tbuckley/cabot-search huggingface dataset:
Response to Letter Regarding Article, “Effect of Warfarin Treatment on Survival of Patients With Pulmonary Arterial Hypertension (PAH) in the Registry to Evaluate Early and Long-Term PAH Disease Management (REVEAL)”
Authors: Ioana R. Preston, Kari E. Roberts, Dave P. Miller, Ginny P. Sen, Mona Selej, Wade W. Benton, Nicholas S. Hill, Harrison W. Farber
Journal: Circulation (2016)

We thank Nikpour et al for highlighting their observational, retrospective study, which suggested, in a multivariate analysis, that anticoagulation of at least 6 months was associated with improved survival in connective disease-associated pulmonary arterial hypertension (PAH). 1 Their results, indeed, are contrary to our US-based (Registry to Evaluate Early and Long-Term PAH Disease Management [REVEAL]) and the EU-based (Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension [COMPERA]) databases, 2,3 both of which suggested lack of (or even possible harm with) anticoagulation in this high-risk population.Acknowledging that these analyses are limited by the lack of randomization, the study by Ngian et al also suffers from several flaws: lack of definition of survival analysis (start at entry in the database, initial diagnosis, or warfarin start); timing of initiation of anticoagulation (at diagnosis, at entry into the database, or later); level of anticoagulation achieved (international normalized ratio); and length of treatment with anticoagulation and tolerability.We also noted that most patients receiving warfarin were receiving combination therapy for PAH, another independent variable in the study by Ngian et al that was associated with improved survival.Most importantly, the lack of information on the start of warfarin therapy raises the possibility of immortal time bias, an issue also raised in the data from the COMPERA report.By examining only new warfarin starts, applying the comprehensive REVEAL score to account for disease severity, and detailing the level (international normalized ratio) and length of anticoagulation, we believe our study accounted for many of the possible confounding factors that limit a database analysis.Acknowledging the unanswered questions and limitations of all the reports to date regarding chronic anticoagulation therapy in connective disease-associated PAH, we commend Nikpour et al on initiating a prospective, randomized, placebo-controlled clinical trial using one of the newer, nonwarfarin anticoagulants.While awaiting the results of this study, we believe that the weight of current evidence strongly implies that warfarin is potentially detrimental in patients with connective disease-associated PAH and that it should not be used in these patients in the absence of strong indications, such as documented thromboembolic disease.
Factors That Promote the Development of Human Breast Cancer
Authors: David B. Thomas
Journal: Environmental Health Perspectives (1983)

Epidemiologic and endocrinologic studies of breast cancer etiology are reviewed in the context of the Moolgavkar two-stage model for mammary carcinogenesis. Promoters are hypothesized to enhance the growth of stem and intermediate cells, and initiators are assumed to cause stem and intermediate cells to give rise to intermediate and tumor cells, respectively. Although all epidemiologic features of breast cancer can be explained in terms of the cellular events supposed by the model, the specific causes of breast cancer are largely unknown. Aberrations in endogenous steroid sex hormones most probably act as promoters, although their exact nature and etiology are unclear. Ionizing radiation is the only known initiator. The two-stage model implies that others exist and that they are responsible for both the international variation in risk of breast cancer, and its familial aggregation. Results of endocrinologic studies suggest either that aberrations in endogenous sex hormones serve as such initiators or are correlated with them, or that familial and international variations in risk are mediated by promoters.
Perioperative evaluation of a patient with abdominal aortic aneurysm
Authors: M. D. Hostetler
Journal: JAMA (1993)

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
Compensation for drug injury
Journal: BMJ (1979)

