tbuckley/cabot-search huggingface dataset:
Hyperglycemia is associated with poor outcomes in patients with acute exacerbations of chronic obstructive pulmonary disease
Authors: Hajer Benabdelghaffar, Tawadoud Khmiss, Soraya Fenniche, Othmen Neffati, Leila Fekih, Dorra Greb, Hela Hassene, Hanene Smadhi, Ines Akrout, Dalinda Belhabib, Mohamed Lamine Megdiche
Journal: European Respiratory Journal (2013)

Hyperglycemia is associated with poor outcomes from pneumonia and myocardial infarction, but its effect on outcomes from acute exacerbations of chronic obstructive pulmonary disease (AECOPD) has not been established. Records of patients admitted with AECOPD during 6 years were reviewed. The patients were grouped according to blood glucose quartile (group 1,  9.0 mmol/l (n = 20). The relative risk (RR) of long inpatient stay was significantly increased in group 3 and 4 with a significant difference. For each 1 mmol/l increase in blood glucose the absolute risk of adverse outcomes increased by 12%, p = 0.004. The risk of adverse outcomes increased with increasing hyperglycaemia independent of age, and COPD severity. Isolation of pathogens from sputum increased with increasing blood glucose. Patients in group 3 and 4 had more hypertension, exacerbation was more severe and frequent with a significant difference. COPD may be considered as a novel risk factor for new onset type 2 diabetes mellitus via pathophysiological alterations and diabetes may act as an independent factor, negatively affecting pulmonary function. Diabetes is associated with an increased risk of disease exacerbations and worsened COPD outcomes. Conclusion:Increasing blood glucose concentrations are associated with adverse clinical outcomes in patients with AECOPD. Tight control of blood glucose reduces mortality in patients in intensive care or following myocardial infarction. A prospective study is required to determine whether control of blood glucose can also improve outcomes from AECOPD.
Genetic Loci Associated With C-Reactive Protein Levels and Risk of Coronary Heart Disease
Authors: Paul Elliott
Journal: JAMA (2009)

Plasma levels of C-reactive protein (CRP) are independently associated with risk of coronary heart disease, but whether CRP is causally associated with coronary heart disease or merely a marker of underlying atherosclerosis is uncertain.To investigate association of genetic loci with CRP levels and risk of coronary heart disease.We first carried out a genome-wide association (n = 17,967) and replication study (n = 13,615) to identify genetic loci associated with plasma CRP concentrations. Data collection took place between 1989 and 2008 and genotyping between 2003 and 2008. We carried out a mendelian randomization study of the most closely associated single-nucleotide polymorphism (SNP) in the CRP locus and published data on other CRP variants involving a total of 28,112 cases and 100,823 controls, to investigate the association of CRP variants with coronary heart disease. We compared our finding with that predicted from meta-analysis of observational studies of CRP levels and risk of coronary heart disease. For the other loci associated with CRP levels, we selected the most closely associated SNP for testing against coronary heart disease among 14,365 cases and 32,069 controls.Risk of coronary heart disease.Polymorphisms in 5 genetic loci were strongly associated with CRP levels (% difference per minor allele): SNP rs6700896 in LEPR (-14.8%; 95% confidence interval [CI], -17.6% to -12.0%; P = 6.2 x 10(-22)), rs4537545 in IL6R (-11.5%; 95% CI, -14.4% to -8.5%; P = 1.3 x 10(-12)), rs7553007 in the CRP locus (-20.7%; 95% CI, -23.4% to -17.9%; P = 1.3 x 10(-38)), rs1183910 in HNF1A (-13.8%; 95% CI, -16.6% to -10.9%; P = 1.9 x 10(-18)), and rs4420638 in APOE-CI-CII (-21.8%; 95% CI, -25.3% to -18.1%; P = 8.1 x 10(-26)). Association of SNP rs7553007 in the CRP locus with coronary heart disease gave an odds ratio (OR) of 0.98 (95% CI, 0.94 to 1.01) per 20% lower CRP level. Our mendelian randomization study of variants in the CRP locus showed no association with coronary heart disease: OR, 1.00; 95% CI, 0.97 to 1.02; per 20% lower CRP level, compared with OR, 0.94; 95% CI, 0.94 to 0.95; predicted from meta-analysis of the observational studies of CRP levels and coronary heart disease (z score, -3.45; P < .001). SNPs rs6700896 in LEPR (OR, 1.06; 95% CI, 1.02 to 1.09; per minor allele), rs4537545 in IL6R (OR, 0.94; 95% CI, 0.91 to 0.97), and rs4420638 in the APOE-CI-CII cluster (OR, 1.16; 95% CI, 1.12 to 1.21) were all associated with risk of coronary heart disease.The lack of concordance between the effect on coronary heart disease risk of CRP genotypes and CRP levels argues against a causal association of CRP with coronary heart disease.
Small Bowel Obstruction: A Review of 456 Cases in a West of Ireland Region
Authors: K S H Cross, J G Johnston
Journal: Journal of the Royal Society of Medicine (1987)

