tbuckley/cabot-search huggingface dataset:
Multiple Biomarkers and Risk of Clinical and Subclinical Vascular Brain Injury
Authors: Aleksandra Pikula, Alexa S. Beiser, Charles DeCarli, Jayandra J. Himali, Stephanie Debette, Rhoda Au, Jacob Selhub, Geoffrey H. Toffler, Thomas J. Wang, James B. Meigs, Margaret Kelly-Hayes, Carlos S. Kase, Philip A. Wolf, Ramachandran S. Vasan, Sudha Seshadri
Journal: Circulation (2012)

Several biomarkers have been individually associated with vascular brain injury, but no prior study has explored the simultaneous association of a biologically plausible panel of biomarkers with the incidence of stroke/transient ischemic attack and the prevalence of subclinical brain injury.In 3127 stroke-free Framingham offspring (age, 59±10 years; 54% female), we related a panel of 8 biomarkers assessing inflammation (C-reactive protein), hemostasis (D-dimer and plasminogen activator inhibitor-1), neurohormonal activity (aldosterone-to-renin ratio, B-type natriuretic peptide, and N-terminal proatrial natriuretic peptides), and endothelial function (homocysteine and urinary albumin/creatinine ratio) measured at the sixth examination (1995-1998) to risk of incident stroke/transient ischemic attack. In a subset of 1901 participants with available brain magnetic resonance imaging (1999-2005), we further related these biomarkers to total cerebral brain volume, covert brain infarcts, and large white-matter hyperintensity volume. During a median follow-up of 9.2 years, 130 participants experienced incident stroke/transient ischemic attack. In multivariable analyses adjusted for stroke risk factors, the biomarker panel was associated with incident stroke/transient ischemic attack and with total cerebral brain volume (P<0.05 for both) but not with covert brain infarcts or white-matter hyperintensity volume (P>0.05). In backward elimination analyses, higher log-B-type natriuretic peptide (hazard ratio, 1.39 per 1-SD increment; P=0.002) and log-urinary albumin/creatinine ratio (hazard ratio, 1.31 per 1-SD increment; P=0.004) were associated with increased risk of stroke/transient ischemic attack and improved risk prediction compared with the Framingham Stroke Risk Profile alone; when the <5%, 5% to 15%, or >15% 10-year risk category was used, the net reclassification index was 0.109 (P=0.037). Higher C-reactive protein (β=-0.21 per 1-SD increment; P=0.008), D-dimer (β=-0.18 per 1-SD increment; P=0.041), total homocysteine (β=-0.21 per 1-SD increment; P=0.005), and urinary albumin/creatinine ratio (β=-0.15 per 1-SD increment; P=0.042) were associated with lower total cerebral brain volume.In a middle-aged community sample, we identified multiple biomarkers that were associated with clinical and subclinical vascular brain injury and could improve risk stratification.
Methotrexate osteopathy in rheumatic disease.
Authors: S J Preston, T Diamond, A Scott, M R Laurent
Journal: Annals of the Rheumatic Diseases (1993)

OBJECTIVE--To determine whether two adults with stress fractures receiving low weekly doses of methotrexate had methotrexate osteopathy. CASE REPORTS--Two adult patients developed features consistent with methotrexate osteopathy while receiving low weekly doses of methotrexate. METHODS--Iliac crest biopsy samples were taken and bone histomorphometry carried out. RESULTS--Symptoms resolved when the methotrexate was discontinued. Bone histology showed changes consistent with osteoblast inhibition by methotrexate. CONCLUSIONS--When given in low doses for prolonged periods, methotrexate may have adverse effects on bone, particularly in post-menopausal women.
Host genetic factors influence disease progression in chronic hepatitis C
Authors: Elizabeth E. Powell, Catherine J. Edwards-Smith, John L. Hay, Andrew D. Clouston, Darrell H. Crawford, Claudia Shorthouse, David M. Purdie, Julie R. Jonsson
Journal: Hepatology (2000)

