tbuckley/cabot-search huggingface dataset:
Definitions of Binge Drinking
Authors: William DeJong
Journal: JAMA (2003)

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
PULMONARY INFARCTION IN HEART DISEASE
Authors: Laurence E. Hines, Jordan T. Hunt
Journal: Annals of Internal Medicine (1941)

Article1 October 1941PULMONARY INFARCTION IN HEART DISEASELAURENCE E. HINES, M.D., F.A.C.P., JORDAN T. HUNT, M.D.LAURENCE E. HINES, M.D., F.A.C.P.Search for more papers by this author, JORDAN T. HUNT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-4-644 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe pathological changes of pulmonary infarction were known to Laennec, but he failed to recognize the relationship between embolism and infarction and called the condition "pulmonary apoplexy." Later, in 1856, Virchow pointed out the rôle of the embolus as the cause of lung infarcts. Over a period of many years numerous clinical, pathological, and experimental studies have established an accepted anatomical and clinical picture for pulmonary infarction. The typical pathological appearance of the lesion cannot be disputed. The necessary rôle of impaired pulmonary circulation in the development of the disease is also well established. The well known clinical syndrome seems...Reference1. HOSAI K: Pulmonary embolism and infarction, Ann. Surg., 1932, xcv, 67. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Received for publication June 25, 1940.From the Department of Medicine, Northwestern University, Chicago, Illinois. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTreatment of the Patient With Refractory Heart FailureThe Peripheral Vascular Dynamics of Bowel FunctionDie LungenembolieHerz und Kreislauf bei OperationenCor pulmonaleHerz und Kreislauf bei OperationenCor pulmonaleDoes Rapid Dehydration in Cardiac Decompensation Produce Thromboembolic Complications?Thromboembolic phenomena associated with rapid diuresis in the treatment of congestive heart failureDicumarol Therapy in Congestive Heart FailureIncidence of thrombo-embolic lesions accompanying myocardial infarctionIncidence of embolic or thrombotic processes during the immediate convalescence from acute myocardial infarction 1 October 1941Volume 15, Issue 4Page: 644-647KeywordsCardiovascular therapyInfarctionLesionsLungsPulmonary diseasesPulmonary embolismStroke ePublished: 1 December 2008 Issue Published: 1 October 1941 PDF downloadLoading ...
Cost-effectiveness of Screening for Lung Cancer—Reply
Authors: Jerome Reich
Journal: JAMA (2003)

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
Histology for Pathologists
Authors: Stephen S. Sternberg
Journal: Annals of Internal Medicine (1992)

Bone marrow, S.N.Wickramasinghe adipose tissue, John J. Brooks and Patricia M.Perosio bone, A. Marion Gurley and Sanford I.Roth skeletal muscle, R Reid Heffner Jr myofibroblast, Walte Schurch et al central nervous system, Gregory N. Fuller and Peter C. Burger peripheral nervous system, Carlos Ortis Hidalgo and Roy O'weller blood vessels, Patrick J.Gallagher normal heart, Margaret E. Billingham reactive lymph nodes, Paul van der Valk and Chris J.L.M. Meijer spleen, J.H.J.M. van Kricken and J.te Velde thymus, Saul Suster and Juan Rosai pituitary and sellar region, P.J. Pernicone et al thyroid, Virginia A. LiVolsi parathyroid glands, Graziella M. Abu Jawdeh and Sanford I.Roth adrenal gland, J.Aidan Carney neuroendocrine system, Ronald A. DeLellis and Yogeshwar Dayal paraganglia, Arthur S. Tischler noral skin, Carlos Urmacher nail, Julian Sanchez Conejo-Mir periodontiu, Minor salivary glands and maxillary sinus, Kenneth D. McClatchey larynx and pharynx, Robert E. Fechner major salivary glands, Fernando Martinez Madrigal and Christian Micheau lungs, Thomas V. Colby and Samuel A. Yousem serous membranes, Darryl Carter et al esophagus, Franco G. DeNardi and Robert H. Riddell stomach, David A. Owen small intestine, Glenn H.Segal and Robert E. Petras colon, Douglas S. Levine and Rodger C. Haggitt vermiform appendix, H. Glenn et al anal canal, Claus Fenger liver, N. Swan et al gallbladder and extrahepatic biliary system, Henry F. Frierson Jr pancreas, James E Oertel et al pediatric kidney, J. Bruce Beckwith adult kidney, urinary bladder and ureter, Victor E. Reuter penis, Jose Barreto et al testis and excretory duct system, Thomas D.Trainer prostate, John E. McNeal ovary, Philip B. Clement uterus, cervix and fallopian tube, Michael R Hendrickson and Richard Kempson placenta, Steven H. Lewis and Kurt Benirschke vulva, Edward J. Wilkinson and Nancy Hardt vagina, Stanley J. Robboy et al breast, Kenneth S. McCarty, Jr and J. Allen Tucker normal eye and ocular adnexa, Mark W. Scroggs and Gordon K. Klintworth ear, Leslie Michaels.
Organization of the Mammalian Metabolome according to Organ Function, Lineage Specialization, and Longevity
Authors: Siming Ma, Sun Hee Yim, Sang-Goo Lee, Eun Bae Kim, Sang-Rae Lee, Kyu-Tae Chang, Rochelle Buffenstein, Kaitlyn N. Lewis, Thomas J. Park, Richard A. Miller, Clary B. Clish, Vadim N. Gladyshev
Journal: Cell Metabolism (2015)
Urologie des praktischen Arztes.
Authors: Felix Schlagintweit
Journal: JAMA (1933)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Latent Myeloproliferative Neoplasm May Underlie Retinal Vein Occlusion In Older Patients
Authors: Katerina Zoi, Christine Zoi, Andreas Giannopoulos, Argyri Gialeraki, Kassiani Giannaki, Niki Rougkala, Panagiotis Theodosiadis, John Vergados, Dimitris Loukopoulos, Nicholas C.P. Cross, Marianna Politou
Journal: Blood (2013)
Abstract 3654: The role of structure-specific endonuclease MUS81 in the induction of cytosolic DNA in tumor cells
Authors: Samantha Ho, Stephan Gasser
Journal: Cancer Research (2014)

