tbuckley/cabot-search huggingface dataset:
Transcutaneous abdominal ultrasonography in the staging of lung cancer
Authors: P. S. Bakke, M. Taule, E. Lillo, G. Melgren, I. J. Magnussen, O. J. Halvorsen
Journal: Thorax (1997)

There is limited information available regarding the relationship between clinical indicators of widespread disease in patients with lung cancer and the findings of transcutaneous ultrasonography.A retrospective survey was made of 279 consecutive patients with lung cancer. By reviewing the patients' records the clinical findings were divided into symptoms, signs, and laboratory tests indicative of metastatic disease. All patients had been examined by abdominal ultrasonography.The patients included 19% with small cell carcinoma. The frequency of abdominal metastases by ultrasonography in those with small cell carcinoma was 40%, in the other patients it was 8%. Regardless of histological group, all the 40 patients with abdominal metastases by ultrasonography had at least one clinical category indicative of widespread disease and 38 (95%) had two or all three clinical categories positive. Fifty nine patients had no clinical indicators of metastases and none of these had abdominal metastases by ultrasonography.The results of this study indicate that abdominal metastases are found in lung cancer patients with clinical findings indicative of widespread disease. No abdominal metastases were found in patients with a negative clinical evaluation. The results indicate that transcutaneous ultrasonography of the abdomen is not necessary in the initial staging if the clinical evaluation is unremarkable.
Comparative Analysis of Alcohol Control Policies in 30 Countries
Authors: Donald A Brand, Michaela Saisana, Lisa A Rynn, Fulvia Pennoni, Albert B Lowenfels
Journal: PLoS Medicine (2007)

Alcohol consumption causes an estimated 4% of the global disease burden, prompting governments to impose regulations to mitigate the adverse effects of alcohol. To assist public health leaders and policymakers, the authors developed a composite indicator-the Alcohol Policy Index-to gauge the strength of a country's alcohol control policies.The Index generates a score based on policies from five regulatory domains-physical availability of alcohol, drinking context, alcohol prices, alcohol advertising, and operation of motor vehicles. The Index was applied to the 30 countries that compose the Organization for Economic Cooperation and Development and regression analysis was used to examine the relationship between policy score and per capita alcohol consumption. Countries attained a median score of 42.4 of a possible 100 points, ranging from 14.5 (Luxembourg) to 67.3 (Norway). The analysis revealed a strong negative correlation between score and consumption (r = -0.57; p = 0.001): a 10-point increase in the score was associated with a one-liter decrease in absolute alcohol consumption per person per year (95% confidence interval, 0.4-1.5 l). A sensitivity analysis demonstrated the robustness of the Index by showing that countries' scores and ranks remained relatively stable in response to variations in methodological assumptions.The strength of alcohol control policies, as estimated by the Alcohol Policy Index, varied widely among 30 countries located in Europe, Asia, North America, and Australia. The study revealed a clear inverse relationship between policy strength and alcohol consumption. The Index provides a straightforward tool for facilitating international comparisons. In addition, it can help policymakers review and strengthen existing regulations aimed at minimizing alcohol-related harm and estimate the likely impact of policy changes.
A randomised, double blind, placebo controlled, multicentre trial of combination therapy with methotrexate plus ciclosporin in patients with active psoriatic arthritis
Authors: A D Fraser
Journal: Annals of the Rheumatic Diseases (2004)

To evaluate the safety and efficacy of adding ciclosporin A (CSA) to the treatment of patients with psoriatic arthritis (PsA) demonstrating an incomplete response to methotrexate (MTX) monotherapy.In a 12 month, randomised, double blind, placebo controlled trial at five centres in three countries, 72 patients with active PsA with an incomplete response to MTX were randomised to receive either CSA (n = 38) or placebo (n = 34). Patients underwent full clinical and radiological assessment and, in addition, high resolution ultrasound (HRUS) was performed at one centre. An intention to treat (last observation carried forward) analysis was employed.Some significant improvements were noted at 12 months in both groups. However, in the active but not the placebo arm there were significant improvements in swollen joint count, mean (SD), from 11.7 (9.7) to 6.7 (6.5) (p<0.001) and C reactive protein, from 17.4 (14.5) to 12.7 (14.3) mg/l (p<0.05) as compared with baseline. The Psoriasis Area and Severity Index (PASI) score improved in the active group (2 (2.3) to 0.8 (1.3)) as compared with placebo (2.2 (2.7) to 1.9 (2.8)), p<0.001, and synovitis detected by HRUS (33 patients, 285 joints) was reduced by 33% in the active group compared with 6% in the placebo group (p<0.05). No improvement in Health Assessment Questionnaire or pain scores was detected.Synovitis detected by HRUS was significantly reduced. Combining CSA and MTX treatment in patients with active PsA, and a partial response to MTX, significantly improves the signs of inflammation but not pain or quality of life.
Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components
Authors: M. Rumelhard, K. Ramgolam, R. Hamel, F. Marano, A. Baeza-Squiban
Journal: European Respiratory Journal (2007)

