tbuckley/cabot-search huggingface dataset:
Essen und Wissen: Eine praktische Ernährungskunde
Journal: JAMA (1949)

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
Benign Histoplasmosis
Authors: R. Leigh, H. E. Thomas
Journal: Thorax (1955)

Histoplasmosis is an infection caused by the fungus Histoplasma capsulatum.This infection may be generalized, in which case it is usually fatal, or localized to the lungs, when survival and eventual calcification of the lesions generally result.Focal lesions are also found.The disease, which occurs chiefly in the North American continent, has been reported 10 times in the United Kingdom.An eleventh case, which was probably contracted in the United States of America, is reported below.Knowledge of histoplasmosis has accrued from investigations of acute cases and research into the aetiology of unusual pulmonary lesions.Opie and McPhedran (1926) found an appreciable number of children with pulmonary radiographic shadows, previously interpreted as tuberculous, who did not react to 1 mg. of tuberculin, and this observation was repeated by many other American workers (Barnard, Amber- son, and Loew, 1931; Nelson, Mitchell, and Brown, 1938; Crimm and Short, 1939; Gass, Murphy, Harrison, Puffer, and Williams, 1941; Gass, Harrison, Puffer, Stewart, and Williams, 1943).In reviewing the chest radiographs of 53,400 men on induction to the American Forces, Long and Stearns (1943) found that both multiple and miliary calcifications were more frequent and more extensive in men from the Middle West than in men from the rest of the country.Zarafonetis and Lindberg (1941) prepared histoplasmin, and surveys of histoplasmin sensitivity were made.Palmer (1945) and Christie and Peterson (1946) suggested that the association of the histoplasmin skin test with calcification is not fortuitous, but that it indicates an infection with H. capsidatum in the past.This was supported by similar investigations (Zwerling and Palmer, 1946; Palmer, 1946; High, Zwerling, and Furcolow, 1947; Dickie and Clark, 1948).Furcolow (1949) described the isolation of H. capsulatum from soft lesions undergoing calcification in two patients with positive histoplasmin and negative tuberculin skin reactions.Schulz (1950) found a calcifying pulmonary lesion containing H. capsulatum in an infant who died of generalized histoplasmosis. DISTRIBUTIONThe original three cases of disseminated histoplasmosis were described by Darling (1906Darling ( , 1908Darling ( , 1909) ) from the Panama Canal zone.The first American case came from the State of Minnesota (Riley and Watson, 1926).Since then cases have been reported from the following countries: Anglo-Egyptian Sudan, Argentina, Australia, Austria,
Uptake of the anti-epidermal growth factor receptor (EGFR) antibody EMD 72000 in tumors of subjects with head and neck squamous cell carcinoma (HNSCC)
Authors: J. Hoffend, A. Mohammed, M. Eisenhut, F. Bosch, A. Dietz, O. Rosen, A. Kovar, D. Weber, J. Tillner, U. Haberkorn
Journal: Journal of Clinical Oncology (2004)

3043 Background: EGFR is a potential therapeutic target in HNSCC. EGFR signaling inhibitors such as EMD 72000, a humanized anti-EGFR monoclonal antibody, have shown the potential for antitumor activity in subjects with EGFR-expressing cancers. However, it is undetermined whether EGFR saturation is a prerequisite for effective treatment. Methods: Accumulation of EMD 72000 in tumors of subjects with histologically confirmed HNSCC was measured, and saturation of EGFR by a single 200-mg dose was assessed. EMD 72000 was radiolabeled with I-123 and 2 mg were administered either simultaneously with (Group A; n = 9) or 24 h after (Group B; n = 5) infusion of 198 mg unlabelled antibody. Single photon emission computerized tomography (SPECT) of the neck, and planar whole body (WB) images were acquired 0.2, 4, 24, and 48 h after injection of radiolabeled EMD 72000. Serum was collected prior to infusion of the unlabelled dose and up to72 h thereafter for determination of pharmacokinetic (PK) parameters of the total antibody. Tumor:background ratios (Tu:B) were obtained from SPECT and normalized time-activity curves for the heart, liver, and WB were obtained from planar images. Tumor expression of EGFR was determined by immunohistochemistry. Results: Fourteen subjects with stage 3 or 4 EGFR+ HNSCC participated in the study. There were no major differences in either EGFR expression or EMD 72000 PK between the study groups, and PK parameters were similar to those seen in other studies. Tumor uptake of EMD 72000 increased in both groups for 24 h. Although Tu:B was greater in group A, which indicated substantial tumor accumulation, peak Tu:B (A 2.9; B 2.4) did not differ significantly between groups. Bloodpool activities were comparable between groups; liver accumulation was slightly but not significantly lower in B. After 48 h, WB retention in A (84%) was significantly (P < 0.05) lower than in B (94%). Conclusions: Tumor accumulation of EMD 72000 suggests potential applications for this antibody in the treatment of HNSCC. However, a single 200-mg dose of EMD 72000 did not completely saturate EGFR in this study. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Merck KGaA Merck KGaA
Defining clinically insignificant prostate cancer
Authors: S. H. Woolf
Journal: JAMA (1996)

