tbuckley/cabot-search huggingface dataset:
Evidence for the Fucoidan/P-Selectin Axis as a Therapeutic Target in Hypoxia-induced Pulmonary Hypertension
Authors: Tatyana Novoyatleva, Baktybek Kojonazarov, Andreas Owczarek, Swathi Veeroju, Nabham Rai, Ingrid Henneke, Mario Böhm, Friedrich Grimminger, Hossein A. Ghofrani, Werner Seeger, Norbert Weissmann, Ralph T. Schermuly
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

Pulmonary arterial hypertension (PAH) is characterized by vascular remodeling and excessive proliferation of pulmonary artery smooth muscle cells (PASMCs). Fucoidan, a polysaccharidic ligand of the adhesion molecule P-selectin, exhibits antiproliferative properties. The effects of the fucoidan/P-selectin axis on vascular remodeling and pulmonary hypertension (PH) after hypoxia remain unexplored.
Abstract 20919: Manipulation-Free Particle Image Velocimetry Method of Screening Drugs Using Human iPSC-Derived Cardiomyocytes
Authors: Sheeja Rajasingh, Andras Czirok, Dona G Isai, Saheli Samanta, Zhigang Zhou, Bahar Barani, Nicholas Drosos, Buddhadeb Dawn, Johnson Rajasingh
Journal: Circulation (2017)

Introduction: Currently available drug screening models are not efficient in detecting cardiac toxicity. Here we demonstrate the in vitro Particle Image Velocimetry (PIV) assays followed by fourier spectrum and heatmap analyses for measuring the impact of different cardiac drugs on the spontaneous beat frequency (SBF) and spontaneous beat amplitude (SBA) of beating cardiomyocytes (CMCs). Hypothesis: Our PIV method of measuring CMCs contractility could be beneficial for drug testing and preclinical screening to detect cardio-toxicity. Methods and Results: The novelty of our system is that we can record the spatiotemporal maturation of human iPSC-derived CMCs at specific positions. We have evaluated the contractility of CMCs with the response to various chemical compounds such as Verapamil (Ca2+ blocker), Isoproterenol (Ca2+ activator), E-4031 (K+ inhibitor) and NS-1643 (K+ activator). Our optically recorded beat patterns were in good agreement with the calcium-imaging signal ( Fig 1 ). Our data also show that Isoproterenol, the β adrenergic agonist influencing intracellular Ca2+ dynamics, induced a substantial and sustained increase in SBF without triggering arrhythmias (Fig 2A, B) . Fourier analysis clearly indicates a shift in the SBF (Fig. 2C , dotted line). Power spectra of consecutive recordings are shown as heat maps ( Fig. 2D ). The reversibility of the Isoproterenol effect is indicated by the SBF returning to the baseline value after drug removal (Fig 2B, E ). Conclusions: We report for the first time the applications of PIV assays for prospective cardiac drug efficacy screening by measuring the contractility of CMCs from the video image without jeopardizing the biology of cells.
Identification and Characterization of Synthetic Viability with ERCC1 Deficiency in Response to Interstrand Crosslinks in Lung Cancer
Authors: Joshua R. Heyza, Wen Lei, Donovan Watza, Hao Zhang, Wei Chen, Jessica B. Back, Ann G. Schwartz, Gerold Bepler, Steve M. Patrick
Journal: Clinical Cancer Research (2018)

