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17beta-hydroxysteroid dehydrogenase type 1 is an independent prognostic marker in breast cancer.

https://arctichealth.org/en/permalink/ahliterature17431
Source
Cancer Res. 2004 Oct 15;64(20):7604-9
Publication Type
Article
Date
Oct-15-2004
Author
Olayiwola O Oduwole
Yan Li
Veli V Isomaa
Anne Mäntyniemi
Anitta E Pulkka
Ylermi Soini
Pirkko T Vihko
Author Affiliation
Biocenter Oulu and Research Center for Molecular Endocrinology, WHO Collaborating Centre for Research on Reproductive Health, Oulu, Finland.
Source
Cancer Res. 2004 Oct 15;64(20):7604-9
Date
Oct-15-2004
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - biosynthesis - genetics
Breast Neoplasms - enzymology - genetics - metabolism - pathology
Estrogen Receptor alpha - biosynthesis - genetics
Estrogen Receptor beta - biosynthesis - genetics
Female
Humans
Immunohistochemistry
In Situ Hybridization
Isoenzymes
Ki-67 Antigen - biosynthesis - genetics
Middle Aged
Neoplasm Staging
Paraffin Embedding
Prognosis
RNA, Messenger - biosynthesis - genetics
Receptor, erbB-2 - biosynthesis - genetics
Research Support, Non-U.S. Gov't
Tumor Markers, Biological - biosynthesis - genetics
Abstract
Estrogens have an important role in the development and progression of breast cancer. 17beta-Hydroxysteroid dehydrogenase type 1 (17HSD1), type 2 (17HSD2), and type 5 (17HSD5) are associated with sex steroid metabolism in normal and cancerous breast tissue. The mRNA expressions of the 17HSD1, 17HSD2, and 17HSD5 enzymes were analyzed in 794 breast carcinoma specimens by using tissue microarrays and normal histologic sections. The results were correlated with the estrogen receptor alpha (ER-alpha) and beta (ER-beta), progesterone receptor, Ki67, and c-erbB-2 expressions analyzed by immunohistochemical techniques and with the Tumor-Node-Metastasis classification, tumor grade, disease-free interval, and survival of the patients. Signals for 17HSD1 mRNA were detected in 16%, 17HSD2 in 25%, and 17HSD5 in 65% of the breast cancer specimens. No association between the 17HSD1, 17HSD2, and 17HSD5 expressions was detected. A significant association was observed between ER-alpha and ER-beta (P = 0.02; odds ratio, 1.96) expressions. There was also a significant inverse association between ER-alpha and 17HSD1 (P = 0.04; odds ratio, 0.53), as well as ER-alpha and 17HSD5 (P = 0.001; odds ratio, 0.35). Patients with tumors expressing 17HSD1 mRNA or protein had significantly shorter overall and disease-free survival than the other patients (P = 0.0010 and 0.0134, log rank). The expression of 17HSD5 was significantly higher in breast tumor specimens than in normal tissue (P = 0.033; odds ratio, 5.56). The group with 17HSD5 overexpression had a worse prognosis than the other patients (P = 0.0146). ER-alpha also associated with survival (P = 0.045). Cox multivariate analyses showed that 17HSD1 mRNA, tumor size, and ER-alpha had independent prognostic significance.
PubMed ID
15492288 View in PubMed
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17Beta-hydroxysteroid dehydrogenase type 2: independent prognostic significance and evidence of estrogen protection in female patients with colon cancer.

https://arctichealth.org/en/permalink/ahliterature18039
Source
J Steroid Biochem Mol Biol. 2003 Nov;87(2-3):133-40
Publication Type
Article
Date
Nov-2003
Author
Olayiwola O Oduwole
Markus J Mäkinen
Veli V Isomaa
Anitta Pulkka
Petra Jernvall
Tuomo J Karttunen
Pirkko T Vihko
Author Affiliation
Biocenter Oulu, Research Center for Molecular Endocrinology, WHO Collaborating Centre for Research on Reproductive Health, P.O. Box 5000, University of Oulu, FIN-90014 Oulu, Finland.
