tbuckley/cabot-search huggingface dataset:
AB0252 ASSOCIATION OF FAT MASS AND ITS DISTRIBUTION WITH BONE MINERAL DENSITY FOR RHEUMATOID ARTHRITIS PATIENTS.
Authors: O. Lamkhanat, H. Azzouzi, B. Touil, I. Linda
Journal: Annals of the Rheumatic Diseases (2020)

Background: Bone mineral density (BMD) and body mass are closely associated. lean mass(LM) and fat mass(FM) account for approximately 95% of body mass[1]. Objectives: We aimed to study the association between body fat mass and its distribution with femoral and lumbar bone mineral density in rheumatoid arthritis (RA) patients. Methods: The present RA population-based cross sectionnel study done on 2019 was part of our rhumatology departement. Clinical data, femoral and lumbar BMD, body fat mass (BFM), android fat mass(AFM), gynoid fat mass (GFM), visceral fat mass (VFM) measured with dual energy X-ray absorptiometry (DXA: Hologic®) and results of laboratory tests were collected. Our statistical analysis was based on descriptive study and linear regression with SPSS20. Results: We included 73 RA patients witch mean age of 52.7+/-11.7, their mean of body mass index was 26.6+/5.8, mean of disease activity score was 2.6+/-0.94 and the mean health assessment questionnaire was 1.14+/0.78. In univariable linear regression, we found a significant association between femoral BMD and (BFM) (p=0.001, béta=0.36, IC:[0.000003-0.00001]), (AFM) (p=0.01, béta=0.29, IC:[0.00001, 0.00008]) and (GFM) (p=0.001, béta= 0.38, IC=[0.000005-0.000088]). There wasn’t any association between (VFM) and femoral BMD. Also we have found a significant association between lumbar spine BMD and BFM (p=0.0002, béta=0.41, IC[0.000003-0.000011]), AFM(p=0.001, béta=0.38, IC[0.000025-0.000094]), GFM(p=0.000018, béta=0.47, IC[0.00003-0.00007] and VFM (p=0.01, béta=0.28, IC[0.000027, 0.000251]). Adjusted on BFM, GFM, AFM and VFM in multiple regression analysis, it seems that the association between GFM, femoral BMD (p=0.02, béta= 0.38, IC[0.000005, 0.000088]. and lumbar spine BMD(p=0.01, béta=0.85, IC[0.000022, 0.000168]), was more significant. Conclusion: The finding of this study confirmed previous studies partly, that genoid fat mass has a positive effect of lumbar and femoral BMD. References: [1 ]S. Yang et al. Association between fat mass, lean mass, and bone loss: the Dubbo osteoporosis epidemiology study . International Osteoporosis Foundation and National Osteoporosis Foundation 2014, osteoporosis int. 2015; 26(4): 1381-6. Disclosure of Interests: None declared
Clarification Regarding Noninferiority and a Discussion of Model Selection and Treatment Effects in Observational Research
Authors: Zachary H. Hopkins, Aaron M. Secrest
Journal: JAMA Dermatology (2020)

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 Dermatology 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 Dermatology journal
Risk score to predict event-free survival after hematopoietic cell transplant for sickle cell disease
Authors: Ruta Brazauskas, Graziana M. Scigliuolo, Hai-Lin Wang, Barbara Cappelli, Annalisa Ruggeri, Courtney D. Fitzhugh, Jane S. Hankins, Julie Kanter, Joerg J. Meerpohl, Julie A. Panepinto, Damiano Rondelli, Shalini Shenoy, Mark C. Walters, John E. Wagner, John F. Tisdale, Eliane Gluckman, Mary Eapen
Journal: Blood (2020)
Tumor biomarkers predict clinical outcome of COVID-19 patients
Authors: Bangshun He, Aifang Zhong, Qiuyue Wu, Xiong Liu, Jie Lin, Chao Chen, Yiming He, Yanju Guo, Man Zhang, Peiran Zhu, Jian Wu, Changjun Wang, Shukui Wang, Xinyi Xia
Journal: Journal of Infection (2020)
High rates of 30-day mortality in patients with cirrhosis and COVID-19
Authors: Massimo Iavarone, Roberta D'Ambrosio, Alessandro Soria, Michela Triolo, Nicola Pugliese, Paolo Del Poggio, Giovanni Perricone, Sara Massironi, Angiola Spinetti, Elisabetta Buscarini, Mauro Viganò, Canio Carriero, Stefano Fagiuoli, Alessio Aghemo, Luca S. Belli, Martina Lucà, Marianna Pedaci, Alessandro Rimondi, Maria Grazia Rumi, Pietro Invernizzi, Paolo Bonfanti, Pietro Lampertico
Journal: Journal of Hepatology (2020)
원저 : 최근 5 년 사이에 발생한 자발성 세균성 복막염의 임상 양상과 배양 균주 및 항균제 내성 추이
Authors: 송희곤, 이한주, 주연호, 정세라, 박영환, 류수형, shin jung woo, 이윤정, 정영화, 이영상, 서동진
Journal: Clinical and Molecular Hepatology (2002)

