tbuckley/cabot-search huggingface dataset:
Breast-Cancer Adjuvant Therapy with Zoledronic Acid
Authors: Robert E. Coleman, Helen Marshall, David Cameron, David Dodwell, Roger Burkinshaw, Maccon Keane, Miguel Gil, Stephen J. Houston, Robert J. Grieve, Peter J. Barrett-Lee, Diana Ritchie, Julia Pugh, Claire Gaunt, Una Rea, Jennifer Peterson, Claire Davies, Victoria Hiley, Walter Gregory, Richard Bell
Journal: New England Journal of Medicine (2011)

Data suggest that the adjuvant use of bisphosphonates reduces rates of recurrence and death in patients with early-stage breast cancer. We conducted a study to determine whether treatment with zoledronic acid, in addition to standard adjuvant therapy, would improve disease outcomes in such patients.In this open-label phase 3 study, we randomly assigned 3360 patients to receive standard adjuvant systemic therapy either with or without zoledronic acid. The zoledronic acid was administered every 3 to 4 weeks for 6 doses and then every 3 to 6 months to complete 5 years of treatment. The primary end point of the study was disease-free survival. A second interim analysis revealed that a prespecified boundary for lack of benefit had been crossed.At a median follow-up of 59 months, there was no significant between-group difference in the primary end point, with a rate of disease-free survival of 77% in each group (adjusted hazard ratio in the zoledronic acid group, 0.98; 95% confidence interval [CI], 0.85 to 1.13; P=0.79). Disease recurrence or death occurred in 377 patients in the zoledronic acid group and 375 of those in the control group. The numbers of deaths--243 in the zoledronic acid group and 276 in the control group--were also similar, resulting in rates of overall survival of 85.4% in the zoledronic acid group and 83.1% in the control group (adjusted hazard ratio, 0.85; 95% CI, 0.72 to 1.01; P=0.07). In the zoledronic acid group, there were 17 confirmed cases of osteonecrosis of the jaw (cumulative incidence, 1.1%; 95% CI, 0.6 to 1.7; P<0.001) and 9 suspected cases; there were no cases in the control group. Rates of other adverse effects were similar in the two study groups.These findings do not support the routine use of zoledronic acid in the adjuvant management of breast cancer. (Funded by Novartis Pharmaceuticals and the National Cancer Research Network; AZURE Current Controlled Trials number, ISRCTN79831382.).
Disrupting the adult globin promoter alleviates promoter competition and reactivates fetal globin gene expression
Authors: Sarah K. Topfer, Ruopeng Feng, Peng Huang, Lana C. Ly, Gabriella E. Martyn, Gerd A. Blobel, Mitchell J. Weiss, Kate G. R. Quinlan, Merlin Crossley
Journal: Blood (2022)
Deleterious Mutations Accumulate Faster in Allopolyploid Than Diploid Cotton (<i>Gossypium</i>) and Unequally between Subgenomes
Authors: Justin L Conover, Jonathan F Wendel
Journal: Molecular Biology and Evolution (2022)

Whole-genome duplication (polyploidization) is among the most dramatic mutational processes in nature, so understanding how natural selection differs in polyploids relative to diploids is an important goal. Population genetics theory predicts that recessive deleterious mutations accumulate faster in allopolyploids than diploids due to the masking effect of redundant gene copies, but this prediction is hitherto unconfirmed. Here, we use the cotton genus (Gossypium), which contains seven allopolyploids derived from a single polyploidization event 1-2 Million years ago, to investigate deleterious mutation accumulation. We use two methods of identifying deleterious mutations at the nucleotide and amino acid level, along with whole-genome resequencing of 43 individuals spanning six allopolyploid species and their two diploid progenitors, to demonstrate that deleterious mutations accumulate faster in allopolyploids than in their diploid progenitors. We find that, unlike what would be expected under models of demographic changes alone, strongly deleterious mutations show the biggest difference between ploidy levels, and this effect diminishes for moderately and mildly deleterious mutations. We further show that the proportion of nonsynonymous mutations that are deleterious differs between the two coresident subgenomes in the allopolyploids, suggesting that homoeologous masking acts unequally between subgenomes. Our results provide a genome-wide perspective on classic notions of the significance of gene duplication that likely are broadly applicable to allopolyploids, with implications for our understanding of the evolutionary fate of deleterious mutations. Finally, we note that some measures of selection (e.g., dN/dS, πN/πS) may be biased when species of different ploidy levels are compared.
Prevalence and Durability of SARS-CoV-2 Antibodies Among Unvaccinated US Adults by History of COVID-19
Authors: Jennifer L. Alejo, Jonathan Mitchell, Amy Chang, Teresa P. Y. Chiang, Allan B. Massie, Dorry L. Segev, Martin A. Makary
Journal: JAMA (2022)

