bluuebunny/crossref_metadata_2025_split huggingface dataset:
Climate change and tuberculosis: an analytical framework
Authors: Saunders Matthew J , Boccia Delia , Khan Palwasha Y , Goscè Lara , Gasparrini Antonio , Clark Rebecca A , Pescarini Julia M , White Richard G , Houben Rein MGJ , Zignol Matteo , Gebreselassie Nebiat , Finn McQuaid C 
Published: February 2025

SummaryClimate change is likely to exacerbate a range of determinants which drive tuberculosis, the world’s leading infectious disease killer. However, tuberculosis is often neglected in wider climate health discussions.Commissioned by the World Health Organization, we developed an analytical framework outlining potential causal relationships between climate change and tuberculosis. We drew on existing knowledge of tuberculosis determinants, identified which are likely to be sensitive to the effects of climate change, and conceptualised the mechanistic pathways through which this might occur. We collated evidence for these pathways through literature reviews. Our reviews found no studies directly linking climate change and tuberculosis, warranting research to build evidence for action.The available evidence supports the existence of plausible links between climate change and tuberculosis, and highlights the need to include tuberculosis in climate risk adaptation and mitigation programmes, and climate-resilient funding and response mechanisms. Further evidence is urgently needed to quantify the effects of climate change on tuberculosis.
Frequency and Predictors of Adolescent Worry for School Gun Violence In the United States: Findings from a Nationally Representative Study
Authors: Kirkland Danielle , Fu Tsung-chieh , Herbenick Debby , Hensel Devon J. 
Published: February 2025

AbstractPurposeWhile school gun violence (SGV) incidents in the United States (U.S.) have risen sharply over the past decade, limited research has examined adolescent worries about SGV. We examined the frequency and correlates of SGV worry in a U.S. nationally representative sample of adolescents.MethodsData were from adolescent participants (14–17 years; N = 1017) in the 2022 National Survey of Sexual Health and Behavior, a nationally representative study of sexual health experiences of people in the U.S. SGV worry was a single 5-point item (not at all worried – extremely worried). We used both weighted descriptive statistics to examine SGV frequency and random intercept mixed effects ordinal regression to examine demographic and background impact on SGV worry.ResultsNearly 75% of adolescents reported some degree of SGV worry; of these, one in five were very or extremely worried. SGV worry was significantly higher for adolescents in younger grades and among racial/ethnic minority youth, as well as for cisgender female and gender minority teens. Adolescents in higher income homes were less worried about SGV. Both teens living in metropolitan locations and teens who reported higher anxiety in the past two weeks noted higher SGV worry.ConclusionsU.S. adolescents have a substantial level of worry about school gun violence. Structural interventions are needed to reduce SGV itself. Moreover, because there are detrimental long-term impacts of prolonged worry, targeted interventions are important for reaching those who are at greatest worry risk, including lower income, race/ethnic minority and gender minority teens.Implications and ConclusionsThree out of every four adolescents in the United States worry about being a victim of school gun violence. Structural interventions to both reduce SGV itself and to reach adolescents at greatest risk for SGV worry are warranted.
Fibroblast growth factor 21 regulates neuromuscular junction innervation through HDAC4 in denervation-induced skeletal muscle atrophy
Authors: Zheng Lirong , Sasaki Takashi , Ni Liyang , Takahashi Yu , Yamauchi Yoshio , Shimizu Makoto , Ryuichiro Sato 
Published: February 2025

AbstractSkeletal muscles undergo atrophy in response to denervation and neuromuscular diseases. Understanding the mechanisms by which denervation drives muscle atrophy is crucial for developing therapies against neurogenic muscle atrophy. Here, we identify muscle-secreted fibroblast growth factor 21 (FGF21) as a key inducer of atrophy following muscle denervation. In denervated skeletal muscles, FGF21 is uniquely upregulated among the FGF family members and acts in an autocrine/paracrine manner to promote muscle atrophy. Silencing FGF21 in muscle prevents denervation-induced muscle wasting by preserving neuromuscular junction (NMJ) innervation. Conversely, forced expression of FGF21 in muscle reduces NMJ innervation, leading to muscle atrophy. Mechanistically, TGFB1 released by denervated fibro-adipogenic progenitors (FAPs) upregulates FGF21 through the JNK/c-Jun axis, which in turn reduces the cytoplasmic level of histone deacetylase 4 (HDAC4), culminating in muscle atrophy. HDAC4 knockdown abolishes the atrophy-resistant effects observed in FGF21-deficient denervated muscles, resulting in muscle atrophy. Our findings reveal a novel role and heretofore unrecognized mechanism of FGF21 in skeletal muscle atrophy, suggesting that inhibiting muscular FGF21 could be a promising strategy for mitigating skeletal muscle atrophy.
Developing Interferon-β as a safe in-vivo experimental-medicine model of human inflammation
Authors: Periche-Tomas Eva , Maclver Claire , Underwood John , Leach Helena , Bone Claudia , Jones Simon , Szomolay Barbara , Triantafilou Kathy , Harrison Neil A. 
Published: February 2025

