tbuckley/cabot-search huggingface dataset:
腫瘍血管系特異的ナノグラフェン酸化物による転移性乳癌のin vivo標的化【Powered by NICT】
Authors: Yang Dongzhi, Feng Liangzhu, A Dougherty Casey, E Luker Kathryn, Chen Daiqin, A Cauble Meagan, M Banaszak Holl Mark, D Luker Gary, D Ross Brian, Liu Zhuang, Hong Hao
Journal: Biomaterials (2016)
Increased delivery of chemotherapy to the vitreous by inhibition of the blood-retinal barrier
Authors: Guillem Pascual-Pasto, Nagore G. Olaciregui, Javier A.W. Opezzo, Helena Castillo-Ecija, Maria Cuadrado-Vilanova, Sonia Paco, Ezequiel M. Rivero, Monica Vila-Ubach, Camilo A. Restrepo-Perdomo, Montserrat Torrebadell, Mariona Suñol, Paula Schaiquevich, Jaume Mora, Guillermo F. Bramuglia, Guillermo L. Chantada, Angel M. Carcaboso
Journal: Journal of Controlled Release (2017)
癌細胞における薬物送達および強化された抗増殖効果のための生分解性リグニン系ナノ粒子のin vitro評価【Powered by NICT】
Authors: Figueiredo Patricia, Lintinen Kalle, Kiriazis Alexandros, Hynninen Ville, Liu Zehua, Bauleth-Ramos Tomas, Rahikkala Antti, Correia Alexandra, Kohout Tomas, Sarmento Bruno, Yli-Kauhaluoma Jari, Hirvonen Jouni, Ikkala Olli, A Kostiainen Mauri, A Santos Helder
Journal: Biomaterials (2017)
Targeting miR-423-5p Reverses Exercise Training–Induced HCN4 Channel Remodeling and Sinus Bradycardia
Authors: Alicia D’Souza, Charles M. Pearman, Yanwen Wang, Shu Nakao, Sunil Jit R.J. Logantha, Charlotte Cox, Hayley Bennett, Yu Zhang, Anne Berit Johnsen, Nora Linscheid, Pi Camilla Poulsen, Jonathan Elliott, Jessica Coulson, Jamie McPhee, Abigail Robertson, Paula A. da Costa Martins, Ashraf Kitmitto, Ulrik Wisløff, Elizabeth J. Cartwright, Oliver Monfredi, Alicia Lundby, Halina Dobrzynski, Delvac Oceandy, Gwilym M. Morris, Mark R. Boyett
Journal: Circulation Research (2017)

Rationale: Downregulation of the pacemaking ion channel, HCN4 (hyperpolarization-activated cyclic nucleotide gated channel 4), and the corresponding ionic current, I f , underlies exercise training–induced sinus bradycardia in rodents. If this occurs in humans, it could explain the increased incidence of bradyarrhythmias in veteran athletes, and it will be important to understand the underlying processes. Objective: To test the role of HCN4 in the training-induced bradycardia in human athletes and investigate the role of microRNAs (miRs) in the repression of HCN4. Methods and Results: As in rodents, the intrinsic heart rate was significantly lower in human athletes than in nonathletes, and in all subjects, the rate-lowering effect of the HCN selective blocker, ivabradine, was significantly correlated with the intrinsic heart rate, consistent with HCN repression in athletes. Next-generation sequencing and quantitative real-time reverse transcription polymerase chain reaction showed remodeling of miRs in the sinus node of swim-trained mice. Computational predictions highlighted a prominent role for miR-423-5p. Interaction between miR-423-5p and HCN4 was confirmed by a dose-dependent reduction in HCN4 3′-untranslated region luciferase reporter activity on cotransfection with precursor miR-423-5p (abolished by mutation of predicted recognition elements). Knockdown of miR-423-5p with anti-miR-423-5p reversed training-induced bradycardia via rescue of HCN4 and I f . Further experiments showed that in the sinus node of swim-trained mice, upregulation of miR-423-5p (intronic miR) and its host gene, NSRP1, is driven by an upregulation of the transcription factor Nkx2.5. Conclusions: HCN remodeling likely occurs in human athletes, as well as in rodent models. miR-423-5p contributes to training-induced bradycardia by targeting HCN4. This work presents the first evidence of miR control of HCN4 and heart rate. miR-423-5p could be a therapeutic target for pathological sinus node dysfunction in veteran athletes.
