tbuckley/cabot-search huggingface dataset:
The Worldwide Pandemic of Asbestos-Related Diseases
Authors: Leslie Stayner, Laura S. Welch, Richard Lemen
Journal: Annual Review of Public Health (2013)

Asbestos-related diseases are still a major public health problem. The World Health Organization (WHO) has estimated that 107,000 people worldwide die each year from mesothelioma, lung cancer, and asbestosis. We review what is known about asbestos use, production, and exposure and asbestos-related diseases in the world today, and we offer predictions for the future. Although worldwide consumption of asbestos has decreased, consumption is increasing in many developing countries. The limited data available suggest that exposures may also be high in developing countries. Mesothelioma is still increasing in most European countries and in Japan but has peaked in the United States and Sweden. Although the epidemic of asbestos-related disease has plateaued or is expected to plateau in most of the developed world, little is known about the epidemic in developing countries. It is obvious that increased asbestos use by these countries will result in an increase in asbestos-related diseases in the future.
In-Home Air Pollution Is Linked to Respiratory Morbidity in Former Smokers with Chronic Obstructive Pulmonary Disease
Authors: Nadia N. Hansel, Meredith C. McCormack, Andrew J. Belli, Elizabeth C. Matsui, Roger D. Peng, Charles Aloe, Laura Paulin, D’Ann L. Williams, Gregory B. Diette, Patrick N. Breysse
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

The effect of indoor air pollutants on respiratory morbidity among patients with chronic obstructive pulmonary disease (COPD) in developed countries is uncertain.The first longitudinal study to investigate the independent effects of indoor particulate matter (PM) and nitrogen dioxide (NO(2)) concentrations on COPD morbidity in a periurban community.Former smokers with COPD were recruited and indoor air was monitored over a 1-week period in the participant's bedroom and main living area at baseline, 3 months, and 6 months. At each visit, participants completed spirometry and questionnaires assessing respiratory symptoms. Exacerbations were assessed by questionnaires administered at clinic visits and monthly telephone calls.Participants (n = 84) had moderate or severe COPD with a mean FEV1 of 48.6% predicted. The mean (± SD) indoor PM(2.5) and NO(2) concentrations were 11.4 ± 13.3 µg/m(3) and 10.8 ± 10.6 ppb in the bedroom, and 12.2 ± 12.2 µg/m(3) and 12.2 ± 11.8 ppb in the main living area. Increases in PM(2.5) concentrations in the main living area were associated with increases in respiratory symptoms, rescue medication use, and risk of severe COPD exacerbations. Increases in NO(2) concentrations in the main living area were independently associated with worse dyspnea. Increases in bedroom NO(2) concentrations were associated with increases in nocturnal symptoms and risk of severe COPD exacerbations.Indoor pollutant exposure, including PM(2.5) and NO(2), was associated with increased respiratory symptoms and risk of COPD exacerbation. Future investigations should include intervention studies that optimize indoor air quality as a novel therapeutic approach to improving COPD health outcomes.
Correlation of desensitisation of platelet activating factor (PAF) receptors with intensity of inflammation and intestinal PAF content during experimental ileitis in guinea pig
Authors: O Jeanneton, M Delvaux, Y Langlois, P Le Bars, J Le Bars, M B Delisle, J Frexinos, L Bueno
Journal: Gut (1998)

To determine the kinetics of platelet activating factor (PAF) and prostaglandin E2 (PGE2) receptor desensitisation during intestinal inflammation induced by trinitrobenzenesulphonic acid (TNB) instillation and to study the relation between receptor regulation, inflammatory lesions, and PAF content of the gut wall.Receptor desensitisation was assessed on isolated smooth muscle cells from the circular layer. PAF content of the intestinal wall was determined by thin layer chromatography and radioimmunoassay.After an acute inflammatory phase on day 1, subacute changes appeared in TNB instilled ileum, with a maximal intensity on day 6. In control animals, PAF 10 nM and PGE2 10 nM provoked a maximal contraction in the range of 24% of cell shortening. On days 1 and 3 after intestinal instillation of TNB, PAF induced contraction was not altered whereas the effect of PGE2 was progressively desensitised (2 logM rightward shift of its concentration-response curve: Cmax = 1 microM; p < 0.01). Between days 4 and 6, the concentration-response curve of PGE2 shifted by only 1 logM (p < 0.05) whereas the curve of PAF induced contraction shifted by 2 logM (Cmax = 1 microM; p < 0.01). The PAF content of the ileal wall was maximal between days 3 and 5 (300 ng/mg tissue). On days 10 and 15, PAF and PGE2 induced contractions were similar to those observed on day 1, and PAF content returned to basal.Inflammation induced by TNB instillation triggers PAF and PGE2 receptor desensitisation; this is dependent on the duration of inflammation and correlates with PAF content in the ileum. This receptor desensitisation may play a protective role by preventing overstimulation of intestinal smooth muscle cells.
The Coronary Arteries in Coarctation of the Aorta
Authors: ZEEV VLODAVER, HENRY N. NEUFELD
Journal: Circulation (1968)

