bluuebunny/crossref_metadata_2025_split huggingface dataset:
GM-CSF Expression and Macrophage Polarization in Joints of Undifferentiated Arthritis Patients Evolving to Rheumatoid Arthritis or Psoriatic Arthritis
Authors: Fuentelsaz-Romero Sara , Cuervo Andrea , Estrada-Capetillo Lizbeth , Celis Raquel , García-Campos Raquel , Ramírez Julio , Sastre Sergi , Samaniego Rafael , Puig-Kröger Amaya , Cañete Juan D 
Published: June 2020

Abstract
Background and Aims: GM-CSF-dependent macrophage polarization hasbeen demonstrated in rheumatoid arthritis (RA). Our aim was to seek diagnostic/prognostic biomarkers for undifferentiated arthritis (UA) by analyzing GM-CSF expression and source, macrophage polarization and density in joints of patients with UA evolving to RA or PsA compared with established RA or PsA, respectively.Methods:Synovial tissue (ST)from patients with UA evolving to RA (UA>RA, n=8), PsA (UA>PsA, n=9), persistent UA (UA, n=16), established RA (n=12) and PsA (n=10), and healthy controls (n=6), were analyzed. Cell source and quantitative expression of GM-CSF and proteins associated with pro-inflammatory (GM-CSF-driven) and anti-inflammatory (M-CSF-driven) macrophage polarization (activin A, TNFα, MMP12 and CD209, respectively) were assessed in ST CD163+ macrophages by multicolor immunofluorescence. GM-CSF and activin A levels were also quantified in paired synovial fluid samples. CD163+ macrophage density was determined in all groups by immunofluorescence.Results:Synovial stromal cells (FAP+ fibroblast, CD90+ endothelial cells) and CD163+ sublining macrophages were the sources of GM-CSF. ST CD163+ macrophages from all groups expressed pro-inflammatory polarization markers (activin A, TNFα and MMP12). Expression of the M-CSF-dependent anti-inflammatory marker CD209 identified two macrophage subsets (CD163+ CD209high and CD163+ CD209low/-). CD209+ macrophages were more abundant in ST from healthy controls and PsA patients, although both macrophage subtypesshowed similar levels of pro-inflammatory markers in all groups. In paired synovial fluid samples, activin A was detected in all patients, with higher levels in UA>RA and RA, while GM-CSF was infrequently detected. ST CD163+ macrophage density was comparable between UA>RA and UA>PsA patients, but significantly higher than in persistent UA and established RA and PsA patients, respectively.Conclusions: GM-CSF is highly expressed by sublining CD90+ FAP+ synovial fibroblasts, CD90+ activated endothelium and CD163+ macrophages in different types of arthritis. The polarization state of ST macrophages was similar in all UA and established arthritis groups, with a predominance of pro-inflammatory GM-CSF-associated markers. CD163+ macrophage density was significantly higher in the UA phases of RA and PsA compared with persistent UA. Taken together, our findings support the idea that GM-CSF is a strong driver of macrophage polarization and a potential therapeutic target not only in RA but also in PsA and all types of UA.
A Genotype-Phenotype Study of High-Resolution FMR1 Nucleic Acid and Protein Analyses in Fragile X Patients With Neurobehavioral Assessments
Authors: Budimirovic Dejan B , Schlageter Annette , Sadic-Filipovic Stela , Protic Dragana , Bram Eran , Mahone E. Mark , Nicholson Kimberly , Culp Kristen , Javanmardi Kamyab , Hadd Andrew , Sharp Kevin , Adayev Tatyana , LaFauci Giuseppe , Dobkin Carl , Zhou Lili , Brown William Ted , Berry-Kravis Elizabeth , Kaufmann Walter E , Latham Gary J 
Published: June 2020