The aim of the current study was to establish the epidermal growth factor receptor (EGFR) ligand expression profile in human airway epithelial cells exposed to either particulate matter (PM) with an aerodynamic diameter &lt;2.5 μm (PM 2.5 ) or its components and the involvement of EGFR ligands in PM 2.5 -provoked airway inflammation. EGFR ligand mRNA and protein expression were studied in a human bronchial epithelial cell line and normal nasal cells exposed to noncytotoxic concentrations of PM 2.5 or its components. The autocrine role of EGFR ligands in airway epithelial cell pro-inflammation was determined by adding conditioned media from PM 2.5 -treated cells to fresh cells and measuring the secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a pro-inflammatory biomarker. PM 2.5 increased amphiregulin, transforming growth factor-α and heparin-binding EGF-like growth factor mRNA expression and protein secretion, with a slight contribution of aqueous metallic compounds and a strong participation of organic components putatively attributed to PM polyaromatic hydrocarbon content. PM 2.5 -induced EGFR ligands were involved in cellular GM-CSF release. The current study revealed upregulation of several epidermal growth factor receptor ligands by airway epithelial cells exposed to particulate matter with an aerodynamic diameter &lt;2.5 μm and their contribution to bronchial epithelial cell granulocyte-macrophage colony-stimulating factor secretion by an autocrine action, suggesting that these ligands could elicit and sustain the particulate matter-induced airway pro-inflammatory response and contribute to bronchial remodelling.
Epidemiological investigation of Pseudomonas aeruginosa isolates from a six-year-long hospital outbreak using high-throughput whole genome sequencing
Authors: L A Snyder, N J Loman, L A Faraj, K Levi, G Weinstock, T C Boswell, M J Pallen, D A Ala’Aldeen
Journal: Eurosurveillance (2013)

Binary file ES_Abstracts_Final_ECDC.txt matches
A Controlled Trial of Sildenafil in Advanced Idiopathic Pulmonary Fibrosis
Authors: David A Zisman, Marvin Schwarz, Kevin J Anstrom, Harold R Collard, Kevin R Flaherty, Gary W Hunninghake
Journal: New England Journal of Medicine (2010)

Sildenafil, a phosphodiesterase-5 inhibitor, may preferentially improve blood flow to well-ventilated regions of the lung in patients with advanced idiopathic pulmonary fibrosis, which could result in improvements in gas exchange. We tested the hypothesis that treatment with sildenafil would improve walk distance, dyspnea, and quality of life in patients with advanced idiopathic pulmonary fibrosis, defined as a carbon monoxide diffusion capacity of less than 35% of the predicted value.We conducted a double-blind, randomized, placebo-controlled trial of sildenafil in two periods. The first period consisted of 12 weeks of a double-blind comparison between sildenafil and a placebo control. The primary outcome was the proportion of patients with an increase in the 6-minute walk distance of 20% or more. Key secondary outcomes included changes in oxygenation, degree of dyspnea, and quality of life. The second period was a 12-week open-label evaluation involving all patients receiving sildenafil.A total of 180 patients were enrolled in the study. The difference in the primary outcome was not significant, with 9 of 89 patients (10%) in the sildenafil group and 6 of 91 (7%) in the placebo group having an improvement of 20% or more in the 6-minute walk distance (P=0.39). There were small but significant differences in arterial oxygenation, carbon monoxide diffusion capacity, degree of dyspnea, and quality of life favoring the sildenafil group. Serious adverse events were similar in the two study groups.This study did not show a benefit for sildenafil for the primary outcome. The presence of some positive secondary outcomes creates clinical equipoise for further research. (Funded by the National Heart, Lung, and Blood Institute and others; ClinicalTrials.gov number, NCT00517933.)
(34) Facial blistering and scarring
Authors: R.A. Marsden
Journal: British Journal of Dermatology (1985)

