tbuckley/cabot-search huggingface dataset:
Lignocaine in experimental myocardial infarction: failure to prevent neutrophil accumulation and ventricular fibrillation and to reduce infarct size
Authors: M. D. LORGERIL, G. ROUSSEAU, A. BASMADJIAN, J.-G. LATOUR
Journal: Cardiovascular Research (1988)

Growing evidence supports the concept that neutrophils accumulating in reperfused ischaemic myocardium play a detrimental role in evolving infarction. Lignocaine, an antiarrhythmic drug commonly used clinically, interferes with neutrophil function in vitro and potentially in vivo. To test the hypothesis that lignocaine may influence infarct size by reducing neutrophil accumulation in reperfused ischaemic myocardium, 31 dogs underwent a 2 h occlusion of the left anterior descending coronary artery, followed by 6 h of reperfusion. One group of dogs received saline (controls) the other a perfusion of lignocaine 0.06 mg·kg−1·min−1 starting 30 min before coronary occlusion and lasting for the duration of the experiment. Blood lignocaine concentrations at the onset of reperfusion were 3.3(0.6) μg·ml−1. 111Indium labelled autologous neutrophils were injected at the time of occlusion and their accumulation in the myocardium measured by digital scintigraphy of heart slices. The area at risk and infarct size were evaluated by planimetry of the heart slices (7 mm) after perfusion of Evans blue dye and triphenyltetrazolium staining. Ventricular fibrillation occurred in six controls and in five dogs receiving lignocaine. The phenomenon occurred early during the occlusion period in the lignocaine group (five dogs) and at reperfusion in controls (five dogs; p<0.05). In the remaining 20 dogs, 10 in each group, a linear correlation was found between myocardial 111In labelled neutrophil and circulating neutrophil counts at the onset of reperfusion (r=0.076, p<0.05) and with infarct size (r=0.96 and 0.74, p<0.05). The myocardial 111In neutrophil counts per cm2 of tissue were statistically similar in controls (9725(1669)) and lignocaine treated dogs (11631(3317)). Infarct size expressed as a percentage of the area at risk was also similar in both groups (controls 36.1(7.1)%; lignocaine 35.8(6.3)%). Thus lignocaine does not reduce infarct size and myocardial neutrophil accumulation after a 2 h coronary occlusion in the dog. Furthermore, these results suggest that lignocaine may induce ventricular fibrillation during coronary occlusion.
Ischemic heart disease and platelet aggregation. The Caerphilly Collaborative Heart Disease Study.
Authors: P C Elwood, S Renaud, D S Sharp, A D Beswick, J R O'Brien, J W Yarnell
Journal: Circulation (1991)

The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men (2,398) aged 49-66 years at the time of study. Platelet aggregation induced by collagen, thrombin, and ADP was measured in fasting blood samples and was related to prevalent angina, past myocardial infarction, and electrocardiographic evidence of ischemic heart disease. A number of subjects had taken aspirin, other nonsteroidal anti-inflammatory drugs, or other drugs affecting platelet aggregation 7 days before blood sample collection; after the exclusion of these subjects, data were available for 1,811 men. No relations were demonstrated with angina, but significant relations were shown between past myocardial infarctions and electrocardiographic evidence of ischemia and ADP-induced aggregation (both primary and secondary) and between electrocardiographic evidence of ischemia and thrombin-induced aggregation. The strongest relation indicated more than a twofold increase in the odds of a past myocardial infarction in subjects of the highest fifth of ADP-induced primary platelet aggregation compared with the lowest fifth. No significant relations were detected with collagen-induced aggregation. Accounting for a number of possible confounding factors had a relatively small impact on the relations between platelet aggregation and ischemic heart disease. Other evidence, including the well-established effect of aspirin on reducing the incidence of ischemic heart disease, indicates that the relations we describe are unlikely to be simply an effect of IHD on platelets.
PMO-204 Assessing risk of adverse outcome in acute lower gastrointestinal bleeding: artificial neural network vs sign guidelines and bleed score
Authors: C H Choi, J Swingland, A Ali, S Bose, L Ayaru
Journal: Gut (2012)

