bluuebunny/crossref_metadata_2025_split huggingface dataset:
Health and Adverse Childhood Experiences Among Homeless Youth
Authors: Barnes Andrew J. , Gower Amy L. , Sajady Mollika , Lingras Katherine A. 
Published: February 2020

Abstract
Background and Objectives Homelessness is associated with health problems and with adverse childhood experiences (ACEs). The risk of chronic health conditions for homeless compared to housed youth, and how this risk interacts with ACEs remains unclear. This study investigated the relationship between ACEs, housing, and child health, and whether: 1) ACEs and health vary by housing context; 2) ACEs and homelessness confer independent health risks; and 3) ACEs interact with housing with regard to adolescent health. Methods Using data from 119,254 8th-11th graders, we tested independent and joint effects of ACEs and past-year housing status (housed, family homelessness, unaccompanied homelessness) on overall health and chronic health conditions, controlling for sociodemographic covariates. Results The prevalence of ACEs varied by housing status, with 34.1% of housed youth experiencing ≥1 ACE vs. 56.3% of family-homeless and 85.5% of unaccompanied-homeless youth. Health status varied similarly. Homelessness and ACEs were independently associated with low overall health and chronic health conditions, after adjusting for covariates. Compared to housed youth, both family-homeless youth and unaccompanied-homeless youth had increased odds of low overall health and chronic physical and/or mental health conditions. All ACE x housing-status interactions were significant (all p<0.001), such that ACE-related health risks were moderated by housing status. Conclusions ACEs and housing status independently predict health status during adolescence beyond other sociodemographic risks. Being homeless unaccompanied is also riskier than being homeless with family, and every additional ACE increases this risk. Clinicians and health systems should advocate for policies that include stable housing as a protective factor.
Experimental infection with the hookworm, Necator americanus, promotes gut microbial diversity in human volunteers with relapsing multiple sclerosis
Authors: Jenkins Timothy , Pritchard David , Tanasescu Radu , Telford Gary , Paraiakovou Marina , Constantinescu Cris , Cantacessi Cinzia 
Published: February 2020

Abstract
Background Helminth-associated changes in gut microbiota composition have been hypothesised to contribute to the immune-suppressive properties of parasitic worms. Multiple sclerosis is an immune-mediated autoimmune disease of the central nervous system whose pathophysiology has been recently linked to alterations of gut microbial communities. Results In the present study we investigated, for the first time, qualitative and quantitative changes in gut microbial composition of human volunteers with remitting multiple sclerosis (RMS) prior to and following experimental infection with the human hookworm, Necator americanus ( N+ ), and following anthelmintic treatment, and compared the findings with data obtained from a cohort of RMS patients subjected to placebo treatment ( PBO ). Bacterial 16S rRNA high-throughput sequencing data revealed significantly decreased microbial alpha diversity in the gut microbiota of PBO compared to N+ subjects over the course of the trial; additionally, we observed significant differences in the abundances of several bacterial taxa with putative immune-modulatory functions between study cohorts. Parabacteroides were significantly expanded in the gut microbiota of N + individuals for which no relapses were recorded at the end of the trial. Conclusions Overall, these data lend support to the hypothesis of a contributory role of parasite-associated alterations in gut microbial composition to the immunomodulatory properties of hookworm parasites.
Shifts in microbial diversity, composition and functionality in the gut and genital microbiome during a natural SIV infection in vervet monkeys
Authors: Jasinska Anna J , Dong Tien S , Lagishetty Venu , Katzka William , Jacobs Jonathan P , Schmitt Christopher , Cramer Jennifer Danzy , Ma Dongzhu , Coetzer Willem G , Grobler J. Paul , Turner Trudy R , Freimer Nelson , Pandrea Ivona , Apetrei Cristian 
Published: February 2020

