bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors associated with trauma recidivism in young children
Authors: Stephens Caroline Q. , Melhado Caroline G. , Shui Amy M. , Yap Ava , Moses Willieford , Jensen Aaron R. , Newton Christopher 
Published: January 2024

BACKGROUND
Trauma recidivism is associated with future trauma-associated morbidity and mortality. Previous evidence suggests that socioeconomic factors predict trauma recidivism in older children (10–18 years); however, risk factors in US children 10 years and younger have not been studied. We sought to determine the factors associated with trauma recidivism in young children 10 years and younger.

METHODS
We conducted a retrospective cohort study of pediatric trauma patients 10 years and younger who presented to a single American College of Surgeons-verified Level I pediatric trauma center from July 1, 2017, to June 30, 2021. All patients were evaluated for prior injury during trauma registry entry. Characteristics at the index injury were collected via chart review. Patients were geocoded to assess Social Vulnerability Index. Logistic regression examined factors associated with recidivism. Best subset selection was used to compare multivariable models and identify the most predictive and parsimonious model. Statistical significance was set at p < 0.05.

RESULTS
Of the 3,518 patients who presented in the study period, 169 (4.8%) experienced a prior injury. Seventy-six percent (n = 128) had one prior injury presentation, 18% (n = 31) had two prior presentations, and 5.9% (n = 10) had three or more. Falls were the most common mechanism in recidivists (63% vs. 52%, p = 0.009). Child physical abuse occurred in 6.5% of patients, and 0.9% experienced penetrating injury. The majority (n = 137 [83%]) were discharged home from the emergency department. There was no significant difference in the frequency of penetrating injury and child physical abuse between recidivists and nonrecidivists. Following logistic regression, the most parsimonious model demonstrated that recidivism was associated with comorbidities, age, falls, injury location, nontransfer, and racialization. No significant associations were found with Social Vulnerability Index and insurance status.

CONCLUSION
Medical comorbidities, young age, injury location, and falls were primarily associated with trauma recidivism. Support for parents of young children and those with special health care needs through injury prevention programs could reduce trauma recidivism in this population.

LEVEL OF EVIDENCE
Prognostic and Epidemiological; Level III.
Ccr2-dependent monocytes exacerbate intestinal inflammation and modulate gut serotonergic signaling following traumatic brain injury
Authors: El Baassiri Mahmoud G. , Raouf Zachariah , Jang Hee-Seong , Scheese Daniel , Duess Johannes W. , Fulton William B. , Sodhi Chhinder P. , Hackam David J. , Nasr Isam W. 
Published: January 2024

BACKGROUND
Traumatic brain injury (TBI) leads to acute gastrointestinal dysfunction and mucosal damage, resulting in feeding intolerance. C-C motif chemokine receptor 2 (Ccr2+) monocytes are crucial immune cells that regulate the gut's inflammatory response via the brain-gut axis. Using Ccr2ko mice, we investigated the intricate interplay between these cells to better elucidate the role of systemic inflammation after TBI.

METHODS
A murine-controlled cortical impact model was used, and results were analyzed on postinjury days 1 and 3. The experimental groups included (1) sham C57Bl/6 wild type (WT), (2) TBI WT, (3) sham Ccr2ko, and (4) TBI Ccr2ko. Mice were euthanized on postinjury days 1 and 3 to harvest the ileum and study intestinal dysfunction and serotonergic signaling using a combination of quantitative real-time polymerase chain reaction, immunohistochemistry, fluorescein isothiocyanate-dextran motility assays, and flow cytometry. Student's t test and one-way analysis of variance were used for statistical analysis, with significance achieved when p < 0.05.

RESULTS
Traumatic brain injury resulted in severe dysfunction and dysmotility of the small intestine in WT mice as established by significant upregulation of inflammatory cytokines iNOS, Lcn2, TNFα, and IL1β and the innate immunity receptor toll-like receptor 4 (Tlr4). This was accompanied by disruption of genes related to serotonin synthesis and degradation. Notably, Ccr2ko mice subjected to TBI showed substantial improvements in intestinal pathology. Traumatic brain injury Ccr2ko groups demonstrated reduced expression of inflammatory mediators (iNOS, Lcn2, IL1β, and Tlr4) and improvement in serotonin synthesis genes, including tryptophan hydroxylase 1 (Tph1) and dopa decarboxylase (Ddc).

