tbuckley/cabot-search huggingface dataset:
Cardiac Imaging in Patients With Ventricular Tachycardia
Authors: Saagar Mahida, Frédéric Sacher, Rémi Dubois, Maxime Sermesant, Frank Bogun, Michel Haïssaguerre, Pierre Jaïs, Hubert Cochet
Journal: Circulation (2017)

Ventricular tachycardia (VT) is a major cause of sudden cardiac death. The majority of malignant VTs occur in patients with structural heart disease. Multimodality imaging techniques play an integral role in determining the underlying etiology and prognostic significance of VT. In recent years, advances in imaging technology have enabled characterization of the structural arrhythmogenic substrate in patients with VT with increasing precision. In parallel with these advances, the role of cardiac imaging has expanded from a largely diagnostic tool to an adjunctive tool to guide interventional approaches for treatment of VT. Invasive and noninvasive imaging techniques, often used in combination, have made it possible to integrate structural and electrophysiological information during VT ablation procedures. An important area of current development is the use of noninvasive imaging techniques based on body surface electrocardiographic mapping to elucidate the mechanisms of VT. In the future, these techniques may provide a priori information on mechanisms of VT in patients undergoing interventional procedures. This review provides an overview of the role of cardiac imaging in patients with VT.
Rituximab maintenance versus observation following abbreviated induction with chemoimmunotherapy in elderly patients with previously untreated chronic lymphocytic leukaemia (CLL 2007 SA): an open-label, randomised phase 3 study
Authors: Caroline Dartigeas, Eric Van Den Neste, Julie Léger, Hervé Maisonneuve, Christian Berthou, Marie-Sarah Dilhuydy, Sophie De Guibert, Stéphane Leprêtre, Marie C Béné, Florence Nguyen-Khac, Rémi Letestu, Florence Cymbalista, Philippe Rodon, Thérèse Aurran-Schleinitz, Jean-Pierre Vilque, Olivier Tournilhac, Béatrice Mahé, Kamel Laribi, Anne-Sophie Michallet, Alain Delmer, Pierre Feugier, Vincent Lévy, Roselyne Delépine, Philippe Colombat, Véronique Leblond
Journal: The Lancet Haematology (2017)
Vigilancia europea de las infecciones de transmisión sexual: una intervención oportuna y adecuada
Authors: K. A. Fenton, J Giesecke, F F Hamers
Journal: Eurosurveillance (2001)

Las infecciones de transmision sexual (ITS), incluida la infeccion por VIH, representan una grave amenaza para la salud y el bienestar de la poblacion europea y exigen una intervencion concertada y sostenida. En los diez ultimos anos, ha aumentado notablemente el numero de casos declarados de ITS, incluida la infeccion por Neisseria gonorrhoeae resistente a los antibioticos (1) y, ultimamente, se han declarado brotes de sifilis en varios estados miembros de la Union Europea (UE) (2,3). Los grupos mas afectados parecen ser los jovenes, los varones homosexuales y las personas con acceso restringido a los servicios de salud (incluidos los preventivos y educativos), siendo los principales factores desencadenantes el aumento de viajes y migracion, unos comportamientos sexuales de alto riesgo y un deterioro en la respuesta sanitaria en la lucha contra las ITS (por ejemplo, en la declaracion de contactos sexuales). Muchas de estas tendencias demograficas y de comportamiento son similares en distintos estados de la UE, como el deseo compartido de desarrollar e implantar programas eficaces de prevencion y control de las ITS.
Evaluating Causality of Gut Microbiota in Obesity and Diabetes in Humans
Authors: Abraham S Meijnikman, Victor E Gerdes, Max Nieuwdorp, Hilde Herrema
Journal: Endocrine Reviews (2017)

