tbuckley/cabot-search huggingface dataset:
Immunotherapy Approved for Endometrial Cancer
Authors: Rebecca Voelker
Journal: JAMA (2021)

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
Medicare Support for Dental and Podiatry Graduate Medical Education Programs
Authors: Candice Chen, YoonKyung Chung, Geoffrey Broadbent, Elizabeth Mertz
Journal: JAMA Network Open (2021)

<h3>Importance</h3> Oral health care faces ongoing workforce challenges that affect patient access and outcomes. While the Medicare program provides an estimated $14.6 billion annually in graduate medical education (GME) payments to teaching hospitals, including explicit support for dental and podiatry programs, little is known about the level or distribution of this public investment in the oral health and podiatry workforce. <h3>Objective</h3> To examine Medicare GME payments to teaching hospitals for dental and podiatry residents from 1998 to 2018, as well as the distribution of federal support among states, territories, and the District of Columbia. <h3>Design, Setting, and Participants</h3> This cross-sectional study was conducted using data from 1252 US teaching hospitals. Data were analyzed from May through August 2020. <h3>Exposures</h3> Dental and podiatry residency training. <h3>Main Outcomes and Measures</h3> Medicare dental and podiatry GME payments were examined. <h3>Results</h3> Among 1252 teaching hospitals, Medicare provided nearly $730 million in dental and podiatry GME payments in 2018. From 1998 to 2018, the number of residents supported more than doubled, increasing from 2340 residents to 4856 residents, for a 2.1-fold increase, while Medicare payments for dental and podiatry GME increased from $279 950 531 to $729 277 090, for a 2.6-fold increase. In 2018, an estimated 3504 of 4856 supported positions (72.2%) were dental. Medicare GME payments varied widely among states, territories, and the District of Columbia, with per capita payments by state, territory, and district population ranging from $0.05 in Puerto Rico to $14.24 in New York, while 6 states received no support for dental or podiatry residency programs. <h3>Conclusions and Relevance</h3> These findings suggest that dental and podiatry GME represents a substantial public investment, and deliberate policy decisions are needed to target this nearly $730 million and growing investment to address the nation’s priority oral and podiatry health needs.
POS0393 FIBRIN DEPOSITION IS AN ACTIVE TRIGGER OF CARTILAGE DEGENERATION IN RHEUMATOID ARTHRITIS
Authors: T. Hügle, S. Nasi, D. Ehirchiou, P. Omoumi, A. So, N. Busso
Journal: Annals of the Rheumatic Diseases (2021)

Background: Fibrin(ogen) maintains inflammation in various disorders but has never been linked to cartilage damage in rheumatoid arthritis (RA) or other forms of inflammatory arthritis. Objectives: To investigate the role of fibrin deposition on cartilage integrity in arthritis. Methods: Fibrin deposition on knee cartilage was analyzed by immunohistochemistry in RA patients and in murine adjuvant-induced arthritis (AIA). In chondrocytes, fibrinogen expression ( Fgα, Fgβ, Fgγ ) and procoagulant activity were evaluated by qRT-PCR and turbidimetry respectively. Fibrin-induced catabolic genes were assessed by qRT-PCR in chondrocytes. Fibrin-mediated chondro-synovial adhesion (CSA) with subsequent cartilage tears was studied in co-cultures of human RA cartilage with autologous synoviocytes, in the AIA model, and by MRI. The link between fibrin and calcification was examined in human RA cartilage stained for calcific deposits and in vitro in fibrinogen-stimulated chondrocytes. Results: Fibrin deposition on cartilage correlated with the severity of cartilage damage in human RA explants and in AIA wildtype (WT) mice, while fibrinogen deficient (Fg -/- ) mice were protected. Accordingly, fibrin upregulated catabolic enzymes ( Adamts5 and Mmp13 ) in chondrocytes. Secondly, CSA was present in fibrin-rich and damaged cartilage in AIA WT but not in Fg -/- mice. In line, autologous human synoviocytes, cultured on RA cartilage explants, adhered exclusively to fibrin-positive degraded areas. Gadolinium-enhanced MRI of human joints showed contrast-enhancement along cartilage surface in RA patients but not in controls. Finally, fibrin co-localized with calcification in human RA cartilage and triggered chondrocyte mineralization inducing pro-calcification genes ( Anx5, Pit1, Pc1 ) and cytokine (IL-6). Although at a much lesser extent, we observed similar fibrin-mediated mechanisms in osteoarthritis (OA). Conclusion: Fibrin deposition directly impacts on cartilage integrity via induction of catabolism, mechanical stress, and calcification. Potentially, fibrin is a key factor of cartilage damage occurring in RA as a secondary consequence of inflammation. Disclosure of Interests: None declared
Melanoma pathology: new approaches and classification*
Authors: I. Yeh, B.C. Bastian
Journal: British Journal of Dermatology (2021)