Abstract Purpose: ERCC1/XPF is a DNA endonuclease with variable expression in primary tumor specimens, and has been investigated as a predictive biomarker for efficacy of platinum-based chemotherapy. The failure of clinical trials utilizing ERCC1 expression to predict response to platinum-based chemotherapy suggests additional mechanisms underlying the basic biology of ERCC1 in the response to interstrand crosslinks (ICLs) remain unknown. We aimed to characterize a panel of ERCC1 knockout (Δ) cell lines, where we identified a synthetic viable phenotype in response to ICLs with ERCC1 deficiency. Experimental Design: We utilized the CRISPR-Cas9 system to create a panel of ERCC1Δ lung cancer cell lines which we characterized. Results: We observe that loss of ERCC1 hypersensitizes cells to cisplatin when wild-type (WT) p53 is retained, whereas there is only modest sensitivity in cell lines that are p53mutant/null. In addition, when p53 is disrupted by CRISPR-Cas9 (p53*) in ERCC1Δ/p53WT cells, there is reduced apoptosis and increased viability after platinum treatment. These results were recapitulated in 2 patient data sets utilizing p53 mutation analysis and ERCC1 expression to assess overall survival. We also show that kinetics of ICL-repair (ICL-R) differ between ERCC1Δ/p53WT and ERCC1Δ/p53* cells. Finally, we provide evidence that cisplatin tolerance in the context of ERCC1 deficiency relies on DNA-PKcs and BRCA1 function. Conclusions: Our findings implicate p53 as a potential confounding variable in clinical assessments of ERCC1 as a platinum biomarker via promoting an environment in which error-prone mechanisms of ICL-R may be able to partially compensate for loss of ERCC1. See related commentary by Friboulet et al., p. 2369
Cost-Effectiveness of Buprenorphine–Naloxone Versus Extended-Release Naltrexone to Prevent Opioid Relapse
Authors: Sean M. Murphy, Kathryn E. McCollister, Jared A. Leff, Xuan Yang, Philip J. Jeng, Joshua D. Lee, Edward V. Nunes, Patricia Novo, John Rotrosen, Bruce R. Schackman
Journal: Annals of Internal Medicine (2018)

Background: Not enough evidence exists to compare buprenorphine–naloxone with extended-release naltrexone for treating opioid use disorder. Objective: To evaluate the cost-effectiveness of buprenorphine–naloxone versus extended-release naltrexone. Design: Cost-effectiveness analysis alongside a previously reported randomized clinical trial of 570 adults in 8 U.S. inpatient or residential treatment programs. Data Sources: Study instruments. Target Population: Adults with opioid use disorder. Time Horizon: 24-week intervention with an additional 12 weeks of observation. Perspective: Health care sector and societal. Interventions: Buprenorphine–naloxone and extended-release naltrexone. Outcome Measures: Incremental costs combined with incremental quality-adjusted life-years (QALYs) and incremental time abstinent from opioids. Results of Base-Case Analysis: Use of the health care sector perspective and a willingness-to-pay threshold of $100 000 per QALY showed buprenorphine–naloxone to be preferable to extended-release naltrexone in 97% of bootstrap replications at 24 weeks and in 85% at 36 weeks. Similar results were obtained with incremental time abstinent from opioids as an outcome and with use of the societal perspective. Results of Sensitivity Analysis: The base-case results were sensitive to the cost of the 2 treatments and the success of randomized treatment initiation. Limitation: Relatively short follow-up for a chronic condition, substantial missing data, no information on patient out-of-pocket and social service costs. Conclusion: Buprenorphine–naloxone is preferred to extended-release naltrexone as first-line treatment when both options are clinically appropriate and patients require detoxification before initiating extended-release naltrexone. Primary Funding Source: National Institute on Drug Abuse, National Institutes of Health.
Abstract 16324: Myocardial Slices to Study the Structural and Functional Plasticity of the Myocardium Following Prolonged Changes in Mechanical Load in vitro
Authors: Samuel A Watson, Filippo Perbellini, Sian E Harding, Cesare M Terracciano
Journal: Circulation (2017)

