tbuckley/cabot-search huggingface dataset:
Nested Case–Control Study of Selected Systemic Autoimmune Diseases in World Trade Center Rescue/Recovery Workers
Authors: M. P. Webber, W. Moir, R. Zeig‐Owens, M. S. Glaser, N. Jaber, C. Hall, J. Berman, B. Qayyum, K. Loupasakis, K. Kelly, D. J. Prezant
Journal: Arthritis & Rheumatology (2015)

Objective To test the a priori hypothesis that acute and chronic work exposures to the World Trade Center (WTC) site on or after September 11, 2001 were associated with risk of new‐onset systemic autoimmune diseases. Methods A nested case–control study was performed in WTC rescue/recovery workers who had received a rheumatologist‐confirmed systemic autoimmune disease diagnosis between September 12, 2001 and September 11, 2013 (n = 59), each of whom was individually matched to 4 randomly selected controls (n = 236) on the basis of year of hire (±1 year), sex, race, and work assignment (firefighter or emergency medical service). Acute exposure was defined according to the earliest time of arrival (morning of 9/11 versus later) at the WTC site, and chronic exposure was defined as duration (number of months) of WTC site–related work. Rheumatologists were blinded with regard to each subject's exposure status. The conditional odds ratios (CORs) with 95% confidence intervals (95% CIs) for incident autoimmune disease were derived from exact conditional logistic regression models. Results Rheumatoid arthritis was the most common autoimmune diagnosis (37% of subjects), followed by spondyloarthritis (22%), inflammatory myositis (14%), systemic lupus erythematosus (12%), systemic sclerosis (5%), Sjögren's syndrome (5%), antiphospholipid syndrome (3%), and granulomatosis with polyangiitis (Wegener's) (2%). The COR for incident autoimmune disease increased by 13% (COR 1.13, 95% CI 1.02–1.26) for each additional month worked at the WTC site. These odds were independent of the association between high acute exposure (working during the morning of 9/11) and disease outcome, which conveyed an elevated, but not statistically significant, risk (COR 1.85, 95% CI 0.86–3.89). Conclusion Prolonged work at the WTC site, independent of acute exposure, was an important predictor of post‐9/11 systemic autoimmune diseases. The WTC Health Program should expand surveillance efforts for those with extended exposures, as early detection can facilitate early treatment, which has been shown to minimize organ damage and improve quality of life.
NICE widens patient group for leukaemia drug
Authors: Z. Kmietowicz
Journal: BMJ (2002)

The National Institute for Clinical Excellence (NICE) has recommended that anyone with chronic myeloid leukaemia who has failed first line therapy or is in the accelerated and blast phase of the disease should have access to the signal transduction inhibitor imatinib (Glivec). This is a wider group of patients than doctors and campaigners originally …
TONSIL PUNCTURE: A NEW METHOD OF INVESTIGATION
Authors: J. Ramsay, C. M. Pearce
Journal: BMJ (1929)

