tbuckley/cabot-search huggingface dataset:
A polygenic risk score and age of diagnosis of COPD
Authors: Jingzhou Zhang, Hanfei Xu, Dandi Qiao, Dawn L. DeMeo, Edwin K. Silverman, George T. O'Connor, Brian D. Hobbs, Josée Dupuis, Michael H. Cho, Matthew Moll
Journal: European Respiratory Journal (2022)

Background Genetic susceptibility may be associated with earlier onset of chronic obstructive pulmonary disease (COPD). We hypothesised that a polygenic risk score (PRS) for COPD would be associated with earlier age of diagnosis of COPD. Methods In 6647 non-Hispanic White (NHW) and 2464 African American (AA) participants from COPDGene, and 6812 participants from the Framingham Heart Study (FHS), we tested the relationship of the PRS and age of COPD diagnosis. Age at diagnosis was determined by: 1) self-reported age at COPD diagnosis or 2) age at visits when moderate-to-severe airflow limitation (Global Initiative for Chronic Obstructive Lung Disease (GOLD) grade 2–4) was observed on spirometry. We used Cox regression to examine the overall and time-dependent effects of the PRS on incident COPD. In the COPDGene study, we also examined the PRS's predictive value for COPD at age &lt;50 years (COPD50) using logistic regression and area under the curve (AUC) analyses, with and without the addition of other risk factors present at early life ( e.g. childhood asthma). Results In Cox models, the PRS demonstrated age-dependent associations with incident COPD, with larger effects at younger ages in both cohorts. The PRS was associated with COPD50 (OR 1.55 (95% CI 1.41–1.71) for NHW, OR 1.23 (95% CI 1.05–1.43) for AA and OR 2.47 (95% CI 2.12–2.88) for FHS participants). In COPDGene, adding the PRS to known early-life risk factors improved prediction of COPD50 in NHW (AUC 0.69 versus 0.74; p&lt;0.0001) and AA (AUC 0.61 versus 0.64; p=0.04) participants. Conclusions A COPD PRS is associated with earlier age of diagnosis of COPD and retains predictive value when added to known early-life risk factors.
Dendritic Nanostructures for Effector Cell Activation to Study Allergic Reactions to Amoxicillin
Authors: Amene Ayane, Sara Benedé, Alba Rodríguez-Nogales, Tahia Fernández, Juan Paris, Maria Rodriguez, Isabel Jiménez, Gador Bogas Herrera, Cristobalina Mayorga, Maria Torres JaÃ©n, Maria Montañez
Journal: Journal of Allergy and Clinical Immunology (2022)
Medicolegal
Journal: JAMA (1927)

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
Frequency and Outcomes of Periprocedural MI in Patients With Chronic Coronary Syndromes Undergoing PCI
Authors: Yasushi Ueki, Tatsuhiko Otsuka, Sarah Bär, Kostantinos C. Koskinas, Dik Heg, Jonas Häner, George C.M. Siontis, Fabien Praz, Lukas Hunziker, Jonas Lanz, Stefan Stortecky, Thomas Pilgrim, Sylvain Losdat, Stephan Windecker, Lorenz Räber
Journal: Journal of the American College of Cardiology (2022)
'Eve' and 'Ecstasy'
Authors: Graeme P. Dowling
Journal: JAMA (1987)

