bluuebunny/crossref_metadata_2025_split huggingface dataset:
In-Hospital Cost Comparison of Triple-Rule-Out Computed Tomography Angiography Versus Standard of Care in Patients With Acute Chest Pain
Authors: Takx Richard A.P. , Wichmann Julian L. , Otani Katharina , De Cecco Carlo N. , Tesche Christian , Baumann Stefan , Mastrodicasa Domenico , Litwin Sheldon E. , Bayer Richard R. , Nance John W. , Suranyi Pal , Jacobs Brian E. , Duguay Taylor M. , Vogl Thomas J. , Carr Christine M. , Schoepf U. Joseph 
Published: February 2020

Purpose:
The purpose of this study was to evaluate the utilization of invasive and noninvasive tests and compare cost in patients presenting with chest pain to the emergency department (ED) who underwent either triple-rule-out computed tomography angiography (TRO-CTA) or standard of care.

Materials and Methods:
We performed a retrospective single-center analysis of 2156 ED patients who presented with acute chest pain with a negative initial troponin and electrocardiogram for myocardial injury. Patient cohorts matched by patient characteristics who had undergone TRO-CTA as a primary imaging test (n=1139) or standard of care without initial CTA imaging (n=1017) were included in the study. ED visits, utilization of tests, and costs during the initial episode of hospital care were compared.

Results:
No significant differences in the diagnosis of coronary artery disease, pulmonary embolism, or aortic dissection were observed. Median ED waiting time (4.5 vs. 7.0 h, P<0.001), median total length of hospital stay (5.0 vs. 32.0 h, P<0.001), hospital admission rate (12.6% vs. 54.2%, P<0.001), and ED return rate to our hospital within 30 days (3.5% vs. 14.6%, P<0.001) were significantly lower in the TRO-CTA group. Moreover, reduced rates of additional testing and invasive coronary angiography (4.9% vs. 22.7%, P<0.001), and ultimately lower total cost per patient (11,783$ vs. 19,073$, P<0.001) were observed in the TRO-CTA group.

Conclusions:
TRO-CTA as an initial imaging test in ED patients presenting with acute chest pain was associated with shorter ED and hospital length of stay, fewer return visits within 30 days, and ultimately lower ED and hospitalization costs.
Pneumothorax Rate and Diagnostic Adequacy of Computed Tomography–guided Lung Nodule Biopsies Performed With 18 G Versus 20 G Needles
Authors: Kolderman Nathan C. , Cheti Dev R. , Hasbrook Connor D. , Forsyth Andrew J. , Coffey Mary P. , Nair Girish B. , Al-Katib Sayf A. 
Published: February 2020

Purpose:
Conflicting data exist with regard to the effect of needle gauge on outcomes of computed tomography (CT)-guided lung nodule biopsies. The purpose of this study was to compare the complication and diagnostic adequacy rates between 2 needle sizes: 18 G and 20 G in CT-guided lung nodule biopsies.

Materials and Methods:
This retrospective cohort study examined CT-guided lung biopsies performed between March 2014 and August 2016 with a total of 550 patients between the ages of 30 and 94. Biopsies were performed using an 18-G or a 20-G needle. Procedure-associated pneumothorax and other complication rates were compared between the 2 groups. Univariate and multiple logistic regression analyses were performed.

Results:
There was no significant difference in pneumothorax rate between 18 G (n=125) versus 20 G (n=425) (rates: 25.6% vs. 28.7%; P=0.50; odds ratio [OR]=0.86; 95% confidence interval [CI]=0.54-1.35), chest tube insertion rate (4.8% vs. 5.6%; P=0.71; OR=0.84; 95% CI=0.34-2.11), or diagnostic adequacy (95% vs. 93%; P=0.36; OR=1.51; 95% CI=0.61-3.72). Multiple logistic regression analysis demonstrated emphysema along the biopsy path (OR=3.12; 95% CI=1.63-5.98) and nodule distance from the pleural surface ≥4 cm (OR=1.85; 95% CI=1.05-3.28) to be independent risk factors for pneumothorax.