The pathophysiology of obesity and obesity-related diseases such as type 2 diabetes mellitus (T2DM) is complex and driven by many factors. One of the most recently identified factors in development of these metabolic pathologies is the gut microbiota. The introduction of affordable, high-throughput sequencing technologies has substantially expanded our understanding of the role of the gut microbiome in modulation of host metabolism and (cardio)metabolic disease development. Nevertheless, evidence for a role of the gut microbiome as a causal, driving factor in disease development mainly originates from studies in mouse models: data showing causality in humans are scarce. In this review, we will discuss the quality of evidence supporting a causal role for the gut microbiome in the development of obesity and diabetes, in particular T2DM, in humans. Considering overlap in potential mechanisms, the role of the gut microbiome in type 1 diabetes mellitus will also be addressed. We will elaborate on factors that drive microbiome composition in humans and discuss how alterations in microbial composition or microbial metabolite production contribute to disease development. Challenging aspects in determining causality in humans will be postulated together with strategies that might hold potential to overcome these challenges. Furthermore, we will discuss means to modify gut microbiome composition in humans to help establish causality and discuss systems biology approaches that might hold the key to unravelling the role of the gut microbiome in obesity and T2DM.
Thrombotic Thrombocytopenic Purpura Misdiagnosed As Autoimmune Cytopenia: Causes of Diagnostic Errors and Consequence on Outcome. Experience of the French Thrombotic Microangiopathies Reference Centre
Authors: Maximilien Grall, Ygal Benhamou, Elie Azoulay, Eric Mariotte, Lionel Galicier, Steven Grange, Virginie Barbay, Dominique Bordessoule, Agnes Veyradier, Paul Coppo
Journal: Blood (2016)
Financial Conflicts of Interest Among Oncology Clinical Pathway Vendors
Authors: Bobby Daly, Peter B. Bach, Ray D. Page
Journal: JAMA Oncology (2017)

all incidence of IRAEs in this series was comparable to rates observed in randomized trials of CPIs for metastatic lung cancer. 1,2Development of grade 2 or higher IRAEs was associated with improved survival, possibly reflecting that patients responding to CPIs likely received more cycles of therapy, which may have in turn predisposed them to the toxic effects.Interestingly, response rates to CPIs in melanoma are significantly higher among patients with treatment-related adverse events, even after adjusting for CPI doses, 3 suggesting that augmentation of the antitumor response may be coupled to anti-self activity.The trend toward increased overall survival with TRT despite significantly fewer patients harboring targetable mutations is intriguing.It has been postulated that lack of antigenic mutations and other mechanisms of immune evasion may underlie resistance to CPIs. 4 In certain situations, radiotherapy may potentiate the efficacy of immunotherapy, even restimulating a durable systemic response in disease that had become refractory to CPIs. 5 A recent single-institution secondary analysis of KEYNOTE-001 6 found that patients who received any radiotherapy prior to pembrolizumab had significantly longer progression-free and overall survival. 6While the few patients in that study who received TRT before pembrolizumab (n = 24; median interval, 11.5 months) had a higher incidence of lowgrade pulmonary toxic effects, there was no difference in grade 3 or higher pneumonitis, consistent with our findings.Limitations of this analysis are that we report a singleinstitution series, and median time between TRT and CPI was 8.6 months.Prospective study is needed, and studies investigating both consolidative CPI after definitive chemoradiotherapy (NCT02768558 and NCT02125461) and concurrent radiotherapy with CPI (NCT03035890 and NCT02599454) are ongoing.Nonetheless, pending prospective validation, our results suggest that TRT does not significantly increase the risk of symptomatic IRAEs, including pneumonitis, compared with CPIs alone.
BET Proteins as Targets for Anticancer Treatment
Authors: Anastasios Stathis, Francesco Bertoni
Journal: Cancer Discovery (2017)

