bluuebunny/crossref_metadata_2025_split huggingface dataset:
Schistosoma mansoniantigen induced innate immune memory features mitochondrial biogenesis and can be inhibited by ovarian produced hormones
Authors: Oviedo Juan Marcos , Cortes-Selva Diana , Marchetti Marco , Gordon Lauren , Gibbs Lisa , Maschek J. Alan , Cox James , Frietze Seth , Amiel Eyal , Fairfax Keke C. 
Published: January 2025

AbstractWe have previously identified thatS. mansoniinfection induces a unique form of myeloid training that protects male but not female mice from high fat diet induced disease. Here we demonstrate that ovarian derived hormones account for this sex specific difference. Ovariectomy of females prior to infection permits metabolic reprogramming of the myeloid lineage, with BMDM exhibiting carbon source flexibility for cellular respiration, and mice protected from systemic metabolic disease. The innate training phenotype of infection can be replicated byin vivoinjection of SEA, and by exposure of bone marrow to SEA in culture prior to macrophage differentiation (Day 0). This protective phenotype is linked to increased chromatin accessibility of lipid and mitochondrial pathways in BMDM including Nrf1 and Tfam, as well as mitochondrial biogenesis. This work provides evidence thatS. mansoniantigens induce a unique form of innate training inhibited by ovarian-derived hormones in females.
Cognitive enrichment preserves retrosplenial parvalbumin density and cognitive function in female 5xFAD mice
Authors: Terstege Dylan J. , Epp Jonathan R. 
Published: January 2025

ABSTRACTBACKGROUNDThe rate of cognitive decline in Alzheimer’s disease (AD) varies considerably from person to person. Numerous epidemiological studies point to the protective effects of cognitive, social, and physical enrichment as potential mediators of cognitive decline in AD; however, there is much debate as to the mechanism underlying these effects. The retrosplenial cortex (RSC) is one of the earliest brain regions with impaired functions during AD pathogenesis, and its activity is affected by cognitive, social, and physical stimulation.METHODSIn the current study, we use the 5xFAD mouse mode of AD to examine the impact of enriched housing conditions on cognitive function in AD and the viability of a particularly vulnerable cell population within the RSC – parvalbumin interneurons (PV-INs).RESULTSEnriched housing conditions improved cognitive performance in 5xFAD mice. These changes in cognitive performance coincided with restored functional connectivity of the RSC and preserved PV-IN density within this region. Along with preserved PV-IN density, there was an increase in the density of perineuronal nets (PNNs) across the RSC of 5xFAD mice housed in enriched conditions. Direct manipulation of PNNs revealed that these extracellular matrix structures protect PV-INs from amyloid toxicity.CONCLUSIONSTogether, these results provide support for the PNN-mediated maintenance of PV-INs in the RSC as a potential mechanism mediating the protective effects of enrichment against cognitive decline in AD.
Childhood maltreatment and brain aging during adulthood
Authors: Fleming Leland L. , Ohashi Kyoko , Enlow Michelle Bosquet , Khoury Jennifer , Klengel Torsten , Lyons-Ruth Karlen , Teicher Martin , Ressler Kerry J. 
Published: January 2025

