bluuebunny/crossref_metadata_2025_split huggingface dataset:
Obesity in HIV infection: host-pathogen interaction
Authors: Savinelli Stefano , Wrigley Kelly Neil E. , Feeney Eoin R. , O'Shea Donal B. , Hogan Andrew E. , Overton Edgar T. , Landay Alan L. , Mallon Patrick W. 
Published: August 2022

Objective:
Both obesity and HIV infection are characterized by a state of chronic inflammation associated with increased morbidity and mortality. This review aims to assess the available literature on immune dysregulation in obesity and people with HIV infection (PWH).

Design:
A systematic review of peer-reviewed literature.

Methods:
We conducted a systematic literature search of PubMed, Embase, Scopus, and international conference abstracts for articles on the epidemiology of obesity in the general population and in PWH and the pathogenesis of obesity with a focus on inflammation and immune activation.

Results:
Of the 631 articles selected after title review, 490 met the inclusion criteria and 90 were included in the final selection. The selected studies highlight the increasing prevalence of obesity in PWH and a substantial role for antiretroviral treatment (ART) in its development. Pathogenesis of obesity and its associated inflammation derives from disturbances in adipose tissue (AT) immune function, focused on T-cell and macrophage function, with a switch to pro-inflammatory immune phenotype and resulting increases in pro-inflammatory chemokines, which contribute to the development of metabolic syndrome. Although dysregulation of these pathways is seen in both obesity and HIV, there remains a lack of human studies on AT inflammation in HIV.

Conclusion:
Obesity is an emerging comorbidity in PWH, with a substantial overlap in immune dysregulation patterns seen in both conditions. How this immune dysfunction impacts on development of metabolic complications for both obesity and HIV infection, and whether targeting of AT-derived inflammation will improve outcomes in PWH requires further study.
Early Detection of First Carpometacarpal Joint Osteoarthritis Using Magnetic Resonance Imaging Assessment in Women With High Hypermobility Scores
Authors: Taylor-Gjevre Regina M. , Nair Bindu , Lourens Joe-Ann , Leswick David , Obaid Haron 
Published: August 2022

Objective
The aim of this study was to explore association between hypermobility and osteoarthritis (OA) at the first carpometacarpal (CMC) joint, using magnetic resonance imaging (MRI) to identify early change in women at high risk of developing OA but without yet established diagnoses.

Methods
For this observational study, 33 women (aged 30–50 years) with self-reported history of maternal hand OA but without personal diagnoses of OA were recruited. Participants completed a 5-point hypermobility questionnaire. The 20 participants with 2 or more positive responses were categorized with “high hypermobility scores.” The remaining 13 were categorized with “low hypermobility scores.” Data collection included functional index, hand pain measure, parity, smoking status, and body mass index. Each participant underwent dominant hand radiographic and MRI examination. Imaging studies were interpreted by assessors blinded to hypermobility score categorization.

Results
No significant differences in age, body mass index, parity, functional index, or pain scores were observed between higher and lower hypermobility score groups. Similarly, there were no significant differences between groups for radiographic changes. However, significantly higher proportions of women with higher hypermobility scores were observed on MRI to have abnormalities of trapezium cartilage (75% vs. 38%), metacarpal cartilage (80% vs. 38%), and trapezium bone (70% vs. 31%); p < 0.05 for all.

Conclusions
First CMC joint structural abnormalities were more frequently observed in women with higher hypermobility scores. Identification of early preradiographic changes in this group supports the concept that early-life joint laxity may contribute to future OA predisposition. Magnetic resonance imaging may be a preferred imaging test for detection of early cartilage changes in people at high risk of CMC joint OA.
Striatal tau burden is increased in APOE-e4+ mild cognitive impairment
Authors: Langley Jason , Dara Sumanth , Bennett Ilana J. , Hu Xiaoping P. ,   the Alzheimer’s Disease Neuroimaging Initiative
Published: August 2022

