tbuckley/cabot-search huggingface dataset:
Clinical Prediction of Pneumonia
Authors: Michael B. Jacobs
Journal: Annals of Internal Medicine (1991)

Letters1 March 1991Clinical Prediction of PneumoniaMichael B. Jacobs, MDMichael B. Jacobs, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-114-5-428 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors:Health care costs are rising, hence the increasing emphasis on a more selective use of high-cost technologic and other ancillary testing. To assist physicians with this task, clinical prediction rules have emerged as a somewhat contrived yet potentially useful tool. At the bedrock of these rules lies the physical examination. The performance of this time-honored labor of our profession may, I fear, be rapidly becoming a lost art. This perception is reinforced by the article by Heckerling and colleagues (1), in which reference is made to a sign of pulmonary consolidation as "decreased" breath sounds. To the...Reference1. Heckerling P, Tape T, and Wigton R. Clinical prediction rule for pulmonary infiltrates. Ann Intern Med. 1990;113:664-70. LinkGoogle Scholar1. Heckerling P, Tape T, and Wigton R. Clinical prediction rule for pulmonary infiltrates. Ann Intern Med. 1990;113:664-70. LinkGoogle Scholar2. Pauker S and Kassirer J. The threshold approach to clinical decision making. N Engl J Med. 1980;302:1109-17. CrossrefMedlineGoogle Scholar1. Heckerling P, Tape T, and Wigton R. Clinical prediction rule for pulmonary infiltrates. Ann Intern Med. 1990;113:664-70. LinkGoogle Scholar1. DeGowin E and DeGowin R. Bedside Diagnostic Examination. 2d edition. New York: The MacMillan Company;1969:298. Google Scholar2. Prior J and Silberstein J. Physical Diagnosis: The History and Examination of the Patient. 4th edition. St. Louis, Missouri: The C.V. Mosby Company;1973:195. Google Scholar3. Heckerling P, Tape T, and Wigton R. Clinical prediction rule for pulmonary infiltrates. Ann Intern Med. 1990;113:664-70. LinkGoogle Scholar4. Pauker S and Kassirer J. The threshold approach to clinical decision making. N Engl J Med. 1980;302:1109-17. CrossrefMedlineGoogle Scholar5. Lee T. Evaluating decision aids: the next painful step [Editorial]. J Gen Intern Med. 1990;5:528-9. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Michael B. Jacobs, MDAffiliations: Stanford Medical Center Stanford, CA 94305 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1991Volume 114, Issue 5Page: 428-429KeywordsFearHealth carePerceptionPneumonia ePublished: 1 December 2008 Issue Published: 1 March 1991 PDF downloadLoading ...
Lowering Risk without Lowering Cholesterol: Implications for National Cholesterol Policy
Authors: Andrew L. Avins
Journal: Annals of Internal Medicine (1996)

Current recommendations for the treatment of hypercholesterolemia include drug therapy for persons at sufficiently elevated risk for coronary heart disease.However, no guidelines incorporate the effects of alternative interventions that decrease risk for coronary heart disease but are not used specifically to alter blood lipids. We did a simulation study to estimate the number of hypercholesterolemic adults who would continue to exceed a high-risk threshold after receiving aspirin, antihypertensive medication, and estrogen-replacement therapy. We found that of all persons who are currently candidates for hypolipidemic medication because they are at high risk for coronary heart disease, 6 to 8 million would no longer have this therapy recommended if the abilities of alternative interventions to reduce risk were considered. Pharmaceutical cost savings associated with alternative interventions range from $3 to $4 billion per year. Current guidelines should be revised to account for this effect.
Penicilloyl-Polylysine Skin Tests and Allergies
Authors: Bernard B. Levine
Journal: JAMA (1966)

<h3>To the Editor:—</h3> The recent Clinical Note "Penicilloyl-Polylysine Skin Test" by Resnik and Shelley (<b>196</b>:740, 1966) describes a patient in whom an anaphylactic reaction to penicilloyl-polylysine (PPL) developed in a skin test, whereas he tolerated oral administration of penicillin without allergic reaction. The authors are, of course, correct in stating that skin testing with PPL carries with it the possible hazard of anaphylaxis and that certain patients with positive PPL tests may receive penicillin without adverse reaction. However, these conclusions should not be taken to indicate that the penicillin skin tests are dangerous or that they have no value. First, it is well-known that skin testing with any allergen carries with it the possibility of an anaphylactic reaction. However, when the minimal dose necessary to elicit a wheal-and-flare reaction is used for testing, the risk of anaphylaxis is negligible, especially when compared to the useful information that these tests
Jejunal Sensitivity to Acid Peptic Digestion
Authors: D. H. Dillard
Journal: JAMA (1963)

