tbuckley/cabot-search huggingface dataset:
Interaction Between House Staff and Attending Physicians
Authors: BOY FRAME
Journal: Annals of Internal Medicine (1982)

Editorials1 March 1982Interaction Between House Staff and Attending PhysiciansBOY FRAME, M.D.BOY FRAME, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-3-372 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptApproved residency training programs differ widely in the emphasis placed on bedside teaching and the extent to which senior attending physicians supervise the care of patients. The increasing use of laboratory and technologic procedures may benefit patients, but often these procedures are unnecessary, not cost effective, and at times harmful. Invasive procedures may be ordered without adequate consideration of the patient's history and findings on physical examination. Important clinical features frequently are not reviewed at the bedside with the senior attending physician; bedside teaching is becoming a lost art in many hospitals. Major decisions on diagnostic investigation and treatment may... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Grosse Pointe Park, Michigan PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCommunication barriers between attending physicians and residentsBeyond “the men of steel”Managerial model of the attending physicianThe chief medical residency in the 1980sGuidelines for Teaching RoundsD.A. VAUGHAN, M.D.Residency TrainingROBERT F. JOHNSON, M.D. 1 March 1982Volume 96, Issue 3Page: 372-373KeywordsDiagnostic medicineHospital medicinePatientsResearch laboratoriesResidency Issue Published: 1 March 1982 PDF downloadLoading ...
Gene-Set Enrichment Analysis (GSEA) of Microarray Data in Patients with HER2-Positive Breast Cancer Treated with Preoperative Chemotherapy Including Trastuzumab.
Authors: C. Shimizu, C. Shimizu, K. Mogushi, K. Tamura, F. Koizumi, M. Ando, T. Kinoshita, H. Tanaka, Y. Fujiawara
Journal: Cancer Research (2009)

Abstract Background: Identification of molecular predictors of response is important in the aspect of personalization of treatment, especially in the era of molecular targeted drugs. Genome-wide analysis such as microarray may be useful in exploring genes related to mechanism of action or resistance to trastuzumab-based treatment.Patients and Methods: 17 HER2-negative and 13 HER2-positve patients with primary breast cancer were enrolled onto this prospective study. HER2 status was determined by HercepTest (3+) or (2+) with gene amplification. The patients were prospectively treated with preoperative chemotherapy (4 cycles of 5FU/epirubicin/cyclophosphamide 500/100/500 mg/m2, q3w, followed by 12 cycles of weekly paclitaxel 80mg/m2. All HER2-positve patients were administered trastuzumab 2mg/kg weekly with paclitaxel. Gene expressions were measured using Affimetrix GeneChip Human Genome U133 Plus 2.0 array in mRNA samples extracted from pretreatment core-needle biopsy specimens. GSEA (www.broad.mit.edu/gsea/msigdb/) were performed to explore gene sets differentially expressed between tumors that achieved pathological complete response (pCR) and those did not (non-pCR). 386 gene sets corresponding to human chromosome and 1454 gene sets named by gene ontology term were examined.Results: The 5 gene sets significantly differentiated HER2-positive and HER2-negative tumors with nominal p-value of &amp;lt;.03 and false-discovery rate (FDR) q-value of &amp;lt;.25 included 3 gene sets located in 17q chromosome including 17q11, indicating the validity of the microarray experiment and GSEA in a relatively small study. Six HER2-positive tumors achieved pCR. We identified 22 and 112 gene sets with nominal p-value of &amp;lt;0.01 and &amp;lt;0.05 that differentiated pCR and non-pCR in HER2-positive tumors, respectively. The top 22 gene sets included gene sets related to regulation of phosphorylation, receptor complex, cell proliferation, cytoplasmic vesicle, regulation of apoptosis and immune response. Other significant gene sets were those related to cell adhesion, signal transduction, cell proliferation and protein homodimerization. We could not identify gene sets which was differentiately expressed in tumors with pCR and non-pCR with FDR q-value of &amp;lt;.25 probablely because of the sample size.Conclusion: Although the results are still exploratory, GSEA seems to be helpful in narrowing down the gene sets from wide range of pathways in molecular network even in a small study if the selected gene sets are biologicaly robust. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 1167.
The isopeptidase USP2a regulates the stability of fatty acid synthase in prostate cancer
Authors: Edgard Graner, Dan Tang, Sabrina Rossi, Antonella Baron, Toshiro Migita, Lisa J Weinstein, Mirna Lechpammer, Dieter Huesken, Johann Zimmermann, Sabina Signoretti, Massimo Loda
Journal: Cancer Cell (2004)
Chemerin aggravates DSS-induced colitis by suppressing M2 macrophage polarization
Authors: Yuli Lin, Xuguang Yang, Wenjie Yue, Xiaofei Xu, Bingji Li, Linlin Zou, Rui He
Journal: Cellular and Molecular Immunology (2014)