AbstractBackgroundThe presence of β-amyloid (Aβ) extracellular plaques and hyper-phosphorylated tau neurofibrillary tangles characterize the pathology of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Individuals carrying the apolipoprotein E-ε4 (APOE-ε4) allele are at increased risk of cognitive decline and developing AD pathology. The 18F-AV1451 radioligand allows for assessment of tau burden in vivo. However, this radioligand also binds with iron and this off-target binding can occlude tau deposition in iron rich gray matter structures such as the putamen and caudate nucleus.MethodsWe employ a MRI measure sensitive to iron, quantitative susceptibility mapping, to control for off-target binding effects of the 18F-AV1451 radioligand and examine tau burden in the striatum. 20 APOE-ε4 negative MCI, 20 APOE-ε4 positive MCI, and 29 APOE-ε4 negative control participants from ADNI were used in this analysis.ResultsIncreased tau pathology (18F-AV1451 PET uptake), after controlling for tissue susceptibility, was found in the putamen and caudate nucleus of APOE-ε4+ MCI participants as compared to APOE-ε4 negative MCI and control participants. Tau burden in the caudate nucleus of the APOE-ε4+ MCI group was correlated with Montreal Cognitive Assessment (MOCA) score with higher caudate tau burden associated with greater cognitive impairment.ConclusionsControlling for iron allows for the assessment of tau burden in iron rich deep gray matter structures. Our findings suggest that APOE-ε4 allele increases the risk of developing AD pathology in the striatum.
How Have Global Scientists Responded to Tackling COVID-19?
Authors: Cao Longbing , Hou Wenfeng 
Published: August 2022

AbstractSince the outbreak of COVID-19, the global scientific communities across almost all countries have made urgent, intensive, and continuous effort on understanding, fighting and modeling the COVID-19 pandemic. COVID-19 research turns out to be the first overwhelming global scientific reaction to significant global crises and threats. This literature analysis report collects and summarizes the profiles, trends, quality and impact of this global scientific response. It collects and analyzes 346,267 scientific references in English, involving researchers from 189 countries and regions in 27 subject areas. The report generates a picture of how global scientists have responded to COVID-19 between Jan 2020 and Mar 2022 in terms of their publication quantity, impact, focused major problems, and research areas and methods over country/region, discipline and time and collaboratively. The report also captures broad-reaching distributions and trends of modeling COVID-19 by AI, data science, analytics, shallow and deep machine learning, epidemic modeling, applied mathematics, and social science methods, etc. We further show the correlations between publication quality and quantity and economic status and COVID-19 infections globally and in major countries and regions. The literature analysis results of this global scientific response to COVID-19 present a comprehensive global, regional and subject-specific picture of the significant cross-disciplinary, cross-country, cross-problem, and cross-technique profiles and differences of the COVID-19 publication quantity and quality. The report also discloses significant imbalances in the COVID-19 research across countries/regions, subject areas, problems, topics, methods, research collaborations, and economic statuses. We share the source and analytical data of this global literature analysis for further research on this unprecedented and future crises.More Information about COVID-19 ModelingThe COVID-19 global scientists response datasetThe COVID-19 global scientists response dataset supporting this report can be found in Kaggle at: https://www.kaggle.com/datasets/datascienceslab/covid19-global-scientists-response, Dataset doi: 10.34740/kaggle/dsv/4077649.More information about COVID-19 modelingInterested readers may refer to the following review on modeling COVID-19 which complements this global literature analysis: Longbing Cao and Qing Liu, COVID-19 Modeling: A Review, 1-103, 2022 (version 2). Accessible at medRxiv: https://www.medrxiv.org/content/10.1101/2022.08.22.22279022v1.More information about COVID-19 modeling, including the analytical results of this report and data and review on COVID-19 can be found at: https://datasciences.org/covid19-modeling.Citation of this reportLongbing Cao and Wenfeng Hou. How have global scientists responded to tackling COVID-19? Full technical report, https://doi.org/10.1101/2022.08.16.22278871, Data Science Lab, University of Technology Sydney, 2022.
Soil variation among natural habitats alters glucosinolate content in a wild perennial mustard
Authors: Wagner Maggie R. , Mitchell-Olds Thomas 
Published: August 2022

