bluuebunny/crossref_metadata_2025_split huggingface dataset:
Harnessing extracellular cold-inducible RNA binding protein by PS-OMe miR130: A promising shield against hemorrhage-induced lung injury
Authors: Hu Zhijian , Li Jingsong , Jacob Asha , Wang Ping 
Published: April 2024

INTRODUCTION
Hemorrhagic shock (HS) poses a life-threatening condition with the lungs being one of the most susceptible organs to its deleterious effects. Extracellular cold-inducible RNA binding protein has emerged as a pivotal mediator of inflammation, and its release has been observed as a case of HS-induced tissue injury. Previous studies unveiled a promising engineered microRNA, designated PS-OMe miR130, which inhibits extracellular cold-inducible RNA binding protein, thereby safeguarding vital organs. In this study, we hypothesized that PS-OMe miR130 serves as a protective shield against HS-induced lung injury by curtailing the overzealous inflammatory immune response.

METHODS
Hemorrhagic shock was induced in male C57BL6 mice by withdrawing blood via a femoral artery cannula to a mean arterial pressure of 30 mm Hg for 90 minutes. The mice were resuscitated with twice the shed blood volume with Ringer's lactate solution. They were then treated intravenously with either phosphate-buffered saline (vehicle) or 62.5 nmol PS-OMe miR130. At 4 hours later, blood and lungs were harvested.

RESULTS
Following PS-OMe miR130 treatment in HS mice, a substantial decrease was observed in serum injury markers including aspartate aminotransferase, alanine transaminase, lactate dehydrogenase, and blood urea nitrogen. Serum interleukin (IL)-6 exhibited a similar reduction. In lung tissues, PS-OMe miR130 led to a significant decrease in the messenger RNA expressions of pro-inflammatory cytokines (IL-6, IL-1β, and tumor necrosis factor α), chemokines (keratinocyte-derived chemokine and macrophage inflammatory protein 2), and an endothelial injury marker, E-selectin. PS-OMe miR130 also produced substantial inhibition of lung myeloperoxidase activity and resulted in a marked reduction in lung injury as evidenced by histological evaluation. This was further confirmed by the observation that PS-OMe miR130 significantly reduced the presence of lymphocyte antigen 6 family member G–positive neutrophils and terminal deoxynucleotidyl transferase dUTP nick end labeling–positive apoptotic cells.

CONCLUSION
PS-OMe miR130 emerges as a potent safeguard against HS-induced lung injury by effectively inhibiting pro-inflammation and injuries, offering a promising therapeutic strategy in such critical clinical condition.
Effect of contextual prediction on emotional word processing: an evidence from ERPNR-D-24-00189
Authors: Li Yulin , Sui Xue , Li Yutong 
Published: April 2024

Objective
This study examined the effect of context on the prediction of emotional words with varying valences. It investigated the neural mechanisms underlying the processing differences of emotion words with different valences in both predictable and unpredictable contexts. Additionally, it aimed to address the conflicting results regarding the processing time in predictive contexts reported in previous studies.

Methods
Participants were instructed to carefully read the text that included the specified emotion words. Event-related potentials elicited by emotional words were measured. To ensure that the participants can read the text carefully, 33% of the texts are followed by comprehension problems. After reading the text, the comprehension questions were answered based on the text content.

Results
The study revealed that the N400 amplitude elicited by an unpredictable context was greater than that elicited by a predictable context. Additionally, the N400 amplitude triggered by positive emotion words was larger than that triggered by negative emotion words. However, there was no significant difference in late positive component amplitude observed between contextual prediction and emotional word valence.

Conclusion
The present study suggests that predictive processing takes place at an intermediate stage of speech processing, approximately 400 ms after stimulus onset. Furthermore, the presence of a predictive context enhances the processing of emotional information. Notably, brain activity is more pronounced during the processing of positive emotional stimuli compared to negative emotional stimuli. Additionally, the facilitative effect of a predictable context diminishes in the advanced phase of Chinese speech comprehension.
The Relationship between microbial population adenosine triphosphate and quantitative polymerase chain reaction bioburdens in diesel fuel microcosms
Authors: Passman Frederick J. , Schmidt Jordan , Nicoletti Danika 
Published: April 2024

