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101 records – page 1 of 11.

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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Age-related changes of cardiac gene expression following myocardial ischemia/reperfusion.

https://arctichealth.org/en/permalink/ahliterature53445
Source
Arch Biochem Biophys. 2003 Dec 15;420(2):268-78
Publication Type
Article
Date
Dec-15-2003
Author
Boris Z Simkhovich
Paul Marjoram
Coralie Poizat
Larry Kedes
Robert A Kloner
Author Affiliation
Heart Institute, Good Samaritan Hospital, Department of Medicine and Division of Cardiovascular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, CA 90017, USA.
Source
Arch Biochem Biophys. 2003 Dec 15;420(2):268-78
Date
Dec-15-2003
Language
English
Publication Type
Article
Keywords
Age Factors
Animals
Apoptosis - genetics
Cardiac Surgical Procedures - methods
Comparative Study
Female
Gene Expression Profiling
Gene Expression Regulation
Myocardial Ischemia - genetics - metabolism
Myocardial Reperfusion
Myocardial Reperfusion Injury - genetics - metabolism
Myocardium - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Signal Transduction
Transcription, Genetic
Abstract
Young and old (4 and 25 months of age, respectively) Fisher 344/Brown Norway hybrid female rats were subjected to four 3 min episodes of ischemia separated by 5 min of reperfusion. Corresponding open-chest sham-operated groups received 32 min of no intervention. All rats were allowed to recover, and 24h later hearts were removed and frozen in liquid nitrogen. Global gene profiling in the ischemic and the non-ischemic areas and in the sham-operated hearts as well was carried out by using Affymetrix Gene Chips. Young ischemic hearts demonstrated down-regulation of gene expression associated with early-remodeling including down-regulation of tissue inhibitor of metalloproteinase 1, decorin, collagen, tropoelastin, and fibulin, as well as decreases in hypertrophy-related transcripts. In contrast, old hearts showed a unique injury-related response, which included up-regulation of mRNAs for proteins associated with hypertrophy or apoptosis (including H36-alpha7 integrin, alpha-actin, tubulin, filamin, connective tissue growth factor, calcineurin, serine protease, and apoptosis inducing factor). These injury-related changes in gene expression could in part explain increased gravity of outcomes of ischemia and myocardial infarction in elderly hearts.
PubMed ID
14654066 View in PubMed
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Aging and the brown Norway rat leydig cell antioxidant defense system.

https://arctichealth.org/en/permalink/ahliterature83080
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Publication Type
Article
Author
Luo Lindi
Chen Haolin
Trush Michael A
Show Matthew D
Anway Matthew D
Zirkin Barry R
Author Affiliation
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205, USA. lluo@jhsph.edu
Source
J Androl. 2006 Mar-Apr;27(2):240-7
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Antioxidants - metabolism
Glutathione Peroxidase - genetics - metabolism
Leydig Cells - enzymology
Male
RNA, Messenger - genetics
Rats
Rats, Inbred BN
Superoxide Dismutase - genetics - metabolism
Testis - growth & development
Transcription, Genetic
Abstract
Previous studies have shown that testosterone production by the Leydig cells of aged Brown Norway rats is reduced from the relatively high levels produced by Leydig cells of young rats and that this reduction is not secondary to decreased serum luteinizing hormone concentration. The free radical theory of aging proposes that imbalance between pro-oxidants and the antioxidant defense system ultimately results in oxidative damage to cellular processes. With this in mind, we hypothesized herein that age-related reductions in steroidogenesis by Brown Norway rat Leydig cells may be associated with the impairment of the antioxidant defense system of these cells. To begin to test this hypothesis, we compared the activities and steady-state mRNA and protein levels of the antioxidant enzymes copper zinc (CuZn) superoxide dismutase (CuZnSOD, SOD1), manganese (Mn) superoxide dismutase (MnSOD, SOD2), and glutathione peroxidase (GPx) and the levels of reduced and oxidized glutathione in Leydig cells isolated from the testes of young (4-month-old) and aged (20-month-old) Brown Norway rats. For some studies, Leydig cells were isolated separately from aged testes that either had regressed because of age-related losses of germ cells or that were nonregressed. SOD (total) and GPx activities were found to decrease significantly with age whether or not the testes were regressed. CuZnSOD and MnSOD mRNA levels decreased with aging, though the magnitude of the decreases were considerably lower than the respective decreases in enzyme activities. GPx mRNA levels also decreased, which is consistent with the decreases seen in enzyme activity. MnSOD protein expression declined with age, and to a lesser extent, CuZnSOD did as well. Reduced and oxidized glutathione also exhibited age-related reductions in cells from both normal and regressed aged testes. The age-related decreases in Leydig cell antioxidant enzyme activities, gene expression, and protein levels and in glutathione were consistent with the hypothesis that the loss of steroidogenic function that accompanies Leydig cell aging may result in part from a decrease in the fidelity of the cellular antioxidant defense system.
PubMed ID
16304208 View in PubMed
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Amplification of HER-2(erbB-2/neu) oncogene as the most significant prognostic factor in a group of Russian breast cancer patients.