Conclusion:
No statistically significant difference in pneumothorax rate or diagnostic adequacy was found between 18-G versus 20-G core biopsy needles. Independent risk factors for pneumothorax include emphysema along the biopsy path and nodule distance from the pleural surface.
Cortical abnormalities and identification for first-episode schizophrenia via high-resolution magnetic resonance imaging
Authors: Liu Lin , Cui Long-Biao , Wu Xu-Sha , Fei Ning-Bo , Xu Zi-Liang , Wu Di , Xi Yi-Bin , Huang Peng , von Deneen Karen M. , Qi Shun , Zhang Ya-Hong , Wang Hua-Ning , Yin Hong , Qin Wei 
Published: February 2020

AbstractIntroEvidence from neuroimaging has implicated abnormal cerebral cortical patterns in schizophrenia. Application of machine learning techniques is required for identifying structural signature reflecting neurobiological substrates of schizophrenia at the individual level. We aimed to detect and develop a method for potential marker to identify schizophrenia via the features of cerebral cortex using high-resolution magnetic resonance imaging (MRI).MethodIn this study, cortical features were measured, including volumetric (cortical thickness, surface area, and gray matter volume) and geometric (mean curvature, metric distortion, and sulcal depth) features. Patients with first-episode schizophrenia (n = 52) and healthy controls (n = 66) were included from the Department of Psychiatry at Xijing Hospital. Multivariate computation was used to examine the abnormalities of cortical features in schizophrenia. Features were selected by least absolute shrinkage and selection operator (LASSO) method. The diagnostic capacity of multi-dimensional neuroanatomical patterns-based classification was evaluated based on diagnostic tests.ResultsMean curvature (left insula and left inferior frontal gyrus), cortical thickness (left fusiform gyrus), and metric distortion (left cuneus and right superior temporal gyrus) revealed both group differences and diagnostic capacity. Area under receiver operating characteristic curve was 0.88, and the sensitivity, specificity, and accuracy of were 94%, 82%, and 88%, respectively. Confirming these findings, similar results were observed in the independent validation. There was a positive association between index score derived from the multi-dimensional patterns and the severity of symptoms (r = 0.40, P < .01) for patients.DiscussionOur findings demonstrate a view of cortical differences with capacity to discriminate between patients with schizophrenia and healthy population. Structural neuroimaging-based measurements hold great promise of paving the road for their clinical utility in schizophrenia.
Trait-similarity and trait-hierarchy jointly determine co-occurrences of resident and invasive ant species
Authors: Wong Mark K. L. , Tsang Toby P. N. , Lewis Owen T. , Guénard Benoit 
Published: February 2020

AbstractInterspecific competition, a dominant process structuring ecological communities, acts on species’ phenotypic differences. Species with similar traits should compete intensely (trait-similarity), while those with traits that confer competitive ability should outcompete others (trait-hierarchy). Either or both of these mechanisms may drive competitive exclusion within a community, but their relative importance and interacting effects are rarely studied. We show empirically that spatial associations (pairwise co-occurrences) between an invasive antSolenopsis invictaand 28 other ant species across a relatively homogenous landscape are explained largely by an interaction of trait-similarity and trait-hierarchy in one morphological trait. We find that increasing trait-hierarchy leads to more negative associations; however these effects are counteracted when species are sufficiently dissimilar (by 37-95%) in their trait ranges. We also show that a model of species co-occurrences integrating trait-similarity and trait-hierarchy consolidates predictions of different theoretical assembly rules. This highlights the explanatory potential of the trait-based co-occurrence approach.
The multiplicity of infection does not affect interactions betweenCryptococcus neoformansand macrophages
Authors: Pline Katherine , Johnston Simon 
Published: February 2020

