tbuckley/cabot-search huggingface dataset:
Automated Review of Electronic Health Records to Assess Quality of Care for Outpatients with Heart Failure
Authors: David W. Baker, Stephen D. Persell, Jason A. Thompson, Neilesh S. Soman, Karen M. Burgner, David Liss, Karen S. Kmetik
Journal: Annals of Internal Medicine (2007)

Background: Electronic health records (EHRs) may be used to assess quality of care. Objective: To evaluate the accuracy of automated review of EHR data to measure quality of care for outpatients with heart failure. Design: Observational study of quality of care for heart failure comparing automated review of EHR data with automated review followed by manual review of electronic notes for patients with apparent quality deficits (hybrid review). Setting: An academic general internal medicine clinic with several years' experience using a commercial EHR. Patients: 517 adults with a qualifying International Classification of Diseases, Ninth Revision, diagnosis of heart failure in their EHR data and 2 or more clinic visits over the past 18 months. Measurements: Left ventricular ejection fraction (LVEF), prescription of a β-blocker and an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) for patients with left ventricular systolic dysfunction (LVEF <0.40) and prescription of warfarin for patients with comorbid atrial fibrillation. Results: Performance based on automated review of EHR data was similar to that based on hybrid review for assessing LVEF measurement (94.6% vs. 97.3%), prescription of β-blockers (90.9% vs. 92.8%), and prescription of ACE inhibitors or ARBs (93.9% vs. 98.7%). However, performance based on automated review was lower than that based on hybrid review for prescription of warfarin for atrial fibrillation (70.4% vs. 93.6%), primarily because automated review did not detect documentation of accepted reasons for not prescribing warfarin. Limitations: The findings may not be applicable to other practices and other EHRs. The authors used EHR data to identify eligible patients, so the study may have excluded some patients with heart failure. Patient charts were manually reviewed only if a provider appeared to fail a quality measure on automated review and did not determine the sensitivity and specificity of automated review according to standard definitions. Conclusions: Automated review of EHR data to measure the quality of care of outpatients with heart failure missed many exclusion criteria for medications documented only in providers' notes. As a result, it sometimes underestimated performance on medication-based quality measures.
DIASTOLIC DYSFUNCTION IS A STRONG PROGNOSTIC PREDICTOR IN ASYMPTOMATIC PATIENTS WITH MODERATE TO SEVERE AORTIC STENOSIS
Authors: Sung-Ji Park, Sung-A Chang, Jin-Oh Choi, Sang-Chol Lee, Seung Woo Park, Pyo Won Park, Jae K. Oh
Journal: Journal of the American College of Cardiology (2011)
Increased expression of cardiac angiotensin II type 1 (AT) receptors decreases myocardial microvessel density after experimental myocardial infarction
Authors: R DEBOER, Y PINTO, A SUURMEIJER, S POKHAREL, E SCHOLTENS, M HUMLER, J SAAVEDRA, F BOOMSMA, W VANGILST, D VANVELDHUISEN
Journal: Cardiovascular Research (2003)

Objective: To study the effects of increased levels of myocardial angiotensin II type 1 (AT1) receptor on microvascular growth following myocardial infarction (MI). Methods: MI was created in transgenic rats (TGR) with a cardioselective overexpression of the AT1 receptor. We used Sprague–Dawley (SD) rats as controls. Some of the rats were treated with the selective AT1 receptor blocker losartan (Los). Rats were sacrificed after 3 weeks. Results: MI caused left ventricular (LV) hypertrophy and LV dysfunction in both SD and TGR, which was prevented by AT1 receptor blockade. Furthermore, MI decreased microvessel density in the non-infarcted myocardium (SD MI: 1653±37/mm2, P<0.01 vs. sham-operated controls), however, microvessel density decreased significantly more in TGR with MI (1298±33/mm2, P<0.01 vs. SD MI). AT1 receptor blockade restored microvessel density (SD MI Los: 2046±195/mm2; TGR MI Los: 1742±47/mm2; P<0.01 vs. untreated). The differences in microvessel density were still present after correction for LV hypertrophy. The increase in microvessel density after AT1 receptor blockade was not accompanied by increased myocardial vascular endothelial growth factor (VEGF) levels. Microvessel density correlated with parameters of myocardial stretch, such as LV end-diastolic pressure (−0.681, P<0.001) and N-ANP (−0.424, P=0.01). Conclusions: Microvessel density after MI is decreased when the AT1 receptor is overexpressed, and this is amenable to AT1 receptor blockade. This suggests that efficacy of AT1 receptor blockers post-MI may not only be due to attenuation of LV remodeling, but also to a stimulatory effect on angiogenesis.
Dendritic cells induce T cell proliferation to synthetic antigens under Ir gene control.
Authors: G H Sunshine, D R Katz, M Feldmann
Journal: The Journal of Experimental Medicine (1980)

