tbuckley/cabot-search huggingface dataset:
Asbestos and man‐made vitreous fibres may not currently contribute to the burden of lung cancer
Authors: S Mandal
Journal: Thorax (2007)

▴ Carel R, Olsson AC, Zaridze D, et al . Occupational exposure to asbestos and man-made vitreous fibre and risk of lung cancer: a multicentre case-control study in Europe. Occup Environ Med2007;64:502–08.

[OpenUrl][1][Abstract/FREE Full Text][2]



Asbestos is an environmental carcinogen and exposure has been linked with the development of lung cancer. The use of asbestos has been partially replaced by man-made vitreous fibres (MMVF). The aim of this case–control study was to quantify the contribution of asbestos and MMVF to the burden …

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Lung cancer risk and solid fuel smoke exposure: a systematic review and meta-analysis
Authors: Om Prakash Kurmi, Pallavi Huma Arya, Kin-Bong Hubert Lam, Tom Sorahan, Jon G. Ayres
Journal: European Respiratory Journal (2012)

The aim of this systematic review was to quantify the impact of biomass fuel and coal use on lung cancer and to explore reasons for heterogeneity in the reported effect sizes. A systematic review of primary studies reporting the relationship between solid fuel use and lung cancer was carried out, based on pre-defined criteria. Studies that dealt with confounding factors were used in the meta-analysis. Fuel types, smoking, country, cancer cell type and sex were considered in sub-group analyses. Publication bias and heterogeneity were estimated. The pooled effect estimate for coal smoke as a lung carcinogen (OR 1.82, 95% CI 1.60–2.06) was greater than that from biomass smoke (OR 1.50, 95% CI 1.17–1.94). The risk of lung cancer from solid fuel use was greater in females (OR 1.81, 95% CI 1.54–2.12) compared to males (OR 1.16, 95% CI 0.79–1.69). The pooled effect estimates were 2.33 (95% CI 1.72–3.17) for adenocarcinoma, 3.58 (1.58–8.12) for squamous cell carcinoma and 1.57 (1.38–1.80) for tumours of unspecified cell type. These findings suggest that in-home burning of both coal and biomass is consistently associated with an increased risk of lung cancer.
Exanthematic pityriasis rubra pilaris
Authors: None Varma, None Logan
Journal: British Journal of Dermatology (1999)

Journal Article Exanthematic pityriasis rubra pilaris Get access S. Varma, S. Varma Department of Dermatology, University Hospital of Wales, Heath Park, Cardiff CF4 4XW, U.K. Search for other works by this author on: Oxford Academic Google Scholar R.A. Logan R.A. Logan Department of Dermatology, Princess of Wales Hospital, Bridgend CF31 1RQ, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 141, Issue 4, 1 October 1999, Pages 769–771, https://doi.org/10.1046/j.1365-2133.1999.03143.x Published: 01 October 1999
Neutrophils Promote Liver Metastasis via Mac-1–Mediated Interactions with Circulating Tumor Cells
Authors: Jonathan D. Spicer, Braedon McDonald, Jonathan J. Cools-Lartigue, Simon C. Chow, Betty Giannias, Paul Kubes, Lorenzo E. Ferri
Journal: Cancer Research (2012)

Although circulating neutrophils are associated with distant metastasis and poor outcome in a number of epithelial malignancies, it remains unclear whether neutrophils play an active causal role in the metastatic cascade. Using in vivo models of metastasis, we found that neutrophils promote cancer cell adhesion within liver sinusoids and, thereby, influence metastasis. Neutrophil depletion before cancer cell inoculation resulted in a decreased number of gross metastases in an intrasplenic model of liver metastasis. This effect was reversed when inflamed neutrophils were co-inoculated with cancer cells. In addition, early adhesion within liver sinusoids was inhibited in the absence of neutrophils and partially restored with a short perfusion of isolated activated neutrophils. Intravital microscopy showed that cancer cells adhered directly on top of arrested neutrophils, indicating that neutrophils may act as a bridge to facilitate interactions between cancer cells and the liver parenchyma. The adhesion of lipopolysaccharide-activated neutrophils to cancer cells was mediated by neutrophil Mac-1/ICAM-1. Our findings, therefore, show a novel role for neutrophils in the early adhesive steps of liver metastasis.
OUTBREAK OF PARALYTIC POLIOMYELITIS IN FINLAND: WIDESPREAD CIRCULATION OF ANTIGENICALLY ALTERED POLIOVIRUS TYPE 3 IN A VACCINATED POPULATION
Authors: T. Hovi, A. Huovilainen, T. Kuronen, T. Pöyry, N. Salama, K. Cantell, E. Kinnunen, K. Lapinleimu, M. Roivainen, M. Stenvik, A. Silander, C.-J. Thoden, S. Salminen, P. Weckström
Journal: The Lancet (1986)
Absence of bacterial colonization of the airways after therapeutic rigid bronchoscopy without stenting
Authors: M Noppen, D. Pierard, M Meysman, R.v Herreweghe, W Vincken
Journal: European Respiratory Journal (2000)

