bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dual‐Band Huygens Source Antennas With Partially Reflective Surfaces
Authors: Kawdungta S. , Torrungrueng D. , Boonpoonga A. , Chou H.‐T. 
Published: November 2022

AbstractThis paper presents an antenna architecture from Huygens sources placed in a middle cavity formed by a metal reflector and a partially reflective surface (PRS) of dielectric superstrates. The proposed antenna is excited by a pair of cross‐feedings to produce two frequency resonances in reflection coefficients and radiate unidirectional patterns. In contrast to conventional designs, the proposed PRS‐supported Huygens source antenna may effectively broaden the bandwidth and increase radiation gains with a low profile, including low cost. Simulation results show broadband radiation characteristics at 2.45 and 5 GHz bands, where the impedance bandwidths are in the ranges of 2.4–2.5 GHz and 4.8–5.8 GHz, respectively. In addition, the measurement results of the antenna prototype validate the simulation results in terms of reflection coefficients and radiation patterns. It is found that the gains are 5.0 dBi (2.45 GHz) and 3.0 dBi (5 GHz), where simulation and measurement results are agreed well for practical applications of wireless communications.
Managing Waldenström’s macroglobulinemia with BTK inhibitors
Authors: Buske Christian , Jurczak Wojciech , Salem Joe-Elie , Dimopoulos Meletios A. 
Published: November 2022

AbstractBruton’s tyrosine kinase (BTK) inhibition is one of the treatment standards for patients with relapsed/refractory Waldenström’s macroglobulinemia (WM) and for patients with WM who are unsuitable for immunochemotherapy (ICT). It offers deep and durable responses with a manageable safety profile that is generally favorable compared with ICT regimens. However, the limitations of the first approved BTK inhibitor (BTKi), ibrutinib, include reduced efficacy in patients lacking the characteristic WM mutation (MYD88L265P) and toxicities related to off-target activity. The risk of atrial fibrillation (AF) and other cardiovascular side effects are a notable feature of ibrutinib therapy. Several next-generation covalent BTKis with greater selectivity for BTK are at various stages of development. In November 2021, zanubrutinib became the first of these agents to be approved by the European Medicines Agency for the treatment of WM. Head-to-head trial data indicate that it has comparable efficacy to ibrutinib for patients with WM overall, although it may be more effective in patients with CXCR4 mutations or wild-type MYD88. In the clinical trial setting, its greater selectivity translates into a reduced risk of cardiovascular side effects, including AF. Acalabrutinib, which is pre-approval in WM, appears to offer similar advantages over ibrutinib in terms of its safety profile. Beyond the next-generation covalent BTKis, non-covalent BTKis are an emerging class with the potential to provide a therapeutic option for patients who relapse on covalent BTKis. In the future, BTKis may be increasingly utilized within combination regimens. Several ongoing trials in WM are investigating the potential for BTKi use in combination with established and novel targeted agents.
Genetic investigation of the contribution of body composition to anorexia nervosa in an electronic health record setting
Authors: Mack Taralynn , Sanchez-Roige Sandra , Davis Lea K. 
Published: November 2022

AbstractAnorexia nervosa (AN) is a psychiatric disorder defined by anthropometric symptoms, such as low body weight, and cognitive-behavioral symptoms, such as restricted eating, fear of weight gain, and distorted body image. Recent studies have identified a genetic association between AN and metabolic/anthropometric factors, including body mass index (BMI). Although the reported associations may be under pleiotropic genetic influences, they may represent independent risk factors for AN. Here we examined the independent contributions of genetic predisposition to low body weight and polygenic risk (PRS) for AN in a clinical population (Vanderbilt University Medical Center biobank, BioVU). We fitted logistic and linear regression models in a retrospective case-control design (123 AN patients, 615 age-matched controls). We replicated the genetic correlations between PRSBMIand AN (p = 1.12 × 10−3, OR = 0.96), but this correlation disappeared when controlling for lowest BMI (p = 0.84, OR = 1.00). Additionally, we performed a phenome-wide association analysis of the PRSANand found that the associations with metabolic phenotypes were attenuated when controlling for PRSBMI. These findings suggest that the genetic association between BMI and AN may be a consequence of the weight-related diagnostic criteria for AN and that genetically regulated anthropometric traits (like BMI) may be independent of AN psychopathology. If so, individuals with cognitive-behavioral symptomatology suggestive of AN, but with a higher PRSBMI, may be under-diagnosed given current diagnostic criteria. Furthermore, PRSBMImay serve as an independent risk factor for weight loss and weight gain during recovery.
Cell-cell contact-driven EphB1 cis- and trans- signalings regulate cancer stem cells enrichment after chemotherapy
Authors: Wang Lujuan , Peng Qiu , Xie Yaohuan , Yin Na , Xu Jiaqi , Chen Anqi , Yi Junqi , Shi Wenhua , Tang Jingqun , Xiang Juanjuan 
Published: November 2022

