tbuckley/cabot-search huggingface dataset:
TULAREMIC PNEUMONIA
Authors: P. G.  BOMAN, A. J.  BIANCO
Journal: Annals of Internal Medicine (1934)

Article1 June 1934TULAREMIC PNEUMONIAP. G. BOMAN, M.D., A. J. BIANCO, M.D.P. G. BOMAN, M.D.Search for more papers by this author, A. J. BIANCO, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-7-12-1491 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptUntil recently many observers have considered the presence of pneumonia in cases of tularemia as an intercurrent infection. Several published necropsy reports refer to more or less extensive bronchopneumonia without directly attributing it to the tularemic infection.Permar and MacLachlan,1in reviewing the reported fatal cases, found that 36 per cent showed pneumonia either clinically or at autopsy and that in 62.5 per cent of the autopsied cases there was diffuse pneumonic involvement. In correlating the pathological reports in published cases with their own observations they believe that tularemic pneumonia presents morphologic changes which are specific for tularemia. These morphologic...Bibliography1. PERMARMACLACHLAN HHWW: Tularemic pneumonia, ANN. INT. MED., 1931, v, 687-698. Google Scholar2. FRANCIS E: Symptoms, diagnosis and pathology of tularemia, Jr. Am. Med. Assoc., 1928, xci, 1155-1161. CrossrefGoogle Scholar3. SANTE LR: Pulmonary infection in tularemia, Am. Jr. Roentgenol., 1931, xxv, 241-242. Google Scholar4. TUREEN LL: Tularemic pneumonia, Jr. Am. Med. Assoc., 1932, xcix, 1501-1502. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Duluth, Minnesota*Read before the Minnesota Society of Internal Medicine, May 15, 1933.From The Duluth Clinic and St. Mary's Hospital. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1934Volume 7, Issue 12Page: 1491-1495KeywordsAutopsyPneumoniaTularemia ePublished: 1 December 2008 Issue Published: 1 June 1934 PDF downloadLoading ...
Viral gastroenteritis
Authors: A. Z. Kapikian
Journal: JAMA (1993)

<h3>SELECTED CASE</h3> An 11-month-old male infant was admitted to the Children's Hospital National Medical Center in Washington, DC, with vomiting and diarrhea. The patient was well until 3 days prior to admission when he had the onset of vomiting ("many times") that was accompanied over the next 2 days with diarrhea (with a maximum of six loose stools per day) and fever, with a maximum rectal temperature of 40.5°C. Physical examination on the day of admission showed a febrile, mildly dehydrated (=5%), irritable but not lethargic infant who had an essentially normal oropharynx, ears, lymph nodes, lungs, and abdomen. While in the hospital, the patient became afebrile the day after admission, did not vomit, but had diarrhea for the first 2 days after admission (two loose stools each day). The illness was managed by restriction of food and oral fluids for about 25 hours, when clear fluids were allowed, and
Shall The Journal be Removed to Washington?
Authors: J. H. Davisson
Journal: JAMA (1891)

<h3>To the Editor:</h3> —Permit me, as a member of the American Medical Association since 1877, to interpose my decided opposition to the removal ofThe Journalto Washington or anywhere East. From my standpoint I cannot see any good reasons for the change, while to the contrary, many sufficient reasons have already been suggested, by many members from different points of the compass, why it<i>should not</i>be removed to Washington, but should remain in the great central interior city of Chicago, where it first saw the light, and where it has served us so well. Los Angeles, Cal., Feb. 19, 1891.
SOCIOLOGY OF MEDICINE
Journal: JAMA (1967)

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
"Halothane Hepatitis"
Authors: Thomas S. Morley
Journal: JAMA (1973)

<h3>To the Editor.—</h3> I was pleased to see Dr. Mathieu's timely and scholarly rebuttal of Dr. Schaffner's unimpressive efforts to diagnose the, as yet, mythical phenomenon, known as "halothane hepatitis."<sup>1</sup>It must be reassuring to many anesthetists to learn that current immunological tests do not indicate the existence of a specific toxic hepatitis due to halothane. Similarly, clinical and pathological data, when unbiased, indicate that "halothane hepatitis" and acute viral hepatitis are indistinguishable. Special mention should be made of clinical and laboratory evidence of "hypersensitivity" such as skin rashes, arthralgias, and eosinphilia, which have been used by "halothane hepatitis" protagonists in an attempt to delineate this supposed condition (<i>Medical Letter</i>, June 9, 1972). Little do they realize, apparently, that<i>all</i>these features are excellent diagnostic indicators of acute viral hepatitis!<sup>2,3</sup> The epidemiology of postoperative hepatitis also hardly points towards the existence of a distinct "halothane hepatitis." Repeated large
Effect of genetic counselling on the prevalence of Huntington's chorea
Authors: C O Carter, M Baraitser
Journal: BMJ (1983)