Cancer is caused by the accumulation of pathogenic alterations of the genome and epigenome that result in permanent changes that disrupt cellular homeostasis. The genes that become corrupted in this process vary among different tumour types, reflecting specific vulnerabilities and dependencies of the cell from which the cancer originated. This also applies to 'melanoma', a cancer that constitutes not one, but multiple diseases that can be separated based on their cell of origin, aetiology, clinical appearance and course, and response to treatment. In this article, we review the current classification of melanoma within distinct evolutionary pathways and the associated genetic alterations. In addition, we review the application of molecular diagnostics to the diagnosis of melanocytic tumours in the context of histopathological assessment.
Prevalence of Asymptomatic SARS-CoV-2 Infection
Authors: Daniel P. Oran, Eric J. Topol
Journal: Annals of Internal Medicine (2020)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly throughout the world since the first cases of coronavirus disease 2019 (COVID-19) were observed in December 2019 in Wuhan, China. It has been suspected that infected persons who remain asymptomatic play a significant role in the ongoing pandemic, but their relative number and effect have been uncertain. The authors sought to review and synthesize the available evidence on asymptomatic SARS-CoV-2 infection. Asymptomatic persons seem to account for approximately 40% to 45% of SARS-CoV-2 infections, and they can transmit the virus to others for an extended period, perhaps longer than 14 days. Asymptomatic infection may be associated with subclinical lung abnormalities, as detected by computed tomography. Because of the high risk for silent spread by asymptomatic persons, it is imperative that testing programs include those without symptoms. To supplement conventional diagnostic testing, which is constrained by capacity, cost, and its one-off nature, innovative tactics for public health surveillance, such as crowdsourcing digital wearable data and monitoring sewage sludge, might be helpful.
OP0279-PARE CHRONIC RHEUMATIC DISEASE (CRD) AND SPORT
Authors: P. Lemesle, L. Poulain, X. Grapton, N. Bouhedja
Journal: Annals of the Rheumatic Diseases (2021)