Abstract

Background. Fragile X syndrome (FXS) is caused by silencing of the FMR1 gene, which encodes a protein with a critical role in synaptic plasticity. The molecular abnormality underlying FMR1 silencing, CGG repeat expansion, is well characterized; however, delineation of the pathway from DNA to RNA to protein using biosamples from well characterized patients with FXS is limited. Since FXS is a common and prototypical genetic disorder associated with intellectual disability (ID) and autism spectrum disorder (ASD), a comprehensive assessment of the FMR1 DNA-RNA-protein pathway and its correlations with the neurobehavioral phenotype is a priority.Methods. We applied nine sensitive and quantitative assays evaluating FMR1 DNA, RNA, and FMRP parameters to a reference set of cell lines representing the range of FMR1 expansions. We then used the most informative of these assays on blood and buccal specimens from cohorts of patients with different FMR1 expansions, with emphasis on those with FXS (N = 42 total, N = 31 with FMRP measurements). The group with FMRP data was also evaluated comprehensively in terms of its neurobehavioral profile, which allowed molecular-neurobehavioral correlations. Results. FMR1 CGG repeat expansions, methylation levels, and FMRP levels, in both cell lines and blood samples, were consistent with previous FMR1 genomic and protein studies. They also demonstrated a high level of agreement between blood and buccal specimens. These assays further corroborated previous reports of the relatively high prevalence of methylation mosaicism. Molecular-neurobehavioral correlations confirmed the inverse relationship between overall severity of the FXS phenotype and decrease in FMRP levels. Other intriguing findings included a potential relationship between diagnosis of FXS with ASD and very low levels of FMRP, compared to FXS without ASD. Conclusions. The results underscore the link between FMR1 expansion, gene methylation, and FMRP deficit. The association between FMRP deficiency and overall severity of the neurobehavioral phenotype invites follow up studies in larger patient cohorts. They would be valuable to confirm and potentially extend our initial findings of a relationship between ASD and other neurobehavioral features and the magnitude of FMRP deficit. Molecular profiling of individuals with FXS may have important implications in research and clinical practice.
Effects of regulatory exercise on lipolysis pathway in obese pre and postmenopausal women
Authors: Park Kyu-Min , Lim Seung-Taek , Sung Kun-Young , Kang Sunghwun 
Published: June 2020

Abstract
Background

The purpose of study was to examine the effects of regulatory resistance exercise for 12 weeks on lipolysis pathway in pre- and post- menopausal women with obesity.
Methods

Twenty-three pre- and post- menopausal women with body fat percentages of 30% or more divided into pre- menopausal group (n = 9) and post- menopausal group (n = 14). All subjects participated in resistance exercise training for 12 weeks. All participant’s anthropometric measurements and physical fitness tests were performed. Protein analyses were performed with subcutaneous fatty tissue extracted, and the samples were analyzed of relevant protein expression changes by using Western blotting. All serum samples were submitted for enzyme-linked immunosorbent assay measurements of adipocyte factors.
Results

After 12 weeks between pre- menopausal and post- menopausal groups ATGL, MGL and PLIN protein expression were significantly lower in the post- menopausal group than in the pre- menopausal group. HSL protein expression were significantly higher in the post- menopausal group than in the pre- menopausal group. In addition, leptin concentration was significantly decreased, and adiponectin concentration was significantly increased after resistance exercise in the post- menopausal group more than pre- menopausal group.
Conclusions

In this study indicates that regular resistance exercise to change of leptin and adiponectin might be release of overall decreased ATGL, HSL, MGL and PLIN expression in subcutaneous fatty tissue, and driving reduction of % fat in the obese post- menopausal group more than obese pre- menopausal group.
LINC00665 enhances tumorigenicity of endometrial carcinoma by interacting with high mobility group AT-hook 1
Authors: Liu Yun , Chang Yue , Cai Yixuan 
Published: June 2020

Abstract
Background: Endometrial carcinoma is a frequently diagnosed cancer among females. LncRNAs are reported to be associated with various cancers. Their biological roles in endometrial carcinoma progression is an emerging scientific area. LINC00665 can exert a significant role in many cancers. Up to now, its potential function in endometrial carcinoma is still poorly known.Method: qRT-PCR was carried out to test expression of LINC00665 and HMGA1. Western blot analysis was carried out to detect protein expression of HMGA1. Cell proliferation was evaluated using Cell Counting Kit-8 (CCK-8) and EdU assay. Flow cytometry assay was used to determine cell apoptosis and cell cycle. Would healing and transwell invasion assay was carried out to test cell migration and invasion. Immunohistochemical staining and HE staining were conducted to assess Ki-67 and tumor growth respectively.Results: Expression of LINC00665 in clinical endometrial carcinoma tissues and cells was obviously up-regulated. Loss of LINC00665 could repress endometrial carcinoma cell viability, induce cell apoptosis and blocked cell cycle in G1 phase. KLE and HHUA cell migration and invasion ability were depressed by LINC00665 shRNA. Decrease of LINC00665 suppressed endometrial carcinoma tumorigenicity in vivo. RIP assay evidenced LINC00665 directly bound with HMGA1 protein. shRNA of HMGA1 obviously restrained endometrial carcinoma cell growth and cell invasion.Conclusions: LINC00665 might promote endometrial carcinoma progression by positively modulating HMGA1.
RNA-sequencing reveals the expression profiles of tsRNAs and their potential carcinogenic role in cholangiocarcinoma
Authors: Yan Li-rong , Wang Ang , Xu Qian , Wang Ben-gang 
Published: June 2020

