tbuckley/cabot-search huggingface dataset:
Self-assessed experience, competence and knowledge of non-invasive ventilation amongst medical trainees
Authors: Mansoor Hameed, Charles Sharp, Philip Mitchelmore
Journal: European Respiratory Journal (2013)

Introduction 

Non-invasive ventilation is a key skill for physicians working on the medical take. COPD is the 2nd most common cause of hospital admission among adults1 and yet in some regions of the United Kingdom, only 40.9% of core medical training programs include respiratory medicine2, thus limiting exposure of trainees to NIV.

Objectives and methods 

We aimed to explore the experience and confidence of core and higher specialty trainees in the UK, and assess their knowledge of indications/management of NIV.

Methods 

A questionnaire was distributed electronically to 7 participating training regions in the UK. Trainees were given questions to self-assess experience and competence in NIV; further questions assessed knowledge.

Results 

194 trainees responded to the questionnaire. Of these 40 were core trainees, with the remainder higher specialty trainees.

Overall 62.9% of trainees stated “extensive” experience of NIV, 34.5% having “limited” exposure. Amongst core trainees only 30% had extensive experience. Overall 63.4% felt independently competent in NIV, but 27.5% of core trainees felt accordingly. In contrast, only 46.9% of trainees felt they could set up and titrate NIV independent of assistance.

The knowledge assessment demonstrated significant gaps in understanding of indications, contra-indications and ongoing titration of NIV amongst all trainees.

Conclusions 

UK trainees demonstrate a discordance between self-assessed experience/confidence with NIV and knowledge/practical ability. This survey identifies a training need for both core and higher specialty trainees.

References 

1 Outcomes Strategy for COPD, DoH, 2011

2 Payne et al, Clinical Medicine 2013, Vol 13, No 1:50-6.
The effects of variation in dietary protein and ethanol on hepatic microsomal drug metabolism in the rat
Authors: Mack C. Mitchell, Esteban Mezey, Willis C. Maddrey
Journal: Hepatology (1981)

The effect of chronic ethanol consumption and variations in dietary protein content on microsomal drug metabolism were studied in rats pair-fed liquid diets containing 10, 20, ro 30% dietary protein with or without ethanol. In vitro drug metabolism was measured by aminopyrine breath tests and aminopyrine blood elimination kinetics. In vitro drug metabolism was assessed by measuring aminopyrine N-demethylase activity in the hepatic microsomal fraction. The rate of elimination of aminopyrine in vivo was increased in all ethanol-fed animals (p less than 0.05) regardless of the protein content of the diet. Animals receiving 10 or 20% protein diets with ethanol showed a 36% increase in drug elimination over pair-fed controls as compared to a 17% increase in drug elimination over controls in animals receiving 30% protein diets. Microsomal aminopyrine N-demethylase activities were similar in ethanol/fed animals and pair-fed controls. Cytochrome P-450 content was increased in all ethanol-fed animals (p less than 0.05) but the increase was not dependent on dietary protein content. These results indicate that the effect of chronic ethanol feeding in enhancing drug metabolism in vivo is influenced by the dietary protein content.
Medical Education in the United States
Authors: Walter S. Wiggins
Journal: JAMA (1961)

Introduction  In presenting this 61st Annual Report on Medical Education, the Council on Medical Education and Hospitals is pleased to express appreciation to the individual medical schools, the Association of American Medical Colleges, governmental agencies and others who provided information important in the preparation of the report. The statistical data were collected for the most part from medical schools through a questionnaire prepared jointly by the staffs of the Council on Medical Education and Hospitals and the Association of American Medical Colleges.  This report presents information primarily related to medical schools and their faculties and students. In order to make the material more readable, most of the statistical data appear in the text in graphic and summary form and the basic tabular material has been included in appendix tables for reference purposes. Where information was available, similar appendix tables have been included for medical schools in Canada.  Medical Schools  The
NF-κB inhibition delays DNA damage–induced senescence and aging in mice
Authors: Jeremy S. Tilstra, Andria R. Robinson, Jin Wang, Siobhán Q. Gregg, Cheryl L. Clauson, Daniel P. Reay, Luigi A. Nasto, Claudette M. St Croix, Arvydas Usas, Nam Vo, Johnny Huard, Paula R. Clemens, Donna B. Stolz, Denis C. Guttridge, Simon C. Watkins, George A. Garinis, Yinsheng Wang, Laura J. Niedernhofer, Paul D. Robbins
Journal: Journal of Clinical Investigation (2012)

