tbuckley/cabot-search huggingface dataset:
Chikungunya Arthritis Mechanisms in the Americas
Authors: Aileen Y. Chang, Karen A. O. Martins, Liliana Encinales, St. Patrick Reid, Marlon Acuña, Carlos Encinales, Christian B. Matranga, Nelly Pacheco, Carlos Cure, Bhavarth Shukla, Teofilo Ruiz Arteta, Richard Amdur, Lisa H. Cazares, Melissa Gregory, Michael D. Ward, Alexandra Porras, Alejandro Rico Mendoza, Lian Dong, Tara Kenny, Ernie Brueggemann, Lydia G. Downey, Priyanka Kamalapathy, Paola Lichtenberger, Orlando Falls, Gary L. Simon, Jeffrey M. Bethony, Gary S. Firestein
Journal: Arthritis & Rheumatology (2017)

To determine if chikungunya virus persists in synovial fluid after infection, potentially acting as a causative mechanism of persistent arthritis. We conducted a cross-sectional study of 38 Colombian participants with clinical chikungunya virus infection during the 2014-2015 epidemic who reported chronic arthritis and 10 location-matched controls without chikungunya virus or arthritis. Prior chikungunya virus infection status was serologically confirmed, and the presence of synovial fluid chikungunya virus, viral RNA, and viral proteins was determined by viral culture, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and mass spectrometry, respectively. Biomarkers were assessed by multiplex analysis. Patients with serologically confirmed chikungunya arthritis (33 of 38 [87%]) were predominantly female (82%) and African Colombian (55%) or white Colombian (33%), with moderate disease activity (mean ± SD Disease Activity Score in 28 joints 4.52 ± 0.77) a median of 22 months after infection (interquartile range 21-23 months). Initial symptoms of chikungunya virus infection included joint pain (97%), swelling (97%), stiffness (91%), and fever (91%). The most commonly affected joints were the knees (87%), elbows (76%), wrists (75%), ankles (56%), fingers (56%), and toes (56%). Synovial fluid samples from all patients with chikungunya arthritis were negative for chikungunya virus on qRT-PCR, showed no viral proteins on mass spectrometry, and cultures were negative. Case and control plasma cytokine and chemokine concentrations did not differ significantly. This is one of the largest observational studies involving analysis of the synovial fluid of chikungunya arthritis patients. Synovial fluid analysis revealed no detectable chikungunya virus. This finding suggests that chikungunya virus may cause arthritis through induction of potential host autoimmunity, suggesting a role for immunomodulating agents in the treatment of chikungunya arthritis, or that low-level viral persistence exists in synovial tissue only and is undetectable in synovial fluid.
Criteria for return to running after anterior cruciate ligament reconstruction: a scoping review
Authors: Alexandre J M Rambaud, Clare L Ardern, Patricia Thoreux, Jean-Philippe Regnaux, Pascal Edouard
Journal: British Journal of Sports Medicine (2018)

Objective To describe the criteria used to guide clinical decision-making regarding when a patient is ready to return to running (RTR) after ACL reconstruction. Design Scoping review. Data sources The MEDLINE (PubMed), EMBASE, Web of Science, PEDro, SPORTDiscus and Cochrane Library electronic databases. We also screened the reference lists of included studies and conducted forward citation tracking. Eligibility criteria for selecting studies Reported at least one criterion for permitting adult patients with primary ACL reconstruction to commence running postoperatively. Results 201 studies fulfilled the inclusion criteria and reported 205 time-based criteria for RTR. The median time from when RTR was permitted was 12 postoperative weeks (IQR=3.3, range 5–39 weeks). Fewer than one in five studies used additional clinical, strength or performance-based criteria for decision-making regarding RTR. Aside from time, the most frequently reported criteria for RTR were: full knee range of motion or &gt;95% of the non-injured knee plus no pain or pain &lt;2 on visual analogue scale; isometric extensor limb symmetry index (LSI)&gt;70% plus extensor and flexor LSI&gt;70%; and hop test LSI&gt;70%. Conclusions Fewer than one in five studies reported clinical, strength or performance-based criteria for RTR even though best evidence recommends performance-based criteria combined with time-based criteria to commence running activities following ACL reconstruction.
Electrocardiographic Changes in a Woman With Anorexia Nervosa
Authors: Ersilia M. DeFilippis, James Yeh
Journal: JAMA Internal Medicine (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Monitoring patients with a resolved hepatitis B virus infection for HBV reactivation
Authors: A. Tamori, R. Kozuka, H. Motoyama, H. Fujii, A. Hagihara, S. Uchida-Kobayashi, H. Morikawa, M. Enomoto, Y. Murakami, N. Kawada
Journal: Journal of Hepatology (2018)
Strong increase of acute HCV infections in HIV-negative men having sex with men
Authors: L. Cotte, M. Astrie, A.-C. Uhres, F. Bailly, S. Radenne, C. Ramiere, C. Brochier, P. Miailhes, M.-A. Trabaud, J.-C. Tardy, M. Godinot, P. Chiarello, O. Guillaud, P. Pradat
Journal: Journal of Hepatology (2018)
Pharmacological induction of hypoxia-inducible transcription factor ARNT attenuates chronic kidney failure
Authors: Björn Tampe, Désirée Tampe, Gunsmaa Nyamsuren, Friederike Klöpper, Gregor Rapp, Anne Kauffels, Thomas Lorf, Elisabeth M. Zeisberg, Gerhard A. Müller, Raghu Kalluri, Samy Hakroush, Michael Zeisberg
Journal: Journal of Clinical Investigation (2018)