ABSTRACTImportanceChildhood maltreatment (CM) is associated with the early onset of psychiatric and medical disorders and accelerated biological aging.ObjectiveTo identify types of maltreatment and developmental sensitive periods that are associated with accelerated adult brain aging.DesignParticipants were mothers of infants recruited from the community into a study assessing the effects of CM on maternal behavior, infant attachment, and maternal and infant neurobiology. Data were collected from July 2015 to November 2019 and were analyzed from July 2023 to October 2024.SettingAcademic medical centers.ParticipantsHigh-quality MRI scans were obtained on 92 of 150 mothers enrolled in the study. The main exclusion criteria for neuroimaging were histories of head trauma with loss of consciousness or concussion, psychotropic use before age 18, pregnancy, and customary MRI exclusions (e.g., metal implant). The primary reasons for non-completion of the neuroimaging study were unwillingness to be scanned, inability to attend the MRI study visit due to work and/or childcare, metal implants, or pregnancy.Main Outcome(s) and Measure(s)The Maltreatment and Abuse Chronology of Exposure scale was used to retrospectively assess the annual severity of exposure to ten types of CM from birth to age 18 years. Brain age was calculated from T1-weighted 3T MRI Scans using a previously published machine learning algorithm. Sensitive periods were identified using random forest regression with conditional inference trees.ResultsForty-nine (53.3%) of the 92 mothers (mean [SD] age, 32.4 [4.3] years) reported experiencing one or more types of CM. Total CM severity was associated with accelerated brain aging (β=0.05, 95% CI, 0.02 to 0.09, p<.005). The most robust type/time risk factors for accelerated brain aging were parental physical abuse between ages 4 to 6 years, witnessing sibling violence between ages 4 to 15 years, parental verbal abuse between ages 10 to 12 years, and parental emotional neglect between ages 16 to 18 years.Conclusions and RelevanceSeveral types of CM between ages 4-18 years were associated with accelerated brain aging. Understanding how these specific types and ages of exposure contribute to accelerated brain aging may provide important insights into preventing key clinical consequences of CM.SUMMARYQuestion:How does childhood adversity relate to brain aging in adulthood, and are there sensitive periods for this association?Findings:In this cohort-based study of adult women, we observed sensitive periods for the association between adult brain aging and five classes of childhood maltreatment: parental physical abuse, parental verbal abuse, parental emotional neglect, and witnessing sibling violence.Meaning:These findings suggest that maltreatment subtype and age at exposure may be important factors contributing to the impact of childhood adversity on brain aging later in life.
Axon Trafficking Counteracts Aberrant Protein Aggregation in Neurons
Authors: Feng Yu , Luan Tongshu , Zhang Zhenda , Wang Wei , Chu Yuanyuan , Wan Sijia , Pan Xiaorong , Li Jie , Liu Yifan , Wang Tong 
Published: January 2025

AbstractDirected axon trafficking of mRNA via ribonucleoprotein complexes (RNPs) is essential for the proper function and survival of neurons. However, the mechanisms governing RNP transport in axons remain poorly understood. Here, we identify Annexin A7 (ANXA7) as a critical adaptor facilitating the retrograde transport of T-cell intracellular antigen 1 (TIA1)-containing RNPs by linking them to the cytoplasmic dynein. Persistent axonal Ca²⁺ elevation disrupts ANXA7’s linker role, causing the detachment of TIA1 granules from dynein, consequently impairing transport and triggering pathological TIA1 aggregation within axons. Similarly, ANXA7 knockdown decouples TIA1 granules from dynein, severely obstructing trafficking and causing pathological aggregation of TIA1 in axons, which culminates in axonopathy and neurodegeneration bothin vitroandin vivo. Conversely, ANXA7 overexpression enhances trafficking and counteracts aberrant aggregation of TIA1-containing RNPs in axons. Our findings elucidate a novel mechanism underlying RNP axonal transport, highlighting its significance in the biology and pathology of central neurons.
Epigenetic Modulation of Host Immunity related genes in Pulmonary Tuberculosis: A Comprehensive Analysis of DNA Methylation Profiles in Peripheral Blood Mononuclear Cells
Authors: Kumar Ankit , Sharma Sumedha , Kaur Jyotdeep , Pal Arnab , Aggarwal Ashutosh Nath , Verma Indu 
Published: January 2025

AbstractBackgroundIn the last few years, there has been increasing evidence in the literature for promoter hypermethylation of various host genes following infection with various pathogens. Therefore, in the present study, the role of epigenetic reprogramming of host cells through DNA methylation was evaluated which indicates that the disease progression takes place through changes in host immune response related genes.ObjectiveTo elucidate the differential genome-wide DNA methylation profile of peripheral blood mononuclear cells in pulmonary tuberculosis (PTB) patients.Materials and methodsTo decipher the methylation profile of PBMCs in PTB patients whole genome bisulphite sequencing was performed using 4 DNA samples from each study group i.e. PTB, healthy controls and diseased controls. Briefly, the samples were subjected to bisulphite conversion followed by library preparation and whole genome bisulphite sequencing. The data then were analysed for differential methylation analysis followed by gene set enrichment analysis to select DMRs for validation by sanger sequencing. Further the GEOR2 online server was used to investigate the mRNA expression of selected genes associated with hypermethylated DMRs in promoter region.ResultsDifferential methylation region analysis was performed for the following comparisons. TB v/s Diseased (Hypermethylated=1756; Hypomethylated=1886), TB v/s Healthy( Hypermethylated=2203; Hypomethylated=2466), Diseased v/s Healthy ( Hypermethylated=1656; Hypomethylated=3936). Further gene set enrichment analysis showed that the hypermetylated regions belonged to genes that are involved in immune responses mainly T cell functioning and T cell mediated immune processes. There were 8 DMR belonging to TAF8,FZD5, HLA-DRB, MIR483, PVRIG, SH2B2, ZAP70, TNFRSF13C simultaneously (n=10 from each study group). mRNA expression analysis with GEOR2 (Datasets used n= 12) revealed significant downregulation of TNFRSF13C, ZAP70, PVRIG Among the selected genes associated with hypermethylated DMRs in promoter region.(e) ConclusionThe altered differential methylation profile of PBMCs from TB patients shows that on onset the active disease there occurs aberrant methylation of expression regulating regions that in turn results in decreased T cell functions and hence suboptimal immune responses in TB
New deep-branching environmental plastid genomes on the algal tree of life
Authors: Jamy Mahwash , Huber Thomas , Antoine Thibault , Ruscheweyh Hans-Joachim , Paoli Lucas , Pelletier Eric , Delmont Tom O. , Burki Fabien 
Published: January 2025