SummaryMajor determinants of the outcome of infection include growth of the pathogen and response of immune cells such as macrophages.Cryptococcus neoformansis a fungal pathogen which may grow within the extracellular environment, or may exploit host macrophages as a niche for replication and dissemination. The clinical outcome of cryptococcal infection varies widely between individuals even when key host and pathogen molecular factors are the same. For a broad range of infections altering pathogen density is known to influence progression and outcome of infection by affecting immune response and pathogen biology (e.g. via innate immune signalling or microbial quorum sensing). Here, using time lapse imaging of murine cell line and human primary macrophagesin vitro, we examined the effect of altering pathogen density on the interactions of macrophages with cryptococci. We find that increasing fungal burden over several orders of magnitude did not increase or decrease phagocytosis by murine J774 macrophage-like cells or human monocyte-derived macrophages, illustrating neither dose-dependent immune activation nor dampening of the phagocytic response. Furthermore, increasing fungal density alone was not sufficient to alter the ability of cryptococci to grow intracellularly and has no significant effect on fungal doubling time for cryptococci that were intracellular or extracellular. This suggested that individual macrophage-Cryptococcusinteractions were not affected by even large changes in fungal density, an important finding in understanding what determines the outcome of cryptococcal infection.
A Versatile Vector System for the Fast Generation of Knock-in Cell Lines with CRISPR
Authors: Perez-Leal Oscar , Nixon-Abell Jonathon , Barrero Carlos A. , Gordon John , Rico Mario C. 
Published: February 2020

ABSTRACTUntil recent advancements in genome editing via CRISPR/Cas9 technology, understanding protein function typically involved artificially overexpressing proteins of interest. Despite that CRISPR/Cas9 has ushered in a new era of possibilities for modifying endogenous genes with labeling tags (knock-in) to more accurately study proteins under physiological conditions, the technique is largely underutilized due to its tedious, multi-step process. Here we outline a homologous recombination system (FAST-HDR) to be used in combination with CRISPR/Cas9 that significantly simplifies and accelerates this process while introducing multiplexing to allow live-cell studies of 3 endogenous proteins within the same cell line. Furthermore, the recombination vectors are assembled in a single reaction that is enhanced for eliminating false positives and reduces the overall creation time for the knockin cell line from~8 weeks to <15 days. Finally, the system utilizes a modular construction to allow for seamlessly swapping labeling tags to ensure flexibility according to the area under study. We validated this new methodology by developing advanced cell lines with 3 fluorescent-labeled endogenous proteins that support high-content phenotypic drug screening without using antibodies or exogenous staining. Therefore, Fast-HDR cell lines provide a robust alternative for studying multiple proteins of interest in live cells without artificially overexpressing labeled proteins.
Next generation cytogenetics: comprehensive assessment of 48 leukemia genomes by genome imaging
Authors: Neveling Kornelia , Mantere Tuomo , Vermeulen Susan , Oorsprong Michiel , van Beek Ronald , Kater-Baats Ellen , Pauper Marc , van der Zande Guillaume , Smeets Dominique , Weghuis Daniel Olde , Stevens-Kroef Marian J , Hoischen Alexander 
Published: February 2020

AbstractSomatic structural variants are important for cancer development and progression. In a diagnostic set-up, especially for hematological malignancies, the comprehensive analysis of all cytogenetic aberrations in a given sample still requires a combination of techniques, such as karyotyping, fluorescencein situhybridization and CNV-microarrays. We hypothesize that the combination of these classical approaches could be replaced by high-resolution genome imaging.Bone marrow aspirates or blood samples derived from 48 patients with leukemia, who received a clinical diagnoses of different types of hematological malignancies, were processed for genome imaging with the Bionano Genomics Saphyr system. In all cases cytogenetic abnormalities had previously been identified using standard of care workflows. Based on these diagnostic results, the samples were divided into two categories: simple cases (<5 aberrations, n=37) and complex cases (≥5 aberrations or an unspecified marker chromosome, n=11). By imaging the labelled ultra-long gDNA molecules (average N50 >250kb), we generated on average ∼280-fold mapped genome coverage per sample. Chromosomal aberrations were called by Bionano Genomics Rare variant pipeline (RVP) specialized for the detections of somatic variants.Per sample, on average a total of 1,454 high confidence SVs were called, and on average 44 (range: 14-130) of those were rarei.e. not present in the population control database. Importantly, for the simple cases, all clinically reported aberrations with variant allele frequencies higher than 10% were detected by genome imaging. This held true for deletions, insertions, inversions, aneuploidies and translocations. The results for the complex cases were also largely concordant between the standard of care workflow and optical mapping, and in several cases, optical mapping revealed higher complexity than previously known. SV and CNV calls detected by optical mapping were more complete than any other previous single test and likely delivered the most accurate and complete underlying genomic architecture. Even complex chromothripsis structures were resolved. Finally, optical mapping also identified multiple novel events, including balanced translocations that lead to potential novel fusion-genes, opening the potential to discover new prognostic and diagnostic biomarkers.The full concordance with diagnostic standard assays for simple cases and the overall great concordance with (previously likely incompletely understood) complex cases demonstrates the potential to replace classical cytogenetic tests with genome imaging. In addition, this holds the potential to rapidly map new fusion genes and identify novel SVs and CNVs as novel potential leukemia drivers.
Hydrogen sulfide exposure reduces thermal set point in zebrafish
Authors: Skandalis Dimitri A. , Dobell Cheryl D. , Shaw Joshua C. , Tattersall Glenn J. 
Published: February 2020