Background: In order to study the state of mind of patients with chronic inflammatory rheumatic disease (CRD) regarding physical/sports activity, excluding household activities despite their quantifiable energy value (MET), the CREER group produces this study. Objectives: Analyze a population in the Ile-de-France region with CRD practicing a physical activity (their motivations, expectations, nature and rhythm). Determine the place of physical activity in the management of an CRD by the rheumatologist (Rh). Methods: 207 patients, 53 yo average, 56% between 50 and 70 years, 60% are women; 97% of the CRD, Rheumatoid arthritis (RA): 57%) or Ankylosing Spondylitis (AS): 40%, low or moderate activity (66%). 10 years evolution (RA) and 11.5 years (AS), corticosteroids RA/AS as follows (34/5 %), NSAIDs (15/52 %), conventional DMARDS (84/30%) or biotherapies (21/43%). Co-morbidities are found for RA/AS in 55% vs 44%, includes high blood pressure 20%, overweight 21%, tobacco 13.5%, other 19%. Results: 7/10 patients are encouraged to engage in physical activity, regardless of gender, age, RA or AS. The most common activity proposed is walking (53%), followed by swimming and/or aquagym (40%) and gym (19%). The practice is regular in 60% more by women, RA=AS, more before 40 yo and after 60 years old (70%). The activity actually practiced is: 1- walking 46.4%, 2- aquatic activities 37%, 3- cycling 29%, 4- home sports 19%. Once/week minimum is good for cycling and swimming, insufficient for walking, very good for sport at home. 50% have been practicing for 3 years. 60% adapt the rhythm to rheumatism. Their motivations are: to maintain one’s health, to de-stress. A discordance exists between Rh/General physician that advise sport 8 times/10 vs 4.5/10. Nevertheless 50% ignore whether he or she is getting worse or better, hence the need for information. Rh needs to communicate more about the interest of physical activity and the absence of deleterious effect on CRD which one patient over two ignores. If 60% of patients modify their activity with CRD, many do not participate in sports because no time, no need, no desire RA=AS. If the activity is supervised, adapted, prescribed is well-known, its application is confidential due to lack of coaches, and of qualified centers. Conclusion: If the main activity practiced by patients and advocated by Rh is walking, the patients go beyond this framework by mobilizing for cycling, walking, swimming and gym. But the reluctance persists and we must, through therapeutic education convince of the benefits of the activity on CRD and its co-morbidities, unknown to 50% of patients. To map lesions, judge the ability and desires are necessary to set goals for duration and frequency of activity. Using connected tools improves compliance. Finally, walking which does not require neither schedule nor equipment (otherwise a cane) should become a first-line prescription. Disclosure of Interests: None declared.
Development and Validation of a Machine Learning Model Using Administrative Health Data to Predict Onset of Type 2 Diabetes
Authors: Mathieu Ravaut, Vinyas Harish, Hamed Sadeghi, Kin Kwan Leung, Maksims Volkovs, Kathy Kornas, Tristan Watson, Tomi Poutanen, Laura C. Rosella
Journal: JAMA Network Open (2021)

<h3>Importance</h3> Systems-level barriers to diabetes care could be improved with population health planning tools that accurately discriminate between high- and low-risk groups to guide investments and targeted interventions. <h3>Objective</h3> To develop and validate a population-level machine learning model for predicting type 2 diabetes 5 years before diabetes onset using administrative health data. <h3>Design, Setting, and Participants</h3> This decision analytical model study used linked administrative health data from the diverse, single-payer health system in Ontario, Canada, between January 1, 2006, and December 31, 2016. A gradient boosting decision tree model was trained on data from 1 657 395 patients, validated on 243 442 patients, and tested on 236 506 patients. Costs associated with each patient were estimated using a validated costing algorithm. Data were analyzed from January 1, 2006, to December 31, 2016. <h3>Exposures</h3> A random sample of 2 137 343 residents of Ontario without type 2 diabetes was obtained at study start time. More than 300 features from data sets capturing demographic information, laboratory measurements, drug benefits, health care system interactions, social determinants of health, and ambulatory care and hospitalization records were compiled over 2-year patient medical histories to generate quarterly predictions. <h3>Main Outcomes and Measures</h3> Discrimination was assessed using the area under the receiver operating characteristic curve statistic, and calibration was assessed visually using calibration plots. Feature contribution was assessed with Shapley values. Costs were estimated in 2020 US dollars. <h3>Results</h3> This study trained a gradient boosting decision tree model on data from 1 657 395 patients (12 900 257 instances; 6 666 662 women [51.7%]). The developed model achieved a test area under the curve of 80.26 (range, 80.21-80.29), demonstrated good calibration, and was robust to sex, immigration status, area-level marginalization with regard to material deprivation and race/ethnicity, and low contact with the health care system. The top 5% of patients predicted as high risk by the model represented 26% of the total annual diabetes cost in Ontario. <h3>Conclusions and Relevance</h3> In this decision analytical model study, a machine learning model approach accurately predicted the incidence of diabetes in the population using routinely collected health administrative data. These results suggest that the model could be used to inform decision-making for population health planning and diabetes prevention.
AB0182 HEMOGLOBIN RATE AS A PREDICTOR OF SUBCLINICAL LEFT VENTRICULAR SYSTOLIC DYSFUNCTION IN RHEUMATOID ARTHRITIS
Authors: Y. Ben Abderrazek, R. Dhahri, W. Lahmar, M. Slouma, B. Louzir, L. Metoui, I. Gharsallah, H. Mahfoudhi, C. Chourabi, W. Fehri
Journal: Annals of the Rheumatic Diseases (2021)