Abstract Genomic DNA is constantly damaged by endogenous and exogenous agents. The DNA damage response (DDR) is vital for recognizing DNA damage and instigating DNA repair reactions to ensure genome stability. MUS81 is a structure-specific endonuclease that is required for resolving stalled replication forks at sites of DNA damage to initiate Homologous Recombination repair. Our preliminary data suggests that the potentially detrimental DNA structures cleaved by MUS81 accumulate in the cytosol of many tumor cells. Furthermore, we found that DNA cleaved by MUS81 induces type I interferon expression in a STING-dependent manner, and initiates an innate immune response in vivo. Cytosolic DNA in tumor cells was also abrogated upon inhibition of DNA damage sensors, ATM/ATR and PARP1. In addition, genetic inhibition of Mus81 in different tumor cells lines impaired expression of cytosolic DNA and type I interferon. In summary, our data suggest that the structure-specific endonuclease MUS81 cleaves damaged nuclear DNA leading to accumulation of genomic DNA in the cytosol of tumor cells, activating immunosurveillance mechanisms. Citation Format: Samantha Ho, Stephan Gasser. The role of structure-specific endonuclease MUS81 in the induction of cytosolic DNA in tumor cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3654. doi:10.1158/1538-7445.AM2014-3654
Commentary: Lessons on functional diseases
Authors: Samy A Azer
Journal: BMJ (2006)

Kenneth Neville's case raises the question whether we should teach general practitioners and medical students about functional oesophageal disorders.1 This question is particularly important now that most medical schools are implementing a problem based or case based curriculum. The philosophy of these courses is to focus on key concepts and reduce detail in the subject matter. Conditions such as rumination syndrome will not be considered important and will be omitted.

Interestingly, major medical textbooks also show a deficiency in this area. For example, the last editions of Harrison's Principles of …
Retrofit Particle Traps Reduce Exposure to Fine Particulate Air Pollution and Prevent Vascular Dysfunction in Man
Authors: Nicholas L. Mills, Magnus Lundback, Stefan Barath, Andrew J. Lucking, Jeremy P. Langrish, Ken Donaldson, Nicholas A. Boon, Thomas Sandstrom, Anders Blomberg, David E. Newby
Journal: Journal of the American College of Cardiology (2009)
Evidence base of clinical diagnosis: Rational, cost effective use of investigations in clinical practice
Authors: R. Winkens
Journal: BMJ (2002)