Abstract
Background: The microbiota plays an important role in HIV pathogenesis in humans. Microbiota can impact health through several pathways such as increasing inflammation in the gut, metabolites of bacterial origin, and microbial translocation from the gut to the periphery which contributes to systemic chronic inflammation, immune activation, and the development of AIDS. Unlike HIV-infected humans, SIV-infected vervet monkeys do not experience gut dysfunction, microbial translocation and chronic immune activation and do not progress to immunodeficiency. Here, we provide the first reported characterization of the microbial ecosystems of the gut and genital tract in a natural nonprogressing host of SIV, wild vervet monkeys from South Africa. Results: We characterized fecal, rectal, vaginal, and penile microbiomes in vervets from populations heavily infected with SIV from diverse locations across South Africa. Geographic site, age, and sex affected the vervet microbiome across different body sites. Fecal and vaginal microbiome showed marked stratification with three enterotypes in fecal samples and two vagitypes, which were predicted functionally distinct within each body site. Bioclimatic factors, biome type, and environmental temperature, influenced microbiomes locally associated with vaginal and rectal mucosa. Several fecal microbial taxa were linked to plasma levels of immune molecules, for example, MIG was positively correlated with Lactobacillus and Escherichia/Shigella and Helicobacter , and IL-10 was negatively associated with Erysipelotrichaceae , Anaerostipes , Prevotella and Anaerovibrio , and positively correlated with Bacteroidetes , and Succinivibrio . During the chronic phase of SIV infection, we observed a significant increase in gut microbial diversity, alterations in community composition (including a decrease in Proteobacteria/ Succinivibrio in the gut) and functionality (including a decrease in genes involved in bacterial invasion of epithelial cells in the gut), and partial reversibility of acute infection-related shifts in microbial abundance. As part of our study, we also developed an accurate predictor of SIV infection using fecal samples. Conclusions: The vervets infected with SIV and humans infected with HIV differ in microbial responses to infection. These responses to SIV infection may aid in preventing microbial translocation and subsequent disease progression in vervets, and may represent host microbiome adaptations to the virus.
Eosinophilic Gastroenteritis as a Cause of Non-Helicobacter pylori, Non-gastrotoxic Drug Ulcers in Children
Authors: Joo Jung Yeon , Cho Jin Min , Yoo In Hyuk , Yang Hye Ran 
Published: February 2020

Abstract
Background: While Helicobacter pylori (H. pylori) ulcers has declined recently, H. pylori-negative and/or gastrotoxic drug-negative peptic ulcers (HNGN-PU) has increased. This study aimed to analyze the etiology of peptic ulcers in children and the differences in clinical, laboratory, endoscopic, and histopathologic findings of peptic ulcers according to etiology, including eosinophilic gastroenteritis (EoGE). Methods: In total, 255 children (157 boys and 98 girls) with peptic ulcers were recruited. The subjects were categorized into 5 groups according to the etiology of the ulcer: 1) H. pylori infection (n = 51); 2) gastrotoxic drugs (n = 18); 3) idiopathic (n = 144); 4) systemic disease (n = 23); 5) EoGE (n = 19). Clinical data were reviewed and analyzed retrospectively. Results: Age at diagnosis, ulcer recurrence, atopic dermatitis history, white blood cell count, blood eosinophil count, platelet count, serum albumin level, iron level, erythrocyte sedimentation rate, and C-reactive protein level differed significantly among the 5 groups (all p < 0.05). Regarding endoscopic findings, multiple ulcers and gastric mucosal nodularity differed among the 5 groups (all p < 0.05). When comparing the EoGE ulcer group with the others, EoGE group revealed older ages (p = 0.022), higher rates of ulcer recurrence (p = 0.018), atopic dermatitis history (p = 0.001), and both blood and tissue eosinophilia (both p = 0.001). Conclusions: EoGE ulcers constituted 10.2% of HNGN-PU in pediatric patients. In children with HNGN-PU, peripheral eosinophilia, ulcer recurrence, and atopic dermatitis history might imply EoGE, necessitating thorough investigation of tissue eosinophils during endoscopic biopsy. Trial registration: 255 children retrospectively registered between between July 2003 and April 2017.
The Developed Patient Healthy Questionnaire-8 with a Greater Impact on Quality of Life Compared with the Somatic Symptom Scale-8 in Functional Dyspepsia
Authors: Yuan Chaoqun , Yong Guizhen , Wang Xi , Xie Ting , Wang Chunyan , Yuan Yuan , He Guobin 
Published: February 2020