Compensation for drug injury about to change.Dissatisfaction with the present system has long been increasing, and the thalidomide tragedy provided the final push.TheRoyalCommission on Civil Liability and Compensation for PersonalInjury (Pearson Commission) was set up in 1973 to consider whether change was necessary and how it might be effected.Its 1978 report re- commended introducing strict liability in tort for injury resulting from all products, including drugs.The recommendations were in line with those produced in Europe by the EEC and the Council of Europe.The EEC has now produced a draft directive (8 December, p 1525), which will probably become law in the next few years. Existing systemAt present in the United Kingdom a person injured by a drug has two ways to attempt to claim compensation: through the law of contract or through the law of tort.Under the law of contract if a person is injured by a drug then the seller is strictly liable-the injured person does not have to prove negligence.But the injured person can make a claim only if he himself had bought the drug, and then only
Demonstration Projects
Authors: Mike Mitka
Journal: JAMA (2008)

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
Clinical Laboratory Diagnosis. Designed for the Use of Students and Practitioners of Medicine.
Journal: JAMA (1924)

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
A QUARTER CENTURY'S PROGRESS IN MEDICAL EDUCATION
Journal: JAMA (1925)

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
Placebos
Authors: P. Sedgwick
Journal: BMJ (2010)

Researchers undertook a randomised, double blind, placebo controlled trial to assess whether calcium supplementation was associated with adverse cardiovascular events.1 Healthy postmenopausal women were recruited and randomly assigned to receive five tablets a day of either 200 mg of elemental calcium or identical placebo. The occurrence of adverse cardiovascular events over a five year period was recorded. Calcium supplementation in healthy postmenopausal women was associated with increased rates of adverse cardiovascular events. Which of the following statements, if any, are true?
Abstract 2647: Analysis of the Anatomical and Electrophysiological Characteristics of Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia Accompanied by the Block in the Upper Common Pathway
Authors: Kenji Morihisa, Hiroshige Yamabe, Yasuaki Tanaka, Takashi Uemura, Hisao Ogawa
Journal: Circulation (2007)

We examined the anatomical and electrophysiological characteristic of the atrioventricular nodal reentrant tachycardia (AVNRT) accompanied by the ventriculo-atrial block during tachycardia, suggesting the presence of upper common pathway in 8 patients. Tachycardia was induced by the atrial burst and/or extrastimulation followed by the AH jump and the earliest atrial electrogram was observed at the His bundle (HB) site in all patients. The HA block was observed after gradual prolongation of the HA interval in 2 patient and abruptly in 6 patients. After administration of isoproterenol, 1:1 HA conduction was resumed in all patients. The tachycardia cycle length, AeHe interval and HeAe interval were 357±89, 275±55 and 80±44 msec, respectively. Single extrastimulus delivered from the HB site reset the tachycardia as soon as it was delivered during late diastole. However, single extrastimulus delivered from the inferior portion of the coronary sinus ostium (I-CSOS) was unable to reset the tachycardia without capturing the earliest atrial electrogram at the HB site, suggesting that atrium is not involved in the circuit. Thus, the longest coupling interval of single extrastimulus that reset the tachycardia at the HB site was significantly longer than that at I-CSOS (347±89 msec vs. 324±109 msec, p=0.012). The following return cycle after extrastimulation at the HB site did not differ from the tachycardia cycle length (357±89 msec, vs. 357±89 msec, p=NS), however, that at I-CSOS was significantly longer than the tachycardia cycle length (398±85 msec, vs. 357±89 msec, p=0.012). Catheter ablation was performed in a stepwise fashion starting at the inferior CSOS. Although the results of single extrastimulation showed that the atrial myocardium at I-CSOS was out of the reentry circuit, ablation near the I-CSOS, distant from HB site, selectively eliminated slow pathway conduction in all patients without impairment of fast pathway conduction. Conclusions: The AVNRT with upper common pathway has the characteristic of relatively long HA interval during tachycardia. Sub-atrial tissue, but not the atrium, extending from the HB site to I-CSOS forms the upper common pathway in AVNRT. It was shown that upper common pathway has an anatomical structure of a certain range.
Protocol Deviations and Reanalyses in Derivative Studies of the PREDIMED Trial
Journal: JAMA Internal Medicine (2018)

