tbuckley/cabot-search huggingface dataset:
Human Ia beta chains and the invariant chain share a common antigenic determinant.
Authors: O J Finn, C J Stackhouse, R S Metzgar
Journal: The Journal of Experimental Medicine (1983)

We have presented evidence that a mouse monoclonal antibody 1,227, which was previously shown to recognize a determinant on the light chains beta 1 and beta 2 of human Ia antigens, also recognizes a determinant on the invariant chain (1) associated with these molecules. Ia-specific proteins were resolved by two-dimensional (2D) PAGE and electrophoretically transferred onto nitrocellulose filters. The presence of a determinant shared between beta 1, beta 2 and I was established using "Western blotting" technique. In addition, we demonstrated that 1,227 can immunoprecipitate isolated beta 1, beta 2, and the invariant chain proteins following their separate elution from SDS-PAGE.
The Day the EHR Died
Authors: Paul Hyman
Journal: Annals of Internal Medicine (2014)

On Being a Doctor15 April 2014The Day the EHR DiedPaul Hyman, MDPaul Hyman, MDFrom Cambridge Health Alliance, Cambridge, Massachusetts.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M13-2749 Audio Reading - “The Day the EHR Died” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "The Day the EHR Died," by P. Hyman. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I was sitting at the computer, reviewing a note in the EHR, when suddenly the software froze. I was just about to begin a full day in clinic.I felt immediate frustration and anger. Each day in my job as a primary care physician is a race that I cannot finish to complete as much as I can from a long list of electronic messages, results, prescriptions, paperwork, telephone calls, and e-mails. For each minute I am unproductive at work, I know I will be working 2 minutes later that night after my family has all gone to sleep.Once ... Author, Article, and Disclosure InformationAffiliations: From Cambridge Health Alliance, Cambridge, Massachusetts.Corresponding Author: Paul Hyman, MD, 454 Broadway, Revere, MA 02151; e-mail, [email protected]org. PreviousarticleNextarticle Advertisement Audio Reading - “The Day the EHR Died” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "The Day the EHR Died," by P. Hyman. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics Cited byThe Electronic Health Record and the Clinical ExaminationEthical Implications of the Electronic Health Record: In the Service of the PatientSnapshot at Mid-stride: Current State of EHRs and Their Use by Clinicians from a CMIO’s PerspectiveThe Impact of the Implementation of the Electronic Medical Record in an Italian University HospitalReport of the AMIA EHR-2020 Task Force on the status and future direction of EHRs 15 April 2014Volume 160, Issue 8Page: 576-577KeywordsChartsComputer softwareComputersElectronic medical recordsEmergency departmentInfectious diseasesPrimary care physiciansThoraxVaccinesVital signs ePublished: 15 April 2014 Issue Published: 15 April 2014 Copyright & PermissionsCopyright © 2014 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Economic evaluation of etanercept in the management of chronic plaque psoriasis
Authors: A. Lloyd, P. Reeves, P. Conway, A. Reynolds, G. Baxter
Journal: British Journal of Dermatology (2008)

The National Institute for Health and Clinical Excellence has recommended that etanercept 25 mg twice weekly (biw) be used in adults with severe plaque psoriasis. However, its economic model did not consider the alternative licensed regimen of etanercept 50 mg biw.To assess the cost-effectiveness of etanercept 50 mg biw for the treatment of chronic plaque psoriasis, and to explore characteristics of patients who benefited most from 50 mg dosing.An economic model was constructed to estimate the incremental cost per quality-adjusted life year (QALY) gained. The model considered patients with chronic plaque psoriasis who had both Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI) of 10 or higher who were unable to take standard systemic therapies. Quality of life gain was estimated from the DLQI responses of patients enrolled in three clinical studies. The model considered expenditure on drugs, monitoring visits, adverse events and inpatient stays. Costs were estimated from the perspective of the U.K. National Health Service over a time period of 10 years.The incremental cost per QALY for etanercept 50 mg biw compared with no systemic therapy was found to be 6217 pounds sterling (95% confidence interval 5396-7486 pounds sterling). The cost-effectiveness of 50 mg dosing was more attractive in patients with baseline PASI > or = 20 (5163 pounds sterling) or baseline DLQI > or = 20 (4599 pounds sterling).This model found the licensed dose regimen of etanercept 50 mg biw to be cost effective in the U.K. This regimen was particularly appropriate for patients with severe disease or poor quality of life at baseline.
Prognostic Implication of Creatine Kinase Elevation Following Elective Coronary Artery Interventions
Authors: Thomas Q. Kong
Journal: JAMA (1997)