Background: The role of rheumatoid arthritis as an ischemic heart disease and heart failure risk factor is well acknowledged even if the physiopathological pathways are still debated. The effect of anemia on myocardial deformation has already been established and a hemoglobin level below 9g/dL was associated with a significantly lower global longitudinal strain (GLS) patients with no history of CVD or chronic inflammatory diseases.[1] Objectives: In the present study, we looked into the effect of anemia and hemoglobin on the myocardial impairement in RA patients. Methods: We conducted a monocentric cross-sectional study between march 2019 and september 2019 on 36 RA patients without any history of cardiovascular disease and non-altered left ventricular ejection fraction in the outpatient population of the rheumatology department of the military hospital of Tunis matched with 36 healthy control subjects. Both groups underwent conventional echocardiography and STE to measure GLS; subclinical left ventricular systolic dysfunction was defined as a GLS &gt; −18%, and a complete blood cell count; anemia was defined as Hemoglobin levels &lt; 12 g/dL for women and &lt; 13 g/dL for men. Results: Myocardial deformation study revealed that rheumatoid arthritis patients had a significantly worse GLS than healthy controls (18.99±2.81% vs 20.42±1.33%; P =.015). We also observed that third of the RA patients had subclinical left ventricular systolic dysfunction. In our report 36% of RA patients were anemic. In our univariate analysis anemia was found to be significantly correlated with GLS (r=−0.368, P =.027) and hemoglobin was found to be the best predictor of subclinical LVSD in our ROC curve analysis (AUC=0.752, 95% CI: 0.577-0.927, P =.02). In our multivariate analysis anemia was the only factor that was independently related to subclinical LVSD (OR: 11.39, 95% CI: 1.57-82.89, P =.016). Figure 1. ROC curve analysis for Hemoglobin as a predictor of subclinical left ventricular systolic dysfunction Conclusion: To our knowledge, this is the first study to look into the relationship between GLS and anemia among RA patients, and now it is safe to say that anemia is yet another added burden on the myocardial function in RA patients that needs to be taken into account when discussing therapeutic action. References: [1]Zhou Q, Shen J, Liu Y, Luo R, Tan B, Li G. Assessment of left ventricular systolic function in patients with iron deficiency anemia by three-dimensional speckle-tracking echocardiography. Anatol J Cardiol. 2017;18(3):194–9. Disclosure of Interests: None declared
Correction: The Sensitivity and Costs of Testing for SARS-CoV-2 Infection With Saliva Versus Nasopharyngeal Swabs
Authors: Mayara Lisboa Bastos, MD, Sara Perlman-Arrow, Dick Menzies, MD, Jonathon R. Campbell, PhD
Journal: Annals of Internal Medicine (2021)

CorrectionsApril 2021Correction: The Sensitivity and Costs of Testing for SARS-CoV-2 Infection With Saliva Versus Nasopharyngeal SwabsFREEThis correction concerns the following article:ReviewsApr 2021The Sensitivity and Costs of Testing for SARS-CoV-2 Infection With Saliva Versus Nasopharyngeal SwabsFREEMayara Lisboa Bastos, MD, Sara Perlman-Arrow, Dick Menzies, MD, and Jonathon R. Campbell, PhDMayara Lisboa Bastos, MDMcGill University and McGill International TB Centre, Montreal, Quebec, Canada, and State University of Rio de Janeiro, Rio de Janeiro, Brazil (M.L.B.), Sara Perlman-ArrowMcGill University, Montreal, Quebec, Canada (S.P.), Dick Menzies, MDMcGill University, McGill International TB Centre, and Montreal Chest Institute, Montreal, Quebec, Canada (D.M.), and Jonathon R. Campbell, PhDMcGill University and McGill International TB Centre, Montreal, Quebec, Canada (J.R.C.).https://doi.org/10.7326/L21-0055 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail In the review by Bastos and colleagues (1), a labeling error in the Figure has been corrected. All estimates remain unchanged and valid. These corrections were made after review of a comment by readers (2).These corrections have been made online.References1. Bastos ML, Perlman-Arrow S, Menzies D, et al. The sensitivity and costs of testing for SARS-CoV-2 infection with saliva versus nasopharyngeal swabs. A systematic review and meta-analysis. Ann Intern Med. 2021;174:501-10. doi:10.7326/M20-6569 LinkGoogle Scholar2. Hill C, Thuret J. The sensitivity and costs of testing for SARS-CoV-2 infection with saliva versus nasopharyngeal swabs [Letter]. Ann Intern Med. 2021;174:582. doi:10.7326/L21-0092 Google Scholar Comments0 CommentsSign In to Submit A Comment PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoThe Sensitivity and Costs of Testing for SARS-CoV-2 Infection With Saliva Versus Nasopharyngeal Swabs Mayara Lisboa Bastos , Sara Perlman-Arrow , Dick Menzies , and Jonathon R. Campbell Metrics Cited byReal-life experience: sensitivity and specificity of nasal and saliva samples for COVID-19 diagnosis April 2021Volume 174, Issue 4Page: 584 ePublished: 20 April 2021 Issue Published: April 2021 Copyright & PermissionsCopyright © 2021 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
POS0205 AMELIORATION OF ENDOTHELIAL DYSFUNCTION WITH JAK INHIBITION IN RHEUMATOID ARTHRITIS: JAK CV-RISK REDUCTION STUDY
Authors: A. Syngle, N. Garg, K. Chauhan
Journal: Annals of the Rheumatic Diseases (2021)