Venkata Viswanadh Edara, PhD; William H. Hudson, PhD; Xuping Xie, PhD; Rafi Ahmed, PhD; Mehul S. Suthar, PhD
Increased risk of MAFLD and Liver Fibrosis in Inflammatory Bowel Disease Independent of Classic Metabolic Risk Factors
Authors: Juan Carlos Rodriguez-Duque, José Luis Calleja, Paula Iruzubieta, Marta Hernández-Conde, Coral Rivas-Rivas, María Isabel Vera, Maria Jose Garcia, Marta Pascual, Beatriz Castro, Agustín García-Blanco, Enrique García-Nieto, Soraya Curiel-del Olmo, María Luisa Cagigal, Lorena Lopez-Montejo, Tatiana Fernández-Lamas, Laura Rasines, José Ignacio Fortea, José Pedro Vaque, Yza Frias, Montserrat Rivero, María Teresa Arias-Loste, Javier Crespo
Journal: Clinical Gastroenterology and Hepatology (2022)

There is conflicting evidence regarding the prevalence of and risk factors for metabolic-associated fatty liver disease (MAFLD) in patients with inflammatory bowel disease (IBD). We aimed to determine MAFLD prevalence and risk factors in IBD patients.Cross-sectional, case-control study included all consecutive IBD patients treated at 2 different university hospitals. Controls were subjects randomly selected from the general population and matched by age, sex, type 2 diabetes status, and body mass index in a 1:2 ratio. MAFLD was confirmed by controlled attenuation parameter. Liver biopsies were collected when MAFLD with significant liver fibrosis was suspected. In addition, age- and fibrosis stage-paired non-IBD patients with biopsy-proven MAFLD served as a secondary control group.Eight hundred thirty-one IBD patients and 1718 controls were included. The prevalence of MAFLD and advanced liver fibrosis (transient elastography ≥9.7 kPa) was 42.00% and 9.50%, respectively, in IBD patients and 32.77% and 2.31%, respectively, in the general population (P < .001). A diagnosis of IBD was an independent predictor of MAFLD (adjusted odds ratio, 1.99; P < .001) and an independent risk factor for advanced liver fibrosis (adjusted odds ratio, 5.55; P < .001). Liver biopsies were obtained from 40 IBD patients; MAFLD was confirmed in all cases, and fibrosis of any degree was confirmed in 25 of 40 cases (62.5%). Body mass index and type 2 diabetes prevalence were significantly lower in IBD-MAFLD patients than in severity-paired patients with biopsy-proven MAFLD.MAFLD and liver fibrosis are particularly prevalent in IBD patients, regardless of the influence of classic metabolic risk factors.
Vitamin D and marine omega 3 fatty acid supplementation and incident autoimmune disease: VITAL randomized controlled trial
Authors: Jill Hahn, Nancy R Cook, Erik K Alexander, Sonia Friedman, Joseph Walter, Vadim Bubes, Gregory Kotler, I-Min Lee, JoAnn E Manson, Karen H Costenbader
Journal: BMJ (2022)