Abstract
Background: To adapt insufficiencies of the Somatic Symptom Scale-8 (SSS-8) measuring somatization in functional dyspepsia (FD) to develop PHQ-8, of which reliability, validity and the effects of somatization evaluated by the developed PHQ-8 on quality of life (QoL) were further assessed.Methods: 612 FD patients completed a 25 items questionnaire. 8 items were selected from 25 items to constitute the PHQ-8 by discrete degree, correlation coefficient, factor analysis and Cronbach coefficient four methods. Reliability and validity for the PHQ-8 and the SSS-8 were compared by principal component and confirmatory factor analysis. The effects of somatization, depression and anxiety on the Nepean Dyspepsia Index (NDI) for QoL were explored by Pearson correlation coefficient and linear regression analysis.Results: Cronbach’s α coefficients for the PHQ-8 and the SSS-8 were 0.601, 0.553, and cumulative contribution rates of three extracted factors were 55.103%, 51.666%, respectively. Somatization evaluated by the PHQ-8(r=0.309, P<0.001) and the SSS-8 (r=0.281, P<0.001) were related to the NDI. The model for the PHQ-8 showed χ2=31.247, RMR=0.01, RMSEA=0.042, GFI=0.984. Linear regression analysis showed that somatization measured by the PHQ-8 (β=0.270, P<0.001), anxiety (β=0.163, P<0.001) and depression (β=0.136, P=0.003) were determinants of the NDI; somatization measured by the SSS-8 (β=0.250, P<0.001), anxiety (β=0.156, P<0.001) and depression (β=0.155, P =0.001) were determinants of the NDI.Conclusions: The developed PHQ-8 had a better reliability and validity, which assessing somatization appeared to have a greater impact on QoL than that of the SSS-8. These results suggested that the developed PHQ-8 might improve to study the effects of somatization on QoL instead of the SSS-8 in specific FD patients.
Exome sequencing for diagnosis of congenital hemolytic anemia
Authors: Mansour-Hendili Lamisse , Aissat Abdelrazak , Badaoui Bouchra , Sakka Mehdi , Gameiro Christine , Ortonne Valérie , Wagner-Ballon Orianne , Pissard Serge , Picard Véronique , Ghazal Khaldoun , Bahuau Michel , Guitton Corinne , Mansour Ziad , Duplan Mylène , Petit Arnaud , Chalumeau Nathalie Costedoat , Michel Marc , Bartolucci Pablo , Moutereau Stéphane , Funalot Benoît , Galactéros Frédéric 
Published: February 2020

Abstract
Background: Congenital hemolytic anemia constitutes a heterogeneous group of rare genetic disorders of red blood cells. Diagnosis is based on clinical data, family history and phenotypic testing, genetic analyses being usually performed as a late step. In this study, we explored 40 patients with congenital hemolytic anemia by whole exome sequencing: 20 patients with hereditary spherocytosis and 20 patients with unexplained hemolysis.Results: A probable genetic cause of disease was identified in 82.5% of the patients (33/40): 100% of those with suspected hereditary spherocytosis (20/20) and 65% of those with unexplained hemolysis (13/20). We found that several patients carried genetic variations in more than one gene (3/20 in the hereditary spherocytosis group, 6/13 fully elucidated patients in the unexplained hemolysis group), giving a more accurate picture of the genetic complexity of congenital hemolytic anemia. In addition, whole exome sequencing allowed us to identify genetic variants in non-congenital hemolytic anemia genes that explained part of the phenotype in 3 patients.Conclusion: The rapid development of next generation sequencing has rendered the genetic study of these diseases much easier and cheaper. Whole exome sequencing use for congenital hemolytic anemia could provide a more precise and quicker diagnosis, improve patients’ healthcare and probably has to be democratized notably for complex cases.
Resistin Induces Chemokine and Matrix Metalloproteinase Production via CAP1 Receptor and Activation of P38-MAPK and NF-κB Signalling Pathways in Human Chondrocytes
Authors: Zhao Cheng-Wu , Song Wen-Xia , Liu Bo , Gao Yu-Hang , Ding Lu , Huang Yi-Fan , Qi Xin 
Published: February 2020