A retrospective study was carried out of 456 patients with small bowel obstruction (SBO). The operative findings of all patients who presented with SBO between 1977 and 1982 were compared and contrasted with those who presented during equivalent periods in the previous three decades. Obstructed hernias still account for the highest percentage of cases. Surprisingly, adhesions as a causative factor are not significantly more common than they were three decades ago, despite the enormous increase in the frequency with which abdominal surgery is now being carried out. The postoperative mortality rate for the period 1977–82 was 14%.
Solitary Fibrous Tumor (Sft): a Registry Program to Assess Frequency and Managemente in Our Country. a Spanish Group for Research on Sarcoma (Geis) Study
Authors: J. Cruz Jurado, C. Valverde Morales, M.A. Vaz, R. Alvarez Alvarez, A. Lopez-Pousa, P. Sancho Marquez, J.A. Carrasco, J. Martinez-Trufero, M.A. Sala Gonzalez, J.L. Arranz, L.M. De Sande González, M.J. Blanco Sanchez, C. Orbegoso, J.A. Pérez-Fidalgo, J. Martinez García, J. Lavernia, I. Sevilla, J.M. Cano, A. Meana, J. Martin Broto
Journal: Annals of Oncology (2014)
The impact of smoking on bronchoalveolar lavage fluid (BALf) amyloid A concentration in patients with sarcoidosis
Authors: Marta Maskey-Warzechowska, Joanna Domagala-Kulawik, Tomasz Urbankowski, Patrycja Nejman-Gryz, Rafal Krenke, Ryszarda Chazan
Journal: European Respiratory Journal (2013)

Serum amyloid A (AA) is known as a marker of inflammation and has been proved to be elevated in patients with sarcoidosis, but data on AA concentration in bronchoalveolar lavage fluid (BALf) in these patients are scarce. Some report higher BALf AA concentrations in patients with sarcoidosis as compared to healthy subjects; moreover, there was a correlation between BALf AA concentration and the stage of the disease. On the other hand, smoking is suspected to have a protective role on the course of sarcoidosis, however this remains a point of controversy.  The aim of our study was to evaluate BALf AA in patients with sarcoidosis in relation to their smoking history.   Material and methods . Forty one patients with sarcoidosis (mean age 42 yrs, range 25-74 yrs) were enrolled. There were 31 never smokers and 10 smokers (two of them active) in the group; the median number of packyears was 8 (range 1-30). BALf AA concentration was assessed by ELISA, (Human SAA ELISA, IBL International, Germany).   Results. The median BALf AA concentration in the whole group was 104 µg/ml (IQR 78-147 µg/ml) and a statistically significant difference between smokers and never-smokers was found - 88 µg/ml (IQR 89-179 µg/ml) vs. 128.5 µg/ml (IQR 67-130 µg/ml), respectively, p = 0.026. No correlations between BALf AA and the BALf cellular composition or the clinical parameters of the disease were found.   Conclusions.  BALF AA seems to be a promising biomarker sarcoidosis. The lower BALf AA concentration in smokers warrants further studies and contributes to the discussion on the role of smoking in this disease.
Nationwide laboratory-based surveillance of invasive beta-haemolytic streptococci in Denmark from 2005 to 2011
Authors: L.M. Lambertsen, H. Ingels, H.C. Schønheyder, S. Hoffmann
Journal: Clinical Microbiology and Infection (2013)