The histological changes found in the coronary arteries in 15 patients with coarctation of the aorta have been described. Qualitative and quantitative studies were performed and the results compared with the findings of a matched control group of patients without heart disease. Severe changes in the intima during early life and even the severe atheroma which appears in young persons are considered to be a reaction to coronary hypertension. The striking thickening of the media in the coronary arteries is also thought to be a reaction to the altered hemodynamic forces. In coarctation of the aorta the coronary arteries are of greater than normal capacity, and it is suggested that this histological feature parallels the increased metabolic requirements of the left ventricle.
Long-Term Survival Among Patients With Hodgkin's Lymphoma Who Developed Breast Cancer: A Population-Based Study
Authors: Michael T. Milano, Huilin Li, Mitchell H. Gail, Louis S. Constine, Lois B. Travis
Journal: Journal of Clinical Oncology (2010)

Purpose The increased risk of breast cancer (BC) among women receiving chest radiotherapy for Hodgkin's lymphoma (HL) is well-established. However, there are no large population-based studies that describe overall survival (OS) and cause-specific survival (CSS) compared with women with first primary BC. Methods For 298 HL survivors who developed BC (HL-BC group) and 405,223 women with a first or only BC (BC-1 group), actuarial OS and CSS were compared, accounting for age, BC stage, hormone receptor status, sociodemographic status, radiation for HL, and other variables. All patients were derived from the population-based Surveillance, Epidemiology, and End Results program. Results OS among patients with HL-BC was significantly inferior that of to patients with BC-1: 15-year OS was 48% versus 69% (P &lt; .0001) for localized BC, and 33% versus 43% (P &lt; .0001) for regional/distant BC. Patients with HL-BC had a significantly increased seven-fold risk (P &lt; .0001) of death from other cancers (ie, not HL or BC) compared with patients with BC-1. Mortality from heart disease among patients with HL-BC with either localized or regional/distant disease was also significantly increased (hazard ratio = 2.22, P = .04; and hazard ratio = 4.28, P = .02, respectively) compared with patients with BC-1. Although 10-year BC-CSS was similar for patients with HL-BC and BC-1 with regional/distant disease, it was inferior for patients with localized BC (82% v 88%, respectively; P = .002). Conclusion Women with HL may survive a subsequent diagnosis of BC, only to experience significant excesses of death from other primary cancers and cardiac disease. Greater awareness of screening for cardiac disease and subsequent primary cancers in patients with HL-BC is warranted.
Outcomes of Children With Intermediate-Risk Neuroblastoma After Treatment Stratified by <i>MYCN</i> Status and Tumor Cell Ploidy
Authors: Rochelle Bagatell, Pavlina Rumcheva, Wendy B. London, Susan L. Cohn, A. Thomas Look, Garrett M. Brodeur, Christopher Frantz, Vijay Joshi, Paul Thorner, P.V. Rao, Robert Castleberry, Laura C. Bowman
Journal: Journal of Clinical Oncology (2005)

The goal of Pediatric Oncology Group 9243 was to improve outcomes for children with intermediate-risk neuroblastoma (NB).Patients were assigned to treatments on the basis of age, tumor MYCN status, and tumor cell ploidy. Children in the less intensive arm A received cyclophosphamide/doxorubicin and surgery. Patients not in complete remission postoperatively were treated with cisplatin/etoposide, cyclophosphamide/doxorubicin, and additional surgery. Patients with less favorable features were assigned to arm B, which consisted of carboplatin, etoposide, ifosfamide, and surgery. Survival rates were determined using an intent-to-treat approach.For arm-A patients, the 6-year event-free survival (EFS) was 86% with an SE of 3%. For arm-B patients, the 6-year EFS was 46% with an SE of 7%. MYCN status was the only statistically significant prognostic variable. Among patients whose tumors were MYCN nonamplified, a trend toward improved EFS was seen in children with hyperdiploid versus diploid tumors. However, many of these children responded well to salvage therapy, and overall survival rates did not differ on the basis of ploidy. Six-year EFS rates for arm B were patients with MYCN nonamplified, hyperdiploid tumors, 86% with an SE of 3%; patients with MYCN nonamplified, diploid tumors, 74% with an SE of 10%; patients with MYCN-amplified, hyperdiploid tumors, 46% with an SE of 15%; and patients with MYCN-amplified, diploid tumors, 22% with an SE of 10%.Outcomes for patients with MYCN-nonamplified, hyperdiploid tumors were excellent. Therapy reductions for these patients merit study. A trend toward less favorable outcomes for patients with MYCN-nonamplified, diploid tumors was observed; more children may need to be evaluated before therapy is reduced for this subgroup. For patients with MYCN-amplified tumors, new strategies are needed.
Declining incidence of surgery for Achilles tendon rupture follows publication of major RCTs: evidence-influenced change evident using the Finnish registry study
Authors: Ville M Mattila, Tuomas T Huttunen, Heidi Haapasalo, Petri Sillanpää, Antti Malmivaara, Harri Pihlajamäki
Journal: British Journal of Sports Medicine (2013)