AbstractBehavioural flexibility allows ectotherms to exploit the environment to govern their metabolic physiology, including in response to environmental stress. Hydrogen sulfide (H2S) is a widespread environmental toxin that can lethally inhibit metabolism. However, H2S can also alter behaviour and physiology, including a hypothesised induction of hibernation-like states characterised by downward shifts of the innate thermal setpoint (anapyrexia). Support for this hypothesis has proved controversial because it is difficult to isolate active and passive components of thermoregulation, especially in animals with high resting metabolic heat production. Here, we directly test this hypothesis by leveraging the natural behavioural thermoregulatory drive of fish to move between environments of different temperatures in accordance with their current physiological state and thermal preference. We observed a decrease in adult zebrafish (Danio rerio) preferred body temperature with exposure to 0.02% H2S, which we interpret as a shift in thermal setpoint. Individuals exhibited consistent differences in shuttling behaviour and preferred temperatures, which were reduced by a constant temperature magnitude during H2S exposure. Seeking lower temperatures alleviated H2S-induced metabolic stress, as measured by reduced rates of aquatic surface respiration rate. Our findings highlight the interactions between individual variation and sublethal impacts of environmental toxins on behaviour.
Comparative analysis of CPI-motif regulation of biochemical functions of actin capping protein
Authors: McConnell Patrick , Mekel Marlene , Kozlov Alexander G. , Mooren Olivia L. , Lohman Timothy M. , Cooper John A. 
Published: February 2020

ABSTRACTThe heterodimeric actin capping protein (CP) is regulated by a set of proteins that contain CP-interacting (CPI) motifs. Outside of the CPI motif, the sequences of these proteins are unrelated and distinct. The CPI motif and surrounding sequences are conserved within a given protein family, when compared to those of other CPI-motif protein families. Using biochemical assays with purified proteins, we compared the ability of CPI-motif-containing peptides from different protein families to a) bind to CP, b) allosterically inhibit barbed-end capping by CP, and c) allosterically inhibit interaction of CP with V-1, another regulator of CP. We found large differences in potency among the different CPI-motif-containing peptides, and the different functional assays showed different orders of potency. These biochemical differences among the CPI-motif peptides presumably reflect interactions between CP and CPI-motif peptides involving amino-acid residues that are conserved but are not part of the strictly defined consensus, as it was originally identified in comparisons of sequences of CPI motifs(1, 2) across all protein families (1, 2). These biochemical differences may be important for conserved distinct functions of CPI-motif protein families in cells with respect to the regulation of CP activity and actin assembly near membranes.
Recombinant human MG53 protein preserves mitochondria integrity in cardiomyocytes during ischemia reperfusion-induced oxidative stress
Authors: Gumpper Kristyn , Ma Hanley , Krishnamurthy Karthikeyan , Zhou Xinyu , Park Ki Ho , Sermersheim Matthew , Zhou Jingsong , Tan Tao , Lin Pei-Hui , Li Lei , Liu Jianxun , Zhu Hua , Ma Jianjie 
Published: February 2020