The aim of this work was to describe national surveillance of invasive beta-haemolytic streptococci (BHS) in Denmark and to report overall trends and major findings by groups and types of BHS causing laboratory-confirmed disease from 2005 to 2011. A total of 3063 BHS isolates were received from 2872 patients. Based on confirmed cases the overall annual incidence increased from 6.2 to 8.9 per 100 000 persons between 2005 and 2011. In 2011 the incidences of group A, B, C and G streptococci were 3.1, 2.3, 0.9 and 2.6 per 100 000 persons, respectively. An increase was observed for all groups of BHS, but in particular for group G in men above 65 years of age. Among group A streptococci (GAS), five T-types (1, 28,12, 3,13,B3264 and B3264) represented 71% and five emm-types (1, 28, 3, 89 and 12) 76% of all isolates. Among group B streptococci (GBS) four types (III, Ia, V, Ib) represented 79% of the isolates. Potential coverage for future vaccines against GAS and GBS disease was 76% compared with the 26-valent GAS vaccine and 89% based on GBS serotypes Ia, Ib, II, III and V. The number of reported cases of invasive BHS disease increased in Denmark from 2005 to 2011. Nationwide laboratory-based surveillance of BHS is required to monitor epidemiological changes, explore potential outbreaks and determine potential vaccine coverage.
Maternal Age and Birth Rank of Women With Breast Cancer2
Authors: K. J. Rothman, B. MacMahon, T. M. Lin, C. R. Lowe, A. P. Mirra, B. Ravnihar, E. J. Salber, D. Trichopoulos, S. Yuasa
Journal: JNCI Journal of the National Cancer Institute (1980)

Journal Article Maternal Age and Birth Rank of Women With Breast Cancer Get access K. J. Rothman, K. J. Rothman 3Department of Epidemiology, School of Public Health, Harvard University, Boston, Mass. 02115. Search for other works by this author on: Oxford Academic PubMed Google Scholar B. MacMahon, B. MacMahon 3Department of Epidemiology, School of Public Health, Harvard University, Boston, Mass. 02115. Search for other works by this author on: Oxford Academic PubMed Google Scholar T. M. Lin, T. M. Lin 4Department of Public Health, College of Medicine, National Taiwan University, Taipei, Taiwan. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. R. Lowe, C. R. Lowe 5Department of Social and Occupational Medicine, Welsh National School of Medicine, University of Wales, Cardiff, Wales. Search for other works by this author on: Oxford Academic PubMed Google Scholar A. P. Mirra, A. P. Mirra 6Central Cancer Registry, São Paulo, Brazil. Search for other works by this author on: Oxford Academic PubMed Google Scholar B. Ravnihar, B. Ravnihar 7Institute of Oncology, Medical Faculty, University of Ljubljana, Ljubljana, Yugoslavia. Search for other works by this author on: Oxford Academic PubMed Google Scholar E. J. Salber, E. J. Salber 8Department of Community Health Sciences, Duke University Medical Center, Durham, N.C. 27710. Search for other works by this author on: Oxford Academic PubMed Google Scholar D. Trichopoulos, D. Trichopoulos 9Department of Hygiene and Epidemiology, University of Athens, Athens, Greece. Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Yuasa S. Yuasa 10Department of Epidemiology, Institute of Public Health, Tokyo, Japan. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 65, Issue 4, October 1980, Pages 719–722, https://doi.org/10.1093/jnci/65.4.719 Published: 01 October 1980 Article history Received: 07 February 1980 Accepted: 14 April 1980 Published: 01 October 1980
ANTAGONIST: Mycobacterium avium subspecies paratuberculosis is a cause of Crohn's disease
Authors: P Quirke
Journal: Gut (2001)

The hypothesis that Mycobacterium paratuberculosis is the cause of Crohn's disease has been with us for over 80 years.1 Yet the hypothesis remains controversial and unproved.2-5 In spite of advances in molecular techniques such as polymerase chain reaction (PCR) which has shed light on the infectious basis of many other diseases (Whipple's disease, Helicobacter pylori , hepatitis C, etc.), the cause of Crohn's disease remains unknown.

The competing hypotheses are widely known:

(1)
:   Genetic predisposition.
(2)
:   Other infectious agents such as measles virus or an unknown agent.
(3)
:   Abnormal autoimmune reaction to antigen(s).
(4)
:   Environmental factors within the gut related either to dietary factors or the microbiological environment.



 There is little controversy over a genetic component to the disease but this hypothesis alone cannot explain the increasing incidence. It appears most likely that the cause of Crohn's disease is a combination of a genetic predisposition to the disease and one or more of the alternative hypotheses. For the infectious disease hypothesis to be proved for any organism, Koch's postulates need to be fulfilled. It is clear that to date these have yet to be met for M paratuberculosis . Van Kruiningen2 has extensively reviewed the data on culture of M paratuberculosis in Crohn's disease, experimental transmission of Crohn's disease, and inoculation with M paratuberculosis , and has found the evidence wanting. There is also no evidence of direct transmission from animal to humans, despite the frequent occurrence of M paratuberculosis (up to 54% in some cattle herds3) and Johne's disease in cattle, its detection in cows milk, and the presence of M paratuberculosis in a number of other animals. High risk groups susceptible to transmission of the disease would be families of cattle and sheep farmers, abattoir workers, veterinary surgeons, and possibly gastroenterologists. To date, there is no such evidence.