<h3>Introduction</h3> The majority of patients with acute lower gastrointestinal bleeding (ALGIB) have a low risk of requiring intervention, rebleeding or death. Nevertheless in routine clinical practice most are admitted to hospital for observation and endoscopy increasing cost of care. There are no risk scores routinely used in clinical practice which differentiate high risk patients who should be admitted to hospital from those who could be managed as outpatients. British Society of Gastroenterology/Scottish intercollegiate guidelines network (SIGN) have published expert opinion based criteria for non-admission but the accuracy of these is unclear. <h3>Methods</h3> The aim of this study was to compare an artificial neural network9s (ANN) performance in distinguishing high-risk from low-risk patients with ALGIB to SIGN guidelines (six clinical variables) and BLEED score (five clinical variables). Data were collected retrospectively from patients with ALGIB who were admitted to the emergency department of a teaching hospital between 2007 and 2010 (n=174). A multi-layered perceptron ANN model using back propagation and logistic activation function with hidden nodes to make a prediction was constructed from 35 clinical and laboratory variables. The ANN was trained and validated internally using leave-one-out method. The primary composite end point was the need for intervention, rebleeding or death. Sensitvity, specificity, predictive values and accuracy were calculated to compare the performance of the scores in predicting the composite end point. <h3>Results</h3> Overall demographics and outcome of the 174 patients identified with ALGIB were: mean age 68 year (range 16–99), male:female 1:1, rebleeding rate (16.1% n=28), 30 day in hospital mortality (2.3% n=4). The most common diagnoses were diverticular disease (36%), haemorrhoids (10%) and colorectal carcinoma (10%). Twenty-three patients (13%) required intervention; endoscopic therapy (n=7), angiographic embolisation (n=8), or surgery (n=8). Notably, only four (2.3%) patients satisfied the SIGN criteria for non-admission. Predictive scores for each tool were: ANN (sensitivity 50%, specificity 83%, PPV 44%, NPV 83%), BLEED (sensitivity 67%, specificity 44%, PPV 28%, NPV 81%) and SIGN (sensitivity 100%, specificity 3%, PPV 25%, NPV 100%). The ANN performed significantly better in predicting the composite outcome (accuracy 0.76, 95% CI 0.70 to 0.83) compared with BLEED (0.49, 95% CI 0.42 to 0.57) and SIGN (0.26, 95% CI 0.20 to 0.33) scores. <h3>Conclusion</h3> A non-endoscopic based artificial neural network model was more accurate than published guidelines/scores in predicting an adverse outcome in patients with ALGIB. <h3>Competing interests</h3> None declared.
ChlVPP/EVA Hybrid Versus the Weekly VAPEC-B Regimen for Previously Untreated Hodgkin’s Disease
Authors: J. A. Radford, A. Z.S. Rohatiner, W. D.J. Ryder, D. P. Deakin, T. Barbui, N. P. Lucie, A. Rossi, D. J. Dunlop, R. A. Cowan, P. M. Wilkinson, R. K. Gupta, R. D. James, J. Shamash, J. Chang, D. Crowther, T. A. Lister
Journal: Journal of Clinical Oncology (2002)

PURPOSE: To test the hypothesis that a chemotherapy regimen of relatively low toxicity and 11 weeks’ duration (doxorubicin, cyclophosphamide, etoposide, vincristine, bleomycin, and prednisolone [VAPEC-B]) is at least as effective in terms of disease control as 6 months’ treatment with chlorambucil, vinblastine, procarbazine, and prednisone/etoposide, vincristine, and doxorubicin (ChlVPP/EVA hybrid), which is associated with a high risk of permanent sterility. PATIENTS AND METHODS: Two hundred eighty-two patients with previously untreated Hodgkin’s disease, clinical stages I/II (plus mediastinal bulk and/or B symptoms) and clinical stages III/IV were randomized at three United Kingdom and one Italian center to receive either six monthly cycles of ChlVPP/EVA hybrid or 11 weekly cycles of VAPEC-B. After chemotherapy and a restaging evaluation, radiotherapy was administered to sites of previous bulk or residual radiographic abnormality before patients were observed off treatment. RESULTS: Further accrual to the trial was halted at the planned third interim analysis in September 1996. After a median follow-up of 4.9 years, freedom from progression (FFP), event-free survival (EFS), and overall survival (OS) are all significantly better in the population treated with ChlVPP/EVA than VAPEC-B, where the comparative 5-year results are 82% and 62% (FFP), 78% and 58% (EFS), and 89% and 79% (OS), respectively. The superiority of ChlVPP/EVA was seen in both low-risk and intermediate/high-risk patients, although subset analysis suggested that ChlVPP/EVA and VAPEC-B produce equivalent results in the best-prognosis patients (Hasenclever score ≤ 2, nonbulky disease). CONCLUSION: Apart from possibly in the best-prognosis group, where results are equivalent, ChlVPP/EVA hybrid produces significantly better FFP, EFS, and OS than VAPEC-B in patients with previously untreated Hodgkin’s disease.
Meetings on Drug Applications
Authors: Lester M. Crawford, Jr
Journal: JAMA (2002)