Historically, fuel microbiology studies have relied on culture data. Potentially relevant but unculturable were not detected. Although adenosine triphosphate (ATP) can quantify total microbial bioburdens in fuels, it cannot differentiate among the taxa present. Quantitative polymerase chain reaction (qPCR) testing promises to fill this gap by quantifying targeted amplicon sequences and thereby detecting both culturable and non-culturable taxa and quantifying specifically targeted taxa. In this study, fluid samples drawn from the fuel, interface, and water phases of fuel over water microcosms were tested for cellular ATP concentration ([cATP]), and qPCR bioburdens. Additionally, surface swab samples from steel corrosion coupon surfaces exposed to each of these three phases were collected and tested for total ATP concentration ([tATP]) and qPCR bioburdens. Statistical relationships between ATP and qPCR bioburdens were examined. Correlation coefficients between the two variables were matrix dependent and ranged from negligible (|r| = 0.2) to strong (|r| = 0.7). When results were categorized into negligible, moderate, and heavy bioburdens, parameter agreement was again matrix dependent. Percent agreement between [ATP] and qPCR gene copies ranged from 11 % to 89 % – with qPCR-bioburden ratings typically being greater than ATP-bioburden ratings.
The Role of Genomic-Informed Risk Assessments in Predicting Dementia Outcomes
Authors: Andrews Shea J. , Jonson Caroline , Fulton-Howard Brian , Renton Alan E , Yokoyama Jennifer S , Yaffe Kristine ,   the Alzheimer’s Disease Neuroimaging Initiative
Published: April 2024

AbstractImportanceBy integrating genetic and clinical risk factors into genomic-informed dementia risk reports, healthcare providers can offer patients detailed risk profiles to facilitate understanding of individual risk and support the implementation of personalized strategies for promoting brain health.ObjectiveTo develop a genomic-informed risk assessment composed of family history, genetic, and clinical risk factors and, in turn, evaluate how the risk assessment predicted incident dementia.DesignThis longitudinal study included data from two clinical case-control cohorts with an average of 6.6 visits. Secondary analyses were conducted from July 2023 - March 2024.SettingData were previously collected across multiple US locations from 1994 to 2023.ParticipantsOlder adults aged 55+ with whole-genome sequencing and dementia-free at baseline.ExposuresAn additive score comprising the modified Cardiovascular Risk Factors, Aging, and Incidence of Dementia Risk Score (mCAIDE), family history of dementia, APOEgenotype, and an AD polygenic risk score.Main Outcome(s) and Measure(s)The risk of progression to all-cause dementia was evaluated using Cox-proportional hazard models (hazard ratios with 95% confidence intervals [OR 9%CI]).ResultsA total of 3,429 older adults were included (aged 75 ± 7 years; 59% female; 75% non-Latino White, 15% Black, 5.2% Latino, 3.6% other, and 0.4% Asian; 27% MCI), with 751 participants progressing to dementia. The most common high-risk indicator was a family history of dementia (56%), followed byAPOE*ε4 genotype (36%), high mCAIDE score (34%), and high AD-PRS (11%). Most participants had at least one high-risk indicator, with 39% having one, 32% two, 9.8% three, and 1% four. The presence of 1, 2, 3, or 4 risk indicators was associated with a doubling (HR = 1.72, CI: 1.34-2.22, p = 2.5e-05), tripling (HR = 3.09, CI: 2.41-3.95, p = 4.4e-19), quadrupling (HR = 4.46, CI: 3.34-5.94, p = 2.2e-24), and a twelvefold increase (HR = 12.15, CI: 7.33-20.14, p = 3.2e-22) in dementia risk.Conclusion & RelevanceWe found that most participants in memory and aging clinics had at least one high-risk indicator for dementia. Furthermore, we observed a dose-response relationship where a greater number of risk indicators was associated with an increased risk of incident dementia.
Light Exposure Differs by Gender in the US: Women Have Less Bright Light Exposure than Men
Authors: Wallace Danielle A. 
Published: April 2024