Montserrat Fitó, MD, PhD; Mònica Guxens, MD; Dolores Corella, DPharm, PhD; Guillermo Sáez, MD, PhD; Ramón Estruch, MD, PhD; Rafael de la Torre, DPharm, PhD; Francesc Francés, MD; Carmen Cabezas, MD; María del Carmen López-Sabater, DPharm, PhD; Jaume Marrugat, MD, PhD; Ana García-Arellano, PhD; Fernando Arós, MD, PhD; Valentina Ruiz-Gutierrez, PhD; Emilio Ros, MD, PhD; Jordi Salas-Salvadó, MD, PhD; Miquel Fiol, MD, PhD; Rosa Solá, MD, PhD; María-Isabel Covas, DPharm, PhD; for the PREDIMED Study Investigators
Subcellular localization of hepatitis B viral core- and X-protein during the cell cycle in human hepatoma Huh7 cells H Sirma, O Rosmorduc, D Kremsdorf and C Br�chot. INSERM U370, CHU Necker, Paris
Journal: Hepatology (1995)

Alcohol induced liver disease or alcoholic liver disease (ALD), a complex trait, encompasses a gamut of pathophysiological alterations in the liver due to continuous exposure to a toxic amount of alcohol (more than 80 g per day). Of all chronic heavy drinkers, only 15–20% develops hepatitis or cirrhosis concomitantly or in succession. Several studies revealed that inter-individual as well as inter-ethnic genetic variation is one of the major factors that predispose to ALD. The role of genetic factors in ALD has long been sought for in ethnically distinct population groups. ALD is fast emerging as an important cause of chronic liver disease in India; even in populations such as “Bengalis” who were “culturally immune” earlier. While the genetic involvement in the pathogenesis of ALD is being sought for in different races, the complex pathophysiology of ALD as well as the knowledge of population level diversity of the relevant alcohol metabolizing and inflammatory pathways mandates the need for well designed studies of genetic factors in ethnically distinct population groups. An array of cytokines plays a critical role as mediators of injury, inflammation, fibrosis and cirrhosis in ALD. We, therefore, studied the association of polymorphisms in five relevant cytokine genes with “clinically significant” ALD in an ethnic “Bengali” population in Eastern India. Compared with “alcoholic” controls without liver disease (n = 110), TNFα −238AA genotype, IL1β −511CC genotype, TGFβ1 − 509CC genotype and IL10 −592AA genotype were significantly overrepresented in ALD patients (n = 181; OR = 2.4 and 95% CI 1.2–5.5, Pgenotype = 0.042, Pallelic = 0.008; OR = 2.7 and 95% CI 1.2–5.9, Pgenotype = 0.018, Pallelic = 0.023; OR = 4.7 and 95% CI 1.7–13.1, Pgenotype = 0.003, Pallelic = 0.014; and OR = 2.2 and 95% CI 1.1–4.8, Pgenotype = 0.04, Pallelic = 0.039 respectively). Moreover a cumulative genetic risk analysis revealed a significant trend for developing ALD with an increase in the number of risk alleles on IL10 and TGFβ1 loci among alcoholics. The risk genotype of IL1β and TGFβ1 also influences the total bilirubin, albumin and alanine aminotransferase levels among alcoholic “Bengalis”. The present study is the first case–control study from Eastern India that comprehensively identified polymorphic markers in TNFα, IL10, IL1β and TGFβ1 genes to be associated with ALD in the Bengali population, accentuating the significance of genetic factors in clinical expressions of ALD.
Cytokine and Estrogen Stimulation of Endothelial Cells Augments Activation of the Surface-Bound Prekallikrein-High Molecular Weight Kininogen Complex: Implications for Hereditary Angioedema (HAE)
Authors: Kusumam Joseph, Baby G. Tholanikunnel, Allen P. Kaplan
Journal: Journal of Allergy and Clinical Immunology (2016)
Massachusetts Medical Society
Authors: E. Gilmore, B. H. Athreya
Journal: New England Journal of Medicine (1960)

