tbuckley/cabot-search huggingface dataset:
Short-term effects of air pollution on health: a European approach using epidemiological time-series data. The APHEA project: background, objectives, design
Authors: K Katsouyanni, D Zmirou, C Spix, J Sunyer, JP Schouten, A Ponka, HR Anderson, Y Le Moullec, B Wojtyniak, MA Vigotti, al. et
Journal: European Respiratory Journal (1995)

Recent studies investigating the adverse health effects of air pollution indicate that effects exist around and below the current national and international air quality guidelines and standards. However, the difficult methodological issues involved, and the diversity of analytical techniques so far applied, hinder direct between-study comparability and the drawing of clear conclusions. The APHEA (Air Pollution on Health: European Approach) project is an attempt to provide quantitative estimates of the short-term health effects of air pollution, using an extensive data base from 10 different European countries, which represent various social, environmental and air pollution situations. Within the framework of the project, the methodology of analysing epidemiological time series data, as well as that of performing meta-analysis, are further developed and standardized. Data have been collected from 15 European cities with a total population exceeding 25 million. The exposure data consist of daily measurements of black smoke, sulphur dioxide, suspended particles, nitrogen dioxide and ozone (each available in several, though not all, cities) from already existing monitoring networks. There is substantial variability in air pollution mixtures and air pollutant levels in participating cities. The mean (24 h) levels of SO2 range 27-327 micrograms.m-3 in the winter season, and those of black smoke range 15-292 micrograms.m-3. The mean (1 h) levels of ozone in the summer season range 32-166 micrograms.m-3. The outcome data are daily counts of total and cause-specific deaths and hospital emergency admissions. Data on potential confounders (mainly meteorological and chronological variables) are also used. There is large diversity in the climatic conditions in the different cities.(ABSTRACT TRUNCATED AT 250 WORDS)
Mechanisms governing the biphasic pattern of gastric emptying after truncal vagotomy and pyloroplasty.
Authors: N J Parr, S Grime, M Critchley, J N Baxter, C R Mackie
Journal: Gut (1988)

The pattern of gastric emptying after truncal vagotomy and drainage is usually biphasic. An early rapid phase is followed by a characteristically abrupt transition to slow emptying. The mechanisms responsible for this pattern were studied in six dogs with truncal vagotomy and pyloroplasty, fitted with a proximal duodenal cannula. Gastric emptying was measured using gamma camera imaging of a radiolabelled 15% dextrose test meal. Sixty one hour studies were done using five designs. (1) With the cannula closed gastric emptying was initially rapid, followed by stasis (emptying at 15 min - 32% (5.3), 60 min - 34% (4.8); mean (SE)). (2) With the cannula open emptying was very rapid (15 min - 76% (4.2) p less than 0.001, 60 min - 88% (2.6) p less than 0.001 ANOVA). (3) Distal duodenal instillation of isotonic saline, at a rate equivalent to gastric emptying with the cannula closed, did not retard this rapid emptying (15 min - 78% (10.6), 60 min - 90% (5.4)). (4) With duodenal instillation of 15% dextrose, gastric emptying remained faster than in studies without diversion (15 min - 50% (7.0) NS, 60 min - 65% (6.8) p less than 0.01), but was slower than during diversion alone (p less than 0.05). (5) Finally, duodenal instillation of 15% dextrose before administration of the test meal produced slower initial emptying without subsequent stasis (15 min - 24% (4.5), 60 min - 47% (10.6)), although the amounts emptied were not significantly different from those with the cannula closed. These results indicate that after truncal vagotomy and pyloroplasty small bowel resistances play a significant role in controlling gastric emptying. Osmoreceptor responses persist after truncal vagotomy, but sympathetic inhibitory responses to small bowel distension are not involved in the regulatory process.
Innate immunity in the lung: how epithelial cells fight against respiratory pathogens
Authors: R. Bals, P.S. Hiemstra
Journal: European Respiratory Journal (2004)