Dendritic cells prepared by a modification of the method of Steinman and Cohn are I-A+ and FcR-. They are extremely potent at activating not only allogeneic T cell proliferation but also antigen-specific syngeneic T cell proliferation. Dendritic cells from nonresponder strains are unable to present antigens to responder X nonresponder T cells, suggesting that they may be a site of Ir gene product expression.
Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography.
Authors: W R Condos, R D Latham, S D Hoadley, A Pasipoularides
Journal: Circulation (1987)

Ten subjects with normal hemodynamics were studied during elective cardiac catheterization with right and left heart multisensor micromanometry to assess hemodynamic responses to the Mueller maneuver. Simultaneous right and left circulatory hemodynamics and left ventricular, pulmonary arterial, and aortic pressures were recorded, in addition to pulmonary arterial and aortic flow velocities. Steady-state cardiac outputs were determined by thermal dilution. Aortic systolic and mean pressures were not significantly changed during the Mueller maneuver, in contrast to a lower diastolic (p = .019) and higher pulse pressure (p = .016). Mean right atrial pressure (+/- SE) decreased from 7 +/- 1 to -17 +/- 4 mm Hg (p = .0002) and the right atrial "x" descent was markedly accentuated. Left ventricular end-diastolic pressure decreased from 12 +/- 4 to -3 +/- 13 mm Hg (p = .0025). Systemic vascular resistance and left ventricular peak positive dP/dt were increased during the Mueller maneuver (p less than .02), cardiac output and stroke volume were reduced (p less than .05), and there was no significant change in heart rate. Right and left peak flow velocities showed a trend toward a bilateral decrease (right, p = .054; left, p greater than .1), and times to peak flow velocity were increased in the pulmonary artery (p = .007) and reduced in the aortic root (p = .03). Normal subjects were studied separately by pulsed Doppler echocardiography. During the sustained Mueller maneuver, the internal jugular and right ventricular dimensions decreased, and superior vena cava Doppler flow was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
Impact of weight on the efficacy and safety of ustekinumab in patients with moderate to severe psoriasis: Rationale for dosing recommendations
Authors: Mark Lebwohl, Newman Yeilding, Philippe Szapary, Yuhua Wang, Shu Li, Yaowei Zhu, Kristian Reich, Richard G. Langley, Kim A. Papp
Journal: Journal of the American Academy of Dermatology (2010)
Abstract 66: Effectiveness Of Cardiac-only CPR Training by Self-learning Video, a 1-hour program, or Both
Authors: Chika Nishiyama, Taku Iwami, Takashi Kawamura, Masahiko Ando, Robert A Berg, Naohiro Yonemoto, Risa Fukuda, Haruyuki Yuasa, Akiko Kada, Hiroyuki Yokoyama, Hiroshi Nonogi
Journal: Circulation (2007)

[Introduction] Despite present efforts to train the general public in CPR, the proportion of bystander CPR is still low. Length of CPR training program and complexity of CPR skills may be barriers to bystander CPR performance. Recently, simple video self-learning has been shown to be an effective CPR training technique. [Objective] To evaluate the effectiveness of cardiac-only CPR training program by a self-learning video, a 1-hour practical course, or both. [Method] Designs : A randomized controlled trial. Participants: General public aged 18 years or older. Intervention: In the video (V) group, participants received the self-learning video before CPR training and then attended a 1-hour cardiac-only CPR training program; in the control (C) group participants attended the training program without a self-learning video. Data collection: Before and immediately after the training, a 2 minute scenario-based test was conducted and CPR skills were recorded. Outcomes: The primary outcome measure was the number of correct chest compressions immediately after the training. We also calculated the achievement of correct chest compressions, which meant the proportion of correct chest compressions in relation to the ideal number of chest compressions based on 2005 CPR guideline. [Result] 214 participants were randomly assigned to V (108) and C (106) groups. Before the training, the proportion of attempting chest compression, attempting AED operation, and calling for an AED, and the total number of chest compressions were significantly grater in the V group. After the training, all measured CPR skills of both groups improved substantially compared with pre-training skills, but there were no differences between groups (Table ). [Conclusion] A self-learning video improved CPR skills. However, a 1-hour practical training course was substantially more effective and the addition of a self-learning video did not improve its effectiveness. Table: CPR Skills of Pre- and Post-training
Decreased ribosomal RNA content and in vitro RNA synthesis in purified bone marrow erythroblasts of patients with idiopathic ineffective erythropoiesis and diguglielmo disease
Authors: GraçA Lourenço, Stephen Embury, Stanley L Schrier, Laurence H. Kedes
Journal: American Journal of Hematology (1978)