Progressive hepatic fibrosis and cirrhosis develops in 20% to 30% of patients with chronic hepatitis C virus (HCV). We propose that host genetic factors influencing fibrogenesis may account for some of the variability in progression of this disease. In progressive fibrosis of other organs, particularly heart and kidney, production of the profibrogenic cytokine, transforming growth factor β1 (TGF-β1), may be enhanced by angiotensin II, the principal effector molecule of the renin-angiotensin system. The inheritance of polymorphisms in TGF-β1, interleukin 10 (IL-10), tumor necrosis factor α (TNF-α), and genes of the renin-angiotensin system was examined in 128 patients with chronic HCV. The influence of genotypes on the stage of hepatic fibrosis was tested after adjustment for potential confounders (age, gender, alcohol consumption, portal inflammation, and steatosis), which may have independent effects on histological severity. The stage of fibrosis was 0 in 30 (23.4%), 1 in 44 (34.4%), 2 in 27 (21.1%), and 3 or 4 in 27 (21.1%). A statistically significant relationship was seen between inheritance of high TGF-β1- and angiotensinogen (AT)-producing genotypes and the development of progressive hepatic fibrosis. This association persisted after correcting for potential confounders. Patients who inherited neither of the profibrogenic genotypes had no or only minimal fibrosis. Knowledge of these polymorphisms may have prognostic significance in patients with chronic HCV and may direct more aggressive therapy towards those patients with an increased risk of disease progression. The documentation of a significant relationship between AT genotype and fibrosis raises the novel suggestion that angiotensin II may be another mediator of extracellular matrix production in the liver.
Effect of Efferent Vagal Stimulation on Coronary Sinus Outflow and Cardiac Work in the Anesthetized Dog
Authors: HSUEH-HWA WANG, MARVIN R. BLUMENTHAL, S. C. WANG
Journal: Circulation Research (1960)

Efferent vagal stimulation in the anesthetized dog with constant ventricular rate caused either no change in coronary sinus outflow and cardiac work, or a decrease in coronary sinus outflow associated with a greater decrease in cardiac work. When the decreases were observed they could best be explained by a negative inotropic effect of vagal stimulation on ventricular muscle, rather than by a direct vasomotor effect of vagal stimulation on the coronary bed. Critical review of apparent divergent results previously reported regarding the effect of vagal stimulation on coronary flow reveals that they are not inconsistent with the above hypothesis.
TCT-36 One-year Clinical Outcomes of Diabetic Patients Treated With Everolimus-Eluting Bioresorbable Vascular Scaffolds: A Pooled Analysis From the ABSORB Cohort B and the ABSORB EXTEND Trials.
Authors: Takashi Muramatsu, Yoshinobu Onuma, Robert J. Van Geuns, Bernard Chevalier, Tejas M. Patel, Ashok Seth, Roberto Diletti, Hector M. Garcia-Garcia, Cécile Dorange, Susan Veldhof, Wai-Fung Cheong, Robert J. Whitbourn, Antonio L. Bartorelli, Alexandre Abizaid, Patrick W. Serruys
Journal: Journal of the American College of Cardiology (2013)
Intestinal GATA4 deficiency protects from diet-induced hepatic steatosis
Authors: Jay V. Patankar, Sascha Obrowsky, Prakash Doddapattar, Gerald Hoefler, Michele Battle, Sanja Levak-Frank, Dagmar Kratky
Journal: Journal of Hepatology (2012)

GATA4, a zinc finger domain transcription factor, is critical for jejunal identity. Mice with an intestine-specific GATA4 deficiency (GATA4iKO) are resistant to diet-induced obesity and insulin resistance. Although they have decreased intestinal lipid absorption, hepatic de novo lipogenesis is inhibited. Here, we investigated dietary lipid-dependent and independent effects on the development of steatosis and fibrosis in GATA4iKO mice.GATA4iKO and control mice were fed a Western-type diet (WTD) or a methionine and choline-deficient diet (MCDD) for 20 and 3 weeks, respectively. Functional effects of GATA4iKO on diet-induced liver steatosis were investigated.WTD-but not MCDD-fed GATA4iKO mice showed lower hepatic concentrations of triglycerides, free fatty acids, and thiobarbituric acid reactive species and had reduced expression of lipogenic as well as fibrotic genes compared with controls. Reduced nuclear sterol regulatory element-binding protein-1c protein levels were accompanied by lower lipogenic gene expression. Oil red O and Sirius Red staining of liver sections confirmed the observed reduction in hepatic lipid accumulation and fibrosis. Immunohistochemical staining revealed an increased number of jejunal glucagon-like peptide 1 (GLP-1) positive cells in GATA4iKO mice. Consequently, we found enhanced phosphorylation of hepatic AMP-activated protein kinase and acetyl-CoA carboxylase alpha.Our results provide strong indications for a protective effect of intestinal GATA4 deficiency on the development of hepatic steatosis and fibrosis via GLP-1, thereby blocking hepatic de novo lipogenesis.
"A NEW DIET FOR PEPTIC ULCER"
Authors: Alexander Jarotzky
Journal: JAMA (1925)

