bluuebunny/crossref_metadata_2025_split huggingface dataset:
Childhood maltreatment and cognitive functioning: the role of depression, parental education, and polygenic predisposition
Authors: Goltermann Janik , Redlich Ronny , Grotegerd Dominik , Dohm Katharina , Leehr Elisabeth J. , Böhnlein Joscha , Förster Katharina , Meinert Susanne , Enneking Verena , Richter Maike , Repple Jonathan , DeVillers Immanuel , Kloecker Marine , Jansen Andreas , Krug Axel , Nenadić Igor , Brosch Katharina , Meller Tina , Stein Frederike , Schmitt Simon , Rietschel Marcella , Streit Fabian , Witt Stephanie H. , Forstner Andreas J. , Nöthen Markus M. , Baune Bernhard T. , Andlauer Till F. M. , Kircher Tilo , Opel Nils , Dannlowski Udo 
Published: August 2020

AbstractChildhood maltreatment is associated with cognitive deficits that in turn have been predictive for therapeutic outcome in psychiatric patients. However, previous studies have either investigated maltreatment associations with single cognitive domains or failed to adequately control for confounders such as depression, socioeconomic environment, and genetic predisposition. We aimed to isolate the relationship between childhood maltreatment and dysfunction in diverse cognitive domains, while estimating the contribution of potential confounders to this relationship, and to investigate gene–environment interactions. We included 547 depressive disorder and 670 healthy control participants (mean age: 34.7 years, SD = 13.2). Cognitive functioning was assessed for the domains of working memory, executive functioning, processing speed, attention, memory, and verbal intelligence using neuropsychological tests. Childhood maltreatment and parental education were assessed using self-reports, and psychiatric diagnosis was based on DSM-IV criteria. Polygenic scores for depression and for educational attainment were calculated. Multivariate analysis of cognitive domains yielded significant associations with childhood maltreatment (η²p = 0.083,P < 0.001), depression (η²p = 0.097,P < 0.001), parental education (η²p = 0.085,P < 0.001), and polygenic scores for depression (η²p = 0.021,P = 0.005) and educational attainment (η²p = 0.031,P < 0.001). Each of these associations remained significant when including all of the predictors in one model. Univariate tests revealed that maltreatment was associated with poorer performance in all cognitive domains. Thus, environmental, psychopathological, and genetic risk factors each independently affect cognition. The insights of the current study may aid in estimating the potential impact of different loci of interventions for cognitive dysfunction. Future research should investigate if customized interventions, informed by individual risk profiles and related cognitive preconditions, might enhance response to therapeutic treatments.
Adaptive immune responses to SARS-CoV-2 infection in severe versus mild individuals
Authors: Zhang Fan , Gan Rui , Zhen Ziqi , Hu Xiaoli , Li Xiang , Zhou Fengxia , Liu Ying , Chen Chuangeng , Xie Shuangyu , Zhang Bailing , Wu Xiaoke , Huang Zhiwei 
Published: August 2020

AbstractThe global Coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has affected more than eight million people. There is an urgent need to investigate how the adaptive immunity is established in COVID-19 patients. In this study, we profiled adaptive immune cells of PBMCs from recovered COVID-19 patients with varying disease severity using single-cell RNA and TCR/BCR V(D)J sequencing. The sequencing data revealed SARS-CoV-2-specific shuffling of adaptive immune repertories and COVID-19-induced remodeling of peripheral lymphocytes. Characterization of variations in the peripheral T and B cells from the COVID-19 patients revealed a positive correlation of humoral immune response and T-cell immune memory with disease severity. Sequencing and functional data revealed SARS-CoV-2-specific T-cell immune memory in the convalescent COVID-19 patients. Furthermore, we also identified novel antigens that are responsive in the convalescent patients. Altogether, our study reveals adaptive immune repertories underlying pathogenesis and recovery in severe versus mild COVID-19 patients, providing valuable information for potential vaccine and therapeutic development against SARS-CoV-2 infection.
Membranous NOX5-derived ROS oxidizes and activates local Src to promote malignancy of tumor cells
Authors: Chen Jie , Wang Yan , Zhang Weimin , Zhao Di , Zhang Lingyuan , Fan Jiawen , Li Jinting , Zhan Qimin 
Published: August 2020