Journal Article (34) Facial blistering and scarring Get access R.A. Marsden R.A. Marsden ST George's Hospital, London SW17 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 113, Issue s29, 1 July 1985, Pages 79–80, https://doi.org/10.1111/j.1365-2133.1985.tb13049.x Published: 01 July 1985
Predictive Utility of Circulating Methylated DNA in Serum of Melanoma Patients Receiving Biochemotherapy
Authors: Takuji Mori, Steven J. O’Day, Naoyuki Umetani, Steve R. Martinez, Minoru Kitago, Kazuo Koyanagi, Christine Kuo, Teh-Ling Takeshima, Robert Milford, He-Jing Wang, Vu D. Vu, Sandy L. Nguyen, Dave S.B. Hoon
Journal: Journal of Clinical Oncology (2005)

Purpose Currently, no validated blood-based assays accurately predict treatment response or outcome in melanoma patients. We hypothesized that methylation of tumor-related genes detected in serum DNA could predict disease outcome and therapeutic response in patients receiving concurrent biochemotherapy (BC) for metastatic melanoma. Patients and Methods American Joint Committee on Cancer stage IV melanoma patients (N = 50) had blood drawn before administration of BC. Patients (n = 47) were classified as BC responders or nonresponders. Responders (n = 23) demonstrated a complete or partial response following BC; nonresponders (n = 24) demonstrated progressive disease. Hypermethylation of Ras association domain family 1 (RASSF1A), retinoic acid receptor-β2 (RAR-β2), and O 6 -methylguanine DNA methyltransferase (MGMT) genes were assessed by methylation-specific polymerase chain reaction. Results Circulating methylated RASSF1A was significantly less frequent for responders (three of 23 patients; 13%) than nonresponders (10 of 24 patients; 42%; P = .028). Patients with RASSF1A, RAR-β2, or at least one serum methylated gene had significantly worse overall survival than patients with no methylated genes (log-rank, P = .013, .021, and .01, respectively). Methylated RASSF1A was the only factor that significantly correlated with overall survival and BC response (risk ratio, 2.38; 95% CI, 1.16 to 4.86; P = .018; odds ratio = 0.21; 95% CI, 0.05 to 0.90; P = .036). Conclusion Detection of circulating methylated DNA in serum can predict response to BC and disease outcome.
Biased Ligands for Better Cardiovascular Drugs
Authors: Scott M. DeWire, Jonathan D. Violin
Journal: Circulation Research (2011)

Drug discovery efforts targeting G-protein-coupled receptors (GPCR) have been immensely successful in creating new cardiovascular medicines. Currently marketed GPCR drugs are broadly classified as either agonists that activate receptors or antagonists that prevent receptor activation by endogenous stimuli. However, GPCR couple to a multitude of intracellular signaling pathways beyond classical G-protein signals, and these signals can be independently activated by biased ligands to vastly expand the potential for new drugs at these classic targets. By selectively engaging only a subset of a receptor's potential intracellular partners, biased ligands may deliver more precise therapeutic benefit with fewer side effects than current GPCR-targeted drugs. In this review, we discuss the history of biased ligand research, the current understanding of how biased ligands exert their unique pharmacology, and how research into GPCR signaling has uncovered previously unappreciated capabilities of receptor pharmacology. We focus on several receptors to illustrate the approaches taken and discoveries made, and how these are steadily illuminating the intricacies of GPCR pharmacology. Discoveries of biased ligands targeting the angiotensin II type 1 receptor and of separable pharmacology suggesting the potential value of biased ligands targeting the β-adrenergic receptors and nicotinic acid receptor GPR109a highlight the powerful clinical promise of this new category of potential therapeutics.
Exercise in the End-Stage Renal Disease Population
Authors: Kirsten L. Johansen
Journal: Journal of the American Society of Nephrology (2007)