Backgrounds/Aims: Recently, treatment failure with the third generation of cephalosporin was increasingly noted in patients with spontaneous bacterial peritonitis (SBP). We therefore were to evaluate the pattern of antibiotic resistance and its clinical significance. Methods: We retrospectively analyzed 580 episodes of SBP occurring between 1995 and 1999. There were 87 episodes of SBP in 1995, 222 in 1998, and 271 in 1999. The pattern of isolated organisms and antibiotic resistance, and prognostic factors for survival, were analyzed. Results: Microorganisms were isolated in 41% of total episodes. The three most frequently isolated organisms were E. coli (48%), K. pneumoniae (15%), and Aeromonas (8%). The percentage of resistant strains to cefotaxime (9%, 14%, 32%) and ciprofloxacin (13%, 21%, 32%) significantly increased. The proportion of E. coli producing extended spectrum β-lactamase (ESBL) also increased significantly (0%, 16%, 33%). The need of secondary antibiotics such as imipenem due to treatment failure was significantly increased from 0% in 1995 to 33% in 1999. Overall in-hospital mortality, however, was not changed (20%, 20%, 24%, respectively). The factor affecting early mortality was renal failure at diagnosis. Prognostic factors for long-term survival were the presence of associated malignancy and ESBL-producing microorganisms. Conclusion: Microorgansims resistant to third generation cephalosporin and quinolone were increasingly isolated over the 5 years in patients with SBP. Measures to prevent in-hospital spread of resistant strains and indiscreet use of antibiotics should therefore be instituted.(Korean J Hepatol 2002;8:61-70)
Clinical and Molecular Spectrum of Nonsyndromic Early‐Onset Osteoarthritis
Authors: Valentin Ruault, Kevin Yauy, Aurélie Fabre, Mélanie Fradin, Julien Van-Gils, Chloé Angelini, Geneviève Baujat, Patricia Blanchet, Silvestre Cuinat, Bertrand Isidor, Christian Jorgensen, Didier Lacombe, Sébastien Moutton, Sylvie Odent, Elodie Sanchez, Sabine Sigaudy, Isabelle Touitou, Marjolaine Willems, Florence Apparailly, David Geneviève, Mouna Barat-Houari
Journal: Arthritis & Rheumatology (2020)

Objective Osteoarthritis (OA) is the most common joint disease worldwide. The etiology of OA is varied, ranging from multifactorial to environmental to monogenic. In a condition called early‐onset OA, OA occurs at an earlier age than is typical in the general population. To our knowledge, there have been no large‐scale genetic studies of individuals with early‐onset OA. The present study was undertaken to investigate causes of monogenic OA in individuals with nonsyndromic early‐onset OA. Methods The study probands were 45 patients with nonsyndromic early‐onset OA who were referred to our skeletal disease center by skeletal dysplasia experts between 2013 and 2019. Criteria for early‐onset OA included radiographic evidence, body mass index ≤30 kg/m 2 , age at onset ≤50 years, and involvement of ≥1 joint site. Molecular analysis was performed with a next‐generation sequencing panel. Results We identified a genetic variant in 13 probands (29%); the affected gene was COL2A1 in 11 , ACAN in 1, and SLC26A2 in 1. After familial segregation analysis, 20 additional individuals were identified. The mean ± SD age at onset of joint pain was 19.5 ± 3.9 years (95% confidence interval 3–47). Eighteen of 33 subjects (55%) with nonsyndromic early‐onset OA and a genetic variant had had at least 1 joint replacement (mean ± SD age at first joint replacement 41 ± 4.2 years; mean number of joint replacements 2.6 per individual), and 21 (45%) of the joint replacement surgeries were performed when the patient was &lt;45 years old. Of the 20 patients age &gt;40 years, 17 (85%) had had at least 1 joint replacement. Conclusion We confirmed that COL2A1 is the main monogenic cause of nonsyndromic early‐onset OA. However, on the basis of genetic heterogeneity of early‐onset OA, we recommend next‐generation sequencing for all individuals who undergo joint replacement prior to the age of 45 years. Lifestyle recommendations for prevention should be implemented.
Monitoring of patients with systemic lupus erythematosus during the COVID-19 outbreak
Authors: Jan Holubar, Moglie Le Quintrec, Hind Letaief, Jean Luc Faillie, Yves-Marie Pers, Christian Jorgensen
Journal: Annals of the Rheumatic Diseases (2020)