Progression of chronic kidney disease associated with progressive fibrosis and impaired tubular epithelial regeneration is still an unmet biomedical challenge because, once chronic lesions have manifested, no effective therapies are available as of yet for clinical use. Prompted by various studies across multiple organs demonstrating that preconditioning regimens to induce endogenous regenerative mechanisms protect various organs from later incurring acute injuries, we here aimed to gain insights into the molecular mechanisms underlying successful protection and to explore whether such pathways could be utilized to inhibit progression of chronic organ injury. We identified a protective mechanism controlled by the transcription factor ARNT that effectively inhibits progression of chronic kidney injury by transcriptional induction of ALK3, the principal mediator of antifibrotic and proregenerative bone morphogenetic protein-signaling (BMP-signaling) responses. We further report that ARNT expression itself is controlled by the FKBP12/YY1 transcriptional repressor complex and that disruption of such FKBP12/YY1 complexes by picomolar FK506 at subimmunosuppressive doses increases ARNT expression, subsequently leading to homodimeric ARNT-induced ALK3 transcription. Direct targeting of FKBP12/YY1 with in vivo morpholino approaches or small molecule inhibitors, including GPI-1046, was equally effective for inducing ARNT expression, with subsequent activation of ALK3-dependent canonical BMP-signaling responses and attenuated chronic organ failure in models of chronic kidney disease, and also cardiac and liver injuries. In summary, we report an organ-protective mechanism that can be pharmacologically modulated by immunophilin ligands FK506 and GPI-1046 or therapeutically targeted by in vivo morpholino approaches.
Television’s <i>The Good Doctor</i> Raises Good Questions
Authors: Abigail Zuger
Journal: JAMA (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
12,13-diHOME: An Exercise-Induced Lipokine that Increases Skeletal Muscle Fatty Acid Uptake
Authors: Kristin I. Stanford, Matthew D. Lynes, Hirokazu Takahashi, Lisa A. Baer, Peter J. Arts, Francis J. May, Adam C. Lehnig, Roeland J.W. Middelbeek, Jeffrey J. Richard, Kawai So, Emily Y. Chen, Fei Gao, Niven R. Narain, Giovanna Distefano, Vikram K. Shettigar, Michael F. Hirshman, Mark T. Ziolo, Michael A. Kiebish, Yu-Hua Tseng, Paul M. Coen, Laurie J. Goodyear
Journal: Cell Metabolism (2018)
A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline
Authors: Mariana G. Tarragó, Claudia C.S. Chini, Karina S. Kanamori, Gina M. Warner, Ariel Caride, Guilherme C. de Oliveira, Micaela Rud, Adrienne Samani, Kyaw Z. Hein, Runqing Huang, Diana Jurk, Dong Seong Cho, James J. Boslett, Jordan D. Miller, Jay L. Zweier, João F. Passos, Jason D. Doles, David J. Becherer, Eduardo N. Chini
Journal: Cell Metabolism (2018)
PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding protein
Authors: Paul M Daniel, Gulay Filiz, Daniel V Brown, Michael Christie, Paul M Waring, Yi Zhang, John M Haynes, Colin Pouton, Dustin Flanagan, Elizabeth Vincan, Terrance G Johns, Karen Montgomery, Wayne A Phillips, Theo Mantamadiotis
Journal: Neuro-Oncology (2018)

