tbuckley/cabot-search huggingface dataset:
Computer Physician Order Entry
Authors: Gilad J. Kuperman
Journal: Annals of Internal Medicine (2004)

Letters20 April 2004Computer Physician Order EntryGilad J. Kuperman, MD, PhD and Richard F. Gibson, MD, PhDGilad J. Kuperman, MD, PhDFrom Partners HealthCare System, Inc., Wellesley, MA 02481, and Providence Health System, Portland, OR 97223.Search for more papers by this author and Richard F. Gibson, MD, PhDFrom Partners HealthCare System, Inc., Wellesley, MA 02481, and Providence Health System, Portland, OR 97223.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-140-8-200404200-00031 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We agree with Dr. Edwards that most of the research thus far on the impact of CPOE applications has been done at academic centers and that more research is needed to understand the challenges in implementing CPOE in institutions of different sizes and staffing models. More papers continue to be published on this topic (1). Our aim was to point out the opportunities and potential benefits that organizations should keep in mind as they struggle with the very real issues of implementation. We further agree that a situation in which physicians' efficiency is negatively affected over an extended ...References1. Metzger J, Fortin J. Computerized Order Entry in Community Hospitals: Lessons from the Field. Oakland, CA: California Health Care Foundation and First Consulting Group; 2003. Google Scholar2. Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, DC: National Academy Pr; 2000. Google Scholar Author, Article, and Disclosure InformationAffiliations: From Partners HealthCare System, Inc., Wellesley, MA 02481, and Providence Health System, Portland, OR 97223. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoComputer Physician Order Entry: Benefits, Costs, and Issues Gilad J. Kuperman and Richard F. Gibson Computer Physician Order Entry David B. Edwards Computer Physician Order Entry Barton M. Nassberg Metrics 20 April 2004Volume 140, Issue 8Page: 669-670KeywordsComputer applicationsComputersComputing systems ePublished: 20 April 2004 Issue Published: 20 April 2004 Copyright & PermissionsCopyright © 2004 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
1034-214 Effects of candesartan and enalapril on atrial endocardial nitric oxide synthase expression in an animal model of pacing induced atrial remodelling
Authors: Fernando Cabestrero, Jose A Cabrera, Elise Courtois, Jose M Rubio, Miguel Orejas, Pedro P Pérez, Ana B Herrera, Antonio López-Farré, Jeronimo Farré
Journal: Journal of the American College of Cardiology (2004)
Usefulness of dried blood samples for quantification and molecular characterization of HBV-DNA
Authors: Rosendo Jardi, Francisco Rodriguez-Frias, Maria Buti, Melanie Schaper, Auristela Valdes, Mariano Martinez, Rafael Esteban, Jaime Guardia
Journal: Hepatology (2004)

The purpose of this study was to assess the use of dried blood spot (DBS) samples for hepatitis B virus (HBV) DNA quantification, HBV genotyping, and detection of G1896A precore mutants and variants in the YMDD polymerase motif. We studied DBS and serum samples from 82 patients with chronic HBV infection (23 hepatitis B e antigen [HBeAg]-positive and 39 HBeAg-negative), 20 HBeAg-inactive carriers, and 15 HBeAg-negative patients under lamivudine therapy (selected from chronic HBV patients). DBS samples consisted of approximately 20 μL of blood applied to 5-mm paper disks. HBV DNA quantification and HBV precore mutant detection were done using real-time polymerase chain reaction, HBV genotyping using restriction fragment length polymorphism, and YMDD variant detection by Inno-lipa assay. DBS and serum results were compared. HBV DNA was detected in a range of 10 2 -10 8 copies/mL, with low intra-assay and inter-assay variation (&lt;10%). Median DBS HBV DNA (copies/mL) was: 3.7 × 10 6 in HBeAg-positive, 6.2 × 10 5 in HBeAg-negative, and 5.5 × 10 2 in inactive carriers ( P &lt; .05). HBV DNA was positive in serum (median 5 × 10 3 copies/mL) but negative in DBS for five inactive carriers. The correlation coefficient between HBV DNA concentration in DBS versus serum samples was r 2 = 0.96 ( P &lt; .001). The sensitivity of HBV DNA detection in DBS samples was 1 log 10 lower than in serum samples. Concordance between DBS and serum for HBV genotyping, and for precore mutant and YMDD variant detection was optimal. DBS storage for 7 days at room temperature and 21 days at −20°C revealed no decrease in HBV DNA levels or integrity. In conclusion , the DBS sample is useful for HBV DNA quantification, genotyping, and detection of precore mutant and YMDD variants. All four determinations can be completed with a single drop of dried blood. (Hepatology 2004;40:133-139.)
Viral Load and CD4 T Cell Percentage Predict Sleep Disturbances in HIV-Infected Children
Authors: I. Okocha, S.B. Foster, M.E. Paul, D.G. Glaze, J.M. Reuben, L.L. Harris, E.N. Cohen, B. Lee, C.A. Kozinetz, H.L. Schwarzwald, M.W. Kline, C.D. Jackson, E.N. Ward, J.E. Fehlis, P.Y. Brouwers, T.L. Miller, L. Himic, F.D. Armstrong, S. Shahzeidi, A.A. Colin, G.B. Scott, D. Asthana, S.E. Lipshultz, W.T. Shearer
Journal: Journal of Allergy and Clinical Immunology (2009)
EFFECTS OF EXOGENOUS ADRENOCORTICOTROPIC HORMONE (ACTH) UPON PITUITARY ACTH CONCENTRATION AFTER PROLONGED CORTISONE TREATMENT AND STRESS*
Authors: Donald A. Holub, Julian I. Kitay, Joseph W. Jailer
Journal: Journal of Clinical Investigation (1959)