ABSTRACTLight is a salient environmental exposure, serving as the primary entraining cue for the circadian system and having other, non-circadian, effects on health. Gender differences in light exposure patterns could contribute to gender differences in health outcomes and would have important implications for sleep and circadian research. Gender differences in real-world light exposure (measured over a week with wrist-worn ActiGraph GT3X+ devices) were investigated in cross- sectional data from the 2011-2014 National Health and Nutrition Examination Survey (NHANES). Measures of time above light threshold (TALT), individual photoperiod (IP), first and last timing of light (FTL and LTL, respectively), and mean light timing revised (MLiTR) at different light intensity thresholds were derived. Gender differences in light exposure were tested using two-sample t-tests, Watson’s two-sample test of homogeneity, and linear regression models. Exploratory analyses to investigate work and physical activity-related factors in relation to bright light exposure were also conducted. A total of 11,318 NHANES participants (age range: 3-80+, 52.2% women) with 6 days of valid actigraphy and light data were included in the analysis. The findings suggest that for every 60 minutes of bright light (≥1,000 lux) that men receive, women receive 39.6 minutes. Men spend approximately 52% more time in bright light than women and this gender difference begins in childhood. The IP of bright light exposure is also longer for men, with earlier first and later last timing of bright light exposure compared to women. These gender differences were robust across ages and between race and ethnicity groups. While further research is needed, these gender differences in light exposure may be due to gender differences in indoor vs. outdoor activities. Future studies of gender differences in response to light exposure should consider light exposure history in study design and analysis. The results of this study may inform future health disparities research and support the importance of the study of light as an important environmental exposure and component of the human exposome.
Clostridioides difficiletransmission: a compartmental model accounting for environmental spore persistence
Authors: Edman-Wallér Jon , Rizzardi Kristina , Jacobsson Gunnar , Gerlee Philip 
Published: April 2024

AbstractObjectiveTo set up a compartmental model, including environmental spore levels, forC. difficiletransmission dynamics in a hospital and determine the effect of preventive interventions on infection and colonization rates.DesignIntervention study within a compartmental mathematical modeling framework.SettingA simulated Swedish 500-bed secondary care hospital.Interventions modeledAntibiotic stewardship, improved isolation of infected patients, improved general cleaning and disinfection.ResultsAntibiotic stewardship had the largest effect on infections, with a 30.6% decrease in infection prevalence. Improved general cleaning and disinfection had the largest effect on colonization (–22.5%) and environmental spore levels (–39.7%). Improved isolation of infected patients had modest effects in comparison.ConclusionsModeling that includes the dynamics of environmental spores can aid our understanding ofC. difficiletransmission within hospitals. Antibiotic stewardship and improved general cleaning and disinfection showed the largest potential for prevention in our modeled setting.
Unveiling Peripheral Immune Dysfunction in Parkinson’s Disease through Analysis of Blood-based Mitochondrial DNA Copy Number
Authors: Wang Longfei , Han Jiru , Fearnley Liam G. , Milton Michael , Rafehi Haloom , Reid Joshua , Gerring Zachary , Masaldan Shashank , Lang Tali , Speed Terence P. , Bahlo Melanie 
Published: April 2024

AbstractMitochondrial dysfunction plays an important role in Parkinson’s disease (PD), with mitochondrial DNA copy number (mtDNA-CN) emerging as a potential marker for mitochondrial health. Our study aimed to assess the association between blood mtDNA-CN and PD, as well as to uncover the underlying mechanisms. Introducing mitoCN, a novel mtDNA-CN estimator adjusting for coverage bias, suitable for large-scale whole-genome sequencing data, we applied it across six cohorts within the Accelerating Medicines Partnership program for Parkinson’s Disease dataset. We investigated the links between blood mtDNA-CN and both PD risk and severity, leveraging comprehensive clinical assessments. Our findings reveal that reduced blood mtDNA-CN levels are associated with heightened PD risk and increased severity of motor symptoms and olfactory dysfunction. However, upon adjusting for blood composition, these associations largely disappeared, indicating a predominant influence of changes in blood variables. Furthermore, using bidirectional Mendelian randomization, we explored causal relationships, finding no evidence of a direct causal relationship between blood mtDNA-CN and PD susceptibility. Thus, even though blood bulk mtDNA-CN correlates with an elevated risk of PD and more severe PD symptoms, our refined analyses and results suggest that peripheral immune dysfunction rather than mitochondrial dysfunction underpins these previously identified associations.
Quality of life, symptom burden and associated factors among lung cancer patients: baseline study of three public hospitals across sub- Saharan Africa
Authors: Ratshikana Mpho , Malale Kija , Murunga Lawrence Atundo , Sayed Abdul-Rauf , Ayeni Oluwatosin , Ginindza Themba G , Dlamini Xolisile , Busakhala Naftali , Mathiba Rofhiwa , Blanchard Charmaine , Tsitsi Merika , Msomi Sabelo , Masalu Nestory , Dhudha Herry O. , Ruff Paul , Graham Anita , Osei-Fofie Daniel 
Published: April 2024