AbstractIschemic injury to the heart causes a loss of mitochondria function due to an increase in oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle and is essential to repair damage to plasma membrane. We have shown thatmg53-/-mice are more susceptible to ischemia-reperfusion injury, whereas treatment with exogenous recombinant human MG53 (rhMG53) reduces both infarct damage and restores cardiac function. This study assesses whether MG53 protects and repairs mitochondria injury after oxidative stress associated with myocardial infarction. We hypothesize that in addition to known cell membrane repair function, MG53 acts as a myokine to protect cardiomyocytes by maintaining mitochondrial function. A combination ofin vivoandin vitroischemia/reperfusion models were used to assess MG53’s effect on mitochondria using biochemical assays and confocal microscopic imaging. Treatment with rhMG53 allowed cells to maintain a healthy mitochondrial membrane potential, reduced release of mitochondrial reactive oxygen species, and mitigated mitophagy. Mitochondrial localization of rhMG53 is mediated by exposure of and interaction with cardiolipin on the mitochondrial membrane. Our data demonstrates that rhMG53 protein preserves mitochondria integrity in cardiomyocytes during ischemia reperfusion-induced oxidative stress.
Predatory colponemids are the sister group to all other alveolates
Authors: Tikhonenkov Denis V. , Strassert Jürgen F. H. , Janouškovec Jan , Mylnikov Alexander P. , Aleoshin Vladimir V. , Burki Fabien , Keeling Patrick J. 
Published: February 2020

AbstractAlveolates are a major supergroup of eukaryotes encompassing more than ten thousand free-living and parasitic species, including medically, ecologically, and economically important apicomplexans, dinoflagellates, and ciliates. These three groups are among the most widespread eukaryotes on Earth, and their environmental success can be linked to unique innovations that emerged early in each group. Understanding the emergence of these well-studied and diverse groups and their innovations has relied heavily on the discovery and characterization of early-branching relatives, which allow ancestral states to be inferred with much greater confidence. Here we report the phylogenomic analyses of 313 eukaryote protein-coding genes from transcriptomes of three members of one such group, the colponemids (Colponemidia), which unambiguously support their monophyly and position as the sister lineage to all other alveolates. Colponemid-related sequences from environmental surveys and our microscopical observations show that colponemids are not common in nature, but diverse and widespread in freshwater habitats around the world. Studied colponemids possess two types of extrusive organelles (trichocysts or toxicysts) for active hunting of other unicellular eukaryotes and potentially play an important role in microbial food webs. Colponemids have generally plesiomorphic morphology and illustrate the ancestral state of Alveolata. We further discuss their importance in understanding the evolution of alveolates as well as origin of myzocytosis and plastids.HighlightsPhylogenomics resolves Colponemidia as a sister group to all other alveolatesThe ancestor of all alveolates was a biflagellate predator feeding by phagocytosisColponemids may illuminate the ancestral states of apicomplexans, dinoflagellates, and ciliatesColponemids are geographically widespread in freshwater habitats
Intimate functional interactions between TGS1 and the Smn complex revealed by an analysis of the Drosophila eye development
Authors: Maccallini Paolo , Bavasso Francesca , Scatolini Livia , Bucciarelli Elisabetta , Noviello Gemma , Lisi Veronica , Palumbo Valeria , D’Angeli Simone , Cacchione Stefano , Cenci Giovanni , Ciapponi Laura , Wakefield James G. , Gatti Maurizio , Raffa Grazia Daniela 
Published: February 2020

AbstractTrimethylguanosine synthase 1 (TGS1) is a conserved enzyme that mediates formation of the trimethylguanosine cap on several RNAs, including snRNAs and telomerase RNA. Previous studies have shown that TGS1 binds the Survival Motor Neuron (SMN) protein, whose deficiency causes spinal muscular atrophy (SMA). In addition, TGS1 depletion results in increased hTR levels and telomere elongation in human cells. Here, we analyzed the roles of theDrosophilaorthologs of the humanTGS1andSMNgenes. We show that theDrosophilaTGS1 protein (dTgs1) physically interacts with all subunits of theDrosophilaSmn complex (Smn, Gem2, Gem3, Gem4 and Gem5), and that a humanTGS1transgene rescues the mutant phenotype caused bydTgs1loss. We demonstrate that bothdTgs1andSmnare required for viability of retinal progenitor cells and that downregulation of these genes leads to a reduced eye size. Importantly, overexpression ofdTgs1partially rescues the eye defects caused by Smn depletion, and vice versa. These results suggest that theDrosophilaeye model can be exploited for screens aimed at the identification of genes and drugs that modify the phenotypes elicited by Tgs1 and Smn deficiency. These modifiers could help to devise new therapies for SMA and diseases caused by telomerase insufficiency.