The human lung is exposed to a large number of airborne pathogens as a result of the daily inhalation of 10,000 litres of air. The observation that respiratory infections are nevertheless rare is testimony to the presence of an efficient host defence system at the mucosal surface of the lung. The airway epithelium is strategically positioned at the interface with the environment, and thus plays a key role in this host defence system. Recognition systems employed by airway epithelial cells to respond to microbial exposure include the action of the toll-like receptors. The airway epithelium responds to such exposure by increasing its production of mediators such as cytokines, chemokines and antimicrobial peptides. Recent findings indicate the importance of these peptides as effector molecules of innate immunity by killing microorganisms, but also as regulators of inflammation, immunity and wound repair. Finally, the clinical relevance of the functions of the airway epithelium in innate immunity is discussed.
Endothelial Cell Senescence in Human Atherosclerosis
Authors: Tohru Minamino, Hideaki Miyauchi, Toshihiko Yoshida, Yasuo Ishida, Hideo Yoshida, Issei Komuro
Journal: Circulation (2002)

Background — The functional changes associated with cellular senescence may be involved in human aging and age-related vascular disorders. We have shown the important role of telomere and telomerase in vascular cell senescence in vitro. Progressive telomere shortening in vivo has been observed in the regions susceptible to atherosclerosis, implying contributions to atherogenesis. However, whether senescent vascular cells are present in the vasculature and contribute to the pathogenesis of atherosclerosis remains unclear. Methods and Results — Senescence-associated β-galactosidase (β-gal) activity was examined in the coronary arteries and the internal mammary arteries retrieved from autopsied individuals who had had ischemic heart diseases. Strong β-gal stainings were observed in atherosclerotic lesions of the coronary arteries but not in the internal mammary arteries. An immunohistochemical analysis using anti-factor VIII antibody demonstrated that β-gal stained cells are vascular endothelial cells. To determine whether endothelial cell senescence causes endothelial dysfunction, we induced senescence in human aortic endothelial cells (HAECs) by inhibiting telomere function and examined the expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) activity. Senescent HAECs exhibited increased ICAM-1 expression and decreased eNOS activity, both of which are alterations implicated in atherogenesis. In contrast, introduction of telomerase catalytic component significantly extended the life span and inhibited the functional alterations associated with senescence in HAECs. Conclusions — Vascular endothelial cells with senescence-associated phenotypes are present in human atherosclerotic lesions, and endothelial cell senescence induced by telomere shortening may contribute to atherogenesis.
Obstructive sleep apnea and hypertrophic cardiomyopathy: A common and potential harmful combination
Authors: Flávia B. Nerbass, Rodrigo P. Pedrosa, Naury J. Danzi-Soares, Luciano F. Drager, Edmundo Arteaga-Fernández, Geraldo Lorenzi-Filho
Journal: Sleep Medicine Reviews (2012)
How do I measure physical activity in my patients? Questionnaires and objective methods
Authors: B E Ainsworth
Journal: British Journal of Sports Medicine (2008)

How do healthcare providers know if their patients are getting enough physical activity to promote good health and to reduce their risks of chronic diseases and injury? The first step is to identify the patient's current level of physical activity using questionnaires and/or motion sensors. Questionnaires assess activity levels by having patients answer a set of questions about the types and amounts of activity performed at some time in the past. Motion sensors assess physical activity by patients wearing a small monitoring device that records their body movement as it occurs. If a provider is interested in determining a patient's caloric energy expenditure, he/she can apply statistical regression models to the questionnaire and motion sensor data to estimate kilocalories. If more precise measures of energy expenditure are desired, a provider can use the isotopic doubly labelled water method to estimate kilocalories; however, this method is costly and is impractical in non-research clinical settings.
Strategies to improve clinical research in surgery through international collaboration
Authors: Kjetil Søreide, Derek Alderson, Anders Bergenfelz, John Beynon, Saxon Connor, Dan L Deckelbaum, Cornelis H Dejong, Jonathan J Earnshaw, Patrick Kyamanywa, Rodrigo O Perez, Yoshiharu Sakai, Desmond C Winter
Journal: The Lancet (2013)
Melanocyte Destruction after Antigen-Specific Immunotherapy of Melanoma
Authors: Cassian Yee, John A. Thompson, Patrick Roche, David R. Byrd, Peter P. Lee, Michael Piepkorn, Karla Kenyon, Mark M. Davis, Stanley R. Riddell, Philip D. Greenberg
Journal: The Journal of Experimental Medicine (2000)

