bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long-term disgust habituation with limited generalisation in care home workers
Authors: Edgar Charlotte , Chan Faye , Armstrong Thomas , Dalmaijer Edwin S. 
Published: September 2023

AbstractCountless workers handle bodily effluvia and body envelope violations every working day, and consequentially face deeply unpleasant levels of disgust. Understanding if and how they adapt can help inform policies to improve worker satisfaction and reduce staff turnover. So far, limited evidence exist that self-reported disgust is reduced (or lower to begin with) among those employed in high-disgust environments. However, it is unclear if this is due to demand effects or translates into real behavioural changes. Here, we tested healthcare assistants (N=32) employed in UK care homes and a control sample (N=50). We replicated reduced self-reported pathogen disgust sensitivity in healthcare workers compared to controls. We also found it negatively correlated with career duration, suggesting long-term habituation. Furthermore, we found that healthcare assistants showed no behavioural disgust avoidance on a web-based preferential looking task (equivalent to eye tracking). Surprisingly, this extended to disgust elicitors found outside care homes, suggesting generalisation of disgust habituation. While we found no difference between bodily effluvia (core disgust) and body envelope violations (gore disgust), generalisation did not extend to other domains: self-reported sexual and moral disgust sensitivity were not different between healthcare assistants and the control group, nor was there a correlation with career duration. In sum, our work confirms that people in high-frequency disgust employment are less sensitive to pathogen disgust. Crucially, we provide preliminary evidence that this is due to a process of long-term habituation with generalisation to disgust-elicitors within the pathogen domain, but not beyond it.
Combined and differential roles of ADD domains of DNMT3A and DNMT3L on DNA methylation landscapes in mouse germ cells
Authors: Kubo Naoki , Uehara Ryuji , Uemura Shuhei , Ohishi Hiroaki , Shirane Kenjiro , Sasaki Hiroyuki 
Published: September 2023

AbstractDNA methyltransferase 3A (DNMT3A) and its catalytically inactive cofactor DNA methyltransferase 3-Like (DNMT3L) proteins form functional heterotetramers to deposit DNA methylation in mammalian germ cells. While both proteins have an ATRX-DNMT3-DNMT3L (ADD) domain that recognizes histone H3 tail unmethylated at lysine-4 (H3K4me0), the combined and differential roles of the domains in the two proteins have not been fully definedin vivo. Here we investigate DNA methylation landscapes in female and male germ cells derived from mice with loss-of-function amino acid substitutions in the ADD domains of DNMT3A and/or DNMT3L. Mutations in either the DNMT3A-ADD or the DNMT3L-ADD domain moderately decreases global CG methylation levels, but to different degrees, in both germ cells. Furthermore, when the ADD domains of both DNMT3A and DNMT3L lose their functions, the CG methylation levels are much more reduced, especially in oocytes, comparable to the impact of theDnmt3a/3Lknockout. In contrast, aberrant accumulation of non-CG methylation occurs at thousands of genomic regions in the double mutant oocytes and spermatozoa. These results highlight the critical role of the ADD-H3K4me0 binding in proper CG and non-CG methylation in germ cells and the various impacts of the ADD domains of the two proteins.
Oxidized LDL regulates efferocytosis through the CD36-PKM2-mtROS pathway
Authors: Zhang Jue , Chang Jackie , Chen Vaya , Beg Mirza Ahmar , Huang Wenxin , Vick Lance , Wang Yaxin , Zhang Heng , Yttre Erin , Gupta Ankan , Castleberry Mark , Zhang Ziyu , Dai Wen , Song Shan , Zhu Jieqing , Yang Moua , Brown Ashley Kaye , Xu Zhen , Ma Yan-Qing , Smith Brian C. , Zielonka Jacek , Traylor James G. , Dhaou Cyrine Ben , Orr A Wayne , Cui Weiguo , Zheng Ze , Chen Yiliang 
Published: September 2023