To determine the prognostic significance of creatine kinase (CK) elevation following elective percutaneous transluminal coronary angioplasty (PTCA).Retrospective cohort study.Tertiary care referral center.A total of 253 consecutive patients with total CK and CK-MB fraction (CK-MB) elevation (case patients) and 120 patients without CK elevation (controls). Control patients had undergone interventions during the same month and year using the same devices.In-hospital and late cardiac mortality, subsequent myocardial infarction, and the combined end point of cardiac mortality or myocardial infarction.Patient groups were similar with respect to age, sex, extent of coronary artery disease, left ventricular function, number of lesions treated by PTCA, and mean duration of follow-up (>3.5 years). Cardiac mortality was significantly greater (P=.02) for patients with CK elevation after PTCA. When patients were categorized according to peak CK elevation, cardiac mortality differed significantly among patient groups (P=.007), with increased cardiac mortality observed for patients with high (>3.0 times normal) and intermediate (1.5 to 3.0 times normal) CK elevations. In multivariate analyses, higher peak CK and lower ejection fraction were the most important predictors of increased cardiac mortality (both, P<.001); the relative risk for cardiac mortality was 1.05 (95% confidence interval, 1.03-1.08) per 100-U/L increment increase in CK.Creatine kinase elevation following elective PTCA is associated with increased late cardiac mortality. This increase in cardiac mortality is independent of clinical variables, severity of heart disease, coronary artery lesion characteristics, interventional devices, and procedural outcomes. Even patients with lesser degrees of CK elevation are at significantly increased risk for late cardiac death.
Decline in NHS productivity over past decade is branded "a myth"
Authors: I. Torjesen
Journal: BMJ (2012)

Official claims that NHS productivity has declined over the past 10 years have been disputed by a leading expert in health policy, who argues that this is a myth and that productivity has probably gone up.

Claims by politicians that NHS productivity is in decline, which are being used by the Conservatives to justify a need for their controversial health reforms, have been based mainly on an analysis by the Office for National Statistics (ONS) showing that overall NHS productivity has fallen by 0.4% a year since 2000 (http://bit.ly/xNn6B7). A National Audit Office report published in 2010 concluded from these figures that this meant that hospital productivity had fallen by around 1.4% a year ( BMJ 2010;341:c7287, doi:10.1136/bmj.c7287).

But Nick Black, from the department of public health and policy at the London School of Hygiene and Tropical Medicine, writing in the Lancet this week (doi:10.1016/S0140-6736(11)61782-0), argues that “rather than declining, …
Visualization of a Pseudomeningocele on Isotope Cisternography
Authors: JANE TUVIA, SUREKHA PATEL, MAHENDRA PATEL, GERARD W. MOSKOWITZ, LESTER LEVY
Journal: Clinical Nuclear Medicine (1988)

Pseudomeningocele, a hernial protrusion of the meninges, most commonly forms in wounds that have been incompletely closed at surgery. They are frequently seen with hydrocephalus, with or without increased intracranial pressure. The authors present a case of an incidental finding of a posterior fossa pseudomeningocele seen on cisternography that was performed because of postoperative hydrocephalus after removal of a cerebellar astrocytoma.
Polyunsaturated fatty acids in treatment of acute remitting multiple sclerosis.
Authors: D Bates, P R Fawcett, D A Shaw, D Weightman
Journal: BMJ (1978)

One hundred and sixteen patients with acute remitting multiple sclerosis (MS) took part in a double-blind controlled trial of treatment with polyunsaturated fatty acids and were randomly allocated to one of four groups. Two groups received linoleic acid, one alone as a spread and one with gamma-linolenic acid in capsules (Naudicelle); and two control groups received oleic acid, one as a spread and one in capsules. Rates of clinical deterioration and frequencies of attacks were not significantly different between treated and control groups. Exacerbations were shorter and less severe in patients receiving a high dose of linoleic acid than in controls, but those receiving a lower dose--that is, Naudicelle--showed no such difference. Thus supplementing the diet with 20 g linoleic acid marginally affected the duration and severity of relapses of MS but had no effect on overall disability. The dose of Naudicelle used provided insufficient supplementation.
Elevated sympathetic nerve activity in patients with accelerated essential hypertension.
Authors: T Matsukawa, T Mano, E Gotoh, M Ishii
Journal: Journal of Clinical Investigation (1993)