Hyperactivation of phosphoinositide 3-kinase (PI3K) signaling is common in cancers, but the precise role of the pathway in glioma biology remains to be determined. Some understanding of PI3K signaling mechanisms in brain cancer comes from studies on neural stem/progenitor cells (NSPCs), where signals transmitted via the PI3K pathway cooperate with other intracellular pathways and downstream transcription factors to regulate critical cell functions.To investigate the role of the PI3K pathway in glioma initiation and development, we generated a mouse model targeting the inducible expression of a PIK3CAH1047A oncogenic mutant and deletion of the PI3K negative regulator, phosphatase and tensin homolog (PTEN), to NSPCs.Expression of a Pik3caH1047A was sufficient to generate tumors with oligodendroglial features, but simultaneous loss of PTEN was required for the development of invasive, high-grade glioma. Pik3caH1047A-PTEN mutant NSPCs exhibited enhanced neurosphere formation which correlated with increased Wnt signaling, while loss of cAMP response element binding protein (CREB) in Pik3caH1047A-Pten mutant tumors led to longer symptom-free survival in mice.Taken together, our findings present a novel mouse model for glioma demonstrating that the PI3K pathway is important for initiation of tumorigenesis and that disruption of downstream CREB signaling attenuates tumor expansion.
TCTAP A-148 Retrograde Approach for Percutaneous Recanalization of Coronary Chronic Total Occlusions; Contribution to Clinical Practice and Its Long-term Results
Authors: Osung Kwon, Pil Hyung Lee, Seung-Whan Lee, Sun Hack Lee, Sangwoo Park, Tae-Oh Kim, Yong-Hoon Yoon, Sang Yong Om, Minsoo Kim, Hanbit Park, Sang-Cheol Cho, Ungjeong Do, Jung Ae Hong, Kyusup Lee, Do-Yoon Kang, Chulhyun Lee, Jung-Min Ahn, Duk-Woo Park, Soo-Jin Kang, Young-Hak Kim, Cheol Whan Lee, Seong-Wook Park, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2018)
P507Noncompact left ventricular myocards and pregnancy
Authors: D Bublikov, G V Serduk, M G Nicolaeva, A P Momot
Journal: Cardiovascular Research (2018)

Conclusion:In summary, our results demonstrate that BAK treatment attenuates IRI by attenuating IR-induced mitochondrial oxidative damage via the activation of SIRT3/PGC-1a signaling.
Corrigendum to “Hepatitis C virus drug resistance associated substitutions and their clinical relevance: Update 2018” [Drug Resist. Updates 37 (March) (2018) 17–39]
Authors: Maria C. Sorbo, Valeria Cento, Velia C. Di Maio, Anita Y.M. Howe, Federico Garcia, Carlo F. Perno, Francesca Ceccherini-Silberstein
Journal: Drug Resistance Updates (2018)
P493The absences of Growth Differentiation Factor 15 aggravates adverse cardiac remodeling upon pressure-overload
Authors: S C A De Jager, J J De Haan, L Bosch, M A D Brans, S J Lee, D W D Kuster, M Mokry, J Van Der Velden, G Pasterkamp, J P G Sluijter
Journal: Cardiovascular Research (2018)

Conclusion: GA activates caspase-8 to cleave N-term of IjBa, leading to decrease of NF-jB activity and hypertrophy, consequently induces autophgy, thereby providing the molecular basis by which
P351The possible participation of telocytes as tissue modulators in normal and pathological human aorta
Authors: L Borges, RSP Falcao, S R Taboga, P S Gutierrez, J B Michel
Journal: Cardiovascular Research (2018)

