid foundation for biotechnological adaptation of a whole-cell approach to recycling carbon wastes into hydrocarbon products. Thus, this study has several repercussions for evolution-, environment- and energy-related areas.
Multivoxel neurofeedback selectively modulates confidence without changing perceptual performance
Authors: Cortese Aurelio , Amano Kaoru , Koizumi Ai , Kawato Mitsuo , Lau Hakwan 
Published: December 2016

AbstractA central controversy in metacognition studies concerns whether subjective confidence directly reflects the reliability of perceptual or cognitive processes, as suggested by normative models based on the assumption that neural computations are generally optimal. This view enjoys popularity in the computational and animal literatures, but it has also been suggested that confidence may depend on a late-stage estimation dissociable from perceptual processes. Yet, at least in humans, experimental tools have lacked the power to resolve these issues convincingly. Here, we overcome this difficulty by using the recently developed method of decoded neurofeedback (DecNef) to systematically manipulate multivoxel correlates of confidence in a frontoparietal network. Here we report that bi-directional changes in confidence do not affect perceptual accuracy. Further psychophysical analyses rule out accounts based on simple shifts in reporting strategy. Our results provide clear neuroscientific evidence for the systematic dissociation between confidence and perceptual performance, and thereby challenge current theoretical thinking.
Photonic Weyl point in a two-dimensional resonator lattice with a synthetic frequency dimension
Authors: Lin Qian , Xiao Meng , Yuan Luqi , Fan Shanhui 
Published: December 2016

AbstractWeyl points, as a signature of 3D topological states, have been extensively studied in condensed matter systems. Recently, the physics of Weyl points has also been explored in electromagnetic structures such as photonic crystals and metamaterials. These structures typically have complex three-dimensional geometries, which limits the potential for exploring Weyl point physics in on-chip integrated systems. Here we show that Weyl point physics emerges in a system of two-dimensional arrays of resonators undergoing dynamic modulation of refractive index. In addition, the phase of modulation can be controlled to explore Weyl points under different symmetries. Furthermore, unlike static structures, in this system the non-trivial topology of the Weyl point manifests in terms of surface state arcs in the synthetic space that exhibit one-way frequency conversion. Our system therefore provides a versatile platform to explore and exploit Weyl point physics on chip.
Heritability of the shape of subcortical brain structures in the general population
Authors: Roshchupkin Gennady V. , Gutman Boris A. , Vernooij Meike W. , Jahanshad Neda , Martin Nicholas G. , Hofman Albert , McMahon Katie L. , van der Lee Sven J. , van Duijn Cornelia M. , de Zubicaray Greig I. , Uitterlinden André G. , Wright Margaret J. , Niessen Wiro J. , Thompson Paul M. , Ikram M. Arfan , Adams Hieab H. H. 
Published: December 2016

AbstractThe volumes of subcortical brain structures are highly heritable, but genetic underpinnings of their shape remain relatively obscure. Here we determine the relative contribution of genetic factors to individual variation in the shape of seven bilateral subcortical structures: the nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen and thalamus. In 3,686 unrelated individuals aged between 45 and 98 years, brain magnetic resonance imaging and genotyping was performed. The maximal heritability of shape varies from 32.7 to 53.3% across the subcortical structures. Genetic contributions to shape extend beyond influences on intracranial volume and the gross volume of the respective structure. The regional variance in heritability was related to the reliability of the measurements, but could not be accounted for by technical factors only. These findings could be replicated in an independent sample of 1,040 twins. Differences in genetic contributions within a single region reveal the value of refined brain maps to appreciate the genetic complexity of brain structures.
A large-scale genome-wide association and meta-analysis identified four novel susceptibility loci for leprosy
Authors: Wang Zhenzhen , Sun Yonghu , Fu Xi’an , Yu Gongqi , Wang Chuan , Bao Fangfang , Yue Zhenhua , Li Jianke , Sun Lele , Irwanto Astrid , Yu Yongxiang , Chen Mingfei , Mi Zihao , Wang Honglei , Huai Pengcheng , Li Yi , Du Tiantian , Yu Wenjun , Xia Yang , Xiao Hailu , You Jiabao , Li Jinghui , Yang Qing , Wang Na , Shang Panpan , Niu Guiye , Chi Xiaojun , Wang Xiuhuan , Cao Jing , Cheng Xiujun , Liu Hong , Liu Jianjun , Zhang Furen 
Published: December 2016

AbstractLeprosy, a chronic infectious disease, results from the uncultivable pathogen Mycobacterium leprae (M. leprae), and usually progresses to peripheral neuropathy and permanent progressive deformity if not treated. Previously published genetic studies have identified 18 gene/loci significantly associated with leprosy at the genome-wide significant level. However as a complex disease, only a small proportion of leprosy risk could be explained by those gene/loci. To further identify more susceptibility gene/loci, we hereby performed a three-stage GWAS comprising 8,156 leprosy patients and 15,610 controls of Chinese ancestry. Four novel loci were identified including rs6807915 on 3p25.2 (P=1.94 × 10−8, OR=0.89), rs4720118 on 7p14.3 (P=3.85 × 10−10, OR=1.16), rs55894533 on 8p23.1 (P=5.07 × 10−11, OR=1.15) and rs10100465 on 8q24.11 (P=2.85 × 10−11, OR=0.85). Altogether, these findings have provided new insight and significantly expanded our understanding of the genetic basis of leprosy.
Temporal pairwise spike correlations fully capture single-neuron information
Authors: Dettner Amadeus , Münzberg Sabrina , Tchumatchenko Tatjana 
Published: December 2016