Symptoms and metabolic abnormalities closely resembling those of hypoadrenalism have been reported following cessation of prolonged treatment with adrenal steroids (1-5).Sudden death following surgery has been reported in association with this syndrome and has been ascribed to fail- ure of the hypothalamic-pituitary-adrenal system to respond to stress (6-9).Since prolonged ad- ministration of corticosteroids produces adrenal atrophy in both man and laboratory animals (7, 10, 11), this failure has been attributed to adrenal insufficiency.Exogenous corticotropin (ACTH) will repair or maintain normal adrenal weight in the cortisone-treated animal (12).Consequently the addition of ACTH in various dosage sched- ules has been advocated for the purpose of main- taining or restoring normal adrenal responsiveness to stress (5,(13)(14)(15)(16).The efficacy of such combined therapy is not firmly established.In addition to producing adrenal atrophy, chronic treatment with steroids results in decreased pituitary ACTH content (17,18).The failure of steroid-treated subjects to respond to stress may therefore reflect pituitary ACTH insufficiency rather than, or in addition to, adrenal insufficiency.ACTH administration, on the other hand, has been shown to increase pituitary ACTH content in the intact rat, despite stimulation of secretion of endogenous steroids (18).For this reason ACTH therapy has been studied in the cortisone- treated animal to determine whether such adjunctive therapy is capable of modifying the pituitary ACTH depletion which follows steroid adminis- tration, and whether it can enhance the pituitary response to stress.
Monitored Isoniazid Prophylaxis for Low-Risk Tuberculin Reactors
Authors: Tom Moulding
Journal: Annals of Internal Medicine (1998)

Letters15 June 1998Monitored Isoniazid Prophylaxis for Low-Risk Tuberculin ReactorsTom Moulding, MDTom Moulding, MDHarbor-UCLA Medical Center; Torrance, CA 90502Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-12_Part_1-199806150-00028 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Decision analyses should be helpful in selecting indications for isoniazid prophylaxis. In reality, however, they are not helpful because they use widely different assumptions that lead to vastly different conclusions. This is demonstrated by the contrasting analyses by Salpeter and colleagues [1], which concluded that isoniazid given to all tuberculin rectors would result in significant savings and large health benefits, and Tsevat and colleagues [2], which concluded that isoniazid reduces life expectancy.Salpeter and associates assumed that the annual rate of the development of tuberculosis would be a constant 0.0006 cases per year, starting with the 15th ...References1. Salpeter SR, Sanders GD, Salpeter EE, Owens DK. Monitored isoniazid prophylaxis for low-risk tuberculin reactors older than 35 years of age: a risk–benefit and cost-effectiveness analysis. Ann Intern Med. 1997; 127:1051-61. Google Scholar2. Tsevat J, Taylor WC, Wong JB, Pauker SG. Isoniazid for the tuberculin reactor: take it or leave it. Am Rev Respir Dis. 1988; 137:215-20. Google Scholar3. Chiba Y. Significance of endogenous reactivation: 30 year follow up of tuberculin convertors. Bulletin of International Union Against Tuberculosis. 1974; 49:321-4. Google Scholar4. Efficacy of various durations of isoniazid preventive therapy for tuberculosis: five years of follow-up in the IUAT trial. International Union Against Tuberculosis-Committee on Prophylaxis. Bull WHO. 1982; 60:555-64. Google Scholar5. Moulding T, Barnes P. Isoniazid for the tuberculin reactor: take it or leave it [Letter]. Am Rev Respir Dis. 1988; 138:489. Google Scholar Author, Article, and Disclosure InformationAffiliations: Harbor-UCLA Medical Center; Torrance, CA 90502 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 June 1998Volume 128, Issue 12_Part_1Page: 1048KeywordsDecision analysisHepatitisIsoniazidLife expectancyProphylaxisTuberculinTuberculin tests Issue Published: 15 June 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
A Neural Network Model for Predicting Pancreas Transplant Graft Outcome
Authors: Susan G Dorsey, Carolyn F Waltz, Laura Brosch, Ingrid Connerney, Eugene J Schweitzer, Stephen T Bartlett
Journal: Diabetes Care (1997)