increased level of immature platelets in acute coronary syndrome (ACS) associated with adverse ischemic outcomes.The mechanisms involved in the regulation of platelet turnover per se remain discussible.The impact of mandatory pharmacological platelet suppression as a cornerstone of antithrombotic therapy of ACS on platelet turnover is poorly understood.Purpose: of the study was to investigate associations between platelet turnover parameters, thrombopoietin (TPO), stromal cell derived factor 1 (SDF1) and myeloproliferative leukemia virus oncogene (MPL) in patients with ST segment elevation myocardial infarction (STEMI), furthermore to characterize key regulatory mechanisms of platelet turnover in STEMI as potential pharmacological target.Methods: We report preliminary results of the on-going study.40 male patients with STEMI were enrolled, and stratified into two groups according to clinical presentation and short-term risk scores.Mean platelet volume (MPV) and MPV to platelet count ratio were used as a surrogate marker of platelet turnover.TPO, SDF1 and MPL were chosen to characterize platelet turnover regulation, and were serially (0-1-7 days) measured with commercially available ELISA kits.Time delays, and rate characteristics were calculated from TPO, SDF1 and MPL time functions.Results: Among already involved patients 37.5% were hemodynamically unstable, with elevated short-term risk of adverse outcomes, and suffered from early MI complications (group 1).The patients of the group 2 were comparatively but insignificantly (p ¼ 0.354) younger, less likely to be a current smoker.Neither platelet count (p ¼ 0.814), nor MPL (0.585), nor their ratio (0.865) were significantly different between the compared groups.Initial levels of TPO were significantly increased in group 1: 331.82 (207.04;477.08) vs 209.06 (153.32;298.91) pg/mL, p ¼ 0.044.Within 7 days TPO levels decreased in both groups with poor and better prognosis, but the mean rate was maximal in unstable patients: 7.5 vs 0.44 pg/mL*day.We detected noticeable negative correlation between TPO, SDF1 levels and MPL (Spearman R -0.437 . . .-0.586, p < 0.05) more substantial in patients with better prognosis: Spearman R -0.614 vs -0.586, p ¼ 0.012.Longer delays in TPO, SDF1 and MPL kinetics were revealed in patients with poor prognosis.Conclusion: In patients with STEMI, thrombopoietin and stromal cell derived factor 1 were inversely associated with platelet turnover parameters.In hemodynamically unstable patients with elevated short-term risk of adverse outcomes, kinetics of key regulators of platelet turnover were characterized by maximal rates and delays.Our findings suggest presence of an alternative regulator of platelet turnover associated with clinically severe course of STEMI.
LONG – TERM RESULTS OF PERORAL ENDOSCOPIC MYOTOMY (POEM) FOR ACHALASIA
Authors: Z Rábeková, Z Vacková, V Lánská, J Spicak, T Hucl, P Štirand, E Kieslichová, J Martínek
Journal: Endoscopy (2018)

POEM has gained trust by proved safety and short-term efficacy and it is considered to be a standard method for treatment of achalasia. The aim of this prospective single-center case series was to assess the long-term clinical outcome of POEM with emphasis on post-POEM reflux evaluated by pH monitoring, endoscopy findings, reflux symptoms and use of PPIs.
Long noncoding RNA miR503HG, a prognostic indicator, inhibits tumor metastasis by regulating the HNRNPA2B1/NF-κB pathway in hepatocellular carcinoma
Authors: Hui Wang, Linhui Liang, Qiongzhu Dong, Lin Huan, Jia He, Botai Li, Chen Yang, Haojie Jin, Lin Wei, Chengtao Yu, Fangyu Zhao, Jinjun Li, Ming Yao, Wenxin Qin, Lunxiu Qin, Xianghuo He
Journal: Theranostics (2018)

