bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Haemagglutinin Genes of the UK Clade 2.3.4.4b H5N1 Avian Influenza Viruses from 2020 to 2022 Retain Strong Avian Phenotype
Authors: Yang Jiayun , Daines Rebecca , Chang Pengxiang , Karunarathna Thusitha K. , Qureshi Mehnaz , Sadeyen Jean-Remy , James Joe , Banyard Ashley C. , Slomka Marek , Brown Ian H. , Iqbal Munir 
Published: July 2024

AbstractSince 2020, the United Kingdom (UK) has suffered repeated epizootics of clade 2.3.4.4b H5 high pathogenicity avian influenza viruses (HPAIVs) in wild birds and poultry, resulting in substantial economic losses due to enforced statutory control. The rapid evolution of H5 HPAIVs continues to raise concern with heightened zoonotic and pandemic risks. The immunodominant haemagglutinin glycoprotein (HA) is crucial for influenza virus receptor binding and pH-induced fusion of viral and cellular membranes. Mutations in HA are frequent due to polymerase error, immune pressure and host adaptation, resulting in antigenic modulation and/or an expansion of host tropism, respectively, ultimately hindering control strategies. We evaluated a comprehensive panel of H5 viruses representing prevalent genotypes from UK outbreaks spanning 2020 to 2022 for HA functionality. HA genes from each genotype were assessed through receptor binding, pH of fusion, thermostability and HA inhibition assays to evaluate factors contributing to zoonotic potential, stability, and antigenicity. The viruses only bound to avian receptors and exhibited fusion at a pH of 5.8, above the pH range (pH 5.0 to 5.5) associated with efficient human-to-human transmission. Therefore, these H5 viruses have low immediate zoonotic threat. Contemporary H5 viruses were more thermostable and showed antigenic drift compared to the earlier 2017-2018 clade 2.3.4.4b H5N8 viruses, and N236D in HA was identified as a significant antigenic epitope. The findings of this study underscore the evolving nature of the HA of these viruses and highlight the importance of ongoing surveillance and characterisation efforts to identify factors that might contribute to zoonotic risk.
Heat-killed probioticLevilactobacillus brevisMKAK9 and its exopolysaccharide promote longevity by modulating aging hallmarks and enhancing immune responses inCaenorhabditis elegans
Authors: Kumar Arun , Saha Manti Kumar , Kumar Vipin , Bhattacharya Anupam , Barge Sagar , Mukherjee Ashis K. , Kalita Mohan C. , Khan Mojibur R. 
Published: July 2024

AbstractBackgroundProteostasis is a critical aging hallmark responsible for removing damaged or misfolded proteins and their aggregates by improving proteasomal degradation through the autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS). Research on the impact of heat-killed probiotic bacteria and their structural components on aging hallmarks and innate immune responses is scarce, yet enhancing these effects could potentially delay age- related diseases.ResultsThis study introduces a novel heat-killedLevilactobacillus brevisstrain MKAK9 (HK MKAK9), along with its exopolysaccharide (EPS), demonstrating their ability to extend longevity by improving proteostasis and immune responses in wild-typeCaenorhabditis elegans. We elucidate the underlying mechanisms through a comprehensive approach involving mRNA- and small RNA sequencing, proteomic analysis, lifespan assays on loss-of- function mutants, and quantitative RT-PCR. Mechanistically, HK MKAK9 and its EPS resulted in downregulation of the insulin-like signaling pathway in a DAF-16-dependent manner, enhancing protein ubiquitination and subsequent proteasomal degradation through activation of the ALP pathway, which is partially mediated by microRNA mir-243. Importantly, autophagosomes engulf ubiquitinylated proteins, as evidenced by increased expression of the autophagy receptorsqst-3, and subsequently fuse with lysosomes, facilitated by increased levels of the lysosome-associated membrane protein (LAMP) lmp-1, suggesting the formation of autolysosomes for degradation of the selected cargo. Moreover, HK MKAK9 and its EPS activated the p38 MAPK pathway and its downstream SKN-1 transcription factor, which are known to regulate genes involved in innate immune response (thn-1,ilys-1,cnc-2,spp-9,spp-21,clec-47, andclec-266) and antioxidation (sod-3andgst-44), thereby reducing the accumulation of reactive oxygen species (ROS) at both cellular and mitochondrial levels. Notably, SOD-3 emerged as a transcriptional target of both DAF-16 and SKN-1 transcription factors.ConclusionOur research sets a benchmark for future investigations by demonstrating that heat-killed probiotic and its specific cellular component, EPS, can downregulate the insulin- signaling pathway, potentially improving the autophagy-lysosome pathway (ALP) for degrading ubiquitinylated proteins and promoting organismal longevity. Additionally, we discovered that increased expression of microRNA mir-243 regulates insulin-like signaling and its downstream ALP pathway. Our findings also indicate that postbiotic treatment may bolster antioxidative and innate immune responses, offering a promising avenue for interventions in aging-related diseases.
RBM10 loss induces aberrant splicing of cytoskeletal and extracellular matrix mRNAs and promotes metastatic fitness
Authors: Krishnamoorthy Gnana P. , Glover Anthony R. , Untch Brian R. , Sigcha-Coello Nickole , Xu Bin , Vukel Dina , Liu Yi , Tiedje Vera , Berman Katherine , Tamarapu Prasanna P. , Acuña-Ruiz Adrian , Saqcena Mahesh , de Stanchina Elisa , Boucai Laura , Ghossein Ronald A. , Knauf Jeffrey A. , Abdel-Wahab Omar , Bradley Robert K. , Fagin James A. 
Published: July 2024