Abstract Ribsomal RNA content and in vitro 3 H‐uridine and 3 H‐thymidine incorporation were examined in purified marrow erythroblasts of patients with idiopathic ineffective eryth‐ ropoiesis (HE) and DiGuglielmo disease (DD) and compared with cells from normal marrows. Whereas H‐thymidine incorporation rates were normal in all patients, 3 H‐uridine incorporation was 42%‐75% of normal in cells from patients examined. Ribosomal RNA content was measured by spectrophotometric scanning of RNA electrophoresed on polyacrylamide gels and corrections made for contamination of the erythroblast preparations with ribosome bearing reticulocytes. In cells from every patient examined RNA content was decreased to 60‐76% of normal. Uridine incorporation and rRNA content of patients with β thalassemia minor and megaloblastic anemia were normal, suggesting that the defects observed in HE and DD were not due to ineffective erythropoiesis per se. Since erythroblast ribosomes may be rate limiting in protein synthesis, we postulate that even a minor decrease in ribosome content might engender the ubiquitous abnormalities reported in erythroid cells in both HE and DD.
An Insider's Guide for Medical Authors and Editors
Authors: Lawrence Grouse
Journal: JAMA (1987)

For a thin paperback with only about 100 pages of text, this little volume packs a wallop. It delivers on the promise of its title by providing readers with authoritative and helpful information from one of the Scientific Editors of the<i>Canadian Medical Association Journal</i>about the medical publication process. The author's term "companion" for the book is fitting. It is a disorganized romp through the intellectual issues of contemporary medical editing and writing. It succeeds best when the author exercises his considerable creative talents. Brief, illustrative vignettes that resemble mini—morality plays bring many otherwise boring technical editorial issues to life. They feature such droll characters as the elitist, hardnosed journal editor Ambrose Relso, MD, and the plodding resident, would-be author, and all-around schlemiel Norman Nojarg, MD. Interesting historical anecdotes presented in the book, such as the origin of symposia as drinking parties, put modern practices in an instructive light.
Conditioned stimuli and the expression of extraversion: Help or hindrance?
Authors: Paul Vezina
Journal: Behavioral and Brain Sciences (1999)

Upon consideration of the unconditioned and particularly the conditioned stimuli that have been proposed to participate in the generation of incentive motivational states and, by extension, of extraversion, the nature of the contribution of NAS DA becomes less clear. Different kinds of conditioned stimuli can also exert strong control over the expression of behavioral sensitization. How might such stimuli affect the ability of experience-dependent processes to introduce stable individual differences in the development and expression of extraversion trait levels?
The “mechanism” of human cognitive variation
Authors: Matthew K. Belmonte
Journal: Behavioral and Brain Sciences (2008)

Abstract The theory of psychosis and autism as diametrical disorders offers a tractable and testable view of normal and abnormal human cognitive variation as a function of opposing traits grouped by their selection for maternal and paternal reproductive fitness. The theory could be usefully rooted and developed with reference to the lower-level perceptual and attentional phenomena from which social cognitive modules are developmentally refined.
Retinoic acid suppresses telomerase activity in HSC-1 human cutaneous squamous cell carcinoma
Authors: M. Kunisada, A. Budiyanto, T. Bito, C. Nishigori, M. Ueda
Journal: British Journal of Dermatology (2005)