AbstractBaseline levels of glucosinolates—important defensive phytochemicals in Brassicaceous plants—are determined by both genotype and the environment. However, the ecological causes of glucosinolate plasticity are not well characterized. Fertilization is known to alter glucosinolate content of Brassica crops, but the effect of naturally-occurring soil variation on glucosinolate content of wild plants is unknown. Here, we conduct greenhouse experiments using Boechera stricta to ask 1) whether soil variation among natural habitats shapes leaf and root glucosinolate profiles; 2) whether such changes are caused by abiotic soil properties, soil microbes, or both; and 3) whether soil-induced glucosinolate plasticity is genetically variable.Total glucosinolate quantity differed up to two-fold between soils from different natural habitats, while the relative amounts of different compounds was less responsive. This effect was due to physico-chemical soil properties rather than microbial communities. We detected modest genetic variation for glucosinolate plasticity in response to soil. In addition, glucosinolate composition, but not quantity, of field-grown plants could be accurately predicted from measurements from greenhouse-grown plants. In summary, soil alone is sufficient to cause plasticity of baseline glucosinolate levels in natural plant populations, which may have implications for the evolution of this important trait across complex landscapes.
Multiclass Semantic Segmentation of Immunostained Breast Cancer Tissue with a Deep-Learning Approach
Authors: Ortega-Ruiz Mauricio Alberto , Roman-Rangel Edgar , Reyes-Aldasoro Constantino Carlos 
Published: August 2022

AbstractThis paper describes a multiclass semantic segmentation of breast cancer images into the following classes: Tumour, Stroma, Inflammatory, Necrosis and Other. The images were stained with Haematoxilin and Eosin and acquired from the Cancer Genome Atlas through the Breast Cancer Semantic Segmentation Challenge. Over 12,000 patches of data and classes were generated from training images with the use of data augmentation.The segmentation was obtained with a U-Net architecture for which the hyperparameters were explored systematically. Optimal values were obtained with batch size = 8, Loss function Adam and 50 epochs, which took over 50 hours to train. Due to this fact and limitations in time, the rest of the parameters were explored with 10 epochs and we speculate that values would increase if 50 epochs would be used. The trained U-Net was applied to unseen images, per-patch and the following metrics were obtained from full scale WSI; Accuracy, Mean Area Under the Curve and Dice Index. No post-processing was applied. The resulting segmentations outperformed the baseline in terms of accuracy for some tissues; Tumour from 0.804 to 0.913, Inflammatory from 0.743 to 0.8364. The data is available from the Grand Challenges website (https://bcsegmentation.grand-challenge.org/) and the code is available from the following GitHub repository (https://github.com/mauOrtRuiz/Breast_Cancer_Sem_Seg).
Impact of the COVID-19 Pandemic on Personal Networks and Neurological Outcomes of People with Multiple Sclerosis: A Case-Control Cross-sectional and Longitudinal Analysis
Authors: Riley Claire S. , Venkatesh Shruthi , Dhand Amar , Doshi Nandini , Kavak Katelyn , Levit Elle E. , Perrone Christopher , Weinstock-Guttman Bianca , Longbrake Erin E. ,   MSReCOV investigators, De Jager Philip L. , Xia Zongqi 
Published: August 2022

ABSTRACTBackgroundThe COVID-19 pandemic has negatively impacted the social fabric of people with multiple sclerosis (pwMS).ObjectiveTo evaluate the associations between personal social network environment and neurological function in pwMS and controls during the COVID-19 pandemic and compare with the pre-pandemic baseline.MethodsWe first analyzed data collected from 8 cohorts of pwMS and control participants during the COVID-19 pandemic (March-December 2020). We then leveraged data collected between 2017-2019 in 3 of the 8 cohorts for longitudinal comparison. Participants completed a questionnaire that quantified the structure and composition of their personal social network, including the health behaviors of network members. We assessed neurological disability using three interrelated patient-reported outcomes: Patient Determined Disease Steps (PDDS), Multiple Sclerosis Rating Scale – Revised (MSRS-R), and Patient Reported Outcomes Measurement Information System (PROMIS)-Physical Function. We identified the network features associated with neurologic disability using paired t-tests and covariate-adjusted regressions.ResultsIn the cross-sectional analysis of the pandemic data from 1130 pwMS and 1250 control participants, higher percent of network members with a perceived negative health influence was associated with greater neurological symptom burden in pwMS (MSRS-R: Beta[95% CI]=2.181[1.082, 3.279], p<.001) and worse physical function in controls (PROMIS-Physical Function: Beta[95% CI]=-5.707[-7.405, -4.010], p<.001). In the longitudinal analysis of 230 pwMS and 136 control participants, the networks of both pwMS and controls experienced an increase in constraint (pwMS p=.006, control p=.001) as well as a decrease in network size (pwMS p=.003, control p<.001), effective size (pwMS p=.007, control p=.013), maximum degree (pwMS p=.01, control p<.001), and percent contacted weekly or less (pwMS p<.001, control p<.001), suggesting overall network contraction during the COVID-19 pandemic. There was also an increase in percentage of kin (p=.003) in the networks of pwMS but not controls during the COVID-19 pandemic when compared to the pre-pandemic baseline. These changes in personal social network due to the pandemic were not associated with worsening neurological disability during the pandemic.ConclusionsOur findings suggest that perceived negative health influences in personal social networks are associated with worse disability in all participants during the COVID-19 pandemic. Despite the perturbation in social environment and connections during the pandemic, the stability in neurological function among pwMS suggests potential resilience.
Polymorphic KIR3DL3 expression modulates tissue-resident and innate-like T cells
Authors: Palmer William H. , Leaton Laura Ann , Codo Ana Campos , Hume Patrick S. , Crute Bergren , Stone Matthew , van Bokhoven Adrie , Tobin Richard P. , McCarter Martin D. , Janssen William J. , Roest James , Zhu Shiying , Petersen Jan , Vivian Julian P. , Rossjohn Jamie , Trowsdale John , Getahun Andrew , Cambier John , Loh Liyen , Norman Paul J. 
Published: August 2022