AbstractMarine algae support the entire ocean ecosystem and greatly impact planetary biology. The availability of algae in culture poorly represents their large environmental diversity, and we still have a limited understanding of their convoluted evolution by endosymbiosis. Here, we performed a phylogeny-guided plastid genome-resolved metagenomic survey ofTaraOceans expeditions. We present a manually curated resource of nearly 700 new non-redundant plastid genomes of environmental pelagic algae. This catalogue vastly expands the plastid genome diversity within major algal groups, often corresponding to algae without closely related reference genomes. We also recovered four genomes, including one near complete, forming a deep-branching plastid lineage of nano-size algae (<5 μm) that we informally named leptophytes. This group is globally distributed and generally rare, although it can reach relatively high abundance notably in the Arctic. Leptophytes encompass the enigmatic marine plastid group DPL2, one of the very few known plastid groups not clearly belonging to any major algal groups and for which only 16S amplicon data is available. Extensive phylogenetic analyses based on 93 plastid genes and gene content comparison firmly place leptophytes together with haptophytes and cryptophytes, although the exact relationships remain ambiguous. Collectively, our study demonstrates that metagenomics can reveal currently hidden diversity of organellar genomes, and shows the importance of including this diversity to improve models for plastid evolution.
Bacterial fitness for plant colonization is influenced by plant growth substrate
Authors: Torres Marta , Price Morgan N. , Kashanova Albina , Kosina Suzanne M. , Zhalnina Kateryna , Northen Trent R. , Deutschbauer Adam M. 
Published: January 2025

SummaryBacteria colonize plants and contribute to their health. Despite advances in our understanding of bacterial plant colonization, the extent to which growth substrate influences the molecular mechanisms enabling bacteria to efficiently colonize plants remains poorly understood.To evaluate if genes important for plant colonization are influenced by substrate, we used randomly barcoded transposon mutagenesis sequencing (RB-TnSeq) inParaburkholderia graminisOAS925, an efficient rhizosphere colonizer, andBrachypodium distachyonplants grown in six different substrates.Of the 382 rhizosphere colonization genes that we identified in strain OAS925, 348 genes (91.1%) are dependent on the growth substrate evaluated, and 34 genes (8.9%) are shared across all the substrates. To further characterize the plant colonization fitness genes, we compared our data to growth in 110 distinctin vitroconditions. To validate our results, we used individual mutants of selected genes and tested them in different growth substrates. We also show the influence of substrate on colonization byP. phytofirmansPsJN,Variovoraxsp. OAS795 andRhizobiumsp. OAE497.Our data confirms that bacterial fitness for plant colonization is strongly influenced by plant growth substrate type, and highlights the importance of taking this parameter into consideration when engineering bacterial strains for improved host colonization.
Quantifying heat exposure and its related mortality in Rio de Janeiro City: evidence to support Rio’s recent heat protocol
Authors: Araujo Morais João Henrique de , Medeiros de Oliveira e Cruz Débora , Saraceni Valeria , Dias Ferreira Caroline , Mateus Oliveira Aguilar Gislani , Gonçalves Cruz Oswaldo 
Published: January 2025