AbstractReactive oxygen species (ROS) localized at the precise subcellular compartments are essential for regulating the activity of signaling proteins. Furthermore, ROS are master regulators of tumor malignant progression that respond to a diverse set of environmental stress, especially hypoxia. NADPH oxidases (NOXs) appear to be activated within discrete subcellular compartments to facilitate local ROS production. However, the subcellular function of NOXs in hypoxic tumor is still unclear. In this study, we demonstrated that NOX5 was greatly upregulated in clinical esophageal squamous cell carcinoma (ESCC) tumors, ESCC cell lines or primary ESCC cells, and elevated NOX5 was correlated to malignancy of ESCC tumors and poor prognosis. NOX5 induced the malignant progression of ESCC by activating Src, especially under hypoxic condition. Mechanistically, we showed that hypoxia promoted the interaction between NOX5 and Pyk2 on cell membrane via facilitating Ca2+-mediated Pyk2 Tyr402 site phosphorylation. Subsequently, Pyk2 acted as a scaffold for c-Abl phosphorylating the catalytic domain of NOX5 Tyr476/478 sites, which in turn upregulated hydrogen peroxide (H2O2) inside the Pyk2/NOX5 complex to oxidize and activate local Src. These findings provide insights into the biological significance of NOX5 in the development of ESCC.
Oxidized-LDL inhibits testosterone biosynthesis by affecting mitochondrial function and the p38 MAPK/COX-2 signaling pathway in Leydig cells
Authors: Jing Jun , Ding Ning , Wang Dandan , Ge Xie , Ma Jinzhao , Ma Rujun , Huang Xuan , Jueraitetibaike Kadiliya , Liang Kuan , Wang Shuxian , Cao Siyuan , Zhao Allan Zijian , Yao Bing 
Published: August 2020

AbstractAbnormal lipid/lipoprotein metabolism induced by obesity may affect spermatogenesis by inhibiting testosterone synthesis in Leydig cells. It is crucial to determine which components of lipoproteins inhibit testosterone synthesis. Circulating oxidized low-density lipoprotein (oxLDL), the oxidized form of LDL, has been reported to be an independent risk factor for decreased serum testosterone levels. However, whether oxLDL has a damaging effect on Leydig cell function and the detailed mechanisms have been rarely studied. This study first showed the specific localization of oxLDL and mitochondrial structural damage in testicular Leydig cells of high-fat diet-fed mice in vivo. We also found that oxLDL reduced the mitochondrial membrane potential (MMP) by disrupting electron transport chain and inhibited testosterone synthesis-related proteins and enzymes (StAR, P450scc, and 3β‑HSD), which ultimately led to mitochondrial dysfunction and decreased testosterone synthesis in Leydig cells. Further experiments demonstrated that oxLDL promoted lipid uptake and mitochondrial dysfunction by inducing CD36 transcription. Meanwhile, oxLDL facilitated COX2 expression through the p38 MAPK signaling pathway in Leydig cells. Blockade of COX-2 attenuated the oxLDL-induced decrease in StAR and P450scc. Our clinical results clarified that the increased serum oxLDL level was associated with a decline in circulating testosterone levels. Our findings amplify the damaging effects of oxLDL and provide the first evidence that oxLDL is a novel metabolic biomarker of male-acquired hypogonadism caused by abnormal lipid metabolism.
Antifungal drug miconazole ameliorated memory deficits in a mouse model of LPS-induced memory loss through targeting iNOS
Authors: Yeo In Jun , Yun Jaesuk , Son Dong Ju , Han Sang-Bae , Hong Jin Tae 
Published: August 2020

AbstractAlzheimer’s disease (AD) is closely related to neuroinflammation, and the increase in inflammatory cytokine generation and inducible nitric oxide synthase (iNOS) expression in the brain of a patient with AD is well known. Excessive cytokines can stimulate iNOS in microglia and astroglia and overproduce nitric oxide, which can be toxic to neurons. The disease–gene–drug network analysis based on the GWAS/OMIM/DEG records showed that miconazole (MCZ) affected AD through interactions with NOS. Inhibiting iNOS can reduce neuroinflammation, thus preventing AD progression. To investigate the prophylactic role of antifungal agent in the AD development, a lipopolysaccharide-induced memory disorder mouse model was used, and cognitive function was assessed by Morris water maze test and passive avoidance test. MCZ treatment significantly attenuated cognitive impairment, suppressed iNOS and cyclooxygenase-2 expression, and activation of astrocyte and microglial BV2 cells, as well as reduced cytokine levels in the brains and lipopolysaccharide-treated astrocytes and microglia BV2 cells. In further mechanism studies, Pull-down assay and iNOS luciferase activity data showed that MCZ binds to iNOS and inhibited transcriptional activity. Our results suggest that MCZ is useful for ameliorating the neuroinflammation-mediated AD progression by blocking iNOS expression.
Mechanism of ribosome rescue by alternative ribosome-rescue factor B
Authors: Chan Kai-Hsin , Petrychenko Valentyn , Mueller Claudia , Maracci Cristina , Holtkamp Wolf , Wilson Daniel N. , Fischer Niels , Rodnina Marina V. 
Published: August 2020