AbstractBackgroundCancer patients in Sub-Saharan Africa (SSA) are diagnosed late partly due to community lack of knowledge about the disease, social and cultural factors, health system challenges, and inadequate health care worker knowledge. These delays in diagnosis as well as inadequate treatment options contribute to the high mortality from lung cancer in SSA. Quality of life (QoL) is an important outcome measure for cancer patients undergoing treatment.ObjectiveTo describe the quality of life among lung cancer patients in three teaching hospitals in SSA.MethodsThis is a prospective cross-sectional study of lung cancer patients at three teaching hospitals in Sub-Saharan Africa (SSA-Kenya (BMC), Tanzania (MTRH) and South Africa (The Lung Laboratory Research and Intervention Unit Helen Joseph Hospital). Trained interviewers collected data on demographics, clinical information and performance status using the Eastern Cooperative Oncological Group Performance Scale (ECOG-PS). Patients’ QoL was assessed using the 30-item European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30).ResultsA total of 210 lung cancer patients consented and were enrolled across the three sites. Global Health Status in this cohort is low, the median score was 41.7 (range: 0-100) and differed between sites. Wits Core patients had higher social functioning, while BMC and MTRH had higher financial difficulty scores. Poor ECOG-PS score (3-4) was associated with poorer Global QoL (GqoL) score (aOR = 2.9; 95% CI: 1.4 - 5.9), and patients with higher symptom burden had poorer GQoL.ConclusionThe QoL among lung cancer patients in the three sites is low. Poor QOL in the study is associated with level of education, performance status, fatigue, pain, dyspnoea, insomnia, loss of appetite and constipation.
Trends in fetal alcohol spectrum disorder (FASD) research: a systematic scoping review and bibliometric analysis
Authors: McQuire Cheryl , Frennessen Nessie Felicia , Parsonage James , Van der Heiden Molly , Troy David , Zuccolo Luisa 
Published: April 2024

AbstractFetal alcohol spectrum disorder (FASD) is a leading cause of neurodevelopmental disability globally. International health and policy organisations have highlighted an urgent need for improved prevention, diagnosis, and support. However, the evidence base needed to inform this is thought to be limited. We conducted a systematic scoping review and bibliometric analysis to describe trends in the volume and characteristics of original research on FASD published between 2000–2023 (Review 1). We compared the volume of published research on FASD to that of other neurodevelopmental disorders (Review 2). Searches were conducted in MEDLINE, Embase, CINAHL, PsychInfo (Review 1) and PubMed (Review 2). Eligible studies were original research articles with FASD terms in the title (Review 1) and all records with FASD, autism, or attention-deficit-hyperactivity disorder terms in the title (Review 2) published between 2000–2023. Data were summarised using descriptive statistics, narrative syntheses, and time-series plots to depict trends in common themes, countries of publication, sample characteristics, and research volume. This review found that FASD remains significantly under-researched. While there has been an increase in the number of original FASD research articles published annually over the last 23-years, this is significantly lower than what would be expected based on comparison with publication trends for other neurodevelopmental conditions, and the wider scientific literature. Further research is needed to understand the needs and impact of FASD across the lifespan and within different populations, to inform evidence-based prevention, policy, and support, and to advance progress in strength-based, stigma-reducing approaches to FASD research and practice.Statements and DeclarationsThe authors declare no conflicts of interest
Discovery of a synthetic small molecule targeting the central regulator ofSalmonellapathogenicity
Authors: Boudrioua Abdelhakim , Joiner Joe D. , Grin Iwan , Kronenberger Thales , Korotkov Vadim S. , Steinchen Wieland , Kohler Alexander , Schminke Sophie , Schulte Julia-Christina , Pietsch Michael , Naini Arun , Kalverkamp Simon , Hotop Sven-Kevin , Coyle Travis , Piselli Claudio , Coles Murray , Rox Katharina , Marschal Matthias , Bange Gert , Flieger Antje , Poso Antti , Brönstrup Mark , Hartmann Marcus D. , Wagner Samuel 
Published: April 2024