ABSTRACTRBM10 modulates transcriptome-wide cassette exon splicing. Loss-of-functionRBM10mutations are enriched in thyroid cancers with distant metastases. Analysis of transcriptomes and genes mis-spliced by RBM10 loss showed pro-migratory and RHO/RAC signaling signatures. RBM10 loss increases cell velocity. Cytoskeletal and ECM transcripts subject to exon-inclusion events included vinculin (VCL), tenascin C (TNC) and CD44. Knockdown of the VCL exon inclusion transcript inRBM10-null cells reduced cell velocity, whereas knockdown of TNC and CD44 exon-inclusion isoforms reduced invasiveness. RAC1-GTP levels were increased inRBM10-null cells. MouseHrasG12V/Rbm1OKOthyrocytes develop metastases that are reversed by RBM10 or by combined knockdown of VCL, CD44 and TNC inclusion isoforms. Thus,RBM10loss generates exon inclusions in transcripts regulating ECM-cytoskeletal interactions, leading to RAC1 activation and metastatic competency. Moreover, a CRISPR-Cas9 screen for synthetic lethality with RBM10 loss identified NFkB effectors as central to viability, providing a therapeutic target for these lethal thyroid cancers.SUMMARYRNA splicing factor mutations are common in cancer but connecting phenotypes to specific misspliced genes has been challenging. We show that RBM10 loss leads to exon inclusions of transcripts regulating ECM-cytoskeletal interactions and RAC1-GTP activation, sufficient to promote metastatic fitness.
A HigB-like toxin promotes non-replicatingSalmonellainside macrophages by inhibiting ribonuclease III
Authors: Choi Soomin , Cho Yong-Joon , Baek Seungwoo , Choi Eunna , Kim Yoon Ki , Lee Eun-Jin 
Published: July 2024

SUMMARYMany bacteria are often resistant to antibiotic treatment because they can slow down their growth rate, thereby attenuating the drug’s effectiveness. A similar growth-rate control is observed in pathogens that infect and persist inside their hosts. The bacterial toxin-antitoxin (TA) system serves as a non-heritable phenotypic switch by slowing down growth through the expression of a toxin component. Here, we investigated a HigB-like type II toxin from the intracellular bacterial pathogenSalmonellaTyphimurium. Unlike other HigB-like toxins that cleave ribosome-bound mRNAs, it does not exhibit endoribonuclease activity. Instead, it inhibits ribonuclease III, which mediates the initial cleavage for rRNA processing, by directly binding to the dsRNA-binding domain of RNase III, thereby decreasing ribosome assembly and bacterial growth. Given that the formation of HigB-like toxin-mediated non-replicatingSalmonellawithin macrophages is RNase III-dependent, persister formation by inhibiting RNase III is a newly identified strategy for pathogens to survive within host cells.
Dynamic stress- and inflammatory-based regulation of psychiatric risk loci in human neurons
Authors: Retallick-Townsley Kayla G. , Lee Seoyeon , Cartwright Sam , Cohen Sophie , Sen Annabel , Jia Meng , Young Hannah , Dobbyn Lee , Deans Michael , Fernandez-Garcia Meilin , Huckins Laura M. , Brennand Kristen J. 
Published: July 2024