Source
J Steroid Biochem Mol Biol. 2003 Nov;87(2-3):133-40
Date
Nov-2003
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - genetics - metabolism
Adult
Aged
Aged, 80 and over
Colonic Neoplasms - enzymology - genetics - pathology
Comparative Study
Estrogens - metabolism
Female
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Humans
Isoenzymes - metabolism
Male
Middle Aged
Neoplasm Staging
Prognosis
Proportional Hazards Models
RNA, Messenger - biosynthesis - genetics
Research Support, Non-U.S. Gov't
Sex Factors
Survival Rate
Abstract
The mRNA expression of 17beta-hydroxysteroid dehydrogenase (17HSD) types 1 and 2 enzymes catalyzing opposite reaction of estrogen metabolism was investigated in colon cancer. Further, the significance of the 17HSD type 2 enzyme as a possible marker of colorectal cancer (CRC) prognosis was studied. In the normal mucosa, 17HSD type 2 mRNA was predominantly expressed in the surface epithelium and in the upper parts of the crypts. In the lamina propria expression was seen in endothelial cells and mononuclear phagocytes. In colorectal tumors, 17HSD type 2 expression was in most cases downregulated. Female patients had significantly more cancers with high 17HSD type 2 mRNA expression (n=11/35; 31%) than male patients (n=3/39; 8%) (P=0.02). We observed a significant impact of 17HSD type 2 mRNA expression on survival in female patients with distal colorectal cancer (n=24), with an overall cumulative 5-year survival rate of 54% in those with low 17HSD type 2 mRNA expression. None of the female patients with high 17HSD type 2 mRNA expression survived (n=11; P=0.0068; log rank 7.32). In male patients, no significant association with survival was observed. Our data provide evidence suggesting that low 17HSD type 2 mRNA expression is an independent marker of favorable prognosis in females with distal colorectal cancer, supporting the presence of gender- and location-related differences in the pathogenesis of colon cancer.
PubMed ID
14672733 View in PubMed
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Abnormal adherence junctions in the heart and reduced angiogenesis in transgenic mice overexpressing mutant type XIII collagen.

https://arctichealth.org/en/permalink/ahliterature53860
Source
EMBO J. 2001 Sep 17;20(18):5153-64
Publication Type
Article
Date
Sep-17-2001
Author
M. Sund
R. Ylönen
A. Tuomisto
R. Sormunen
J. Tahkola
A P Kvist
S. Kontusaari
H. Autio-Harmainen
T. Pihlajaniemi
Author Affiliation
Collagen Research Unit, Biocenter Oulu, Department of Medical Biochemistry, University of Oulu, PL 5000, 90014 Oulu, Finland.
Source
EMBO J. 2001 Sep 17;20(18):5153-64
Date
Sep-17-2001
Language
English
Publication Type
Article
Keywords
Adherens Junctions - ultrastructure
Animals
Collagen - genetics - metabolism - physiology
Embryonic and Fetal Development
Fetus - abnormalities - blood supply
Heart - embryology
Heart Defects, Congenital - pathology
Mice
Mice, Transgenic
Mutation
Myocardium - ultrastructure
Neovascularization, Physiologic
Phenotype
Placenta - abnormalities - blood supply
RNA, Messenger - biosynthesis
Research Support, Non-U.S. Gov't
Survival Analysis
Abstract
Type XIII collagen is a type II transmembrane protein found at sites of cell adhesion. Transgenic mouse lines were generated by microinjection of a DNA construct directing the synthesis of truncated alpha1(XIII) chains. Shortened alpha 1(XIII) chains were synthesized by fibroblasts from mutant mice, and the lack of intracellular accumulation in immunofluorescent staining of tissues suggested that the mutant molecules were expressed on the cell surface. Transgene expression led to fetal lethality in offspring from heterozygous mating with two distinct phenotypes. The early phenotype fetuses were aborted by day 10.5 of development due to a lack of fusion of the chorionic and allantoic membranes. The late phenotype fetuses were aborted by day 13.5 of development and displayed a weak heartbeat, defects of the adherence junctions in the heart with detachment of myofilaments and abnormal staining for the adherence junction component cadherin. Decreased microvessel formation was observed in certain regions of the fetus and the placenta. These results indicate that type XIII collagen has an important role in certain adhesive interactions that are necessary for normal development.