Current strategies for the immunotherapy of melanoma include augmentation of the immune response to tumor antigens represented by melanosomal proteins such as tyrosinase, gp100, and MART-1. The possibility that intentional targeting of tumor antigens representing normal proteins can result in autoimmune toxicity has been postulated but never demonstrated previously in humans. In this study, we describe a patient with metastatic melanoma who developed inflammatory lesions circumscribing pigmented areas of skin after an infusion of MART-1-specific CD8(+) T cell clones. Analysis of the infiltrating lymphocytes in skin and tumor biopsies using T cell-specific peptide-major histocompatibility complex tetramers demonstrated a localized predominance of MART-1-specific CD8(+) T cells (>28% of all CD8 T cells) that was identical to the infused clones (as confirmed by sequencing of the complementarity-determining region 3). In contrast to skin biopsies obtained from the patient before T cell infusion, postinfusion biopsies demonstrated loss of MART-1 expression, evidence of melanocyte damage, and the complete absence of melanocytes in affected regions of the skin. This study provides, for the first time, direct evidence in humans that antigen-specific immunotherapy can target not only antigen-positive tumor cells in vivo but also normal tissues expressing the shared tumor antigen.
Automated eukaryotic gene structure annotation using EVidenceModeler and the Program to Assemble Spliced Alignments
Authors: Brian J Haas, Steven L Salzberg, Wei Zhu, Mihaela Pertea, Jonathan E Allen, Joshua Orvis, Owen White, C Robin Buell, Jennifer R Wortman
Journal: Genome biology (2008)

Abstract EVidenceModeler (EVM) is presented as an automated eukaryotic gene structure annotation tool that reports eukaryotic gene structures as a weighted consensus of all available evidence. EVM, when combined with the Program to Assemble Spliced Alignments (PASA), yields a comprehensive, configurable annotation system that predicts protein-coding genes and alternatively spliced isoforms. Our experiments on both rice and human genome sequences demonstrate that EVM produces automated gene structure annotation approaching the quality of manual curation.
Predictive Capacity of Three Comorbidity Indices in Estimating Mortality After Surgery for Colon Cancer
Authors: Robert B. Hines, Chakrapani Chatla, Harvey L. Bumpers, John W. Waterbor, Gerald McGwin, Ellen Funkhouser, Christopher S. Coffey, James Posey, Upender Manne
Journal: Journal of Clinical Oncology (2009)

Although, for patients with cancer, comorbidity can affect the timing of cancer detection, treatment, and prognosis, there is little information relating to the question of whether the choice of comorbidity index affects the results of studies. Therefore, to compare the association of comorbidity with mortality after surgery for colon cancer, this study evaluated the Adult Comorbidity Evaluation-27 (ACE-27), the National Institute on Aging (NIA) and National Cancer Institute (NCI) Comorbidity Index, and the Charlson Comorbidity Index (CCI).The study population consisted of colon cancer patients (N = 496) who underwent surgery at the University of Alabama at Birmingham Hospital from 1981 to 2002. Hazard ratios (HRs) with 95% CIs were obtained using the method of Cox proportional hazards for the three comorbidity indices in predicting overall and colon cancer-specific mortality. The point estimates obtained for comorbidity and other risk factors across the three models were compared.For each index, the highest comorbidity burden was significantly associated with poorer overall survival (ACE-27: HR = 1.63; 95% CI, 1.24 to 2.15; NIA/NCI: HR = 1.83; 95% CI, 1.29 to 2.61; CCI: HR = 1.46; 95% CI, 1.14 to 1.88) as well as colon cancer-specific survival. For the other risk factors, there was little variation in the point estimates across the three models.The results obtained from these three indices were strikingly similar. For patients with severe comorbidity, all three indices were statistically significant in predicting shorter survival after surgery for colon cancer.
Nicotine Strongly Activates Dendritic Cell–Mediated Adaptive Immunity
Authors: Alexandra Aicher, Christopher Heeschen, Mariette Mohaupt, John P. Cooke, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Circulation (2003)