ABSTRACTMacrophage efferocytosis, the process by which phagocytes engulf and remove apoptotic cells (ACs), plays a critical role in maintaining tissue homeostasis. Efficient efferocytosis prevents secondary necrosis, mitigates chronic inflammation, and impedes atherosclerosis progression. However, the regulatory mechanisms of efferocytosis under atherogenic conditions remain poorly understood. We previously demonstrated that oxidized LDL (oxLDL), an atherogenic lipoprotein, induces mitochondrial reactive oxygen species (mtROS) in macrophages via CD36. In this study, we demonstrate that macrophage mtROS facilitate continual efferocytosis through a positive feedback mechanism. However, oxLDL disrupts continual efferocytosis by dysregulating the internalization of ACs. This disruption is mediated by an overproduction of mtROS. Mechanistically, oxLDL/CD36 signaling promotes the translocation of cytosolic PKM2 to mitochondria, facilitated by the chaperone GRP75. Mitochondrial PKM2 then binds to Complex III of the electron transport chain, inducing mtROS production. This study elucidates a novel regulatory mechanism of efferocytosis in atherosclerosis, providing potential therapeutic targets for intervention.SUMMARYMacrophages clear apoptotic cells through a process called efferocytosis, which involves mitochondrial ROS. However, the atherogenic oxidized LDL overstimulates mitochondrial ROS via the CD36-PKM2 pathway, disrupting continual efferocytosis. This finding elucidates a novel molecular mechanism that explains defects in efferocytosis, driving atherosclerosis progression.
Colonization of larval zebrafish (Danio rerio) with adherent-invasiveEscherichia coliprevents recovery of the intestinal mucosa from drug-induced colitis
Authors: Flores Erika , Dutta Soumita , Bosserman Rachel , van Hoof Ambro , Krachler Anne-Marie 
Published: September 2023

ABSTRACTInflammatory bowel disease (IBD) is a broad term for a range of chronic intestinal disorders, including Crohn’s disease and ulcerative colitis. The global prevalence of IBD is rising, with over one million patients affected in the US alone. Adherent-invasiveE. coli(AIEC) is a pathobiont frequently found in IBD biopsies. AIEC adhere to and invade epithelial cells, and can survive inside phagocytesin vitro. However, how AIEC contribute to IBDin vivoremains unclear. Here, we established a larval zevbrafish (Danio rerio) model to study the interplay between pre-existing intestinal inflammation and AIEC colonization of the gut. We used the pro-inflammatory drug dextran sulfate sodium (DSS) to induce colitis. This was followed by food-borne infection of larvae with AIEC using the protozoanParamecium caudatum, a natural prey, as a vehicle.We show that AIEC more robustly colonizes the zebrafish gut, and persists for longer, compared to non-pathogenicE. coli. In addition, DSS induced colitis increases both bacterial burden and persistence in the larval gut. We benchmark our model against existing rodent models using two mutants deficient in the known AIEC virulence factors FimH and IbeA, which have virulence defects in both rodent and the larval zebrafish model. Finally, we show that AIEC colonization exacerbates DSS induced colitis and prevents recovery from inflammation. In conclusion, we established a high-throughput, genetically tractable model to study AIEC–host interactions in the context of chronic inflammation.IMPORTANCEAlthough inflammatory bowel diseases are on the rise, a lot remains to be learned about the link between IBD severity and the underlying cause. Although host genetics, microbiome, and environmental factors have all been shown to correlate with the development of IBD, cause and effect are difficult to disentangle in this context. For example, AIEC is a known pathobiont found in IBD patients, but it remains unclear if gut inflammation during IBD facilitates colonization with AIEC, or if AIEC colonization makes the host more susceptible towards pro-inflammatory stimuli. To develop successful therapeutics, it is critical to understand the mechanisms that contribute to AIEC infections in a susceptible host. Here, we show that the larval zebrafish model recapitulates key features of AIEC infections in other animal models, and can be utilized to address these gaps in knowledge.
The RU486-dependent activation of the GeneSwitch system in adult muscles leads to severe adverse effects in Drosophila
Authors: Zappia Maria Paula , Damschroder Deena , Westacott Anton , Wessells Robert J. , Frolov Maxim V. 
Published: September 2023