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Medical schools in sub-Saharan Africa
Authors: Fitzhugh Mullan, Seble Frehywot, Francis Omaswa, Eric Buch, Candice Chen, S Ryan Greysen, Travis Wassermann, Diaa ElDin ElGaili Abubakr, Magda Awases, Charles Boelen, Mohenou Jean-Marie Isidore Diomande, Delanyo Dovlo, Josefo Ferro, Abraham Haileamlak, Jehu Iputo, Marian Jacobs, Abdel Karim Koumaré, Mwapatsa Mipando, Gottleib Lobe Monekosso, Emiola Oluwabunmi Olapade-Olaopa, Paschalis Rugarabamu, Nelson K Sewankambo, Heather Ross, Huda Ayas, Selam Bedada Chale, Soeurette Cyprien, Jordan Cohen, Tenagne Haile-Mariam, Ellen Hamburger, Laura Jolley, Joseph C Kolars, Gilbert Kombe, Andre-Jacques Neusy
Journal: The Lancet (2010)
Do we need to screen for latent TB when initiating a methotrexate treatment
Authors: Victoria Sadovici, Lucia Mazur-Nicorici, Virginia Salaru, Tatiana Rotaru, Snejana Vetrila, Mariana Cebanu, Minodora Mazur
Journal: European Respiratory Journal (2013)

In rheumatology, the reactivation of pulmonary tuberculosis (TB) is a significant problem, especially in patients treated tumor necrosis factor antagonists. Simultaneously, it is unclear if DMARDS as methotrexate (MTX) could enhance the risk of TB reactivation in rheumatoid arthritis (RA).  The aim: To investigate the risk of TB reactivation in RA treated with MTX and low doses of corticosteroids.  Methods: The study included patients fulfilling the ACR criteria for RA, treated with MTX 15 mg weekly or MTX plus corticosteroids max 10 mg daily prednisolone equivalent. All subjects were screened for TB antecedents and undergone quantiFERON-TB Gold (QTF) test and chest radiography. The subjects were reevaluated after 12 months for pulmonary TB reactivation.  Results: The cohort included 44 patients, mean age 52,04±9,2 (range 29-62) years, female rate 93,2%, mean duration of disease - 9,36 years, activity of RA – mean DAS28 - 3,4 p.  From all patients, 31 received MTX and 13 MTX plus corticosteroids (mean dose 6,15 mg). Mean duration of MTX treatment was 5,36 years (mean dose 11,47 mg/week).  It was established that 11 patients had positive QTF and 2 patients - nodular lesions, confirmed as pulmonary TB.  At reevaluation, 1 subject presenting at the first visit positive QTF and normal chest radiography, treated with MTX 10 mg weekly and 5 mg prednisolone/day, developed bilateral nodular infiltrates and positive BAAR test.  Conclusions: The use of MTX in the RA treatment may be a risk factor for TB reactivation in high prevalence populations. It is necessary to screen the patients benefiting from MTX treatment with QTF test and chest radiography.
Point: Impaired Fasting Glucose: The Case for the New American Diabetes Association Criterion
Authors: Jonathan E. Shaw, Paul Z. Zimmet, K. George M.M. Alberti
Journal: Diabetes Care (2006)

In 1979 and 1980, both the National Diabetes Data Group (1) and the World Health Organization (WHO) (2) formally defined a postchallenge state of glucose tolerance that lay between what was considered normal and diabetic. This state was defined as an elevated 2-h plasma glucose with a nondiabetic fasting glucose level and was termed “impaired glucose tolerance” (IGT). Those individuals falling within the new IGT range were known to have an increased risk of future diabetes and of cardiovascular disease (CVD). It took almost another 20 years to officially recognize that a similar category existed for elevated, but nondiabetic, fasting glucose levels.

In 1997 and 1999, the American Diabetes Association (ADA) and the WHO, respectively, added the term “impaired fasting glucose” (IFG) (with the WHO using “impaired fasting glycemia”) to the available diagnostic categories (3,4). It was defined as a fasting plasma glucose (FPG) of 110–125 mg/dl (6.1–6.9 mmol/l). While it was clear that FPG values below the diabetes threshold were predictive of future diabetes and CVD, it was less obvious where the appropriate cut point between normal and IFG status should lie.