of age, intercurrent disease, and tumour staging, results in a hospital mortality nearer 10% as shown in several recent British studies.24Indeed, in the latter quarter of the Lancaster series mortality has been reduced to 7o% with no sig- nificant variation according to cell type.5
Do polyunsaturated fatty acids ameliorate hepatic steatosis in obese mice by SREPB-1 suppression or by correcting essential fatty acid deficiency
Authors: Naoya Yahagi, Motohiro Sekiya, Hitoshi Shimano
Journal: Hepatology (2004)

Alwayn et al. insightfully argue that the high value of mead acid (20:3 n-9) / arachidonic acid (20:4 n-6) ratio (M/A) in livers from our animals indicates severe deficiency in essential fatty acids, and that the model we employed is therefore close to hepatic steatosis due to essential fatty acid deficiency (EFAD). It depends on how one defines EFAD considering that M/A > 0.4 could be another criterion.1 Overall, EFAD animal models are generally made by feeding them for several weeks diets without essential fatty acids, while the duration is only one week in our protocol for ob/ob mice. In fact, according to our preliminary data, feeding with the basal fat-free diet one week was not long enough to see an appreciable increase in liver triglyceride contents in C57BL/6J mice. Besides, it has been well established that fatty livers observed in ob/ob homozygous mice are caused by increased lipogenesis mediated through sustained activation of SREBP-1c,2 which presumably originates from hyperphagia. Thus, it is unlikely that EFAD played a major role in the development of steatosis in our ob/ob model. However, this does not exclude the possibility that SREBP-1 could be involved in the pathogenesis of steatosis associated with EFAD. Fat-free diet is a key factor for maximum dietary induction of SREBP-1c and essential fatty acids specifically suppress the expression of mature SREBP-1 protein as others and we previously showed.3 It is plausible that EFAD induces hepatic SREBP-1c, which contributes to the development of steatosis.
Manual of Chemistry. A Guide to Lectures and Laboratory Work for Beginners in Chemistry. A Text-book specially adapted for Students of Pharmacy and Medicine.
Journal: JAMA (1898)

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
Urinary Excretion of Vanilmandelic Acid in Patients with Arterial Hypertension
Journal: JAMA (1963)

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
Adenylate-Cyclase VI Transforms Ventricular Cardiomyocytes Into Biological Pacemaker Cells
Authors: Arjang Ruhparwar
Journal: Circulation (2007)