AbstractRobust genetic systems to control the expression of transgenes in a spatial and temporal manner are a valuable asset for researchers. The GeneSwitch system induced by the drug RU486 has gained widespread use in the Drosophila community. However, some concerns were raised as negative effects were seen depending on the stock, transgene, stage and tissue under study. Here, we characterized the adverse effects triggered by activating the GeneSwitch system in adult muscles using theMHC-GS-GAL4driver. When a control, mockUAS-RNAitransgene was induced by feeding adult flies with RU486, we found that the overall muscle structure, including myofibrils and mitochondrial shape, was significantly disrupted and led to a significant reduction in the lifespan. Remarkably, lifespan was even shorter when two copies of the driver were used even without the mockUAS-RNAitransgene. Thus, researchers should be cautious when interpreting the results given the adverse effects we found when inducing RU486-dependentMHC-GS-GAL4in adult muscles. To counter the impact of these effects we recommend setting up additional control groups, such as a mock UAS-RNAi transgene, to validate the findings when using this inducible genetic system, as comparing the phenotypes between RU486-treated and untreated animals could be insufficient.
Endogenous Opioid Signaling Regulates Proliferation of Spinal Cord Ependymal Cells
Authors: Yue Wendy W.S. , Touhara Kouki K. , Toma Kenichi , Duan Xin , Julius David 
Published: September 2023

AbstractAfter injury, mammalian spinal cords develop scars to seal off the damaged area and prevent further injury. However, excessive scarring can hinder neural regeneration and functional recovery (1, 2). These competing actions underscore the importance of developing therapeutic strategies to dynamically modulate the extent of scar formation. Previous research on scar formation has primarily focused on the role of astrocytes, but recent evidence suggests that ependymal cells also participate. Ependymal cells normally form the epithelial layer encasing the central canal, but they undergo massive proliferation and differentiation into astroglia following certain types of injury, becoming a core component of scars (3–7). However, the mechanisms regulating ependymal proliferationin vivoin both healthy and injured conditions remain unclear. Here, we uncover an intercellular kappa (κ) opioid signaling pathway that controls endogenous ependymal proliferation. Specifically, we detect expression of the κ opioid receptor, OPRK1, in a functionally under-characterized cell type called cerebrospinal fluid-contacting neurons (CSF-cNs). We also discover a neighboring cell population that express the cognate ligand, prodynorphin (PDYN). Importantly, OPRK1 activation excites CSF-cNs, and systemic administration of a κ antagonist enhances ependymal proliferation in uninjured spinal cords in a CSF-cN-dependent manner. Moreover, injecting a κ agonist reduces the proliferation induced by dorsal hemisection. Altogether, our data suggest a regulatory mechanism whereby PDYN+cells tonically release κ opioids to stimulate CSF-cNs, which in turn suppress ependymal proliferation. This endogenous pathway provides a mechanistic basis for the potential use of κ opiates in modulating scar formation and treating spinal cord injuries.
Analysis of citation dynamics reveals that you do not receive enough recognition for your influential science
Authors: Arabi Salsabil , Ni Chaoqun , Hutchins B. Ian 
Published: September 2023

AbstractDuring career advancement and funding allocation decisions in biomedicine, reviewers have traditionally depended on journal-level measures of scientific influence like the impact factor. Prestigious journals are thought to pursue a reputation of exclusivity by rejecting large quantities of papers, many of which may be meritorious. It is possible that this process could create a system whereby some influential articles are prospectively identified and recognized by journal brands but most influential articles are overlooked. Here, we measure the degree to which journal prestige hierarchies capture or overlook influential science. We quantify the fraction of scientists’ articles that would receive recognition because (a) they are published in journals above a chosen impact factor threshold, or (b) they are at least as well-cited as articles appearing in such journals. We find that the number of papers cited as frequently as those published in high impact factor journals vastly exceeds the number of papers these prestigious journals publish. At the investigator level, this phenomenon extends across gender, racial, and career stage groupings of scientists. We also find that approximately half of researchers never publish in a venue with an impact factor above 15, which under journal-level evaluation regimes may exclude them from consideration for opportunities. Many of these researchers publish equally influential work, however, raising the possibility that the traditionally chosen journal-level measures that are routinely considered under decision-making norms, policy, or law, may recognize as little as 10-20% of the work that warrants recognition.
A Quantitative Genetic Model of Background Selection in Humans
Authors: Buffalo Vince , Kern Andrew D. 
Published: September 2023