AbstractReactivation of chemotherapy-induced dormant cancer cells is the main cause of relapse and metastasis. The molecular mechanisms underlying remain to be elucidated. In this study, we introduced a cellular model that mimics the process of cisplatin responsiveness in NSCLC patients. We found that during the process of dormancy and reactivation induced by cisplatin, NSCLC cells underwent sequential EMT-MET with enrichment of cancer stem cells. The ATAC-seq combined with motif analysis revealed that OCT4-SOX2-TCF-NANOG motifs were associated with the enrichment of cancer stem cells induced by chemotherapy. Gene expression profiling suggested a dynamic regulatory mechanism during the process of enrichment of cancer stem cells, where Nanog showed upregulation in the dormant state and SOX2 showed upregulation in the reactivated state. Further, we showed that EphB1 and p-EphB1 showed dynamic expression in the process of cancer cell dormancy and reactivation, where the expression profiles of EphB1 and p-EphB1 showed negatively correlated. In the dormant EMT cells which showed disrupted cell-cell contacts, ligand-independent EphB1 promoted entry of lung cancer cells into dormancy through activating p-p38 and downregulating E-cadherin. On the contrary, in the state of MET, in which cell-cell adhesion was recovered, interactions of EphB1 and ligand EphrinB2 in trans promoted the stemness of cancer cells through upregulating Nanog and Sox2. In conclusion, lung cancer stem cells were enriched during the process of cellular response to chemotherapy. EphB1 cis- and trans- signalings function in the dormant and reactivated state of lung cancer cells respectively. It may provide a therapeutic strategy that target the evolution process of cancer cells induced by chemotherapy.
PRDM15 interacts with DNA-PK-Ku complex to promote radioresistance in rectal cancer by facilitating DNA damage repair
Authors: Yu Yue , Liu Tingting , Yu Guanyu , Wang Hang , Du Zhipeng , Chen Yuanyuan , Yang Nan , Cao Kun , Liu Chunlei , Wan Zhijie , Shen Hui , Gao Fu , Yang Yanyong , Zhang Wei 
Published: November 2022

AbstractNeoadjuvant radiotherapy is a standard treatment for locally advanced rectal cancer, however, resistance to chemoradiotherapy is one of the main obstacles to improving treatment outcomes. The goal of this study was to explore the role of PRDM15 involved in the radioresistance of colorectal cancer and to clarify the underlying mechanism. In present study, we demonstrated that, after DNA damage, PRDM15 was upregulated and localized to DNA damage sites, co-localizing with γ-H2AX. Knockdown of PRDM15 inhibited DNA damage repair and increased radiosensitivity in colorectal cancer cells. Mechanistically, PRDM15 promoted DNA repair by interacting with DNA-PKcs and Ku70/Ku80 complex. In preclinical models of rectal cancer, knockdown of PRDM15 sensitized cell derived xenograft and patient derived xenograft to radiotherapy. In 80 rectal cancer patients treated with neoadjuvant chemoradiotherapy, higher PRDM15 expression was observed associated with weaker tumor regression and poorer prognosis. Our findings revealed that inhibiting PRDM15 was potent to overcome radioresistance through abrogating DNA repair in colorectal cancer cells. Additionally, the expression level of PRDM15 could be applied to predict radiotherapy responsiveness and the outcome of neoadjuvant radiotherapy in rectal cancer patients.
BNIP3-dependent mitophagy safeguards ESC genomic integrity via preventing oxidative stress-induced DNA damage and protecting homologous recombination
Authors: Zhao Qian , Liu Kun , Zhang Lin , Li Zheng , Wang Liang , Cao Jiani , Xu Youqing , Zheng Aihua , Chen Quan , Zhao Tongbiao 
Published: November 2022