CONCLUSION
Our study reveals a critical role for Ccr2+ monocytes in modulating intestinal homeostasis after TBI. Ccr2+ monocytes aggravate intestinal inflammation and alter gut-derived serotonergic signaling. Therefore, targeting Ccr2+ monocyte-dependent responses could provide a better understanding of TBI-induced gut inflammation. Further studies are required to elucidate the impact of these changes on brain neuroinflammation and cognitive outcomes.
Procedural sedation of adult patients in the emergency department: a best practice implementation project
Authors: Pickens Jessica , Garbo Candon 
Published: January 2024

ABSTRACT

Introduction:
The emergency department is a fast-paced and complex health care setting, where critical care is provided to patients of all ages. However, various environmental factors, such as high patient volumes, overburdened staff, and frequent nurse turnover, can hinder the use of evidence-based practices during procedural sedation. Proper patient monitoring is essential to prevent adverse events during procedural sedation.

Objectives:
The goal of this implementation project was to enhance compliance with best practices for patient monitoring during procedural sedation in the emergency department.

Methods:
The project used the JBI Model of Evidence-Based Healthcare and JBI's Getting Research into Practice (GRiP) tool for implementing evidence-based monitoring practices for adult patients during procedural sedation in the emergency department. A baseline audit was conducted to assess current practice against evidence-based recommendations, followed by the implementation of strategies to improve compliance with best practices. The project concluded with a follow-up audit to determine any improvement in practice.

Results:
The baseline audit revealed 81% overall compliance with evidence-based practice. Three barriers were identified, namely, lack of staff education, increased turnover rate of nurses, and the need for nurses to be mobile during procedural sedation. Strategies were implemented to improve compliance with evidence-based practice. The follow-up audit showed an overall improvement of 95% after project implementation.

Conclusions:
The project improved best practices for patient monitoring during procedural sedation in the emergency department. However, more work remains to be done to ensure the sustainability of the best practices, including monitoring of end-tidal capnography and vital sign assessment.
Interactive effects of intrinsic and extrinsic factors on metabolic rate
Authors: Glazier Douglas S. , Gjoni Vojsava 
Published: January 2024

Metabolism energizes all biological processes, and its tempo may importantly influence the ecological success and evolutionary fitness of organisms. Therefore, understanding the broad variation in metabolic rate that exists across the living world is a fundamental challenge in biology. To further the development of a more reliable and holistic picture of the causes of this variation, we review several examples of how various intrinsic (biological) and extrinsic (environmental) factors (including body size, cell size, activity level, temperature, predation and other diverse genetic, cellular, morphological, physiological, behavioural and ecological influences) can interactively affect metabolic rate in synergistic or antagonistic ways. Most of the interactive effects that have been documented involve body size, temperature or both, but future research may reveal additional ‘hub factors’. Our review highlights the complex, intimate inter-relationships between physiology and ecology, knowledge of which can shed light on various problems in both disciplines, including variation in physiological adaptations, life histories, ecological niches and various organism-environment interactions in ecosystems. We also discuss theoretical and practical implications of interactive effects on metabolic rate and provide suggestions for future research, including holistic system analyses at various hierarchical levels of organization that focus on interactive proximate (functional) and ultimate (evolutionary) causal networks.
This article is part of the theme issue ‘The evolutionary significance of variation in metabolic rates’.
Individual variation in thermally induced plasticity of metabolic rates: ecological and evolutionary implications for a warming world
Authors: Gvoždík Lumír 
Published: January 2024