Background— Antigen-presenting cells (APCs) such as monocytes and dendritic cells (DCs) stimulate T-cell proliferation and activation in the course of adaptive immunity. This cellular interaction plays a role in the growth of atherosclerotic plaques. Nicotine has been shown to increase the growth of atherosclerotic lesions. Therefore, we investigated whether nicotine can stimulate APCs and their T cell–stimulatory capacity using human monocyte–derived DCs and murine bone marrow–derived DCs as APCs. Methods and Results— Nicotine dose-dependently (10 −8 to 10 −4 mol/L) induced DC expression of costimulatory molecules (ie, CD86, CD40), MHC class II, and adhesion molecules (ie, LFA-1, CD54). Moreover, nicotine induced a 7.0-fold increase in secretion of the proinflammatory T H 1 cytokine interleukin-12 by human DCs. These effects were abrogated by the nicotinic receptor antagonist α-bungarotoxin and mecamylamine, respectively. The effects of nicotine were mediated in part by the phosphorylation of the PI3 kinase downstream target Akt and the mitogen-activated kinases ERK and p38 MAPK. Nicotine-stimulated APCs had a greater capacity to stimulate T-cell proliferation and cytokine secretion, as documented by mixed lymphocyte reactions and ovalbumin-specific assays with ovalbumin-transgenic DO10.11 mice. In a murine model of atherosclerosis, nicotine significantly enhanced the recruitment of DCs to atherosclerotic lesions in vivo. Conclusions— Nicotine activates DCs and augments their capacity to stimulate T-cell proliferation and cytokine secretion. These effects of nicotine may contribute to its influence on the progression of atherosclerotic lesions.
A Comparison of DNA Copy Number Profiling Platforms
Authors: Joel Greshock, Bin Feng, Cristina Nogueira, Elena Ivanova, Ilana Perna, Katherine Nathanson, Alexei Protopopov, Barbara L. Weber, Lynda Chin
Journal: Cancer Research (2007)

Abstract The accurate mapping of recurring DNA copy number aberrations (CNAs), a hallmark feature of the cancer genome, has facilitated the discovery of tumor suppressor genes and oncogenes. Microarray-based assays designed to detect these chromosomal copy number alterations on a genome-wide and high-resolution scale have emerged as a cornerstone technology in the genomic era. The diversity of commercially available platforms prompted a systematic comparison of five copy number profiling assays for their ability to detect 2-fold copy number gain and loss (4n or 1n, respectively) as well as focal high-amplitude CNAs. Here, using a collection of established human melanoma cell lines, we defined the reproducibility, absolute signals, signal to noise, and false-positive and false-negative rates for each of the five assays against ground truth defined by spectral karyotyping, in addition to comparing the concordance of CNA detection by two high-resolution Agilent and Affymetrix microarray platforms. Our analyses concluded that the Agilent's 60-mer oligonucleotide microarray with probe design optimized for genomic hybridization offers the highest sensitivity and specificity (area under receiver operator characteristic curve &amp;gt;0.99), whereas Affymetrix's single nucleotide polymorphism microarray seems to offer better detection of CNAs in gene-poor regions. Availability of these comparison results should guide study design decisions and facilitate further computational development. [Cancer Res 2007;67(21):10173–80]
Glucagonlike Peptide 1–Based Drugs and Pancreatitis: Clarity at Last, but What About Pancreatic Cancer?
Authors: Belinda Gier, Peter C. Butler
Journal: JAMA Internal Medicine (2013)