To determine if an abnormality exists in the sympathetic nervous system of patients with accelerated hypertension, we recorded muscle sympathetic nerve activity (MSNA) from the tibial nerve by microneurography in eight benign essential hypertensives and seven accelerated essential hypertensives. Basal MSNA, plasma renin activity, and plasma angiotensin II levels were significantly higher in accelerated hypertensives than in benign hypertensives (P < 0.05). To clarify the relationship between the renin-angiotensin axis and sympathetic nervous system in the accelerated hypertensives, we measured the MSNA after 7 d of oral administration of captopril (75 mg/d) for antihypertensive treatment in the benign hypertensives and accelerated hypertensives. After administering captopril, the arterial pressure decreased significantly in the benign hypertensives and accelerated hypertensives with decreases in plasma angiotensin II levels, and the decreases in arterial pressure were greater in the accelerated hypertensive than in the benign hypertensives. After captopril administration, the MSNA decreased significantly in the accelerated hypertensives but did not change in the benign hypertensives. Thus, in accelerated hypertensives, sympathetic tone is elevated, and the elevated sympathetic tone is closely related to the activated renin-angiotensin axis tone.
β-Blockers in Congestive Heart Failure: A Bayesian Meta-Analysis
Authors: James M. Brophy, Lawrence Joseph, Jean L. Rouleau
Journal: Annals of Internal Medicine (2001)

Congestive heart failure is an important cause of patient morbidity and mortality. Although several randomized clinical trials have compared beta-blockers with placebo for treatment of congestive heart failure, a meta-analysis quantifying the effect on mortality and morbidity has not been performed recently.The MEDLINE, Cochrane, and Web of Science electronic databases were searched from 1966 to July 2000. References were also identified from bibliographies of pertinent articles.All randomized clinical trials of beta-blockers versus placebo in chronic stable congestive heart failure were included.A specified protocol was followed to extract data on patient characteristics, beta-blocker used, overall mortality, hospitalizations for congestive heart failure, and study quality.A hierarchical random-effects model was used to synthesize the results. A total of 22 trials involving 10 135 patients were identified. There were 624 deaths among 4862 patients randomly assigned to placebo and 444 deaths among 5273 patients assigned to beta-blocker therapy. In these groups, 754 and 540 patients, respectively, required hospitalization for congestive heart failure. The probability that beta-blocker therapy reduced total mortality and hospitalizations for congestive heart failure was almost 100%. The best estimates of these advantages are 3.8 lives saved and 4 fewer hospitalizations per 100 patients treated in the first year after therapy. The probability that these benefits are clinically significant (>2 lives saved or >2 fewer hospitalizations per 100 patients treated) is 99%. Both selective and nonselective agents produced these salutary effects. The results are robust to any reasonable publication bias.beta-Blocker therapy is associated with clinically meaningful reductions in mortality and morbidity in patients with stable congestive heart failure and should be routinely offered to all patients similar to those included in trials.
NK cells link obesity-induced adipose stress to inflammation and insulin resistance
Authors: Felix M Wensveen, Vedrana Jelenčić, Sonja Valentić, Marko Šestan, Tamara Turk Wensveen, Sebastian Theurich, Ariella Glasner, Davor Mendrila, Davor Štimac, F Thomas Wunderlich, Jens C Brüning, Ofer Mandelboim, Bojan Polić
Journal: Nature Immunology (2015)
Effect of Cocaine on Left Ventricular Function
Authors: Prabodh M. Mehta, Terry A. Grainger, Robert M. Lust, Assad Movahed, Jarrett Terry, M.G.F. Gilliland, Stanley R. Jolly
Journal: Circulation (1995)