AbstractMost human killer cell immunoglobulin-like receptors (KIR) are expressed by Natural Killer (NK) cells and recognize HLA class I molecules as ligands. Uniquely, KIR3DL3 is a conserved but polymorphic inhibitory KIR recognizing a B7 family ligand, HHLA2, and is implicated for immune checkpoint targeting. Because the expression profile and biological function of KIR3DL3 remained elusive, we searched extensively for KIR3DL3 transcripts, revealing expression is highly enriched in γδ and CD8+ T cells rather than NK cells. These KIR3DL3 expressing cells are rare in the blood and thymus, but more common in the lungs and digestive tract. High resolution flow cytometry and single cell transcriptomics showed that peripheral blood KIR3DL3+ T cells have an activated transitional memory phenotype and are hypofunctional. The TCR usage is biased towards genes from early rearranged TCR-α variable segments or Vδ1 chains. Whereas we detected no impact of KIR3DL3 polymorphism on ligand binding, variants in the proximal promoter and at residue 86 can reduce expression. Together, we demonstrate that KIR3DL3 is upregulated in response to unconventional T cell stimulation and that individuals may vary in their ability to express KIR3DL3. These results have implications for the personalized targeting of KIR3DL3/HHLA2 checkpoint inhibition.
Single molecule long-read real-time amplicon-based sequencing ofCYP2D6: a proof-of-concept with hybrid haplotypes
Authors: Dong Rachael , Thamilselvan Megana , Foo Jerome Clifford , DeJarnette Jacqueline , Hu Xiuying , Henriques Beatriz Carvalho , Wang Yabing , Wallace Keanna , Sivapalan Sudhakar , Buchner Avery , Yavorskyy Vasyl , Martens Kristina , Maier Wolfgang , Henigsberg Neven , Hauser Joanna , Cattaneo Annamaria , Mors Ole , Rietschel Marcella , Pfeffer Gerald , Aitchison Katherine J. 
Published: August 2022