歯槽骨再生用の骨代替としてコラゲナーゼをカプセル化したヒドロキシアパタイト‐硫酸カルシウム‐ヒアルロン酸複合体
Authors: Subramaniam Sadhasivam, Fang Yen-Hsin, Sivasubramanian Savitha, Lin Feng-Huei, Lin Chun-pin
Journal: Biomaterials (2016)
同所性乳癌マウスモデルにおけるドセタキセルを負荷したタキサン結合ペプチド修飾高分子ミセルの前臨床評価【Powered by NICT】
Authors: Logie Jennifer, N Ganesh Ahil, M Aman Ahmed, S Al-awar Rima, S Shoichet Molly
Journal: Biomaterials (2017)
STING Requires the Adaptor TRIF to Trigger Innate Immune Responses to Microbial Infection
Authors: Xin Wang, Tanmay Majumdar, Patricia Kessler, Evgeny Ozhegov, Ying Zhang, Saurabh Chattopadhyay, Sailen Barik, Ganes C. Sen
Journal: Cell Host & Microbe (2017)
Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7–9
Authors: Shlomi Matetzky, Dov Freimark, Micha S Feinberg, Ilya Novikov, Shmuel Rath, Babeth Rabinowitz, Elieser Kaplinsky, Hanoch Hod
Journal: Journal of the American College of Cardiology (1999)
Antimicrobial resistance: The complex challenge of measurement to inform policy and the public
Authors: Didier Wernli, Peter S. Jørgensen, Stephan Harbarth, Scott P. Carroll, Ramanan Laxminarayan, Nicolas Levrat, John-Arne Røttingen, Didier Pittet
Journal: PLoS Medicine (2017)

Antimicrobial resistance (AMR) is developing in many pathogenic bacteria, threatening to compromise the effectiveness of crucial medical treatments.• Member States of the United Nations (UN) have reiterated their commitment to tackle AMR at the UN General Assembly held in New York City on 21 September 2016.The main challenge is now implementation of the Global Action Plan (GAP) adopted by the World Health Organization (WHO) in 2015.• There are currently large information gaps about the global governance of AMR regarding both the magnitude of the problem and national responses.• Expanding national and subnational monitoring by integrating measurements ranging from assessments of drivers of AMR to responses can increase political buy-in, societal participation, and implementation of agreed policies.• WHO should lead the way to expand monitoring of progress regarding AMR control, but a broad coalition of global health actors is needed to build a robust approach in a significant number of countries.Antimicrobial resistance (AMR) is increasing in a wide range of pathogens, causing morbidity and mortality globally, and threatening modern medicine.While the long-term impact of AMR on human societies remains uncertain [1], the conservation of antimicrobials' effectiveness has become an urgent priority.Tackling this ubiquitous problem requires coordination among countries and across sectors that include human and animal health, the environment,
A Sensitized IGF1 Treatment Restores Corticospinal Axon-Dependent Functions
Authors: Yuanyuan Liu, Xuhua Wang, Wenlei Li, Qian Zhang, Yi Li, Zicong Zhang, Junjie Zhu, Bo Chen, Philip R. Williams, Yiming Zhang, Bin Yu, Xiaosong Gu, Zhigang He
Journal: Neuron (2017)
FRI0173 Correlation between assymetric dimethylarginine and homocysteine levels in patients with rheumatoid arthritis
Authors: T Dimitroulas, J Hodson, A Sandoo, K Douglas, J Smith, G Kitas