Energy metabolism is a fundamental property of life providing the energy for all processes and functions within an organism. As it is temperature-dependent, it mediates the effects of changing climate on ectotherm fitness and population dynamics. Though resting metabolic rate is a highly labile trait, part of its variation is individually consistent. Recent findings show that resting metabolic rate contains consistent variation not only in the elevations (intercepts) but also in the slopes of individual thermal dependence curves, challenging the thermal dependence assumption for this trait in several ectotherm taxa. I argue that among-individual variation in thermal metabolic curves represents a previously undetected component of ectotherm response to climate change, potentially affecting their adaptive capacity and population resilience under increasing stochasticity of thermal environment. Future studies need to examine not only the amount of among-individual variation in thermal metabolic curves across phylogenetic contexts but also other aspects concerning its mechanisms and adaptive significance to improve predictions about the impact of climate change on ectotherm population dynamics.
This article is part of the theme issue ‘The evolutionary significance of variation in metabolic rates’.
A historical sequence deletion in a commonly usedBacillus subtilischromosome integration vector generates undetected loss-of-function mutations
Authors: Dierksheide K. Julia , Li Gene-Wei 
Published: January 2024

AbstractSince the 1980s, chromosome-integration vectors have been used as a core method of engineeringBacillus subtilis. One of the most frequently used vector backbones contains chromosomally derived regions that direct homologous recombination into theamyElocus. Here, we report a gap in the homology region inherited from the originalamyEintegration vector, leading to erroneous recombination in a subset of transformants and a loss-of-function mutation in the downstream gene. Internal to the homology arm that spans the 3′ portion ofamyEand the downstream geneldh, an unintentional 227-bp deletion generates two crossover events. The major event yields the intended genotype, but the minor event, occurring in ∼10% of colonies, results in a truncation ofldh, which encodes lactate dehydrogenase. Although both types of colonies test positive foramyEdisruption by starch plating, the potential defect in fermentative metabolism may be left undetected and confound the results of subsequent experiments.
Deep Learning Analysis on Images of iPSC-derived Motor Neurons Carrying fALS-genetics Reveals Disease-Relevant Phenotypes
Authors: Atmaramani Rahul , Dreossi Tommaso , Ford Kevin , Gan Lin , Mitchell Jana , Tu Shengjiang , Velayutham Jeevaa , Zeng Haoyang , Chickering Michael , Soare Tom , Sivanandan Srinivasan , Conrad Ryan , Bao Yujia , Akle Santiago , Liu Jonathan , Redmond Stephanie , Guo Syuan-Ming , Conrad Patrick , Yi Flora , Atkeson Nick , Xu Difei , McMorrow Aidan , Hergenreder Emiliano , Hari Mukund , Sandakli Ahmed , Mittal Nitya , Zhang Liyuan , Topol Aaron , Hartley Brigham , Lam Elaine , Krauel Eva-Maria , Karaletsos Theofanis , Labow Mark , Hargreaves Richard , Trotter Matthew , Biswas Shameek , Pisco Angela Oliveira , Kaykas Ajamete , Koller Daphne , Sances Samuel 
Published: January 2024

SummaryAmyotrophic lateral sclerosis (ALS) is a devastating condition with very limited treatment options. It is a heterogeneous disease with complex genetics and unclear etiology, making the discovery of disease-modifying interventions very challenging. To discover novel mechanisms underlying ALS, we leverage a unique platform that combines isogenic, induced pluripotent stem cell (iPSC)-derived models of disease-causing mutations with rich phenotyping via high-content imaging and deep learning models. We introduced eight mutations that cause familial ALS (fALS) into multiple donor iPSC lines, and differentiated them into motor neurons to create multiple isogenic pairs of healthy (wild-type) and sick (mutant) motor neurons. We collected extensive high-content imaging data and used machine learning (ML) to process the images, segment the cells, and learn phenotypes. Self-supervised ML was used to create a concise embedding that captured significant, ALS-relevant biological information in these images. We demonstrate that ML models trained on core cell morphology alone can accurately predict TDP-43 mislocalization, a known phenotypic feature related to ALS. In addition, we were able to impute RNA expression from these image embeddings, in a way that elucidates molecular differences between mutants and wild-type cells. Finally, predictors leveraging these embeddings are able to distinguish between mutant and wild-type both within and across donors, defining cellular, ML-derived disease models for diverse fALS mutations. These disease models are the foundation for a novel screening approach to discover disease-modifying targets for familial ALS.
Information-based rhythmic transcranial magnetic stimulation accelerates learning during auditory working memory training
Authors: Whittaker Heather T. , Khayyat Lina , Fortier-Lavallée Jessica , Laverdière Megan , Bélanger Carole , Zatorre Robert J. , Albouy Philippe 
Published: January 2024