The accumulation of cellular damage, including DNA damage, is thought to contribute to aging-related degenerative changes, but how damage drives aging is unknown. XFE progeroid syndrome is a disease of accelerated aging caused by a defect in DNA repair. NF-κB, a transcription factor activated by cellular damage and stress, has increased activity with aging and aging-related chronic diseases. To determine whether NF-κB drives aging in response to the accumulation of spontaneous, endogenous DNA damage, we measured the activation of NF-κB in WT and progeroid model mice. As both WT and progeroid mice aged, NF-κB was activated stochastically in a variety of cell types. Genetic depletion of one allele of the p65 subunit of NF-κB or treatment with a pharmacological inhibitor of the NF-κB–activating kinase, IKK, delayed the age-related symptoms and pathologies of progeroid mice. Additionally, inhibition of NF-κB reduced oxidative DNA damage and stress and delayed cellular senescence. These results indicate that the mechanism by which DNA damage drives aging is due in part to NF-κB activation. IKK/NF-κB inhibitors are sufficient to attenuate this damage and could provide clinical benefit for degenerative changes associated with accelerated aging disorders and normal aging.
The effect of flufenamic acid on gastrointestinal myoelectrical activity and transit time in dogs
Authors: G Farrugia, S Nitecki, G J Harty, M Camilleri, J H Szurszewski
Journal: Gut (1998)

Flufenamic acid, a fenamate, has been shown to alter markedly the membrane potential of small intestinal smooth muscle and increase intracellular calcium in single cells.To determine the effects of flufenamic acid on myoelectrical motor activity and gastrointestinal transit in the intact animal.Myoelectrical motor activity was recorded via seromuscular platinum electrodes sutured at regular intervals in the stomach and throughout the small intestine. Fasted and fed gastrointestinal transit was assessed using technetium-99m (99mTc) as the radioactive marker linked to 1 mm amberlite pellets or added to the meal.Flufenamic acid (600 mg, intravenously) induced intense spike activity in the small intestine. The mean duration of irregular spike activity was 250 (7) minutes. Spike activity was more pronounced in the lower small intestine. Flufenamic acid also accelerated initial gastric emptying and markedly shortened transit time in the small intestine. In the fasted state the 50% transit time in the small intestine was 54 (8) minutes with infusion of flufenamic acid compared with 105 (10) minutes in the control group; in the fed state 99mTc first reached the colon at 220 (10) minutes compared with 270 (12) minutes in the control group.Flufenamic acid had marked effects on both myoelectrical motor complex activity and small intestinal transit in the dog. The observed effects suggest that flufenamic acid may be of potential use as a prokinetic agent.
Oral administration of the probiotic<i>Lactobacillus fermentum</i>VRI-003 and mucosal immunity in endurance athletes
Authors: A J Cox, D B Pyne, P U Saunders, P A Fricker
Journal: British Journal of Sports Medicine (2008)

To evaluate the ability of a probiotic Lactobacillus fermentum VRI-003 (PCC) to enhance the mucosal immune system of elite athletes.A double-blind, placebo-controlled, crossover trial was conducted over a 4-month period of winter training. PARTICIPANTS; 20 healthy elite male distance runners.PCC was given at a daily dose of 1.26 x 10(10) as a freeze-dried powder in gelatin capsules. Placebo capsules contained an inert excipient.Treadmill performance (monthly), mucosal and systemic immunity (monthly), training (daily) and illness (daily) were assessed. Serum cytokine levels, salivary IgA levels and incidence, duration and severity of respiratory tract infections were measured.Subjects reported less than half the number of days of respiratory symptoms during PCC treatment (30 days) compared with placebo (72 days, p<0.001). Illness severity was also lower for episodes occurring during the PCC treatment (p = 0.06). There were no significant differences in the mean change in salivary IgA and IgA1 levels, or in interleukin (IL)4 and IL12 levels, between treatments. However, PCC treatment elicited a twofold (p = 0.07) greater change in whole-blood culture interferon gamma (IFNgamma) compared with placebo. No substantial changes in running performance measures were seen over the study period.Prophylactic administration of PCC was associated with a substantial reduction in the number of days and severity of respiratory illness in a cohort of highly trained distance runners. Maintenance of IFNgamma levels may be one mechanism underpinning the positive clinical outcomes.
Effect of Molecular Therapeutics on Liver Regeneration in a Murine Model
Authors: George Van Buren, Anthony D. Yang, Nikolaos A. Dallas, Michael J. Gray, Sherry J. Lim, Ling Xia, Fan Fan, Ray Somcio, Yan Wu, Daniel J. Hicklin, Lee M. Ellis
Journal: Journal of Clinical Oncology (2008)