Long noncoding RNAs (lncRNAs) have been associated with hepatocellular carcinoma (HCC), but the underlying molecular mechanisms of their specific association with hepatocarcinogenesis have not been fully explored. Methods: miR503HG was identified by microarray and validated by real-time PCR. Survival analysis was evaluated using the Kaplan-Meier method and assessed using the log-rank test. In vitro and in vivo assays were preformed to explore the biological effects of miR503HG in HCC cells. The interaction of miR503HG with HNRNPA2B1 was identified by RNA pull-down and RNA immunoprecipitation. Expression of HNRNPA2B1 was examined by western blotting, immunofluorescence and immunohistochemical analyses, while HNRNPA2B1 ubiquitination was detected by immunoprecipitation. Results: We have identified 713 differentially expressed lncRNAs in 12 pairs of HCC tissues compared with corresponding noncancerous liver tissues. One of these lncRNAs, miR503HG, the host gene of miR503, is markedly decreased in HCC. Expression level of miR503HG is significantly associated with the time to recurrence and overall survival and is an independent risk factor for recurrence and survival. Enhanced expression of miR503HG could noticeably inhibit HCC invasion and metastasis in vitro and in vivo. Further investigation suggested that miR503HG could specifically interact with the heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1). miR503HG promoted HNRNPA2B1 degradation via the ubiquitin-proteasome pathway, which reduced the stability of p52 and p65 mRNA, and simultaneously suppressed the NF-κB signaling pathway in HCC cells. In addition, miR503HG can function synergistically with miR503 to inhibit HCC migration. Conclusion: Our findings support a role for miR503HG in tumor recurrence risk and survival prediction in HCC patients. We demonstrate a novel mechanism by which miR503HG inhibits the NF-κB signaling pathway and exerts its metastatic tumor suppression function through modulating the ubiquitination status of HNRNPA2B1.
Increased DNA methylation variability in rheumatoid arthritis-discordant monozygotic twins
Authors: Amy P. Webster, Darren Plant, Simone Ecker, Flore Zufferey, Jordana T. Bell, Andrew Feber, Dirk S. Paul, Stephan Beck, Anne Barton, Frances M. K. Williams, Jane Worthington
Journal: Genome Medicine (2018)

Rheumatoid arthritis is a common autoimmune disorder influenced by both genetic and environmental factors. Epigenome-wide association studies can identify environmentally mediated epigenetic changes such as altered DNA methylation, which may also be influenced by genetic factors. To investigate possible contributions of DNA methylation to the aetiology of rheumatoid arthritis with minimum confounding genetic heterogeneity, we investigated genome-wide DNA methylation in disease-discordant monozygotic twin pairs.Genome-wide DNA methylation was assessed in 79 monozygotic twin pairs discordant for rheumatoid arthritis using the HumanMethylation450 BeadChip array (Illumina). Discordant twins were tested for both differential DNA methylation and methylation variability between rheumatoid arthritis and healthy twins. The methylation variability signature was then compared with methylation variants from studies of other autoimmune diseases and with an independent healthy population.We have identified a differentially variable DNA methylation signature that suggests multiple stress response pathways may be involved in the aetiology of the disease. This methylation variability signature also highlighted potential epigenetic disruption of multiple RUNX3 transcription factor binding sites as being associated with disease development. Comparison with previously performed epigenome-wide association studies of rheumatoid arthritis and type 1 diabetes identified shared pathways for autoimmune disorders, suggesting that epigenetics plays a role in autoimmunity and offering the possibility of identifying new targets for intervention.Through genome-wide analysis of DNA methylation in disease-discordant monozygotic twins, we have identified a differentially variable DNA methylation signature, in the absence of differential methylation in rheumatoid arthritis. This finding supports the importance of epigenetic variability as an emerging component in autoimmune disorders.
Quantitative assessment of regional left ventricular wall motion from real-time 3D echocardiography: Effects of dual-triggered contrast enhancement tested against cardiac magnetic resonance
Authors: Cristiana Corsi, P. Coon, S. Goonewardena, L. Weinert, T. S. Polonsky, L. Sugeng, E. G. Caiani, Claudio Lamberti, R. M. Lang, V. Mor Avi
Journal: Journal of the American College of Cardiology (2006)
Applications of RNA Indexes for Precision Oncology in Breast Cancer
Authors: Liming Ma, Zirui Liang, Hui Zhou, Lianghu Qu
Journal: Genomics Proteomics & Bioinformatics (2018)

Abstract Precision oncology aims to offer the most appropriate treatments to cancer patients mainly based on their individual genetic information. Genomics has provided numerous valuable data on driver mutations and risk loci; however, it remains a formidable challenge to transform these data into therapeutic agents. Transcriptomics describes the multifarious expression patterns of both mRNAs and non-coding RNAs (ncRNAs), which facilitates the deciphering of genomic codes. In this review, we take breast cancer as an example to demonstrate the applications of these rich RNA resources in precision medicine exploration. These include the use of mRNA profiles in triple-negative breast cancer (TNBC) subtyping to inform corresponding candidate targeted therapies; current advancements and achievements of high-throughput RNA interference (RNAi) screening technologies in breast cancer; and microRNAs as functional signatures for defining cell identities and regulating the biological activities of breast cancer cells. We summarize the benefits of transcriptomic analyses in breast cancer management and propose that unscrambling the core signaling networks of cancer may be an important task of multiple-omic data integration for precision oncology.