Abstract Objective To investigate whether vitamin D and marine derived long chain omega 3 fatty acids reduce autoimmune disease risk. Design Vitamin D and omega 3 trial (VITAL), a nationwide, randomized, double blind, placebo controlled trial with a two-by-two factorial design. Setting Nationwide in the United States. Participants 25 871 participants, consisting of 12 786 men ≥50 years and 13 085 women ≥55 years at enrollment. Interventions Vitamin D (2000 IU/day) or matched placebo, and omega 3 fatty acids (1000 mg/day) or matched placebo. Participants self-reported all incident autoimmune diseases from baseline to a median of 5.3 years of follow-up; these diseases were confirmed by extensive medical record review. Cox proportional hazard models were used to test the effects of vitamin D and omega 3 fatty acids on autoimmune disease incidence. Main outcome measures The primary endpoint was all incident autoimmune diseases confirmed by medical record review: rheumatoid arthritis, polymyalgia rheumatica, autoimmune thyroid disease, psoriasis, and all others. Results 25 871 participants were enrolled and followed for a median of 5.3 years. 18 046 self-identified as non-Hispanic white, 5106 as black, and 2152 as other racial and ethnic groups. The mean age was 67.1 years. For the vitamin D arm, 123 participants in the treatment group and 155 in the placebo group had a confirmed autoimmune disease (hazard ratio 0.78, 95% confidence interval 0.61 to 0.99, P=0.05). In the omega 3 fatty acids arm, 130 participants in the treatment group and 148 in the placebo group had a confirmed autoimmune disease (0.85, 0.67 to 1.08, P=0.19). Compared with the reference arm (vitamin D placebo and omega 3 fatty acid placebo; 88 with confirmed autoimmune disease), 63 participants who received vitamin D and omega 3 fatty acids (0.69, 0.49 to 0.96), 60 who received only vitamin D (0.68, 0.48 to 0.94), and 67 who received only omega 3 fatty acids (0.74, 0.54 to 1.03) had confirmed autoimmune disease. Conclusions Vitamin D supplementation for five years, with or without omega 3 fatty acids, reduced autoimmune disease by 22%, while omega 3 fatty acid supplementation with or without vitamin D reduced the autoimmune disease rate by 15% (not statistically significant). Both treatment arms showed larger effects than the reference arm (vitamin D placebo and omega 3 fatty acid placebo). Study registration ClinicalTrials.gov NCT01351805 and NCT01169259
From the Congressional Office of Technology Assessment
Journal: JAMA (1989)

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
Medical News
Journal: JAMA (1910)

<h3>ILLINOIS</h3><h3>Quarantine Hospital for Moline.—</h3> Plans have been formulated by Dr. August H. Arp, health commissioner of Moline for a new isolation hospital to be built immediately in the rear of the Moline City Hospital. The building will be of brick and two stories in height. <h3>The Glidden Hospital.—</h3> The De Kalb City Medical Society has selected property just south of the city limits for the Glidden Hospital, for which James F. Glidden left a bequest of $25,000.—The late Col. Isaac L. Elwood, DeKalb, in his will, made provision for the payment of $25,000 to the institution. <h3>Cases Dismissed.—</h3> The trial of Dr. William Hecker, Watseka, at Portage, Wis., charged with being responsible for the drowning of his wife at Fox Lake in August, was concluded, October 7, by the dismissal of the case.—In the case of Dr. Thomas D. Doan, Scottville, charged with an attempt to produce abortion, the jury
Government Services
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
Interdependencies of cellular and humoral immune responses in heterologous and homologous SARS‐CoV‐2 vaccination
Authors: Moritz M. Hollstein, Lennart Münsterkötter, Michael P. Schön, Armin Bergmann, Thea M. Husar, Anna Abratis, Abass Eidizadeh, Meike Schaffrinski, Karolin Zachmann, Anne Schmitz, Jason S. Holsapple, Hedwig Stanisz‐Bogeski, Julie Schanz, Andreas Fischer, Uwe Groß, Andreas Leha, Andreas E. Zautner, Moritz Schnelle, Luise Erpenbeck
Journal: Allergy (2022)