Objectives Acute Achilles tendon ruptures are common among highly active people. Recently published studies have provided increasing evidence to support non-surgical treatment. This study aimed to assess the incidence trends of surgically treated, acute Achilles tendon ruptures. Our hypothesis, based on the recent literature showing no difference in functional results between surgical and non-surgical treatment, was that the incidence of surgery would be declining. Methods We conducted a nationwide hospital register-based study. All patients 18 years of age or older with a diagnosis of acute Achilles tendon injury, and treated with Achilles tendon repair from 1987 to 2011 in Finland were included in the study. Results During the 25-year study period in Finland, a total of 15 252 patients received surgical treatment for an acute Achilles tendon rupture. The incidence of surgical treatment of acute Achilles tendon rupture in men was 11.1/100 000 person-years in 1987 and 20.5/100 000 person-years in 2011. The corresponding figures in women were 2.5/100 000 person-years in 1987 and 4.2/100 000 person-years in 2011. The highest rates occurred in 2008 in men and 2007 in women, and since then the decrease has been 42% in men and 55% in women. Conclusions During the past few years, the rate of surgically treated acute Achilles tendon ruptures has declined remarkably. The findings of the present study indicate that orthopaedic surgeons have chosen more often non-surgical treatment option for acute Achilles ruptures. This can be considered as an example, how high-quality scientific evidence can lead to a rapid change in clinical practice.
Comparison of Radioimmunoprecipitation With Luciferase Immunoprecipitation for Autoantibodies to GAD65 and IA-2 
Authors: Peter D. Burbelo, Hiroki Hirai, Alexandra T. Issa, Albert Kingman, Åke Lernmark, Sten-A. Ivarsson, Abner L. Notkins, Michael J. Iadarola
Journal: Diabetes Care (2010)

OBJECTIVE To compare the sensitivity and specificity of luciferase immunoprecipitation (LIPS) with radioimmunoprecipitation (RIP) for the measurement of autoantibodies to the type 1 diabetes autoantigens glutamic acid decarboxylase 65 (GAD65) and insulinoma-associated protein (IA)-2β. RESEARCH DESIGN AND METHODS Sera from 49 type 1 diabetic patients and 100 nondiabetic control subjects from Diabetes Antibody Standardization Program 2007 were used to screen for autoantibodies to GAD65. An additional 200 type 1 diabetic patients and 200 nondiabetic control subjects were used to validate the GAD65 results and screen for autoantibodies to IA-2β. RESULTS LIPS showed equal sensitivity and specificity to RIP for detecting autoantibodies to GAD65 and IA-2β. Receiver-operating characteristic analysis revealed that the detection of autoantibodies to GAD65 and IA-2β by LIPS and RIP were not statistically different. CONCLUSIONS The LIPS assay does not require the use of radioisotopes or in vitro transcription/translation and is a practical alternative at the clinical level for the RIP assay.
Two Varieties of Plasma Imipramine Curves in Psychotic Depressions and Normal Controls
Authors: GEORGE G. HAYDU, ANDREAS DHRYMIOTIS, GERTRUDE P. QUINN
Journal: American Journal of Psychiatry (1967)