There are pathological similarities between Johne's disease and Crohn's disease but there are also many features that are not found. These are eloquently detailed by Van Kruiningen2 and will not be …
Granulocyte-macrophage colony-stimulating factor with induction treatment of acute myelogenous leukemia.
Authors: D R Adkins, R A Brown, J F DiPersio
Journal: Journal of Clinical Oncology (1997)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1997.15.2.862 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 9053516 Granulocyte-macrophage colony-stimulating factor with induction treatment of acute myelogenous leukemia. D R AdkinsxD R AdkinsSearch for articles by this author , R A BrownxR A BrownSearch for articles by this author , J F DiPersioxJ F DiPersioSearch for articles by this author https://doi.org/10.1200/JCO.1997.15.2.862 PDF "Granulocyte-macrophage colony-stimulating factor with induction treatment of acute myelogenous leukemia.." Journal of Clinical Oncology, 15(2), pp. 862–863© 1997 by American Society of Clinical Oncology
Cystic fibrosis registry: A preliminary report of CF patient from NRITLD
Authors: Soheila Khalilzadeh, Mohammad Reza Bloorsaz, Nooshin Baghaie, Elaheh Heydarian Fard, Maryam Hassanzad
Journal: European Respiratory Journal (2012)

Introduction:  Cystic fibrosis is an inherited chronic disease that affects the lungs and digestive system of about 70,000 children and adults in the worldwide.To Create more accurate picture of current state of Iranian CF patients, we started to collect and register the data of CF cases at pediatric Pulmonary ward of Masih Daneshvari Hospital.  Material and Method:  This cross-sectional study was performed on 66 CF patients aged 0-18 years (mean: 14.46 yrs) to describe the demographics, clinical features and outcome among patients hospitalized in Masih Daneshvari Hospital from (2000-2011). 56% of the patients, had Consanguinity marriage and 10.6% had family history of CF in one sibling .Regarding the age at the onset of symptoms, in 33.4% the symptoms was started at the newborn period but only in 9% diagnosis was made at this period. For all patients HRCT of the lung was performed and the dominant finding was Bronchiectasis in 92.70%. Bacteriological findings of cases detected P.A in 68.18% cases, Staph.a in 6.06% cases, AsP.F in 6.06% cases, Candida in 4.54% cases, B.Cepasia in 1.51%. According to the ABPA diagnostic criteria 4 patients diagnosed with ABPA. 17% of the patients are candidate for lung transplantation and 3 patients underwent lung transplantation. Out of 66 cases 19 cases expired due to respiratory failure.  Considering the result of our study and high rate of morbidity and mortality in our cases, we propose that CF registry and evaluation of the disease progression by means of a routine monitoring will increase the survival and improve quality of life of the patients.
Methotrexate Restores Regulatory T Cell Function Through Demethylation of the FoxP3 Upstream Enhancer in Patients With Rheumatoid Arthritis
Authors: Adam P. Cribbs, Alan Kennedy, Henry Penn, Parisa Amjadi, Patricia Green, Jordan E. Read, Fionula Brennan, Bernard Gregory, Richard O. Williams
Journal: Arthritis & Rheumatology (2015)