The relation of carbon disulphide (CS2) exposure to risk factors for ischaemic heart disease was recently examined using data from a 1979 cross sectional study of 410 male textile workers, of whom 165 were exposed and 245 were unexposed to CS2. Average eight hour CS2 exposure concentrations ranged from 0.6 to 11.8 ppm by job title category among the exposed workers. A significant and positive linear trend in low density lipoprotein cholesterol concentration (LDLc) and diastolic blood pressure with increasing CS2 exposure was found after adjustment for potential confounders. When exposure was examined as a categorical variable (none, low, moderate, and high), the high exposure group had an adjusted mean LDLc that was 0.32 mmol/l greater than the non-exposed group (p = 0.02), and an adjusted mean diastolic blood pressure that was 3.16 mm Hg greater than the non-exposed group (p = 0.09). The effect of CS2 on diastolic blood pressure was strengthened in analyses limited to exposed workers: the high exposure group had an adjusted mean diastolic blood pressure that was 5 mm Hg greater than that of the low exposed group (p = 0.03). Triglyceride, high density lipoprotein cholesterol, and fasting glucose concentration, and systolic blood pressure were not affected by exposure. Blood lead concentration was positively associated with systolic and diastolic blood pressure. The results indicate that relatively modest exposure to CS2 may raise LDLc concentration and diastolic blood pressure and suggest mechanisms by which exposure to CS2 may influence risk of ischaemic heart disease. Also the results provide further support for the hypothesis of a possible association between blood lead concentration and blood pressure.
Clinical Concepts of Infectious Diseases.
Authors: Leighton E. Cluff, Joseph Eggleston Johnson
Journal: Annals of Internal Medicine (1978)

This volume is an update and expanded sequel to the first edition, published in 1972.It tries to offer a "perspective of the approaches important for thinking about problems in infectious diseases and caring for patients".In keeping with this objective, this book is not a "cookbook" dealing with all the eventualities of the field of clinical infectious disease.The editors have devoted the first eight chapters to basic host defences, microbial virulence factors, and the interaction of the two that leads to clinically apparent disease.A new chapter on clinical epidemiology clarifies this approach to disease states for the nonepidemiologist.The ensuing six chapters deal with the signs and symptoms by which various infectious agents may be suspected clinically, including acute and prolonged fever, septic shock, and the dermatologic and hematologic manifestations of infection.A review of the many factors that influence the rate of recovery from infection raises useful points for evaluation of patients' response to therapy.Thirteen chapters detail selected problems in clinical infectious diseases, which include viral respiratory infections, infectious mononucleosis, acute and chronic pulmonary infections, urinary tract infections, hepatitis, meningitis and endocarditis.New to this volume are chapters
Abstract 14842: Satellite Based Urban Land Cover and Proximity to Urban Center are Independent Predictors of Hypertension in a Southeast Asian Population
Authors: Mohan Thanikachalam, Kevin J Lane, Jahnavi Sunderarajan, Vijaykumar Harivanzan, Sadagopan Thanikachalam
Journal: Circulation (2014)

Background: Urbanization is linked to higher prevalence of cardiovascular disease (CVD). Hypertension (HTN) is a major risk factor for CVD. In this study we assess the impact of urbanization on prevalence of HTN in a population-based study in South India. Methods: In the cross-sectional analysis 8080 participants (mean age 42 years; 58% women) spread over 65 x 80 km area constituted the study sample. MODIS satellite derived land cover data at a 1 km x 1 km resolution was obtained and joined to each participant’s geolocated residential position in ArcGIS to assign urban and rural (crops, trees, shrubs and grass land cover) designations. Simultaneously, participants’ residential position in relation to urban center was assessed. The study included sytolic (SBP) and diastolic (DBP) blood pressure, anthropometric, socioeconomic, psycosocial, physcial activity assessemnts and blood work. HTN was defined as SBP ≥ 140 or DBP ≥ 90 or reported history of HTN. Results: Based on the land cover data the mean SBP and DBP (mmHg) in men (SBP: 131 ± 21; DBP: 81 ± 12) and women (SBP: 125 ± 20; DBP: 77 ± 11) living in urban environment were significantly higher when compared to men (SBP: 122 ± 18; DBP: 77 ± 11) and women (SBP: 117 ± 18; DBP: 74 ± 10) in rural environments [p &lt; 0.001]. There was a significantly higher prevalence of HTN in urban men (42.1%) when compared to rural men (26.4%) [p &lt; 0.001]. Similarly, the prevalence of HTN was higher in urban women (28.3%), when compared to rural women (19.1%) [p &lt; 0.001]. After controlling for age, BMI, smoking, blood sugar, LDL and socioeconomic, physical activity, anxiety and stress levels, both men (OR = 1.94; 95% CI: 1.64, 2.9) and women (OR = 1.51; 95% CI: 1.28, 1.8) living in urban land cover were more likely to have HTN compared to those living in non-urban land cover. In the proximity analysis after multivariate adjustments, men (OR = 2.25; 95%CI: 1.78, 2.83) and women (OR = 1.87; 95%CI: 1.47, 2.38) residing within 0-20 km distance from urban center had significantly higher odds of HTN than the 60-80 km reference group. Conclusions: Living in an urban environment is associated with increased prevalence of HTN independent of other risk factors. Future research is needed to determine what components of the urban environment contribute to increased levels of HTN.
Abstract 3135: Impact Of PCI On The Clinical Burden Of Atherothrombotic Disease. An Analysis From The NHLBI Dynamic Registry
Authors: Warren K Laskey, Faith Selzer, Evan Mokwe, David Holmes, Spencer King, Howard Cohen, James Slater, Jean-Francois Tanguay, Elizabeth Holper, David Williams, Katherine Detre
Journal: Circulation (2007)