<h3>In Reply.</h3> —From a public health perspective, preventing the emergence and transmission of MDR TB in the community through the measures we described is more effective than trying to prevent the development of active TB in those individuals already infected. However, we acknowledge that managing patients infected with isoniazid- and rifampin-resistant strains of<i>Mycobacterium tuberculosis</i>, for which there is no demonstrable effective preventive therapy, is difficult and needs consideration. In answer to Dr Kirkland's questions: First, the CDC's recommendations for the management of persons exposed to MDR TB have not changed since their 1992 publication.<sup>1</sup>We continue to strongly recommend alternative preventive therapy (ie, multidrug regimens with drugs other than isoniazid or rifampin) for contacts of MDR TB patients who have (1) a high likelihood of having been infected with the drugresistant<i>M tuberculosis</i>strain and (2) a high likelihood of progressing to active TB. The possibility of preventive therapy
EIS officers: medical detectives
Authors: M. F. Goldsmith
Journal: JAMA (1990)

WHEN LISTERIOSIS struck the neonatal unit in a Costa Rican hospital about a year ago, the CDC sent Anne Schuckit, MD, to find out why. The young Epidemic Intelligence Service (EIS) officer had investigated one other major outbreak at the time, but it offered little direct guidance for how to approach the new problem. Yet she knew what to do, and no more infants in that hospital became ill. Tackling outbreaks of diseases as diverse as Schuckit's first encounter with a rapidly transmitted pathogen—which turned out to be sporotrichosis, a fungal infection—and her second, the<i>Listeria</i>bacterium, is par for the EIS course. Founding the EIS in 1951, Alexander Langmuir, MD, set up a 2-year training and service program designed to accomplish three objectives: (1) to help the CDC implement its mission to prevent and control communicable diseases, (2) to increase the number of field-trained epidemiologists in the United States,
Index to advertisers
Journal: JAMA (1974)

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
Informing physicians about promising new treatments for severe disease
Journal: JAMA (1990)

<h3>To the Editor.—</h3> In addition to its relevance regarding treatment, the article by Drs Steinbrook and Lo<sup>1</sup>is timely in regard to the issue of the dissemination of other medical intelligence to physicians. The spread of information after the recent discovery of the association between tryptophan use and the eosinophilia-myalgia syndrome is illustrative. After our initial report to the Centers for Disease Control and the New Mexico Department of Health and Environment on October 26, 1989, an article headlined "Three N.M. Women Contract Unusual Medical Syndrome" appeared in the<i>Albuquerque Journal</i>on November 7, 1989. Word quickly spread across the nation by means of newspaper reports. On November 11, 1989, after 55 cases had been reported in nine states, the Food and Drug Administration warned consumers temporarily to stop using tryptophan; on November 14, 1989, New Mexico banned the sale of the substance. Although a report<sup>2</sup>appeared
Why information?
Authors: Joseph O'Rourke
Journal: Behavioral and Brain Sciences (1999)