AbstractAcross the human genome, there are large-scale fluctuations in genetic diversity caused by the indirect effects of selection. This “linked selection signal” reflects the impact of selection according to the physical placement of functional regions and recombination rates along chromosomes. Previous work has shown that purifying selection acting against the steady influx of new deleterious mutations at functional portions of the genome shapes patterns of genomic variation. To date, statistical efforts to estimate purifying selection parameters from linked selection models have relied on classic Background Selection theory, which is only applicable when new mutations are so deleterious that they cannot fix in the population. Here, we develop a statistical method based on a quantitative genetics view of linked selection, that models how polygenic additive fitness variance distributed along the genome increases the rate of stochastic allele frequency change. By jointly predicting the equilibrium fitness variance and substitution rate due to both strong and weakly deleterious mutations, we estimate the distribution of fitness effects (DFE) and mutation rate across three geographically distinct human samples. While our model can accommodate weaker selection, we find evidence of strong selection operating similarly across all human samples. Although our quantitative genetic model of linked selection fits better than previous models, substitution rates of the most constrained sites disagree with observed divergence levels. We find that a model incorporating selective interference better predicts observed divergence in conserved regions, but overall our results suggest uncertainty remains about the processes generating fitness variation in humans.
A tale of caution: How endogenous viral elements affect virus discovery in transcriptomic data
Authors: Brait Nadja , Hackl Thomas , Morel Côme , Exbrayat Antoni , Gutierrez Serafín , Lequime Sebastian 
Published: September 2023

AbstractLarge-scale metagenomic and -transcriptomic studies have revolutionized our understanding of viral diversity and abundance. In contrast, endogenous viral elements (EVEs), remnants of viral sequences integrated into host genomes, have received limited attention in the context of virus discovery, especially in RNA-Seq data. EVEs resemble their original viruses, a challenge that makes distinguishing between active infections and integrated remnants difficult, affecting virus classification and biases downstream analyses. Here, we systematically assess the effects of EVEs on a prototypical virus discovery pipeline, evaluate their impact on data integrity and classification accuracy, and provide some recommendations for better practices.We examined EVEs and exogenous viral sequences linked to Orthomyxoviridae, a diverse family of negative-sense segmented RNA viruses, in 13 genomic and 538 transcriptomic datasets of Culicinae mosquitoes. Our analysis revealed a substantial number of viral sequences in transcriptomic datasets. However, a significant portion appeared not to be exogenous viruses but transcripts derived from EVEs. Distinguishing between transcribed EVEs or exogenous virus sequences was especially difficult in samples with low viral abundance. For example, three transcribed EVEs showed full-length segments, devoid of frameshift and nonsense mutations, exhibiting sufficient mean read depths that qualify them as exogenous virus hits. Mapping reads on a host genome containing EVEs before assembly somewhat alleviated the EVE burden, but it led to a drastic reduction of viral hits and reduced quality of assemblies, especially in regions of the viral genome relatively similar to EVEs.Our study highlights that our knowledge of the genetic diversity of viruses can be altered by the underestimated presence of EVEs in transcriptomic datasets, leading to false positives and altered or missing sequence information. Thus, recognizing and addressing the influence of EVEs in virus discovery pipelines will be key to enhancing our ability to capture the full spectrum of viral diversity.
Equine herpesvirus 4 infected domestic horses associated with Sintashta spoke-wheeled chariots around 4,000 years ago
Authors: Lebrasseur Ophélie , More Kuldeep Dilip , Orlando Ludovic 
Published: September 2023