To the Editor:—  I would like to call to your attention an article in the April 13 issue ofThe Journalentitled Colon Interposition for Treatment of Benign and Malignant Constricting Esophageal Lesions ( 184 :114). On pages 118 and 119 the authors state, It has been noted in the past by Ivy et al, Dragsted, and Vaughn, Wangensteen, and Dillard and Merendino that the jejunum is especially sensitive to acid peptic digestion. I am sure this represents an oversight which can happen so easily in this day and age when there are so many references regarding any one subject. However, if one rereads the article written by Dillard and Merendino in 1956, 1 one finds that the conclusions derived from the reported studies indicate exactly the opposite point of view. These studies showed that there is no inherent increased sensitivity of the mucosa of the jejunum to acid peptic digestion
Estimating Health Expenditure Growth Under Managed Competition
Authors: Robert H. Miller
Journal: JAMA (1995)

The estimated impact of health system reform proposals on health expenditures influences the health system reform debate. Health expenditure growth rate (HEGR) estimates are particularly critical because small differences in rates over time create large differences in health expenditures. There currently is no hard scientific basis for estimating the impact of managed care/managed competition legislation and market developments on the HEGR. For the 1994 health system reform debate, the two leading nonpartisan modelers developed qualitative scenarios about future health system developments in which managed care/managed competition would have little or no impact on the HEGR. We conclude that there are alternative plausible scenarios, based on current health system changes interacting with potential legislation, in which managed care/managed competition will substantially lower the HEGR. We recommend that simulation models should provide a range of estimates that better reflect both market trends and the profound uncertainty about the effects of health system reform.
Smoking while Wearing a Nicotine Patch
Authors: Murray A. Mittleman
Journal: Annals of Internal Medicine (1995)

Letters15 March 1995Smoking while Wearing a Nicotine PatchMurray A. MittlemanMurray A. MittlemanSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-122-6-199503150-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In a recent letter, Warner and Little [1] reported a case of myocardial infarction occurring in a patient wearing a nicotine patch. They concluded that “smoking. combined with nicotine patch use may trigger myocardial infarction.” In response to this letter, Kafka [2] wrote that “the problem with this patient was not that he was wearing a nicotine patch but rather that he was smoking.”These letters raise several important points about clinical observation, interpretation of associations, and causation in individual cases. First, new observations by astute clinicians alert the medical community to associations between exposure and disease ...References1. Warner JG, Little WC. Myocardial infarction in a patient who smoked while wearing a nicotine patch (Letter). Ann Intern Med. 1994; 120:695. Google Scholar2. Kafka HP. Heart attacks, smoking, and the nicotine patch (Letter). Ann Intern Med. 1994; 121:389. Google Scholar3. Rothman KJ. Modern Epidemiology. Boston: Little, Brown; 1986. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 March 1995Volume 122, Issue 6Page: 476-477KeywordsMyocardial infarctionNicotine Issue Published: 15 March 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Dysfunctional Smad Signaling Contributes to Abnormal Smooth Muscle Cell Proliferation in Familial Pulmonary Arterial Hypertension
Authors: Xudong Yang, Lu Long, Mark Southwood, Nung Rudarakanchana, Paul D. Upton, Trina K. Jeffery, Carl Atkinson, Hailan Chen, Richard C. Trembath, Nicholas W. Morrell
Journal: Circulation Research (2005)

