tbuckley/cabot-search huggingface dataset:
Management of osteoarthritis (OA) with an unsupervised home based exercise programme and/or patient administered assessment tools. A cluster randomised controlled trial with a 2x2 factorial design
Authors: P Ravaud, B Giraudeau, I Logeart, J S Larguier, D Rolland, R Treves, L Euller-Ziegler, B Bannwarth, M Dougados
Journal: Annals of the Rheumatic Diseases (2004)

<b>Background:</b> Diary recording of pain and disabling activities in osteoarthritis (OA) is widely recommended, but, to our knowledge, its impact on symptoms has not been investigated. Exercise programmes have been shown to be effective when patients are closely supervised by nurses or physiotherapists; however, data are lacking on the efficacy of an unsupervised home based exercise regimen in patients with OA. <b>Objectives:</b> To evaluate the clinical efficacy of patient administered assessment tools and an unsupervised home based exercise programme alone or in combination in patients with OA. <b>Methods:</b> The study was a 24 week, open cluster randomised controlled trial with a factorial design. Rheumatologists (n = 867) were assigned to four groups according to the treatment given: standardised tools (ST; n = 220), exercises (EX; n = 213), both tools and exercises (ST+EX; n = 213), or usual care (n = 221). Each rheumatologist was to enrol four patients who met the American College of Rheumatology criteria for OA (three with knee OA, one with hip OA). "Tools" consisted of weekly recording of pain and disabling activities in a diary. A home based exercise programme was performed daily at least four times per week with the aid of videotape and booklet. In addition to exercise and asessment, all patients received 12.5 mg or 25 mg of the non-steroidal anti-inflammatory drug rofecoxib once daily. Outcome variables were: pain (measured on a visual analogue scale, 0–100); Western Ontario and McMaster Universities Osteoarthritis Index, function subscale (0–100); and patient assessment of the quality of care (0–100). <b>Results:</b> Overall, 2957 patients with OA (2216 knee, 741 hip) were included. After 24 weeks, both pain and function improved in the ST, EX, ST+EX, and usual care groups (mean (SD) −17 (27), −20 (29), −15 (27), −19 (29); and −11 (19), −12 (19), −10 (19), −11 (20), respectively), without significant differences between groups. However, patients in the EX and ST+EX groups were more likely to agree that their rheumatologist had done his best to preserve their functional and physical activities. <b>Conclusion:</b> Although patients' assessments favoured the exercise programme, results from this study failed to demonstrate a short term symptomatic effect of the two non-pharmacological treatments (weekly recording of condition and exercise) in patients with OA concurrently receiving nonsteroidal anti-inflammatory drugs.
Erythropoietin receptor. Subunit structure and activation.
Authors: A D D'Andrea, L I Zon
Journal: Journal of Clinical Investigation (1990)

Physiologic role oferythropoietin in erythroid differentiation Erythropoietin (EPO)' is a 34-kD glycoprotein hormone which is the primary regulator of human erythropoiesis.A cDNA encoding EPO has been isolated (1), and recombinant EPO with oligosaccharide moieties identical to the natural ma- terial is available (2).EPO is synthesized and released by the kidney, and it circulates to the bone marrow where it stimu- lates resident erythroid progenitors via a specific receptor (3).EPO as a pharmacologic agent has clearly demonstrated effi- cacy in anemic states such as kidney failure (4, 5).In vivo, EPO causes a rapid rise in hematocrit in 7-10 d.Despite the availability of purified recombinant EPO, little is known regarding the interaction of EPO and the erythropoi- etin receptor (EPO-R) or the physiologic mechanisms by which EPO causes cells to undergo proliferation or differentia- tion.This is largely due to the lack of adequate quantities of EPO-R for in-depth biochemical study.Only small numbers of surface EPO-R (< 1,000) are present on normal erythroblasts and erythroleukemia cells.EPO provides a proliferative signal to the Burst-forming unit-erythroid (BFU-E), an early EPO- responsive erythroid progenitor, and a differentiative signal to the colony-forming unit-erythroid (CFU-E), a later EPO-re- sponsive erythroid progenitor (3).These two classes of EPO- responsive cells are clearly different populations since they can be separated by unit gravity sedimentation and more recently have been purified to homogeneity (6).The purpose of this review is to describe the recent advances in our understanding of EPO-R physiology, derived from the cloning of the EPO-R cDNA.Structure ofthe EPO-R Before the cloning of the EPO-R cDNA, investigators have used radiolabeled EPO to demonstrate specific binding to cells derived from the erythroid lineage.These cells include normal erythroid progenitors, virally transformed spleen cells (i.e., Friend cells), murine and human erythroleukemia cells, and cells from human fetal liver.Since there is 80% protein homol- ogy between the murine and human EPO polypeptide, most of
Incidence of hyperkalaemia induced by indomethacin in a hospital population.
Authors: A Zimran, M Kramer, M Plaskin, C Hershko
Journal: BMJ (1985)

As there was only marginal improvement she was transferred for hyper- baric oxygen treatment to the nearby naval recompression unit at Ports- mouth.Treatment began within two hours after her initial collapse.She underwent 285 minutes of alternating oxygen and air treatment beginning at a pressure of 2-8 bar (atmosphere absolute).2After 90 minutes she suddenly became conscious and responded to simple instructions.Neurological exam- ination yielded normal results.She made a full recovery with no neurological sequelae but with a retrograde amnesia of about two hours.1
Incidental Finding of Parathyroid Adenoma With 11C-Choline PET/CT
Authors: Paola Mapelli, Elena Busnardo, Patrizia Magnani, Massimo Freschi, Maria Picchio, Luigi Gianolli, Cristina Messa
Journal: Clinical Nuclear Medicine (2012)

Positron emission tomography/computed tomography (PET/CT) with 11C-choline is an established diagnostic tool for restaging prostate cancer patients with biochemical failure after primary treatment. In the present case, 11C-choline PET/CT was performed in a prostate cancer patient with skeletal metastases, treated with hormonal therapy. In addition to the detection of pathologic uptake at prostate and vertebra, 11C-choline uptake occurred in the neck. The finding was suggestive for a parathyroid adenoma on subsequent ultrasound, then finally confirmed by parathyroid scintigraphy and histopathological analysis performed after hemithyroidectomy.
European regulators urge commission to tighten regulations on doctors' cross border working
Authors: C. Dyer
Journal: BMJ (2010)

Doctors’ regulators from 23 countries in Europe are pressing the European Commission to tighten the requirements for doctors who practise outside their home country, to protect patients.

They want more stringent safety requirements to be imposed when the commission reviews the 2005 European directive on the mutual recognition of medical qualifications in 2012.

The move comes after concerns about the language skills of foreign doctors employed by locum agencies in the United Kingdom and the reciprocal arrangements that allow doctors registered in another European Union country to be registered by the UK regulator, the …
Essentials of Infectious Diseases
Authors: Jerry D. Smilack
Journal: JAMA (1986)

The goal of this book is to provide clinicians with a pragmatic approach to the evaluation and treatment of infected patients, while at the same time presenting this information in a concise and authoritative manner. Such an intention is admirable, but, in the case of this book, unrealized. After a few introductory chapters, this volume follows a format oriented around infection sites and syndromes (central nervous system, cardiovascular, etc). Each chapter touches on microbial etiology, epidemiology, pathophysiology, clinical manifestations, methods of diagnosis, treatment, and prognosis. In a volume of modest size (slightly over 400 pages), such discussions must be brief, and, at times, telegraphic. As a result, I believe this book's value is severely limited. For example, important differences between subdural empyema and epidural abscess are summarily dismissed; Lyme disease, cat-scratch disease, and Rocky Mountain spotted fever are barely mentioned; discussion of toxic shock syndrome is limited to two sentences;
The future of medical education in South Africa
Authors: R. Hoffenberg
Journal: BMJ (1997)

When I left South Africa in 1968 academic medicine was flourishing. The best graduates wanted to pursue academic careers and there was fierce competition for posts in teaching hospitals. Although not in itself a manifestation of profound research the world's first heart transplant had revealed just how sophisticated medicine was in the country. The general medical scene was less satisfactory. Few black doctors were being trained—seven in 1966; 11 in 1967; 10 in 1968—and the distribution of doctors was grossly distorted in favour of white suburbs. This inequality of service was reflected in patterns of health and disease.

At the end of 1995 I returned to join an advisory group set up by the minister of health, Dr N C Zuma, to try to restore a badly depleted and demoralised academic sector. What I found was extremely depressing. The status of academic medicine had declined seriously, the teaching hospitals had been deprived of funds, salaries for academics and those working in the public sector were quite inadequate with a resultant haemorrhage into private practice. Vast numbers of doctors had emigrated. The mix of private and public medicine had changed completely. Only 39% of health expenditure went to the public sector, 61% to the private; one third of all hospital beds were in the private sector.

The new minister was determined to do something about the unequal …
Science, medicine, and the future: Susceptibility to infection
Authors: D. Kwiatkowski
Journal: BMJ (2000)

Genetic factors explain, at least in part, why some people resist infection more successfully than others. Rare gene disruptions cause fatal vulnerability to specific microbes, but more subtle differences are common and arise from minor variation in many genes. Recent advances in the human genome project and in high throughput genotyping technology will make it feasible within the next decade to screen the whole genome for genetic factors that determine susceptibility to HIV and AIDS, malaria, and tuberculosis. This will help to identify critical pathways of host defence and generate novel strategies for disease prevention. Understanding the evolutionary impact of infectious disease on the human genome may shed light on the origins of other common diseases, particularly those with an atopic or autoimmune component.

Historical accounts of the plague tell of individuals who survived unscathed in households where almost everyone else died. Each winter, British hospital wards are full of infants requiring oxygen therapy for bronchiolitis, but most infants infected with the same virus have little more than a runny nose. Over a million African children die each year of malaria, but many more remain in relatively good health despite being continually infected with the parasite.

To what extent does our genetic make up determine the different ways that we respond to the same infectious agent? This is difficult to answer because of the many other contributory factors involved, such as previous health, acquired immunity, and variability in the pathogen. Epidemiological analysis of the genetic component is confounded by environmental factors that cause familial clustering and is further complicated by the many different genes that are likely to be involved. Nevertheless, there is compelling evidence for a genetic component, including twin studies of tuberculosis,1 leprosy,2 malaria,3 and Helicobacter pylori infection4 and a large survey that found …
Thallium reinjection demonstrates viable myocardium in regions with reverse redistribution.
Authors: J A Marin-Neto, V Dilsizian, J A Arrighi, N M Freedman, P Perrone-Filardi, S L Bacharach, R O Bonow
Journal: Circulation (1993)

BACKGROUND The clinical significance and pathophysiological mechanisms of reverse redistribution on stress-redistribution thallium-201 myocardial scintigraphy in patients with chronic coronary artery disease are unclear. Recent studies have shown that thallium-201 reinjection is a useful technique for the detection of myocardial viability in chronic coronary artery disease. In this investigation we determined whether thallium reinjection distinguishes viable from nonviable myocardium in regions with reverse redistribution. METHODS AND RESULTS We studied 39 patients with chronic stable coronary artery disease (age, 60 +/- 10 years), all of whom demonstrated reverse redistribution on standard exercise-redistribution thallium single-photon emission computed tomography (SPECT). Reverse redistribution was defined as &gt; or = 10% decrease in relative thallium-201 activity between stress and redistribution images and included either the worsening of a perfusion defect apparent on post-stress images or the appearance of a new defect on the redistribution images. Thallium reinjection was performed immediately after the 3- to 4-hour redistribution study. Of 39 regions with reverse redistribution, 32 (82%) showed enhanced thallium-201 activity (&gt; or = 10% increase) after reinjection. In the other 7 regions (18%), the scintigraphic defect persisted after reinjection. Abnormal Q waves were present in only 8 of 32 (25%) regions with enhanced thallium-201 uptake after reinjection compared with 5 of 7 (71%) regions not responding to reinjection (P &lt; .05). Akinetic or dyskinetic wall motion was present in 3 of 32 (9%) regions showing enhanced uptake after reinjection, in contrast with 5 of 7 (71%) regions not responding to reinjection (P &lt; .01). Critically stenosed or totally occluded coronary arteries supplied 24 of 29 (83%) regions with enhanced thallium-201 uptake after reinjection but only 2 of 7 (28%) regions not showing a positive response to reinjection (P &lt; .05). Collateral circulation was detected in 23 of 29 (79%) regions with a positive thallium reinjection effect but in only 1 of the other 7 regions (P &lt; .01). Sixteen of the 39 patients also underwent positron emission tomography using 18F-fluorodeoxyglucose (FDG) to assess glucose utilization and H2(15)O to assess regional blood flow. The 14 regions with reverse redistribution that responded to reinjection with enhanced thallium uptake all showed either normal patterns of FDG uptake and flow or an ischemic pattern with increased FDG uptake relative to flow. Reduced FDG uptake and reduced flow values were seen in the two regions not responding to thallium reinjection. CONCLUSIONS These observations indicate that reverse redistribution in chronic coronary artery disease usually reflects viable myocardium, critically dependent upon collateral circulation.
T cell depletion in untreated adult coeliac disease.
Authors: D P O'Donoghue, M Lancaster-Smith, P Laviniere, P J Kumar
Journal: Gut (1976)

The proportional and absolute numbers of circulating thymus dependent lymphocytes (T cells) were reduced in untreated patients with coeliac disease but were normal after treatment with a gluten free diet. There was an inverse correlation between circulating T cell numbers and jejunal intraepithelial lymphocytes. This evidence suggests a possible role for T cells in the pathogenesis of coeliac disease and is a further example of disturbed cell mediated immunity in this condition.
T-cell responses and hypersensitivity to influenza and egg antigens among adults with asthma immunized with the influenza vaccine
Authors: R Miller
Journal: Journal of Allergy and Clinical Immunology (2003)

<h2>Abstract</h2><h3>Background</h3> The American Lung Association Asthma Clinical Research Centers (ALA-ACRC) reported that the inactivated influenza vaccine is safe for patients with asthma and recommended its use to reduce the morbidity associated with infection. <h3>Objective</h3> Because the ALA-ACRC's recommendation would include vaccination of all patients with asthma, including those with severe asthma and first-time vaccinees, we conducted a parallel study to address whether patients with asthma who report bronchospasm after vaccination might be demonstrating a hypersensitivity response to the vaccine. <h3>Methods</h3> Thirty-two adult patients with asthma from the ALA-ACRC cohort were recruited. Subjects were randomly assigned to receive influenza vaccine or placebo and then recorded asthma symptoms and peak expiratory flow rates for 14 days. On day 14, influenza vaccine and egg antigen–induced mononuclear cell proliferation and IFN-γ, IL-5, and IL-4 production were measured and compared with symptoms. <h3>Results</h3> Increased influenza but not egg antigen–induced mononuclear cell proliferation was present among vaccinated subjects. These responses were unrelated to asthma exacerbations after vaccine. There were no differences in cytokine production in response to either influenza or egg antigen in association with asthma exacerbations. <h3>Conclusions</h3> Episodes of bronchospasm after influenza vaccination do not seem related to hypersensitivity to the vaccine.
A CASE OF APLASTIC ANEMIA.
Authors: LEROY CRUMMER
Journal: JAMA (1907)

The recent and carefully prepared report of a case of aplastic anemia by Lavenson<sup>1</sup>embraces a thorough review of the literature and renders a detailed consideration of this disease unnecessary, but the cases are still so rare that it is deemed of importance to report every case. <h3>History.</h3> —Miss F. S., aged 18, was seen through the kindness of Dr. H. B. Jennings, of Council Bluffs, Iowa. She was one of a large family of girls and with no trace of hereditary impairment. She had always been well, save for some slight gastrointestinal symptoms so common in girls of this age. In April, 1907, she had an attack of generalized muscular pain, which under salicylate treatment immediately improved. No attention was directed toward the tonsils during this illness. A month later she again complained of pain in the limbs and body. These pains were neither constant nor severe. Up
Calories, Growth and the Quality of Life
Authors: John D. Crawford
Journal: New England Journal of Medicine (1971)