O'Brien &amp; Opie's admirably sharp hypothesis gains some of its force by ignoring distinctions in murky areas. I attempt to agitate the waters by suggesting that process and vehicle theories are not so different, that classicism can support a vehicle theory, and that several of the key concepts underlying their theory are less clear than depicted. The connection to information I find especially tenuous. Finally, I address the implications of their theory for unconscious thought.
PHILADELPHIA LETTER.
Journal: JAMA (1883)

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
The After-Treatment of Operations: A Manual for Practitioners and House Surgeons.
Journal: JAMA (1930)

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
Generic Substitution
Authors: Sheldon S. Stoffer
Journal: JAMA (1981)

<h3>To the Editor.—</h3> In previous correspondence (1978;240:1241) we indicated that generic drugs are often dispensed with misleading labeling. In most cases, the consumer's medication was switched to a generic drug without his knowledge or consent and a look-alike generic medication dispensed with a label bearing the brand name and occasionally a cryptic "GEq." We recently encountered a prescription with two new variations on this troublesome theme. A patient of ours was switched to a generic levothyroxine sodium preparation without her knowledge and consent. The prescription label mentioned only the brand name with the designation "GEq." Inside the bottle we found two physically different generic tablets. A side label read: "This is the same medication you have been getting; color, size, or shape may appear different." We have recently provided data demonstrating that generic levothyroxine tablets may differ substantially from each other and from a brand name product (1980;244:1704). Clearly, not
Errata
Journal: Allergy (2004)

AllergyVolume 59, Issue 11 p. 1241-1241 Free Access Errata First published: 01 October 2004 https://doi.org/10.1111/j.1398-9995.2004.00759.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat In (1), the following error was published on page 753. F. A. Puccio, N. R. Lynch, O. Noga, A. Noda, I. Hagel, E. López, R. López, L. Caraballo, D. Mercado, M.C. DiPrisco The author listing was wrong and should have read: F. A. Puccio, N. R. Lynch, O. Noya, A. Noda, I. Hagel, E. López, R. López, L. Caraballo, D. Mercado, M.C. DiPrisco In (2), the following error was published on page 788. E. Nucera, D. Schiavino, E. Pollastrini, R. Manna, M. De Lillo, A. Buonomo, C. Roncallo, G. Patriarca The author listing was wrong and should have read: E. Nucera, D. Schiavino, E. Pollastrini, R. Manna, M. Di Lillo, A. Buonomo, C. Roncallo, G. Patriarca References 1 Puccio FA, Lynch NR, Noga O, Noda A, Hagel I, López E, López R, Caraballo L, Mercado D, DiPrisco MC. Importance of including Blomia tropicalis in the routine diagnosis of Venezuelan patients with persistent allergic symptoms. Allergy 2004; 59: 753– 756. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 2 Nucera E, Schiavino D, Pollastrini E, Manna R, De Lillo M, Buonomo A, Roncallo C, Patriarca G. Tolerance induction to rofecoxib in a patient with Bartter's syndrome. Allergy 2004; 59: 788– 789. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Volume59, Issue11November 2004Pages 1241-1241 ReferencesRelatedInformation
Septic Shock
Authors: Jacob Fine
Journal: JAMA (1964)

In THIS STATEMENT I will undertake to demonstrate that when traumatic shock fails to yield to appropriate treatment, death occurs because of the injury produced by a persisting deficiency of flow in the splanchnic circulation. Furthermore, as a corollary of this proposition, evidence will be given that treatment to improve flow in this area can succeed in relieving the state of shock when all other methods fail. This thesis will be stated in the form of an argument, followed by the evidence in support of it and, finally, by a summing up in which other views are considered. <h3>The Argument</h3> The critical feature common to all forms of traumatic shock is an acute and persisting deficiency of flow through the peripheral vessels. The longer it persists, the more likely the resulting injury will become irreversible, in which case death will follow in a matter of hours. The threat to life
Cardiac complications of protein-sparing modified fasting
Authors: J. M. Brown
Journal: JAMA (1978)