Introduction: The myocardium displays structural & functional plasticity to changes in load. Overload leads to depressed contractility & Ca2+ handling which, when coupled with fibrosis & remodeling...
Outcomes and Side Effect Profile of Ponatinib in Treatment of Chronic Myeloid Leukemia (CML): A Retrospective Single-Center Experience
Authors: Onyee Chan, Chetasi Talati, Leidy Isenalumhe, Michael Fradley, Samantha Shams, Javier Pinilla Ibarz, Kendra L. Sweet
Journal: Blood (2018)
Publisher Correction: Myelodysplastic syndrome progression to acute myeloid leukemia at the stem cell level
Authors: Jiahao Chen, Yun-Ruei Kao, Daqian Sun, Tihomira I. Todorova, David Reynolds, Swathi-Rao Narayanagari, Cristina Montagna, Britta Will, Amit Verma, Ulrich Steidl
Journal: Nature Medicine (2018)
E2F1 Is a Biomarker of Selinexor Resistance in Relapsed/Refractory Multiple Myeloma Patients
Authors: Alessandro Lagana, Seongjee Park, Donna Edwards, Violetta Leshchenko, Marsha Crochiere, Yosef Landesman, David Melnekoff, Itai Beno, Deepak Perumal, Deepu Madduri, Joshua Richter, Ajai Chari, Hearn Jay Cho, Bart Barlogie, Sundar Jagannath, Joel Dudley, Samir Parekh
Journal: Blood (2018)
Abstract 16062: Extracorporeal Life Support in Cardiogenic Shock: Impact of Microinvasive Approach on Outcome
Authors: Vincenzo Tarzia, Lorenzo Bagozzi, Giacomo Bortolussi, Roberto Bianco, Jonida Bejko, Fabio Zanella, Tomaso Bottio, Gino Gerosa
Journal: Circulation (2016)

Introduction: Extracorporeal Life Support (ECLS) is a well-established treatment of Refractory Cardiogenic Shock (RCS). A correct timing is the key to the prevention of MultiOrgan Dysfunction Syndr...
Fibrostenotic eosinophilic esophagitis might reflect epithelial lysyl oxidase induction by fibroblast-derived TNF-α
Authors: Yuta Kasagi, Kara Dods, Joshua X. Wang, Prasanna M. Chandramouleeswaran, Alain J. Benitez, Fiona Gambanga, Jonathan Kluger, Tokunbo Ashorobi, Jonathan Gross, John W. Tobias, Andres J. Klein-Szanto, Jonathan M. Spergel, Antonella Cianferoni, Gary W. Falk, Kelly A. Whelan, Hiroshi Nakagawa, Amanda B. Muir
Journal: Journal of Allergy and Clinical Immunology (2018)
Opioid Use Is NOT Associated with in-Hospital Mortality Among Patients with Sickle CELL Disease in the United States: Findings from the National Inpatient Sample
Authors: Oladimeji Akinola Akinboro, Stanley Nwabudike, Camille Edwards, Diana Cirstea, Nana Oduraa Addo-Tabiri, Michael Voisine, Hassan Yameen, Adetola A. Kassim
Journal: Blood (2018)
m6A modification controls the innate immune response to infection by targeting type I interferons
Authors: Roni Winkler, Ella Gillis, Lior Lasman, Modi Safra, Shay Geula, Clara Soyris, Aharon Nachshon, Julie Tai-Schmiedel, Nehemya Friedman, Vu Thuy Khanh Le-Trilling, Mirko Trilling, Michal Mandelboim, Jacob H. Hanna, Schraga Schwartz, Noam Stern-Ginossar
Journal: Nature Immunology (2018)
The trends in incidence of primary liver cancer caused by specific etiologies: Results from the Global Burden of Disease Study 2016 and implications for liver cancer prevention
Authors: Zhenqiu Liu, Yanfeng Jiang, Huangbo Yuan, Qiwen Fang, Ning Cai, Chen Suo, Li Jin, Tiejun Zhang, Xingdong Chen
Journal: Journal of Hepatology (2018)
Hepatic Endothelial Notch Activation Protects against Liver Metastasis by Regulating Endothelial-Tumor Cell Adhesion Independent of Angiocrine Signaling
Authors: Sebastian A. Wohlfeil, Verena Häfele, Bianca Dietsch, Kai Schledzewski, Manuel Winkler, Johanna Zierow, Thomas Leibing, Mona Malek Mohammadi, Joerg Heineke, Carsten Sticht, Victor Olsavszky, Philipp-Sebastian Koch, Cyrill Géraud, Sergij Goerdt
Journal: Cancer Research (2018)