3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy"), a synthetic analogue of 3,4-methylenedioxyamphetamine, has been the center of recent debate over its potential for abuse vs its use as a psychotherapeutic agent. Following its emergency classification in Schedule 1 by the Drug Enforcement Administration in 1985, 3,4-methylenedioxyethamphetamine (MDEA,"Eve") has appeared as MDMA's legal replacement. MDMA is thought to be safe by recreational users and by psychotherapists who support its use. The details of five deaths associated with the use of MDMA and MDEA are reported. In three patients, MDMA or MDEA may have contributed to death by the induction of arrhythmias in individuals with underlying natural disease. In another patient, use of MDMA preceded an episode of bizarre and risky behavior that resulted in accidental death. In another patient, MDMA was thought to be the immediate cause of death. Death as a consequence of the use of these drugs appears to be rare, but it does occur; this outcome may be more common in individuals with underlying cardiac disease. (<i>JAMA</i>1987;257:1615-1617)
Atrial Fibrillation and Dementia: A Report From the AF-SCREEN International Collaboration
Authors: Léna Rivard, Leif Friberg, David Conen, Jeffrey S. Healey, Trygve Berge, Giuseppe Boriani, Axel Brandes, Hugh Calkins, A. John Camm, Lin Yee Chen, Josep Lluis Clua Espuny, Ronan Collins, Stuart Connolly, Nikolaos Dagres, Mitchell S.V. Elkind, Johan Engdahl, Thalia S. Field, Bernard J. Gersh, Taya V. Glotzer, Graeme J. Hankey, Joseph A. Harbison, Karl Georg Haeusler, Mellanie T. Hills, Linda S.B. Johnson, Boyoung Joung, Paul Khairy, Paulus Kirchhof, Derk Krieger, Gregory Y.H. Lip, Maja-Lisa Løchen, Malini Madhavan, Georges H. Mairesse, Joan Montaner, George Ntaios, Terence J. Quinn, Michiel Rienstra, Mårten Rosenqvist, Roopinder K. Sandhu, Breda Smyth, Renate B. Schnabel, Stavros Stavrakis, Sakis Themistoclakis, Isabelle C. Van Gelder, Ji-Guang Wang, Ben Freedman
Journal: Circulation (2022)

Growing evidence suggests a consistent association between atrial fibrillation (AF) and cognitive impairment and dementia that is independent of clinical stroke. This report from the AF-SCREEN International Collaboration summarizes the evidence linking AF to cognitive impairment and dementia. It provides guidance on the investigation and management of dementia in patients with AF on the basis of best available evidence. The document also addresses suspected pathophysiologic mechanisms and identifies knowledge gaps for future research. Whereas AF and dementia share numerous risk factors, the association appears to be independent of these variables. Nevertheless, the evidence remains inconclusive regarding a direct causal effect. Several pathophysiologic mechanisms have been proposed, some of which are potentially amenable to early intervention, including cerebral microinfarction, AF-related cerebral hypoperfusion, inflammation, microhemorrhage, brain atrophy, and systemic atherosclerotic vascular disease. The mitigating role of oral anticoagulation in specific subgroups (eg, low stroke risk, short duration or silent AF, after successful AF ablation, or atrial cardiopathy) and the effect of rhythm versus rate control strategies remain unknown. Likewise, screening for AF (in cognitively normal or cognitively impaired patients) and screening for cognitive impairment in patients with AF are debated. The pathophysiology of dementia and therapeutic strategies to reduce cognitive impairment warrant further investigation in individuals with AF. Cognition should be evaluated in future AF studies and integrated with patient-specific outcome priorities and patient preferences. Further large-scale prospective studies and randomized trials are needed to establish whether AF is a risk factor for cognitive impairment, to investigate strategies to prevent dementia, and to determine whether screening for unknown AF followed by targeted therapy might prevent or reduce cognitive impairment and dementia.
提高对银屑病遗传学和结构变异的理解
Journal: British Journal of Dermatology (2022)

Journal Article 提高对银屑病遗传学和结构变异的理解 Get access British Journal of Dermatology, Volume 186, Issue 2, 1 February 2022, Page e103, https://doi.org/10.1111/bjd.20931 Published: 01 February 2022
Association News
Journal: JAMA (1933)

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
Mechanisms and functions of cellular senescence
Authors: Nicolás Herranz, Jesús Gil
Journal: Journal of Clinical Investigation (2018)