Bromodomain and extraterminal domain (BET) proteins are epigenetic readers that regulate gene expression and are involved in cancer pathogenesis. Over the last years, several BET inhibitors have been developed and clinically tested. Results from the first clinical trials show limited single-agent activity in a small subset of patients with hematologic malignancies and in NUT carcinoma. Adverse events have been observed and may limit treatment compliance. Here, we review the preclinical rationale for targeting BET proteins in cancer and the preliminary results from clinical trials, and outline future directions for the use of BET inhibitors as antitumor agents.Significance: BET inhibitors represent a new class of anticancer agents. Results from the first clinical trials confirm the antitumor potential of BET inhibitors, but their efficacy as single agents seems to be limited. Based on preclinical data, combination therapies with other anticancer agents and the development of a new generation of compounds may open new possibilities for targeting BET proteins as effective anticancer strategies. Cancer Discov; 8(1); 24-36. ©2017 AACR.
Ventriculopleural Shunt Dysfunction Due to a Loculated Pleural Collection Demonstrated on SPECT/CT Imaging
Authors: Jeremy Szajer, Roberto Russo, Robert Mansberg
Journal: Clinical Nuclear Medicine (2017)

A 35-year-old woman presented with increasing drowsiness on a background of childhood meningitis and hydrocephalus managed with a ventriculopleural shunt. Her cerebral CT and chest radiograph were unchanged from previous imaging and did not identify significant pathology. Because of clinical suspicion of cerebrospinal fluid shunt dysfunction, she was referred for a cerebrospinal fluid shunt study, which demonstrated tracer accumulation within a loculated pleural collection in the left costophrenic recess.
Potential cardiac risk of immune‐checkpoint blockade as anticancer treatment: What we know, what we do not know, and what we can do to prevent adverse effects
Authors: Paolo Spallarossa, Giovanni Meliota, Claudio Brunelli, Eleonora Arboscello, Pietro Ameri, Christian Cadeddu Dessalvi, Francesco Grossi, Martino Deidda, Donato Mele, Matteo Sarocchi, Andrea Bellodi, Rosalinda Madonna, Giuseppe Mercuro
Journal: Medicinal Research Reviews (2017)

Abstract Cancer immunotherapy has become a well‐established treatment option for some cancers after the development of a family of drugs targeting the so‐called immune checkpoints, such as CTLA4 and PD‐1 with PD‐L1. These co‐receptors/ligands inhibit the activation of T‐cell, thus preventing an excessive inflammatory response. Tumors exploit these pathways to induce immune tolerance to themselves. Thus, the main effect of checkpoint‐blocking drugs is to awake an immune response primarily directed against cancer cells. Nonetheless, as the immune response elicited by these drugs is not completely tumor‐specific, their use may actually cause several adverse effects, including adverse cardiovascular effects. In this review, we will discuss the principles and potentiality of immunotherapy for cancer treatment, the experimental and clinical data on the role of CTLA4 and PD‐1 with PD‐L1 as immune‐checkpoints in the cancer environment and in the cardiovascular system, and strategies aimed at preventing possible cardiovascular adverse effects of immune‐checkpoint blockers.
Abstract 14212: P22 Protein Cage Nanoparticles targeted With RGD Enhance Detection of Vascular Inflammation
Authors: Hisanori Kosuge, Masaki Uchida, Toshinobu Saito, Janice Lucon, Shefah Qazi, Trevor Douglas, Michael V McConnell
Journal: Circulation (2016)