The impoitant points noted as a result of this experiment -are as follows:(ai) If a normal or leukaemic blood be placed in the chamber and irradiated as described-, complete loss of all phagocytic power in the polymorphs is observed within about thirty-five nliinlutes.(h)) This loss of phagocytic power appears to be quite peimanent.The experiment was varied in different ways and samples of blood given time to recover before examinlation, but no return of phagocytic power could be detected. (c) In passing', it was noted that in fresh unirradiated bloods pliagocvtic power was possessed only by the relatively mature forms of polymorphonuclear and hyaline leucocytes.It is of iinterest that myeloblasts, myelocytes, and -transitionals appear tQ have no phaagocyti6 powver towards the usual types of bacteria. (d) The lethial effect appeared to begin upon the polymorphs at about tlhe same poinit, whetlher in norimal or leukaemic bloods.Thus the experiments with the pa.raffin block appeared clearly to demonstrate a directly destructive effect by the rays on the white cells, anid also that this destructi-e effect was prIoduced mainlly, if lnot enitirely, bv the secondarv raliations aiid not bv the original lhard rays.Somiie sulecess w-ith this method in vitro at once suiggested apl)lications of the test for plhagocvtic l)pvoer uloii the white cells of patienits undergoing deep therapy treatmiient.Dir:ect T'ests upon I rradiulted Patietnts.InI this respect the first fact to be observed wi-as that if blood fromn a leukaemic lpatient be taken twenty-four hiours after deep therapy treatment and, as already described, ntixed with staphvlococci, a considerable numiiber of the p)olmorplhs, althouglh they stain quite ilolmallv, will be founld tb lave lost their plhagocytic p)ower.The test was tliere- ftre sy-stematically applied to patielnts during actual irradiation.It was found that, whltever part of the body ,was irradiated, wvithin about twi-enty miiinutes the percentage of actively phlagocvtic polymorplhs began to fall.If the test was repeated at intervals a few otlher importanit poinits could be noted-niamely: (a) After full irradiation of the spleen in, for example, a case of splenomedullary leukaemia, althouglh the first treatmernt will result in loss of phagocytic power in a considerable number of the polymorphs, the percentage varying according to the dose given and the width of the field irradiated, the proportion of white cells which disappear from the circulating blood within the next few hours is much less than this, and it takes a few days for all these damaged cells to be i'emoved from the circulation.
Molecular Prediction of Response to 5-Fluorouracil and Interferon-α Combination Chemotherapy in Advanced Hepatocellular Carcinoma
Authors: Yukinori Kurokawa, Ryo Matoba, Hiroaki Nagano, Masato Sakon, Ichiro Takemasa, Shoji Nakamori, Keizo Dono, Koji Umeshita, Noriko Ueno, Shin Ishii, Kikuya Kato, Morito Monden
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The prognosis of hepatocellular carcinoma (HCC) is very poor, particularly in patients with tumors that have invaded the major branches of the portal vein. Combination chemotherapy with intra-arterial 5-fluorouracil and subcutaneous interferon-α has shown promising results for such advanced HCC, but it is important to develop the ability to accurately predict chemotherapeutic responses. Experimental Design: We analyzed the expression of 3,080 genes using a polymerase chain reaction-based array in 20 HCC patients who were treated with combination chemotherapy after reduction surgery. After unsupervised analyses, a supervised classification method for predicting chemotherapeutic responses was constructed. To minimize the number of predictive genes, we used a random permutation test to select only significant (P &amp;lt; 0.01) genes. A leave-one-out cross-validation confirmed the gene selection. We also prepared an additional 11 cases for validation of predictive performance. Results: Hierarchical clustering analysis and principal component analysis with all 3,080 genes revealed distinct gene expression patterns in responders (those with complete response or partial response) and nonresponders (those with stable disease or progressive disease) to the combination chemotherapy. Using a weighted-voting classification method with either all genes or only significant genes as assessed by permutation testing, the objective responses to treatment were correctly predicted in 17 of 20 cases (accuracy, 85%; positive predictive value, 100%; negative predictive value, 80%). Moreover, patients in the validation dataset could be classified into two distinct prognostic groups using 63 predictive genes. Conclusions: Molecular analysis of 63 genes can predict the response of patients with advanced HCC and major portal vein tumor thrombi to combination chemotherapy with 5-fluorouracil and interferon-α.
Evolution of galactoglycerolipid biosynthetic pathways – From cyanobacteria to primary plastids and from primary to secondary plastids
Authors: Dimitris Petroutsos, Souad Amiar, Heni Abida, Lina-Juana Dolch, Olivier Bastien, Fabrice Rébeillé, Juliette Jouhet, Denis Falconet, Maryse A. Block, Geoffrey I. McFadden, Chris Bowler, Cyrille Botté, Eric Maréchal
Journal: Progress in Lipid Research (2014)
The Relationship Between Financial Incentives and Quality of Diabetes Care in Ontario, Canada
Authors: Tara Kiran, J. Charles Victor, Alexander Kopp, Baiju R. Shah, Richard H. Glazier
Journal: Diabetes Care (2012)