AbstractEmbryonic stem cells (ESCs) have a significantly lower mutation load compared to somatic cells, but the mechanisms that guard genomic integrity in ESCs remain largely unknown. Here we show that BNIP3-dependent mitophagy protects genomic integrity in mouse ESCs. Deletion of Bnip3 increases cellular reactive oxygen species (ROS) and decreases ATP generation. Increased ROS in Bnip3−/− ESCs compromised self-renewal and were partially rescued by either NAC treatment or p53 depletion. The decreased cellular ATP in Bnip3−/− ESCs induced AMPK activation and deteriorated homologous recombination, leading to elevated mutation load during long-term propagation. Whereas activation of AMPK in X-ray-treated Bnip3+/+ ESCs dramatically ascended mutation rates, inactivation of AMPK in Bnip3−/− ESCs under X-ray stress remarkably decreased the mutation load. In addition, enhancement of BNIP3-dependent mitophagy during reprogramming markedly decreased mutation accumulation in established iPSCs. In conclusion, we demonstrated a novel pathway in which BNIP3-dependent mitophagy safeguards ESC genomic stability, and that could potentially be targeted to improve pluripotent stem cell genomic integrity for regenerative medicine.
Antigenic sin of wild-type SARS-CoV-2 vaccine shapes poor cross-neutralization of BA.4/5/2.75 subvariants in BA.2 breakthrough infections
Authors: Ju Bin , Fan Qing , Wang Miao , Liao Xuejiao , Guo Huimin , Wang Haiyan , Ge Xiangyang , Liu Lei , Zhang Zheng 
Published: November 2022

AbstractWith declining SARS-CoV-2-specific antibody titers and increasing numbers of spike mutations, the ongoing emergence of Omicron subvariants causes serious challenges to current vaccination strategies. BA.2 breakthrough infections have occurred in people who have received the wild-type vaccines, including mRNA, inactivated, or recombinant protein vaccines. Here, we evaluate the antibody evasion of recently emerged subvariants BA.4/5 and BA.2.75 in two inactivated vaccine-immunized cohorts with BA.2 breakthrough infections. Compared with the neutralizing antibody titers against BA.2, marked reductions are observed against BA.2.75 in both 2-dose and 3-dose vaccine groups. In addition, although BA.2 breakthrough infections induce a certain cross-neutralization capacity against later Omicron subvariants, the original antigenic sin phenomenon largely limits the improvement of variant-specific antibody response. These findings suggest that BA.2 breakthrough infections seem unable to provide sufficient antibody protection against later subvariants such as BA.2.75 in the current immunization background with wild-type vaccines.
Electricity consumption variation versus economic structure during COVID-19 on metropolitan statistical areas in the US
Authors: Wang Jinning , Li Fangxing , Cui Hantao , Shi Qingxin , Mingee Trey 
Published: November 2022

AbstractThe outbreak of novel coronavirus disease (COVID-19) has resulted in changes in productivity and daily life patterns, and as a result electricity consumption (EC) has also shifted. In this paper, we construct estimates of EC changes at the metropolitan level across the continental U.S., including total EC and residential EC during the initial two months of the pandemic. The total and residential data on the state level were broken down into the county level, and then metropolitan level EC estimates were aggregated from the counties included in each metropolitan statistical area (MSA). This work shows that the reduction in total EC is related to the shares of certain industries in an MSA, whereas regardless of the incidence level or economic structure, the residential sector shows a trend of increasing EC across the continental U.S. Since the MSAs account for 86% of the total population and 87% of the total EC of the continental U.S., the analytical result in this paper can provide important guidelines for future social-economic crises.
How people wake up is associated with previous night’s sleep together with physical activity and food intake
Authors: Vallat Raphael , Berry Sarah E. , Tsereteli Neli , Capdevila Joan , Khatib Haya Al , Valdes Ana M. , Delahanty Linda M. , Drew David A. , Chan Andrew T. , Wolf Jonathan , Franks Paul W. , Spector Tim D. , Walker Matthew P. 
Published: November 2022