AbstractRhythmic transcranial magnetic stimulation (rhTMS) has been shown to enhance auditory working memory manipulation, specifically by boosting theta oscillatory power in the dorsal auditory pathway during task performance. It remains unclear whether these enhancements i) persist beyond the period of stimulation, ii) if they can accelerate learning and iii) if they would accumulate over several days of stimulation. In the present study, we investigated the lasting behavioural and electrophysiological effects of applying rhTMS over the left intraparietal sulcus (IPS) throughout the course of seven sessions of cognitive training on an auditory working memory task. Fourteen neurologically healthy participants took part in the training protocol with an auditory working memory task while being stimulated with either theta (5Hz) rhTMS or sham TMS. Electroencephalography (EEG) was recorded before, throughout five training sessions and after the end of training to assess to effects of rhTMS on behavioural performance and on oscillatory entrainment of the dorsal auditory network. We show that this combined approach enhances theta oscillatory activity within the fronto-parietal network and causes improvements in auditory working memory performance. We show that compared to individuals who received sham stimulation, cognitive training can be accelerated when combined with optimized rhTMS, and that task performance benefits can outlast the training period by up to 3 days. Furthermore, we show that there is increased theta oscillatory power within the recruited dorsal auditory network during training, and that sustained EEG changes can be observed up to 3 days following stimulation. The present study improves our understanding of the causal dynamic interactions supporting auditory working memory. Our results constitute an important proof of concept for the potential translational impact of non-invasive brain stimulation protocols and provide preliminary data for developing optimized rhTMS and training protocols that could be implemented in clinical populations.
Molecular, physiological and functional features underlying cortical thinning related to antipsychotic medication use
Authors: Tuominen Lauri , Armio Reetta-Liina , Hansen Justine Y. , Walta Maija , Koutsouleris Nikolaos , Laurikainen Heikki , Salokangas Raimo K.R. , Misic Bratislav , Hietala Jarmo 
Published: January 2024

AbstractUse of antipsychotic medication is related to thinning of the cerebral cortex, but the underlying mechanisms of this effect remain largely unknown. Here, we investigated potential mechanisms across multiple levels of description, from molecular and physiological factors to whole-brain functional patterns. We first analyzed a single site discovery sample of patients (N=131) with early psychosis for whom antipsychotic related cortical thinning was estimated based on lifetime exposure to antipsychotics. Findings were replicated using data from a large (N≥2168) ENIGMA meta-analysis. We discovered that antipsychotic related cortical thinning is associated with a number of neurotransmitter systems, most notably the serotonin system, physiological measures, and functional networks and neural oscillatory power distributions typical for regions subserving higher cognition. At the functional level, antipsychotic related cortical thinning affects regions involved in executive function and motivation, but not perception. These results show how molecular, physiological, and large-scale functional patterns underlie antipsychotic related cortical thinning.
A Comparative Machine Learning Study of Connectivity-Based Biomarkers of Schizophrenia
Authors: Shevchenko Victoria , Benn R. Austin , Scholz Robert , Wei Wei , Pallavicini Carla , Klatzmann Ulysse , Alberti Francesco , Satterthwaite Theodore D. , Wassermann Demian , Bazin Pierre-Louis , Margulies Daniel S. 
Published: January 2024