To the Editor:  —InThe Journal, Sept. 20, 1924, was published the work of Dr. Warren Coleman in which he proposes the use of raw white of egg and olive oil or butter fat given separately, as a quite new diet for peptic ulcer.  This diet was proposed by me in an article published in Russian in 1910 (Dietetic Treatment of Ulcer of the Stomach, Russk. Vrach , 1910, No. 51, p. 1979), and in German in 1911 (Ueber die diatetische Behandlung von Ulcus ventriculi, St. Petersburg med. Wchnschr.  36 :13, 1911). I also published an article about this method in 1916 ( Russk. Vrach , 1916, No.23), as well as a separate volume in 1918 (Treatment of Ulcer of the Stomach, St. Petersburg, 1918) and an article in 1923 ( Vrach. Gaz. , 1923, Nos. 17-18, p. 386). The diet has since been successfully used in the clinic that I direct and in several
Too much medicine is not just a problem of rich countries
Authors: A. Jain
Journal: BMJ (2015)

South Asia needs better recognition of the manifestations and drivers of overdiagnosis

One memory of medical school stays with me. It was our first day in clinical medicine, and we would be meeting a widely respected and feared professor. “Why have you taken up medicine?” he asked each one of us. Idealistic aspirations of serving the society and making a difference to the world came up.

“A barber does greater service to society than you ever will as a doctor,” he said emphatically. “You are here to make money.”

I found this reality difficult to accept then, but his words ring true as I observe medical practice today. Last year the personal account of an Australian physician volunteering in India blew the lid off the practice whereby doctors receive a commission of 10-30% for referrals to diagnostic centres and to specialists.1 Doctors refer to this “cut practice” as essential to set up shop and run their business, but it has led to rampant abuse of investigations and unnecessary procedures. What makes the situation more deplorable is that patients largely pay for healthcare from their own pockets, and the increased costs are …
The Practice of Quality
Authors: P. Wilcock
Journal: BMJ (1996)

Richard Joss, Maurice Kogan Open University Press, £14.99, pp 215 ISBN 0 335 19395 1

The Practice of Quality 

Donald Irvine, Sally Irvine Radcliffe, £16.50, pp 206 ISBN 1 85775 073 X

Written from very different perspectives, these books come at a time when traditional paradigms of quality are being increasingly questioned. The Irvines' book is based on their extensive experience of working in primary care, while Joss and Kogan's more detailed research account analyses their three year study of a sample of the hospital and community services funded by the Department of Health to test the relevance of total quality management principles to health care.

Both books focus on the dynamic of improving health care rather than merely taking snapshots of its current quality. They build …
Predicting mortality from cervical cancer after negative smear test results.
Authors: G. J. van Oortmarssen, J. D. Habbema, M. van Ballegooijen
Journal: BMJ (1992)