Chemerin is present in various inflammatory sites and is closely involved in tissue inflammation. Recent studies have demonstrated that chemerin treatment can cause either anti-inflammatory or pro-inflammatory effects according to the disease model being investigated. Elevated circulating chemerin was recently found in patients with inflammatory bowel disease (IBD); however, the role of chemerin in intestinal inflammation remains unknown. In this study, we demonstrated that the administration of exogenous chemerin (aa17–156) aggravated the severity of dextran sulfate sodium (DSS)-induced colitis, which was characterized by higher clinical scores, extensive mucosal damage and significantly increased local and systemic production of pro-inflammatory cytokines, including IL-6, TNF-α and interferon (IFN-γ). Interestingly, chemerin did not appear to influence the magnitudes of inflammatory infiltrates in the colons, but did result in significantly decreased colonic expression of M2 macrophage-associated genes, including Arginase 1 (Arg-1), Ym1, FIZZ1 and IL-10, following DSS exposure, suggesting an impaired M2 macrophage skewing in vivo. Furthermore, an in vitro experiment showed that the addition of chemerin directly suppressed M2 macrophage-associated gene expression and STAT6 phosphorylation in IL-4-stimulated macrophages. Significantly elevated chemerin levels were found in colons from DSS-exposed mice and from ulcerative colitis (UC) patients and appeared to positively correlate with disease severity. Moreover, the in vivo administration of neutralizing anti-chemerin antibody significantly improved intestinal inflammation following DSS exposure. Taken together, our findings reveal a pro-inflammatory role for chemerin in DSS-induced colitis and the ability of chemerin to suppress the anti-inflammatory M2 macrophage response. Our study also suggests that upregulated chemerin in inflamed colons may contribute to the pathogenesis of IBD.
Research misconduct revisited
Authors: M. Fitzpatrick
Journal: BMJ (2011)

OBJECTIVE: To determine which proposed risk factor, work activity (industrial v clerical), body mass index (BMI), or other demographic factors had the most influence on the prevalence of median mononeuropathy at the wrist, and if there was an interaction between the risk factors. METHODS: This was a cross sectional study of active workers at five different worksites; four were industrial sites and one was clerical. 527 workers were recruited--164 clerical and 363 industrial. The presence of a median mononeuropathy in either hand was measured by electrodiagnostic techniques comparing median and ulnar sensory latencies. RESULTS: 30% of workers had an abnormality of the median sensory nerve at the wrist (34% of the industrial v 21% of the clerical workers). The adjusted risk for industrial workers was twice that of clerical workers. Obese workers (BMI &gt; 29) were four times more likely to present with a median mononeuropathy than workers who were normal or slender (BMI &lt; 25). There was no significant interaction between BMI and worksite in relation to median mononeuropathy. Increasing age was also related to an increased risk of median mononeuropathy. CONCLUSIONS: Obesity, industrial work, and age are independent risk factors that influence the prevalence of median mononeuropathies among active workers.
SOME ORIGINAL BLOOD PRESSURE OBSERVATIONS
Authors: VIRGIL C. KINNEY
Journal: JAMA (1923)