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Rheumatoid Arthritis is a chronic inflammatory condition associated with increased cardiovascular disease (CVD) morbidity and mortality due to high coronary and cerebral atherosclerotic burden. Assymetric dimethylarginine (ADMA) – the most potent endogenous inhibitor of nitric oxide synthase - is an emerging marker of endothelial dysfunction and CVD in several conditions such as coronary artery disease and diabetes mellitus. ADMA levels are higher in RA patients compared to controls suggesting a role in the development of atherosclerosis. In addition ADMA is involved in the metabolism of honocysteine (Hcy) which is considered a novel, non-traditional CVD risk factor contributing to excess CVD risk in this population. <h3>Objectives</h3> The aim of our study was to determine whether asymmetric dimethylarginine (ADMA) levels are associated with Hcy and methylenetetrahydrofolate reductase (MTHFR) C677T (rs1801133) gene variants in patients with RA. <h3>Methods</h3> Serum ADMA and Hcy levels were measured in 201 RA individuals [155 (77.1%) females, median age 67 years (interquartile range 59–73)]. The MTHFR C677T polymorphism was assessed by using the LightCyclerTM System. Initially, ADMA was compared across the categories of MTHFR using a one-way analysis of variance (ANOVA), followed by a multivariate model, which accounted for Hcy, age, erythrocyte sedimentation rate (ESR), and homeostatic model assessment (HOMA). <h3>Results</h3> In univariable analysis, ADMA differed significantly across the categories of MTHFR (p=0.037). Patients with the MTHFR 677TT genotype had the highest ADMA levels, with a mean of 0.62 (SE =0.03), significantly higher than either those patients carrying the MTHFR 677CT (0.55, SE =0.01) or the MTHFR 677CC (0.55, SE=0.01) genotype (p=0.042) in both cases. In the multivariable model, Hcy (p=0.022) and ESR (p&lt;0.001) were found to have significant positive associations with ADMA but the relationship between MTHFR gene variants and ADMA was found to be non-significant (p=0.102). <h3>Conclusions</h3> The results of our study indicate an association between ADMA and Hcy in patients with RA without any genetic background as no relationship was established between ADMA and MTHFR gene variants. Abnormal metabolism of Hcy and dimethylarginines may interfere with each other resulting in endothelial dysfunction and accelerated atherosclerosis in RA individuals. <h3>References</h3> Dimitroulas T, Sandoo A, Hodson J, Smith J, Douglas K, Kitas G. MTHFR C677T Polymorphism but not DDAH gene variants are associated with Assymetric Dimethylarginine (ADMA) in RA. Ann Rhem Dis 2014;72(Suppl 2):333. Perna M, Roman MJ, Alpert DR, Crow MK, Lockshin MD, Sammaritano L, et al. Relationship of asymmetric dimethylarginine and homocysteine to vascular aging in systemic lupus erythematosus patients. Arthritis Rheum 2010;62:1718–22. <h3>Disclosure of Interest</h3> None declared
Distinct Subcortical Volume Alterations in Pediatric and Adult OCD: A Worldwide Meta-and Mega-Analysis (vol , pg , 2016)
Authors: Yoshinari Abe, Pino Alonso, Stephanie H. Ameis, Paul D. Arnold, Nuria Bargallo, Marcelo C. Batistuzzo, Francesco Benedetti, Jan C. Beucke, Premika S. W. Boedhoe, Irene Bollettini, Anushree Bose, Silvia Brem, Geraldo F. Busatto, Anna Calvo, Rosa Calvo, Danielle C. Cath, Yuqi Cheng, Kang Ik K. Cho, Sara Dallaspezia, Froukje E. de Vries, Stella J. de Wit, Damiaan Denys, Yu Fang, Kate D. Fitzgerald, Martine Fontaine, Jean-Paul Fouche, Monica Gimenez, Patricia Gruner, Gregory L. Hanna, Derrek P. Hibar, Marcelo Q. Hoexter, Hao Hu, Chaim Huyser, Keisuke Ikari, Neda Jahanshad, Norbert Kathmann, Christian Kaufmann, Sabin Khadka, Kathrin Koch, Jun Soo Kwon, Luisa Lazaro, Yanni Liu, Christine Lochner, Rachel Marsh, Ignacio