Unresectable metastatic colorectal cancer (CRC) can be rendered resectable with systemic chemotherapy in approximately 20% of cases. Most patients with metastatic CRC receive chemotherapy with the addition of targeted therapy with anti-vascular endothelial growth factor (VEGF) or anti-epidermal growth factor receptor (EGFR) antibodies. We sought to determine whether anti-VEGF receptor (VEGFR) or anti-EGFR therapy would impair liver regeneration after partial hepatectomy (PH) in mice.Mice underwent either 66% PH or sham laparotomy. In the first experiment, mice in the PH group were randomly assigned to receive daily intraperitoneal injections of monoclonal antibodies (MoABs) to murine VEGFR-2 or nonspecific MoABs (control). In the second experiment, mice in the PH group were randomly assigned to receive intraperitoneal injections of antimurine EGFR or nonspecific (control) MoABs. In both experiments, therapy was initiated the day before surgery and continued until the mice were killed on day 5. Livers were collected and processed.Anti-VEGFR-2 therapy slightly impaired liver regeneration and hepatic cell proliferation compared with control. Hematoxylin and eosin staining showed no differences in liver morphology. CD105 staining showed decreased levels of activated endothelium in livers in the VEGFR-2 MoAB group. VEGFR-2 MoAB therapy decreased the levels of the cell cycle regulators cyclin D1 and cyclin D3 and the regenerative cytokine interleukin-6. Anti-EGFR therapy had no effect on liver regeneration or cellular proliferation.Anti-VEGFR-2 therapy slightly impaired liver regeneration in this murine model, whereas anti-EGFR therapy had no effect on liver regeneration.
Dengue viruses and mononuclear phagocytes. II. Identity of blood and tissue leukocytes supporting in vitro infection
Authors: SB Halstead, EJ O'Rourke, AC Allison
Journal: The Journal of Experimental Medicine (1977)

Studies were made on the identity of human and monkey mononuclear leukocytes permissive to antibody-enhanced dengue 2 virus (D2V) infection. In cultures of peripheral blood leukocytes (PBL) inoculated immediately after separation, it was concluded that only mononuclear phagocytes support dengue infection. This is based upon observations that D2V-permissive cells were resistant to 1,200 rads, were both plastic adherent and nonadherent, were removed when passed through nylon wool columns in 10 percent fetal bovine serum or 100 percent autologous serum, and were destroyed by incubation with 100 μg/ml particulate silica. On direct immunofluorescence staining, perinuclear dengue antigen was visualized at 24 h, becoming maximal at 60 h. Antigen-containing cells had ample cytoplasm, ruffled cytoplasmic membrane, and 73 percent were actively phagocytic. As further evidence of the infection of mononuclear phagocytes, antibody-enhanced D2V replication was observed in bone marrow cultures from five of five rhesus monkeys, but not in cell cultures of spleen, thymus, or lymph nodes prepared from the same animals. It is hypothesized that dengue virus complexed with non-neutralizing antibody is internalized by immune phagocytosis in a mononuclear phagocyte with a defective virus-destroying mechanism. Dengue permissiveness may depend upon cellular immaturity since bone marrow leukocytes could be infected even when held for 4 days before infection while PBL held for this time decreased in permissiveness. In vitro antibody-dependent infection of mononuclear phagocytes should prove useful as a model for study of immunopathologic mechanisms in human dengue.
Association Between Inpatient Surveillance and Venous Thromboembolism Rates After Hospital Discharge
Authors: Carla N. Holcomb, Aerin DeRussy, Joshua S. Richman, Mary T. Hawn
Journal: JAMA Surgery (2015)