OBJECTIVE We assessed the impact of a diabetes incentive code introduced for primary care physicians in Ontario, Canada, in 2002 on quality of diabetes care at the population and patient level. RESEARCH DESIGN AND METHODS We analyzed administrative data for 757,928 Ontarians with diabetes to examine the use of the code and receipt of three evidence-based monitoring tests from 2006 to 2008. We assessed testing rates over time and before and after billing of the incentive code. RESULTS One-quarter of Ontarians with diabetes had an incentive code billed by their physician. The proportion receiving the optimal number of all three monitoring tests (HbA1c, cholesterol, and eye tests) rose gradually from 16% in 2000 to 27% in 2008. Individuals who were younger, lived in rural areas, were not enrolled in a primary care model, or had a mental illness were less likely to receive all three recommended tests. Patients with higher numbers of incentive code billings in 2006–2008 were more likely to receive recommended testing but also were more likely to have received the highest level of recommended testing prior to introduction of the incentive code. Following the same patients over time, improvement in recommended testing was no greater after billing of the first incentive code than before. CONCLUSIONS The diabetes incentive code led to minimal improvement in quality of diabetes care at the population and patient level. Our findings suggest that physicians who provide the highest quality care prior to incentives may be those most likely to claim incentive payments.
Bronchoscopic Microsampling Method for Measuring Drug Concentration in Epithelial Lining Fluid
Authors: Koichi Yamazaki, Shigeaki Ogura, Akitoshi Ishizaka, Toshinari Oh-hara, Masaharu Nishimura
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

Direct measurement of the concentration of antimicrobial agents in bronchial epithelial lining fluid (ELF) would allow for a more informed approach to appropriate dosing of antimicrobial agents for respiratory tract infections. In this study, we determined the time versus concentration profile in ELF after an oral administration of levofloxacin, using recently developed bronchoscopic microsampling probes. These probes could be repeatedly and safely inserted through the fiberoptic bronchoscope in normal healthy volunteers. The concentration of levofloxacin in ELF was 43.4% of the corresponding serum value at 1 hour, reached the same level at 2 hours, decreased in a similar manner as that in serum, and returned to undetectable levels at 24 hours. It exceeded minimal inhibitory concentrations of Staphylococcus aureus (0.25 microg/ml), Klebsiella species (0.5 microg/ml), and Haemophilus influenzae (0.06 microg/ml) after 6 hours. The experimental procedure was well tolerated, and no complications were observed. In conclusion, bronchoscopic microsampling is a feasible and promising method for measuring antimicrobial concentrations in the target sites of respiratory tracts directly and repeatedly.
Siglecs and Immune Regulation
Authors: Shiv Pillai, Ilka Arun Netravali, Annaiah Cariappa, Hamid Mattoo
Journal: Annual Review of Immunology (2012)

Sialic acid-binding Ig-like lectins, or Siglecs, vary in their specificity for sialic acid-containing ligands and are mainly expressed by cells of the immune system. Many Siglecs are inhibitory receptors expressed in innate immune cells that regulate inflammation mediated by damage-associated and pathogen-associated molecular patterns (DAMPs and PAMPs). This family also includes molecules involved in adhesion and phagocytosis and receptors that can associate with the ITAM-containing DAP12 adaptor. Siglecs contribute to the inhibition of immune cells both by binding to cis ligands (expressed in the same cells) and by responding to pathogen-derived sialoglycoconjugates. They can help maintain tolerance in B lymphocytes, modulate the activation of conventional and plasmacytoid dendritic cells, and contribute to the regulation of T cell function both directly and indirectly. Siglecs modulate immune responses, influencing almost every cell in the immune system, and are of relevance both in health and disease.
Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)
Authors: Giacomo Ruotolo, Carl-Göran Ericsson, Cristina Tettamanti, Fredrik Karpe, Lars Grip, Bertil Svane, Jan Nilsson, Ulf de Faire, Anders Hamsten
Journal: Journal of the American College of Cardiology (1998)
PERFLUOROALKYL ACIDS: What Is the Evidence Telling Us?
Authors: Kellyn S. Betts
Journal: Environmental Health Perspectives (2007)