AbstractHow people wake up and regain alertness in the hours after sleep is related to how they are sleeping, eating, and exercising. Here, in a prospective longitudinal study of 833 twins and genetically unrelated adults, we demonstrate that how effectively an individual awakens in the hours following sleep is not associated with their genetics, but instead, four independent factors: sleep quantity/quality the night before, physical activity the day prior, a breakfast rich in carbohydrate, and a lower blood glucose response following breakfast. Furthermore, an individual’s set-point of daily alertness is related to the quality of their sleep, their positive emotional state, and their age. Together, these findings reveal a set of non-genetic (i.e., not fixed) factors associated with daily alertness that are modifiable.
Charge-separation driven mechanism via acylium ion intermediate migration during catalytic carbonylation in mordenite zeolite
Authors: Chen Wei , Tarach Karolina A. , Yi Xianfeng , Liu Zhiqiang , Tang Xiaomin , Góra-Marek Kinga , Zheng Anmin 
Published: November 2022

AbstractBy employing ab initio molecular dynamic simulations, solid-state NMR spectroscopy, and two-dimensional correlation analysis of rapid scan Fourier transform infrared spectroscopy data, a new pathway is proposed for the formation of methyl acetate (MA) via the acylium ion (i.e.,CH3 − C ≡ O+) in 12-membered ring (MR) channel of mordenite by an integrated reaction/diffusion kinetics model, and this route is kinetically and thermodynamically more favorable than the traditional viewpoint in 8MR channel. From perspective of the complete catalytic cycle, the separation of these two reaction zones, i.e., the C-C bond coupling in 8MR channel and MA formation in 12MR channel, effectively avoids aggregation of highly active acetyl species or ketene, thereby reducing undesired carbon deposit production. The synergistic effect of different channels appears to account for the high carbonylation activity in mordenite that has thus far not been fully explained, and this paradigm may rationalize the observed catalytic activity of other reactions.
How Carvedilol activates β2-adrenoceptors
Authors: Benkel Tobias , Zimmermann Mirjam , Zeiner Julian , Bravo Sergi , Merten Nicole , Lim Victor Jun Yu , Matthees Edda Sofie Fabienne , Drube Julia , Miess-Tanneberg Elke , Malan Daniela , Szpakowska Martyna , Monteleone Stefania , Grimes Jak , Koszegi Zsombor , Lanoiselée Yann , O’Brien Shannon , Pavlaki Nikoleta , Dobberstein Nadine , Inoue Asuka , Nikolaev Viacheslav , Calebiro Davide , Chevigné Andy , Sasse Philipp , Schulz Stefan , Hoffmann Carsten , Kolb Peter , Waldhoer Maria , Simon Katharina , Gomeza Jesus , Kostenis Evi 
Published: November 2022

AbstractCarvedilol is among the most effective β-blockers for improving survival after myocardial infarction. Yet the mechanisms by which carvedilol achieves this superior clinical profile are still unclear. Beyond blockade of β1-adrenoceptors, arrestin-biased signalling via β2-adrenoceptors is a molecular mechanism proposed to explain the survival benefits. Here, we offer an alternative mechanism to rationalize carvedilol’s cellular signalling. Using primary and immortalized cells genome-edited by CRISPR/Cas9 to lack either G proteins or arrestins; and combining biological, biochemical, and signalling assays with molecular dynamics simulations, we demonstrate that G proteins drive all detectable carvedilol signalling through β2ARs. Because a clear understanding of how drugs act is imperative to data interpretation in basic and clinical research, to the stratification of clinical trials or to the monitoring of drug effects on the target pathway, the mechanistic insight gained here provides a foundation for the rational development of signalling prototypes that target the β-adrenoceptor system.
Drivers of recent decline in dust activity over East Asia
Authors: Wu Chenglai , Lin Zhaohui , Shao Yaping , Liu Xiaohong , Li Ying 
Published: November 2022