TOXIC HAZARDS*Recovery after Accidental Ingestion of a Fatal Dose of Brompheniramine Tablets†Brompheniramine‡ is parabromdylamine maleate and is closely related to chlorpheniramine. Recently, there have been a few reports of its use in a number of allergic conditions.1 2 3 The only side reactions reported in these series were mild drowsiness, slight feeling of dizziness, heartburn and macular eruptions that disappeared in about three days' time. The toxic effects of various antihistamines, in general, have been known for a long time, and there have been several reports of ingestion of toxic doses of antihistamines, most with recovery but some with a . . .
Doctors Don't Believe It—Why Should You? Facts and Fallacies About Health with Practical Guidance for the Layman
Journal: JAMA (1941)

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
Intravascular erythrophagocytosis
Authors: H D Friedman, R A Dracker
Journal: JAMA (1991)

A previously healthy 8-year-old boy developed severe hemolytic anemia several days after uneventful chickenpox. He presented shortly after cold exposure with a hematocrit of 0.12, hemoglobinuria, and a white blood cell count of 26 × 10<sup>9</sup>/L. His presentation and laboratory findings strongly suggested postinfectious cold agglutinin disease of IgM type.<sup>1(pp526-527)</sup>The peripheral blood film at admission (Figure) was striking for erythrophagocytosis by 9% of 22 × 10<sup>9</sup>/L segmented neutrophils, erythrocyte agglutination, and a rosette-like arrangement of erythrocytes about segmented neutrophils. Intravascular erythrophagocytosis appears to serve as an auxiliary means of sequestering and destroying erythrocytes and occurs during excessive opsonization of intravascular erythrocytes<sup>1(pp98-101)</sup>and when splenic and hepatic macrophages are overwhelmed.<sup>2,3</sup>Nonneoplastic diseases associated with intravascular erythrophagocytosis include two types of disorders: (1) those with an abundance of altered erythrocytes (as in sickle cell crisis<sup>4</sup>and Heinz-body hemolytic anemia<sup>5,6</sup>) and (2) those
Metallothionein in Rabbit Kidneys Preserved for Transplantation
Authors: Carl Gustaf Elinder, Goran Lundgren, Monica Nordberg, Brita Palm, Magnus Piscator
Journal: Environmental Health Perspectives (1984)

Thirteen rabbits were given repeated cadmium injections to achieve cadmium concentrations in kidney cortex ranging from 0.05 to 1 mmole Cd/kg wet weight. Another four animals served as controls. One kidney from each animal was frozen directly to -70 degrees C whereas the other kidney was kept for 24 hr at +4 degrees C in a preservative (Sachs' solution) to simulate conditions for preservation of human donor kidneys before transplantation. Protein binding of cadmium, zinc and copper in kidney homogenates and the concentration of metallothionein (MT) were measured in the kidney that was frozen directly and in the kidney that had been preserved. No gross differences in either the protein binding of cadmium, zinc and copper or in the MT content were seen between the directly frozen and preserved kidneys from the same animal. This indicates that MT is not rapidly broken down in rabbit kidneys which have been preserved similarly to human donor kidneys for 24 hr in a standard preservative solution prior to a transplantation.
Clinical Cytogenetics
Authors: Park S. Gerald
Journal: JAMA (1972)

This text provides the reader with an exhaustive coverage of the human cytogenetics literature. Notwithstanding its comprehensive nature, it is couched in very elementary language. All subjects are approached with a simplicity that demands little previous knowledge on the reader's part. The first 90 pages provide background information on cell division, the postulated mechanisms producing chromosome disorders, and detailed descriptions of sex chromatin (the Barr body) and its neutrophilic equivalent (the drumstick). Most of the remaining pages are devoted to a remarkably exhaustive listing of the clinical features associated with various chromosome disorders. The incredibly comprehensive nature of this coverage is attested by the more than 1,600 literature citations in the bibliography. There are many lengthy, but highly readable tables in which the clinical findings associated with each major variety of chromosome lesion have been assembled. Given a specific cytologic abnormality, it is a simple matter to locate what has