Focus | What Is the Evidence Telling Us?I t was 2000 when the scientific community first became widely aware that perfluorooctanyl sulfonate (PFOS), then the key ingredient in 3M Company's popular Scotchgard stain repellent, was being found at extremely low levels throughout the environment and the human population.Since that time, environmental scientists and toxicologists have begun paying much more attention to PFOS, its sister compound perfluorooctanoic acid (PFOA; known for its use in DuPont's Teflon products), and other members of the family of perfluoroalkyl acids (PFAAs).As more tests have been conducted, the research has revealed that laboratory animals respond in vastly different ways to PFAAs and related compounds, which can make it difficult to pinpoint the mechanisms underlying the responses.However, toxicologists are making headway in their understanding of these compounds, an important fact in light of new research suggesting that the levels being found in both people and animals may have an impact on their health.The tremendous variation in the speed with which humans and laboratory animals can eliminate PFOA is one example of why understanding how the compounds are processed in the body poses such a formidable challenge."You go from hours for the female rat, to days for the male rat, to months for the monkey, to almost four years in humans," explains Jennifer Seed, a branch chief with the EPA Office of Pollution Prevention and Toxics."We truly don't understand what are the biological events that drive this difference," says Christopher Lau, a lead research biologist with the EPA National Health and Environmental Effects Research Laboratory (NHEERL)."Are there binding protein differences?Do humans have a different set of transporters that is not the same as in animals?"Lau terms these gaps in understanding "a black hole."These gaps render the toxicologist's goal of extrapolating from one species to another "a very complex state of affairs," as Seed puts it.For this reason, deciphering the human risk posed by exposure to PFAAs is a major challenge, Lau says."We need to go to the next level to identify the underlying events that drive the adverse effects," he says.
Millions Dead: How Do We Know and What Does It Mean? Methods Used in the Comparative Risk Assessment of Household Air Pollution
Authors: Kirk R. Smith, Nigel Bruce, Kalpana Balakrishnan, Heather Adair-Rohani, John Balmes, Zoë Chafe, Mukesh Dherani, H. Dean Hosgood, Sumi Mehta, Daniel Pope, Eva Rehfuess
Journal: Annual Review of Public Health (2014)

In the Comparative Risk Assessment (CRA) done as part of the Global Burden of Disease project (GBD-2010), the global and regional burdens of household air pollution (HAP) due to the use of solid cookfuels, were estimated along with 60+ other risk factors. This article describes how the HAP CRA was framed; how global HAP exposures were modeled; how diseases were judged to have sufficient evidence for inclusion; and how meta-analyses and exposure-response modeling were done to estimate relative risks. We explore relationships with the other air pollution risk factors: ambient air pollution, smoking, and secondhand smoke. We conclude with sensitivity analyses to illustrate some of the major uncertainties and recommendations for future work. We estimate that in 2010 HAP was responsible for 3.9 million premature deaths and ∼4.8% of lost healthy life years (DALYs), ranking it highest among environmental risk factors examined and one of the major risk factors of any type globally.
Diagnostic value of microtympanometry in primary care.
Authors: R. A. de Melker
Journal: BMJ (1992)

To determine the reliability, validity, and feasibility of a new hand held microtympanometer.Comparison of microtympanometry by two independent observations of a general practitioner and a nurse, and against a validated reference instrument.Primary care health centre of a school for the deaf in the United States.111 schoolchildren receiving a regular check up.Tympanometry with the Grason Stadler 28, classified with a slightly modified Jerger's classification.Interobserver reliability was 0.95 (Cohen's kappa). Results of microtympanometry were highly comparable with results of the reference instrument (likelihood ratio of positive results, 161.2).The microtympanometer could be used in general practice: it is hand held, child friendly, easy to handle, and accurate.
Interleukin-10, age and acute lung injury genetics: the action is in the interaction
Authors: J. D. Christie
Journal: European Respiratory Journal (2006)

A cute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are important public health issues, and both incidence and mortality increase with age [1].Given that only a moderate percentage of individuals with the same level of exposure develop ALI/ ARDS, it is logical to investigate whether inherent interindividual variation will, in part, determine the risk of ALI/ARDS.Better understanding of the genetic factors influencing both risk of developing ALI/ARDS and outcomes following ALI/ ARDS may aid in the identification of high-risk individuals, suggest areas for laboratory research and lead to the development of more specific, targeted pharmacogenomic strategies for treatment and prevention [2].
An exploratory population-based case-control study of primary biliary cirrhosis
Authors: Denise Howel, Colin M. Fischbacher, Raj S. Bhopal, Jackie Gray, Jane V. Metcalf, Oliver F. James
Journal: Hepatology (2000)