AbstractUnder a climate change scenario, extreme heat episodes show an increase in frequency and intensity, with a scaling impact in Latin American cities. Recently, Rio de Janeiro City developed its heat protocol, using the amount of hours spent over specific heat thresholds as its trigger metric. This study gathers mortality data by 17 different causes in Rio, in a 12.5 year period (2012-2024). We use Distributed Lag Non-Linear Models (DLNM) to assess the relationship between different heat exposure metrics to mortality among the young (< 65) and elderly (>=65y), including a novel metric called Heat Area Above a Threshold (HAAT). In the study period, there were 466,121 deaths in the city from natural causes. Deaths due to diabetes, hypertensive diseases, Alzheimer’s/dementia, renal failure and even undetermined deaths were strongly associated with extreme heat episodes, especially among the elderly. The proposed HAAT metric showed better performance on explaining mortality for most causes (10 out of the 17), when compared to temperature or heat index, or commonly used heat wave definitions. The results dialogue with Rio’s heat protocol, evaluating the cut-off points defined and proposing simpler definitions using the HAAT metric. An exposure to a HAAT of 64°C*h increases mortality by natural causes by 50%, and 91.2°C*h already doubles the mortality risk. Main strengths of the study lie on the comparison of different heat exposure metrics and the investigation of cause-specific mortality in a period when recent and remarkable heat waves occurred. There is still fragility when considering a compound index such as the Heat Index, and social and spatial differences on heat-related mortality should also be considered in future models. The proposed metric, however, appears as a relevant indicator to distinguish unusually warm days that lead to elevated mortality, and could guide definitions for Heat Warning Systems.
Computable Phenotypes for Respiratory Viral Infections in theAll of UsResearch Program
Authors: Waxse Bennett J , Carrillo Fausto Andres Bustos , Tran Tam C , Mo Huan , Ricotta Emily E , Denny Joshua C 
Published: January 2025

ABSTRACTElectronic health records (EHRs) contain rich temporal data about infectious diseases, but an optimal approach to identify infections remains undefined. Using theAll of UsResearch Program, we developed computable phenotypes for respiratory viruses by integrating billing codes, prescriptions, and laboratory results within 90-day episodes. Phenotypes computed from 265,222 participants yielded cohorts ranging from 238 (adenovirus) to 28,729 (SARS-CoV-2) cases. Virus-specific billing codes showed varied sensitivity (8-67%) and high positive predictive value (90-97%), except for influenza virus and SARS-CoV-2 where lower PPV (69-70%) improved with increasing billing codes. Identified infections exhibited expected seasonal patterns and virus proportions when compared with CDC data. This integrated approach identified episodic disease more effectively than individual components alone and demonstrated utility in identifying severe infections. The method enables large-scale studies of host genetics, health disparities, and clinical outcomes across episodic diseases.
Mitochondrial Ca2+flickers on endoplasmic reticulum (ER)-mitochondrial contact sites to suppress store-operated Ca2+entry
Authors: Lin Yu-Chiao , Tsai Feng-Chiao 
Published: January 2025

SummarySuccessful Ca2+signaling requires appropriate Ca2+storage and buffering by endoplasmic reticulum (ER) and mitochondria. Recent research has elucidated how Ca2+storage in ER is controlled by STIM1-mediated store-operated Ca2+entry (SOCE). However, how cells employ mitochondrial Ca2+buffering to maintain Ca2+homeostasis has remained elusive. Here, with the use of mitochondria-tethered Ca2+sensor, we noticed local Ca2+flickering within individual mitochondria. Those Ca2+flickers were generated on ER-mitochondrial contact sites (EMC), as indicated by their downregulation under EMC breakdown and upregulation under EMC induction. Surprisingly, EMC breakdown increased SOCE while EMC induction reduced SOCE. Further investigations revealed that EMC effect on SOCE was not through biological functions of mitochondria or through STIM1 regulators, but via IP3R-VDAC1-driven mitochondrial Ca2+flickers on EMC. Those flickers depleted peri-EMC Ca2+inside ER, resulting in STIM1 sequestration around EMC to cause SOCE reduction. Moreover, EMC breakdown also increased availability of STIM1 to bind with microtubule plus ends, preventing STIM1 over-activation and SOCE upregulation. Overall, ER, mitochondria and microtubules constitute a self-sufficient system to control Ca2+homeostasis, driven by mitochondrial Ca2+flickers to reduce SOCE and to prevent intracellular Ca2+overload.
Postnatal reduction of eIF4E overexpression in D1-SPNs ameliorates KCNQ dysfunction, hyperexcitability and ASD-like behaviours
Authors: Aaltonen Alina , Tamaki Ayu , Ramón Andrés Peris , Borgkvist Anders , Santini Emanuela 
Published: January 2025