Background To determine whether alterations in left ventricular (LV) function after a cocaine infusion are due to reduced myocardial contractility or changes in loading conditions, we examined LV function in 30 morphine-sedated, closed-chest dogs. We also wanted to determine the time course of the effects of cocaine on LV function after the infusion was stopped. Methods and Results Two-dimensional echocardiography and hemodynamics provided LV fractional shortening and end-systolic wall stress data. Radionuclide ventriculography was also performed. Four groups of dogs received saline or cocaine infusions of 10, 30, or 100 μg · kg −1 · min −1 . Cocaine was infused for 90 minutes with ECG and arterial pressure monitoring. Animals were monitored for an additional 120 minutes after the infusion ended. Arterial pressure rose over the course of the experiment in all four groups, but saline and cocaine 10 μg · kg −1 · min −1 did not significantly change ejection fraction. Cocaine 30 and 100 μg · kg −1 · min −1 acutely increased arterial pressure and heart rate but decreased ejection fraction from 0.64±0.06 to 0.45±0.08 and from 0.65±0.10 to 0.46±0.11, respectively. Additionally, cocaine 100 μg · kg −1 · min −1 decreased fractional shortening from 36±9% to 23±12%. However, cocaine 30 and 100 μg · kg −1 · min −1 also increased wall stress from 42±15 to 65±11 g/cm 2 and from 37±15 to 90±33 g/cm 2 , respectively. These results were analyzed by use of the relation between wall stress and fractional shortening as an index of contractility. Fractional shortening after cocaine infusion was displaced downward as a result of increased wall stress rather than changes in contractility. In addition, alteration of afterload with phenylephrine (6 μg/kg) and sodium nitroprusside (10 μg/kg) before and during infusion of cocaine 100 μg · kg −1 · min −1 showed similar regression lines for wall stress to fractional shortening. Conclusions Ejection-phase indexes of LV function were reduced by cocaine in this model of conscious, sedated dogs, but effects were attributable to increased wall stress rather than to reduced myocardial contractility. These effects persisted for at least 2 hours after the infusion was stopped.
Hepatic alcohol dehydrogenase activity in alcoholic subjects with and without liver disease.
Authors: F Vidal, J Perez, J Morancho, B Pinto, C Richart
Journal: Gut (1990)

Alcohol dehydrogenase activity was measured in samples of liver tissue from a group of alcoholic and non-alcoholic subjects to determine whether decreased liver alcohol dehydrogenase activity is a consequence of ethanol consumption or liver damage. The alcoholic patients were classified further into the following groups: control subjects with no liver disease (group 1), subjects with non-cirrhotic liver disease (group 2), and subjects with cirrhotic liver disease (group 3). The non-alcoholic subjects were also divided, using the same criteria, into groups 4, 5, and 6, respectively. The analysis of the results showed no significant differences when mean alcohol dehydrogenase activities of alcoholic and non-alcoholic patients with similar degrees of liver pathology were compared (groups 1 v 4, 2 v 5, and 3 v 6. Alcohol dehydrogenase activity was, however, severely reduced in patients with liver disease compared with control subjects. Our findings suggest that alcohol consumption does not modify hepatic alcohol dehydrogenase activity. The reduction in specific alcohol dehydrogenase activity in alcoholic liver disease is a consequence of liver damage.
What Is the Optimal Chest Compression Depth During Out-of-Hospital Cardiac Arrest Resuscitation of Adult Patients?
Authors: Ian G. Stiell, Siobhan P. Brown, Graham Nichol, Sheldon Cheskes, Christian Vaillancourt, Clifton W. Callaway, Laurie J. Morrison, James Christenson, Tom P. Aufderheide, Daniel P. Davis, Cliff Free, Dave Hostler, John A. Stouffer, Ahamed H. Idris
Journal: Circulation (2014)