AbstractTo crack the neural code and read out the information neural spikes convey, it is essential to understand how the information is coded and how much of it is available for decoding. To this end, it is indispensable to derive from first principles a minimal set of spike features containing the complete information content of a neuron. Here we present such a complete set of coding features. We show that temporal pairwise spike correlations fully determine the information conveyed by a single spiking neuron with finite temporal memory and stationary spike statistics. We reveal that interspike interval temporal correlations, which are often neglected, can significantly change the total information. Our findings provide a conceptual link between numerous disparate observations and recommend shifting the focus of future studies from addressing firing rates to addressing pairwise spike correlation functions as the primary determinants of neural information.
Oscillatory integration windows in neurons
Authors: Gupta Nitin , Singh Swikriti Saran , Stopfer Mark 
Published: December 2016

AbstractOscillatory synchrony among neurons occurs in many species and brain areas, and has been proposed to help neural circuits process information. One hypothesis states that oscillatory input creates cyclic integration windows: specific times in each oscillatory cycle when postsynaptic neurons become especially responsive to inputs. With paired local field potential (LFP) and intracellular recordings and controlled stimulus manipulations we directly test this idea in the locust olfactory system. We find that inputs arriving in Kenyon cells (KCs) sum most effectively in a preferred window of the oscillation cycle. With a computational model, we show that the non-uniform structure of noise in the membrane potential helps mediate this process. Further experiments performed in vivo demonstrate that integration windows can form in the absence of inhibition and at a broad range of oscillation frequencies. Our results reveal how a fundamental coincidence-detection mechanism in a neural circuit functions to decode temporally organized spiking.
Evidence for spin-to-charge conversion by Rashba coupling in metallic states at the Fe/Ge(111) interface
Authors: Oyarzún S. , Nandy A. K. , Rortais F. , Rojas-Sánchez J.-C. , Dau M.-T. , Noël P. , Laczkowski P. , Pouget S. , Okuno H. , Vila L. , Vergnaud C. , Beigné C. , Marty A. , Attané J.-P. , Gambarelli S. , George J.-M. , Jaffrès H. , Blügel S. , Jamet M. 
Published: December 2016

AbstractThe spin–orbit coupling relating the electron spin and momentum allows for spin generation, detection and manipulation. It thus fulfils the three basic functions of the spin field-effect transistor. However, the spin Hall effect in bulk germanium is too weak to produce spin currents, whereas large Rashba effect at Ge(111) surfaces covered with heavy metals could generate spin-polarized currents. The Rashba spin splitting can actually be as large as hundreds of meV. Here we show a giant spin-to-charge conversion in metallic states at the Fe/Ge(111) interface due to the Rashba coupling. We generate very large charge currents by direct spin pumping into the interface states from 20 K to room temperature. The presence of these metallic states at the Fe/Ge(111) interface is demonstrated by first-principles electronic structure calculations. By this, we demonstrate how to take advantage of the spin–orbit coupling for the development of the spin field-effect transistor.
Hepatitis C Virus Infection of Cultured Human Hepatoma Cells Causes Apoptosis and Pyroptosis in Both Infected and Bystander Cells
Authors: Kofahi H. M. , Taylor N. G. A. , Hirasawa K. , Grant M. D. , Russell R. S. 
Published: December 2016

AbstractIndividuals infected with hepatitis C virus (HCV) are at high risk of developing progressive liver disease, including cirrhosis and hepatocellular carcinoma (HCC). How HCV infection causes liver destruction has been of significant interest for many years, and apoptosis has been proposed as one operative mechanism. In this study, we employed a tissue culture-adapted strain of HCV (JFH1T) to test effects of HCV infection on induction of programmed cell death (PCD) in Huh-7.5 cells. We found that HCV infection reduced the proliferation rate and induced caspase-3-mediated apoptosis in the infected cell population. However, in addition to apoptosis, we also observed infected cells undergoing caspase-1-mediated pyroptosis, which was induced by NLRP3 inflammasome activation. By co-culturing HCV-infected Huh-7.5 cells with an HCV-non-permissive cell line, we also demonstrated induction of both apoptosis and pyroptosis in uninfected cells. Bystander apoptosis, but not bystander pyroptosis, required cell-cell contact between infected and bystander cells. In summary, these findings provide new information on mechanisms of cell death in response to HCV infection. The observation that both apoptosis and pyroptosis can be induced in bystander cells extends our understanding of HCV-induced pathogenesis in the liver.
AECHL-1 targets breast cancer progression via inhibition of metastasis, prevention of EMT and suppression of Cancer Stem Cell characteristics
Authors: Dasgupta Aparajita , Sawant Mithila A. , Kavishwar Gayatri , Lavhale Manish , Sitasawad Sandhya 
Published: December 2016

AbstractTriple negative breast cancer (TNBC) features among the most aggressive manifestations of cancer due to its enhanced metastatic potential and immunity to therapeutics which target hormone receptors. Under such scenarios, anti-cancer compounds with an ability to influence multiple targets, or an entire process, will have an advantage over specific signal transduction inhibitors. To counter the metastatic threat it is essential to target cellular components central to the processes of cancer cell migration and adaptation. Our previous work on a novel triterpenoid, AECHL-1, explored its anti-cancer potential, and linked it to elevated ER stress in cancer cells, while its anti-angiogenic potential was credited for its ability to manipulate the cytoskeleton. Here, we broaden its range of action by showing that it curbs the metastatic ability of TNBC cells, bothin vitroin MDA-MB-231 cell line andin vivo, in mouse models of metastasis. AECHL-1 does so by disrupting the cytoskeletal network, and also suppressing NF-κB and β-Catenin mediated key molecular pathways. These activities also contributed to AECHL-1 mediated suppression of TGF-β/TNF-α induced Epithelial to Mesenchymal Transition (EMT) and cancer stem cell characteristic. Thus, we present AECHL-1 as a promising therapeutic inhibitor of metastatic disease.