Following airway stenting, bacterial colonization of the airways with potentially pathogenic micro-organisms occurs within 4 weeks after treatment in the majority of patients. The objective of this study was to prospectively investigate whether nonstenting therapeutic rigid bronchoscopy (using laser, cryotherapy, mechanical dilatation or debridement) is followed by airway colonization or infection. Protected specimen brush sampling of the central airways and quantitative culture were performed immediately prior to, and 4 weeks after nonstenting therapeutic rigid bronchoscopy in 20 consecutive patients with central airway lesions. Prior to therapeutic bronchoscopy, airway colonization/infection was present in nine of 20 (45%) patients. In these nine patients, 10 different potential pathogens were identified: Streptococcus pneumoniae (four cases), Pseudomonas aeruginosa (three), Haemophilus influenzae (two), and Serratia marcescens (one). Eight of these nine patients had a history of postobstructive infections, of which three were currently being treated with antibiotics. Four weeks following therapeutic bronchoscopy, airway colonization/infection was present in five of 20 (25%) patients, each of whom had airway colonization/infection prior to bronchoscopy. In three of these five patients, the same organisms were found 4 weeks after bronchoscopy as at baseline bronchoscopy. In two of five patients new organisms were identified: one case of Streptococcus viridans and one case of Haemophilus parainfluenzae, both considered to be nonpathogens. In four of nine patients with airway colonization/infection prior to bronchoscopy, the airways were clear of micro-organisms after the procedure. The authors conclude that: 1) nonstenting therapeutic rigid bronchoscopy is not complicated by airway colonization or infection by new potential pathogens; and 2) therapeutic rigid bronchoscopy led to clearing of airway colonization/infection in almost half of the patients studied.
Dual Mechanisms for Lysophosphatidic Acid Stimulation of Human Ovarian Carcinoma Cells
Authors: Y.-L. Hu, C. Albanese, R. G. Pestell, R. B. Jaffe
Journal: JNCI Journal of the National Cancer Institute (2003)