Background: Cardiovascular (CV) disease is the leading cause of premature mortality and sudden death in Rheumatoid Arthritis (RA). Conventional CV risk factors and disease specific risk factors are responsible for endothelial dysfunction (ED) in RA. ED is the barometer of CV health and key initial event in atherosclerosis. Tofacitinib, a JAK inhibitor, is in clinical use since 2012 and has had the most extensive development program in RA, but its impact on ED has not yet been explored in humans. Objectives: To investigate the impact of tofacitinib on endothelial dysfunction in RA Methods: 40 RA patients fulfilling the 2010 Rheumatoid Arthritis classification criteria with active disease (DAS28&gt;3.2) were randomized to receive 24 weeks of treatment with Tofacitinib (5mg bd, n=20) and placebo (n=20) as an adjunct to existing stable antirheumatic drugs. Primary endpoints included endothelial dysfunction assessed by FMD using Angiodefender and lipids were estimated at baseline and after 12 weeks of treatment. The secondary end points included: DAS28, ESR, CRP, HAQ-DI and cardiovascular risk using SCORE chart assessed at week 0 and 12. Results: At baseline, endothelial function was impaired and levels of inflammatory measures were elevated in both groups. CV risk SCORE was high and HAQ-DI was impaired at baseline. After treatment, FMD improved significantly in the tofacitinib group from (8.16±1.38% to 10.98±2.33%, p≤0.05) as compared to placebo (7.12±0.25% to 8.04±0.30%, p=0.35) (Fig. 1A). DAS28 (Fig. 1B), ESR and CRP (Fig. 1C) levels improved significantly in tofacitinib group as compared to placebo (p≤0.05). Tofacitinib significantly decreased HAQ-DI and SCORE (Fig. 1D) values as compared to placebo. There was significant increase in HDL (p≤0.05) after treatment with tofacitinib as compared to placebo. After 12 weeks of treatment, FMD and HDL increased by 34.55% and 13.58% respectively where as DAS28, ESR and CRP decreased by 37.40%, 36.10% and 76.59% respectively in the tofacitinib group. Significant negative correlation was observed between FMD and DAS28 (r= -0.50, p≤0.05) and CRP (r= -52, p≤0.05) after treatment with tofacitinib where as no such correlation was found in placebo group. Figure 1. Impact of Tofacitinib on FMD, DAS 28, CRP &amp; SCORE Conclusion: First study to show that tofacitinib, apart from its anti inflammatory activity, improves endothelial dysfunction and cardiovascular risk in RA. Thus, JAK inhibition with tofacitinib has vasculoprotective and cardioprotective effect mediated through anti-inflammatory and probably other mechanisms. This study would stimulate further research in exploring the vasculoprotective and cardioprotective potential of tofacitinib in RA. References: [1]Tofacitinib reversed endothelial dysfunction in rheumatoid arthritis: mechanistic insights from the rat adjuvant-induced arthritis model. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2747 Disclosure of Interests: None declared