ABSTRACTThe prenatal environment can alter neurodevelopmental and clinical trajectories, markedly increasing risk for psychiatric disorders in childhood and adolescence. To understand if and how fetal exposures to stress and inflammation exacerbate manifestation of genetic risk for complex brain disorders, we report a large-scale context-dependent massively parallel reporter assay (MPRA) in human neurons designed to catalogue genotype x environment (GxE) interactions. Across 240 genome-wide association study (GWAS) loci linked to ten brain traits/disorders, the impact of hydrocortisone, interleukin 6, and interferon alpha on transcriptional activity is empirically evaluated in human induced pluripotent stem cell (hiPSC)-derived glutamatergic neurons. Of ∼3,500 candidate regulatory risk elements (CREs), 11% of variants are active at baseline, whereas cue-specific CRE regulatory activity range from a high of 23% (hydrocortisone) to a low of 6% (IL-6). Cue-specific regulatory activity is driven, at least in part, by differences in transcription factor binding activity, the gene targets of which show unique enrichments for brain disorders as well as co-morbid metabolic and immune syndromes. The dynamic nature of genetic regulation informs the influence of environmental factors, reveals a mechanism underlying pleiotropy and variable penetrance, and identifies specific risk variants that confer greater disorder susceptibility after exposure to stress or inflammation. Understanding neurodevelopmental GxE interactions will inform mental health trajectories and uncover novel targets for therapeutic intervention.
Impact of Equilibrative Nucleoside Transporters TgAT1, TgENT1, and TgENT3 onToxoplasma gondiiInfection and Differentiation
Authors: Goerner Amber , Messina Gabriel , Drogalis Beckham Lea , Martorelli Di Genova Bruno 
Published: July 2024

AbstractThe protozoan parasiteToxoplasma gondiirelies on its host for essential metabolites, including purines, which it cannot synthesize de novo. This study investigates the roles of equilibrative nucleoside transporters (TgENTs), specifically TgAT1, TgENT1, and TgENT3, across different developmental stages ofT. gondii. Utilizing protein-protein BLAST and position-specific iterated BLAST, we identified six genes in theT. gondiigenome with high sequence similarity to human andPlasmodium falciparumENTs, focusing on TgENT1, TgENT3, and TgAT1 due to their expression in tachyzoites and homology to the nucleoside domain.Our results demonstrate that TgENT3 plays a crucial role during chronic infection, as TgENT3 deletion reduced tissue cysts by 50%. The double knockout of TgAT1 and TgENT3 (ΔTgAT1ΔTgENT3) failed to differentiate into bradyzoites under alkaline stress, indicating that both transporters are important for differentiation. Upregulation of TgENT1 transcripts in ΔTgAT1ΔTgENT3 parasites suggests a compensatory mechanism among TgENTs.Conditional deletion of TgENT1 revealed its critical role in parasite growth and replication, with auxin-treated parasites showing reduced replication and long-term growth defects. Localization studies using immunofluorescence assays confirmed TgENT1’s association with the plant-like vacuole (PLVAC) membrane, distinguishing it from other ENTs typically found at the plasma membrane.These findings highlight the distinct and overlapping functions of TgENTs inT. gondii, emphasizing their potential as therapeutic targets for toxoplasmosis. Our study contributes to the broader understanding of nucleoside transporter functions in protozoans and suggests new avenues for drug development targeting ENT function to impair parasite survival and infection.
Isolating perturbative QCD splittings in heavy-ion collisions
Authors: Cunqueiro Leticia , Pablos Daniel , Soto-Ontoso Alba , Spousta Martin , Takacs Adam , Verweij Marta 
Published: July 2024