Abstract Background Homologous and heterologous SARS‐CoV‐2 vaccinations yield different spike protein‐directed humoral and cellular immune responses. This study aimed to explore their currently unknown interdependencies. Methods COV‐ADAPT is a prospective, observational cohort study of 417 healthcare workers who received vaccination with homologous ChAdOx1 nCoV‐19, homologous BNT162b2 or with heterologous ChAdOx1 nCoV‐19/BNT162b2. We assessed humoral (anti‐spike‐RBD‐IgG, neutralizing antibodies, and avidity) and cellular (spike‐induced T‐cell interferon‐γ release) immune responses in blood samples up to 2 weeks before (T1) and 2–12 weeks following secondary immunization (T2). Results Initial vaccination with ChAdOx1 nCoV‐19 resulted in lower anti‐spike‐RBD‐IgG compared with BNT162b2 (70 ± 114 vs. 226 ± 279 BAU/ml, p &lt; .01) at T1. Booster vaccination with BNT162b2 proved superior to ChAdOx1 nCoV‐19 at T2 (anti‐spike‐RBD‐IgG: ChAdOx1 nCoV‐19/BNT162b2 2387 ± 1627 and homologous BNT162b2 3202 ± 2184 vs. homologous ChAdOx1 nCoV‐19 413 ± 461 BAU/ml, both p &lt; .001; spike‐induced T‐cell interferon‐γ release: ChAdOx1 nCoV‐19/BNT162b2 5069 ± 6733 and homologous BNT162b2 4880 ± 7570 vs. homologous ChAdOx1 nCoV‐19 1152 ± 2243 mIU/ml, both p &lt; .001). No significant differences were detected between BNT162b2‐boostered groups at T2. For ChAdOx1 nCoV‐19, no booster effect on T‐cell activation could be observed. We found associations between anti‐spike‐RBD‐IgG levels (ChAdOx1 nCoV‐19/BNT162b2 and homologous BNT162b2) and T‐cell responses (homologous ChAdOx1 nCoV‐19 and ChAdOx1 nCoV‐19/BNT162b2) from T1 to T2. Additionally, anti‐spike‐RBD‐IgG and T‐cell response were linked at both time points (all groups combined). All regimes yielded neutralizing antibodies and increased antibody avidity at T2. Conclusions Interdependencies between humoral and cellular immune responses differ between common SARS‐CoV‐2 vaccination regimes. T‐cell activation is unlikely to compensate for poor humoral responses.
Emergency Dermatology
Authors: Ashish C. Bhatia
Journal: JAMA (2012)

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
CD4 T cell-intrinsic STING signaling controls the differentiation and effector functions of T<sub>H</sub>1 and T<sub>H</sub>9 cells
Authors: Isis Benoit-Lizon, Elise Jacquin, Thaiz Rivera Vargas, Corentin Richard, Aurélie Roussey, Ludivine Dal Zuffo, Tiffany Martin, Andréa Melis, Daria Vinokurova, Sayyed Hamed Shahoei, Alvaro Baeza Garcia, Cassandre Pignol, Stéphane Giorgiutti, Raphaël Carapito, Romain Boidot, Frédérique Végran, Richard A Flavell, Bernhard Ryffel, Eric R Nelson, Pauline Soulas-Sprauel, Toby Lawrence, Lionel Apetoh
Journal: Journal for ImmunoTherapy of Cancer (2022)