PubMed ID
11566879 View in PubMed
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Abnormal regulation of the LDL-R and HMG CoA reductase genes in subjects with familial hypercholesterolemia with the "French Canadian mutation".

https://arctichealth.org/en/permalink/ahliterature211598
Source
Atherosclerosis. 1996 Jul;124(1):103-17
Publication Type
Article
Date
Jul-1996
Author
L. Yu
S. Qiu
J. Genest
Author Affiliation
Cardiovascular Genetics Laboratory, Clinical Research Institute of Montréal, Québec Canada.
Source
Atherosclerosis. 1996 Jul;124(1):103-17
Date
Jul-1996
Language
English
Publication Type
Article
Keywords
Anticholesteremic Agents - pharmacology - therapeutic use
Canada - epidemiology
Cells, Cultured
Enzyme Induction
Enzyme Inhibitors - pharmacology - therapeutic use
Ethnic Groups - genetics
Female
Fibroblasts - metabolism
France - ethnology
Gene Expression Regulation - drug effects
Haploidy
Humans
Hydroxymethylglutaryl CoA Reductases - genetics
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Hyperlipoproteinemia Type II - drug therapy - ethnology - genetics
Lipoproteins, LDL - metabolism
Lovastatin - pharmacology - therapeutic use
Male
Prevalence
RNA, Messenger - biosynthesis - genetics
Receptors, LDL - genetics - metabolism
Sequence Deletion
Transcription, Genetic
Treatment Failure
Abstract
Familial hypercholesterolemia (FH) is seen with high frequency in the province of Québec, Canada. A large deletion (> 10 kb) of the 5'-end of the low density lipoprotein receptor (LDL-R) gene is the major mutation of the LDL-R in FH subjects in Québec (approximately 60% of FH subjects). No mRNA is produced from the allele bearing the mutation, and cellular cholesterol obtained by receptor-mediated endocytosis is under the control of the non-deletion allele. We have previously reported that some patients with the 10-kb deletion (approximately 9%) fail to respond to the hydroxymethylglutaryl coenzyme A reductase (HMG CoA reductase) inhibitor class of medications. We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. We determined mRNA levels by RNase protection assay in skin fibroblasts obtained from controls (n = 3) and FH subjects with the > 10-kb deletion (responders, n = 3; non responders, n = 3; to drug therapy). We measured 125I-LDL binding on skin fibroblasts grown in the presence of lipoprotein-deficient serum with or without 1 microM lovastatin, using 10 micrograms/mL of 125I-LDL protein. Control subjects exhibited coordinate regulation of the LDL-R and HMG CoA reductase genes in response to lovastatin, 0.1-25 microM, for 0-24 h. Correlation coefficients between mRNA levels of both genes were > 0.9 in controls and FH subjects. However, by linear regression analysis, the corresponding slopes for the correlation between both genes were 0.98 (controls), 3.36 and 3.63 (FH responders and non-responders), indicating a pattern of dissociated but still coordinate regulation in FH subjects. The magnitude of increase of mRNA levels of the LDL-R gene was approximately five-fold over LPDS in controls, two-fold in FH responders and two-fold in non-responders. Binding studies using 125I-LDL reveal that a control subject and all responders had a 2-2.5-fold increase in binding to cell surface receptors but two out of three FH non-responders showed no increase in binding in response to 1 microM lovastatin. The LDL-R and HMG CoA reductase genes are expressed in coordinate regulation in fibroblasts from subjects with FH due to the > 10-kb deletion, but with a proportionately greater up-regulation of the HMG CoA reductase gene. Some subjects, with FH caused by the > 10-kb deletion of the LDL-R gene, who fail to respond to HMG CoA reductase inhibitors have abnormal LDL receptor binding activity at the cell surface in response to lovastatin in vitro.
PubMed ID
8800498 View in PubMed
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Adrenomedullin gene expression in the rat heart is stimulated by acute pressure overload: blunted effect in experimental hypertension.