Introduction:  The 60-nm protein cage of the bacteriophage P22 has promising properties for molecular/cellular imaging when loaded with imaging agents and targeting ligands. We evaluated RGD-conjugated P22 for macrophage imaging in vitro and in murine carotid arteries.   Methods:  1)  In vitro : Mouse macrophage cells (RAW 264.7) were incubated for both 4 and 24 hours with P22 loaded with Gadolinium (Gd , 0.1mM) plus the RGD peptide bound through a decorating (Dec) protein (P22-RGD-Dec-Gd). The same conditions were used for two controls: P22-wtDec-Gd (w/o RGD) and P22-Gd (w/o RGD or wtDec). After washing in PBS, cells were scanned with 3T MRI using spin echo sequence (TR/TE=400ms/11ms, slice thickness=1mm, FOV=12cm, matrix=256x256).  2)  In vivo : FVB mice (N=18) underwent induction of diabetes and hyperlipidemia, followed by carotid ligation to develop macrophage-rich atherosclerotic lesions. Two weeks post carotid ligation, mice were injected with RGD-targeted (P22-RGD-Dec-Cy5.5) or non-targeted control (P22-wtDec-Cy5.5) via tail vein (4 nmol/mouse) and scanned by in-vivo fluorescence imaging for up to 48 hours (FMT, Visen, Bedford, MA). After in vivo imaging, carotid arteries were harvested and scanned ex vivo (Maestro, Cri, Woburn MA).   Results:  In vitro MRI (Fig 1) showed higher signal to noise ratio in cells incubated with RGD-targeted P22 compared to cells with non-targeted P22 (4 hour; 1.3x, 24 hour; 1.1x). In vivo fluorescence molecular tomography showed the accumulation of both targeted and non-targeted P22 in carotid arteries. Ex vivo fluorescence imaging (Fig 2) demonstrated significant 75% signal enhancement in atherosclerotic lesions of RGD-targeted P22 compared to non-targeted control (0.021 ± 0.003 vs. 0.012 ± 0.002 counts/second, p   Conclusions:  Both in vitro and in vivo studies show RGD enhances P22 molecular/cellular imaging of macrophages. P22 with RGD-targeting can detect high-risk biological activity in vascular inflammation.
Impact of comorbidities on patient outcomes after interferon-free therapy-induced viral eradication in hepatitis C
Authors: Javier Ampuero, Carlota Jimeno, Rosa Quiles, José Miguel Rosales, Susana Llerena, Nieves Palomo, Patricia Cordero, Francisco Javier Serrano, Juan José Urquijo, José María Moreno-Planas, Guillermo Ontanilla, Marta Hernández, Aída Ortega-Alonso, Marta Maraver, Martín Bonacci, Ángela Rojas, Blanca Figueruela, Xavier Forns, Raúl J. Andrade, José Luis Calleja, Moisés Diago, Isabel Carmona, Manuel de la Mata, María Buti, Javier Crespo, Juan Manuel Pascasio, José María Navarro, Javier Salmerón, Manuel Romero-Gómez
Journal: Journal of Hepatology (2017)
Blood Test Results—Pronto
Authors: Rebecca Voelker
Journal: JAMA (2017)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Use of the Kidney Failure Risk Equation to Determine the Risk of Progression to End-stage Renal Disease in Children With Chronic Kidney Disease
Authors: Erica Winnicki, Charles E. McCulloch, Mark M. Mitsnefes, Susan L. Furth, Bradley A. Warady, Elaine Ku
Journal: JAMA Pediatrics (2017)