The emergence and spread of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the resulting COVID-19 disease, have had a tremendous impact on public health and the world economy. Thus far, COVID-19 does not appear to be more severe in immunocompromised patients, but relevant data are scarce.1 Conversely to what was initially thought, patients with systemic lupus erythematosus (SLE) are also involved.2 3 In an article by Mathian et al ,4 some severe forms of COVID-19 infection were described in 17 patients with SLE, particularly in those with renal failure or obesity. This greater susceptibility might arise from dysregulation of ACE2 and interferon expression.5 At the same time, hydroxychloroquine (HCQ), the reference standard-of-care treatment for SLE, has emerged as a potential treatment option for COVID-19. HCQ has shown the potential to inhibit the viral replication in vitro, and several clinical trials are under way to evaluate its clinical efficacy.6 Building on the report of Mathian et al ,4 we would like to share our experience from another French university centre to further the discussion of SLE patient outcomes during the COVID-19 outbreak. Here we aim to address COVID-19 disease progression …
Clinical effectiveness of pharmacist-led versus conventionally delivered antiviral treatment for hepatitis C virus in patients receiving opioid substitution therapy: a pragmatic, cluster-randomised trial
Authors: Andrew Radley, Marijn de Bruin, Sarah K Inglis, Peter T Donnan, Adrian Hapca, Stephen T Barclay, Andrew Fraser, John F Dillon
Journal: The Lancet. Gastroenterology & hepatology (2020)
AB0098 THE EFFECT OF MALT1-DEFICIENCY ON THE EFFECTOR PHASE OF EXPERIMENTAL AUTOIMMUNE ARTHRITIS
Authors: T. Nemeth, K. Futosi, J. Ruland, A. Mocsai
Journal: Annals of the Rheumatic Diseases (2020)

Background: The paracaspase Malt1 is a cysteine protease, which forms a complex leading to the activation of the in proinflammatory transcription factor NF-κB in lymphocytes with CARMA1 and Bcl10. Previously, we showed that the myeloid equivalent of CARMA1, Card9 is important in neutrophils in Fcγ receptor-mediated cytokine release together with Bcl10 and Malt1. In line with these findings, we observed a significant decrease in the severity of autoantibody-triggered arthritis in the absence of Card9 and Bcl10. Objectives: Our aim was to directly investigate whether the genetic deficiency of Malt1, the third component of the complex altered the process of the K/BxN serum transfer arthritis (that resembles to the effector phase of rheumatoid arthritis). Methods: We used wild type and Malt1 –/– mice for our experiments. Autoantibody-mediated arthritis was induced by a single intraperitoneal injection of K/BxN serum. Clinical signs of joint inflammation were scored on a scale based on the cardinal inflammatory clues for two weeks. Ankle thickness was measured by a spring-loaded caliper. Results: Similar to the deficiency of the other two components of the complex, Malt1 –/– mice showed a partial, but significant decrease in the macroscopic joint inflammation compared to arthritic serum-treated wild type animals during the entire experimental process. In line with this phenomenon, Malt1 –/– animals had reduced autoantibody-triggered ankle thickening. Conclusion: Our results show that Malt1 seems to be an important molecule in the development and progression of experimental autoantibody-induced arthritis in mice, highlighting the role of the molecule as a potential therapeutic target in the future. Disclosure of Interests: None declared
Sex Differences in Right Ventricular–Pulmonary Arterial Coupling in Pulmonary Arterial Hypertension
Authors: Khodr Tello, Manuel J. Richter, Athithan Yogeswaran, Hossein A. Ghofrani, Robert Naeije, Rebecca Vanderpool, Henning Gall, Ryan J. Tedford, Werner Seeger, Tim Lahm
Journal: American Journal of Respiratory and Critical Care Medicine (2020)

affect case fatality (6).These findings are in line with a previous trial that demonstrated reduced intubation rates in the most hypoxemic patients (3) and that mortality is not affected by HFNC put forward the complexity of SARS-CoV-2 infection, in which the underlying lungs do not hold typical features of acute respiratory distress syndrome (7, 8).Instead, acute fibrinous and organizing pneumonia with organizing intraalveolar fibrin associated with notorious endothelial injury can be found in postmortem biopsies (7, 8).Moreover, the proportion of pulmonary embolism and acute kidney and myocardial injury are reported in much higher proportions than in typical acute respiratory distress syndrome (9).Finally, this study highlights that HFNC was as safe as standard oxygen in a large cohort of patients with COVID-19.
Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis
Authors: Gonzalo Artiach, Miguel Carracedo, Oscar Plunde, Craig E. Wheelock, Silke Thul, Peter Sjövall, Anders Franco-Cereceda, Andres Laguna-Fernandez, Hildur Arnardottir, Magnus Bäck
Journal: Circulation (2020)