https://arctichealth.org/en/permalink/ahliterature222515
Source
Neoplasma. 1993;40(1):35-9
Publication Type
Article
Date
1993
Author
E N Imyanitov
O I Chernitsa
O M Serova
I F Nikoforova
G F Pluzhnikova
P G Knyazev
Author Affiliation
N.N. Petrov Research Institute of Oncology, Laboratory of Molecular Genetics of Cancer, St. Petersburg, Russia.
Source
Neoplasma. 1993;40(1):35-9
Date
1993
Language
English
Publication Type
Article
Keywords
Blotting, Northern
Blotting, Southern
Breast Neoplasms - genetics - pathology
Chi-Square Distribution
Chromosomes, Human, Pair 17
DNA - analysis - isolation & purification
Female
Follow-Up Studies
Gene Amplification
Gene Expression Regulation, Neoplastic
Genes, p53
Humans
Menopause
Middle Aged
Oncogene Proteins v-erbB
Oncogene Proteins, Viral - genetics
Oncogenes
Prognosis
RNA - analysis - isolation & purification
Receptor, erbB-2
Receptors, Estrogen - biosynthesis
Receptors, Progesterone - biosynthesis
Retroviridae Proteins, Oncogenic - genetics
Russia
Transcription, Genetic
Abstract
Amplification of HER-2(erbB-2/neu) oncogene was detected in 36 of 142 (25%) breast carcinomas (BC) RNA expression was examined in 42 carcinomas, in 10 of them overexpression was revealed. Amplification was matched by overexpression. No association was found between the increased number of HER-2(erbB-2/neu) copies and tumor size, lymph node involvement, stage of disease, age of onset, and estrogen and progesterone receptor level. HER-2(erbB-2/neu) amplification was shown to be of independent prognostic significance in the group of 32 BC patients with sufficient follow-up (more than 40 months). Six of 7 HER-2(erbB-2/neu) amplification-positive patients and only 2 of 25 HER-2(erbB-2/neu) amplification-negative ones relapsed (p
PubMed ID
7688867 View in PubMed
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Antisignature oligonucleotides and their analogs as inhibitors of mollicutes-cofactors of HIV.

https://arctichealth.org/en/permalink/ahliterature7746
Source
Mikrobiol Z. 1997 Mar-Apr;59(2):3-11
Publication Type
Article
Author
I H Skrypal'
V V Babychev
L P Panchenko
O V Iehorov
K S Korobkova
I Ia Dubei
D M Fedoriak
A S Shalamai
Author Affiliation
Institute of Microbiology and Virology, Kyiv, Ukraine.
Source
Mikrobiol Z. 1997 Mar-Apr;59(2):3-11
Language
English
Publication Type
Article
Keywords
Acholeplasma laidlawii - drug effects - genetics
Base Sequence
DNA, Bacterial - drug effects - genetics
Depression, Chemical
HIV-1
Molecular Sequence Data
Mycoplasma fermentans - drug effects - genetics
Oligonucleotides, Antisense - pharmacology
Protein Biosynthesis - drug effects
RNA, Bacterial - drug effects - genetics
RNA, Ribosomal, 16S - drug effects - genetics
Transcription, Genetic - drug effects
rRNA Operon - drug effects - genetics
Abstract
Inhibition of mollicutes by synthetic oligonucleotides and their analogs complementary to specific "signature" regions of 16S rRNA and corresponding sequences of ribosomal operon DNA was studied. It was shown that antisignature oligonucleotides inhibited transcription in vitro for above 79% interacting specifically with ribosomal operon and non-specific with DNA-dependent RNA-polymerase. The inhibition efficiency depended on oligonucleotide sequence and type of modification. Translation in vitro was suppressed most efficiently (up to 60%) by oligonucleotides complementary to 3'-end region of 16S rRNA, also depending on their modification. Translation in vivo was inhibited most efficiently (up to 73%) by thiophosphate analogs of oligonucleotides complementary to sequences 499-507 and 523-532 of 16S rRNA responsible for binding of ribosomal "core" protein S4 starting the assembly of 30S ribosome subunit. With the simultaneous use of the last two oligonucleotides, the growth of mollicutes in SM IMV-72 medium rich in exogenous sources of nucleosides was suppressed for over 90%. It is supposed that under conditions where mollicutes have no free access to starting materials for their own synthesis of nucleic acid these nucleotides could suppress microorganisms completely. Antisignature oligonucleotides are considered as superspecific agents not leading to the development of resistance of mollicutes and believed to be the main future remedy against diseased caused by microorganisms lacking the system of nucleoside synthesis.
PubMed ID
9177600 View in PubMed
Less detail