The report of the ADA’s 1997 Expert Committee on the Diagnosis and Classification of Diabetes (3) cites several earlier studies on which the cut point of 110 mg/dl (6.1 mmol/l) was based. The first is, in fact, the origin of both the name, IFG, and the cut point (5). In an analysis of the Paris Prospective Study, Charles et al. (5) selected a group of people just below the then fasting diabetes threshold of 140 mg/dl (7.8 mmol/l) from the cohort to determine whether elevated, nondiabetic fasting glucose levels were comparable to IGT in predicting incident diabetes. To make the comparison with IGT even handed, they chose a fasting glucose cut point that would include …
European Union plans electronic health card to guarantee treatment
Authors: R. Watson
Journal: BMJ (2002)

Plans are being finalised to introduce new electronic health cards that will guarantee their holders emergency medical treatment throughout the European Union. The cards are designed to replace the cumbersome E111 health forms and reduce paperwork and red tape.

The credit-style cards would contain several standardised features, just as the European passport now does, enabling them to be easily recognisable by health authorities and professionals throughout the union.

The initiative is not designed to give patients any new rights. The European Commission, which proposed the scheme earlier …
Larval therapy for leg ulcers (VenUS II): randomised controlled trial
Authors: J. C Dumville, G. Worthy, J M. Bland, N. Cullum, C. Dowson, C. Iglesias, J. L Mitchell, E A. Nelson, M. O Soares, D. J Torgerson
Journal: BMJ (2009)

<h3>Background</h3> The Quality of Life Instrument for Chronic Diseases (QLICD)-COPD (V2.0) was designed to assess the health condition of patients with chronic obstructive pulmonary disease (COPD). The objective of this study was to evaluate the quality of life (QOL) of patients, the influential clinical factors and the relationships between QOL and clinical objective indicators. <h3>Methods</h3> Two hundred and sixty-one inpatients with COPD in the acute exacerbation stage were evaluated using the QLICD-COPD (V2.0) and data on clinical objective indicators were collected. The relationships between QOL and the clinical objective indicators were determined using canonical correlation analysis. <h3>Results</h3> The standardised scores for the patients in four domains, namely, physical function, psychological function, social function and a disease-specific module, were 49.00±12.91, 59.89±13.51, 68.59±11.94 and 51.84±13.58, respectively. The total score for the QOL of patients was 57.17±10.26. Two pairs of canonical variables were statistically significant (r<sub>1</sub>=0.35, p&lt;0.0001; r<sub>2</sub>=0.26, p&lt;0.05). These variables accounted for 45.8% and 33.8% of the variance, respectively. The levels of total protein, albumin, serum sodium and alkaline phosphatase and the percentages of neutrophils and lymphocytes were correlated with the QOL, with correlation coefficients ranging from −0.435 to 0.675. <h3>Conclusion</h3> Clinicians should pay close attention to the levels of total protein, albumin, serum sodium and alkaline phosphatase and the percentages of neutrophils and lymphocytes to improve the QOL of patients.
Resistance of CD7-deficient Mice to Lipopolysaccharide-induced Shock Syndromes
Authors: Gregory D. Sempowski, David M. Lee, Richard M. Scearce, Dhavalkumar D. Patel, Barton F. Haynes
Journal: The Journal of Experimental Medicine (1999)