Introduction . The addition of percutaneous coronary intervention (PCI) to the treatment options for patients with atherothrombotic (AT) coronary heart disease (CHD) has resulted in considerable debate regarding its overall clinical benefit. Although rates of “hard” clinical endpoints have been used as measures of both clinical outcome and disease burden, a comprehensive, clinically relevant measure of disease burden in the general population of patients undergoing PCI is lacking. Hypothesis . A comprehensive measure of AT clinical burden in patients undergoing PCI can be used to detect the qualitative and quantitative impact of PCI over time. Methods . Four distinct cohorts (Waves) of ~ 2,000 patients each participating in the NHLBI Dynamic Registry beginning in 1997 (Wave 1) and terminating in 2005 (Wave 4) and surviving to hospital discharge comprise the study population (n= 7,750). A composite clincally relevant measure of AT disease burden over the year following PCI was defined as: any death, myocardial infarction (MI), hospitalization for recurrent angina (A) or congestive heart failure (HF), stroke, any repeat PCI or coronary bypass surgery. Cumulative event rates, expressed as the presence of any of the above-cited components by one year, were calculated using Kaplan-Meier statistics. Comparison of rates across Waves was accomplished using Cochran- Mantel-Haenszel method. Results. see Table Exclusion of patients requiring PCI for restenosis did not substantially change the overall AT burden. Conclusion. There was a statistically significant decrease in AT disease burden over the time studied. However, the burden of disease in patients undergoing PCI remains substantial for 25% of patients. This measure of AT burden may be of clinical value in assessing the contribution of PCI to patient outcomes and strongly supports more comprehensive treatment strategies for patients following PCI. Component and composite rates at one year
Diagnostic Recognition of Genetic Disease.
Authors: William L. Nyhan, Nadia A. Sakati
Journal: Annals of Internal Medicine (1988)

This book discusses the diagnosis and management of genetically determined diseases. Genetics are also discussed, but the major focus is on diagnosis. Patients with genetically determined disorders have clinical pictures that cross most of the boundaries of subspecialty practice, and are frequently seen by a variety of physicians. The pediatrician will often be the first to come in contact with these patients, but internists are increasingly concerned with these patients, especially those with inborn errors of metabolism. The hematologist may be the first to see a patient with Fanconi anemia, and the gynecologist, the patient with Turner's syndrome. In brief this book emphasizes the diagnosis of various genetic diseases in relation to different medical specialties.
Clinical and immunological determinants of severe/refractory asthma (SRA): association with Staphylococcal superantigen-specific IgE antibodies
Authors: M. L. Kowalski, M. Cieślak, C. A. Pérez-Novo, J. S. Makowska, C. Bachert
Journal: Allergy (2010)

To cite this article: Kowalski ML, Cieślak M, Pérez-Novo CA, Makowska JS, Bachert C. Clinical and immunological determinants of severe/refractory asthma (SRA): association with Staphylococcal superantigen-specific IgE antibodies. Allergy 2011; 66: 32–38. Background: Demographic and immunological determinants of severe refractory asthma (SRA) are not well characterized. Because Staphylococcus aureus enterotoxins with superantigenic activity have been associated with upper and lower airway inflammation, we aimed to evaluate the association of sensitization to Staphylococcal enterotoxins with asthma severity and various asthma phenotypes. Methods: The study included 109 patients with SRA diagnosed according to the American Thoracic Society Workshop 2000, and 101 patients with nonsevere asthma, followed for at least 12 months. Specific IgE to Staphylococcus enterotoxins and total IgE and eosinophil cationic protein concentrations were measured in serum with immunoassays. Findings: A significant risk for severe asthma was associated with female gender [Odds Ratio (OR) = 2.04], history of wheezing in childhood (OR = 2.47), presence of hypersensitivity to aspirin (OR = 1.96) and with body mass index (OR = 3.08). The mean level of enterotoxin-specific IgE was 3-fold higher in patients with severe asthma when compared to patients with nonsevere asthma (P = 0.01). Serum-specific IgE to enterotoxins was significantly associated with low respiratory function parameters (FEV1, FEV1/FVC and MEF 25/75) and increased airway reversibility in response to albuterol. The presence of specific IgE to enterotoxin carried a significant risk for patients to have serum total IgE level above 100 kU/l (OR = 7.84). Interpretation: Specific immunological response to enterotoxins is associated with clinical and immunological parameters of asthma severity, suggesting a role for Staphylococcal enterotoxins in the asthma pathogenesis.