A correct interpretation of blood pressure findings is becoming a matter of the greatest importance. The time has gone by when the mere knowledge of a patient's systolic blood pressure was all that was necessary in order to arrive at a correct diagnosis. In the study of cardiovascular renal diseases, we find many diversified and interesting phenomena. These are each varied and distinct factors, but so closely related that they must all be taken into consideration if we are to arrive at intelligent conclusions. We have alterations (1) in the composition of the blood itself which are caused either by changes in the corpuscular content, by variations in the blood viscosity, or by circulating toxins; (2) in the venous pressure; (3) in the cardiac rhythm, and (4) of the greatest importance, and either temporary or permanent, in the caliber of the arterial venous and capillary circulation. <h3>SAME SYSTOLIC PRESSURE IN</h3>
Tc-99m HMPAO Brain SPECT Imaging in Children With Acute Cerebellar Ataxia
Authors: Pi-Lien Hung, Shu-Hua Huang, Chao-Ching Huang, Song-Chei Huang, Ying-Chao Chang
Journal: Clinical Nuclear Medicine (2008)

We prospectively evaluated consecutive cases of acute cerebellar ataxia in children to identify brain perfusion SPECT features associated with acute cerebellar ataxia and to correlate the brain SPECT findings to clinical severity and prognosis.Among the 10 consecutive children with acute cerebellar ataxia, 7 had abnormal Tc-99m HMPAO brain SPECT findings (4 cerebellar hypoperfusion, 5 unilateral cortical and/or subcortical hypoperfusion, and 1 unilateral cortical hyperperfusion), in contrast to no abnormalities disclosed by CT or MR imagings. Furthermore, the extent of brain perfusion SPECT abnormalities correlated significantly with the clinical severity and the recovery time of cerebellar ataxia. Sixty percent of children with acute cerebellar ataxia had cortical and/or subcortical involvement, which implied the wider involvement of acute cerebellar ataxia than what has been thought.The present data suggest that Tc-99m HMPAO brain SPECT is a sensitive modality for providing prognostic information in childhood acute cerebellar ataxia.
Morphology and functions of astrocytes cultured on water-repellent fractal tripalmitin surfaces
Authors: Wei-wei Hu, Zhe Wang, Shan-shan Zhang, Lei Jiang, Jing Zhang, Xiangnan Zhang, Qun-fang Lei, Hyun-Joo Park, Wen-jun Fang, Zhong Chen
Journal: Biomaterials (2014)
Experimental Study and Clinical Use of Epinephrine for Treatment of Low Cardiac Output Syndrome
Authors: LAURENCE H. COFFIN, JAY L. ANKENEY, EDWARD M. BEHELER
Journal: Circulation (1966)

Epinephrine in doses of 0.5 to 1.0 µg/kg/ min has been shown experimentally to augment cardiac output, with increases in both hepatosplanchnic and peripheral blood flow. At these concentrations, the primary effect of epinephrine is cardiotonic, without measurable vasoconstriction. Larger doses produce significant vasoconstriction with a decrease in cardiac output and a reduction in peripheral venous return. The mean rate of excess lactate accumulation was noted to be increased during epinephrine administration in animals with intact circulation, in spite of increased peripheral and hepatosplanchnic blood flow and oxygen consumption. With the heart and lungs functionally excluded by a pump oxygenator, low doses of epinephrine produced no "excess lactate," even though peripheral constriction was measured. Clinical experience indicates that continuous infusion of 0.1 to 0.5 µg/kg/min of epinephrine is effective in the treatment of postoperative low cardiac output syndrome.
Commentary: Do preterm infants need thyroxine replacement?
Authors: C G D Brook
Journal: BMJ (1996)

The interpretation of thyroid function tests in babies, especially in premature babies, is difficult. In adults the thyroid gland secretes thyroxine which can be deiodinated peripherally to generate iodothyronines that are more (triiodothyronine) or less (reverse triiodothyronine) potent than the parent compound. Triiodothyronine has three to four times the metabolic potency of thyroxine, and 80% is derived from peripheral conversion, the remainder coming from the thyroid gland. In the fetus serum triiodothyronine concentrations are low throughout gestation because the fetus preferentially converts the thyroxine its own thyroid gland produces and that which it acquires from the mother to reverse triiodothyronine, which is inactive. Clearly there has to be a switch at birth but, as …
Heparin and Deep Venous Thrombosis
Authors: P. A. ROUTLEDGE
Journal: Annals of Internal Medicine (1988)