AbstractEquine viral outbreaks have disrupted the socio-economic life of past human societies up until the late 19th century, and continue to be of major concern to the horse industry today. With a seroprevalence of 60-80%, equine herpesvirus 4 (EHV-4) is the most common horse pathogen on the planet. Yet, its evolutionary history remains understudied. Here, we screen the sequenced data of 264 archaeological horse remains to detect the presence of EHV-4. We recover the first ancient EHV-4 genome with 4.2X average depth-of-coverage from a specimen excavated in the Southeastern Urals and dated to the Early Bronze Age period, approximately 3,900 years ago. The recovery of an EHV-4 virus outside of the upper respiratory tract not only points to an animal particularly infected, but also highlights the importance of post-cranial bones in pathogen characterisation. Bayesian phylogenetic reconstruction provides a minimal time estimate for EHV-4 diversification to around 4,000 years ago, a time when modern domestic horses spread across the Central Asian steppes together with spoke-wheeled Sintashta chariots, or earlier. The analyses also considerably revise the diversification time of the two EHV-4 subclades from the 16th century based solely on modern data to nearly a thousand years ago. Our study paves the way for a robust reconstruction of the history of non-human pathogens and their impact on animal health.
Do gender, age and tenure matter when behaving unethically for organizations: Meta-analytic review on organizational identity and unethical pro-organizational behavior
Authors: Dadaboyev Sherzodbek Murodilla Ugli , Paek Soyon , Choi Sungwon 
Published: September 2023

PurposeThis research aims to clarify the relationship between organizational identification and employees’ unethical pro-organizational behavior, which has been a topic of mixed findings in previous empirical studies. To address this issue, a meta-analytic review was conducted, focusing on the influence of key individual differences such as gender, age and organizational tenure on the relationship between organizational identification and unethical pro-organizational behavior.Design/methodology/approachThe study utilizes large scholarly databases including Google Scholar, PsycINFO, Business Source Premier and ProQuest Dissertations to identify relevant studies. A total of 31 independent samples with a combined sample size of 8,861 participants were included in the analysis.FindingsThe results showed that the estimated average correlation between organizational identification and unethical pro-organizational behavior after corrected for measurement unreliability was 0.188 (p < 0.001, 95% [CI: 0.125, 0.251]). Gender demonstrated a significant moderating effect (estimate = 0.004, p < 0.05, 95% [CI: 0.000, 0.007]), suggesting that there is stronger association between organizational identification and unethical pro-organizational behavior among male participants. Neither age nor organizational tenure had significant effect on organizational identification-unethical pro-organizational behavior relations.Originality/valueThis study revealed that the organizational identification-unethical pro-organizational behavior link was positive, and the relationship was stronger among male participants than their female counterparts. Age and organizational tenure show no significant impact on unethical pro-organizational behavior. These contribute to The authors' understanding of organizational identification-unethical pro-organizational behavior relationship, as well as identifying its boundary conditions. The study suggests directions for future research and implications for managers and practitioners.
Impact of family supportive leadership on taking charge behaviour: resource-gain-development framework perspective
Authors: Jin Shan , Fu Xiaoxia , Yan Yanling 
Published: September 2023

Purpose
Based on the resource-gain-development framework, this study aims to explore the mediating mechanism of work–family enrichment (WFE) and psychological distress, and the potential positive effect of co-worker support, on employees’ work behaviour.

Design/methodology/approach
Data was obtained via a three-stage survey with 400 frontline employees from 13 distinct industries.

Findings
This study found that family-supportive leadership (FSL) has a positive impact on employees’ taking charge behaviour (TCB). WFE and psychological distress partially mediated the effect of FSL on TCB and WFE and psychological distress played a serial mediating role between FSL and TCB. Co-worker support positively moderated the relationship between FSL and WFE, TCB and psychological distress.

Research limitations/implications
Managers should consider the problems and difficulties that employees may encounter in completing their work tasks and performance and minimise the interference of non-work factors on employees’ work status. Organisations should also facilitate diversity training for managers to respond to employees’ work and life problems and display family support behaviour.

Originality/value
This study confirmed the role of FSL in WFE, psychological distress and TCB. The results can provide guidance for managers to motivate employees’ TCB.