Abstract 1744 Arjang Ruhparwar, Klaus Kallenbach, Univ of Heidelberg, Heidelberg, Germany; Gunnar Klein, Mahyar E Makoui, Christoph Bara, Hannover Medical School, Hannover, Germany; Daniel C Sigg, Medtronic Inc., Minneapolis, MN; Axel Haverich, Hannover Medical School, Hannover, Germany; Matthias Karck, University of Heidelberg, Heidelberg, Germany; Michael Niehaus, Hannover Medical School, Hannover, Germany Arjang Ruhparwar, 2007 Finalist and Presenting Author
Contents
Authors: Vladimir Lenin, S Friedman, E Larrea, I Echeverria, Jose-I.-I Riezu-Boj, R Aldabe, L Guembe, I Sola, M Civeira, P Sarobe, J Prieto, A Lok, D Gardiner, C He ´zode, E Lawitz, M Bourlie, ` Re, G Everson, P Marcellin, M Rodriguez-Torres, S Pol, L Serfaty, T Eley, S.-P Huang, J Li, M Wind-Rotolo, F Yu, F Mcphee, D Grasela, C Pasquinelli, L Allweiss, T Volz, M Lu, K Giersch, T Bornscheuer, A Lohse, J Petersen, H Ma, K Klumpp, S Fletcher, M Dandri, C Chasela, A Kourtis, P Wall, J Drobeniuc, C King, H Thai, E Teshale, M Hosseinipour, S Ellington, M Codd, D Jamieson, R Knight, P Fitzpatrick, S Kamili, I Hoffman, D Kayira, N Mumba, D Kamwendo, F Martinson, W Powderly, C.-G Teo, C Van Der Horst, V Mom, Z.-H Lu, X.-W Liao, Y Han, C Pichoud, Q.-M Gong, D.-H Zhang, Y Zhang, P Deny, F Zoulim, X.-X Zhang, W Yi, C Pan, J Hao, Y Hu, M Liu, L Li, D Liang, Z Younossi, M Singer, H Mir, L Henry, S Hunt, M Helbig, L Mancke, S Polywka, J Pollok, J Taylor, M Jover-Cobos, L Noiret, K Lee, V Sharma, A Habtesion, M Romero-Gomez, N Davies, R Jalan, C Bosoi, C Zwingmann, H Marin, C Parent-Robitaille, J Huynh, M Tremblay, C Rose, S Augustin, L Milla, A Gonza ´lez, M Martell, A Gelabert, A Segarra, X Serres, R Esteban, J Genesca, E Levesque, F Saliba, D Samuel, O Guillaud, J Dumortier, R Sobesky, D Debray, P Wolf, C Vanlemmens, F Durand, Y Calmus, C Duvoux, S Dharancy, N Kamar, K Boudjema, P Bernard, G.-P Pageaux, E Salame, J Gugenheim, A Lachaux, D Habes, S Radenne, J Hardwigsen, O Chazouille, ` Res, J.-M Trocello, F Woimant, P Ichai, S Branchereau, O Soubrane, D Castaing, E Jacquemin, J.-C Duclos-Valle, L Xu, S Beckebaum, S Iacob, G Wu, G Kaiser, A Radtke, C Liu, I Kabar, H Schmidt, V Cicinnati, N Razumilava, S Gradilone, R Smoot, J Mertens, S Bronk, A Sirica, G Gores, F Turati, D Trichopoulos, J Polesel, F Bravi, M Rossi, R Talamini, S Franceschi, M Montella, A Trichopoulou, C Vecchia, P Lagiou, L Grønbaek, H Vilstrup, P Jepsen, C Schramm, I Wahl, C Weiler-Normann, K Voigt, C Wiegard, C Glaubke, E Bra ¨hler, B Lo, M Rose, D Raptis, P Limani, J Jang, U Ungethu, C Tschuor, R Graf, P.-A Clavien, L Pawella, M Hashani, E Eiteneuer, M Renner, R Bartenschlager, P Schirmacher, B Straub
Journal: Journal of Hepatology (2014)
Star Treatment
Authors: Irvin S. Bauer
Journal: Annals of Internal Medicine (1999)

On Being a Patient2 March 1999Star TreatmentIrvin S. BauerIrvin S. Bauer82 West 12th Street; New York, NY 10011 (Bauer)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-5-199903020-00019 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I wet my bed. That's how it all starts. “It was an accident,” I tell myself. I am embarrassed. No more water before bed; maybe I was drinking too much beer. I am resolved. I am good. In the morning … the bed is wet. Peeing in the bed? Humiliation. Hide it from my wife. Put a towel down. Stay on my side. Don't turn. Give up sleep. Mention it to one of my pals, boyhood friend, like a brother, big-time CEO.“Go to see my doctor. We've just given him a big grant. He's been anointed by a major ... Author, Article, and Disclosure InformationAffiliations: 82 West 12th Street; New York, NY 10011 (Bauer)Corresponding Author: Irvin S. Bauer, 82 West 12th Street, New York, NY 10011. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByLife on the Receiving End: A Qualitative Analysis of Health Providers??? Illness Narratives 2 March 1999Volume 130, Issue 5Page: 447-449KeywordsBladderBloodCystoscopyEjaculationHematologic testsHemorrhagePenisShouldersUltrasound imagingUrine Issue Published: 2 March 1999 CopyrightCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Contents
Authors: W Lohse, K Takano, M Tsukiyama-Kohara, Y Hayashi, M Hirata, Y Satoh, C Tokunaga, Y Tateno, T Hayashi, N Hishima, M Funata, M Sudoh, M Berzsenyi, D Woollard, C Mclean, S Preiss, V Perreau, M Beard, D Bowden, B Cowie, S Li, A Mijch, S Roberts, C Virus Infec- Tion Zeremski, G Hooker, M Shu, E Winkelstein, Q Brown, D Des Jarlais, L Tobler, B Rehermann, M Busch, B Edlin, A Talal, C Manns, S Zeuzem, A Sood, Y Lurie, M Cornberg, H Klinker, P Buggisch, M Rössle, H Hinrichsen, I Merican, Y Ilan, S Mauss, S Abu- Mouch, A Horban, T Müller, C Welsch, R Chen, R Faruqi, L Pedicone, H Wedemeyer, Encephalopathy Guevara, M Baccaro, B Gómez-Ansón, G Frisoni, C Testa, A Torre, J Molinuevo, L Rami, G Pereira, E Sotil, J Córdoba, V Arroyo, P Ginès
Journal: Journal of Hepatology (2011)
Correction: Ipilimumab plus nivolumab for patients with metastatic uveal melanoma: a multicenter, retrospective study
Authors: Charles Ferte, Benjamin Frey, Markus Hecht, Rainer Fietkau, Nora Sundahl, Florian Putz, Andrea Lancia, Angela Rouyar, Marina Milic, Alexandre Carré, Enzo Battistella, Emilie Alvarez Andres, Stéphane Niyoteka, Edouard Romano, Jérôme Durand-Labrunie, Sophie Bockel, Rastilav Bahleda, Charlotte Robert, Celine Boutros, Maria Vakalopoulou, Nikos Paragios, Piet Ost, Udo Gaipl
Journal: Journal for ImmunoTherapy of Cancer (2020)
Withdrawal of antihypertensive therapy
Authors: S. G. Chrysant
Journal: JAMA (1978)