Letters and Corrections1 March 1988Heparin and Deep Venous ThrombosisP. A. ROUTLEDGE, N. J. SCOLDINGP. A. ROUTLEDGESearch for more papers by this author, N. J. SCOLDINGSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-108-3-488_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In their comparison of subcutaneous and continuous intravenous heparin in the treatment of acute deep venous thrombosis, Doyle and coworkers (1) show similar degrees of efficacy (in terms of prevention of pulmonary embolism) and incidence of adverse effects in the two treatment groups.However, it is clear that the subcutaneous group achieved significantly better anticoagulation than the intravenous group (mean + SE activated partial thromboplastin times 59.8 ± 1.4 s and 53.4 ± 1.2 s respectively,P= 0.001) throughout the 7-day period of heparin treatment. The discrepancy was even greater in the first 3 days of...References1. DOYLETURPIEHIRSH DAJ. Adjusted subcutaneous heparin or continuous intravenous heparin in patients with acute deep venous thrombosis: a randomized trial. Ann Intern Med. 1987;107:441-5. LinkGoogle Scholar2. WALKERSHAWTHOMPSONCUMMINGTHOMAS MJGJM. Subcutaneous calcium heparin versus intravenous sodium in the treatment of established acute deep venous thrombosis; a prospective randomised trial. Br Med J. 1987;294:1189-92. CrossrefMedlineGoogle Scholar3. HULLRASKOBHIRSH RGJ. Continuous intravenous heparin compared with intermittent subcutaneous heparin in the initial treatment of proximal vein thrombosis. N Engl J Med. 1986;315:1109-14. CrossrefMedlineGoogle Scholar4. FENNERTYRENOWDENSCOLDINGBENTLEYCAMPBELLROUTLEDGE ASNDIP. Guidelines to control heparin treatment. Br Med J. 1986;292:579-80. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: P. A. ROUTLEDGE; N. J. SCOLDINGAffiliations: University of Wales College of Medicine Heath Park, Cardiff CF4 4XN United Kingdom PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCardiac predictors of death after non-cardiac surgery: Authors' replyAnticoagulants in venous thromboembolism.Anticoagulants in venous thromboembolism: Authors' reply 1 March 1988Volume 108, Issue 3Page: 488-489KeywordsDeep vein thrombosisHeparinPartial thromboplastin timePulmonary embolism ePublished: 1 December 2008 Issue Published: 1 March 1988 PDF downloadLoading ...
Bronchoalveolar lavage in patients with mild and severe rheumatoid lung disease.
Authors: D M Gilligan, C M O'Connor, K Ward, D Moloney, B Bresnihan, M X FitzGerald
Journal: Thorax (1990)

The reported prevalence of interstitial lung disease in patients with rheumatoid arthritis has varied from 10% to 50%, yet less than 5% of patients with arthritis develop severe fibrosing interstitial lung disease. This suggests that subclinical disease may not always presage progressive disease. Bronchoalveolar lavage fluid from patients with rheumatoid arthritis and either clinically evident interstitial lung disease or subclinical disease was examined for the presence of factors with a putative role in the development of interstitial fibrosis. Patients with subclinical disease were identified by prospective radiographic and lung function screening of 93 patients with rheumatoid arthritis. Fourteen patients were identified in this manner and an association between subclinical disease and smoking history was noted. Eleven patients with established interstitial lung disease had increased neutrophils (p less than 0.05), collagenase, and type III procollagen N terminal peptide levels (p less than 0.01) in the bronchoalveolar lavage fluid. Preliminary characterisation of the bronchoalveolar lavage collagenase suggested that it originated from neutrophils. Ten patients with subclinical interstitial lung disease underwent bronchoalveolar lavage. Of these, one had increased neutrophils and two had increased collagenase concentrations--abnormalities associated with advanced interstitial lung disease and a poor prognosis. These results suggest that in arthritis patients with evidence of subclinical pulmonary interstitial disease bronchoalveolar lavage might be useful in identifying those who may require careful monitoring in the hope that early treatment will prevent severe fibrosis.
Jackson Lab Update
Authors: E. Blume
Journal: JNCI Journal of the National Cancer Institute (1989)