https://arctichealth.org/en/permalink/ahliterature54511
Source
Endocrinology. 1997 Jun;138(6):2636-9
Publication Type
Article
Date
Jun-1997
Author
H. Romppanen
M. Marttila
J. Magga
O. Vuolteenaho
P. Kinnunen
I. Szokodi
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Endocrinology. 1997 Jun;138(6):2636-9
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Animals
Argipressin - pharmacology
Atrial Natriuretic Factor - biosynthesis
Blood Pressure - drug effects
Heart - physiology - physiopathology
Heart Failure, Congestive - metabolism
Heart Ventricles
Humans
Hypertension - metabolism - physiopathology
Male
Myocardium - metabolism
Natriuretic Peptide, Brain
Peptide Biosynthesis
Peptides
RNA, Messenger - biosynthesis
Rats
Rats, Inbred Strains
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Time Factors
Transcription, Genetic - drug effects
Abstract
The levels of adrenomedullin (ADM), a newly discovered vasodilating and natriuretic peptide, are elevated in plasma and ventricular myocardium in human congestive heart failure suggesting that cardiac synthesis may contribute to the plasma concentrations of ADM. To examine the time course of induction and mechanisms regulating cardiac ADM gene expression, we determined the effect of acute and short-term cardiac overload on ventricular ADM mRNA and immunoreactive ADM (ir-ADM) levels in conscious rats. Acute pressure overload was produced by infusion of arginine8-vasopressin (AVP, 0.05 microg/kg/min, i.v.) for 2 h into 12-week-old hypertensive TGR(mREN-2)27 rats and normotensive Sprague-Dawley (SD) rats. Hypertension and marked left ventricular hypertrophy were associated with 2.2-times higher ir-ADM levels in the left ventricular epicardial layer (178 +/- 36 vs. 81 +/- 23 fmol/g, P
PubMed ID
9165059 View in PubMed
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Alveolar macrophages of allergic resistant and susceptible strains of rats show distinct cytokine profiles.

https://arctichealth.org/en/permalink/ahliterature15450
Source
Clin Exp Immunol. 2001 Oct;126(1):9-15
Publication Type
Article
Date
Oct-2001
Author
J. Sirois
E Y Bissonnette
Author Affiliation
Département de médecine, Centre de recherche, Hôpital Laval, Institut universitaire de cardiologie et de pneumologie de l'Université Laval, Sainte-Foy, Canada.
Source
Clin Exp Immunol. 2001 Oct;126(1):9-15
Date
Oct-2001
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Animals
Asthma - immunology
Bronchoalveolar Lavage Fluid - immunology
Cells, Cultured
Comparative Study
Cytokines - biosynthesis - genetics
Hypersensitivity, Immediate - immunology
Interleukins - biosynthesis - genetics
Macrophage Inflammatory Protein-1 - biosynthesis - genetics
Macrophages, Alveolar - immunology
Nitric Oxide - biosynthesis
Ovalbumin - administration & dosage - immunology
RNA, Messenger - biosynthesis
Rats
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Th1 Cells - immunology
Th2 Cells - immunology
Tumor Necrosis Factor-alpha - biosynthesis - genetics
Abstract
Brown Norway rats are widely used as a model of asthma, whereas Sprague Dawley rats do not develop allergic reactions under the same conditions. Given the importance of alveolar macrophages (AM) in down-regulating cellular immune responses in the lung, we postulated that the different susceptibilities in the development of airway allergic reactions in these rat strains may be related to functional differences in their AM. We investigated the production of important mediators in asthma, namely tumour necrosis factor (TNF), interleukin-10 (IL-10), IL-12, IL-13, nitric oxide (NO) and macrophage inflammatory protein-1alpha (MIP-1alpha), by AM of unsensitized Sprague Dawley and Brown Norway rats. AM were purified by adherence and stimulated with OX8 (anti-CD8 antibody) or LPS. OX8 stimulation significantly increased the release of TNF, IL-10 and NO in both strains of rats, whereas MIP-1alpha and IL-12 release were increased in Brown Norway rats only. Interestingly, stimulated AM from Sprague Dawley rats released significantly more TNF and less IL-10, IL-12, IL-13, MIP-1alpha and NO compared with AM from Brown Norway rats. These differences were also observed at the mRNA level, except for TNF. Thus, AM from Brown Norway and Sprague Dawley rats are functionally different. Furthermore, LPS- and OX8-stimulated AM from Brown Norway rats produce more Th2 type cytokines (IL-10 and IL-13) than AM from Sprague Dawley rats, suggesting that these cells may play an important role in creating a cytokine milieu that may favour the development of allergic reactions.