The interaction of tumor cells with organ-specific endothelial cells (EC) is an important step during metastatic progression. Notch signaling in organ-specific niches has been implicated in mediating opposing effects on organotropic metastasis to the lungs and the liver, respectively. In this study, we scrutinized the role of endothelial Notch activation during liver metastasis. To target hepatic EC (HEC), a novel EC subtype-specific Cre driver mouse was generated. Clec4g-Cretg/wt mice were crossed to Rosa26N1ICD-IRES-GFP to enhance Notch signaling in HEC (NICDOE-HEC). In NICDOE-HEC mice, hepatic metastasis of malignant melanoma and colorectal carcinoma was significantly reduced. These mice revealed reduced liver growth and impaired metabolic zonation due to suppression of hepatic angiocrine Wnt signaling. Hepatic metastasis, however, was not controlled by angiocrine Wnt signaling, as deficiency of the Wnt cargo receptor Wls in HEC of WlsHEC-KO mice did not affect hepatic metastasis. In contrast, the hepatic microvasculature in NICDOE-HEC mice revealed a special form of sinusoidal capillarization, with effacement of endothelial zonation functionally paralleled by reduced tumor cell adhesion in vivo. Notably, expression of endothelial adhesion molecule ICAM1 by HEC was significantly reduced. Treatment with an anti-ICAM1 antibody significantly inhibited tumor cell adhesion to HEC in wild-type mice confirming that Notch controls hepatic metastasis via modulation of HEC adhesion molecules. As endothelial Notch activation in the lung has been shown to promote lung metastasis, tumor therapy will require approaches that target Notch in an organ-, cell type-, and context-specific manner. SIGNIFICANCE: Manipulation of Notch signaling in the endothelium has opposing, organ-specific effects on metastasis to the lung and the liver, demonstrating that this pathway should be targeted in a cell- and context-specific fashion.
Genetic Data from Nearly 63,000 Women of European Descent Predicts DNA Methylation Biomarkers and Epithelial Ovarian Cancer Risk
Authors: Yaohua Yang, Lang Wu, Xiang Shu, Yingchang Lu, Xiao-Ou Shu, Qiuyin Cai, Alicia Beeghly-Fadiel, Bingshan Li, Fei Ye, Andrew Berchuck, Hoda Anton-Culver, Susana Banerjee, Javier Benitez, Line Bjørge, James D. Brenton, Ralf Butzow, Ian G. Campbell, Jenny Chang-Claude, Kexin Chen, Linda S. Cook, Daniel W. Cramer, Anna deFazio, Joe Dennis, Jennifer A. Doherty, Thilo Dörk, Diana M. Eccles, Digna Velez Edwards, Peter A. Fasching, Renée T. Fortner, Simon A. Gayther, Graham G. Giles, Rosalind M. Glasspool, Ellen L. Goode, Marc T. Goodman, Jacek Gronwald, Holly R. Harris, Florian Heitz, Michelle A. Hildebrandt, Estrid Høgdall, Claus K. Høgdall, David G. Huntsman, Siddhartha P. Kar, Beth Y. Karlan, Linda E. Kelemen, Lambertus A. Kiemeney, Susanne K. Kjaer, Anita Koushik, Diether Lambrechts, Nhu D. Le, Douglas A. Levine, Leon F. Massuger, Keitaro Matsuo, Taymaa May, Iain A. McNeish, Usha Menon, Francesmary Modugno, Alvaro N. Monteiro, Patricia G. Moorman, Kirsten B. Moysich, Roberta B. Ness, Heli Nevanlinna, Håkan Olsson, N. Charlotte Onland-Moret, Sue K. Park, James Paul, Celeste L. Pearce, Tanja Pejovic, Catherine M. Phelan, Malcolm C. Pike, Susan J. Ramus, Elio Riboli, Cristina Rodriguez-Antona, Isabelle Romieu, Dale P. Sandler, Joellen M. Schildkraut, Veronica W. Setiawan, Kang Shan, Nadeem Siddiqui, Weiva Sieh, Meir J. Stampfer, Rebecca Sutphen, Anthony J. Swerdlow, Lukasz M. Szafron, Soo Hwang Teo, Shelley S. Tworoger, Jonathan P. Tyrer, Penelope M. Webb, Nicolas Wentzensen, Emily White, Walter C. Willett, Alicja Wolk, Yin Ling Woo, Anna H. Wu, Li Yan, Drakoulis Yannoukakos, Georgia Chenevix-Trench, Thomas A. Sellers, Paul D.P. Pharoah, Wei Zheng, Jirong Long
Journal: Cancer Research (2018)