Many of the known benefits of exercise in the general population are of particular relevance to the ESRD population. In addition, the poor physical functioning that is experienced by patients who are on dialysis is potentially addressable through exercise interventions. The study of exercise in the ESRD population dates back almost 30 yr, and numerous interventions, including aerobic training, resistance exercise training, and combined training programs, have reported beneficial effects. Recently, interventions during hemodialysis sessions have become more popular and have been shown to be safe. The risks of exercise in this population have not been rigorously studied, but there have been no reports of serious injury as a result of participation in an exercise training program. It is time that we incorporate exercise into the routine care of patients who are on dialysis, but identification of an optimal training regimen or regimens, according to patient characteristics or needs, is still needed to facilitate implementation of exercise programs.
Carbon Source and Myc Expression Influence the Antiproliferative Actions of Metformin
Authors: Shiva Javeshghani, Mahvash Zakikhani, Shane Austin, Miguel Bazile, Marie-José Blouin, Ivan Topisirovic, Julie St-Pierre, Michael N. Pollak
Journal: Cancer Research (2012)

Epidemiologic and experimental data have led to increased interest in possible roles of biguanides in cancer prevention and/or treatment. Prior studies suggest that the primary action of metformin is inhibition of oxidative phosphorylation, resulting in reduced mitochondrial ATP production and activation of AMPK. In vitro, this may lead to AMPK-dependent growth inhibition if AMPK and its effector pathways are intact or to an energetic crisis if these are defective. We now show that the effect of exposure of several transformed cell lines to metformin varies with carbon source: in the presence of glutamine and absence of glucose, a 75% decrease in cellular ATP and an 80% decrease in cell number is typical; in contrast, when glucose is present, metformin exposure leads to increased glycolysis, with only a modest reduction in ATP level and cell number. Overexpression of myc was associated with sensitization to the antiproliferative effects of metformin, consistent with myc involvement in "glutamine addiction". Our results reveal previously unrecognized factors that influence metformin sensitivity and suggest that metformin-induced increase in glycolysis attenuates the antiproliferative effects of the compound.
Hemodialysis Vascular Access Dysfunction
Authors: Prabir Roy-Chaudhury, Vikas P. Sukhatme, Alfred K. Cheung
Journal: Journal of the American Society of Nephrology (2006)

Hemodialysis vascular access dysfunction is a major cause of morbidity and hospitalization in the hemodialysis population. The major cause of hemodialysis vascular access dysfunction is venous stenosis as a result of neointimal hyperplasia. Despite the magnitude of the clinical problem, however, there has been a paucity of novel therapeutic interventions in this field. This is in marked contrast to a recent plethora of targeted interventions for the treatment of arterial neointimal hyperplasia after coronary angioplasty. The reasons for this are two-fold. First there has been a relative lack of cellular and molecular research that focuses on venous neointimal hyperplasia in the specific setting of hemodialysis vascular access. Second, there have been inadequate efforts by the nephrology community to translate the recent advances in molecular and interventional cardiology into therapies for hemodialysis vascular access. This review therefore (1) briefly examines the different forms of hemodialysis vascular access that are available, (2) describes the pathology and pathogenesis of hemodialysis vascular access dysfunction in both polytetrafluoroethylene grafts and native arteriovenous fistulae, (3) reviews recent concepts about the pathogenesis of vascular stenosis that could potentially be applied in the setting of hemodialysis vascular access dysfunction, (4) summarizes novel experimental and clinical therapies that could potentially be used in the setting of hemodialysis vascular access dysfunction, and, finally, (5) offers some broad guidelines for future innovative translational and clinical research in this area that hopefully will reduce the huge clinical morbidity and economic costs that are associated with this condition.
Severe Symptomatic Tricuspid Valve Regurgitation Due to Permanent Pacemaker or Implantable Cardioverter-Defibrillator Leads
Authors: Grace Lin, Rick A. Nishimura, Heidi M. Connolly, Joseph A. Dearani, Thoralf M. Sundt, David L. Hayes
Journal: Journal of the American College of Cardiology (2005)
Mechanical Ventilation Affects Local and Systemic Cytokines in an Animal Model of Acute Respiratory Distress Syndrome
Authors: DAVIDE CHIUMELLO, GORSEV PRISTINE, ARTHUR S. SLUTSKY
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