Lysophosphatidic acid (LPA), at concentrations present in ascitic fluid, indirectly stimulates the growth of malignant ovarian tumors by increasing the expression of vascular endothelial growth factor (VEGF) in ovarian cancer cells. We investigated whether LPA could also directly promote ovarian tumor growth by increasing the level of cyclin D1, a key G1-phase checkpoint regulator, which thereby increases cell proliferation.Expression of cyclin D1 and LPA receptors (EDG4 and EDG7) was determined in six ovarian cancer cell lines (including OVCAR-3 cells) and immortalized ovarian surface epithelial cells (IOSE-29). Cyclin D1 promoter activity was measured in LPA-treated OVCAR-3 cells cotransfected with cyclin D1 promoter-driven luciferase constructs and cDNA expression plasmids for IkappaBalphaM (a nuclear factor kappaB [NFkappaB] super-repressor).Four of six cancer cell lines, including OVCAR-3, overexpressed cyclin D1 protein relative to levels in IOSE-29 cells. LPA treatment increased cyclin D1 protein in a dose- and time-dependent manner in OVCAR-3 cells but not in IOSE-29 cells. LPA stimulated cyclin D1 promoter activity (3.0-fold, 95% confidence interval [CI] = 2.7-fold to 3.3-fold). Mutation of the NFkappaB-binding site in the cyclin D1 promoter to block NFkappaB binding and expression of IkappaBalphaM, which binds NFkappaB and inhibits its binding to the promoter, markedly diminished LPA stimulation of cyclin D1 promoter activity (activity stimulated only 1.4-fold, 95% CI = 1.1-fold to 1.7-fold, and 0.7-fold, 95% CI = 0.6-fold to 0.8-fold, respectively). EDG4 was overexpressed in all cancer cell lines studied relative to that in IOSE-29 cells, but EDG7 was overexpressed in only two lines.Dual mechanisms are probably involved in LPA stimulation of ovarian tumor growth in vivo. In addition to the previously characterized indirect mechanism that increases angiogenesis via VEGF, LPA may directly increase the level of cyclin D1 in ovarian cancer cells, increasing their proliferation.
Deficient HBD-3 in the Skin of Atopic Dermatitis (AD) Patients Increases Susceptibility to Recurrent Viral Skin Infections
Authors: M.D. Howell, J.E. Streib, N. Novak, T. Bieber, M. Boguniewicz, S. Pastore, G. Girolomoni, D.Y.M. Leung
Journal: Journal of Allergy and Clinical Immunology (2006)
Prevention of Iatrogenic Atrial Tachycardia After Ablation of Atrial Fibrillation
Authors: Carlo Pappone, Francesco Manguso, Gabriele Vicedomini, Filippo Gugliotta, Ornella Santinelli, Amedeo Ferro, Simone Gulletta, Simone Sala, Nicoleta Sora, Gabriele Paglino, Giuseppe Augello, Eustachio Agricola, Alberto Zangrillo, Ottavio Alfieri, Vincenzo Santinelli
Journal: Circulation (2004)

Circumferential pulmonary vein ablation (CPVA) is effective in curing atrial fibrillation (AF), but new-onset left atrial tachycardia (AT) is a potential complication. We evaluated whether a modified CPVA approach including additional ablation lines on posterior wall and the mitral isthmus would reduce the incidence of AT after PV ablation.A total of 560 patients (291 men, 52%; age, 56.5+/-7.3 years) entered the study; 280 were randomized to CPVA alone (group 1) and 280 to modified CPVA (group 2). The primary end point was freedom from AT after the procedure. In group 1, 28 patients (10%) experienced new-onset AT, and 41 (14.3%) experienced recurrent AF. In group 2, 11 patients (3.9%) experienced AT, and 36 (12.9%) had recurrent AF. Group 1 was more likely to experience AT than group 2 (P=0.005). Freedom from AF after ablation was similar in both groups (P=0.57). Among those in group 1, gap-related macroreentrant AT was documented in 23 of the 28 patients (82%), and focal AT was found in 5 (18%). In group 2, gap-related macroreentrant AT was found in 8 of the 11 patients (73%), and focal AT was seen in 3 (27%). Two patients in group 1 and 1 patient in group 2 had both AT and AF. The strongest predictor of AT was the presence of gaps (P<0.001).Modified CPVA is as effective as CPVA in preventing AF but is associated with a lower risk of developing incessant AT.
CROSS-IDIOTYPIC SPECIFICITY AMONG MONOCLONAL I<scp>G</scp>M PROTEINS WITH ANTI-γ-GLOBULIN ACTIVITY
Authors: H. G. Kunkel, V. Agnello, F. G. Joslin, R. J. Winchester, J. D. Capra
Journal: The Journal of Experimental Medicine (1973)

Through the use of absorbed idiotypic antisera prepared against single isolated monoclonal IgM anti-γ-globulins, partial cross-idiotypic specificity was demonstrated with other IgM anti-γ-globulins. Such antisera classified these proteins into at least three groups. The major group which included 60% of the anti-γ-globulins was particularly homogeneous. The anti-γ-globulin specific antigens were detected best in hemagglutination and hemagglutination inhibition systems. They were not found in monoclonal IgM proteins that lacked anti-γ-globulin activity although related antigens were detected at low concentrations in pooled immunoglobulin preparations as well as in heterogeneous anti-Rh antibodies. Several lines of evidence were obtained indicating that the antibody combining site was involved in the specific determinants. Attempts were made to analyze the fine specificity of each anti-γ-globulin for the Fc fragment of different subclasses of human immunoglobulins as well as those of other species. Differences were observed but these were not readily related to the cross-specificity antigens. The anti-γ-globulin specific antigens were very analogous to those previously described for monoclonal IgM cold agglutinins. Although each protein could be distinguished from all the others on the basis of individual idiotypic antigens, the antigens common to the specific groups of proteins with each of these activities were prominent and readily detected with multiple antisera. The results indicate basic similarities between proteins of a given activity even in unrelated individuals.
Prevention of sudden cardiac death: return to sport considerations in athletes with identified cardiovascular abnormalities
Authors: M S Link
Journal: British Journal of Sports Medicine (2009)