Mutations in the bone morphogenetic protein type II receptor gene ( BMPR2 ) are the major genetic cause of familial pulmonary arterial hypertension (FPAH). Although smooth muscle cell proliferation contributes to the vascular remodeling observed in PAH, the role of BMPs in this process and the impact of BMPR2 mutation remains unclear. Studies involving normal human pulmonary artery smooth muscle cells (PASMCs) suggest site-specific responses to BMPs. Thus, BMP-4 inhibited proliferation of PASMCs isolated from proximal pulmonary arteries, but stimulated proliferation of PASMCs from peripheral arteries, and conferred protection from apoptosis. These differences were not caused by differential activation of BMP signaling pathways because exogenous BMP-4 led to phosphorylation of Smad1, p38 MAPK , and ERK1/2 in both cell types. However, the proproliferative effect of BMP-4 on peripheral PASMCs was found to be p38 MAPK /ERK-dependent. Conversely, overexpression of dominant-negative Smad1 converted the response to BMP-4 in proximal PASMCs from inhibitory to proliferative. Furthermore, we confirmed that proximal PASMCs harboring kinase domain mutations in BMPR2 are deficient in Smad signaling and are unresponsive to the growth suppressive effect of BMP-4. Moreover, we show that the pulmonary vasculature of patients with familial and idiopathic PAH are deficient in the activated form of Smad1. We conclude that defective Smad signaling and unopposed p38 MAPK /ERK signaling, as a consequence of mutation in BMPR2 , underlie the abnormal vascular cell proliferation observed in familial PAH.
Globulin correction of the albumin gradient: Correlation with measured serum to ascites colloid osmotic pressure gradients
Authors: John C. Hoefs
Journal: Hepatology (1992)

The albumin difference or gradient between serum ascites is presumed to be an effective estimate of the colloid osmotic pressure gradient, although this has never been directly demonstrated. The colloid osmotic pressure gradient is controlled by the degree of portal hypertension. Thus the albumin gradient is clinically useful in detecting patients with ascites caused by portal hypertension, although some overlap in such patients' albumin gradients exists compared with those of patients without portal hypertension. Part of this overlap is related to the inverse correlation of the albumin gradient with serum globulin; globulins also contribute to colloid osmotic pressure. The ability to calculate colloid osmotic pressure in serum and ascites with albumin and globulin concentration or to correct the albumin gradient for the impact of globulins might improve the clinical usefulness of the ascitic fluid analysis in determining the presence of portal hypertension in ascitic patients with borderline albumin gradients. Thus we developed equations to calculate colloid osmotic pressure from multivariate discriminate analyses of albumin and globulin concentrations in serial dilution samples of pooled serum and subsequently validated these equations, along with older methods of calculating colloid osmotic pressure. In an initial set of dilution experiments, globulin concentration was closely correlated with the colloid osmotic pressure to albumin concentration ratio (r = 0.956; p less than 0.001). Multivariate discriminate analysis yielded an equation for calculating colloid osmotic pressure from albumin (A) and globulin (G) concentration with a ratio of colloid osmotic pressure to albumin (calculated colloid osmotic pressure = A(1.058G + 0.163A + 3.11) and two other equations.(ABSTRACT TRUNCATED AT 250 WORDS)
GENERALIZED EDEMA IMMEDIATELY FOLLOWING INSULIN CONTROL IN DIABETES MELLITUS
Authors: R. B. GIBSON
Journal: JAMA (1925)

A pronounced generalized edema occurring in diabetic patients immediately following desugarization of the urine with insulin therapy was observed five times last year in this clinic. The edema promptly disappeared after treatment with potassium bicarbonate and potassium chlorid, 0.6 gm. each three times a day with meals. Thus far we have found no case reports in this country of this annoying untoward effect of insulin control in diabetes. However, edema with insulin therapy has been noted in the German clinics. Hagedorn<sup>1</sup>explains an increase in weight of insulin patients with cessation of the diabetic symptoms as partly a water retention. Edema induced by insulin is reported by von Jaksch-Wartenhorst,<sup>2</sup>by von Noorden and Isaac,<sup>3</sup>and by Klein.<sup>4</sup>It may be mentioned that these writers employed insulin preparations made in Europe, which may have been more effective in inducing water retention through less complete removal of proteins
A Restricted Materia Medica List
Authors: William J. Robinson
Journal: JAMA (1910)