Primary biliary cirrhosis (PBC) is a disease of unknown etiology, with unexplained geographical variation. Various exposures have been suggested as triggers for disease development—possibly in susceptible individuals, but the evidence was not always well founded. We therefore conducted a population-based case-control study in Northeast England to investigate these and other exposures. All cases incident during 1993 to 1995 in a defined area of Northeast England were identified, and age- and sex-matched population controls were identified from primary care population registers. Cases and controls were sent postal self-completion questionnaires covering medical history and lifestyle. Information was received from 100 cases and 223 controls. The familial tendency of PBC was found to be less marked than has been claimed: Only weak associations were found with other autoimmune diseases. Among factors considered previously, no significant associations were found with surgical procedures, events in pregnancy, past infections, vaccinations, and medications. No significant associations were found for previously unconsidered lifestyle factors (drinking alcohol, previous pets, or stressful events), but there was an unexpected association with past smoking (ever smoked: 76% in cases vs. 57% in controls, odds ratio 2.4; smoked for 20 years or more: 64% vs. 35%, odds ratio 3.5). There were also unexpected significant associations with psoriasis (13% in cases vs. 3% in controls, odds ratio 4.6) and eczema (3% in cases vs. 11% in controls, odds ratio 0.13). These findings merit further investigation.
Identification and Functional Characterization of a Novel Unspliced Transcript Variant of <i>HIC-1</i> in Human Cancer Cells Exposed to Adverse Growth Conditions
Authors: Abdul Matin Mondal, Sivasamy Chinnadurai, Kamal Datta, Shyam S. Chauhan, Subrata Sinha, Parthaprasad Chattopadhyay
Journal: Cancer Research (2006)

Abstract The wild-type p53 gene has been widely implicated in the regulation of hypermethylated in cancer-1 (HIC-1) transcription, a master growth regulatory gene with multiple promoters and, consequently, multiple alternatively spliced transcripts. We investigated the role of p53 (wild type and mutant, both endogenous and exogenous) in modulating the various HIC-1 transcripts. We discovered a novel unspliced HIC-1 transcript, identified as “f” in leukocytes and in the human cell lines U87MG (wild-type p53), U373MG (mutant p53), MCF-7 (wild-type p53), HeLa (p53 degraded by HPV18-E6 oncoprotein), and Saos-2 (p53 null). This transcript is initiated from a new transcription start site and has an intervening stop codon that would result in a possibly truncated 22-amino-acid polypeptide. When U87MG (wild-type p53) and MCF-7 cells (wild-type p53) were exposed to adverse growth conditions of serum starvation or treated with the chemotherapeutic agent cisplatin, cells underwent apoptosis and cell cycle arrest accompanied by increase in p53 and HIC-1 transcript levels. Although the increase of the HIC-1-spliced transcripts followed the increase of p53, increase in f transcript coincided with declining p53 and HIC-1 transcript and protein levels. Moreover, the levels of HIC-1 f transcript were not induced by exogenously transfected wild-type p53 in p53-mutated U373MG and p53-null Saos-2 cells, unlike the spliced transcripts that code for full-length HIC-1 protein. These findings suggest a working model wherein the status of f transcript, which is not under direct transcriptional control of wild-type p53, may influence the level of HIC-1 protein in cancer cells. (Cancer Res 2006; 66(21): 10466-77)
Hamster Respiratory Carcinogenesis Induced by Benzo[α]pyrene and Different Dose Levels of Ferric Oxide2
Authors: Arthur R. Sellakumar, Ruggero Montesano, Umberto Saffiotti, David G. Kaufman
Journal: JNCI Journal of the National Cancer Institute (1973)

Journal Article Hamster Respiratory Carcinogenesis Induced by Benzo[α]pyrene and Different Dose Levels of Ferric Oxide Get access Arthur R. Sellakumar, Arthur R. Sellakumar Search for other works by this author on: Oxford Academic PubMed Google Scholar Ruggero Montesano, Ruggero Montesano Search for other works by this author on: Oxford Academic PubMed Google Scholar Umberto Saffiotti, Umberto Saffiotti Search for other works by this author on: Oxford Academic PubMed Google Scholar David G. Kaufman David G. Kaufman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 50, Issue 2, February 1973, Pages 507–510, https://doi.org/10.1093/jnci/50.2.507 Published: 01 February 1973 Article history Received: 05 September 1972 Accepted: 11 October 1972 Published: 01 February 1973