Cellular senescence is a highly stable cell cycle arrest that is elicited in response to different stresses. By imposing a growth arrest, senescence limits the replication of old or damaged cells. Besides exiting the cell cycle, senescent cells undergo many other phenotypic alterations such as metabolic reprogramming, chromatin rearrangement, or autophagy modulation. In addition, senescent cells produce and secrete a complex combination of factors, collectively referred as the senescence-associated secretory phenotype, that mediate most of their non–cell-autonomous effects. Because senescent cells influence the outcome of a variety of physiological and pathological processes, including cancer and age-related diseases, pro-senescent and anti-senescent therapies are actively being explored. In this Review, we discuss the mechanisms regulating different aspects of the senescence phenotype and their functional implications. This knowledge is essential to improve the identification and characterization of senescent cells in vivo and will help to develop rational strategies to modulate the senescence program for therapeutic benefit.
Validation of the geriatric vulnerability score in older patients with ovarian cancer: an analysis from the GCIG-ENGOT-GINECO EWOC-1 study
Authors: Claire Falandry, Fanny Pommeret, Laurence Gladieff, Fabien Tinquaut, Domenica Lorusso, Marie-Ange Mouret-Reynier, Véronique D'Hondt, Delphine Mollon-Grange, Anne Floquet, Sophie Abadie-Lacourtoisie, Pierre-Emmanuel Brachet, Laetitia Stefani, Frédérique Rousseau, Jean-Sébastien Frenel, Francesco Del Piano, Marja Komulainen, Thomas Warkus, Olivier Trédan, Eric Pujade-Lauraine, Gilles Freyer
Journal: The Lancet Healthy Longevity (2022)
GW28-e0969 A study on the mechanism of the Caveolin-1 in Ginsenoside Rb1 against the intrinsic aging of mouse brain
Authors: Bin Zhou, Dinghui Liu, Shujie Yu, Lin Wu, Min Wang, Yesheng Ling, Yong Liu, Baoshun Hao, Lin Chen, Xiaoxian Qian
Journal: Journal of the American College of Cardiology (2017)
Reye Syndrome Surveillance—United States, 1989
Journal: JAMA (1991)

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
FATIGUE AND DISEASE
Journal: JAMA (1926)

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
Nurturing care: promoting early childhood development
Authors: Pia R Britto, Stephen J Lye, Kerrie Proulx, Aisha K Yousafzai, Stephen G Matthews, Tyler Vaivada, Rafael Perez-Escamilla, Nirmala Rao, Patrick Ip, Lia C H Fernald, Harriet MacMillan, Mark Hanson, Theodore D Wachs, Haogen Yao, Hirokazu Yoshikawa, Adrian Cerezo, James F Leckman, Zulfiqar A Bhutta
Journal: The Lancet (2016)
Efficacy of anifrolumab across organ domains in patients with moderate-to-severe systemic lupus erythematosus: a post-hoc analysis of pooled data from the TULIP-1 and TULIP-2 trials
Authors: Eric F Morand, Richard A Furie, Ian N Bruce, Edward M Vital, Maria Dall'Era, Emmanuelle Maho, Lilia Pineda, Raj Tummala
Journal: The Lancet Rheumatology (2022)
CD40L-armed oncolytic herpes simplex virus suppresses pancreatic ductal adenocarcinoma by facilitating the tumor microenvironment favorable to cytotoxic T cell response in the syngeneic mouse model
Authors: Ruikun Wang, Jingru Chen, Wei Wang, Zhuoqian Zhao, Haoran Wang, Shiyu Liu, Fan Li, Yajuan Wan, Jie Yin, Rui Wang, Yuanke Li, Cuizhu Zhang, Hongkai Zhang, Youjia Cao
Journal: Journal for ImmunoTherapy of Cancer (2022)

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant cancers worldwide. Despite the promising outcome of immune checkpoint inhibitors and agonist antibody therapies in different malignancies, PDAC exhibits high resistance due to its immunosuppressive tumor microenvironment (TME). Ameliorating the TME is thus a rational strategy for PDAC therapy. The intratumoral application of oncolytic herpes simplex virus-1 (oHSV) upregulates pro-inflammatory macrophages and lymphocytes in TME, and enhances the responsiveness of PDAC to immunotherapy. However, the antitumor activity of oHSV remains to be maximized. The aim of this study is to investigate the effect of the CD40L armed oHSV on the tumor immune microenvironment, and ultimately prolong the survival of the PDAC mouse model.The membrane-bound form of murine CD40L was engineered into oHSV by CRISPR/Cas9-based gene editing. oHSV-CD40L induced cytopathic effect and immunogenic cell death were determined by microscopy and flow cytometry. The expression and function of oHSV-CD40L was assessed by reporter cell assay. The oHSV-CD40L was administrated intratumorally to the immune competent syngeneic PDAC mouse model, and the leukocytes in TME and tumor-draining lymph node were analyzed by multicolor flow cytometry. Intratumoral cytokines were determined by ELISA.Intratumoral application of oHSV-CD40L efficiently restrained the tumor growth and prolonged the survival of the PDAC mouse model. In TME, oHSV-CD40L-treated tumor accommodated more maturated dendritic cells (DCs), which in turn activated T helper 1 and cytotoxic CD8+ T cells in an interferon-γ-dependent and interleukin-12-dependent manner. In contrast, the regulatory T cells were significantly reduced in TME by oHSV-CD40L treatment. Repeated dosing and combinational therapy extended the lifespan of PDAC mice.CD40L-armed oncolytic therapy endues TME with increased DCs maturation and DC-dependent activation of cytotoxic T cells, and significantly prolongs the survival of the model mice. This study may lead to the understanding and development of oHSV-CD40L as a therapy for PDAC in synergy with immune checkpoint blockade.
Erratum
Journal: Journal of the American Society of Nephrology (2021)