To compare the results of a neural network versus a logistic regression model for predicting early (0-3 months) pancreas transplant graft survival or loss.This study was a cross-sectional, secondary analysis of demographic and clinical data from 117 simultaneous pancreas-kidney (SPK), 35 pancreas-after-kidney (PAK), and 8 pancreas-transplant-alone (PTA) patients (n = 160). The majority of patients were men (57%) and were white (90.1%), with a mean age of 39 +/- 8.09 years. Of the patients, 23 (14.4%) experienced early graft loss, which included any loss owing to technical or immunological causes, and death with a functional graft. Data were analyzed with a logistic regression model for multivariate analysis and a backpropagation neural network (BPNN) model.A total of 12 predictor variables were chosen from literature and transplant surgeon recommendations. A logistic model with all predictor variables included correctly classified 93.53% of cases. Model sensitivity was 35.71%; specificity was 100% (pseudo-R2 0.24). Of the predictors, history of alcohol abuse (odds ratio [OR] 32.39; 95% CI 1.67-626.89), having a PAK or PTA (OR 13.6; 95% CI 2.20-84.01), and use of a nonlocal organ procurement center (OPO) (OR 4.51; 95% CI 0.78-25.96) were most closely associated with early graft loss. The BPNN model with the same 12 predictor variables correctly predicted 92.50% of cases (R2 0.71). Model sensitivity was 68%; specificity was 96%. Of the predictors, the three variables most closely associated with graft outcome in this model were recipient/donor weight difference >50 lb, having a PAK or PTA, and use of a nonlocal OPO.First, the BPNN model correctly predicted 92.5% of graft outcomes versus the logistic model (93.53%). Second, the BPNN model rendered more accurate predictions (>0.70 = loss; <0.30 = survival) versus the logistic model (>0.50 = loss; <0.50 = survival). Third, the BPNN model was more sensitive (68%) than the logistic model (35.71%) to graft failures and demonstrated an almost threefold increase in explained variance (R2 = 0.71 vs. 0.24). These results suggest that the BPNN model is a more powerful tool for predicting early pancreas graft loss than traditional multivariate statistical models.
Relation of parental history of early myocardial infarction to the level of apoprotein B in men.
Authors: F Cambien, J M Warnet, A Jacqueson, P Ducimetiere, J L Richard, J R Claude
Journal: Circulation (1987)

The relations between parental history of early myocardial infarction and plasma lipids and apoproteins have been examined in a population of 4045 middle-aged (20 to 60 years old) working men at the initial examination of the Paris Prospective Study 2. Subjects with a history of myocardial infarction, angina pectoris, or peripheral arterial disease or those treated with hypolipidemic drugs were excluded from the analysis. The numbers of subjects with a paternal or maternal history of early myocardial infarction were 123 and 30, respectively. After adjustment for age, cigarette consumption, alcohol consumption, and body mass index, subjects with parental history of myocardial infarction had higher levels of total cholesterol (p less than .01), low-density lipoprotein (LDL) cholesterol (p less than .01), and apoprotein B (APOB) (p less than .0001) and a lower level of high-density lipoprotein (HDL) cholesterol (p less than .05) than subjects with no parental history of myocardial infarction. On the other hand, apoprotein A1 (APOA1) and triglyceride levels were not different between the two groups. The ratios of HDL/total cholesterol and APOA1/APOB were also lower in presence of parental myocardial infarction (p less than .001 and p less than .01, respectively). When a discriminant analysis was performed, only APOB level was related to parental myocardial infarction. The results for paternal and maternal history were very similar and were grouped for the analysis. We conclude that part of the known relationship between parental history of myocardial infarction and coronary heart disease could be mediated by an increased APOB level.
Cryptosporidium, chronic diarrhoea and the proximal small intestinal mucosa.
Authors: A D Phillips, A G Thomas, J A Walker-Smith
Journal: Gut (1992)