We have previously shown, in a cohort of untreated rheumatoid arthritis (RA) patients, that the suppressive function of Treg cells is defective. However, other studies in cohorts of patients with established RA have shown that Treg cell function is normal. We hypothesized that treatment may restore Treg cell function and lead to reduced disease activity. The aim of this study was to investigate whether treatment with methotrexate (MTX) can result in epigenetic changes that lead to restoration of the Treg cell suppressive function in RA.Peripheral blood samples from RA patients were assessed using (3) H-thymidine incorporation to measure Treg cell suppression of T cell proliferation, and by enzyme-linked immunosorbent assay to determine Treg cell suppression of interferon-γ production. CTLA-4 and FoxP3 expression was measured by flow cytometry and quantitative polymerase chain reaction (qPCR) in Treg cells from healthy individuals and RA patients. CD4+ T cells isolated from healthy individuals were cultured with interleukin-2 (IL-2), IL-6, and tumor necrosis factor α in the presence or absence of MTX, and FoxP3 expression was determined using qPCR and flow cytometry. Methylation of the FOXP3 upstream enhancer was analyzed by bisulfite sequencing PCR.Defective Treg cell function was observed only in RA patients who had not been treated with MTX, whereas Treg cells from MTX-exposed RA patients had restored suppressive function. This restored suppression was associated with increased expression of FoxP3 and CTLA-4 in Treg cells. Bisulfite sequencing PCR of Treg cells cultured in MTX revealed a significant reduction in methylation of the FOXP3 upstream enhancer.This study identifies a novel mechanism of action of MTX, in which treatment of RA patients with MTX restores defective Treg cell function through demethylation of the FOXP3 locus, leading to a subsequent increase in FoxP3 and CTLA-4 expression.
Oncostatin M in the anti-inflammatory response
Authors: A F Wahl, P M Wallace
Journal: Annals of the Rheumatic Diseases (2001)

Oncostatin M (OM) is a pleiotropic cytokine of the interleukin 6 family, whose in vivo properties and physiological function remain in dispute and poorly defined. These in vivo studies strongly suggest that OM is anabolic, promoting wound healing and bone formation, and anti-inflammatory. In models of inflammation OM is produced late in the cytokine response and protects from lipopolysaccharide (LPS)-induced toxicities, promoting the re-establishment of homoeostasis by cooperating with proinflammatory cytokines and acute phase molecules to alter and attenuate the inflammatory response. Administration of OM inhibited bacterial LPS-induced production of tumour necrosis factor α and septic lethality in a dose dependent manner. Consistent with these findings, in animal models of chronic inflammatory disease OM potently suppressed inflammation and tissue destruction in murine models of rheumatoid arthritis and multiple sclerosis. T cell function and antibody production were not impaired by OM treatment. Taken together, these data indicate that the activities of this cytokine in vivo are anti-inflammatory without concordant immunosuppression.
Risk factors for second acute myeloid leukemia/myelodysplastic syndrome among survivors of non-Hodgkin lymphoma
Authors: C J K Lam, R E Curtis, G M Dores, E A Engels, N E Caporaso, A Polliack, J L Warren, H A Young, P H Levine, A F Elmi, J F Fraumeni, M A Tucker, L M Morton
Journal: Leukemia (2015)
A Model for Brief Intervention with Couples Based on Projective Identification
Authors: STANLEY I. GREENSPAN, FORTUNE V. MANNINO
Journal: American Journal of Psychiatry (1974)

Projective identification is a mechanism that has been described by many observers from different perspectives in a variety of settings. It has been most frequently associated with rather disturbed families as an interpersonal mechanism involved in distorted perceptions, identifications, and communication. The authors illustrate how this mechanism manifests itself in couples with relatively intact, although neurotic, personality organizations and how it interferes with their capacity to resolve problems and experience joint interpersonal growth. They suggest that a short-term treatment approach with such couples may usefully organize itself around the identification and correction of the perceptual distortions involved in projective identification.
Chromosome Aberrations and Sister Chromatid Exchanges in Chinese Hamster Cells Exposed to Various Chemicals 2
Authors: Syuiti Abe, Motomichi Sasaki
Journal: JNCI Journal of the National Cancer Institute (1977)

To evaluate its usefulness for detection of mutagenicity and oncogenicity of chemicals, the frequency of chromosome aberrations and sister chromatid exchanges (SCE) was examined in cultured Chinese hamster cells exposed to 33 kinds of chemical agents, including 2 aromatic hydrocarbons, 7 amine derivatives, 3 phenols, 6 carboxylic acid derivatives, 4 azo compounds, 7 heterocyclic compounds, and 4 other types of agents. Among them, 7 chemicals, including 5 known oncogens (N-n-butyl-N-nitrosourethan, N-methyl-N-nitrosourea, beta-propiolacton, methylazoxymethanol acetate, and propane sultone) and 2 non-oncogens (potassium sorbate and sodium benzoate) were inducers of aberrations and/or SCE, although the effective doses for the last two agents were considerably higher. The mutagenic activities estimated by chromosome aberrations were not necessarily the same for a given chemical when estimated by SCE. Slightly to moderately increased rates of SCE or aberrations were noticed among the other 26 chemicals. However, these values were usually without a clear dose relationship.