Abstract
Background: Recently, the incidence of cholangiocarcinoma (CCA) has gradually increased. As CCA has a poor prognosis, the ideal survival rate is scarce for patients. The abnormal expressed tsRNA may regulate the progression of a variety of tumors, and tsRNA is expected to become a new diagnostic marker of cancer. However, the expression of tsRNA is obscure and should be elucidated in CCA.Methods: We collected CCA tissues and adjacent normal tissues from three patients. High-throughput RNA-seq was utilized to determine the overall expression profiles of tsRNA in CCA and adjacent normal tissues and to screen the tsRNAs that were differentially expressed. The biological effects and potential signaling pathways of dysregulated tsRNAs between the CCA and adjacent normal tissues were explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses.Results: High-throughput RNA-seq totally demonstrated 535 dysregulated tsRNAs, of which 241 tsRNAs were upregulated and 294 tsRNAs were downregulated in CCA compared with adjacent normal tissues (|log2 (fold change)| >=1 and p value< 0.05). GO and KEGG enrichment analyses indicated that the target genes of dysregulated tRFs (tRF-34-JJ6RRNLIK898HR, tRF-38-0668K87SERM492V, tRF-39-0668K87SERM492E2) were mainly enriched in the Notch signaling pathway, Hippo signaling pathway, and cAMP signaling pathway and in growth hormone synthesis, secretion and action.Conclusion: Differentially expressed tRFs in CCA are enriched in many pathways associated with neoplasms, which may impact the progression of CCA.
From Passive Surveillance to Response: Suriname's Steady Efforts to Implement Maternal Death Surveillance and Response (MDSR)
Authors: Kodan Lachmi R. , Verschueren Kim J.C. , Boerstra Geertje E. , Gajadien Inder , Mohamed Robert S. , Olmtak Lily D. , Mohan Satish R. , Bloemenkamp Kitty W.M. 
Published: June 2020

Abstract
Background Maternal death surveillance and response (MDSR) is essential in preventing avoidable maternal deaths. The cycle starts by accurately capturing maternal deaths with a surveillance system, followed by an audit to give insight into the underlying causes and "lessons learned." Subsequently, recommendations are formulated and targeted multisectoral responses such as quality of care improvement strategies, including clinical guidelines update, health promotion interventions, research to fulfill knowledge gaps, enabling policies and legislation and interventions addressing social determinants. Finally, continuous evaluation and monitoring close the MDSR cycle. We aim to describe the MDSR implementation process in Suriname to share valuable lessons with other countries.Methods We provide an overview of the evolvement from improved maternal death surveillance, toward review, response, and monitoring to fulfill the MDSR cycle in Suriname. Findings Middle-income country Suriname called for many years for improved surveillance and review, and in 2000 the first action was commenced by extension of maternal death case capturing from death certificates to active hospital surveillance. Consequently, the maternal mortality ratio increased in the following years. However, not the full MDSR cycle was completed in 2015, and local health care providers initiated the next step of the MDSR cycle with the installation of a national maternal death review committee (MaMS). Since then, the committee reviews each maternal death applying the "no blame, no shame" culture, formulates, and disseminates recommendations. Collaboration with the Ministry of Health (MOH), Bureau of Public Health (BOG), and the Pan American Health Organization (PAHO) should ensure progress to the sustainable implementation of MDSR. Committee MaMS demonstrates that maternal death review and recommended high impact interventions can only be effectively implemented and sustained, through strong professional and government commitment and practical, solution-oriented responses. Conclusions Crucial elements for a successful MDSR implementation are Commitment, "no blame, no shame" Culture, Coordination, Collaboration, and Communication (5 C's).We hope that describing this process toward successful nationwide MDSR implementation, with its facilitators and barriers, is helpful for other countries with similar ambitions.
Efficacy Of Unsupervised Home-Based Pulmonary Rehabilitation For Patients With Chronic Obstructive Pulmonary Disease
Authors: Lee Jang Ho , Lee Hyang Yi , Jang Youngwon , Lee Jae Seung , Oh Yeon-Mok , Lee Sang-do , Lee Sei Won 
Published: June 2020