DNA methylation is instrumental for gene regulation. Global changes in the epigenetic landscape have been recognized as a hallmark of cancer. However, the role of DNA methylation in epithelial ovarian cancer (EOC) remains unclear. In this study, high-density genetic and DNA methylation data in white blood cells from the Framingham Heart Study (
Comparative Studies Reveal Robust HbF Induction By Editing of HBG1/2 Promoters or BCL11A Erythroid-Enhancer in Human CD34+ Cells but That BCL11A Erythroid-Enhancer Editing Is Associated with Selective Reduction in Erythroid Lineage Reconstitution in a Xenotransplantation Model
Authors: Kai-Hsin Chang, Minerva Sanchez, Jack Heath, Edouard deDreuzy, Scott Haskett, Abigail Vogelaar, Kiran Gogi, Jen Da Silva, Tongyao Wang, Andrew Sadowski, Gregory Gotta, Jamaica Siwak, Ramya Viswanathan, Katherine Loveluck, Hoson Chao, Eric Tillotson, Aditi Chalishazar, Abhishek Dass, Frederick Ta, Emily Brennan, Diana Tabbaa, Eugenio Marco, John A Zuris, Deepak Reyon, Meltem Isik, Ari Friedland, Terence Ta, Fred Harbinski, Georgia Giannoukos, Sandra Teixeira, Christopher J Wilson, Charlie Albright, Haiyan Jiang
Journal: Blood (2018)
Recurrent Bullous Eruption in a Young Woman
Authors: Robin Reschke, Konstantin Dumann, Mirjana Ziemer
Journal: JAMA Dermatology (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 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
Eltrombopag Improves Hematopoiesis in Patients with Low to Intermediate-2 Risk Myelodysplastic Syndrome (MDS)
Authors: Alana Vicente, Fernanda Gutierrez-Rodrigues, Valentina Giudice, Zhijie Wu, Sachiko Kajigaya, Maria del Pilar Fernandez Ibanez, Maher Albitar, Barbara Weinstein, Katherine R. Calvo, Danielle M. Townsley, Phillip Scheinberg, Cynthia E. Dunbar, Neal S. Young, Thomas Winkler
Journal: Blood (2018)
Proton pump inhibitors negatively impact survival of PD-1 inhibitor based therapies in metastatic melanoma patients
Authors: K. Homicsko, G. Richtig, F. Tuchmann, Z. Tsourti, D. Hanahan, G. Coukos, M. Wind-Rotolo, E. Richtig, P. Zygoura, C. Holler, U. Dafni, O.A. Michielin
Journal: Annals of Oncology (2018)

Background: PD1 inhibitors as well as PD1/CTLA4 combinations have shown remarkable efficacy in the first-line treatment of metastatic melanoma. The impact of many concomitant medications on the clinical outcomes from PD1 based therapies remains elusive.
House dust mite drives proinflammatory eicosanoid reprogramming and macrophage effector functions
Authors: Fiona D. R. Henkel, Antonie Friedl, Mark Haid, Dominique Thomas, Tiffany Bouchery, Pascal Haimerl, Marta de los Reyes Jiménez, Francesca Alessandrini, Carsten B. Schmidt‐Weber, Nicola L. Harris, Jerzy Adamski, Julia Esser‐von Bieren
Journal: Allergy (2018)