AbstractAlternative ribosome-rescue factor B (ArfB) rescues ribosomes stalled on non-stop mRNAs by releasing the nascent polypeptide from the peptidyl-tRNA. By rapid kinetics we show that ArfB selects ribosomes stalled on short truncated mRNAs, rather than on longer mRNAs mimicking pausing on rare codon clusters. In combination with cryo-electron microscopy we dissect the multistep rescue pathway of ArfB, which first binds to ribosomes very rapidly regardless of the mRNA length. The selectivity for shorter mRNAs arises from the subsequent slow engagement step, as it requires longer mRNA to shift to enable ArfB binding. Engagement results in specific interactions of the ArfB C-terminal domain with the mRNA entry channel, which activates peptidyl-tRNA hydrolysis by the N-terminal domain. These data reveal how protein dynamics translate into specificity of substrate recognition and provide insights into the action of a putative rescue factor in mitochondria.
Single cell electron collectors for highly efficient wiring-up electronic abiotic/biotic interfaces
Authors: Yu Yang-Yang , Wang Yan-Zhai , Fang Zhen , Shi Yu-Tong , Cheng Qian-Wen , Chen Yu-Xuan , Shi Weidong , Yong Yang-Chun 
Published: August 2020

AbstractBy electronically wiring-up living cells with abiotic conductive surfaces, bioelectrochemical systems (BES) harvest energy and synthesize electric-/solar-chemicals with unmatched thermodynamic efficiency. However, the establishment of an efficient electronic interface between living cells and abiotic surfaces is hindered due to the requirement of extremely close contact and high interfacial area, which is quite challenging for cell and material engineering. Herein, we propose a new concept of a single cell electron collector, which isin-situbuilt with an interconnected intact conductive layer on and cross the individual cell membrane. The single cell electron collector forms intimate contact with the cellular electron transfer machinery and maximizes the interfacial area, achieving record-high interfacial electron transfer efficiency and BES performance. Thus, this single cell electron collector provides a superior tool to wire living cells with abiotic surfaces at the single-cell level and adds new dimensions for abiotic/biotic interface engineering.
Life histories determine divergent population trends for fishes under climate warming
Authors: Wang Hui-Yu , Shen Sheng-Feng , Chen Ying-Shiuan , Kiang Yun-Kae , Heino Mikko 
Published: August 2020

AbstractMost marine fish species express life-history changes across temperature gradients, such as faster growth, earlier maturation, and higher mortality at higher temperature. However, such climate-driven effects on life histories and population dynamics remain unassessed for most fishes. For 332 Indo-Pacific fishes, we show positive effects of temperature on body growth (but with decreasing asymptotic length), reproductive rates (including earlier age-at-maturation), and natural mortality for all species, with the effect strength varying among habitat-related species groups. Reef and demersal fishes are more sensitive to temperature changes than pelagic and bathydemersal fishes. Using a life table, we show that the combined changes of life histories upon increasing temperature tend to facilitate population growth for slow life-history populations, but reduce it for fast life-history ones. Within our data, lower proportions (25–30%) of slow life-history fishes but greater proportions of fast life-history fishes (42–60%) show declined population growth rates under 1 °C warming. Together, these findings suggest prioritizing sustainable management for fast life-history species.
Reassessment of the distinctive geometry of Staphylococcus aureus cell division
Authors: Saraiva Bruno M. , Sorg Moritz , Pereira Ana R. , Ferreira Mário J. , Caulat Léo C. , Reichmann Nathalie T. , Pinho Mariana G. 
Published: August 2020