Venous thromboembolism (VTE) surveillance practices in hospitals, but not adherence to Surgical Care Improvement Program VTE prophylaxis measures, have been reported to explain the variation in VTE rates in hospitals.To examine the relationship between inpatient surveillance testing for VTE and postdischarge VTE rates at the hospital level to determine whether more frequent inpatient surveillance is associated with reduced occurrence of postdischarge VTEs.Retrospective study of a US national cohort of Veterans Affairs (VA) patients. National VA Surgical Quality Improvement Program outcome data were linked to VA administrative data on patients undergoing inpatient surgery from 2005 to 2009 and were included in the Surgical Care Improvement Program VTE measurement population.Surveillance was identified using Current Procedural Terminology codes for diagnostic VTE imaging. Relationships between hospital-level surveillance and VTE rates were assessed with Pearson correlation coefficients, and the postdischarge VTE rate was modeled using linear regression, adjusting for hospital volume, inpatient VTE rate, inpatient surveillance rate, and case mix.Of 25 975 patients at 79 VA facilities, 296 (1.4%) experienced a VTE during the index hospitalization, and 114 (0.4%) experienced a postdischarge VTE within 30 days after surgery. The median length of stay was 11 days for those with a positive surveillance test result and 9 days for those with a negative test result. There was a positive correlation between inpatient surveillance and inpatient VTE rates (R = 0.33, P = .003) but no significant correlation of inpatient surveillance with either postdischarge surveillance (R = 0.11, P = .29) or postdischarge VTE rates (R = 0.03, P = .76). In an adjusted regression model of the postdischarge VTE rate, only the inpatient VTE rate was significant (β = 0.13, P = .05).Hospitals with higher VTE surveillance rates have higher inpatient VTE rates but not decreased postdischarge VTE rates. However, hospitals with higher inpatient VTE rates have higher postdischarge VTE rates, which suggests that surveillance may be influenced by higher observed rates and not surveillance practices alone.
Quality Versus Quantity: Assessing Individual Research Performance
Authors: José-Alain Sahel
Journal: Science Translational Medicine (2011)

Evaluating individual research performance is a complex task that ideally examines productivity, scientific impact, and research quality--a task that metrics alone have been unable to achieve. In January 2011, the French Academy of Sciences published a report on current bibliometric (citation metric) methods for evaluating individual researchers, as well as recommendations for the integration of quality assessment. Here, I draw on key issues raised by this report and comment on the suggestions for improving existing research evaluation practices.
Perceptions of Appropriateness of Care Among European and Israeli Intensive Care Unit Nurses and Physicians
Authors: Ruth D. Piers, Elie Azoulay, Bara Ricou, Freda DeKeyser Ganz, Johan Decruyenaere, Adeline Max, Andrej Michalsen, Paulo Azevedo Maia, Radoslaw Owczuk, Francesca Rubulotta, Pieter Depuydt, Anne-Pascale Meert, Anna K. Reyners, Andrew Aquilina, Maarten Bekaert, Nele J. Van Den Noortgate, Wim J. Schrauwen, Dominique D. Benoit
Journal: JAMA (2011)

LINICIANS PERCEIVE THE CARE they provide as inappropriate when they feel that it clashes with their personal beliefs and/or professional knowledge. 15][6][7][8] ICU physicians may be troubled by a perceived lack of power to make the clinical decision that most benefits a specific patient. 5A survey among 504 Eu-
Fourth European Conference on Infections in Leukaemia (ECIL-4): guidelines for diagnosis, prevention, and treatment of invasive fungal diseases in paediatric patients with cancer or allogeneic haemopoietic stem-cell transplantation
Authors: Andreas H Groll, Elio Castagnola, Simone Cesaro, Jean-Hugues Dalle, Dan Engelhard, William Hope, Emmanuel Roilides, Jan Styczynski, Adilia Warris, Thomas Lehrnbecher
Journal: The Lancet Oncology (2014)
Evaluation of Protein in Dietary Management of Diabetes Mellitus
Authors: Judith Wylie-Rosett
Journal: Diabetes Care (1988)

Establishing appropriate recommendations for protein intake in the management of diabetes requires examination of the role that dietary protein plays in overall health, in the control of diabetes, and in the risks to health posed by diabetes. Achieving metabolic control and delaying and/or preventing diabetic complications have previously been established as primary goals for the dietary management of diabetes. Although the primary function of dietary protein is for growth and tissue maintenance, dietary protein may play a role in the regulation of glucose metabolism and in the development of diabetic renal complications. Approximately half of protein intake is considered to be available as glucose. Dietary composition also affects secretion of insulin and counterregulatory hormones. One-third of individuals with insulin-dependent diabetes and one-fifth of those with non-insulin-dependent diabetes develop nephropathy within 15 yr after the diagnosis of diabetes. High protein intake and hyperglycemia can increase the glomerular filtration rate and the work load of the kidney. There is growing evidence from clinical studies that the progression of renal disease is delayed by early protein restriction. More studies are needed to assess early risk of diabetic nephropathy and to determine whether protein restriction alters the course of diabetic nephropathy. A dietary intake of between 12 and 20% protein provides flexibility in food selection but exceeds actual needs. The adult Recommended Dietary Allowance of 0.8 g/kg body wt should provide guidance for determining desired protein intake for individuals with diabetes.
A1 adenosine receptor deficiency or inhibition reduces atherosclerotic lesions in apolipoprotein E deficient mice
Authors: Bunyen Teng, Jonathan D. Smith, Michael E. Rosenfeld, Peggy Robinet, Mary E. Davis, R. Ray Morrison, S. Jamal Mustafa
Journal: Cardiovascular Research (2014)