<h3>Importance</h3> The kidney failure risk equation (KFRE) has been shown to accurately estimate progression to kidney failure in adults with chronic kidney disease (CKD). Use of the KFRE in children with CKD, if accurate, would help to optimize planning for end-stage renal disease (ESRD) care. <h3>Objective</h3> To determine whether the KFRE adequately discriminates the risk of ESRD in children with CKD. <h3>Design, Setting, and Participants</h3> This retrospective cohort study included 603 children with an estimated glomerular filtration rate of less than 60 mL/min/1.73 m<sup>2</sup>in the Chronic Kidney Disease in Children study, a national multicenter observational study. Data were collected from January 1, 2005, through July 31, 2013, and analyzed from September 30, 2016, through September 8, 2017. <h3>Exposures</h3> The primary predictive factors were the 4-variable (age, sex, bedside Schwartz estimated glomerular filtration rate, and ratio of albumin to creatinine levels) and 8-variable (4 variables plus serum calcium, phosphate, bicarbonate, and albumin levels) KFREs, which provide 1-, 2-, and 5-year estimates of the risk of progression to ESRD. <h3>Main Outcomes and Measures</h3> Time to ESRD. The Cox proportional hazards model was used to examine the association between the KFRE score and time to ESRD. C statistics were used to discriminate ESRD risk by the KFRE, with a value of greater than 0.80 indicating strong discrimination. <h3>Results</h3> Of the 603 children included in the study, 378 were boys (62.7%) and 225 were girls (37.3%); median age at study entry was 12 years (interquartile range, 8-15 years). Median estimated glomerular filtration rate was 44 mL/min/1.73 m<sup>2</sup>. Four hundred fifty-seven participants (75.8%) had a nonglomerular cause of CKD. Median observation time was 3.8 years (interquartile range, 1.7-6.2 years); 144 (23.9%) developed ESRD within 5 years of enrollment. The 4-variable KFRE scores discriminated risk of ESRD, with C statistics of 0.90, 0.86, and 0.81 for the 1-, 2-, and 5-year risk scores, respectively. Results were similar using the 8-variable equation. <h3>Conclusions and Relevance</h3> The KFRE is a simple tool that provides excellent discrimination of the risk of ESRD. Results suggest that the KFRE could be incorporated into the clinical care of children with CKD to aid in anticipatory guidance, timing of referral for transplant evaluation, and planning for dialysis access.
Hepatocyte Growth Factor Improves the Therapeutic Efficacy of Human Bone Marrow Mesenchymal Stem Cells via RAD51
Authors: Eun Ju Lee, Injoo Hwang, Ji Yeon Lee, Jong Nam Park, Keun Cheon Kim, Gi-Hwan Kim, Chang-Mo Kang, Irene Kim, Seo-Yeon Lee, Hyo-Soo Kim
Journal: Molecular Therapy (2017)

Human embryonic stem cell-derived mesenchymal stem cells (hE-MSCs) have greater proliferative capacity than other human mesenchymal stem cells (hMSCs), suggesting that they may have wider applications in regenerative cellular therapy. In this study, to uncover the anti-senescence mechanism in hE-MSCs, we compared hE-MSCs with adult bone marrow (hBM-MSCs) and found that hepatocyte growth factor (HGF) was more abundantly expressed in hE-MSCs than in hBM-MSCs and that it induced the transcription of RAD51 and facilitated its SUMOylation at K70. RAD51 induction/modification by HGF not only increased telomere length but also increased mtDNA replication, leading to increased ATP generation. Moreover, HGF-treated hBM-MSCs showed significantly better therapeutic efficacy than naive hBM-MSCs. Together, the data suggest that the RAD51-mediated effects of HGF prevent hMSC senescence by promoting telomere lengthening and inducing mtDNA replication and function, which opens the prospect of developing novel therapies for liver disease. Human embryonic stem cell-derived mesenchymal stem cells (hE-MSCs) have greater proliferative capacity than other human mesenchymal stem cells (hMSCs), suggesting that they may have wider applications in regenerative cellular therapy. In this study, to uncover the anti-senescence mechanism in hE-MSCs, we compared hE-MSCs with adult bone marrow (hBM-MSCs) and found that hepatocyte growth factor (HGF) was more abundantly expressed in hE-MSCs than in hBM-MSCs and that it induced the transcription of RAD51 and facilitated its SUMOylation at K70. RAD51 induction/modification by HGF not only increased telomere length but also increased mtDNA replication, leading to increased ATP generation. Moreover, HGF-treated hBM-MSCs showed significantly better therapeutic efficacy than naive hBM-MSCs. Together, the data suggest that the RAD51-mediated effects of HGF prevent hMSC senescence by promoting telomere lengthening and inducing mtDNA replication and function, which opens the prospect of developing novel therapies for liver disease.
Intensive Lifestyle Intervention for Type 2 Diabetes—Reply
Authors: Mathias Ried-Larsen, Mette Yun Johansen, Bente Klarlund Pedersen
Journal: JAMA (2017)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal