tbuckley/cabot-search huggingface dataset:
Campaign to revitalise academic medicine
Authors: Kerr L White
Journal: BMJ (2004)

Crisis in UK academia affects academic medicine too Editor—Academic medicine is in a woeful state. 1–3 But this is only part of the crisis affecting UK academia as a whole. Pumping funds into academic medicine alone 1–4 without tackling fundamental issues would only worsen the situation. “Top class researchers make excellent teachers, and students benefit from the enhanced quality of the education they receive.” 5 But the assessment of these two core university activities, by the research assessment exercise (RAE) and the Quality Assurance Agency’s audit and review processes respectively, is totally separate, generating serious conflict. Carrying such immense funding implications compared with the Quality Assurance Agency’s process, the research assessment exercise wins over education every time. That clinical practice is assessed by a third process only increases the tension, so the saying “a successful clinical academic is one who doesn’t see patients” becomes a truism and not just a pathetic old joke. Preparing for the next research assessment exercise, research staff are being offered inducements to remain in post, and for institutions hoping to do better “100 new chairs [have been] created in a bid to lift RAE scores.” 5 Universities are also shedding staff who are inevitably not so research competitive because of their contribution to education and clinical practice. This cull— now cyclical—creates a hostile environment that is devastating to morale, damages education, and wrecks research teams. The conflict between service, education, and research is old but lies at the heart of the academic crisis and our leaders have let us down by failing to grapple with it. Linking the assessment of academic activities that are currently treated entirely separately is crucial. Only then can the natural synergy between education, research, and clinical work that originally attracted many people into academia be regained. Without it, UK academia will continue to deteriorate.
Ciprofloxacin Levels When Receiving Sucralfate
Authors: Jae H. Yuk
Journal: JAMA (1989)

<h3>To the Editor.—</h3> Ciprofloxacin by oral administration has recently gained considerable popularity in the treatment of serious deep-seated infections in clinically stable patients because of its intense microbiological activity against most<i>Enterobacteriaceae</i>and<i>Pseudomonas aeruginosa</i>organisms and its excellent bioavailability, at least in healthy volunteers. There remains, however, a paucity of bioavailability data on ciprofloxacin and other fluoroquinolones in ill patients, particularly those who are receiving other drugs. It has been demonstrated in normal volunteers that aluminum- and magnesium-containing compounds (eg, antacids) decrease the mean peak concentrations of a single 500-mg dose of ciprofloxacin from 1.7 to 0.1 μg/mL and urine recovery from 24% to 2.1%, presumably because of chelate formation.<sup>1</sup>Morever, in a recent report,<sup>2</sup>sucralfate, an aluminum-containing compound, significantly reduced the bioavailability of norfloxacin. Here, we report on six elderly patients who received 750 mg of ciprofloxacin by mouth, one of whom was also receiving 1
"Stress" Polycythemia and Hypertension
Authors: Alfred C. Emery
Journal: JAMA (1974)

Thirteen of 478 patients whose blood volumes were measured within a two-year period demonstrated "stress" polycythemia; each of these patients had sustained systolic or diastolic hypertension of varying severity. In five patients, antihypertensive (sympatholytic) therapy was associated with remission of the "stress" polycythemia. One half of the patients studied in the present series, and 47% of those previously reported had severe cardiovascular disease; 71% of the latter patients also had arterial hypertension. These findings strongly suggest that "stress" polycythemia should not be considered a "benign" condition meriting therapy with phlebotomy or tranquilizing drugs. Patients with arterial pressure elevation should be treated vigorously with close observation for control of hypertension and remission of the polycythemia. (<i>JAMA</i>229:159-162, 1974)
Syntactic Measures of Bias (and a Perspective on the Essential Issue of Bioethics)
Authors: Tihamer Toth-Fejel, Chris Dodsworth, Jennifer Lahl
Journal: The American Journal of Bioethics (2007)

Click to increase image sizeClick to decrease image size Notes 1. It is true that programmers themselves might mislead or make mistakes, but programs are less likely to be biased when they are open source—biases can be detected (and fixed) by anyone reading the code.
COLOR CODED TISSUE CHARACTERIZATION BY 40 MHZ INTRAVASCULAR ULTRASOUND RELIABLY IDENTIFIES PLAQUE COMPOSITION COMPARISON WITH 64 SLICE COMPUTED TOMOGRAPHY
Authors: Makoto Utsunomiya, Masato Nakamura, Mami Nakanishi, Tadashi Araki, Masaki Hori, Nobutaka Ikeda, Kunihiko Makino, Hideki Itaya, Naohiko Nemoto, Raisuke Iijima, Hidehiko Hara, Takuro Takagi, Kaoru Sugi
Journal: Journal of the American College of Cardiology (2011)
Mouse Model of Colonic Adenoma-Carcinoma Progression Based on Somatic <i>Apc</i> Inactivation
Authors: Takao Hinoi, Aytekin Akyol, Brian K. Theisen, David O. Ferguson, Joel K. Greenson, Bart O. Williams, Kathleen R. Cho, Eric R. Fearon
Journal: Cancer Research (2007)

Abstract Mutations in the adenomatous polyposis coli (APC) gene are pivotal in colorectal tumorigenesis. Existing mouse intestinal tumor models display mainly small intestinal lesions and carcinomas are rare. We defined human CDX2 sequences conferring colon epithelium-preferential transgene expression in the adult mouse. Mice carrying a CDX2P-NLS Cre recombinase transgene and a loxP-targeted Apc allele developed mainly colorectal tumors, with carcinomas seen in 6 of 36 (17%) of mice followed for 300 days. Like human colorectal lesions, the mouse tumors showed biallelic Apc inactivation, β-catenin dysregulation, global DNA hypomethylation, and aneuploidy. The predominantly distal colon and rectal distribution of tumors seen in mice where one Apc allele was inactivated in epithelial cells from distal ileum to rectum suggests that regional differences in the intestinal tract in the frequency and nature of secondary genetic and epigenetic events associated with adenoma outgrowth have a contributing role in determining where adenomas develop. The presence of large numbers of small intestine tumors seemed to inhibit colorectal tumor development in the mouse, and gender-specific effects on tumor multiplicity in the distal mouse colon and rectum mimic the situation in humans where males have a larger number of advanced adenomas and carcinomas in the distal colon and rectum than females. The mouse model of colon-preferential gene targeting described here should facilitate efforts to define novel factors and mechanisms contributing to human colon tumor pathogenesis, as well as work on tumor-promoting environmental factors and agents and strategies for cancer prevention and treatment. [Cancer Res2007;67(20):9721–30]
INTESTINAL ANASTOMOSIS—BY A NEW METHOD, WITHOUT PLATES AND WITH BUT TWO KNOTS—EITHER SILK OR CATGUT SUTURES MAY BE USED.Read before the Section of Surgery aud Anatomy at the Forty-fourth Annual Meeting of the American Medical Association.
Authors: M. E. CONNELL
Journal: JAMA (1893)

When through injury or disease it is found necessary to exclude or remove a portion of the intestinal canal, the question of restoration of its continuity which comes to the surgeon, and how or which is the best method to accomplish this desired result is one of great importance. Many methods are now in the surgical field; but we cannot have one too many if all are good, and the surgeon must familiarize himself with one method or be equally proficient in all, in case of an emergency, such as gunshot wounds or strangulated hernia. The universal interest which has been manifested in the plate operation and its modifications, indicate very clearly that any method which promises an improvement in the technique of intestinal surgery, whether in suturing or the saving of time, will be gladly welcomed by the profession. It is now more than a year ago that I
Irish committee backs genetically modified crops
Authors: D. Payne
Journal: BMJ (2000)

The Irish government committee charged with coming up with a coordinated position on biotechnology has come out in favour of developing genetic modification techniques, recommending both that field trials of genetically modified organisms continue and that government agencies encourage cultivation of genetically modified crops.

The report has dismayed environmental campaigners. The interdepartmental body was set up in March 1999 after a spate of unfavourable reports about the technology and growing public unease throughout Europe about the spread …
Acitretin treatment for hidradenitis suppurativa: a prospective series of 17 patients
Authors: Ł. Matusiak, A. Bieniek, J.C. Szepietowski
Journal: British Journal of Dermatology (2014)

The management of hidradenitis suppurativa (HS) is still challenging, and new treatment methods are necessary. Acitretin seems to be a promising agent in HS management; however, literature data are limited.To investigate the clinical efficacy of acitretin monotherapy in 17 patients with long-standing and recalcitrant HS. Simultaneously, an assessment of quality of life was carried out.The study was conducted with a group of 17 patients with HS. Patients were treated with acitretin for up to 9 months and examined at baseline, after 1 month, and then every 3 months from baseline. The clinical extent of disease severity was measured with the HS Severity Index (HSSI), Hurley scoring system, Physician's Global Assessment and Dermatology Life Quality Index (DLQI).Nine patients (53%) finished the whole 9 months of acitretin treatment. The mean acitretin dose was 0·56 ± 0·08 mg kg(-1) daily. A significant improvement of clinical manifestation (HSSI, DLQI) was observed after only 1 month of therapy, and further improvement was recorded during the next few months. Overall, eight subjects (47%) fulfilled the criteria for response (HSSI ≥ 50% reduction from baseline). The dropout rate was 47%, due mostly to drug ineffectiveness and adverse events. Discontinuation of treatment resulted in deterioration or relapse of HS 2-8 months after acitretin cessation, in all but one patient.HS treatment with acitretin seems to be a promising method of disease management. However, due to the high daily dosage, its usage may be limited.
Stimulation of lamina propria lymphocytes by intestinal epithelial cells: evidence for recognition of nonclassical restriction elements.
Authors: A Panja, A Barone, L Mayer
Journal: The Journal of Experimental Medicine (1994)

We have addressed the restriction elements involved in the interaction of lamina propria lymphocytes (LPL) and intestinal epithelial cells using the model of primary mixed cell culture reaction. Whereas peripheral blood T cells proliferate in response to both allogeneic non T cells and class II antigen-bearing intestinal epithelial cells (non T cells &amp;gt; epithelial cells), LP T cells appear to proliferate preferentially in response to intestinal epithelial cells. The interaction between these cells does not appear to be restricted by conventional products of the major histocompatibility complex as neither monoclonal antibodies to class I nor to class II antigens inhibit the mixed cell cultures, whereas they are inhibitory in conventional mixed lymphocyte reactions. Furthermore, treatment of epithelial cells with interferon gamma fails to augment the cells' ability to induce proliferation of LPL while successfully enhancing proliferation of peripheral blood T cells in parallel cultures. Taken together, these data suggest that alternate restriction elements or mucosa-specific accessory molecules may exist on intestinal epithelial cells that are preferentially recognized by LPLs. Such a distinct regulatory network may be critical to the maintenance of immunologic homeostasis in the gut.
Comparison of Salmeterol and Albuterol-induced Bronchoprotection Against Adenosine Monophosphate and Histamine in Mild Asthma
Authors: DAVID A. TAYLOR, MARIANNE W. JENSEN, SARAH L. AIKMAN, JEANETTE G. HARRIS, PETER J. BARNES, BRIAN J. O'CONNOR
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Short-acting β2-agonists provide greater protection to bronchoconstriction induced by adenosine-5 ′ -monophosphate (AMP) than does methacholine. Because AMP produces bronchoconstriction through release of mediators from mast cells, and methacholine directly constricts airway smooth muscle, this suggests that β2-agonists stabilize mast cells in vivo. This in vivo property has not been demonstrated with long-acting β2-agonists. We undertook two double-blind, randomized, crossover, placebo-controlled studies to investigate the effects of salmeterol and albuterol on airway responsiveness (AR) to AMP and histamine in patients with mild asthma. In the first study, 19 patients attended on four occasions to inhale salmeterol 50 μ g or placebo 2 h before challenge with AMP or histamine. In the second study 16 patients (13 of whom had participated in the first study) were studied in a similar fashion but inhaled albuterol 400 μ g or placebo 30 min prior to challenge. Salmeterol reduced AR to AMP and histamine by 3.4 ± 0.3 and 3.9 ± 0.3 doubling doses, respectively (NS). In contrast, albuterol demonstrated a greater protective effect on AMP than on histamine, reducing AR by 5.1 ± 0.3 and 3.8 ± 0.2 doubling doses, respectively (p < 0.005). Thus, in contrast to albuterol, salmeterol did not demonstrate mast-cell stabilizing properties in vivo at a time corresponding to maximal bronchodilatation. These findings might be explained by the unique pharmacologic profile of salmeterol in combination with the differential β2-adrenoceptor pharmacology of bronchial mast cells and bronchial smooth muscle.
Increasing email consultations may marginalise more people
Authors: G. Wong
Journal: BMJ (2001)

The findings recorded in this report may be summarized briefly: Following single intravenous injections of sodium p-aminohippurate its plasma concentration fell very rapidly (from about 36 to 2 mgm./100 cc. in 90 minutes). This was due principally to distribution and excretion of the compound. Since PAR was excreted by the renal tubules in addition to glomerular filtration, 43.3 to 69.7 per cent of the amount administered intravenously appeared in the urine within the first hour thereafter. In order to maintain a uniform plasma concentration over a long period of time the preferable mode of administration was by venoclysis, although both the subcutaneous and intramuscular routes were used for this purpose. The oral route of administration neither gave nor maintained adequate plasma concentrations of the compound, except for the determination of renal plasma flow. Administered orally, 20.9 to 41.0 per cent of a dose of PAH was excreted in the urine and only 4.1 to 13.4 per cent appeared in the feces, leaving 54.9 to 72.5 per cent of the drug unaccounted for. That the compound was not hydrolyzed to any notable extent in the gastrointestinal tract was indicated by the following information: 1) trypsin and carboxypolypeptidases did not hydrolyze the compound <i>in vitro.</i> 2) If this hydrolysis had occurred <i>in vivo</i> the p-aminobenzoic acid formed thereby would have been rapidly absorbed resulting in a relatively high plasma concentration of the aromatic amino compounds and an overall renal clearance lower than that of PAH at any plasma concentration. As was actually the case only low plasma concentrations of PAH occurred following its oral administration. Renal clearance data obtained in such experiments supported the conclusion that all the diazotizable material was probably PAH. The fact that the dogs did not conjugate the material precluded that as a mode of alteration of the molecule. Our experiments indicated that very little if any PAH was bound on plasma proteins. While equilibration of the material between the blood cellular elements and plasma occurred quickly, approximately 75 per cent of the drug remained in the plasma. The rat was capable of conjugating PAH, but this occurred more slowly than was the case for sulfathiazole, sulfamethazine, sulfadiazine or sulfamerazine tested similarly in this laboratory (10). It is likely that this information is more directly referable to the human than is the similar finding in dogs. Our experiments substantiate the conclusions of others that sodium p-aminohippurate can be used satisfactorily to measure Tm and renal plasma flow. PAH did not antagonize the bacteriostatic activity of sulfanilamide even though one of its components is p-aminobenzoic acid which characteristically has that property. This observation has a very material bearing on the combined use of sulfonamides with penicillin and PAH in highly refractory diseases of bacterial origin. The toxicological aspects of this problem are being reported in a separate communication (7).
Subacute sclerosing panencephalitis: detection of measles virus RNA in appendix lymphoid tissue before clinical signs.
Authors: J G Fournier, P Lebon, M Bouteille, F Goutieres, S Rozenblatt
Journal: BMJ (1986)

An appendix removed 15 days before onset of symptoms of subacute sclerosing panencephalitis was examined retrospectively for measles virus ribonucleic acid (RNA). Tissue sections hybridised in situ to a cloned measles virus probe of deoxyribonucleic acid specific for nucleocapsid protein showed that many cells of the lymphoid tissue contained measles virus RNA. In contrast, only a few infected lymphoid cells were detected in three out of six seropositive controls and none in three seronegative infants. A widespread chronic viral infection of the immune system, established after measles, may promote or even initiate nerve cell infection in subacute sclerosing panencephalitis.
Physician Substance Abuse
Authors: Sally Satel
Journal: JAMA (2005)