Jackson Lab Update Elaine Blume Elaine Blume Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 17, 6 September 1989, Page 1285, https://doi.org/10.1093/jnci/81.17.1285 Published: 06 September 1989
Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques
Authors: Bernhard Schieffer, Elisabeth Schieffer, Denise Hilfiker-Kleiner, Andres Hilfiker, Petri T. Kovanen, Maija Kaartinen, Jörg Nussberger, Wolfgang Harringer, Helmut Drexler
Journal: Circulation (2000)

Background —Patients with an activated renin-angiotensin system (RAS) or genetic alterations of the RAS are at increased risk of myocardial infarction (MI). Administration of ACE inhibitors reduces the risk of MI, and acute coronary syndromes are associated with increased interleukin 6 (IL-6) serum levels. Accordingly, the present study evaluated the expression of angiotensin II (Ang II) in human coronary atherosclerotic plaques and its influence on IL-6 expression in patients with coronary artery disease. Methods and Results —Immunohistochemical colocalization of Ang II, ACE, Ang II type 1 (AT 1 ) receptor, and IL-6 was examined in coronary arteries from patients with ischemic or dilated cardiomyopathy undergoing heart transplantation (n=12), in atherectomy samples from patients with unstable angina (culprit lesion; n=8), and in ruptured coronary arteries from patients who died of MI (n=13). Synthesis and release of IL-6 was investigated in smooth muscle cells and macrophages after Ang II stimulation. Colocalization of ACE, Ang II, AT 1 receptor, and IL-6 with CD68-positive macrophages was observed at the shoulder region of coronary atherosclerotic plaques and in atherectomy tissue of patients with unstable angina. Ang II was identified in close proximity to the presumed rupture site of human coronary arteries in acute MI. Ang II induced synthesis and release of IL-6 shortly after stimulation in vitro in macrophages and rat smooth muscle cells. Conclusions — Ang II, AT 1 receptor, and ACE are expressed at strategic sites of human atherosclerotic coronary arteries, suggesting that Ang II is produced primarily by ACE within coronary plaques. The observation that Ang II induces IL-6 and their colocalization with the AT 1 receptor and ACE is consistent with the notion that the RAS may contribute to inflammatory processes within the vascular wall and to the development of acute coronary syndromes.
IUD vs Hysterectomy
Authors: Rebecca Voelker
Journal: JAMA (1998)

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
Adrenal Apoplexy Following Electronarcosis Therapy
Authors: Mark D. Altschule
Journal: New England Journal of Medicine (1955)

ARECENT review of the subject of adrenal apoplexy1 listed convulsions among the causes of that syndrome. It is known that massive adrenal hemorrhage occurs in occasional patients with severe epilepsy; indeed, this lesion may even be the cause of death in status epilepticus.2 , 3 In a psychotic patient studied at this hospital adrenal apoplexy developed in association with prolonged induced seizures; it was therefore considered of interest to review available information on the relation of convulsions to adrenal hemorrhage.Case ReportH. T. H., a native-born spinster, first entered the McLean Hospital in August, 1945, at the age of 73, with . . .
Passive Smoking and Uptake of Carbon Monoxide in Flight Attendants
Authors: Douglas B. Duncan
Journal: JAMA (1984)

<h3>To the Editor.—</h3> There is concern about the health effects of passive smoking.<sup>1</sup>Because of concern among flight attendants about passive exposure to cigarette smoke during work on commercial aircraft, a preliminary investigation was conducted to search for an increase in expired air (end tidal) carbon monoxide in flight attendants after work. Expired air (end tidal) carbon monoxide was chosen because carbon monoxide concentration is known to vary linearly with the rate of cigarette burning in an environment.<sup>2</sup> Volunteers gave their informed consent after the nature of the procedures had been explained to them. Nonsmoking volunteer flight attendants filled out health history questionnaires before flight and recorded their observations during flight. Expired air (end tidal) carbon monoxide was measured before and after each flight for each volunteer. All flights were "turnaround" flights from Los Angeles to Honolulu and back. These flights were of about five hours' duration in