PubMed ID
11678894 View in PubMed
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The anti-inflammatory action of methotrexate is not mediated by lymphocyte apoptosis, but by the suppression of activation and adhesion molecules.

https://arctichealth.org/en/permalink/ahliterature13769
Source
Clin Immunol. 2005 Feb;114(2):154-63
Publication Type
Article
Date
Feb-2005
Author
Andrew Johnston
Johann Eli Gudjonsson
Hekla Sigmundsdottir
Björn Runar Ludviksson
Helgi Valdimarsson
Author Affiliation
Department of Immunology, Landspitali University Hospital, 101 Reykjavik, Iceland.
Source
Clin Immunol. 2005 Feb;114(2):154-63
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Adenosine - pharmacology
Anti-Inflammatory Agents - pharmacology
Antigens, Bacterial - immunology
Apoptosis - drug effects - immunology
Cell Adhesion Molecules - antagonists & inhibitors - immunology
Flow Cytometry
Fucosyltransferases - biosynthesis - genetics
Humans
Integrins - immunology
Intercellular Adhesion Molecule-1 - genetics - immunology
Leucovorin - pharmacology
Lymphocyte Activation - drug effects - immunology
Membrane Glycoproteins - genetics - immunology
Methotrexate - pharmacology
RNA - chemistry - genetics
RNA, Messenger - biosynthesis - genetics
Receptors, Interleukin-2 - antagonists & inhibitors - immunology
Research Support, Non-U.S. Gov't
Reverse Transcriptase Polymerase Chain Reaction
Streptococcus pyogenes - immunology
T-Lymphocytes - cytology - drug effects - immunology
Abstract
Low-dose methotrexate (MTX) is an established and highly effective treatment for severe psoriasis and rheumatoid arthritis; however, its mechanism of action remains unclear. We investigated the effects of low-dose MTX on antigen-stimulated peripheral blood mononuclear cells and explored through which cellular pathways these effects are mediated. We show that MTX caused a dose-dependent suppression of T cell activation and adhesion molecule expression, and this was not due to lymphocyte apoptosis. The suppression of intercellular adhesion molecule (ICAM)-1 was adenosine and folate-dependent, while MTX suppression of the skin-homing cutaneous lymphocyte-associated antigen (CLA) was adenosine-independent. The effect of MTX on CLA, but not ICAM-1, required the constant presence of MTX in cultures. Thus, the suppression of T cell activation and T cell adhesion molecule expression, rather than apoptosis, mediated in part by adenosine or polyglutamated MTX or both, are important mechanisms in the anti-inflammatory action of MTX.
PubMed ID
15639649 View in PubMed
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Association between IL-1beta/TNF-alpha-induced glucocorticoid-sensitive changes in multiple gene expression and altered responsiveness in airway smooth muscle.

https://arctichealth.org/en/permalink/ahliterature10091
Source
Am J Respir Cell Mol Biol. 2001 Dec;25(6):761-71
Publication Type
Article
Date
Dec-2001
Author
H. Hakonarson
E. Halapi
R. Whelan
J. Gulcher
K. Stefansson
M M Grunstein
Author Affiliation
DeCode Genetics, Reykjavik, Iceland. hakonh@decode.is
Source
Am J Respir Cell Mol Biol. 2001 Dec;25(6):761-71
Date
Dec-2001
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Animals
Asthma - physiopathology
Comparative Study
Dexamethasone - pharmacology
Gene Expression Profiling
Gene Expression Regulation - drug effects
Interleukin-1 - pharmacology
Isoproterenol - pharmacology
Muscle Contraction - drug effects
Muscle Relaxation - drug effects
Muscle, Smooth - cytology - drug effects - metabolism
Oligonucleotide Array Sequence Analysis
RNA, Messenger - biosynthesis
Rabbits
Research Support, U.S. Gov't, P.H.S.