Abstract
BackgroundResistin is an adipokine also detected higher expression in serum and synovial fluid of patients with knee osteoarthritis (KOA). Resistin is known to be related closely to insulin resistance and inflammation. However, the pathogenic role of resistin in KOA remain unclear. Purpose of the study is to investigate whether resistin induces KOA by binding to functional receptor adenylyl cyclase-associated protein 1 (CAP1) and activating the p38 mitogen-activated protein kinase (p38-MAPK) and nuclear factor-κB (NF-κB) signalling pathways in human chondrocytes. MethodsWe enrolled 103 patients with radiographic KOA and 86 healthy participants as controls. The levels of resistin in serum and synovial fluid (SF) were determined via enzyme-linked immunosorbent assay (ELISA). CAP1 expression in cartilage tissues (21 samples of KOA cartilage and 10 samples of healthy hip cartilage) was measured using immunohistochemistry (IHC), quantitative real-time polymerase chain reaction ( qRT-PCR ), and western blotting assays. Effects of resistin on chondrocytes and CAP1 were evaluated via qRT-PCR and co-immunoprecipitation . The roles of CAP1, p38-MAPK, and NF-κB signalling pathways in the development of KOA were evaluated via adenovirus-mediated CAP1 short hairpin RNA, qRT-PCR, western blotting, and ELISA. Results﻿Expression of resistin in serum and SF was elevated in severe radiographic KOA. CAP1 levels were higher in KOA cartilage and were positively correlated with resistin expression. Resistin promoted increased expression of CCL3, CCL4, MMP13, and ADAMTS-4 through CAP1 receptor. Resistin also directly bound to CAP1 as confirmed by co-immunoprecipitation. CAP1 knockdown in chondrocytes attenuated resistin-induced expression of CCL3, CCL4, MMP13, and ADAMTS-4 and activation of the p38-MAPK and NF-κB signalling pathways . ConclusionsOur study shows that resistin bound to CAP1 and upregulated the expression of proinflammatory cytokines and matrix-degrading enzymes via p38-MAPK and NF-κB signalling pathways in human chondrocytes.
Clinical manifestations including the EULAR Sjögren's Syndrome Disease Activity Index in anti-Ro52/SS-A antibody-seropositive patients with Sjögren's syndrome
Authors: Nakamura Hideki , Morimoto Shimpei , Shimizu Toshimasa , Takatani Ayuko , Nishihata Shin-ya , Kawakami Atsushi 
Published: February 2020