Archaeal amoA and ureC genes and their transcriptional activity in the Arctic Ocean.

https://arctichealth.org/en/permalink/ahliterature267632
Source
Sci Rep. 2014;4:4661
Publication Type
Article
Date
2014
Author
Estelle Pedneault
Pierre E Galand
Marianne Potvin
Jean-Éric Tremblay
Connie Lovejoy
Source
Sci Rep. 2014;4:4661
Date
2014
Language
English
Publication Type
Article
Keywords
Archaea - genetics
Archaeal Proteins - classification - genetics - metabolism
Arctic Regions
Gene Expression Profiling
Nitrates - metabolism
Oceans and Seas
Oxidoreductases - classification - genetics - metabolism
Phylogeny
RNA, Ribosomal, 16S - genetics - metabolism
Transcription, Genetic
Urease - classification - genetics - metabolism
Abstract
Thaumarchaeota and the gene encoding for a subunit of ammonia monooxygenase (amoA) are ubiquitous in Polar Seas, and some Thaumarchaeota also have a gene coding for ureC, diagnostic for urease. Using quantitative PCR we investigated the occurrence of genes and transcripts of ureC and amoA in Arctic samples from winter, spring and summer. AmoA genes, ureC genes and amoA transcripts were always present, but ureC transcripts were rarely detected. Over a 48 h light manipulation experiment amoA transcripts persisted under light and dark conditions, but not ureC transcripts. In addition, maxima for amoA transcript were nearer the surface compared to amoA genes. Clone libraries using DNA template recovered shallow and deep amoA clades but only the shallow clade was recovered from cDNA (from RNA). These results imply environmental control of amoA expression with direct or indirect light effects, and rare ureC expression despite its widespread occurrence in the Arctic Ocean.
Notes
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Erratum In: Sci Rep. 2015;5:1178626149188
PubMed ID
24722490 View in PubMed
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Autoantibodies against aromatic L-amino acid decarboxylase in autoimmune polyendocrine syndrome type I.

https://arctichealth.org/en/permalink/ahliterature48227
Source
J Clin Endocrinol Metab. 1997 Jan;82(1):147-50
Publication Type
Article
Date
Jan-1997
Author
E S Husebye
G. Gebre-Medhin
T. Tuomi
J. Perheentupa
M. Landin-Olsson
J. Gustafsson
F. Rorsman
O. Kämpe
Author Affiliation
Department of Internal Medicine, University Hospital, Uppsala University, Sweden. eystein.husebye@medicin.uu.se
Source
J Clin Endocrinol Metab. 1997 Jan;82(1):147-50
Date
Jan-1997
Language
English
Publication Type
Article
Keywords
Adult
Animals
Aromatic-L-Amino-Acid Decarboxylases - genetics - immunology
Autoantibodies - blood
Diabetes Mellitus, Type 1 - immunology
Electrophoresis, Polyacrylamide Gel
Female
Finland
Humans
Islets of Langerhans - enzymology
Male
Polyendocrinopathies, Autoimmune - enzymology - immunology
Protein Biosynthesis
Rats
Research Support, Non-U.S. Gov't
Sweden
Transcription, Genetic
Abstract
Patients with autoimmune polyendocrine syndrome type I (APS I) have autoantibodies against the enzyme aromatic L-amino acid decarboxylase (AADC) of pancreatic beta-cells. The aim of the present study was to investigate the presence of anti-AADC antibodies in a large cohort of patients with APS I, and in patients with isolated insulin-dependent diabetes mellitus (IDDM). We found autoantibodies against AADC in 35 of 69 patients (51%) with APS I but in none of 138 patients with isolated IDDM or 91 healthy controls. Among the patients with APS I, anti-AADC antibodies were more often found in those with hepatitis (11/12, 92%), than in those without hepatitis (24/57, 42%) (P = 0.003). Similarly, of 15 patients with vitiligo, 12 (80%) had anti-AADC antibodies, compared with 23/54 (43%) without vitiligo (P = 0.021). Of the 9 APS I patients with IDDM, 5 had antibodies against both AADC and glutamate decarboxylase, 2 against AADC only, and 2 against glutamate decarboxylase only. Interestingly, AADC is present in relatively large amounts in the liver, where its function is unknown. Thus, an autoimmune reactivity against AADC may be involved in the pathogenesis of autoimmune chronic active hepatitis and vitiligo in APS I patients, whereas the role of AADC in the development of IDDM in these patients remains to be determined.
PubMed ID
8989249 View in PubMed
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101 records – page 1 of 11.