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Lung Function Response to Cold Air Challenge in Asthmatic and Healthy Children of 2–5 Years of Age
Authors: KIM G. NIELSEN, HANS BISGAARD
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

The aim of the study was to assess feasibility, sensitivity, specificity, predictive value, and repeatability of cold, dry air challenge (CACh) as a diagnostic test for asthma in young children 2 to 5 yr of age. Response to a 4-min single-step isocapnic CACh was measured in 38 asthmatics and 29 control subjects. Specific airway resistance (sRaw) by whole body plethysmography was the primary outcome. In addition, lung function was measured as respiratory resistance by the interrupter technique (Rint) and respiratory resistance and reactance at 5 Hz (Rrs5, Xrs5) by the impulse oscillation technique. At baseline, lung function measures differed significantly between asthmatics and healthy control subjects. CACh was readily performed in young children. Response was expressed as change from baseline in numbers of within-subject standard deviation (SDw). Hyperresponsiveness defined as change in lung function of more than 3 SDw was detected by sRaw in 26 of 38 asthmatics versus 2 of 29 control subjects, by Rint in 12 of 38 asthmatics versus 1 of 29 control subjects, by Xrs5 in 9 of 38 asthmatics versus zero of 29 control subjects and by Rrs5 in 7 of 38 asthmatics versus 1 of 29 control subjects. Thus sRaw had the highest sensitivity (68%). Specificity ranged from 93 to 100%. The correlation coefficient between sRaw responses to CACh repeated within 8 wk was 96%. In conclusion, CACh is feasible in young children age 2 to 5 yr. Whole body plethysmography (sRaw) was superior in separating asthmatics from healthy control subjects. Change in sRaw in response to CACh may be used as a diagnostic test for asthma in young children.
Role of myofibroblasts in vascular remodelling: focus on restenosis and aneurysm
Authors: A. Forte, A. Della Corte, M. De Feo, F. Cerasuolo, M. Cipollaro
Journal: Cardiovascular Research (2010)

Myofibroblasts (MFs) are contractile cells deriving from a multiplicity of resident cells and/or circulating progenitors that are known to play a key role in wound healing. They were first discovered and analysed in the early 1970s in granulation tissue. Since their first identification, the role of MF and their mechanisms of differentiation have been highlighted in a number of diseases, including organ fibrosis and tumours, with particular attention devoted to the liver, kidney, and pulmonary fibrosis. The aim of this review is to summarize the current evidence for the role played by MFs in two frequent vascular diseases related to the remodelling of the vascular wall: the different forms of arterial restenosis and the most common forms of thoracic aortic aneurysm. The in-depth knowledge of the molecular pathways involved in MF differentiation, contraction, and survival/apoptosis could contribute to the identification of novel therapeutic strategies for anti-fibrotic and anti-remodelling therapy of vascular diseases in which these cells are involved.
A NOTE ON THE ABSENCE OF ADRENALIN IN MALIGNANT RENAL HYPERNEPHROMAS
Authors: Clyde Brooks
Journal: The Journal of Experimental Medicine (1911)

The results of these experiments show, in short, that, by the method employed, adrenalin could neither be demonstrated in the specimen of blood, nor in either of the two specimens of malignant hypernephroma, nor in the specimen of metastatic tissue from the adrenal tumor which closely resembled a malignant hypernephroma. The results agree with those of Greer and Wells in showing that no adrenalin is found in malignant renal hypernephromas; and the further observation is made that no adrenalin content of the blood of a patient with malignant renal hypernephroma could be shown by the rabbit uterus strip test. Those rare tumors which arise from medullary adrenal tissue might be expected to contain adrenalin; but as pointed out by Greer and Wells, since the ordinary malignant renal hypernephroma arises from adrenal rests which consist of cortical tissue, and since the cortex of adrenal contains no adrenalin, no adrenalin should be expected in the tumors arising from such cortical tissue.