Signal Transduction - drug effects - physiology
Trachea - cytology - drug effects - metabolism
Transcription Factors - genetics - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Abstract
The pleiotropic cytokines interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha have been implicated in the pathophysiology of asthma. To elucidate the role of these cytokines in the pro-asthmatic state, the effects of IL-1beta and TNF-alpha on airway smooth muscle (ASM) responsiveness and ASM expression of multiple genes, assessed by high-density oligonucleotide array analysis, were examined in the absence and presence of the glucocorticoid dexamethasone (DEX). Administration of IL-1beta/TNF-alpha increased ASM contractility to acetylcholine and impaired ASM relaxation to isoproterenol. These pro-asthmatic- like changes in ASM responsiveness were associated with IL-1beta/ TNF-alpha-induced mRNA expression of a host of proinflammatory genes that regulate transcription, cytokines and chemokines, cellular adhesion molecules, and various signal transduction molecules that regulate ASM responsiveness. In the presence of DEX, the changes induced in ASM responsiveness were abrogated, and most of the IL-1beta/TNF-alpha-mediated changes in proinflammatory gene expression were repressed, although mRNA expression of a small number of genes was enhanced by DEX. Collectively, the observations support the concept that, together with its role as a regulator of airway tone, in response to IL-1beta/TNF-alpha, the ASM expresses a host of glucocorticoid-sensitive genes that contribute to the altered structure and function of the airways in the pro-asthmatic state. We speculate that glucocorticoid-sensitive, cytokine-induced pathways involved in ASM cell signaling represent important targets for new therapeutic interventions.
PubMed ID
11726403 View in PubMed
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Association of radiation-induced genes with noncancer chronic diseases in Mayak workers occupationally exposed to prolonged radiation.

https://arctichealth.org/en/permalink/ahliterature263140
Source
Radiat Res. 2015 Mar;183(3):249-61
Publication Type
Article
Date
Mar-2015
Author
Michael Abend
Tamara Azizova
Kerstin Müller
Harald Dörr
Sven Doucha-Senf
Helmut Kreppel
Galina Rusinova
Irina Glazkova
Natalia Vyazovskaya
Kristian Unger
Herbert Braselmann
Viktor Meineke
Source
Radiat Res. 2015 Mar;183(3):249-61
Date
Mar-2015
Language
English
Publication Type
Article
Keywords
Chronic Disease - epidemiology
Dose-Response Relationship, Radiation
Female
Gamma Rays
Gene Expression Regulation - radiation effects
Humans
Male
MicroRNAs - biosynthesis
Nuclear Power Plants
Occupational Exposure
RNA, Messenger - biosynthesis
Radiation Injuries
Russia
Abstract
We examined the association of gene expression with noncancer chronic disease outcomes in Mayak nuclear weapons plant workers who were exposed to radiation due to their occupation. We conducted a cross-sectional study with selection based on radiation exposure status of Mayak plant workers living in Ozyorsk who were alive in 2011 and either exposed to: combined incorporated Plutonium-239 ((239)Pu) and external gamma-ray exposure (n = 82); external gamma-ray exposure alone (n = 18); or were unexposed (n = 50) of Ozyorsk residents who provided community-based professional support for plant personnel and who were alive in 2011. Peripheral blood was taken and RNA was isolated and then converted into cDNA and stored at -20°C. In a previous analysis we screened the whole genome for radiation-associated candidate genes, and validated 15 mRNAs and 15 microRNAs using qRT-PCR. In the current analysis we examined the association of these genes with 15 different chronic diseases on 92 samples (47 males, 45 females). We examined the radiation-to-gene and gene-to-disease associations in statistical models stratified by gender and separately for each disease and exposure. We modeled radiation