Background Activation of telomerase is crucial for the continued growth and progression of cancer cells. In a previous study, we showed that telomerase is frequently activated in skin tumours. Objective Because retinoic acid (RA) plays an important role in the growth and differentiation of keratinocytes and as RA has some preventive and therapeutic effects on human skin cancers, we examined the effect of RA on the telomerase activity of HSC‐1 human cutaneous squamous cell carcinoma cells. Results Treatment of HSC‐1 cells with all‐trans RA (ATRA) significantly suppressed their telomerase activity. The suppression of telomerase activity was obvious at day 4 and was maximal at day 5 after the start of treatment with RA. This suppression was reversible as removal of ATRA allowed the recovery of telomerase activity. The suppression of telomerase activity correlated with the decreased expression of mRNA of human telomerase catalytic subunit (hTERT), the rate‐limiting determinant of enzyme activity. The production of c‐myc and of Sp1 proteins, transcription factors regulating hTERT expression, was not suppressed in HSC‐1 cells by ATRA, but phosphorylation of extracellular signal‐regulated kinases (ERK)1/2 and of the serine/threonine kinase Akt was significantly suppressed. Phosphorylation of the epidermal growth factor receptor, which regulates hTERT expression in HSC‐1 cells, was not altered by ATRA. Conclusions These data indicate that RA is effective in inhibiting telomerase activity in HSC‐1 cells. Suppression of ERK1/2 and Akt activation is presumed to be involved in the RA‐induced suppression of hTERT.
Are clinical trial data shared sufficiently today? Yes
Authors: J. Castellani
Journal: BMJ (2013)

The AllTrials campaign asks for all trials to be registered and their results published. <b>Ben Goldacre</b> (doi:10.1136/bmj.f1880) says we need the evidence to make informed decisions about medicines. <b>John Castellani</b> says mandatory disclosure could affect patient privacy, stifle discovery, and allow competitors or unscrupulous actors to use the information
HEMOBILIA, CHOLECYSTITIS, AND GASTROINTESTINAL BLEEDING WITH RUPTURE OF LIVER
Authors: Harry J. Epstein
Journal: JAMA (1952)

Subcutaneous rupture of the liver is not a rarity. Our case is of particular interest on account of the complications of hemobilia, hemorrhagic cholecystitis, gastrointestinal bleeding, hemothorax, and hydropneumopericardium, with complete recovery. The over-all mortality from hepatic rupture in general remains about 60%, that from massive rupture being higher (60% to 80% ).1  REPORT OF A CASE  R. G., 9 years of age, a white male child, sustained a severe injury to the abdomen and lower right portion of the chest at 5 p. m. on Feb. 9, 1951, when he fell from his sled into a jagged rock-filled creek. He was brought into the office 20 minutes later in a state of collapse. Shock therapy was immediately carried out with favorable response. X-rays were taken of the abdomen to determine the presence of air under the diaphragm and because of possible fracture of the ribs. The x-rays were all
Cyclooxygenase-2 Inhibits T Helper Cell Type 9 Differentiation during Allergic Lung Inflammation via Down-regulation of IL-17RB
Authors: Hong Li, Matthew L. Edin, J. Alyce Bradbury, Joan P. Graves, Laura M. DeGraff, Artiom Gruzdev, Jennifer Cheng, Ryan T. Dackor, Ping Ming Wang, Carl D. Bortner, Stavros Garantziotis, Anton M. Jetten, Darryl C. Zeldin
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

Helper CD4(+) T cell subsets, including IL-9- and IL-10-producing T helper cell type 9 (Th9) cells, exist under certain inflammatory conditions. Cyclooxygenase (COX)-1 and COX-2 play important roles in allergic lung inflammation and asthma. It is unknown whether COX-derived eicosanoids regulate Th9 cells during allergic lung inflammation.To determine the role of COX metabolites in regulating Th9 cell differentiation and function during allergic lung inflammation.COX-1(-/-), COX-2(-/-), and wild-type (WT) mice were studied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of Th9 differentiation using flow cytometry, cytokine assays, confocal microscopy, real-time PCR, and immunoblotting. In addition, the role of specific eicosanoids and their receptors was examined using synthetic prostaglandins (PGs), selective inhibitors, and siRNA knockdown.Experimental endpoints were not different between COX-1(-/-) and WT mice; however, the percentage of IL-9(+) CD4(+) T cells was increased in lung, bronchoalveolar lavage fluid, lymph nodes, and blood of allergic COX-2(-/-) mice relative to WT. Bronchoalveolar lavage fluid IL-9 and IL-10, serum IL-9, and lung IL-17RB levels were significantly increased in allergic COX-2(-/-) mice or in WT mice treated with COX-2 inhibitors. IL-9, IL-10, and IL-17RB expression in vivo was inhibited by PGD2 and PGE2, which also reduced Th9 cell differentiation of murine and human naive CD4(+) T cells in vitro. Inhibition of protein kinase A significantly increased Th9 cell differentiation of naive CD4(+) T cells isolated from WT mice in vitro.COX-2-derived PGD2 and PGE2 regulate Th9 cell differentiation by suppressing IL-17RB expression via a protein kinase A-dependent mechanism.
Hypoxia- and non-hypoxia-related pulmonary hypertension — Established and new therapies
Authors: H GHOFRANI, R VOSWINCKEL, F REICHENBERGER, N WEISSMANN, R SCHERMULY, W SEEGER, F GRIMMINGER
Journal: Cardiovascular Research (2006)