AbstractCYP2D6 is a widely expressed human xenobiotic metabolizing enzyme, best known for its role in the hepatic phase I cytochrome P450 enzyme system, where it metabolizes ∼20% of medications. It is also expressed in other organs including the brain, where its potential role in physiology and mental health traits and disorders is under further investigation. Owing to the presence of homologous pseudogenes in theCYP2Dlocus and transposable repeat elements in the intergenic regions, the gene encoding the CYP2D6 enzyme,CYP2D6, is one of the most hypervariable known human genes - with more than 165 core haplotypes. Haplotypes include structural variants, with a subtype of these known as hybrid haplotypes or fusion genes comprising part ofCYP2D6and part of its adjacent pseudogene,CYP2D7. The fusion genes are particularly challenging to identify. High fidelity (HiFi) single molecule real-time (SMRT) long-read sequencing can cover wholeCYP2D6haplotypes in a single continuous sequence, and is therefore ideal for structural variant detection. In addition, it is highly accurate and suitable for novel haplotype identification, which is necessary as newCYP2D6haplotypes are continuously being discovered, and many more likely remain to be identified in relatively understudied populations such as Indigenous Peoples. The aim of the present work was to develop an efficient and accurate HiFi SMRT amplicon-based method capable of detecting the full range ofCYP2D6haplotypes including fusion genes. We report proof-of-concept for 24 amplicons including three positive controls, aligned to fusion gene haplotypes, with prior cross-validation data. Amplicons withCYP2D7-D6fusion genes, including positive controls, aligned to the*13subhaplotypes predicted (*13F, *13A2) with 100% accuracy, with the exception of one that aligned at 99.9%. Alignment of the*68was 100% and above 99.9% to theCYP2D6*68partial sequences EU5300606 and JF307779, respectively. The best alignments for the remainingCYP2D6-2D7fusion genes were ≥99.7% (to 3 significant figures). Lower percentage alignment forCYP2D6-2D7fusion genes may reflect imperfect PCR optimization and/or the possibility that we may have haplotypes not yet in public databases. Further work on these is in progress. Moreover, we have adapted this method for non-hybrid haplotypes. This technique could therefore suffice for the characterization of the full range ofCYP2D6haplotypes. The method that we have developed could be extended to other complex loci and to other species in a multiplexed high throughput assay.
Mitochondrial decline in the ageing old world primate retina: little evidence for difference between the centre and periphery
Authors: Kam Jaimie Hoh , Shinhmar Harpreet , Powner Michael Barry , JohnHayes Matthew , Aboelnour Asmaa , Jeffery Glen 
Published: August 2022

AbstractMitochondrial decline is a key feature of ageing. The retina has more mitochondria than any other tissue and ages rapidly. To understand human retinal ageing it is critical to examine old world primates that have similar visual systems to humans, and do so across central and peripheral regions, as there is evidence for early central decline. Hence, we examine mitochondrial metrics in young and ageing Macaca fascicularis retinae. In spite of reduced ATP with age, primate mitochondrial complex activity did not decline. But mitochondrial membrane potentials were reduced significantly, and concomitantly, mitochondrial membrane permeability increased. The mitochondrial marker Tom20 declined significantly, consistent with reduced mitochondria number, while VDAC, a voltage dependent anion channel and diffusion pore associated with apoptosis increased significantly. In spite of these clear age-related changes, there was almost no evidence for regional differences between the centre and the periphery.Primate cones do not die with age, but many showed marked structural decline with vacuous spaces in proximal inner segments normally occupied by endoplasmic reticulum (ER), that regulate mitochondrial autophagy. In many peripheral cones, ER was displaced by the nucleus that transposed across the outer limiting membrane and could become embedded in mitochondrial populations. These data are consistent with significant changes in retinal mitochondria in old world primate ageing but provide little if any evidence that aged central mitochondria suffer more than those in the periphery.
Single cell atlas of Xenoturbella bocki highlights the limited cell-type complexity of a non-vertebrate deuterostome lineage
Authors: Robertson Helen E. , Sebe-Pedros Arnau , Saudemont Baptiste , Loe Mie Yann , Zakrzewski Anne , Grau-Bové Xavier , Mailhe Marie-Pierre , Schiffer Philipp , Telford Maximilian J. , Marlow Heather 
Published: August 2022

AbstractEvidence for a sister relationship between Xenacoelomorpha and Ambulacraria (Xenambulacraria) has revived the longstanding debate surrounding the complexity of the Urdeuterostomian and Urbilaterian ancestors and has led to a reassessment of early bilaterian features. Employing whole organism single-cell RNA-seq in the marine xenacoelomorph worm Xenoturbella bocki, we show that Xenambulacrarian nerve nets share regulatory features and a peptidergic identity with those found in cnidarians and protostomes. We also suggest that Xenacoelomorpha muscles are likely to have evolved their “smooth” phenotype convergently. Furthermore, we identify pigmented cells as a potential synapomorphy of the Xenambulacraria. Taken together, these data are consistent with a simplification from an ancestral urbilaterian/urdeuterostomian body plan and a non-centralized nerve net, minimally differentiated contractile cells and evidence of deuterostome cell-type synapomorphies.