Abstract
Background: Pulmonary rehabilitation (PR) is a well-established treatment for chronic obstructive pulmonary disease (COPD). The standard protocol for PR requires frequent hospital visits, which can be difficult for patients. We performed this study to assess whether unsupervised home-based PR (HBPR) is effective for patients with COPD.Methods: This investigation was a prospective cohort study. After assessing the outcome data, including the results of a COPD assessment test (CAT); the body mass index, airflow obstruction, dyspnea, and exercise capacity (BODE) index; a pulmonary function test; the modified Medical Research Council (mMRC) dyspnea scale; and the 6-min walking test (6MWT), specialists imparted education to patients about unsupervised HBPR. Patients who exercised more than three times per week were classified as the compliant group, and the others were categorized as the noncompliant group. Changes in the outcomes were compared between the compliant and noncompliant groups.Results: 41 patients were enrolled in this study. After 8 weeks of unsupervised HBPR, there were significant improvements in CAT scores, BODE index, and forced expiratory volume in 1 s among patients in the compliant group compared with those in the noncompliant group. Moreover, their CAT and mMRC scores improved significantly after 8 weeks compared with those at baseline. On the other hand, patients in the noncompliant group showed no significant improvement in any of the outcomes.Conclusions: Unsupervised HBPR can be effective for compliant patients with COPD. We recommend unsupervised HBPR for patients with COPD even when regular hospital visits for PR are not possible.Trial registration: NCT03754881
The association of Coronavirus Disease-19 mortality and prior bacille Calmette-Guerin vaccination: a robust ecological evaluation using unsupervised machine learning
Authors: Brooks Nathan A , Puri Ankur , Garg Sanya , Nag Swapnika , Kaka Noshir , Zemmel Rodney W. , Corbo Jacomo , Turabi Anas El , Hegarty Paul K. , Kamat Ashish M. 
Published: June 2020

Abstract
Population-level data have suggested that bacille Calmette-Guerin (BCG) vaccination may lessen the severity of Coronavirus Disease-19 (COVID-19) prompting clinical trials in this area. Some reports have demonstrated conflicting results. We performed a robust, ecologic analysis comparing COVID-19 related mortality (CSM) between strictly selected countries based on BCG vaccination program status utilizing publicly available databases and machine learning to define the association between active BCG vaccination programs and CSM. Validation was performed using linear regression and country-specific modeling. CSM was lower for 80% of similarly clustered countries with a BCG vaccination policy for at least the preceding 15 years (BCG15). CSM increased significantly for each increase in the percent population over age 65. The total population of a country and BCG15 were significantly associated with improved CSM. There was a consistent association between countries with a BCG vaccination for the preceding 15 years, but not other vaccination programs, and CSM.
Physalis alkekengi var. franchetii extracts exert anti-tumour effects on non-small cell lung cancer and multiple myeloma by inhibiting STAT3 signalli
Authors: Fu Yufei , Zhu Fanfan , Ma Zhongjun , Lv Bin , Wang Xi , Dai Chunyan , Ma Xiaoqiong , Liu Pei , Lv Hang , Chen Xin , Shen Li , Chen Zhe 
Published: June 2020

Abstract
Background: Physalis alkekengi var. franchetii is an herb that possesses various ethnopharmacological applications. Herein, our current study focuses on the anti-tumour effect of the combination of various physalins, which are regarded as the most representative secondary metabolites from calyces of Physalis alkekengi var. franchetii.Methods: We mainly investigated the anti-tumour activity of the physalins extracted from Physalis alkekengi var. franchetii on both solid and haematologic cancers. The main cells used in this study were NCI-H1975 and U266 cells. The major assays used were the CCK8 assay, western blot analyses, an immunofluorescence assay, the Annexin V assay, and xenograft mouse model.Results: The results showed that physalins exhibited strong anti-tumoural effect on both non-small cell lung cancer (NSCLC) and multiple myeloma (MM) cells by suppressing the constitutive STAT3 activity and further inhibiting the downstream target genes expression of STAT3 signalling, resulting in the enhanced apoptosis of tumour cells. Moreover, physalins significantly reduced tumour growth in xenograft models of lung cancer.Conclusions: Collectively, these findings demonstrated that the physalins from Physalis alkekengi var. franchetii may potentially act as chemopreventive or chemotherapeutic agents for NSCLC and MM by inhibiting the STAT3 signalling pathway. It is promising that the present study served as a guide to further explore the precise mechanism of Physalis alkekengi var. franchetii in cancer treatment.
The effect of flushing on lead concentrations in drinking water
Authors: Budgen Jack , Flack Anna 
Published: June 2020