Abstract
Background: Relationship between anti-Ro52/SS-A antibody (anti-Ro52) and clinical manifestation of Sjögren's syndrome (SS) was sporadically described regarding involvement of internal organs.Objectives: To determine the clinical factors relevant to anti-Ro52 with SS.Methods: We conducted a retrospective study of subjects with suspected SS (n=149), patients with rheumatoid arthritis (RA) (n=62), and healthy subjects (n=50). We analyzed components of the American-European Consensus Group (AECG) criteria, Raynaud's phenomenon (RP), anti-centromere antibody (ACA), serum IgG, rheumatoid factor, and the EULAR Sjögren's Syndrome Disease Activity Index (ESSDAI).Results: Among the 149 suspected SS subjects, 115 subjects were classified as having SS. Anti-Ro52 was observed in 70 SS patients (60.9%), of whom 31 patients had markedly elevated anti-Ro52 (>500 U/ml). In the SS group, three patients with anti-Ro60−/anti-Ro52+ and 17 patients without anti-Ro were observed. Compared to ACA, the relevance of positive anti-Ro52 toward positive anti-Ro60 was significantly higher (p<0.05). We observed relevance between the anti-Ro52 concentration and anti-Ro60 that was significantly affected by xerophthalmia, xerostomia, ACA seropositivity, RP, serum IgG level, and RF. The anti-Ro52 concentration well discriminated six clinical factors (ROC AUC >0.75) for ACA seropositivity, ESSDAI score ≥1, and RF or moderately high serum IgG, focus score ≥1, and anti-La/SS-B antibody seropositivity (ROC AUC >0.7). A linear relationship between the ESSDAI score and anti-Ro52 was observed.Conclusion: Significant relevance between anti-Ro52 and anti-Ro60 as well as significant items including the ESSDAI regarding the anti-Ro52 concentration was revealed. Regarding relevance toward anti-Ro60, anti-Ro52 had a higher association than ACA.(246/250 words)
Drug Safety of Benzodiazepines in Patients with Chronic Obstructive Pulmonary Disease
Authors: Liao Yi-Hsiang , Chen Liang-Yu , Liao Kuang-Ming , Chen Chung-Yu 
Published: February 2020

Abstract
Many comorbidities, including depression, anxiety, dyspnea, and insomnia, occur in patients with chronic obstructive pulmonary disease (COPD). These patients may be prescribed benzodiazepines (BZDs). However, there are some concerns that benzodiazepines increase the risk of drug overdose, hypercapnic respiratory failure, acute exacerbation and increased mortality. The aim of our study was to evaluate the drug safety of BZDs in patients with COPD. We used the National Health Insurance Research Database (NHIRD) in Taiwan from 2002 to 2016 to perform a retrospective cohort study. We enrolled patients who were exposed to the first prescription of BZDs, non-BZDs or a combination (mix user) after COPD diagnosis. We performed 1:1:1:1 propensity score matching in three groups. The outcomes were COPD with acute exacerbation and all-cause mortality. Poisson regression analysis was performed to evaluate the incidence rate ratios (IRRs) for the outcomes in the groups. After propensity score matching, there were 2856 patients in each group. After adjusting for confounding factors, we found that compared to BZD users, non-BZD and mix users had nonsignificant differences in outpatient management of acute exacerbations, hospitalization management of acute exacerbations, emergency department management of acute exacerbations and all-cause mortality. Using BZDs or non-BZDs is safe in terms of COPD exacerbation. However, BZD, non-BZD, and mix users showed increased COPD-related respiratory events compared to nonusers.
Preoperative adjuvant therapy for locally advanced and recurrent/metastatic gastrointestinal stromal tumors: a retrospective study
Authors: Qi Jing , Liu He-li , Ren Feng , Liu Sheng , Shi Wei , Liu Wei-Hang , Cai Gao-Qiang , Liao Guo-Qing 
Published: February 2020