While stimulator of interferon genes (STING) activation in innate immune cells of the tumor microenvironment can result in CD8 T cell-dependent antitumor immunity, whether STING signaling affects CD4 T-cell responses remains elusive.Here, we tested whether STING activation modulated the effector functions of CD4 T cells in vivo by analyzing tumor-infiltrating CD4 T cells and evaluating the contribution of the CD4 T cell-derived cytokines in the antitumor activity of the STING ligand 2'3'-cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) in two mouse tumor models. We performed ex vivo experiments to assess the impact of STING activation on CD4 T-cell differentiation and investigate the underlying molecular mechanisms. Finally, we tested whether STING activation enhances TH9 cell antitumor activity against mouse melanoma upon adoptive transfer.We found that activation of STING signaling cell-intrinsically enhances the differentiation and antitumor functions of TH1 and TH9 cells by increasing their respective production of interferon gamma (IFN-γ) and interleukin-9. IRF3 and type I interferon receptors (IFNARs) are required for the STING-driven enhancement of TH1 cell differentiation. However, STING activation favors TH9 cell differentiation independently of the IFNARs/IRF3 pathway but through mammalian target of rapamycin (mTOR) signaling, underscoring that STING activation differentially affects the fate of distinct CD4 T-cell subsets. The therapeutic effect of STING activation relies on TH1 and TH9-derived cytokines, and STING activation enhances the antitumor activity of TH9 cells upon adoptive transfer.Our results reveal the STING signaling pathway as a therapeutic target to boost CD4 T-cell effector functions and antitumor immunity.
Hyperimmune immunoglobulin for hospitalised patients with COVID-19 (ITAC): a double-blind, placebo-controlled, phase 3, randomised trial
Authors: Mark N. Polizzotto, Jacqueline Nordwall, Abdel G. Babiker, Andrew Phillips, David M. Vock, Nnakelu Eriobu, Vivian Kwaghe, Roger Paredes, Lourdes Mateu, Srikanth Ramachandruni, Rajeev Narang, Mamta K. Jain, Susana M. Lazarte, Jason V. Baker, Anne E.P. Frosch, Garyfallia Poulakou, Konstantinos N. Syrigos, Gretchen S. Arnoczy, Natalie A. McBride, Philip A. Robinson, Farjad Sarafian, Sanjay Bhagani, Hassan S. Taha, Thomas Benfield, Sean T.H. Liu, Anastasia Antoniadou, Jens Ulrik Stæhr Jensen, Ioannis Kalomenidis, Adityo Susilo, Prasetyo Hariadi, Tomas O. Jensen MD, Jose Luis Morales-Rull, Marie Helleberg, Sreenath Meegada, Isik S. Johansen, Daniel Canario, Eduardo Fernández-Cruz, Simeon Metallidis, Amish Shah, Aki Sakurai, Nikolaos G. Koulouris, Robin Trotman, Amy C. Weintrob, Daria Podlekareva, Usman Hadi, Kathryn M. Lloyd, Birgit Thorup Røge, Sho Saito, Kelly Sweerus, Jakob J. Malin, Christoph Lübbert, Jose Muñoz, Matthew J. Cummings, Marcelo H. Losso, Dan Turner, Kathryn Shaw-Saliba, Robin Dewar, Helene Highbarger, Perrine Lallemand, Tauseef Rehman, Norman Gerry, Dona Arlinda, Christina C. Chang, Birgit Grund, Michael R. Holbrook, Horace P. Holley, Fleur Hudson, Laura A. McNay, Daniel D. Murray, Sarah L. Pett, Megan Shaughnessy, Mary C. Smolskis, Giota Touloumi, Mary E. Wright, Mittie K. Doyle, Sharon Popik, Christine Hall, Roshan Ramanathan, Huyen Cao, Elsa Mondou, Todd Willis, Joseph V. Thakuria, Leman Yel, Elizabeth Higgs, Virginia L. Kan, Jens D. Lundgren, James D. Neaton, H. Clifford Lane
Journal: The Lancet (2022)
Gastric pyogenic granuloma: rare entity, usual therapy
Authors: Marco Bassi, Elisa Righi, Emanuele Dabizzi, Stefania Ghersi, Pasquale Apolito, Stefano Landi, Vincenzo Cennamo
Journal: Endoscopy (2022)

Lobular capillary hemangioma, known as pyogenic granuloma, is a benign vascular tumor that generally appears on the skin or in the oral cavity but rarely occurs in the gastrointestinal tract, where it can cause bleeding [1]. Although gastric pyogenic granuloma is rarely reported in the literature, (up to 2016, approximately 50 cases of gastrointestinal pyogenic granuloma in the English literature had been indexed on MEDLINE, including a few cases of gastric involvement), the actual incidence is probably higher [2] [3].
HYPERSUSCEPTIBILITY AND TRANSMITTED IMMUNITY.
Journal: JAMA (1906)

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
Anaphylaxis Management by Location: data from the Cross-Canada Anaphylaxis Registry (C-CARE)
Authors: Marina Delli Colli, Luca Delli Colli, Adnan Al Ali, Sofianne Gabrielli, Ann Clarke, Judy Morris, Jocelyn Gravel, Rod Lim, Edmond Chan, Ran Goldman, Andrew O, Jennifer Gerdts, Derek Chu, Julia Upton, Elana Hochstadter, Adam Bretholz, Christine McCusker, Xun Zhang, Shira Benor, Elinor Simons, Elissa Abrams, Jennifer Protudjer, Moshe Ben-Shoshan
Journal: Journal of Allergy and Clinical Immunology (2022)