The goal of this study was to determine whether the A1 adenosine receptor (AR) plays a role in atherosclerosis development and to explore its potential mechanisms.Double knockout (DKO) mice, deficient in the genes encoding A1 AR and apolipoprotein E (apoE), demonstrated reduced atherosclerotic lesions in aortic arch (en face), aortic root, and innominate arteries when compared with apoE-deficient mice (APOE-KO) of the same age. Treating APOE-KO with an A1 AR antagonist (DPCPX) also led to a concentration-dependent reduction in lesions. The total plasma cholesterol and triglyceride levels were not different between DKO and APOE-KO; however, higher triglyceride was observed in DKO fed a high-fat diet. DKO also had higher body weights than APOE-KO. Plasma cytokine concentrations (IL-5, IL-6, and IL-13) were significantly lower in DKO. Proliferating cell nuclear antigen expression was also significantly reduced in the aorta from DKO. Despite smaller lesions in DKO, the composition of the innominate artery lesion and cholesterol loading and efflux from bone marrow-derived macrophages of DKO were not different from APOE-KO.The A1 AR may play a role in the development of atherosclerosis, possibly due to its pro-inflammatory and mitogenic properties.
Vitamin D May Not Improve Lipid Levels
Authors: Manish P. Ponda, Xiaohua Huang, Mouneer A. Odeh, Jan L. Breslow, Harvey W. Kaufman
Journal: Circulation (2012)

Vitamin D deficiency is highly prevalent and is associated with dyslipidemia and cardiovascular disease. The impact of correcting vitamin D deficiency on blood lipids, strong cardiovascular disease prognostic factors, is unknown.To determine relationships between 25-hydroxyvitamin D levels and lipids, we analyzed 4.06 million deidentified patient laboratory test results from September 2009 through February 2011. We performed a cross-sectional study of this population to determine associations between 25-hydroxyvitamin D levels and lipids across clinically defined strata. We also conducted a retrospective cohort study of vitamin D deficient patients to investigate how changes in 25-hydroxyvitamin D levels relate to changes in lipid levels. After exclusions, 107 811 patients with serial testing were selected for cross-sectional analysis. Compared with vitamin D deficient patients (<20 ng/mL), those with optimal levels (≥30 ng/mL) had lower mean total cholesterol (-1.9 mg/dL; 95% confidence interval [95% CI], -1.2 to -2.7; P<0.0001), lower low-density lipoprotein cholesterol (-5.2 mg/dL; 95% CI, -4.5 to -5.8; P<0.0001), higher high-density lipoprotein cholesterol (4.8 mg/dL; 95% CI, 4.5-5.0; P<0.0001), and lower triglycerides (-7.5 mg/dL; 95% CI, -6.2 to -8.7; P<0.0001). For the retrospective cohort analysis, raising vitamin D levels from <20 to ≥30 ng/mL (n=6260), compared with remaining at <20 ng/mL (n=2332), was associated with a mean increase in total cholesterol (0.77 mg/dL; 95% CI, 0.18-1.36; P=0.01) and high-density lipoprotein cholesterol (0.42 mg/dL; 95% CI, 0.08-0.76; P=0.02) but nonsignificant changes in low-density lipoprotein cholesterol (0.32 mg/dL; 95% CI, -0.01 to 0.66; P=0.06) and triglycerides (0.04 mg/dL; 95% CI, -2.16 to 2.23 mg/dL; P=0.97).Although vitamin D deficiency is associated with an unfavorable lipid profile in cross-sectional analyses, correcting for a deficiency might not translate into clinically meaningful changes in lipid concentrations; however, data from intervention trials are required to confirm these findings.