Abstract
Background Preoperative imatinib mesylate therapy for gastrointestinal stromal tumors (GISTs) is controversial. This study aimed to explore the clinical efficacy and optimal duration of preoperative imatinib mesylate (IM) therapy in patients with locally advanced and recurrent/metastatic GISTs. Methods We retrospectively examined patients who received preoperative imatinib mesylate therapy from January 2013 to December 2018 at Xiangya Hospital, Central South University and the Second Xiangya Hospital of Central South University, China. Clinical data, including the results of tests for mutations in KIT and PDGFR, findings from regularly conducted re-examinations, abdominal enhanced computed tomography/magnetic resonance imaging data, responses to imatinib, progression-free survival and overall cancer-specific survival, were recorded. Results A total of 25 patients were enrolled in our study, including 18 with a locally advanced GIST and 7 with recurrent or metastatic GISTs. Their ages ranged from 22 to 70 years (M:F = 1.6:0.9), with a mean age of 50.48±12.51 years. The tumor locations included the stomach (56.0%), rectum (16.0%), enterocoelic/retroperitoneal sites (12.0%) and the small intestine (12.0%). Based on testing for mutations in KIT and PDGFR, 22 patients received 400 mg/d KIT, and 3 patients received 600 mg/d PDGFR. The median duration of preoperative IM therapy was 8.96±4.81 months, ranging from 3 to 26 months. According to the Choi criteria, 24 patients achieved a partial response (PR), and 1 patient had stable disease (SD). All patients underwent surgery after preoperative IM therapy, and no postoperative complications appeared. The 2-year PFS and 5-year PFS were 92% and 60%, respectively, and the total 5-year cancer-specific survival (CSS) was 92%. Conclusion Preoperative imatinib therapy is feasible for locally advanced and recurrent/metastatic GISTs and can effectively shrink the tumor size, allow organ sparing and avoid extensive organ resection. Moreover, the optimal duration of preoperative IM therapy in patients with locally advanced and recurrent/metastatic GISTs was 8.96±4.81 months, ranging from 3 to 26 months, and gastric GISTs had a better response to preoperative IM therapy than did non-gastric GISTs.
Origin of a novel CYP20A1 transcript isoform through multiple Alu exaptations creates a potential miRNA sponge
Authors: Bhattacharya Aniket , Jha Vineet , Singhal Khushboo , Fatima Mahar , Singh Dayanidhi , Chaturvedi Gaura , Dholakia Dhwani , Kutum Rintu , Pandey Rajesh , Bakken Trygve E. , Seth Pankaj , Pillai Beena , Mukerji Mitali 
Published: February 2020

Abstract
Background: Primate-specific Alus contribute to transcriptional novelties in conserved gene regulatory networks. Alu RNAs are present at elevated levels in stress conditions and consequently leads to transcript isoform specific functional role modulating the physiological outcome. One of the possible mechanisms could be Alu nucleated mRNA-miRNA interplay. Result: Using combination of bioinformatics and experiments, we report a transcript isoform of an orphan gene, CYP20A1 ( CYP20A1_Alu-LT ) through exaptation of 23 Alus in its 9kb 3’UTR. CYP20A1_Alu-LT , confirmed by 3’RACE, is an outlier in length and expressed in multiple cell lines. We demonstrate its presence in single nucleus RNA-seq of ~16000 human cortical neurons (including rosehip neurons). Its expression is restricted to the higher primates. Most strikingly, miRanda predicts ~4700 miRNA recognition elements (MREs; with threshold< -25kcal/mol) for ~1000 miRNAs, which have majorly originated within the 3’UTR-Alus post exaptation. We hypothesized that differential expression of this transcript could modulate mRNA-miRNA networks and tested it in primary human neurons where CYP20A1_Alu-LT is downregulated during heat shock response and upregulated upon HIV1-Tat treatment. CYP20A1_Alu-LT could possibly function as a miRNA sponge as it exhibits features of a sponge RNA such as cytosolic localization and ≥10 MREs for 140 miRNAs. Small RNA-seq revealed expression of nine miRNAs that can potentially be sponged by CYP20A1_Alu-LT in neurons. Additionally, CYP20A1_Alu-LT expression was positively correlated (low in heat shock and high in Tat) with 380 differentially expressed genes that contain cognate MREs for these nine miRNAs. This set is enriched in genes involved in neuronal development and hemostasis pathways. Conclusion: We demonstrate a potential role for CYP20A1_Alu-LT as miRNA sponge through preferential presence of MREs within Alus in a transcript isoform specific manner. This highlights a novel component of Alu-miRNA mediated transcriptional modulation leading to physiological homeostasis.