AbstractStaphylococcus aureus is generally thought to divide in three alternating orthogonal planes over three consecutive division cycles. Although this mode of division was proposed over four decades ago, the molecular mechanism that ensures this geometry of division has remained elusive. Here we show, for three different strains, that S. aureus cells do not regularly divide in three alternating perpendicular planes as previously thought. Imaging of the divisome shows that a plane of division is always perpendicular to the previous one, avoiding bisection of the nucleoid, which segregates along an axis parallel to the closing septum. However, one out of the multiple planes perpendicular to the septum which divide the cell in two identical halves can be used in daughter cells, irrespective of its orientation in relation to the penultimate division plane. Therefore, division in three orthogonal planes is not the rule in S. aureus.
Metal 3D printing technology for functional integration of catalytic system
Authors: Wei Qinhong , Li Hangjie , Liu Guoguo , He Yingluo , Wang Yang , Tan Yen Ee , Wang Ding , Peng Xiaobo , Yang Guohui , Tsubaki Noritatsu 
Published: August 2020

AbstractMechanical properties and geometries of printed products have been extensively studied in metal 3D printing. However, chemical properties and catalytic functions, introduced by metal 3D printing itself, are rarely mentioned. Here we show that metal 3D printing products themselves can simultaneously serve as chemical reactors and catalysts (denoted as self-catalytic reactor or SCR) for direct conversion of C1 molecules (including CO, CO2 and CH4) into high value-added chemicals. The Fe-SCR and Co-SCR successfully catalyze synthesis of liquid fuel from Fischer-Tropsch synthesis and CO2 hydrogenation; the Ni-SCR efficiently produces syngas (CO/H2) by CO2 reforming of CH4. Further, the Co-SCR geometrical studies indicate that metal 3D printing itself can establish multiple control functions to tune the catalytic product distribution. The present work provides a simple and low-cost manufacturing method to realize functional integration of catalyst and reactor, and will facilitate the developments of chemical synthesis and 3D printing technology.
An inducible circular RNA circKcnt2 inhibits ILC3 activation to facilitate colitis resolution
Authors: Liu Benyu , Ye Buqing , Zhu Xiaoxiao , Yang Liuliu , Li Huimu , Liu Nian , Zhu Pingping , Lu Tiankun , He Luyun , Tian Yong , Fan Zusen 
Published: August 2020

AbstractGroup 3 innate lymphoid cells (ILC3) are an important regulator for immunity, inflammation and tissue homeostasis in the intestine, but how ILC3 activation is regulated remains elusive. Here we identify a new circular RNA (circRNA) circKcnt2 that is induced in ILC3s during intestinal inflammation. Deletion of circKcnt2 causes gut ILC3 activation and severe colitis in mice. Mechanistically, circKcnt2, as a nuclear circRNA, recruits the nucleosome remodeling deacetylase (NuRD) complex onto Batf promoter to inhibit Batf expression; this in turn suppresses Il17 expression and thereby ILC3 inactivation to promote innate colitis resolution. Furthermore, Mbd3−/−Rag1−/− and circKcnt2−/−Rag1−/− mice develop severe innate colitis following dextran sodium sulfate (DSS) treatments, while simultaneous deletion of Batf promotes colitis resolution. In summary, our data support a function of the circRNA circKcnt2 in regulating ILC3 inactivation and resolution of innate colitis.
A scalable CRISPR/Cas9-based fluorescent reporter assay to study DNA double-strand break repair choice
Authors: Roidos Paris , Sungalee Stephanie , Benfatto Salvatore , Serçin Özdemirhan , Stütz Adrian M. , Abdollahi Amir , Mauer Jan , Zenke Frank T. , Korbel Jan O. , Mardin Balca R. 
Published: August 2020

AbstractDouble-strand breaks (DSBs) are the most toxic type of DNA lesions. Cells repair these lesions using either end protection- or end resection-coupled mechanisms. To study DSB repair choice, we present the Color Assay Tracing-Repair (CAT-R) to simultaneously quantify DSB repair via end protection and end resection pathways. CAT-R introduces DSBs using CRISPR/Cas9 in a tandem fluorescent reporter, whose repair distinguishes small insertions/deletions from large deletions. We demonstrate CAT-R applications in chemical and genetic screens. First, we evaluate 21 compounds currently in clinical trials which target the DNA damage response. Second, we examine how 417 factors involved in DNA damage response influence the choice between end protection and end resection. Finally, we show that impairing nucleotide excision repair favors error-free repair, providing an alternative way for improving CRISPR/Cas9-based knock-ins. CAT-R is a high-throughput, versatile assay to assess DSB repair choice, which facilitates comprehensive studies of DNA repair and drug efficiency testing.
Control of seed formation allows two distinct self-sorting patterns of supramolecular nanofibers
Authors: Kubota Ryou , Nagao Kazutoshi , Tanaka Wataru , Matsumura Ryotaro , Aoyama Takuma , Urayama Kenji , Hamachi Itaru 
Published: August 2020