We examined the hypothesis that injurious ventilatory strategies (large tidal volume [Vt] and/or low positive end-expiratory pressure [PEEP]) would increase release of inflammatory mediators into the lung and into the systemic circulation in a lung injury model. Lung injury was induced in 40 anesthetized paralyzed Sprague-Dawley rats (350 ± 2 g) by hydrochloric acid instillation (pH 1.5, 2.5 ml/kg). Rats were then randomized into five groups (n = 8): (1) high-volume zero PEEP (HVZP): Vt, 16 ml/ kg; (2) high-volume PEEP (HVP): Vt, 16 ml/kg, PEEP, 5 cm H2O; (3) low-volume zero PEEP (LVZP): Vt, 9 ml/kg; (4) low-volume PEEP (LVP): Vt, 9 ml/kg, PEEP, 5 cm H2O; (5) same settings as (4) plus a recruitment maneuver performed every hour (LVPR). Respiratory rate was adjusted to maintain normocapnia and fraction of inspired oxygen (Fi O2 ) was 1. Cytokine concentrations (tumor necrosis factor-alpha [TNF- α ] and macrophage inflammatory protein-2 [MIP-2]) were measured by ELISA. All animals in the LVZP group died before the end of the experiment. After 4 h of ventilation, the HVZP group had similar lung fluid TNF- α concentrations compared with the HVP group: 1,861 ± 333 pg/ml versus 1,259 ± 189 pg/ml; and much higher serum concentrations: 692 ± 74 pg/ml versus 102 ± 31 pg/ml (p < 0.05). An identical pattern was found for MIP-2. These results suggest that the particular ventilatory strategy can affect the release of cytokines into the systemic circulation, a finding that may have relevance for the development of multisystem organ failure.
Serum Levels of the Interleukin-1 Receptor Family Member ST2 Predict Mortality and Clinical Outcome in Acute Myocardial Infarction
Authors: Masahisa Shimpo, David A. Morrow, Ellen O. Weinberg, Marc S. Sabatine, Sabina A. Murphy, Elliott M. Antman, Richard T. Lee
Journal: Circulation (2004)

Background— Mechanically overloaded cardiomyocytes secrete a soluble interleukin-1 receptor family member called ST2. Serum levels of ST2 are associated with prognosis in nonischemic heart failure, but the predictive value of ST2 in patients with acute myocardial infarction is unknown. Methods and Results— ST2 levels were measured in serum from 810 patients with acute myocardial infarction in the Thrombolysis In Myocardial Infarction (TIMI) 14 (362 patients) and Enoxaparin and TNK-tPA With or Without GPIIb/IIIa Inhibitor as Reperfusion Strategy in STEMI (ENTIRE)-TIMI 23 (448 patients) clinical trials. Baseline levels of ST2 were significantly higher in those patients who died (0.379 versus 0.233 ng/mL, P =0.0001) or developed new congestive heart failure (0.287 versus 0.233 ng/mL, P =0.009) by 30 days. In an analysis of outcomes at 30 days by ST2 quartiles, both death ( P =0.001) and the combined death/heart failure end point ( P =0.001) showed a significant graded association with levels of ST2; furthermore, in-hospital death ( P =0.003) and death/heart failure ( P =0.004) were also significantly associated with higher ST2 levels. In a logistic regression analysis that controlled for important clinical factors, increasing levels of ST2 remained associated with death at 30 days ( P =0.047). ST2 levels rose during the first day after infarction and were maximal at 12 hours; ST2 levels at 12 hours were also independently associated with death at 30 days ( P &lt;0.001). Conclusions— Serum levels of the interleukin-1 receptor family member ST2 predict mortality and heart failure in patients with acute myocardial infarction. These data suggest that ST2 may be a useful biomarker and that this novel inflammatory receptor may play a role in cardiac pathophysiology.
Efficacy of Pet-Ct in Evaluation of Response in Locally Advanced Non-Small Cell Lung Cancer
Authors: S. Roy, S. Pathy, R. Kumar, B.K. Mohanti, V. Raina, A. Jaiswal, A. Malhotra, S. Thulkar, A. Mohan, S. Mathur, D. Behera
Journal: Annals of Oncology (2014)