AbstractIt is essential to understand the factors driving the recent decline of dust activity in East Asia for future dust projections. Using a physically-based dust emission model, here we show that the weakening of surface wind and the increasing of vegetation cover and soil moisture have all contributed to the decline in dust activity during 2001 to 2017. The relative contributions of these three factors to the dust emission reduction during 2010–2017 relative to 2001 are 46%, 30%, and 24%, respectively. Much (78%) of the dust emission reduction is from barren lands, and a small fraction (4.6%) of the reduction is attributed to grassland vegetation increase that is partly ascribed to the ecological restoration. This suggests that the ecological restoration plays a minor role in the decline of dust activity. Rather, the decline is mainly driven by climatic factors, with the weakening of surface wind playing the dominant role.
Consistent diel activity patterns of forest mammals among tropical regions
Authors: Vallejo-Vargas Andrea F. , Sheil Douglas , Semper-Pascual Asunción , Beaudrot Lydia , Ahumada Jorge A. , Akampurira Emmanuel , Bitariho Robert , Espinosa Santiago , Estienne Vittoria , Jansen Patrick A. , Kayijamahe Charles , Martin Emanuel H. , Lima Marcela Guimarães Moreira , Mugerwa Badru , Rovero Francesco , Salvador Julia , Santos Fernanda , Spironello Wilson Roberto , Uzabaho Eustrate , Bischof Richard 
Published: November 2022

AbstractAn animal’s daily use of time (their “diel activity”) reflects their adaptations, requirements, and interactions, yet we know little about the underlying processes governing diel activity within and among communities. Here we examine whether community-level activity patterns differ among biogeographic regions, and explore the roles of top-down versus bottom-up processes and thermoregulatory constraints. Using data from systematic camera-trap networks in 16 protected forests across the tropics, we examine the relationships of mammals’ diel activity to body mass and trophic guild. Also, we assess the activity relationships within and among guilds. Apart from Neotropical insectivores, guilds exhibited consistent cross-regional activity in relation to body mass. Results indicate that thermoregulation constrains herbivore and insectivore activity (e.g., larger Afrotropical herbivores are ~7 times more likely to be nocturnal than smaller herbivores), while bottom-up processes constrain the activity of carnivores in relation to herbivores, and top-down processes constrain the activity of small omnivores and insectivores in relation to large carnivores’ activity. Overall, diel activity of tropical mammal communities appears shaped by similar processes and constraints among regions reflecting body mass and trophic guilds.
Integrating transcription factor occupancy with transcriptome-wide association analysis identifies susceptibility genes in human cancers
Authors: He Jingni , Wen Wanqing , Beeghly Alicia , Chen Zhishan , Cao Chen , Shu Xiao-Ou , Zheng Wei , Long Quan , Guo Xingyi 
Published: November 2022

AbstractTranscriptome-wide association studies (TWAS) have successfully discovered many putative disease susceptibility genes. However, TWAS may suffer from inaccuracy of gene expression predictions due to inclusion of non-regulatory variants. By integrating prior knowledge of susceptible transcription factor occupied elements, we develop sTF-TWAS and demonstrate that it outperforms existing TWAS approaches in both simulation and real data analyses. Under the sTF-TWAS framework, we build genetic models to predict alternative splicing and gene expression in normal breast, prostate and lung tissues from the Genotype-Tissue Expression project and apply these models to data from large genome-wide association studies (GWAS) conducted among European-ancestry populations. At Bonferroni-correctedP < 0.05, we identify 354 putative susceptibility genes for these cancers, including 189 previously unreported in GWAS loci and 45 in loci unreported by GWAS. These findings provide additional insight into the genetic susceptibility of human cancers. Additionally, we show the generalizability of the sTF-TWAS on non-cancer diseases.
The non-catalytic role of DNA polymerase epsilon in replication initiation in human cells
Authors: Vipat Sameera , Gupta Dipika , Jonchhe Sagun , Anderspuk Hele , Rothenberg Eli , Moiseeva Tatiana N. 
Published: November 2022

AbstractDNA polymerase epsilon (PolE) in an enzyme essential for DNA replication. Deficiencies and mutations in PolE cause severe developmental abnormalities and cancers. Paradoxically, the catalytic domain of yeast PolE catalytic subunit is dispensable for survival, and its non-catalytic essential function is linked with replicative helicase (CMG) assembly. Less is known about the PolE role in replication initiation in human cells. Here we use an auxin-inducible degron system to study the effect of POLE1 depletion on replication initiation in U2OS cells. POLE1-depleted cells were able to assemble CMG helicase and initiate DNA synthesis that failed shortly after. Expression of POLE1 non-catalytic domain rescued this defect resulting in slow, but continuous DNA synthesis. We propose a model where in human U2OS cells POLE1/POLE2 are dispensable for CMG assembly, but essential during later steps of replication initiation. Our study provides some insights into the role of PolE in replication initiation in human cells.