There are no more fundamental attributes of childhood than growth and happiness. A major sector of our food industry specializes in products for the young designed to promote their physical growth; we support an enormous educational system devoted to cultivating intellectual growth, and the recent intense focus on improving the environment needs no emphasis. When one of a child's vital systems fails we physicians are confronted by a trying philosophical question: Is a treatment applicable if its promise is only to sustain life falling short of restoring growth or, even if capable of that, only at considerable sacrifice to the . . .
Plasma gaba-like activity in rats with hepatic encephalopathy is due to gaba and taurine
Authors: Jill E. Maddison, Dorothy K. Leong, Peter R. Dodd, Graham A.R. Johnston
Journal: Hepatology (1990)

Significant discrepancy exists between radioreceptor and high–performance liquid chromatographic estimates of plasma GABA concentrations in animal models of hepatic encephalopathy. A possible explanation for this discrepancy is the presence in plasma of a substance that can inhibit [ 3 H]–GABA binding but is not GABA itself. The aim of this study was to determine whether any of the amino acids that are increased in the plasma of animal models of acute and chronic hepatic encephalopathy (glutamine, glutamate, phenylalanine, tyrosine, citrulline and taurine) can significantly inhibit [ 3 H]–GABA binding and contribute to the GABA–like activity of plasma aliquots. At final assay concentrations equivalent to plasma concentrations found in hepatic encephalopathy, only taurine was found to significantly inhibit [ 3 H]–GABA binding to whole rat brain synaptosomal membranes (36% inhibition at 30 μmol/L final assay concentration). The concentration of taurine that resulted in 50% inhibition (final assay concentration) was 158 μmol/L, corresponding to a plasma concentration of 1.58 mmol/L. Taurine inhibition of [ 3 H]–GABA binding was competitive because the receptor density was unaltered, but the receptor affinity decreased with increasing concentration of taurine. Plasma GABA–like activity (determined by radioreceptor assay) and plasma GABA and taurine concentrations (determined by high–performance liquid chromatography) were measured in 18 rats with acute or chronic hepatic encephalopathy and 9 control rats. Plasma GABA–like activity and plasma GABA and taurine concentrations were significantly increased in rats with hepatic encephalopathy compared with control rats. A comparison of the percent inhibition of [ 3 H]–GABA binding expected by known concentrations (determined by high–performance liquid chromatography) of taurine and GABA in each plasma sample indicated that the inhibition of [ 3 H]–GABA binding by plasma aliquots could be entirely attributed to the presence of GABA and taurine in plasma. Therefore the plasma “GABA–like factor” in animal models of hepatic encephalopathy is taurine. The implications of this finding to the pathogenesis of hepatic encephalopathy are unknown at present.
Setting domain boundaries for convergence of biological and psychological perspectives on cognitive coordination in schizophrenia
Authors: J. P. Ginsberg
Journal: Behavioral and Brain Sciences (2003)

Abstract The claim that the disorganized subtype of schizophrenia results from glutamate hypofunction is enhanced by consideration of current subtypology of schizophrenia, symptom definition, interdependence of neurotransmitters, and the nature of the data needed to support the hypothesis. Careful specification clarifies the clinical reality of disorganization as a feature of schizophrenia and increases the utility of the subtype.
Etiology of Decline in General Practice
Authors: Robert J. Haggerty
Journal: JAMA (1963)

MY TASK is not to make a diagnosis. That has been done by others more experienced than I.1,2Decline in general practice is a fact. It is more difficult, however, to determine the etiology of this decline.  In the history of knowledge of causes of disease, we have moved a long way from the era of one cause for each illness. While the pneumococcus is indeed a cause of pneumonia, its entry into the lung is sometimes preceded by an acute alcoholic bout resulting from many factors, known and unknown—physiologic, social, and psychologic—in the patient's background. So it is in the etiology of the decline of general practice—the concept of multiple rather than unitary causation must be invoked.  Most of us have our pet theory as to the cause of this decline. The figure on the following page illustrates the clear association between decline in per cent of physicians