AbstractFunctional connectivity holds promise as a biomarker of psychiatric disorders. Yet, its high dimensionality, combined with small sample sizes in clinical research, increases the risk of overfitting when the aim is prediction. Recently, low-dimensional representations of the connectome such as macroscale cortical gradients and gradient dispersion have been proposed, with studies noting consistent gradient and dispersion differences in psychiatric conditions. However, it is unknown which of these derived measures has the highest predictive capacity and how they compare to raw connectivity. Our study evaluates which connectome features — functional connectivity, gradients, or gradient dispersion — best identify schizophrenia. Figure 1 summarizes this work.Surprisingly, our findings indicate that functional connectivity outperforms its low-dimensional derivatives such as cortical gradients and gradient dispersion in identifying schizophrenia. Additionally, we demonstrated that the edges which contribute the most to classification performance are the ones connecting primary sensory regions.
Beta-Cell Pyroptosis – A Burning Flame in Type 1 Diabetes?
Authors: Frørup Caroline , Svane Cecilie Amalie Søndergaard , Henriksen Kristine , Kaur Simranjeet , Størling Joachim 
Published: January 2024

AbstractImmune-mediated destruction of the beta-cells in the pancreatic islets of Langerhans is the underlying cause of type 1 diabetes (T1D). Despite decades of research, the exact mechanisms involved at the beta-cell level during the development of disease remain poorly understood. This includes the mode(s) of beta-cell death and signaling events implicated in exacerbating local islet inflammation and immune cell infiltration, commonly known as insulitis. In disease models, beta-cell apoptosis seems to be the predominant cell death form which has led to the general assumption that beta cells mostly die by apoptosis in T1D. However, apoptosis is an anti-inflammatory programmed cell death mechanism, and this dogma is therefore challenged by the pathogenetic nature of T1D, as a progressive increase in islet inflammation is seen. This infers that other modes of beta-cell death that inherently increase insulitis may predominate. One such mechanism could be the newly characterized form of programmed cell death; pyroptosis (from the Greek “fire–falling”). Pyroptosis is characterized by gasdermin-mediated cell lysis with a bursting release of pro-inflammatory factors. Beta-cell death by pyroptosis in T1D may therefore offer a plausible explanation for the exacerbated paracrine islet inflammation that spreads during the progression of insulitis. Here, we briefly debate the evidence supporting beta-cell pyroptosis in T1D as a central mechanism of islet inflammation and beta-cell demise. The paper intends to challenge the current understanding of beta-cell destruction to move the field forward. Importantly, we present experimental data from human islets and EndoC-βH5 cells that directly support beta-cell pyroptosis as a rational death mechanism in T1D. We suggest a model of beta-cell demise in T1D in which pyroptosis plays a prominent role in concert with other cell death mechanisms. As the role of pyroptosis in disease is still in its infancy, we hope also to inspire researchers working in other disease fields.
Arf GTPase-activating protein ASAP1 specifically binds to 440-kD ankyrin-B
Authors: Li Yubing , Zhao Yipeng , He Yaojun , Zhang Mingjie , Chen Keyu 
Published: January 2024

AbstractThe 440-kD giant ankyrin-B (gAnkB) exclusively localizes to axons and is essential for axon development. However, proteins that specifically bind to gAnkB but not to other isoforms of ankyrins are poorly understood. Here, we discovered that an Arf GTPase-activating protein ASAP1 and ASAP2 specifically binds to a short and disordered sequence unique to gAnkB. Biochemical studies showed that the SH3 domain of ASAP1 binds to a 12-residue, positively charged peptide fragment from gAnkB. The high-resolution structure of the ASAP1-SH3 domain in complex with the gAnkB peptide revealed the mechanism underlying this non-canonical SH3 domain-mediated target recognition. Further structural and bioinformatic analysis revealed additional previously unknown ASAP1-SH3 binding partners including Clasp1 and Clasp2, both of which are well-known microtubule regulators. Among all known ASAP1-SH3 binders including those identified in the current study, gAnkB has the strongest affinity in binding to ASAP1. Our results suggest that ASAP1 may function together with gAnkB in regulating axonal cytoskeletons.