Background— The 2010 American Heart Association guidelines suggested an increase in cardiopulmonary resuscitation compression depth with a target &gt;50 mm and no upper limit. This target is based on limited evidence, and we sought to determine the optimal compression depth range. Methods and Results— We studied emergency medical services–treated out-of-hospital cardiac arrest patients from the Resuscitation Outcomes Consortium Prehospital Resuscitation Impedance Valve and Early Versus Delayed Analysis clinical trial and the Epistry-Cardiac Arrest database. We calculated adjusted odds ratios for survival to hospital discharge, 1-day survival, and any return of circulation. We included 9136 adult patients from 9 US and Canadian cities with a mean age of 67.5 years, mean compression depth of 41.9 mm, and a return of circulation of 31.3%, 1-day survival of 22.8%, and survival to hospital discharge of 7.3%. For survival to discharge, the adjusted odds ratios were 1.04 (95% CI, 1.00–1.08) for each 5-mm increment in compression depth, 1.45 (95% CI, 1.20–1.76) for cases within 2005 depth range (&gt;38 mm), and 1.05 (95% CI, 1.03–1.08) for percentage of minutes in depth range (10% change). Covariate-adjusted spline curves revealed that the maximum survival is at a depth of 45.6 mm (15-mm interval with highest survival between 40.3 and 55.3 mm) with no differences between men and women. Conclusions— This large study of out-of-hospital cardiac arrest patients demonstrated that increased cardiopulmonary resuscitation compression depth is strongly associated with better survival. Our adjusted analyses, however, found that maximum survival was in the depth interval of 40.3 to 55.3 mm (peak, 45.6 mm), suggesting that the 2010 American Heart Association cardiopulmonary resuscitation guideline target may be too high. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00394706.
Reduction of cerebral perfusion precedes rise of intracranial pressure in rats with ischemic fulminant liver failure
Authors: Vijay Shah, Steve Webster, Jeanne Gottstein, Andres T. Blei
Journal: Hepatology (1993)

In fulminant liver failure, brain edema may progress to intracranial hypertension. However, the rise in intracranial pressure is a late event in this sequence. We investigated the relationship between cerebral perfusion and development of intracranial hypertension in a well-characterized model of fulminant liver failure, the rat subjected to hepatic devascularization (n = 11). In addition, we examined the effects of hyperglycemia on the development of brain edema because high blood glucose level can exacerbate other forms of brain edema, as seen in stroke. Intracranial pressure was continuously monitored with a cisterna magna catheter; relative changes in blood flow were continuously assessed with a Doppler flow probe on the internal carotid artery. Cerebral perfusion decreased by 62%, with the greatest reduction before the onset of increased intracranial pressure. Intracranial pressure did not change until 2 hr before death, at which time it increased exponentially. Brain water in fulminant liver failure rats was significantly increased compared with that in controls. Hyperglycemia (200 to 220 mg/dI) had no effect on time elapsed until loss of corneal reflex, percentage of brain water, maximal intracranial pressure or pattern of change in cerebral perfusion compared with euglycemia (80 to 100 mg/dI). Sham-operated animals showed no changes in measured parameters. We conclude that a linear reduction in cerebral perfusion precedes the rise of intracranial pressure in this model, a decrease that may reflect changes in brain metabolic activity at the time that brain edema develops. Carotid blood flow monitoring may be a useful noninvasive tool for the detection of cerebral events in fulminant liver failure. (Hepatology 1993;17:1117-1121.)
Investigational treatments: process, payment, and priorities
Authors: R. A. Burt
Journal: JAMA (1997)

To the Editor.  —In his Clinical Decision Making article on investigational treatments, Dr Eddy1maintains a misconception that could have damaging consequences in small-population studies when he states that randomization is the best way to ensure similarity of the patient groups.  As clinical trials experts, statisticians, and epidemiologists have stressed repeatedly, the purpose of randomization in randomized controlled trials is to minimize the effect of unconscious bias,2to reduce the bias in assigning patients to treatment,3to ensure the absence of confounding by selection bias,4and to ensure that at the outset the trial groups differ only by chance.5As they have warned, randomization will not ensure an equal distribution of risk factors or other relevant patient characteristics to each treatment group3and does not maximize equality of the groups.5Randomization is not the best way of producing equality,4but it does
Inexpensive one-way screen.
Authors: E S Barton
Journal: BMJ (1972)

mean level of serum vitamin B12 among smokers is significantly less than among non-smokers.They discuss various factors which may have affected the serum B12 level, but they do not mention folate deficiency, which is common during pregnancy.Low serum Bi2 levels have been observed in over 40% of patients with megaloblastic anaemia due to folate deficiency, and the levels rise slowly to within the normal range on treatment with folic acid alone.1 2 As Dr.McGarry and Miss Andrews have not published the serum folate levels in their group of pregnant women, it is not possible to draw conclusions from the B12 levels unless all the women were taking folic acid.-Iam, etc.,