OBJECTIVE--To assess the relative protection against death from cervical cancer after two or more negative smear test results and compare it with the protection against invasive cancer estimated by an International Agency for Research on Cancer (IARC) working group in an analysis of data from 10 large screening programmes. DESIGN--Comparison of risk of death from cervical cancer after two or more negative smear results with the risk in unscreened women by using a model constructed with data from the British Columbia screening programme. MAIN OUTCOME MEASURES--Mortality from and incidence of invasive cancer. RESULTS--In women with two negative smear results estimates of protection against cervical cancer were about 50% higher when lethal invasive cancer was used as the criterion rather than all invasive cancer. This difference was due to these women being more likely to attend for further tests at which invasive cancer could be detected: screen detected cancer has a better prognosis than clinically diagnosed cancer. Screening intervals could be longer than three years: screening women aged 35-64 every five years was predicted to result in a 90% reduction in mortality from cervical cancer. CONCLUSION--Because protection from mortality is higher than protection from disease and because of the high costs and negative side effects of frequent screening, screening intervals should be longer than three years.
The definition, classification, and prognosis of chronic kidney disease: a KDIGO Controversies Conference report
Authors: Andrew S. Levey, Paul E. de Jong, Josef Coresh, Meguid El Nahas, Brad C. Astor, Kunihiro Matsushita, Ron T. Gansevoort, Bertram L. Kasiske, Kai-Uwe Eckardt
Journal: Kidney International (2010)
PREDICTORS OF SIX MONTH REPEAT REVASCULARIZATION FOLLOWING PERIPHERAL VASCULAR INTERVENTION: OBSERVATIONS FROM THE BLUE CROSS BLUE SHIELD OF MICHIGAN CARDIOVASCULAR CONSORTIUM
Authors: Herbert D. Aronow, Khan Munir, Theodore L. Schreiber, Thomas P. Davis, Timothy J. Nypaver, P. Michael Grossman
Journal: Journal of the American College of Cardiology (2011)
Carcinoid Tumors of the Gastrointestinal Tract
Authors: Faith A. Weidner
Journal: JAMA (1981)

CARCINOID tumors have attracted much attention because of their endocrine activity and the unique symptoms that may result from their existence. Once considered benign, their malignant potential is now well appreciated.<sup>1</sup>Radiologically, these relatively uncommon tumors can present a variety of appearances that are a reflection of both tumor growth and secondary tissue reaction. Preoperative diagnosis is notoriously difficult and requires a synthesis of clinical, laboratory, and radiological data. The incidence of carcinoid tumors based on autopsy studies ranges from 0.08% to 1.36%. They are derived from cellular elements originating in the primitive neural-crest ectoderm. These cells migrate to several areas and belong to a family sharing the features of amine content, precursor uptake, and decarboxylation (APUD).<sup>2</sup>Therefore, these carcinoid APUD neoplasms can occur in the gastrointestinal (GI) tract, GI derivatives (pancreatobiliary tract), and primordial GI derivatives (lungs, genitourinary tract, thymus). A consistently positive relationship between carcinoid neoplasms
Paying Research Subjects: An Analysis of Current Policies
Authors: Neal Dickert, Ezekiel Emanuel, Christine Grady
Journal: Annals of Internal Medicine (2002)

Background: Few data are available on guidelines used by research organizations to make decisions about paying subjects. Objective: To analyze existing guidance regarding payment of research subjects and to identify common characteristics and areas for further research. Design: Descriptive content analysis of policies. Measurements: Written policies and rules of thumb about paying subjects from 32 U.S. research organizations. Results: Of 32 organizations, 37.5% had written guidelines about paying subjects; all but 1 reported having rules of thumb. Few (18.8%) were able to provide a confident estimate of the proportion of studies that pay subjects. Organizations reported that investigators and institutional review boards make payment decisions and that both healthy and ill subjects in some studies are paid for their time (87%), for inconvenience (84%), for travel (68%), as incentive (58%), or for incurring risk (32%). Most organizations require that payment be prorated (84%) and described in the consent document (94%). Conclusions: Most organizations pay some research subjects, but few have written policies on payment. Because investigators and institutional review boards make payment decisions with little specific guidance, standards vary.
Hyperactivity: A Lead-Induced Behavior Disorder
Authors: E. K. Silbergeld, A. M. Goldberg
Journal: Environmental Health Perspectives (1974)

Mice were exposed to lead from birth by substituting solutions of lead acetate for the drinking water of their mothers. The suckling mice were thus exposed to lead through their mother's milk and, at weaning, directly through the drinking water. Controls received equal concentrations of sodium acetate. No deaths of offspring or mothers occurred during the first 90 days of exposure. It has been suggested recently that lead exposure may account for some incidences of behavior disorders in children. Levels of motor activity of individual offspring were measured from weaning until 70 days of age in specially designed activity cages. Lead-treated mice were more than three times as active as age-matched or size-matched controls. Treated and control animals were administered drugs currently used in the treatment and diagnosis of hyperactivity in children. All control animals responded as expected to all drugs used in this study. However, lead-treated mice responded paradoxically to d- and l-amphetamine, methylphenidate, and phenobarbital. That is, the CNS stimulants suppressed their hyperactivity while phenobarbital exacerbated the lead-induced hyperactivity. These findings suggest that lead produces an animal model of hyperactivity which may have clinical relevance and which may explain some cases of hyperactivity in children.
RAF around the Edges — The Paradox of BRAF Inhibitors
Authors: Ashani T. Weeraratna
Journal: New England Journal of Medicine (2012)