Martinez-Zalacain, David Mataix-Cols, Jose M. Menchon, Euripedes C. Miguel, Luciano Minuzzi, Astrid Morer, Takashi Nakamae, Tomohiro Nakao, Janardhanan C. Narayanaswamy, Fabrizio Piras, Federica Piras, Christopher Pittenger, Y. C. Janardhan Reddy, Joao R. Sato, H. Blair Simpson, Lianne Schmaal, Noam Soreni, Carles Soriano-Mas, Gianfranco Spalletta, Dan J. Stein, Michael C. Stevens, Philip R. Szeszko, Paul M. Thompson, David F. Tolin, Dick J. Veltman, Ganesan Venkatasubramanian, Odile A. van den Heuvel, Ysbrand D. van der Werf, Guido A. van Wingen, Susanne Walitza, Zhen Wang, Jian Xu, Xiufeng Xu, Je-Yeon Yun, Qing Zhao
Journal: American Journal of Psychiatry (2017)
Phenolic Glycolipid Facilitates Mycobacterial Escape from Microbicidal Tissue-Resident Macrophages
Authors: C.J. Cambier, Seónadh M. O’Leary, Mary P. O’Sullivan, Joseph Keane, Lalita Ramakrishnan
Journal: Immunity (2017)

Mycobacterium tuberculosis (Mtb) enters the host in aerosol droplets deposited in lung alveoli, where the bacteria first encounter lung-resident alveolar macrophages. We studied the earliest mycobacterium-macrophage interactions in the optically transparent zebrafish. First-responding resident macrophages phagocytosed and eradicated infecting mycobacteria, suggesting that to establish a successful infection, mycobacteria must escape out of the initially infected resident macrophage into growth-permissive monocytes. We defined a critical role for mycobacterial membrane phenolic glycolipid (PGL) in engineering this transition. PGL activated the STING cytosolic sensing pathway in resident macrophages, inducing the production of the chemokine CCL2, which in turn recruited circulating CCR2+ monocytes toward infection. Transient fusion of infected macrophages with CCR2+ monocytes enabled bacterial transfer and subsequent dissemination, and interrupting this transfer so as to prolong mycobacterial sojourn in resident macrophages promoted clearing of infection. Human alveolar macrophages produced CCL2 in a PGL-dependent fashion following infection, arguing for the potential of PGL-blocking interventions or PGL-targeting vaccine strategies in the prevention of tuberculosis. VIDEO ABSTRACT.
New approach in delivering chemotherapy: locoregional treatment for recurrent glioblastoma (rGBM).
Authors: A Boiardi, M Eoli, A Salmaggi, E Lamperti, A Botturi, G Broggi, M Bartolomei, A Silvani
Journal: Journal of experimental & clinical cancer research (2003)

The treatment of GBM tumor recurrence is generally a hopeless challenge, since recurred tumor is resistant to the most common therapeutic efforts. Some partial results can be achieved by targeting local disease control, in view of the fact that 95% of recurrences occur locally. We present results concerning three pilot studies, all performed in recurrent GBM patients who underwent second surgery and have been treated systemically with temozolomide and locally through an Ommaya reservoire according to the following schedules: a) in 20 rGBM, 4 mg novantrone was delivered day 1,5 every 30 days; in 26 rGBM, 4 mg novantrone was delivered every 20 days in association with locoregional radioimmunotherapy (RIT); in 12 rGBM pegylated liposomal doxorubicin 4 mg was delivered day 1,5,10,15,20 with 20 days interval. Results seem very promising since there is an extension of disease free and survival, both of more than 50 % if results are evaluated in relation with the most frequent data of the literature.