Sudden cardiac death in the athlete is uncommon but extremely visible. In athletes under age 30, genetic heart disease, including hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and ion channel disorders account for the majority of the deaths. Commotio cordis, involving blunt trauma to the chest leading to ventricular fibrillation, is also a leading cause of sudden cardiac death in young athletes. As the athlete ages, coronary atherosclerosis contributes to an increasing incidence of sudden death during sporting activities. For athletes with aborted sudden death or arrhythmia-related syncope, an implantable cardioverter defibrillator is generally indicated, and they should be restricted from most competitive sports. Participation in competitive athletics for athletes with heart disease should generally follow the recently published 36th Bethesda Conference Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities.
Psychological profiles of patients with upper gastrointestinal symptomatology induced by non-steroidal anti-inflammatory drugs.
Authors: A Juby, P Davis
Journal: Annals of the Rheumatic Diseases (1991)

Eighty three patients with classical or definite rheumatoid arthritis taking non-steroidal anti-inflammatory drugs (NSAIDs) were studied in an attempt to determine whether a patient9s personality and psychological profile might contribute to the development of NSAID induced gastrointestinal symptomatology. It was found that the personality profile of the group of 45 asymptomatic patients was similar to that of a previously reported control group. In contrast, the 37 patients with gastrointestinal symptoms attributed to NSAIDs had a significantly higher mean score for free floating anxiety, depression, and somatisation than controls, suggesting that a patient9s personality may influence the development of NSAID induced gastric symptoms.
Prediagnostic Circulating Sex Hormones Are Not Associated with Mortality for Men with Prostate Cancer
Authors: Boris Gershman, Irene M. Shui, Meir Stampfer, Elizabeth A. Platz, Peter H. Gann, Howard L. Sesso, Natalie DuPre, Edward Giovannucci, Lorelei A. Mucci
Journal: European Urology (2013)
Major histocompatibility complex class I related molecules control the development of CD4+8- and CD4-8- subsets of natural killer 1.1+ T cell receptor-alpha/beta+ cells in the liver of mice.
Authors: T Ohteki, H R MacDonald
Journal: The Journal of Experimental Medicine (1994)

Normal mouse liver contains prominent subsets of CD4+8- and CD4-8- T cell receptor (TCR)-alpha/beta+ cells with intermediate TCR levels. We show here that these cells express the natural killer (NK)1.1 surface antigen and have a restricted TCRV beta repertoire that is highly skewed to V beta 7 and V beta 8. Surprisingly, both CD4+8- and CD4-8- subsets of NK1.1+TCR-alpha/beta+ cells are absent in the liver of beta 2-microglobulin deficient mice, which do not express major histocompatibility complex (MHC) class I or "class I-like" molecules. Analysis of reciprocal radiation bone marrow chimeras established with beta 2-microglobulin deficient and wild-type mice demonstrates that MHC class I expression on radiosensitive (presumably hematopoietic) cells is required for the development of NK1.1+TCR-alpha/beta+ cells in the liver. In the liver of MHC class II deficient mice, the CD4+8- and CD4-8- subsets of NK1.1+TCR-alpha/beta+ cells develop normally. Collectively our data suggest that NK1.1+TCR-alpha/beta+ cells in liver require interaction with a MHC class I-related ligand on hematopoietic cells for their development. This unusual property of liver T cells is shared by a subset of CD4-8-NK1.1+TCR-alpha/beta+ thymocytes, suggesting a common lineage independent of the mainstream of T cell development.
RNA-MEDIATED NEUROMUSCULAR DISORDERS
Authors: Laura P.W. Ranum, Thomas A. Cooper
Journal: Annual Review of Neuroscience (2006)