Plasma imipramine determinations were done in 29 newly hospitalized patients with psychotic depression and in nine normal controls after single oral administrations of 100 mg. of the drug. Two types of curves were found which differed significantly at seven and 24 hours after drug administration. Patients with low oral curves (type A) also had significantly lower plasma imipramine at two hours after intramuscular administration than patients with high oral curves (type B) had. All patients with psychotic involutional depression, as well as normal controls (with one exception), exhibited type A curve. Patients evidencing depressions with manic-depressive psychoses had mainly type B curves. The results are discussed from the point of view of drug binding and metabolism differing according to the functional condition of the central nervous system in the depressions.
Compressing drug development timelines in oncology using phase '0' trials
Authors: Shivaani Kummar, Robert Kinders, Larry Rubinstein, Ralph E. Parchment, Anthony J. Murgo, Jerry Collins, Oxana Pickeral, Jennifer Low, Seth M. Steinberg, Martin Gutierrez, Sherry Yang, Lee Helman, Robert Wiltrout, Joseph E. Tomaszewski, James H. Doroshow
Journal: Nature reviews. Cancer (2007)
Increased urinary leukotriene excretion in patients with cardiac ischemia. In vivo evidence for 5-lipoxygenase activation.
Authors: M Carry, V Korley, J T Willerson, L Weigelt, A W Ford-Hutchinson, P Tagari
Journal: Circulation (1992)

Experimental cardiac ischemia in some animal models results in the activation of the enzyme 5-lipoxygenase and the subsequent production of leukotrienes, potent proinflammatory lipid mediators, by the affected myocardium. Furthermore, prototype antileukotriene drugs can show some beneficial effects on infarct size and cardiac function in these models. Accordingly, urinary excretion of leukotriene E4 (LTE4), the major urinary metabolite of peptide leukotrienes in humans, was measured in patients admitted to the hospital with evidence of acute myocardial ischemia to assess in vivo release of 5-lipoxygenase products during and after the ischemic episode.Urinary leukotriene excretion was measured by reversed-phase high-performance liquid chromatography and specific radioimmunoassay on admission with acute chest pain and again on day 3 in the following patient groups: acute myocardial infarction (AMI), AMI and clinical evidence of early reperfusion after treatment with recombinant tissue-type plasminogen activator (rt-PA), diagnosis of unstable angina (UA) based on clinical history and coronary arteriography, controls with nonischemic chest pain who underwent coronary arteriography, and age-matched controls and normal hospital employees. In 16 patients with diagnosis of AMI, LTE4 excretion on admission (331 +/- 99 pg/mg creatinine sulfate; mean +/- SEM) was considerably higher than that measured on day 3 (195 +/- 59 pg/mg creatinine sulfate). In a subgroup of seven subjects treated with rt-PA resulting in early reperfusion, day 1 excretion was similar (215 +/- 50 pg/mg) but had significantly declined by day 3 (65 +/- 16 pg/mg; p less than 0.01). Urinary LTE4 excretion at admission for chest pain was also elevated in 14 patients having unstable angina (UA; 370 +/- 125 pg LTE4/mg creatinine sulfate). This had declined significantly (p less than 0.05) by day 3 (at which time chest pain had resolved) to 94 +/- 31 pg/mg creatinine sulfate, an excretion rate comparable with that measured in eight similarly aged subjects (64 +/- 12 pg/mg creatinine).This study suggests that peptide leukotrienes are released during episodes of myocardial ischemia and provides clinical evidence for involvement of their biosynthetic enzyme, 5-lipoxygenase, during and after acute myocardial infarction and unstable angina attacks. Thus, potent and specific orally active leukotriene biosynthesis inhibitors may have therapeutic potential in limiting myocardial damage and functional abnormalities after acute ischemia.
Onychomycosis due to <i>Scopulariopsis brevicaulis:</i> clinical features and response to systemic antifungals
Authors: A. TOSTI, B.M. PIRACCINI, C. STINCHI, S. LORENZI
Journal: British Journal of Dermatology (1996)

Six cases of Scopulariopsis onychomycosis, including four patients with onychomycosis exclusively caused by Scopulariopsis brevicaulis and two patients with a mixed nail infection (S. brevicaulis + Tricophyton rubrum and S. brevicaulis + T. interdigitale), are reported. Four patients presented with a typical distal subungual onychomycosis characterized by subungual hyperkeratosis and onycholysis of the distal nail plate. In two patients, Scopulariopsis infection produced a total dystrophic onychomycosis associated with painful periungual inflammation. Three patients were treated with four pulses of itraconazole, 400 mg daily for 1 week a month, and three patients with terbinafine, 250 mg daily for 4 months. The mycological examination 8 months after discontinuation of treatment showed that one patient was mycologically cured whereas the remaining five patients still carried S. brevicaulis in their nails. The clinical examination at the end of the follow-up period showed a complete cure of the nail abnormalities in only one patient.
MCP-1 Contributes to Arteriovenous Fistula Failure
Authors: Julio P. Juncos, Joseph P. Grande, Lu Kang, Allan W. Ackerman, Anthony J. Croatt, Zvonimir S. Katusic, Karl A. Nath
Journal: Journal of the American Society of Nephrology (2010)