We define a new strategy to scan jet substructure in heavy-ion collisions. The scope is multifold: (i) test the dominance of vacuum jet dynamics at early times, (ii) capture the transition from coherent to incoherent jet energy loss, and (iii) study elastic scatterings in the medium, which are either hard and perturbative or soft and responsible for jet thermalization. To achieve that, we analyze the angular distribution of the hardest splitting, θhard, above a transverse momentum scale, ktmin, in high-pt jets. Sufficiently high values of ktmin target the regime in which the observable is uniquely determined by vacuumlike splittings and energy loss, leaving the jet substructure unmodified compared to proton-proton collisions. Decreasing ktmin enhances the sensitivity to the relation between energy loss and the intrajet structure and, in particular, to observe signatures of color decoherence at small angles. At wider angles it also becomes sensitive to hard elastic scatterings with the medium and, therefore, the perturbative regime of medium response. Choosing ktmin≈0 leads to order one effects of nonperturbative origin such as hadronization and, potentially, soft scatterings responsible for jet thermalization. We perform a comprehensive analysis of this observable with three state-of-the-art jet-quenching Monte Carlo event generators. Our study paves the way for defining jet observables in heavy-ion collisions dominated by perturbative QCD and thus calculable from first principles.

Published by the American Physical Society
2024
Na[GeF5]·2HF: the first quarternary phase in the H–Na–Ge–F system
Authors: Bockmair Valentin , Hoch Constantin , Schusterbauer Irina , Kornath Andreas J. 
Published: July 2024

The structure of cis- or trans-bridged [GeF5]− anionic chains have been investigated [Mallouk et al. (1984). Inorg. Chem.
23, 3160–3166] showing the first crystal structures of μ-F-bridged pentafluorogermanates. Herein, we report the second crystal structure of trans-pentafluorogermanate anions present in the crystal structure of sodium trans-pentafluorogermanate(IV) bis(hydrogen fluoride), Na[GeF5]·2HF. The crystal structure [orthorhombic Pca21, a = 12.3786 (3), b = 7.2189 (2), c = 11.4969 (3) Å and Z = 8] is built up from infinite chains of trans-linked [GeF6]2− octahedra, extending along the b axis and spanning a network of pentagonal bipyramidal distorted Na-centred polyhedra. These [NaF7] polyhedra are linked in a trans-edge fashion via hydrogen fluoride molecules, in analogy to already known sodium hydrogen fluorides and potassium hydrogen fluorides.
Managing macromolecular crystallographic data with a laboratory information management system
Authors: Daniel Edward , Wierenga Rik K. , Lehtiö Lari 
Published: July 2024

Protein crystallography is an established method to study the atomic structures of macromolecules and their complexes. A prerequisite for successful structure determination is diffraction-quality crystals, which may require extensive optimization of both the protein and the conditions, and hence projects can stretch over an extended period, with multiple users being involved. The workflow from crystallization and crystal treatment to deposition and publication is well defined, and therefore an electronic laboratory information management system (LIMS) is well suited to management of the data. Completion of the project requires key information on all the steps being available and this information should also be made available according to the FAIR principles. As crystallized samples are typically shipped between facilities, a key feature to be captured in the LIMS is the exchange of metadata between the crystallization facility of the home laboratory and, for example, synchrotron facilities. On completion, structures are deposited in the Protein Data Bank (PDB) and the LIMS can include the PDB code in its database, completing the chain of custody from crystallization to structure deposition and publication. A LIMS designed for macromolecular crystallography, IceBear, is available as a standalone installation and as a hosted service, and the implementation of key features for the capture of metadata in IceBear is discussed as an example.
How does cyber incivility affect work withdrawal? The mediating role of basic need satisfaction and burnout and moderating role of conscientiousness
Authors: Ju Boreum (Jenny) , Pak Sunjin 
Published: July 2024