exposure as gamma or (239)Pu on both the continuous and categorical scales. Unconditional logistic regression was used to calculate odds ratios (OR), 95% confidence intervals (CI), and the concordance for genes that were significantly associated with radiation exposure and a specific disease outcome were identified. Altogether 12 mRNAs and 9 microRNAs appeared to be significantly associated with 6 diseases, including thyroid diseases (3 genes, OR: 1.2-5.1, concordance: 71-78%), atherosclerotic diseases (4 genes, OR: 2.5-10, concordance: 70-75%), kidney diseases (6 genes, OR: 1.3-8.6, concordance: 69-85%), cholelithiasis (3 genes, OR: 0.2-0.3, concordance: 74-75%), benign tumors [1 gene (AGAP4), OR: 3.7, concordance: 81%] and chronic radiation syndrome (4 genes, OR: 2.5-4.3, concordance: 70-99%). Further associations were found for systolic blood pressure (6 genes, OR: 3.7-10.6, concordance: 81-88%) and body mass index [1 gene (miR-484), OR: 3.7, concordance: 81%]. All associations were gender and exposure dependent. These findings suggest that gene expression changes observed after occupational prolonged radiation exposures may increase the risk for certain noncancer chronic diseases.
PubMed ID
25706777 View in PubMed
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Availability of in vitro vitellogenin assay for screening of estrogenic and anti-estrogenic activities of environmental chemicals.

https://arctichealth.org/en/permalink/ahliterature81228
Source
Environ Sci. 2006;13(3):161-83
Publication Type
Article
Date
2006
Author
Iguchi Taisen
Irie Fumi
Urushitani Hiroshi
Tooi Osamu
Kawashima Yukio
Roberts Mike
Norrgren Leif
Hutchinson Thomas
Author Affiliation
National Institutes of Natural Sciences, National Institute for Basic Biology, Okazaki Institute for Integrative Bioscience, 5-1 Higashiyama, Myodaiji, Okazaki 444-8787, Japan. taisen@nibb.ac.jp
Source
Environ Sci. 2006;13(3):161-83
Date
2006
Language
English
Publication Type
Article
Keywords
Animals
Cells, Cultured
Charadriiformes
Chickens
Coturnix
Environmental Pollutants - analysis
Enzyme-Linked Immunosorbent Assay - methods
Estrogens - analysis
Fishes
Hepatocytes - drug effects - metabolism
RNA, Messenger - biosynthesis - genetics
Vitellogenins - analysis - biosynthesis - genetics
Xenopus laevis
Abstract
Vitellogenin (VTG) protein, VTG mRNA, other egg yolk proteins, vitelline envelope proteins and their mRNAs are produced in the liver of oviparous species by stimulation of endogenous estrogen and exogenous estrogenic chemicals. The VTG assay based on enzyme-linked immunosorbent assay (ELISA) has been widely used for many fish species to screen estrogenic and anti-estrogenic activities of chemicals and sewage effluents using immature fish and/or male fish. In order to reduce the number of fish for screening of estrogenicity and anti-estrogenicity of chemicals, primary cultured fish hepatocytes can be used. In fact, primary cultured hepatocytes have been successfully used for the detection of estrogenic and anti-estrogenic activities of environmental chemicals in selected OECD fish species, e.g., medaka (Oryzias latipes) and rainbow trout (Oncorhynchys mykiss) together with other fish species such as Atlantic salmon (Salmo salar L.), Siberian sturgeon (Acipenser baeri), tilapia (Oreochromis mossambicus), carp (Cyprinus carpio), bream (Abramis brama), Carassius auratus, silver eel (Anguilla anguilla L.), and channel catfish (Ictalurus punctanus). In terms of hepatocyte assays relating to other taxa, these include frogs such as Xenopus laevis and the common green frog (Rana esculenta), chickens (Gallus domesticus) and herring gulls (Larus argentatus). VTG mRNA measurement by quantitative reverse transcription-polymerase chain reaction has also been successfully applied in the primary cultured hepatocytes of various species.
PubMed ID
16883298 View in PubMed
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66 records – page 1 of 7.