AbstractAn imbalance between the direct and indirect pathways of the striatum has been implicated in the pathophysiology of ASD, which corresponds with an increase in repetitive behaviours and hyperactivity. The ASD risk geneEIF4Epromotes translation, and its overexpression in mice increases repetitive behaviours and hyperactivity. We used the eIF4E-transgenic mouse model of ASD to study cell-type specific disruptions in the direct and indirect pathways using fibre photometry, electrophysiology, conditional gene silencing, and behavioural analysis. We found that direct pathway SPNs activity increased during exploratory behaviour and identified D1-SPN hyperexcitability and reduced KCNQ channel function in striatal slices. Reduction of eIF4E specifically in the D1-SPNs of adult mice normalised KCNQ function, D1-SPN hyperexcitability and ameliorated repetitive and hyperactive behaviours. Our results highlight the critical role of eIF4E in ASD-associated motor behaviours, elucidate cell-specific mechanisms driving hyperactivity and provide new insight into potential therapeutic targets for ASD and other neurodevelopmental disorders. Overall, this study underscores the translational potential of modulating protein synthesis pathways to address core motor symptoms in ASD.
Unleashing service recovery excellence: exploring the power of dimensional autonomy and thriving at work as catalysts during COVID-19
Authors: Farid Hasan , Zhang Yang , Tian Ming , Lu Shiyao 
Published: January 2025

PurposeThis study explores how three-dimensional job autonomy (decision-making, work method and work scheduling) affects employees’ thriving at work and service recovery performance in the hospitality industry during COVID-19.Design/methodology/approachThis study utilized cross-sectional dyadic data from 287 frontline workers in the Chinese hospitality sector and analyzed it with Analysis of Moment Structures (AMOS) and the PROCESS macro.FindingsThe findings indicate that three-dimensional autonomy has a direct impact on thriving and an indirect effect on service recovery performance (SRP) through thriving, and the relationship between three-dimensional autonomy and thriving is moderated by SOCV19R.Originality/valueThis study addresses the existing gap in research regarding the various aspects of autonomy. It explores how distinct dimensions of autonomy affect employees’ thriving at work and, in turn, influence their ability to excel in service recovery. Furthermore, it sheds light on how the unique circumstances of COVID-19, as represented by SOCV19R, play a role in understanding the dynamics between different forms of autonomy and employees’ thriving.
Grey system theory in supply chain: emerging hotspots and trends
Authors: Jiang Peng , Dong Zhaohu , Sun Hong , Song Yingchun , Zou Qingqing 
Published: January 2025

PurposeSupply chains, as prototypical uncertain systems, are crucial for national security and socioeconomic development. Grey system theory (GST) is an effective tool for addressing uncertainties and has played a pivotal role in related research within the supply chain domain. This study aims to systematically summarize the research achievements and knowledge structures pertaining to GST in supply chain studies. Current and potential research hotspots are also analyzed.Design/methodology/approachCiteSpace is used to conduct a bibliometric analysis of 1,617 articles sourced from the Web of Science (WOS). The analysis aims to summarize the current state of research and the knowledge structure in the field. A strategic diagram incorporating two data indicators, namely, novelty and concern, is constructed based on keyword clustering to identify and analyze current and potential research hotspots.FindingsStudies utilizing GST to guide supply chain practices have attracted the interest of scholars from 205 research institutions across 85 countries and regions globally, which earned recognition from 183 high-level academic journals. In this field, the School of Economics and Management at Nanjing University of Aeronautics and Astronautics stands out as a core research institution, with Professor Deng Julong, who is the founder of GST, being the most frequently cited scholar. Current research hotspots are complex equipment supply chains, drivers and challenges in supply chain management, supply chain risk management, closed-loop supply chain and supply chain operation in the big data era. In addition, emerging research hotspots include digital and intelligent logistics technology, sustainable supplier management, determinants and flexibility of supply chain contracts, supply chain strategy, purchase management, grey prediction of demand and consumption, grey forecasting and economy efficiency, China-specific issues and grey model construction.Originality/valueThe bibliometric analysis reveals the current state and knowledge structure of research in this field. Previous studies on research hotspots have primarily relied on subjective judgments, which lacked empirical data support. This study constructs a strategic diagram incorporating two data indicators, namely, novelty and concern, to provide a more objective and reliable analysis of research hotspots.