The recent success of BRAF inhibitors represents a great stride forward for melanoma research. When used to treat patients with melanoma who harbor the BRAF V600E mutation, these inhibitors lead to the remission of even advanced lesions. However, resistance to BRAF inhibitors emerges within months. Of added concern is the development of secondary tumors, most commonly cutaneous squamous-cell carcinomas and keratoacanthomas, in response to BRAF inhibition.1 In this issue of the Journal, Su et al. found that BRAF inhibition leads to increased MAPK (mitogen-activated protein kinase) signaling and secondary tumor development when another oncogene, HRAS, is activated.2 This is due . . .
A STUDY OF THE INFLUENCE OF EXPERIMENTAL DESIGN ON CLINICAL OUTCOME IN DRUG RESEARCH
Authors: BURTON S. GLICK, REUBEN MARGOLIS
Journal: American Journal of Psychiatry (1962)

Examination of the research designs in 34 published papers (35 separate studies) dealing with the chlorpromazine treatment of chronic, hospitalized schizophrenic patients, reveals the following: 1. Those studies which included within their structure the double-blind, placebo-controlled technique showed significantly lower clinical improvement rates than those which did not. 2. No significant relationship was found between the various dosage levels used and clinical improvement rates, nor could a differential in dosage levels between single- and double-blind studies be established. 3. Long term studies showed significantly higher clinical improvement rates than did short term studies, demonstrating that duration of therapy, as well as degree of "blindness," may be a very meaningful variable in determining clinical outcome. 4. Duration of therapy was significantly related to degree of "blindness" in that only 1 of 11 double-blind studies was long term and only 4 of 16 single-blind studies were short term. 5. Long term, single-blind studies showed appreciably higher clinical improvement rates than did short term, double-blind studies. The very meager number of long term, double-blind studies (1 only) and, to a lesser extent, of short term, single-blind studies prevented us from differentiating between degree of "blindness" and duration of therapy regarding their relative impact on improvement rates. Thus, no clear-cut, certain evidence could be adduced either to support or nullify the contention that the double-blind, placebo-controlled method is, per se, a necessity for the "accurate" clinical evaluation of a drug. Further research and experimentation on this problem are urgently needed. 6. Considering improvement rates as a reflection of the observer's subjective attitude toward a drug, and using publication dates as a rough index of the chronological order in which the studies were performed, we were unable to demonstrate a general decline in improvement rates with the passage of time. Thus we could not validate the commonly held belief of a progression from an initial overenthusiasm to a later realism in the subjective evaluation of a drug. 7. Running like a thread through many of our results was the apparent importance of duration of therapy in determining improvement rates. This is one variable which, in particular, must be taken into account in any study of the relative scientific efficacy of the double-blind method.
Long-Term Nasogastric Feeding Tube
Authors: Larry E. Davis
Journal: JAMA (1969)

<h3>To the Editor:—</h3> Dr. Picard's nasogastric tube design is indeed similar to ours. However, in comatose patients we found aspiration of the small mercury bag to be a problem when passing the soft Penrose tube soley by gravity. To correct this, the Penrose tubing was modified to allow a conventional Levin tube to serve as a passing guide.
Neuroinfectious Diseases
Authors: Avindra Nath
Journal: JAMA Neurology (2014)

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Is Refractory Epilepsy Due to Genetically Determined Resistance to Antiepileptic Drugs?
Authors: Timothy A. Pedley, Michio Hirano
Journal: New England Journal of Medicine (2003)

Failure to respond to antiseizure drugs is the usual basis for defining intractable epilepsy, although there is a lack of consensus about what constitutes drug resistance and when this determination can be made.1,2 At least 30 percent of patients with epilepsy in North America and western Europe continue to have seizures despite drug treatment.3 The figure may be even higher in adults with localization-related epilepsy.4 This situation has not changed despite the introduction of a number of antiseizure drugs in the past decade. Refractory epilepsy is associated with memory loss, lower levels of school performance, depression, impaired psychosocial skills, . . .