Myotonic dystrophy type 1 (DM1) is caused by a CTG expansion mutation located in the 3' untranslated portion of the dystrophica myotonin protein kinase gene. The identification and characterization of RNA-binding proteins that interact with expanded CUG repeats and the discovery that a similar transcribed but untranslated CCTG expansion in an intron causes myotonic dystrophy type 2 (DM2) have uncovered a new type of mechanism in which microsatellite expansion mutations cause disease through an RNA gain-of-function mechanism. This review discusses RNA pathogenesis in DM1 and DM2 and evidence that similar mechanisms may play a role in a growing number of dominant noncoding expansion disorders, including fragile X tremor ataxia syndrome (FXTAS), spinocerebellar ataxia type 8 (SCA8), SCA10, SCA12, and Huntington's disease-like 2 (HDL2).
Microalbuminuria as a Risk Predictor in Diabetes: The Continuing Saga
Authors: George L. Bakris, Mark Molitch
Journal: Diabetes Care (2014)

OBJECTIVE The rationale for this study was to review the data on microalbuminuria (MA), an amount of albumin in the urine of 30–299 mg/day, in patients with diabetes in the context of cardiovascular risk and development of kidney disease. The objective was to review the pathophysiology of MA in patients with diabetes and review the data from trials regarding MA in the context of risk for cardiovascular events or kidney disease progression. RESEARCH DESIGN AND METHODS Data sources were all PubMed-referenced articles in English-language peer-reviewed journals since 1964. Studies selected had to have a minimum 1-year follow-up and be either a randomized trial linking MA to cardiovascular or kidney disease outcome, a meta-analysis/systematic review, or a large observational cohort study. RESULTS The data suggest that MA is a risk marker for cardiovascular events and possibly for kidney disease development. Its presence alone, however, does not indicate established kidney disease, especially if the estimated glomerular filtration rate is &amp;gt;60 mL/min/1.73 m2. An increase in MA, when blood pressure and other risk factors are controlled, portends a poor prognosis for kidney outcomes over time. Early in the course of diabetes, aggressive risk factor management focused on glycemic and blood pressure goals is important to delay kidney disease development and reduce cardiovascular risk. CONCLUSIONS MA is a marker of cardiovascular disease risk and should be monitored per guidelines once or twice a year for progression to macroalbuminuria and kidney disease development, especially if plasma glucose, lipids, and blood pressure are at guideline goals.
Correlates of 1-Year Prospective Outcome in Bipolar Disorder: Results From the Stanley Foundation Bipolar Network
Authors: Willem A. Nolen, David A. Luckenbaugh, Lori L. Altshuler, Trisha Suppes, Susan L. McElroy, Mark A. Frye, Ralph W. Kupka, Paul E. Keck, Gabriele S. Leverich, Robert M. Post
Journal: American Journal of Psychiatry (2004)

The purpose of the study was to examine potential correlates of outcome in patients treated for bipolar disorder.During a 1-year period, 258 patients with DSM-IV bipolar disorder or schizoaffective disorder were rated with the prospective NIMH-Life Chart Method, which characterizes each day in terms of the severity of manic and depressive symptoms on the basis of patients' mood-related impairment in their usual educational, social, or occupational roles. Mean ratings for the severity of mania, depression, and overall bipolar illness and the number of manic, depressive, and overall illness episodes were calculated. Potential risk factors were assessed at the start of the study, and multivariate linear regression analysis was used to determine the correlates of the six 1-year outcome measures.Three of the six outcome measures were largely independent of each other and were used in the analysis. The mean rating for severity of mania was associated with comorbid substance abuse, history of more than 10 prior manic episodes, and poor occupational functioning at study entry. The mean rating for severity of depression was associated with a history of more than 10 prior depressive episodes and poor occupational functioning at study entry. The total number of overall illness episodes was associated with a positive family history of drug abuse, a history of prior rapid cycling, and poor occupational functioning. In addition, the mean rating for severity of mania and the total number of overall illness episodes were both initially associated with a history of childhood abuse, but these relationships were lost with the addition of other illness variables to the analysis.Clinicians who treat patients with bipolar disorder should consider a family history of drug abuse, a history of childhood abuse, prior course of illness, comorbid substance abuse, and occupational functioning in determining prognosis and setting goals for further treatment.