AbstractBackgroundInflammation is increasingly implicated in a wide range of neuropsychiatric disorders ranging from depression through age- and infection-related cognitive decline to dementia. Arguably, the most important evidence supporting an aetiological role for inflammation in these conditions in humans has come from studies of patients receiving IFN- α therapeutically or longitudinal follow-up of patients after naturalistic infections (e.g., hepatitis C). These experimental medicine-type approaches have identified a discrete set of brain regions e.g. amygdala-hippocampus-hypothalamus, insula and anterior cingulate as well as dopamine-rich subcortical structures that are particularly sensitive to systemic inflammation. Coupled with renewed interest in developing novel immune-targeted therapies for neuropsychiatric disorders as diverse as depression and neurodegenerative disorders, this has highlighted the urgent need for a safe, reliable in-vivo experimental medicine model of inflammation that can be used across the age range. To date, this need has been partially addressed by access to short-acting forms of Interferon-alpha or human (GMP) grade lipopolysaccharide (LPS). However, unpegylated IFN-α is no longer commercially available and the costs and cardiovascular monitoring requirements of low-dose (i.e. 0.8-1ng/Kg i.v. endotoxin) LPS are prohibitive and particularly challenging to use in older or more vulnerable populations.AimDevelop a new experimental model of human inflammation that elicits robust sickness responses within a few hours but with minimal cardiovascular effects, thus avoiding the need for continuous cardiac monitoring and ensuring applicability across diverse experimental contexts and participant groups from the young to the elderly.MethodsUsing a randomized, placebo-controlled, repeated measures cross-over design, physiological, behavioural, immune and transcriptomic responses were collected from 30 healthy volunteers (15 young [18-34] and 15 old [60-75]) following both IFN-β (EXTAVIA® [100 µg]) and saline (placebo) injections.ResultsIFN-β induced a robust systemic immune response, evidenced by significant increases in temperature, heart rate, immune cell activation (lymphocytes, monocytes and neutrophils) and levels of IFN-β, IL-10 and TNF-α cytokines. These physiological changes were accompanied by significant increases in negative mood, tiredness, tension and sickness symptoms aa well as by a decrease in vigour.ConclusionsFN-β is a safe and robust new experimental model of mild acute inflammation, This minimally invasive and effective design can induce transient changes in systemic inflammation in healthy individuals from 18-75. A more refined, ecologically valid model similar to the mild inflammation typically reported in psychiatric disorders like depression or cognitive impairment.
Intracellular Trafficking SNARE Protein, Syntaxin-6, is a Modifier of Prion and Tau Pathogenesisin vivoand in Cellular Models
Authors: Hill Elizabeth , Patel Mitali , Ribes Juan M , Linehan Jacqueline , Zhang Fuquan , Farmer Michael , Jakubcova Tatiana , Hamdan Shyma , Tomlinson Andrew , Ercolani Tiziana , Schmidt Christian , Ahmed Parvin , Thirlway George , Purro Silvia , Argentina Fabio , Marinho Aline T , Jones Emma , Kaye Nicholas , Fitzhugh Craig , de Silva Rohan , Jackson Graham S , Brandner Sebastian , Kloehn Peter , Collinge John , Cunningham Thomas J , Mead Simon 
Published: February 2025