The association between Cryptosporidium, chronic diarrhoea and a proximal small intestinal mucosal enteropathy was reviewed over a six and a half year period. One hundred and twenty three children with cryptosporidiosis and no clinical evidence of immune deficiency were identified. 50% of children excreting only Cryptosporidium had chronic diarrhoea. Most cases (63%) of chronic diarrhoea occurred in the first two years of life. A mild to moderate enteropathy was present in all nine children undergoing a small intestinal biopsy and seven showed the presence of Cryptosporidium adhering to villous epithelium. All patients eventually recovered spontaneously. Cryptosporidium is a cause of chronic diarrhoea and a proximal small intestinal mucosal enteropathy in children without immune deficiency. Screening for the parasite should be part of the investigative procedures in children with chronic diarrhoea.
Entourage: the immune microenvironment following follicular lymphoma
Authors: B E Wahlin, B Sander, B Christensson, B Østenstad, H Holte, P D Brown, C Sundström, E Kimby
Journal: Blood Cancer Journal (2012)

In follicular lymphoma, nonmalignant immune cells are important. Follicular lymphoma depends on CD4+ cells, but CD8+ cells counteract it. We hypothesized that the presence of follicular lymphoma is associated with higher CD4+ than CD8+ cell numbers in the tumor microenvironment but not in the immune system. Using flow cytometry, pre-treatment and follow-up CD4/CD8 ratios were estimated in the bone marrow, blood and lymph nodes of untreated follicular lymphoma patients in two independent data sets (N(1)=121; N(2)=166). The ratios were analyzed for their relation with bone marrow lymphoma involvement. Bone marrows were also investigated with immunohistochemistry. In either data set, the bone marrow CD4/CD8 ratios were higher in bone marrows involved with lymphoma (P=0.043 and 0.0002, respectively). The mean CD4/CD8 ratio was 1.0 in uninvolved and 1.4 in involved bone marrows. Also higher in involved bone marrows were CD4/CD56 and CD3CD25/CD3 ratios. No blood or lymph node ratios differed between bone marrow-negative and -positive patients. Sequential samples showed increased bone marrow CD4/CD8 ratios in all cases of progression to bone marrow involvement. Immunohistochemistry showed CD4+, CD57+, programmed death-1+, forkhead box protein 3+ and CD21+ cells accumulated inside the lymphoma infiltrates, whereas CD8+, CD56+ and CD68+ cells were outside the infiltrates. This study provides evidence in vivo that the microenvironment changes upon follicular lymphoma involvement.
Hapten-induced Colitis Is Associated with Colonic Patch Hypertrophy and T Helper Cell 2–Type Responses
Authors: Taeko Dohi, Kohtaro Fujihashi, Paul D. Rennert, Koichi Iwatani, Hiroshi Kiyono, Jerry R. McGhee
Journal: The Journal of Experimental Medicine (1999)

To investigate the potential involvement of T helper (Th)2-type responses in murine models of intestinal inflammation, we used trinitrobenzene sulfonic acid (TNBS)–hapten to induce inflammatory bowel disease in situations where Th1-type responses with interferon (IFN)-γ synthesis are either diminished or do not occur. Intracolonic administration of TNBS to either normal (IFN-γ+/+) or Th1-deficient IFN-γ knockout (IFN-γ−/−) BALB/c mice resulted in significant colitis. In IFN-γ−/− mice, crypt inflammation was more severe than in IFN-γ+/+ mice and was accompanied by hypertrophy of colonic patches with a lymphoepithelium containing M cells and distinct B and T cell zones resembling Peyer's patches. Hapten-specific, colonic patch T cells from both mouse groups exhibited a Th2 phenotype with interleukin (IL)-4 and IL-5 production. TNBS colitis in normal mice treated with anti–IL-4 antibodies or in IL-4−/− mice was less severe than in either IFN-γ+/+ or IFN-γ−/− mice. Our findings now show that the Th2-type responses in TNBS colitis are associated with colonic patch enlargement and inflammation of the mucosal layer and may represent a model for ulcerative colitis.
Scientific Psychology: Principles and Approaches
Authors: Saul Rosenzweig
Journal: JAMA (1965)