PurposeThe purpose of this study was to explore the effects of cyber incivility on adverse work outcomes of work withdrawal and turnover intention. Specifically, we draw on self-determination theory and conservation of resources theory to examine the mediating roles of basic need satisfaction and burnout in the relationship between cyber incivility and work outcomes.Design/methodology/approachWe used Mplus 7.4 software with a maximum likelihood robust (MLR) estimator to test the structural equation modeling. We followed Anderson and Gerbing’s guidelines to test the hypotheses.FindingsThe results based on time-lagged data from 685 full-time workers in the United States provide support for the hypotheses that cyber incivility is indirectly associated with work withdrawal and turnover intention through basic need satisfaction and burnout. We also found that for individuals with high conscientiousness, the negative direct effect of cyber incivility on basic need satisfaction and the positive indirect effects of cyber incivility on work withdrawal and turnover intention through basic need satisfaction and burnout are stronger than for individuals with lower conscientiousness.Originality/valueOur research revealed that when employees experience cyber incivility, they enter a defensive mode to protect their already stretched resources from unfulfilled basic need satisfaction. Specifically, experiencing cyber incivility interferes with meeting basic need satisfaction and leads to burnout, which, in turn, triggers defensive work withdrawal and turnover intention.
Corporate governance effectiveness and firm performance in global crisis: evidence from GCC countries
Authors: Alshdaifat Sajead Mowafaq , Abdul Hamid Mohamad Ali , Ab Aziz Noor Hidayah , Saidin Saidatunur Fauzi , Alhasnawi Mushtaq Yousif 
Published: July 2024

Purpose
This study aims to examine the impact of corporate governance (CG) effectiveness measured by board and audit committee index on firm performance of nonfinancial listed firms in Gulf Cooperation Council (GCC) countries, pre- and during the global crisis of COVID-19.

Design/methodology/approach
The analysis used 2,238 observations from nonfinancial firms listed on GCC countries' stock exchange, covering the period from 2017 to 2022, using a fixed effect panel regression model. The data for this study were manually collected from the annual reports of 373 GCC-listed firms.

Findings
The results demonstrate that the board's effectiveness index has a positive influence solely on accounting-based performance (return on assets) pre- and during the COVID-19 crisis. However, in terms of audit committee effectiveness, the results show a positive impact on market-based performance (Tobin’s Q) both pre- and during the COVID-19 crisis. Additional analysis indicates that the effectiveness of both the board and audit committee is more notable in larger firms compared to smaller firms.

Practical implications
This study is crucial for investors, regulators, managers and governments tackling the financial impacts of global crises like COVID-19. Its comprehensive evaluation of board and audit committee effectiveness guides policymakers and practitioners in enhancing CG for profit and wealth maximization.

Originality/value
This study offers novel evidence detailing the impact of CG effectiveness on firm performance over an extended period, encompassing the COVID-19 period and using a comprehensive index. In addition, this study was conducted in a unique CG setting, focusing on six emerging GCC countries.
A viewpoint on the impact of fundamental attribution error in organizational learning
Authors: Carpenter Rob E. , Damlaj Wafa , Silberman Dave 
Published: July 2024

Purpose
To explore the Fundamental Attribution Error (FAE) bias as a potential impediment to organizational learning and to develop a conceptual model for practitioners and scholars to consider.

Design/methodology/approach
Our methodology includes a review and adoption of concepts from social cognition, organizational psychology, and learning theory to examine the role of FAE bias in organizational learning.

Findings
FAE bias is characterized by providing implicit support for fostering employee cynicism and resistance behaviors and facilitates ongoing cognitive cycles that hinder collaborative learning and knowledge sharing.

Practical implications
By understanding the role of FAE bias in organizational learning, leaders can develop strategies to mitigate the negative impact of FAE bias on organizational learning dynamics and enhance a social cycle that can improve the organization's learning culture.

Social implications
This viewpoint highlights that FAE bias in the workplace can lead to a breakdown in how individuals process emotions (affect), actions (behavior) and thoughts (cognition) in social scenarios, exacerbating employee cynicism and resistance, which in turn undermines effective collaboration, communication and the overall social fabric essential for organizational learning.

Originality/value
This viewpoint presents a novel perspective by linking FAE bias directly to cognitive cycles that can impede organizational learning processes through cynicism and resistance behavior, which we propose should be proactively considered by organizations leveraging learning as a key management strategy.