AbstractSyntaxin-6, a SNARE protein involved in intracellular protein trafficking, is a proposed risk factor for sporadic prion disease, progressive supranuclear palsy and Alzheimer’s disease. However, no study has validated its functional role in these diseases, explored the disease stage at which it is acting nor its mechanism of action. Here, we show that syntaxin-6 acts at early stages of prion disease in experimental mice by increasing disease transmission risk following inoculation with low prion doses. Conversely, syntaxin-6 does not affect prion propagation kinetics or toxicity during established disease. Syntaxin-6 manipulation in cellular models profoundly alters the subcellular distribution and morphologies of disease-related PrP and modifies prion export. Furthermore, syntaxin-6 knockout in a transgenic tauopathy mouse model exerts protective effects on numerous physiological, behavioural and neuropathological outcome measures. Therefore, our studies firmly establish syntaxin-6 as a modifier of prion and tau pathogenesis, providing key insights into a fundamental mechanism of neurodegeneration.
Lysyl-phosphatidylglycerol promotes cell-to-cell interaction and biofilm formation ofStaphylococcus aureusas a biofilm matrix component
Authors: Sugimoto Shinya , Hara Keiichiro , Taketomi Yoshitaka , Nagasaki Yuki , Sato Chikara , Murakami Makoto , Kinjo Yuki 
Published: February 2025

AbstractBiofilms formed byStaphylococcus aureuscontribute significantly to persistent infections and antibiotic resistance, driven by the unique composition of their extracellular matrix. While previous studies highlighted extracellular DNA, proteins, and polysaccharides as key components, the role of phospholipids in biofilm architecture remains underexplored. This study identifies extracellular phospholipids, including lysyl-phosphatidylglycerol (Lys-PG), phosphatidylglycerol, and cardiolipin (CL), as critical structural elements inS. aureusbiofilms. Bacterial phospholipase A1(PLA1) that cleaves the acyl ester bond at thesn-1 position of phospholipids effectively dispersed pre-formed biofilms and prevented new biofilm formation by hydrolyzing extracellular phospholipids, without affecting bacterial growth or exhibiting cytotoxicity. Microscopy analyses confirmed that PLA1disrupts membranous nanostructures, including extracellular vesicles and nanofilaments, integral to biofilm stability. Lipidomic analysis revealed an enrichment of Lys-PG and CL in the biofilm matrix. Lys-PG promotes bacterial aggregation by acting as a molecular glue, mediated through electrostatic and hydrophobic interactions. Deletion of themprFgene, responsible for Lys-PG synthesis, significantly impaired biofilm formation, confirming its essential role. These findings reveal a "moonlighting" function of phospholipids in biofilm architecture, providing insights into biofilm biology and presenting PLA1as a promising tool for biofilm control.SignificanceBiofilms, dense bacterial communities, pose significant challenges across medical, industrial, and daily life contexts. Understanding their formation mechanisms is crucial for developing effective strategies against them. We investigated biofilm matrix components inS. aureusbiofilms, focusing on phospholipids. Our study reveals the presence and significance of Lys-PG in the biofilm matrix, acting as a crucial factor in biofilm formation and maintenance. Through biochemical, lipidomic, and genetic analyses, we demonstrate the role of Lys-PG in facilitating cell-to-cell contacts, contributing to the robustness and thickness ofS. aureusbiofilms. These findings shed light on the physiological function of extracellular phospholipids in bacterial biofilms and suggest targeting Lys-PG and its synthetic mechanism as a promising strategy for biofilm control.
Drivers of avian genomic change revealed by evolutionary rate decomposition
Authors: Duchêne David A. , Chowdhury Al-Aabid , Yang Jingyi , Iglesias-Carrasco Maider , Stiller Josefin , Feng Shaohong , Gilbert M. Thomas P. , Zhang Guojie , Tobias Joseph A. , Ho Simon Y. W. 
Published: February 2025

SummaryModern bird diversity spans a striking array of forms, behaviours, and ecological roles. Analyses of molecular evolutionary rates can reveal the links between genomic and phenotypic change, but disentangling the drivers of rate variation has been difficult across large numbers of whole-genomes. Using comprehensive estimates of traits and evolutionary rates across a family-level phylogeny of birds, we show that clutch size, generation length, and beak shape are dominant predictors of genome-wide mutation rates. To identify the major axes of evolutionary rate variation, we employ covariance matrix eigendecomposition from rates estimated for branches of the avian phylogeny and across genomic loci. We find that the majority of rate variation occurs along the terminal branches of the phylogeny associated with extant families of birds. Additionally, we use principal components analyses to show that several axes of variation are linked with rapid evolution in microchromosomes immediately after the Cretaceous–Palaeogene transition. These apparent pulses of evolution are consistent with major changes in evolutionary rates in the machineries for meiosis, heart performance, and RNA splicing, surveillance, and translation. They also correlate with the diversification of ecological niches reflected in increased tarsus length. Collectively, our analyses paint a nuanced picture of avian evolutionary rates through time, revealing that the ancestors of the most diverse lineages of birds underwent major genomic changes related to mutation, gene usage, and niche expansion near the beginning of the Palaeogene period.
Boosting Brainpower in Ageing: Task-Specific and Transfer Effects of tDCS-Enhanced Working Memory Training
Authors: León-Correa Esteban , Ruhnau Philipp , Balani Alex , Qureshi Adam , Tse Dorothy , Makris Stergios 
Published: February 2025