Abstract Background Eicosanoid lipid mediators play key roles in type 2 immune responses, for example in allergy and asthma. Macrophages represent major producers of eicosanoids and they are key effector cells of type 2 immunity. We aimed to comprehensively track eicosanoid profiles during type 2 immune responses to house dust mite ( HDM ) or helminth infection and to identify mechanisms and functions of eicosanoid reprogramming in human macrophages. Methods We established an LC ‐ MS / MS workflow for the quantification of 52 oxylipins to analyze mediator profiles in human monocyte‐derived macrophages ( MDM ) stimulated with HDM and during allergic airway inflammation ( AAI ) or nematode infection in mice. Expression of eicosanoid enzymes was studied by qPCR and western blot and cytokine production was assessed by multiplex assays. Results Short (24 h) exposure of alveolar‐like MDM ( aMDM ) to HDM suppressed 5‐ LOX expression and product formation, while triggering prostanoid (thromboxane and prostaglandin D 2 and E 2 ) production. This eicosanoid reprogramming was p38‐dependent, but dectin‐2‐independent. HDM also induced proinflammatory cytokine production, but reduced granulocyte recruitment by aMDM . In contrast, high levels of cysteinyl leukotrienes (cys LT s) and 12‐/15‐ LOX metabolites were produced in the airways during AAI or nematode infection in mice. Conclusion Our findings show that a short exposure to allergens as well as ongoing type 2 immune responses are characterized by a fundamental reprogramming of the lipid mediator metabolism with macrophages representing particularly plastic responder cells. Targeting mediator reprogramming in airway macrophages may represent a viable approach to prevent pathogenic lipid mediator profiles in allergy or asthma.
Associations of Body Mass and Fat Indexes With Cardiometabolic Traits
Authors: Joshua A. Bell, David Carslake, Linda M. O’Keeffe, Monika Frysz, Laura D. Howe, Mark Hamer, Kaitlin H. Wade, Nicholas J. Timpson, George Davey Smith
Journal: Journal of the American College of Cardiology (2018)

Body mass index (BMI) is criticized for not distinguishing fat from lean mass and ignoring fat distribution, leaving its ability to detect health effects unclear. The aim of this study was to compare BMI with total and regional fat indexes from dual-energy x-ray absorptiometry in their associations with cardiometabolic traits. Duration of exposure to and change in each index across adolescence were examined in relation to detailed traits in young adulthood. BMI was examined alongside total, trunk, arm, and leg fat indexes (each in kilograms per square meter) from dual-energy x-ray absorptiometry at ages 10 and 18 years in relation to 230 traits from targeted metabolomics at age 18 years in 2,840 offspring from the Avon Longitudinal Study of Parents and Children. Higher total fat mass index and BMI at age 10 years were similarly associated with cardiometabolic traits at age 18 years, including higher systolic and diastolic blood pressure, higher very low-density lipoprotein and low-density lipoprotein cholesterol, lower high-density lipoprotein cholesterol, higher triglycerides, and higher insulin and glycoprotein acetyls. Associations were stronger for both indexes measured at age 18 years and for gains in each index from age 10 to 18 years (e.g., 0.45 SDs [95% confidence interval: 0.38 to 0.53] in glycoprotein acetyls per SD unit gain in fat mass index vs. 0.38 SDs [95% confidence interval: 0.27 to 0.48] per SD unit gain in BMI). Associations resembled those for trunk fat index. Higher lean mass index was weakly associated with traits and was not protective against higher fat mass index. The results of this study support abdominal fatness as a primary driver of cardiometabolic dysfunction and BMI as a useful tool for detecting its effects.
Bayesian Hierarchical Models
Authors: Anna E. McGlothlin, Kert Viele
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 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