AbstractThe enteric pathogenSalmonella entericaserovar Typhimurium relies on the activity of effector proteins to invade, replicate, and disseminate into host epithelial cells and other tissues, thereby causing disease. Secretion and injection of effector proteins into host cells is mediated by dedicated secretion systems, which hence represent major virulence determinants. Here, we report the identification of a synthetic small molecule with drug-like properties, C26, which suppresses the secretion of effector proteins, and consequently hinders bacterial invasion of eukaryotic cells. C26 binds to and inhibits HilD, the transcriptional regulator of the major secretion systems. While sharing the same binding pocket as the previously described long-chain fatty acid ligands, C26 inhibits HilD with a unique binding mode and a distinct mechanism. We provide evidence for target engagement within infected eukaryotic cells and present analogs with improved potency and suitability as scaffolds to develop anti-virulence agents againstSalmonellainfections in humans and animals.
Testing models of cell cortex wave generation by Rho GTPases
Authors: Chomchai Dom , Leda Marcin , Golding Adriana , von Dassow George , Bement William M. , Goryachev Andrew B. 
Published: April 2024

SummaryThe Rho GTPases pattern the cell cortex in a variety of fundamental cell-morphogenetic processes including division, wound repair, and locomotion. It has recently become apparent that this patterning arises from the ability of the Rho GTPases to self-organize into static and migrating spots, contractile pulses, and propagating waves in cells from yeasts to mammals1. These self-organizing Rho GTPase patterns have been explained by a variety of theoretical models which require multiple interacting positive and negative feedback loops. However, it is often difficult, if not impossible, to discriminate between different models simply because the available experimental data do not simultaneously capture the dynamics of multiple molecular concentrations and biomechanical variables at fine spatial and temporal resolution. Specifically, most studies typically provide either the total Rho GTPase signal or the Rho GTPase activity as reported by various sensors, but not both. Therefore, it remains largely unknown how membrane accumulation of Rho GTPases (i.e., Rho membrane enrichment) is related to Rho activity. Here we dissect the dynamics of RhoA by simultaneously imaging both total RhoA and active RhoA in the regime of acute cortical excitability2, characterized by pronounced waves of Rho activity and F-actin polymerization3-5. We find that within nascent waves, accumulation of active RhoA precedes that of total RhoA, and we exploit this finding to distinguish between two popular theoretical models previously used to explain propagating cortical Rho waves.
Post-transcriptional regulatory pre-complex assembly drives timely cell-state transitions during differentiation
Authors: Komori Hideyuki , Rastogi Geeta , Bugay John Paul , Luo Hua , Lin Sichun , Angers Stephane , Smibert Craig A. , Lipshitz Howard D. , Lee Cheng-Yu 
Published: April 2024

AbstractComplexes that control mRNA stability and translation promote timely cell-state transitions during differentiation by ensuring appropriate expression patterns of key developmental regulators. TheDrosophilaRNA-binding protein Brain tumor (Brat) promotes degradation of target transcripts during the maternal-to-zygotic transition in syncytial embryos and in uncommitted intermediate neural progenitors (immature INPs). We identified Ubiquitin-specific protease 5 (Usp5) as a Brat interactor essential for the degradation of Brat target mRNAs in both cell types. Usp5 promotes Brat-dedadenylase pre-complex assembly in mitotic neural stem cells (neuroblasts) by bridging Brat and the scaffolding components of deadenylase complexes lacking their catalytic subunits. The adaptor protein Miranda binds the RNA-binding domain of Brat, limiting its ability to bind target mRNAs in mitotic neuroblasts. Cortical displacement of Miranda activates Brat-mediated mRNA decay in immature INPs. We propose that the assembly of an enzymatically inactive and RNA-binding-deficient pre-complex poises mRNA degradation machineries for rapid activation driving timely developmental transitions.