AbstractSelf-sorting double network hydrogels comprising orthogonal supramolecular nanofibers have attracted attention as artificially-regulated multi-component systems. Regulation of network patterns of self-sorted nanofibers is considered as a key for potential applications such as optoelectronics, but still challenging owing to a lack of useful methods to prepare and analyze the network patterns. Herein, we describe the selective construction of two distinct self-sorting network patterns, interpenetrated and parallel, by controlling the kinetics of seed formation with dynamic covalent oxime chemistry. Confocal imaging reveals the interpenetrated self-sorting network was formed upon addition ofO-benzylhydroxylamine to a benzaldehyde-tethered peptide-type hydrogelator in the presence of lipid-type nanofibers. We also succeed in construction of a parallel self-sorting network through deceleration of seed formation using a slow oxime exchange reaction. Through careful observation, the formation of peptide-type seeds and nanofibers is shown to predominantly occur on the surface of the lipid-type nanofibers via highly dynamic and thermally-fluctuated processes.
Short-term calorie restriction enhances DNA repair by non-homologous end joining in mice
Authors: Ke Zhonghe , Firsanov Denis , Spencer Brianna , Seluanov Andrei , Gorbunova Vera 
Published: August 2020

AbstractCalorie restriction (CR) improves health, reduces cancer incidence and extends lifespan in multiple organisms including mice. CR was shown to enhance base excision repair and nucleotide excision repair pathways of DNA repair, however, whether CR improves repair of DNA double-strand breaks has not been examined in in vivo system. Here we utilize non-homologous end joining (NHEJ) reporter mice to show that short-term CR strongly enhances DNA repair by NHEJ, which is associated with elevated levels of DNA-PK and SIRT6.
The electrode tortuosity factor: why the conventional tortuosity factor is not well suited for quantifying transport in porous Li-ion battery electrodes and what to use instead
Authors: Nguyen Tuan-Tu , Demortière Arnaud , Fleutot Benoit , Delobel Bruno , Delacourt Charles , Cooper Samuel J. 
Published: August 2020

AbstractThe tortuosity factor of porous battery electrodes is an important parameter used to correlate electrode microstructure with performance through numerical modeling. Therefore, having an appropriate method for the accurate determination of tortuosity factors is critical. This paper presents a numerical approach, based on simulations performed on numerically-generated microstructural images, which enables a comparison between two common experimental methods. Several key issues with the conventional “flow through” type tortuosity factor are highlighted, when used to characterise electrodes. As a result, a new concept called the “electrode tortuosity factor” is introduced, which captures the transport processes relevant to porous electrodes better than the “flow through” type tortuosity factor. The simulation results from this work demonstrate the importance of non-percolating (“dead-end”) pores in the performance of real electrodes. This is an important result for optimizing electrode design that should be considered by electrochemical modelers. This simulation tool is provided as an open-source MATLAB application and is freely available online as part of the TauFactor platform.
Statistics of the NiCoCr medium-entropy alloy: Novel aspects of an old puzzle
Authors: Pei Zongrui , Li Rui , Gao Michael C. , Stocks G. Malcolm 
Published: August 2020

AbstractWe study the K-state phenomenon in the NiCoCr medium-entropy alloy using first-principles techniques jointly with the efficient Wang–Landau Monte Carlo and simulated annealing algorithms. Our theoretical results successfully explain the existence of the peak around 940 K in the experimental specific heat curve that characterizes the K-state phenomenon and give a fine picture of its atomic origin. The peak is caused by the maximum change of the local configurations characterized by the short-range-order (SRO) parameters at that temperature. The maximum change in SRO parameters is dominated by the nearest-neighbor interactions of atoms but substantially tuned by the many-body interactions. One surprising aspect revealed by the reciprocal-space SRO parameters is that the Ni–Co pair distribution is not random even above the ordering transition temperature, dramatically different from Ni–Cr and Co–Cr, indicating the system cannot be treated as a pseudo binary alloy. This prototypical example shows the complicated nature of multicomponent alloys, different from binary alloys. Our methods can be directly used to study the important K-state phenomenon observed in a number of other composition-concentrated alloys regardless of their number of components.