<h3>To the Editor.—</h3> We read with some concern the article "Withdrawal of Antihypertensive Therapy: Hypertensive Crisis in Renovascular Hypertension" by Strauss et al (238:1734, 1977). Our experience with clonidine hydrochloride in both essential and renovascular hypertension has been different in the sense that under controlled circumstances we have not seen any arterial pressure overshoot on sudden clonidine withdrawal after short-term and long-term clonidine administration (235:2717, 1976). While a withdrawal syndrome may well occur, it would be interesting to know whether the drug or the patient was unique. Further, we wonder what percentage these three cases represent among all hypertensive patients managed similarly. Our<sup>1</sup>studies in experimental animals have shown that when clonidine is given, even in small amounts, into a peripheral vascular bed, it produces vasoconstriction secondary to its α-adrenergic receptor agonistic effects. Yet, when it is given systemically, the peripheral effect is outweighed by the central effect,<sup>2</sup>
Introduction
Journal: JAMA (1992)

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
Blood Glucose and Coronary Artery Disease in Nondiabetic Patients
Authors: Christopher Nielson, Theodore Lange, Nicholas Hadjokas
Journal: Diabetes Care (2006)

OBJECTIVE—Nondiabetic patients were studied to determine whether modest elevations in blood glucose may be associated with a greater incidence of coronary artery disease (CAD). RESEARCH DESIGN AND METHODS—Baseline morning blood glucose determinations were evaluated with respect to subsequent coronary disease using records from 24,160 nondiabetic patients. CAD was identified from myocardial infarction, new diagnoses of angina, or new prescriptions for nitroglycerin that occurred more than a year after baseline glucose determinations. RESULTS—Of 24,160 patients studied, 3,282 patients developed CAD over a total analysis time at risk of 77,048 years. Higher baseline morning glucose (100–126 vs. &amp;lt;100 mg/dl) was associated with a 53.9% greater myocardial infarction incidence rate, an 18.6% greater acute coronary syndrome incidence rate, and a 26.4% greater number of new prescriptions for nitrates (all P &amp;lt; 0.05). A Cox proportional hazards model with adjustment for age, BMI, sex, creatinine, lipids, smoking, and medications showed that elevated fasting glucose was associated with an increased hazard for new CAD (hazard ratio 1.13 [95% CI 1.05–1.21], glucose &amp;gt;100 vs. &amp;lt;100 mg/dl). Kaplan-Meier analysis showed that elevated baseline glucose was associated with a progressive increase risk of CAD with time. CONCLUSIONS—Patients with higher baseline blood glucose levels in the absence of diabetes and after adjustment for covariants have a significantly greater risk for development of CAD.
Myoglobinuria following aminocaproic acid administration
Authors: R. A. Rizza
Journal: JAMA (1976)

<h3>To the Editor.—</h3> ε-Aminocaproic acid (EACA), a specific inhibitor of plasminogen activation, was originally used in low dosage as an antifibrinolytic agent and is now being employed in higher doses in the treatment of hereditary angioneurotic edema. We have recently encountered a 24-year-old woman receiving high doses of EACA who had rhabdomyolysis and myoglobinuria. <h3>Report of a Case.—</h3> The patient, previously reported in detail by Little and Bell,<sup>1</sup>has had recurrent painful subcutaneous hemorrhages ascribed to DNA sensitivity for sixteen years. She was initially treated with chloroquine, but approximately seven years ago hemorrhages recurred with increasing frequency. The chloroquine regimen was discontinued, and she was treated with EACA (5 gm when she was symptomatic followed by 1 gm every hour for a maximum of 12 hours). This regimen was followed episodically, at most four to five times per month. After her most recent hemorrhage a course of continuous EACA