Aortic valve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing of the aortic valve as a consequence of thickening and calcification of the aortic valve leaflets. The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular prevention have recently been demonstrated in a large randomized, controlled trial. In addition, n-3 PUFAs serve as the substrate for the synthesis of specialized proresolving mediators, which are known by their potent beneficial anti-inflammatory, proresolving, and tissue-modifying properties in cardiovascular disease. However, the effects of n-3 PUFA and specialized proresolving mediators on AVS have not yet been determined. The aim of this study was to identify the role of n-3 PUFA-derived specialized proresolving mediators in relation to the development of AVS.Lipidomic and transcriptomic analyses were performed in human tricuspid aortic valves. Apoe-/- mice and wire injury in C57BL/6J mice were used as models for mechanistic studies.We found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified regions compared with calcified regions. Liquid chromatography tandem mass spectrometry-based lipid mediator lipidomics identified that the n-3 PUFA-derived specialized proresolving mediator resolvin E1 was dysregulated in calcified regions and acted as a calcification inhibitor. Apoe-/- mice expressing the Caenorhabditis elegans Fat-1 transgene (Fat-1tg×Apoe-/-), which enables the endogenous synthesis of n-3 PUFA and increased valvular n-3 PUFA content, exhibited reduced valve calcification, lower aortic valve leaflet area, increased M2 macrophage polarization, and improved echocardiographic parameters. Finally, abrogation of the resolvin E1 receptor ChemR23 enhanced disease progression, and the beneficial effects of Fat-1tg were abolished in the absence of ChemR23.n-3 PUFA-derived resolvin E1 and its receptor ChemR23 emerge as a key axis in the inhibition of AVS progression and may represent a novel potential therapeutic opportunity to be evaluated in patients with AVS.
Development and validation of an automated radiomic CT signature for detecting COVID-19
Authors: Akshayaa Vaidyantahan, Julien Guiot, Louis Deprez, Fadila Zerka, Denis Danthine, Anne-Noëlle Frix, Marie Thys, Monique Henket, Grégory Canivet, Stéphane Mathieu, Evanthia Eftaxia, Philippe Lambin, Nathan Tsoutzidis, Benjamin Miraglio, Sean Walsh, Michel Moutschen, Renaud Louis, Paul Meunier, Vos Wims, Ralph Leijnaar, Pierre Lovinfosse
Journal: European Respiratory Journal (2020)
Molecular Tumor Boards in Clinical Practice
Authors: Claudio Luchini, Rita T. Lawlor, Michele Milella, Aldo Scarpa
Journal: Trends in cancer (2020)

Next-generation sequencing (NGS) application in clinical practice requires the implementation of molecular tumor boards (MTBs). Starting from a systematic review of literature, we discuss the MTB-related key points: MTB aims and composition, types of tumors to discuss, types of molecular analyses, methods for classifying actionability, appropriate turnaround time, and cost management. Next-generation sequencing (NGS) application in clinical practice requires the implementation of molecular tumor boards (MTBs). Starting from a systematic review of literature, we discuss the MTB-related key points: MTB aims and composition, types of tumors to discuss, types of molecular analyses, methods for classifying actionability, appropriate turnaround time, and cost management.
Covid-19: Sweden should have done more, says architect of country’s strategy
Authors: Jacqui Wise
Journal: BMJ (2020)

The epidemiologist responsible for Sweden’s controversial lighter lockdown policy has conceded that the country could have done more to curb the spread of covid-19.

Sweden has a far higher death rate from covid-19 than its neighbouring Scandinavian countries, which imposed stricter measures.

In an interview with Swedish Radio, Anders Tegnell agreed with the interviewer that too many people had died in the country.1 “There is quite obviously a potential for improvement in what we have done in Sweden,” he said.