"Scientific Psychology" is a misleadingly brief title for this book, and even its subtitle is too vague to remedy the difficulty. "Philosophical Issues of a Scientific Psychology" would have come closer to defining the aim and the scope of this work to which 30 psychologists and philosophers have contributed. The editors are, fittingly, Wolman, a psychologist with a philosophical leaning, and Nagel, a philosopher with an appetite for psychology. To the medical reader there will be little here of scientific interest in the specifically experimental or clinical senses. But if the physician or researcher who turns to these pages is prepared for deliberating with Jean Piaget about the possibilities of an empirical genetics of epistemology (in which the naïve child informs his naïve elders about how they got to think as they do); with Anatol Rapoport about the uses of mathematics in psychology; with Benbow Ritchie about "an incurable vagueness
ROLE OF LACTIC ACID IN DENTAL CARIES
Authors: Benjamin F. Miller
Journal: JAMA (1941)

<h3>To the Editor:—</h3> InThe Journalof January 4 there is a communication from Dr. J. Lewis Blass, who in Correspondence discusses the studies of Neuwirth and Klosterman on the production of lactic acid by oral micro-organisms after the introduction of concentrated carbohydrate into the mouth. Dr. Blass states: "Control experiments by these workers demonstrate that this rapid production of lactic acid in the oral cavity can be ascribed to the activity of oral micro-organisms. Thus, for the first time now there is not only a demonstration of the production of acids in the oral cavity but also a demonstration of the production of a definite acid—lactic acid." Dr. Blass mentions that Neuwirth and Klosterman (<i>Proc. Soc. Exper. Biol. &amp; Med.</i><b>45</b>:464 [Oct.] 1940) employed the ultramicro method for lactic acid developed by Muntz and myself, but he neglects to point out that subsequent to the development of this
Statin-Associated Myopathy with Normal Creatine Kinase Levels
Authors: Mark H. Hyman
Journal: Annals of Internal Medicine (2003)

Letters17 June 2003Statin-Associated Myopathy with Normal Creatine Kinase LevelsMark H. Hyman, MDMark H. Hyman, MDUniversity of California, Los Angeles; Los Angeles, CA 90025 (Hyman)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-138-12-200306170-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The article by Phillips and colleagues (1) and the accompanying editorial by Grundy (2) highlight a clinical experience many of us have had. Are the authors aware of any data, or in their clinical experience have they found any other noninvasive testing, such as serum aldolase level, that might identify patients who are experiencing creatine kinasenegative statin myopathy?References1. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, . Statin-associated myopathy with normal creatine kinase levels. Ann Intern Med. 2002;137:581-5. [PMID: 12353945] LinkGoogle Scholar2. Grundy SM. Can statins cause chronic low-grade myopathy? [Editorial]. Ann Intern Med. 2002;137:617-8. [PMID: 12353951] LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: University of California, Los Angeles; Los Angeles, CA 90025 (Hyman) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoStatin-Associated Myopathy with Normal Creatine Kinase Levels Paul S. Phillips , Richard H. Haas , Sergei Bannykh , Stephanie Hathaway , Nancy L. Gray , Bruce J. Kimura , Georgirene D. Vladutiu , John D.F. England , and Can Statins Cause Chronic Low-Grade Myopathy? Scott M. Grundy Statin-Associated Myopathy with Normal Creatine Kinase Levels Josh Torgovnick and Edward Arsura Statin-Associated Myopathy with Normal Creatine Kinase Levels Emil Toma and Maude Loignon Statin-Associated Myopathy with Normal Creatine Kinase Levels Louis Evan Teichholz Statin-Associated Myopathy with Normal Creatine Kinase Levels Paul S. Phillips and Richard H. Haas Metrics Cited ByDietary Fat Intake: Promotion of Disease in Carotid Artery Disease: Lipid Lowering Versus Side Effects of StatinsTesting for Stain-induced MyopathyCurrent awareness: Pharmacoepidemiology and drug safety 17 June 2003Volume 138, Issue 12Page: 1007KeywordsCreatineCreatine kinaseStatins ePublished: 17 June 2003 Issue Published: 17 June 2003 CopyrightCopyright © 2003 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Congenital heart block: development of late-onset cardiomyopathy, a previously underappreciated sequela
Authors: Jeffrey P Moak, Karyl S Barron, Thomas J Hougen, Henry B Wiles, Seshadri Balaji, Narayanswami Sreeram, Mark H Cohen, Aaron Nordenberg, George F Van Hare, Richard A Friedman, Maria Perez, Frank Cecchin, Daniel S Schneider, Rodrigo A Nehgme, Jill P Buyon
Journal: Journal of the American College of Cardiology (2001)