Abstract
Current Environmental Health Standing Committee (enHealth) advice recommends flushing kitchen taps for 30 seconds each morning, because lead can leach into water that has been in contact with brass plumbing fittings for an extended period. A study of 108 Sydney households identified that a five to ten second flush was sufficient to reduce lead concentrations below the Australian Drinking Water Guidelines (ADWG) in all kitchen tap water samples. This supports a change to enHealth recommendations, as a five to ten second flush not only meets public health requirements but is also more realistic for customers to achieve and increases water savings.
Gut Barrier Proteins Mediate Liver Regulation by the Effects of Serotonin on the Non-Alcoholic Fatty Liver Disease
Authors: Zhang Ke , Li Xue , Wang Xian , Zheng Hongyu , Tang Shusheng , Lu Lin , Ma Xi 
Published: June 2020

:
Serotonin (5-hydroxytryptamine, 5-HT) has been recognized as a potent pro-inflammatory
mediator. Increasing the bioavailability and preventing the formation of 5-HT can reduce the inflammatory
response in the body. Moreover, 5-HT is considered as an important central physiologic mediator
of intestinal function by regulating intestinal motility, permeability, and other functions. The dysfunction
of intestinal serotonergic system causes intestinal barrier damage and further leads to the increase
of bacterial endotoxin (LPS) translocation into the liver, which contributes to the development
of non-alcoholic fatty liver disease (NAFLD). In addition, increasing the expression of serotonin reuptake
transporter (SERT) and decreasing the expression of tryptophan hydroxylase1 (TPH1) can relieve
the symptoms of NAFLD. Tryptophan (TRP), as a precursor of 5-HT synthesis, plays an important role
in gut homeostasis and energy metabolism. Previous studies have found that TRP supplementation
aggravates fatty liver degeneration by producing 5-HT, which activates mTOR signaling pathway in
mice fed a high fat and high fructose diet. However, recent researches reveal that TRP supplementation
stabilizes the intestinal barrier damage by increasing the expression of occludin and reduces the accumulation
of fatty acids in liver. Although the effects of TRP supplementation on NAFLD are not clear
and the specific mechanism needs to be further explored. A better understanding of the mechanisms of
5-HT on the liver and gut may open new therapeutic strategies in NAFLD.
Potential Novel Benefits of Sodium Restriction in Chronic Kidney Disease
Authors: Valtuille Rodolfo 
Published: June 2020

:Chronic kidney disease is a global public health issue, and it has been considered as the epidemic of the 21st century. Therefore, all initiatives addressed to slow down the evolution and complications of this condition should be well received. While the effects of salt reduction on cardiovascular disease have some controversial issues, in chronic kidney disease, such a policy is beneficial in multiple aspects. In chronic kidney disease patients, dietary sodium restriction is regularly recommended to control extracellular fluid expansion, hypertension and cardiovascular risk. Instead, the effects of sodium reduction on chronic kidney disease progression are still controversial. In the last years, potentially beneficial effects of a low sodium diet on chronic kidney disease evolution have emerged. Firstly, recent magnetic resonance-based findings of increased Na depots in skin and muscle associated with renal function, ageing and sodium intake open a vast body of investigation as a potential tool for monitoring effects of sodium restriction. In this narrative review, we also discussed novel aspects of sodium restriction in chronic kidney disease to manage metabolic acidosis as well as renal effects on fibroblast growth factor 23 or gut microbiota. Beyond current evidence, these approaches showed that common findings of kidney failure environment such as sodium -sensitivity, micro-inflammation, arterial stiffness metabolic acidosis and sarcopenia could be delayed controlling dietary sodium. Additional studies are now needed in populations with chronic kidney disease to confirm these new findings, addressed to slow down the evolution and complications of this condition.