<h3>To the Editor:—</h3> The action of the National Confederation of State Medical Examining and Licensing Boards in advising the restriction of materia medica examinations to a comparatively small number of drugs is to be highly commended. It is certainly better to know one hundred drugs well than to know one thousand badly. You are of course right in your assumption that the list will hardly please everybody. I cannot truthfully say that it pleases me absolutely; for in my opinion it contains some drugs which in a restricted list might as well be omitted, and it does not contain some drugs which are of sufficient importance to be contained even in a select list. But this is not the point of this letter. The point is a mild criticism of the classification of the drugs. Emanating from such a high body greater care should have been taken in classifying the
NEITHER SERUM VITAMIN D NOR CALCIUM LEVELS ARE ASSOCIATED WITH FLUORSOCOPIC SEVERITY OF CORONARY ARTERY CALCIFICATION AMONG PATIENTS UNDERGOING DIAGNOSTIC CORONARY ANGIOGRAPHY
Authors: Tami L. Bair, Heidi May, Brigham Smith, Shadi Karabsheh, Qunyu P. Li, Anwar Tandar, Jeffrey Anderson, Donald Lappe, J. Muhlestein
Journal: Journal of the American College of Cardiology (2013)
Cardiovascular status in young patients with insulin-dependent diabetes mellitus.
Authors: T R Kimball, S R Daniels, P R Khoury, R A Magnotti, A M Turner, L M Dolan
Journal: Circulation (1994)

Although the existence of diabetic cardiomyopathy in adults is firmly established, the presence of cardiac abnormalities in young diabetic patients is not universally accepted. We sought to determine the early stages of cardiac derangement and whether they are associated with renal dysfunction.Thirty-nine patients (29 boys; mean age, 17.6 +/- 3.4 years) with insulin-dependent diabetes mellitus underwent echocardiography and timed overnight urine collection. Echocardiographic evaluation consisted of left ventricular mass, performance (shortening fraction, velocity of circumferential fiber shortening, stroke volume, and cardiac index), preload (end-diastolic dimension and volume), after-load (end-systolic wall stress and systemic vascular resistance), and contractility (velocity of fiber shortening relative to wall stress). Creatinine clearance and albumin excretion were measured from the urine sample. Glycosylated hemoglobin levels were measured; height and weight were measured; and Quetelet index (weight/height2) was calculated. These data were compared with control data. Left ventricular mass (26 +/- 6 versus 22 +/- 6 g/ht2.7, P < .01), the indexes of performance, blood pressure, and contractility (0.14 +/- 0.14 versus 0.003 +/- 0.03 circumference/s, P < .0003) were significantly higher in the diabetic patients than in control subjects. To evaluate the correlates of left ventricular mass and contractility in the diabetic patients, univariate and multiple regression analyses were performed. Significant univariate correlations of mass included albumin excretion (r = .36, P < .02), glycosylated hemoglobin (r = .35, P < .04), and stroke volume (r = .34, P < .03). A multivariate model included Quetelet index, albumin excretion, and duration of diabetes. Significant univariate correlations of contractility included insulin dosage (r = -.36, P < .02), creatinine clearance (r = .40, P < .02), and Quetelet index (r = .34, P < .03). A multivariate model included insulin dosage and creatinine clearance.Early onset of diabetes mellitus is associated with increased left ventricular mass, performance, contractility, and blood pressure. These cardiovascular findings are correlated with increased creatinine clearance and microalbuminuria. These relations suggest that alterations in cardiovascular and renal function may occur in parallel in adolescents with insulin-dependent diabetes mellitus.
Abstract 3662: FGFR2 gene amplification and overexpression frequently occur in squamous cell carcinomas of the lung
Authors: Ryutaro Kikuchi, Cheng-long Huang, Makoto Sonobe, Masashi Kobayashi, Naoto Imamura, Marika Horiuchi, Jiro Kitamura, Masashi Ishikawa, Hiroshi Date
Journal: Cancer Research (2012)