ABSTRACTAgeing is associated with neural alterations that impair cognitive abilities, particularly working memory (WM)—the capacity to temporarily store and manipulate information essential for daily functioning. Transcranial Direct Current Stimulation (tDCS) has shown promise in enhancing WM in older adults by modulating cortical excitability and promoting neuroplasticity. However, findings on the combined effects of tDCS and WM training remain inconsistent, particularly regarding transfer effects to non-trained WM tasks (near transfer) or other cognitive domains (far transfer).This study examined the behavioural and neural effects of tDCS on distinct WM phases (encoding, retention/manipulation, recall) in older adults. Over three weeks, participants underwent six sessions of adaptive WM training paired with tDCS targeting the left dorsolateral prefrontal cortex (DLPFC). Neural activity was assessed via EEG, focusing on theta and alpha bands. Participants were divided into tDCS and placebo groups and completed two WM tests, the Letter Span and Corsi Test, with retention and manipulation conditions.Results showed no additional behavioural or neural benefits of tDCS. However, both groups exhibited near-transfer effects that persisted one-month post-training. Neural changes varied by task: the Letter Span showed increased alpha power during manipulation, indicating enhanced maintenance of information during that phase, while the Corsi Test showed reduced left-hemisphere theta power during recall, reflecting reduced hemispheric asymmetry.Inter-individual variability likely contributed to inconsistencies and a lack of correlations between outcomes. These findings highlight the importance of personalised tDCS protocols and suggest adaptive WM training can yield enduring cognitive and neural benefits in older adults.
Histone Lysine Crotonylation Regulates Long-Term Memory Storage
Authors: Mukherjee Utsav , Basu Budhaditya , Beyer Stacy E. , Ghodsi Saaman , Robillard Nathan , Vanrobaeys Yann , Taylor Eric B. , Abel Ted , Chatterjee Snehajyoti 
Published: February 2025

AbstractHistone post-translational modifications (PTMs), particularly lysine acetylation (Kac), are critical epigenetic regulators of gene transcription underlying long-term memory consolidation. Beyond Kac, several other non-acetyl acylations have been identified, but their role in memory consolidation remains unknown. Here, we demonstrate histone lysine crotonylation (Kcr) as a key molecular switch of hippocampal memory storage. Spatial memory training induces distinct spatiotemporal patterns of Kcr induction in the dorsal hippocampus of mice. Through genetic and pharmacological manipulations, we show that reducing hippocampal Kcr levels impairs long-term memory, while increasing Kcr enhances memory. Utilizing single-nuclei multiomics, we delineate that Kcr enhancement during memory consolidation activates transcription of genes involved in neurotransmission and synaptic function within hippocampal excitatory neurons. Cell-cell communication analysis further inferred that Kcr enhancement strengthens glutamatergic signaling within principal hippocampal neurons. Our findings establish Kcr as a novel epigenetic mechanism governing memory consolidation and provide a foundation for therapeutic strategies targeting memory-related disorders.
Metabolically flexible microorganisms rapidly establish glacial foreland ecosystems
Authors: Ricci Francesco , Bay Sean K. , Nauer Philipp A. , Wong Wei Wen , Ni Gaofeng , Jimenez Luis , Jirapanjawat Thanavit , Leung Pok Man , Bradley James A. , Eate Vera M. , Hall Montgomery , Stubbusch Astrid , Fernández-Marin Beatriz , de los Ríos Asunción , Cook Perran L.M. , Schroth Martin H. , Chiri Eleonora , Greening Chris 
Published: February 2025