Cut and Paste: Efficient Homology-Directed Repair of a Dominant Negative KRT14 Mutation via CRISPR/Cas9 Nickases
Authors: Thomas Kocher, Patricia Peking, Alfred Klausegger, Eva Maria Murauer, Josefina Piñón Hofbauer, Verena Wally, Thomas Lettner, Stefan Hainzl, Michael Ablinger, Johann Wolfgang Bauer, Julia Reichelt, Ulrich Koller
Journal: Molecular Therapy (2017)

With the ability to induce rapid and efficient repair of disease-causing mutations, CRISPR/Cas9 technology is ideally suited for gene therapy approaches for recessively and dominantly inherited monogenic disorders. In this study, we have corrected a causal hotspot mutation in exon 6 of the keratin 14 gene (KRT14) that results in generalized severe epidermolysis bullosa simplex (EBS-gen sev), using a double-nicking strategy targeting intron 7, followed by homology-directed repair (HDR). Co-delivery into EBS keratinocytes of a Cas9 D10A nickase (Cas9n), a predicted single guide RNA pair specific for intron 7, and a minicircle donor vector harboring the homology donor template resulted in a recombination efficiency of >30% and correction of the mutant KRT14 allele. Phenotypic correction of EBS-gen sev keratinocytes was demonstrated by immunofluorescence analysis, revealing the absence of disease-associated K14 aggregates within the cytoplasm. We achieved a promising safety profile for the CRISPR/Cas9 double-nicking approach, with no detectable off-target activity for a set of predicted off-target genes as confirmed by next generation sequencing. In conclusion, we demonstrate a highly efficient and specific gene-editing approach for KRT14, offering a causal treatment option for EBS.
PCSK9 Inhibitors and the Choice Between Innovation, Efficiency, and Affordability
Authors: Daniel B. Mark, Kevin A. Schulman
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
虚弱と特定高齢者における心血管疾患の罹患率と死亡率のリスク:メタ分析と探索的メタ回帰分析からの結果【Powered by NICT】
Authors: Veronese Nicola, Cereda Emanuele, Stubbs Brendon, Solmi Marco, Luchini Claudio, Manzato Enzo, Sergi Giuseppe, Manu Peter, Harris Tamara, Fontana Luigi, Strandberg Timo, Amieva Helene, Dumurgier Julien, Elbaz Alexis, Tzourio Christophe, Eicholzer Monika, Rohrmann Sabine, Moretti Claudio, D’Ascenzo Fabrizio, Quadri Giorgio, Polidoro Alessandro, Lourenco Roberto Alves, Moreira Virgilio Garcia, Sanchis Juan, Scotti Valeria, Maggi Stefania, U Correll Christoph
Journal: Ageing Research Reviews (2017)
Association Between Mitochondrial DNA Haplogroup Variation and Autism Spectrum Disorders
Authors: Dimitra Chalkia, Larry N. Singh, Jeremy Leipzig, Maria Lvova, Olga Derbeneva, Anita Lakatos, Dexter Hadley, Hakon Hakonarson, Douglas C. Wallace
Journal: JAMA Psychiatry (2017)

<h3>Importance</h3> Autism spectrum disorders (ASD) are characterized by impairments in social interaction, communication, and repetitive or restrictive behavior. Although multiple physiologic and biochemical studies have reported defects in mitochondrial oxidative phosphorylation in patients with ASD, the role of mitochondrial DNA (mtDNA) variation has remained relatively unexplored. <h3>Objective</h3> To assess what impact mitochondrial lineages encompassing ancient mtDNA functional polymorphisms, termed haplogroups, have on ASD risk. <h3>Design, Setting, and Participants</h3> In this cohort study, individuals with autism and their families were studied using the Autism Genetic Resource Exchange cohort genome-wide association studies data previously generated at the Children's Hospital of Philadelphia. From October 2010 to January 2017, we analyzed the data and used the mtDNA single-nucleotide polymorphisms interrogated by the Illumina HumanHap 550 chip to determine the mtDNA haplogroups of the individuals. Taking into account the familial structure of the Autism Genetic Resource Exchange data, we then determined whether the mtDNA haplogroups correlate with