Abstract Introduction: To date, only a few genetic abnormalities have been reported to be involved in tumorigenesis of squamous cell carcinomas (SqCCs) of the lung. Recently, fibroblast growth factor receptor (FGFR) 1 gene amplification was identified as a potential target for treatment in approximately 20% of SqCCs. In order to identify the clinical significance of FGFR family (FGFR1, FGFR2, FGFR3, and FGFR4) in SqCC, we performed a clinical study on the FGFR family in patients with non-small cell lung cancers (NSCLCs). Methods: Consecutive 138 NSCLC patients were studied. Gene expressions of FGFR family were evaluated by quantitative real-time RT-PCR. Intratumoral protein expressions of FGFR1, FGFR2, and Ki-67 were evaluated by immunohistochemistry. Gene amplifications of FGFR1 and FGFR2 were investigated by FISH. In addition, mutations of EGFR (exon 19-22) and KRAS (exon 1) were also investigated using either PCR-SSCP or PCR-RFLP, confirmed by direct sequencing. Results: Among 138 NSCLCs, 91 tumors were adenocarcinoma, 37 tumors were SqCCs, and 10 tumors were other types. Regarding FGFR gene expressions in NSCLCs, The FGFR2 gene expression was significantly higher in NSCLCs with both wild-type EGFR and wild-type KRAS than in NSCLCs with either mutant EGFR or mutant KRAS (P = 0.0012). FGFR2 gene expression was significantly higher in SqCCs than in adenocarcinomas (P &amp;lt; 0.0001). Furthermore, the FGFR2 gene expression was the highest among the gene expressions of FGFR family in SqCC. In contrast, no significant difference was observed in FGFR1 gene expression in relation to tumor histology. Regarding FGFR protein expressions in NSCLCs, the intratumoral FGFR2 protein expression significantly correlated with the FGFR2 gene expression (P &amp;lt; 0.0001, r = 0.5492), and the intratumoral FGFR2 protein expression was also significantly higher in SqCCs than in adenocarcinomas (P = 0.0008). Furthermore, the FGFR2 protein expression significantly correlated with Ki-67 proliferation index (P &amp;lt; 0.0001, r = 0.4677). In FISH analysis, FGFR1 gene amplification was detected in 34.3% (12/35) of SqCCs, and FGFR2 gene amplification was detected in 22.9% (8/35) of SqCCs. Furthermore, the Ki-67 proliferation index was significantly higher in SqCCs with FGFR2 gene amplification than in SqCCs without FGFR2 gene amplification (P = 0.0069). Conclusions: FGFR2 gene amplification and overexpression frequently occur and correlate with the tumor proliferation in SqCCs of the lung. FGFR2 could be a potential molecular target for the treatment of SqCCs of the lung as well as FGFR1. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3662. doi:1538-7445.AM2012-3662
A Five-Gene Signature and Clinical Outcome in Non–Small-Cell Lung Cancer
Authors: Hsuan-Yu Chen, Sung-Liang Yu, Chun-Houh Chen, Gee-Chen Chang, Chih-Yi Chen, Ang Yuan, Chiou-Ling Cheng, Chien-Hsun Wang, Harn-Jing Terng, Shu-Fang Kao, Wing-Kai Chan, Han-Ni Li, Chun-Chi Liu, Sher Singh, Wei J. Chen, Jeremy J.W. Chen, Pan-Chyr Yang
Journal: New England Journal of Medicine (2007)

Current staging methods are inadequate for predicting the outcome of treatment of non–small-cell lung cancer (NSCLC). We developed a five-gene signature that is closely associated with survival of patients with NSCLC.
Recognition of a mycobacteria-specific epitope in the 65-kD heat-shock protein by synovial fluid-derived T cell clones.
Authors: J S Gaston, P F Life, P J Jenner, M J Colston, P A Bacon
Journal: The Journal of Experimental Medicine (1990)

Adjuvant arthritis in rats is induced by a T cell clone specific for amino acids 180-188 of the mycobacterial 65-kD heat-shock protein, and synovial T cell responses to this same Ag have been noted in human arthritis. We have isolated 65-kD Ag-specific T cell clones from synovial fluid mononuclear cells of a patient with acute arthritis, which, unlike the corresponding PBMC, showed a marked proliferative response to the 65-kD Ag. Using synthetic peptides corresponding to the whole sequence of the 65-kD Ag, all the clones were shown to recognize an epitope present in the first NH2-terminal peptide (amino acids 1-15), with no response to the adjacent peptide (amino acids 6-22) or to any other peptide. The complete dominance of this epitope in the response to the 65-kD Ag was shown by documenting responses to the peptide in PBMC obtained after recovery from the arthritis. This epitope, like that recognized by the rat arthritogenic T cell clone, is in a portion of the 65-kD sequence that is not conserved between bacteria and eukaryotes, so that in this case, joint inflammation could not be attributed to bacteria-induced T cell clones cross-reacting with the self 65-kD Ag.