Cardiovascular abnormalities developed in a patient during a proteinsparing modified fasting diet. Syncope was the complaint at the time of examination. Hypotension, persistent QT<i>c</i>interval prolongation, and a low QRS voltage were observed before the development of refractory ventricular tachycardia. At autopsy, antemortem thrombi were attached to the left ventricular endocardium and a fenestrated aortic valvule. Strick proteinsparing modified fasting is not without risk of sudden death even with close medical supervision. (<i>JAMA</i>240:120-122, 1978)
Effects of single ethanol administration on hepatic ornithine decarboxylase induction and polyamine metabolism
Authors: T TANAKA
Journal: Hepatology (1991)

The effects of a single ethanol administration on ornithine decarboxylase induction, polyamine metabolism and DNA synthesis in rat liver after partial hepatectomy were studied. Ethanol given 1 hr before partial hepatectomy at the dose of 2, 3 or 5 gm/kg body wt inhibited the increase in ornithine decarboxylase activity and that in the putrescine level in the liver 4 hr after partial hepatectomy. The hepatectomy increased the amount of ornithine decarboxylase messenger RNA expressed, and this amount was unaffected by ethanol administration. Further, ethanol did not accelerate the degradation of ornithine decarboxylase 4 hr after partial hepatectomy, indicating that the inhibition of ornithine decarboxylase activity caused by ethanol was not caused by a decrease in the ornithine decarboxylase messenger RNA level or by the acceleration of ODC degradation. The single dose of ethanol inhibited [3H]thymidine incorporation into the hepatic DNA 24 hr after partial hepatectomy. The suppression of [3H]thymidine incorporation was partially reversed by the administration of putrescine. These results suggested that ethanol inhibits the increase in ornithine decarboxylase activity after transcription, suppressing the accumulation of putrescine, which prevents DNA synthesis in response to hepatectomy. (HEPATOLOGY 1991;14:696–700.)
Increased Nitric Oxide in Exhaled Gas as an Early Marker of Lung Inflammation in a Model of Sepsis
Authors: Thomas E. Stewart, Franco Valenza, Sergio P. Ribeiro, Avraham D. Wener, George Volgyesi, J. Brendan M. Mullen, Arthur S. Slutsky
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Nitric Oxide (NO) has been implicated in the pathologic vasodilation of sepsis. Because NO can be measured in the exhaled gas of animals and humans, we hypothesized that increases in exhaled NO would occur in a septic model. Using a blinded design, 10 male Sprague-Dawley rats (300 to 400 g) were anesthetized, paralyzed, tracheotomized, and randomized (5/group) to receive an intravenous injection of either lipopolysaccharide (LPS) (Salmonella typhosa, 20 mg/kg) or placebo (equal volume of saline). Thereafter, exhaled gas was collected and measurements of NO concentration were made using chemiluminescence every 20 min for 300 min during ventilation (RR 40 breaths/min, Vt 3 ml, PEEP 0, FiO2 0.21). Another group of 10 animals (5 LPS; 5 control) were treated in the same fashion and then killed at 240 min and an arterial blood sample obtained for blood gas and TNFα determinations. Pressure volume (PV) curves were constructed and lungs removed, preserved, and submitted for histologic evaluation. LPS-treated rats had lower mean arterial pressures than the control group, p < 0.0001. No significant differences in static lung compliance and PV curves were found in the two groups. TNFα levels were greater in the LPS group (1.40 ± 0.24 ng/ml) versus control group (0.09 ± 0.04 ng/ml), p < 0.001. By contrast to the control group, exhaled NO concentration rose in all LPS-treated rats at approximately 100 min and at about 160 min reached a plateau that was 6 times greater than control levels (p < 0.0001). There was greater interstitial, airspace, and total lung injury in the LPS group (p = 0.01). Hypotension alone was not responsible for the rise in exhaled NO because no increase in NO was noted over 300 min in another two rats that did not receive LPS and that were slowly exsanguinated to maintain mean systemic arterial pressure 40 to 60 mm Hg. In two rats that were completely exsanguinated at 240 min we observed marked increases in exhaled NO concentration compared with LPS-treated rats with intact circulation. We conclude that in this model of sepsis, increases in exhaled NO concentration originate in the lungs and appear to be a relatively early marker of lung inflammation.