ASD risk. <h3>Main Outcomes and Measures</h3> Odds ratios of mitochondrial haplogroup as predictors of ASD risk. <h3>Results</h3> Of 1624 patients with autism included in this study, 1299 were boys (80%) and 325 were girls (20%). Families in the Autism Genetic Resource Exchange collection (933 families, encompassing 4041 individuals: 1624 patients with ASD and 2417 healthy parents and siblings) had been previously recruited in the United States with no restrictions on age, sex, race/ethnicity, or socioeconomic status. Relative to the most common European haplogroup HHV, European haplogroups I, J, K, O-X, T, and U were associated with increased risk of ASD, as were Asian and Native American haplogroups A and M, with odds ratios ranging from 1.55 (95% CI, 1.16-2.06) to 2.18 (95% CI, 1.59-3) (adjusted<i>P</i>&lt; .04). Hence, mtDNA haplogroup variation is an important risk factor for ASD. <h3>Conclusions and Relevance</h3> Because haplogroups I, J, K, O-X, T, and U encompass 55% of the European population, mtDNA lineages must make a significant contribution to overall ASD risk.
Clinical and biological characteristics of the French COBRA cohort of adult subjects with asthma
Authors: Marina Pretolani, David Soussan, Isabelle Poirier, Gabriel Thabut, Michel Aubier
Journal: European Respiratory Journal (2017)

The COhort of BRonchial obstruction and Asthma (COBRA) is a longitudinal cohort that involves 12 French academic institutions. DNA, serum samples and clinical data are collected at entry and every 6 months thereafter. Of 1080 patients with asthma recruited between 2007 and 2015, 401 had mild/moderate and 613 had severe asthma. In cross-sectional analyses, compared with patients with milder disease, patients with severe asthma had more symptoms, exacerbations, hospitalisations and visits to the emergency department during the preceding 12 months, higher numbers of blood eosinophils, and more comorbidities. More than 60% of patients with severe asthma were therapy-uncontrolled at entry, and 152 of them were being treated with omalizumab. In addition, patients with asthma who had the highest eosinophilia levels (&gt;300/mm<sup>3</sup>) had shorter asthma duration, lower lung function, and higher rates of severe exacerbations and unacceptable asthma control than patients with lower eosinophil counts. Longitudinal analyses performed in 427 patients with asthma with at least three differential blood cell counts demonstrated that both eosinophil numbers and eosinophil increase over time were associated with the number of exacerbations occurring until the next visit and with Juniper score. Studies with the COBRA cohort will help to improve knowledge concerning the risk and biological factors associated with asthma severity and to better understand their influence on the disease trajectory.
Differences between BCL2-break positive and negative follicular lymphoma unraveled by whole-exome sequencing
Authors: A Zamò, J Pischimarov, M Schlesner, P Rosenstiel, R Bomben, H Horn, T Grieb, T Nedeva, C López, A Haake, J Richter, L Trümper, C Lawerenz, W Klapper, P Möller, M Hummel, D Lenze, M Szczepanowski, L Flossbach, M Schreder, V Gattei, G Ott, R Siebert, A Rosenwald, E Leich
Journal: Leukemia (2017)
EASI p-EASI: Utilizing a combination of serum biomarkers offers an objective measurement tool for disease severity in atopic dermatitis patients
Authors: Judith L. Thijs, Julia Drylewicz, Renée Fiechter, Ian Strickland, Matthew A. Sleeman, Athula Herath, Richard D. May, Catharina A.F.M. Bruijnzeel-Koomen, Edward F. Knol, Barbara Giovannone, Marjolein S. de Bruin-Weller, Stefan Nierkens, Dirk Jan Hijnen
Journal: Journal of Allergy and Clinical Immunology (2017)
Global Obesity Epidemic Worsening
Authors: M.J. Friedrich
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 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