Vascular access dysfunction compromises the care of patients on chronic hemodialysis. Elucidating the mechanisms of such dysfunction and devising strategies that may interrupt neointimal hyperplasia and relevant pathogenetic pathways are essential. Here, we show that, in the venous segment of a murine model of an arteriovenous fistula, monocyte chemoattractant protein-1 (MCP-1) mRNA and protein increase, accompanied by increased activity of the transcription factors NF-κB and AP-1. Genetic deficiency of MCP-1 proved markedly protective in this murine model, reflected by increased fistula patency 6 weeks after its formation, decreased venous wall thickness, and increased luminal area. An early effect of MCP-1 deficiency was the attenuation of the marked induction of CCL5 (RANTES) that occurred in this model, a chemokine recently recognized as a critical participant in vascular injury. Finally, in a rat model of an arteriovenous fistula, we localized expression of MCP-1 to the endothelium, proliferating smooth muscle cells and infiltrating leukocytes. In summary, marked upregulation of MCP-1 occurs in the venous segment of an arteriovenous fistula in rodents, and this vasculopathic chemokine contributes to failure of the fistula.
First blast of the trumpet against the monstrous regiment of scientists (with apologiesto John Knox)
Authors: A.W. McKenzie
Journal: British Journal of Dermatology (1986)

Journal Article First blast of the trumpet against the monstrous regiment of scientists (with apologiesto John Knox) Get access A.W. McKenzie A.W. McKenzie The Skin Department, Norfolk and Norwich Hospital, Norwich NR1 3SR, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 115, Issue 5, 1 November 1986, Page 637, https://doi.org/10.1111/j.1365-2133.1986.tb05778.x Published: 01 November 1986
The accuracy of a dry gas meter to monitor ventilation during exercise
Authors: A. Bonen, A. N. Belcastro
Journal: British Journal of Sports Medicine (1974)

Several reports (Cunningham, 1969; Henry and Katch, 1972; Mayhew, 1973; Wilmore, 1968; Wilmore and Costill, 1974) have described procedures to measure pulmonary ventilation (Ne) continuously during exercise from a Parkinson-Cowan-CD4 dry gas meter (PC-CD4). Since the accuracy of the calculated oxygen consumption is determined in part by the accuracy of the measured Ve, it is critical that the PC-CD4 readings
<i>Helicobacter pylori</i> Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor
Authors: Jacqueline H. Dickson, Anna Grabowska, Mohamad El-Zaatari, John Atherton, Susan A. Watson
Journal: Cancer Research (2006)

Abstract Both gastrin and Helicobacter pylori have been shown capable of up-regulating gene expression and protein shedding of heparin-binding epidermal growth factor (HB-EGF). Furthermore, the bacteria have previously been shown to induce serum hypergastrinemia in infected individuals. The aim of this work was to assess the extent to which the ability of H. pylori to up-regulate expression of HB-EGF can be attributed to its effect on gastrin. Gastric cells, transfected with either gastrin small interfering RNA or antisense plasmid or the gastrin/cholecystokinin-2 receptor (CCK-2R), were cultured for 24 hours with H. pylori+/−, a CCK-2R antagonist. Gene expression levels were measured using reverse transcription-PCR, whereas protein changes were measured using ELISA, Western blotting, and immunofluorescence. H. pylori induced significantly higher levels of HB-EGF gene expression and ectodomain shedding in the CCK-2R-transfected cells than the vector control (P &amp;lt; 0.01). Addition of the CCK-2R inhibitor significantly decreased gene and shedding up-regulation. Gastrin down-regulation reduced the effect of the bacteria on HB-EGF gene and protein expression levels. Endogenous gastrin and CCK-2R expression were also found to be significantly up-regulated in all cell lines as a result of exposure to H. pylori (P &amp;lt; 0.02). Gastric mucosal tissue from H. pylori–infected individuals had significantly higher CCK-2R expression levels than noninfected (P &amp;lt; 0.003), and in hypergastrinemic mice, there was an increase in HB-EGF-expressing cells in the gastric mucosa and colocalization of HB-EGF with CCK-2R-positive enterochromaffin-like cells. In conclusion, gastrin and the CCK-2R play significant roles in the induction of HB-EGF gene and protein expression and ectodomain shedding by H. pylori. (Cancer Res 2006; 66(15): 7524-31)