CD7 is an immunoglobulin superfamily molecule involved in T and natural killer (NK) cell activation and cytokine production. CD7-deficient animals develop normally but have antigen-specific defects in interferon (IFN)-γ production and CD8+ CTL generation. To determine the in vivo role of CD7 in systems dependent on IFN-γ, the response of CD7-deficient mice to lipopolysaccharide (LPS)-induced shock syndromes was studied. In the high-dose LPS-induced shock model, 67% of CD7-deficient mice survived LPS injection, whereas 19% of control C57BL/6 mice survived LPS challenge (P &amp;lt; 0.001). CD7-deficient or C57BL/6 control mice were next injected with low-dose LPS (1 μg plus 8 mg D-galactosamine [D-gal] per mouse) and monitored for survival. All CD7-deficient mice were alive 72 h after injection of LPS compared with 20% of C57BL/6 control mice (P &amp;lt; 0.001). After injection of LPS and D-gal, CD7-deficient mice had decreased serum IFN-γ and tumor necrosis factor (TNF)-α levels compared with control C57BL/6 mice (P &amp;lt; 0.001). Steady-state mRNA levels for IFN-γ and TNF-α in liver tissue were also significantly decreased in CD7-deficient mice compared with controls (P &amp;lt; 0.05). In contrast, CD7-deficient animals had normal liver interleukin (IL)-12, IL-18, and interleukin 1 converting enzyme (ICE) mRNA levels, and CD7-deficient splenocytes had normal IFN-γ responses when stimulated with IL-12 and IL-18 in vitro. NK1.1+/ CD3+ T cells are known to be key effector cells in the pathogenesis of toxic shock. Phenotypic analysis of liver mononuclear cells revealed that CD7-deficient mice had fewer numbers of liver NK1.1+/CD3+ T cells (1.5 ± 0.3 × 105) versus C57BL/6 control mice (3.7 ± 0.8 × 105; P &amp;lt; 0.05), whereas numbers of liver NK1.1+/CD3− NK cells were not different from controls. Thus, targeted disruption of CD7 leads to a selective deficiency of liver NK1.1+/ CD3+ T cells, and is associated with resistance to LPS shock. These data suggest that CD7 is a key molecule in the inflammatory response leading to LPS-induced shock.
Does Adjuvant Vaccine Therapy Really Have Activity in Malignant Melanoma?
Authors: Keith Wheatley, Natalie J. Ives, Paul Lorigan
Journal: Journal of Clinical Oncology (2007)

interferon (IFN) versus low-dose IFN plus allogeneic melanoma lysate vaccine as representing “the first time a randomized large-scale trial of a vaccine regimen has demonstrate d... activity” in the adjuvant melanoma setting, and suggest that “low-dose IFN was probably not solely responsible” for any activity observed. However, since publication, an individual patient data meta-analysis presented recently at the 2007 Annual Meeting of the American Society of Clinical Oncology (ASCO; Chicago, IL) 2 provides no evidence that low-dose IFN is any less effective than high-dose. The hazard ratio (HR) for high-dose IFN is 0.90 (95% CI, 0.80 to 1.02;P .1), and the HR for low-dose IFN is also 0.90 (95% CI, 0.80 to 1.01; P .07). Nor is this finding new. While Mitchell et al quote two qualitative systematic reviews in their discussion, they fail to mention a quantitative published data meta-analysis from 2003, 3 which also showed no dose effect on overall survival (high-dose HR 0.90, low-dose HR 0.90). Thus, it is entirely plausible that the “indistinguishable” survival of patients in the highdose IFN and low-dose IFN plus vaccine arms of their study is due to the similar efficacy of low-dose and high-dose IFN, with the vaccine making no contribution. Furthermore, at the 2007 Annual Meeting of ASCO, a trial of a vaccine in stage III melanoma patients reported adverse survival in the vaccine arm (P .04). 4 We therefore consider that caution should be exercised in interpreting the trial by Mitchell and colleagues as providing any evidence of benefit for adjuvant vaccine therapy in melanoma. Also, as the authors point out, the trial was not large enough to demonstrate equivalence, but no idea (ie, HR with CI) of the range of uncertainty of the treatment effect is presented. We calculate them to
A to Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance—Part 31
Authors: M Gleeson, J C Siegler, L M Burke, S J Stear, L M Castell
Journal: British Journal of Sports Medicine (2012)

This issue deals with the increasingly interesting topic of probiotics and also, slightly out of alphabetical order, with pycnogenol, a product usually associated with pine bark. Probiotics are food supplements containing live microorganisms. They modify intestinal microbiota in a way that enables beneficial bacteria to increase. An additional benefit is that probiotics in sufficient quantities also tend to decrease those species of bacteria which are considered harmful. It is suggested that this situation produces many potential benefits for the health and functioning of the digestive system, and also has a beneficial effect on immune function. In the short review below, the effects of probiotics and their efficacy in reducing infection incidence (or symptom severity/duration) in athletes are summarised. Pycnogenol supplementation has previously been considered to have a range of beneficial effects, including antioxidant and anti-inflammatory properties.

### M Gleeson

Probiotics are food supplements that contain live microorganisms which when administered in adequate amounts can confer a health benefit on the host.1 There is now a reasonable body of evidence that regular consumption of probiotic strains that are proven to survive gut transit can modify the population of the gut-dwelling bacteria (microbiota) and influence immune function2,–,5 though it should be noted that such effects are dose- and strain-dependent. Probiotics modify the intestinal microbiota such that the numbers of beneficial bacteria increase and usually numbers of species considered harmful are decreased. Such changes have been associated with a range of potential benefits to the health and functioning …