AbstractAn overriding question in ecology is how new ecosystems form. This question can be tested by studying colonisation of environments with little to no pre-existing life. Here, we investigated the functional basis of microbial colonisation in the forelands of a maritime Antarctic and an alpine Swiss retreating glacier, by integrating quantitative ecology, genome-resolved metagenomics, and biogeochemical measurements. Habitat generalists and opportunists rapidly colonize both forelands and persist across soil depth and decadal chronosequences that serve as proxies for temporal community dynamics. These microbes are metabolically flexible chemotrophic aerobes that overcome oligotrophic conditions by using both organic and inorganic compounds, including atmospheric trace gases and sulfur substrates, for energy and carbon acquisition. They co-exist with metabolically flexible early-colonising opportunists and metabolically restricted later-colonising specialists, including photosynthetic Cyanobacteria, ammonia-oxidising archaea, and obligate predatory and symbiotic bacteria, that exhibit narrower habitat distributions. Analysis of 589 species-level metagenome-assembled genomes reveals early colonisation both by generalists and opportunists is strongly associated with metabolic flexibility. Field- and laboratory-based biogeochemical measurements reveal the activity of metabolically flexible microbes rapidly commenced in the forelands. Altogether, these findings suggest primary succession in glacial foreland soils is driven by self-sufficient metabolically flexible bacteria that mediate chemosynthetic primary production and likely provide a more hospitable soil environment for subsequent colonisation.
The neural basis of creative thought: An activation likelihood estimation meta-analysis involving over 17,000 participants
Authors: Chan Melody M.Y. , Lambon Ralph Matthew A. , Robinson Gail A. 
Published: February 2025

AbstractHumans can create impressive art, make major scientific breakthroughs, and generate creative solutions that solve everyday life problems. But how are these creative activities supported by the brain? This question is of great scientific interest but remains unanswered. New hypotheses, grounded in converging evidence from cognitive neuroscience, are needed to guide breakthroughs in understanding the neural basis of creative thought. It has long been suggested that creativity is a distinct mental function. However, converging clinical-cognitive neuroscience evidence is starting to suggest that creative thought is not functionally distinct but, instead, might arise from general purpose cognitive mechanisms supporting semantic cognition, controlled episodic memory retrieval, and executive mechanisms (i.e.,Cognitive Cornerstones Hypothesis; Chan et al., 2023). Results from this large-scale activation likelihood estimation (ALE) meta-analysis, based on 787 experiments with 10,357 foci from 17,228 healthy adult participants, showed that the brain regions implicated in creativity tasks heavily overlap with the brain regions implicated in the cognitive cornerstones of creative thought (i.e., pre-existing knowledge and executive mechanisms). These striking results suggest that innovative insights will arise from considering the roles of these fundamental cognitive functions and their interactions in supporting creative thought.
Search for Highly Ionizing Particles in
pp
Collisions during LHC Run 2 Using the Full MoEDAL Detector
Authors: Acharya B. , Alexandre J. , Benes P. , Bergmann B. , Bertolucci S. , Bevan A. , Brancaccio R. , Branzas H. , Burian P. , Campbell M. , Cecchini S. , Cho Y. M. , de Montigny M. , De Roeck A. , Ellis J. R. , Fairbairn M. , Felea D. , Frank M. , Hays J. , Hirt A. M. , Ho D. L.-J. , Hung P. Q. , Janecek J. , Kalliokoski M. , Lacarrère D. H. , Leroy C. , Levi G. , Margiotta A. , Maselek R. , Maulik A. , Mauri N. , Mavromatos N. E. , Mieskolainen M. , Millward L. , Mitsou V. A. , Mukhopadhyay A. , Musumeci E. , Ostrovskiy I. , Ouimet P.-P. , Papavassiliou J. , Patrizii L. , Păvălaş G. E. , Pinfold J. L. , Popa L. A. , Popa V. , Pozzato M. , Pospisil S. , Rajantie A. , Ruiz de Austri R. , Sahnoun Z. , Sakellariadou M. , Sakurai K. , Sarkar S. , Semenoff G. , Shaa A. , Sirri G. , Sliwa K. , Soluk R. , Spurio M. , Staelens M. , Suk M. , Tenti M. , Togo V. , Tuszyński J. A. , Upreti A. , Vento V. , Vives O. ,   MoEDAL Collaboration
Published: February 2025

This search for magnetic monopoles (MMs) and high electric charge objects (HECOs) with spins 0, 1/2, and 1, uses for the first time the full MoEDAL detector, exposed to 6.46  fb−1 proton-proton collisions at 13 TeV. The results are interpreted in terms of Drell-Yan and photon-fusion pair production. Mass limits on direct production of MMs of up to 10 Dirac magnetic charges and HECOs with electric charge in the range 10e to 400e, were achieved. The charge limits placed on MM and HECO production are currently the strongest in the world. MoEDAL is the only LHC experiment capable of being directly calibrated for highly ionizing particles using heavy ions and with a detector system dedicated to definitively measuring magnetic charge.

Published by the American Physical Society
2025