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A constitutional unconjugated hyperbilirubinemia combined with indocyanine green intolerance: A new functional disorder?
Authors: Hideki Ohkubo, Kunio Okuda, Shinji Iida
Journal: Hepatology (1981)

The kinetics of plasma clearance of indocyanine green and bromosulfophthalein were studied in 49 consecutive patients with chronic unconjugated hyperbilirubinemia. Forty-four patients had Gilbert's syndrome whereas five patients had impaired hepatic uptake of indocyanine green and virtually normal hepatic bromosulfophthalein uptake. There was no difference in bilirubin metabolism between the two groups. A family study of the patients with impaired indocyanine green uptake revealed that the defect appears to be transmitted as an autosomal dominant trait associated with inheritance of impaired bilirubin metabolism. These patients manifest a noval disorder of organic anion transport which, like Gilbert's syndrome, is also characterized by chronic milk unconjugated hyperbilirubinemia.
Evidence for defects in the trafficking and translocation of GLUT4 glucose transporters in skeletal muscle as a cause of human insulin resistance.
Authors: W T Garvey, L Maianu, J H Zhu, G Brechtel-Hook, P Wallace, A D Baron
Journal: Journal of Clinical Investigation (1998)

Insulin resistance is instrumental in the pathogenesis of type 2 diabetes mellitus and the Insulin Resistance Syndrome. While insulin resistance involves decreased glucose transport activity in skeletal muscle, its molecular basis is unknown. Since muscle GLUT4 glucose transporter levels are normal in type 2 diabetes, we have tested the hypothesis that insulin resistance is due to impaired translocation of intracellular GLUT4 to sarcolemma. Both insulin-sensitive and insulin-resistant nondiabetic subgroups were studied, in addition to type 2 diabetic patients. Biopsies were obtained from basal and insulin-stimulated muscle, and membranes were subfractionated on discontinuous sucrose density gradients to equilibrium or under nonequilibrium conditions after a shortened centrifugation time. In equilibrium fractions from basal muscle, GLUT4 was decreased by 25-29% in both 25 and 28% sucrose density fractions and increased twofold in both the 32% sucrose fraction and bottom pellet in diabetics compared with insulin-sensitive controls, without any differences in membrane markers (phospholemman, phosphalamban, dihydropyridine-binding complex alpha-1 subunit). Thus, insulin resistance was associated with redistribution of GLUT4 to denser membrane vesicles. No effects of insulin stimulation on GLUT4 localization were observed. In non-equilibrium fractions, insulin led to small GLUT4 decrements in the 25 and 28% sucrose fractions and increased GLUT4 in the 32% sucrose fraction by 2.8-fold over basal in insulin-sensitive but only by 1.5-fold in both insulin-resistant and diabetic subgroups. The GLUT4 increments in the 32% sucrose fraction were correlated with maximal in vivo glucose disposal rates (r = +0.51, P = 0.026), and, therefore, represented GLUT4 recruitment to sarcolemma or a quantitative marker for this process. Similar to GLUT4, the insulin-regulated aminopeptidase (vp165) was redistributed to a dense membrane compartment and did not translocate in response to insulin in insulin-resistant subgroups. In conclusion, insulin alters the subcellular localization of GLUT4 vesicles in human muscle, and this effect is impaired equally in insulin-resistant subjects with and without diabetes. This translocation defect is associated with abnormal accumulation of GLUT4 in a dense membrane compartment demonstrable in basal muscle. We have previously observed a similar pattern of defects causing insulin resistance in human adipocytes. Based on these data, we propose that human insulin resistance involves a defect in GLUT4 traffic and targeting leading to accumulation in a dense membrane compartment from which insulin is unable to recruit GLUT4 to the cell surface.