By 3 June there had been 4542 covid-19 related deaths in Sweden, whereas the number was only 580 in Denmark, 321 in Finland, and 237 in Norway, the latest figures from the John …
Covid-19: Hydroxychloroquine does not benefit hospitalised patients, UK trial finds
Authors: Ingrid Torjesen
Journal: BMJ (2020)

Hydroxychloroquine does not reduce the risk of dying or improve other outcomes in hospitalised patients treated for covid-19, preliminary results from the UK RECOVERY trial have shown.

Announcing the results, Martin Landray, the study’s deputy chief investigator, said, “We have concluded that there is no beneficial effect of hydroxychloroquine in patients hospitalised with covid-19. We have therefore decided to stop enrolling participants to the hydroxychloroquine arm with immediate effect.”

The data show the death rate at 28 days in covid-19 patients taking hydroxychloroquine is 25.7% compared with 23.5% in patients provided with only usual hospital care (hazard ratio 1.11 (95% confidence interval 0.98-1.26); P=0.10). So far 1542 patients in the trial have been randomised to hydroxychloroquine and 3132 patients randomised to usual care alone.

There was also no evidence that hydroxychloroquine impacted on length of …
Abstract 14082: Clinical, Echocardiographic, and Hemodynamic Factors in Predicting Response to Fluid Challenge During Right Heart Catheterization
Authors: Nima Moghaddam, Nawal Al-Gubaisi, John R Swiston, Robert D Levy, Lisa Lee, Victor F Huckell, Nathan W Brunner
Journal: Circulation (2017)

Background: Fluid challenge during right heart catheterization (RHC) has emerged as an adjunctive measure to differentiate pulmonary arterial hypertension from pulmonary hypertension (PH) related t...
Phase 3 Trial of RNAi Therapeutic Givosiran for Acute Intermittent Porphyria
Authors: Manisha Balwani, Eliane Sardh, Paolo Ventura, Paula Aguilera Peiró, David C. Rees, Ulrich Stölzel, D. Montgomery Bissell, Herbert L. Bonkovsky, Jerzy Windyga, Karl E. Anderson, Charles Parker, Samuel M. Silver, Siobán B. Keel, Jiaan-Der Wang, Penelope E. Stein, Pauline Harper, Daphne Vassiliou, Bruce Wang, John Phillips, Aneta Ivanova, Janneke G. Langendonk, Raili Kauppinen, Elisabeth Minder, Yutaka Horie, Craig Penz, Jihong Chen, Shangbin Liu, John J. Ko, Marianne T. Sweetser, Pushkal Garg, Akshay Vaishnaw, Jae B. Kim, Amy R. Simon, Laurent Gouya
Journal: New England Journal of Medicine (2020)

Up-regulation of hepatic delta-aminolevulinic acid synthase 1 (ALAS1), with resultant accumulation of delta-aminolevulinic acid (ALA) and porphobilinogen, is central to the pathogenesis of acute attacks and chronic symptoms in acute hepatic porphyria. Givosiran, an RNA interference therapy, inhibits ALAS1 expression.In this double-blind, placebo-controlled, phase 3 trial, we randomly assigned symptomatic patients with acute hepatic porphyria to receive either subcutaneous givosiran (2.5 mg per kilogram of body weight) or placebo monthly for 6 months. The primary end point was the annualized rate of composite porphyria attacks among patients with acute intermittent porphyria, the most common subtype of acute hepatic porphyria. (Composite porphyria attacks resulted in hospitalization, an urgent health care visit, or intravenous administration of hemin at home.) Key secondary end points were levels of ALA and porphobilinogen and the annualized attack rate among patients with acute hepatic porphyria, along with hemin use and daily worst pain scores in patients with acute intermittent porphyria.A total of 94 patients underwent randomization (48 in the givosiran group and 46 in the placebo group). Among the 89 patients with acute intermittent porphyria, the mean annualized attack rate was 3.2 in the givosiran group and 12.5 in the placebo group, representing a 74% lower rate in the givosiran group (P<0.001); the results were similar among the 94 patients with acute hepatic porphyria. Among the patients with acute intermittent porphyria, givosiran led to lower levels of urinary ALA and porphobilinogen, fewer days of hemin use, and better daily scores for pain than placebo. Key adverse events that were observed more frequently in the givosiran group were elevations in serum aminotransferase levels, changes in serum creatinine levels and the estimated glomerular filtration rate, and injection-site reactions.Among patients with acute intermittent porphyria, those who received givosiran had a significantly lower rate of porphyria attacks and better results for multiple other disease manifestations than those who received placebo. The increased efficacy was accompanied by a higher frequency of hepatic and renal adverse events. (Funded by Alnylam Pharmaceuticals; ENVISION ClinicalTrials.gov number, NCT03338816.).