Zhang L, Chen Q, Chen Z, Wang Y, Gamboa JL, Ikizler TA, Garibotto G, and Mitch WE: Mechanisms Regulating Muscle Protein Synthesis in CKD. J Am Soc Nephrol 31: [2573–2587][1], 2020; doi: <https://doi.org/10.1681/ASN.2019121277>. On [Figure 6A][2], the “H3K34me3” labels are incorrect; the
THE JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
Journal: JAMA (1910)

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
Limited, But Not Eliminated, Excess Long-Term Morbidity in Stage I-IIA Hodgkin Lymphoma Treated With Doxorubicin, Bleomycin, Vinblastine, and Dacarbazine and Limited-Field Radiotherapy
Authors: Ingemar Lagerlöf, Helena Fohlin, Gunilla Enblad, Bengt Glimelius, Christina Goldkuhl, Marzia Palma, Lisa Åkesson, Ingrid Glimelius, Daniel Molin
Journal: Journal of Clinical Oncology (2022)

Balancing disease control and toxicity from chemotherapy and radiotherapy (RT) when treating early-stage classical Hodgkin lymphoma (cHL) is important. Available data on long-term toxicity after RT for cHL mostly refer to RT techniques no longer in use. We aimed to describe long-term toxicity from modern limited-field (LF)-RT after two or four cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD).This study included all patients with cHL treated with two or four cycles of ABVD and 30 Gy LF-RT during 1999-2005 in Sweden. Patients (n = 215) and comparators (n = 860), matched for age, gender, and region of residence, were cross-checked against national health registries for malignancies, diseases of the circulatory system (DCS), and diseases of the respiratory system (DRS) from the day of diagnosis of cHL.The risk of a malignancy was higher for patients than comparators, hazard ratio (HR) 1.5 (95% CI, 1.0 to 2.4), as was the risk for DCS 1.5 (95% CI, 1.1 to 2.0) and for DRS 2.6 (95% CI, 1.6 to 4.3). The median follow-up was 16 years (range, 12-19 years). Of individual diagnoses in DCS, only venous thromboembolism was statistically significantly elevated. If the first 6 months (ie, time of active treatment for cHL) were excluded and censoring at relapse of cHL or diagnosis of any malignancy, the increased HR for venous thromboembolism diminished. Most of the excess risk for DRS consisted of asthma, HR 3.5 (95% CI, 1.8 to 6.8). Patients diagnosed with DRS were significantly younger than comparators.Compared with toxicity from earlier RT techniques, excess morbidity was not eliminated, but lower than previously reported. The elevated risk of DRS was driven by diagnosis of asthma, which could in part be explained by misdiagnosis of persisting pulmonary toxicity.
Chronic Spontaneous Urticaria patients under Treatment with Omalizumab: Our Experience
Authors: María Cervera García, Diana Perez-Alzate, Isabel Torres Rojas, Natalia Blanca López, Ana Prieto-Moreno, Paula López-Gonzalez, Elisa Haroun, Maria Vázquez de la Torre, Maria Luisa Somoza Alvarez, Carlos Blanco, Maria Luisa Quiñones, Francisco Javier Ruano
Journal: Journal of Allergy and Clinical Immunology (2022)