Pulmonary hypertension can occur as an isolated disease affecting the lung vessels only, in association with underlying hypoxic lung disorders, or due to chronic thromboembolic disease. Pulmonary hypertension caused by pulmonary venous congestion will not be focused on in this review. Regardless of the underlying disease, chronic cor pulmonale is associated with progressive clinical deterioration and a poor prognosis in most cases. The aim of specific therapies for pulmonary hypertension is to reduce pulmonary vascular resistance and thereby improve right ventricular function. Currently, three classes of drugs (prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors) are approved for the treatment of pulmonary arterial hypertension (PAH) in a defined patient population (group I according to the recent WHO classification). However, these medications may also lower pulmonary vascular resistance in patients with associated lung diseases (e.g. chronic obstructive pulmonary disease or lung fibrosis) and significant pulmonary hypertension, for whom these drugs are not yet approved. As non-selective vasodilators may induce gas-exchange disturbances, which preclude their long term use in these patients, such substances should be avoided in the hypoxemic patient. In this article we provide an update of the current understanding of hypoxia- and non-hypoxia-related pulmonary hypertension, addressing both the pathophysiological understanding of different disease aetiologies as well as the therapeutic options currently available.
Abnormal expression of the genes involved in cytokine networks and mitochondrial function in systemic juvenile idiopathic arthritis identified by DNA microarray analysis
Authors: S Ishikawa, T Mima, C Aoki, N Yoshio-Hoshino, Y Adachi, T Imagawa, M Mori, M Tomiita, N Iwata, T Murata, M Miyoshi, S Takei, Y Aihara, S Yokota, K Matsubara, N Nishimoto
Journal: Annals of the Rheumatic Diseases (2008)

Objectives: Systemic juvenile idiopathic arthritis (sJIA) is a rheumatic disease in childhood characterised by systemic symptoms and a relatively poor prognosis. Peripheral leukocytes are thought to play a pathological role in sJIA although the exact cause of the disease is still obscure. In this study, we aimed to clarify cellular functional abnormalities in sJIA. Methods: We analysed the gene expression profile in peripheral leukocytes from 51 patients with sJIA, 6 patients with polyarticular type JIA (polyJIA) and 8 healthy children utilising DNA microarrays. Gene ontology analysis and network analysis were performed on the genes differentially expressed in sJIA to clarify the cellular functional abnormalities. Result: A total of 3491 genes were differentially expressed in patients with sJIA compared to healthy individuals. They were functionally categorised mainly into a defence response group and a metabolism group according to gene ontology, suggesting the possible abnormalities in these functions. In the defence response group, molecules predominantly constituting interferon (IFN)γ and tumour necrosis factor (TNF) network cascades were upregulated. In the metabolism group, oxidative phosphorylation-related genes were downregulated, suggesting a mitochondrial disorder. Expression of mitochondrial DNA-encoded genes including cytochrome c oxidase subunit 1(MT-CO1) and MT-CO2 were suppressed in patients with sJIA but not in patients with polyJIA or healthy children. However, nuclear DNA-encoded cytochrome c oxidases were intact. Conclusion: Our findings suggest that sJIA is not only an immunological disease but also a metabolic disease involving mitochondria disorder.
Colorectal-Cancer Screening — Coming of Age
Authors: Theodore R. Levin, Douglas A. Corley
Journal: New England Journal of Medicine (2013)

The Minnesota Colorectal Cancer Control Study showed 20 years ago that the annual use of the guaiac fecal occult-blood test decreased mortality from colorectal cancer by 33%.1 A few years later, colorectal-cancer screening was endorsed by multidisciplinary guidelines2 and was covered by insurance,3 leading to an increase in the performance of colorectal-cancer screening tests. Two articles in this issue of the Journal provide evidence of what colorectal-cancer screening can accomplish over the long term.4,5 Nishihara and colleagues4 found decreased risks of colorectal cancer and death from colorectal cancer associated with screening colonoscopy and sigmoidoscopy, following two well-described prospective cohorts . . .