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21 records – page 1 of 3.

An outbreak of Listeria monocytogenes serotype 3a infections from butter in Finland.

https://arctichealth.org/en/permalink/ahliterature198523
Source
J Infect Dis. 2000 May;181(5):1838-41
Publication Type
Article
Date
May-2000
Author
O. Lyytikäinen
T. Autio
R. Maijala
P. Ruutu
T. Honkanen-Buzalski
M. Miettinen
M. Hatakka
J. Mikkola
V J Anttila
T. Johansson
L. Rantala
T. Aalto
H. Korkeala
A. Siitonen
Author Affiliation
Department of Infectious Disease Epidemiology, National Public Health Institute, FIN-00300 Helsinki, Finland. outi.lyytikainen@ktl. fi.
Source
J Infect Dis. 2000 May;181(5):1838-41
Date
May-2000
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Butter - microbiology
Case-Control Studies
Child
Cross Infection - epidemiology
Dairying
Disease Outbreaks
Female
Finland - epidemiology
Humans
Incidence
Listeria monocytogenes - classification
Listeriosis - epidemiology - etiology - transmission
Male
Middle Aged
Serotyping
Abstract
In February 1999, an outbreak of listeriosis caused by Listeria monocytogenes serotype 3a occurred in Finland. All isolates were identical. The outbreak strain was first isolated in 1997 in dairy butter. This dairy began delivery to a tertiary care hospital (TCH) in June 1998. From June 1998 to April 1999, 25 case patients were identified (20 with sepsis, 4 with meningitis, and 1 with abscess; 6 patients died). Patients with the outbreak strain were more likely to have been admitted to the TCH than were patients with other strains of L. monocytogenes (60% vs. 8%; odds ratio, 17.3; 95% confidence interval, 2.8-136.8). Case patients admitted to the TCH had been hospitalized longer before cultures tested positive than had matched controls (median, 31 vs. 10 days; P=.008). An investigation found the outbreak strain in packaged butter served at the TCH and at the source dairy. Recall of the product ended the outbreak.
PubMed ID
10823797 View in PubMed
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Characterization of estrogen-dependent growth of cultured MCF-7 human breast-cancer cells expressing 17beta-hydroxysteroid dehydrogenase type 1.

https://arctichealth.org/en/permalink/ahliterature22400
Source
Int J Cancer. 1996 Nov 27;68(5):600-4
Publication Type
Article
Date
Nov-27-1996
Author
M M Miettinen
M H Poutanen
R K Vihko
Author Affiliation
Biocenter Oulu, Department of Clinical Chemistry, University of Oulu, Finland.
Source
Int J Cancer. 1996 Nov 27;68(5):600-4
Date
Nov-27-1996
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - genetics - metabolism - pathology
Cell Division - drug effects
Estrogens - pharmacology
Female
Gene Expression Regulation, Neoplastic - drug effects
Gene Transfer Techniques
Humans
Hydroxysteroid Dehydrogenases - biosynthesis - genetics
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
17beta-hydroxysteroid dehydrogenase (17HSD) type I converts the weakly active estrogen, estrone, into highly active estradiol. In addition to being essential for gonadal estradiol biosynthesis, the enzyme is also expressed in a significant proportion of breast tumors. In order to study the role of the enzyme in estrogen-dependent growth of breast cancer, MCF-7 breast-cancer cells stably expressing human 17HSD type I were generated. In control MCF-7 cells a very low 17HSD activity was observed and, in line with its low estrogenic activity, estrone was devoid of the growth-enhancing effect of estradiol. The presence of the enzyme in the stably transfected MCF-7 cells resulted in a rapid conversion of estrone into estradiol but did not alter the estrogen-receptor concentration in the cells. However, in transfected cells, estrone had a growth-promoting effect practically identical to that of estradiol. The presence or absence of 17HSD type I in breast-cancer cells may therefore be decisive with regard to estrogen exposure and the estrogen-responsive growth of breast-cancer tissues.
PubMed ID
8938141 View in PubMed
Less detail

Cholesterol-lowering diet and mortality from coronary heart-disease.

https://arctichealth.org/en/permalink/ahliterature255179
Source
Lancet. 1972 Dec 30;2(7792):1418-9
Publication Type
Article
Date
Dec-30-1972

Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study.

https://arctichealth.org/en/permalink/ahliterature247140
Source
Int J Epidemiol. 1979 Jun;8(2):99-118
Publication Type
Article
Date
Jun-1979
Author
O. Turpeinen
M J Karvonen
M. Pekkarinen
M. Miettinen
R. Elosuo
E. Paavilainen
Source
Int J Epidemiol. 1979 Jun;8(2):99-118
Date
Jun-1979
Language
English
Publication Type
Article
Keywords
Adipose Tissue - analysis
Adult
Blood pressure
Cholesterol - blood
Clinical Trials as Topic
Coronary Disease - epidemiology - prevention & control
Diet
Fatty Acids - analysis
Finland
Humans
Male
Middle Aged
Obesity - complications
Phospholipids - blood
Smoking - complications
Triglycerides - blood
Abstract
A controlled intervention trial, with the purpose of testing the hypothesis that the incidence of coronary heart disease (CHD) could be decreased by the use of serum-cholesterol-lowering (SCL) diet, was carried out in 2 mental hospitals near Helsinki in 1959--71. The subjects were hospitalized middle-aged men. One of the hospitals received the SCL diet, i.e. a diet low in saturated fats and cholesterol and relatively high in polyunsaturated fats, while the other served as the control with a normal hospital diet. Six years later the diets were reversed, and the trial was continued another 6 years. The use of the SCL diet was associated with markedly lowered serum-cholesterol values. The incidence of CHD, as measured by the appearance of certain electrocardiographic patterns and by the occurrence of coronary deaths, was in both hospitals during the SCL-diet periods about half that during the normal-diet periods. An examination of a number of potential confounding variables indicated that the changes in them were small and failed to account for the considerable reduction in the incidence of CHD. It is concluded that the use of the serum-cholesterol-lowering diet exerted a substantial preventive effect on CHD.
PubMed ID
393644 View in PubMed
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Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on bone material properties.

https://arctichealth.org/en/permalink/ahliterature98159
Source
J Biomech. 2010 Apr 19;43(6):1097-103
Publication Type
Article
Date
Apr-19-2010
Author
Mikko A J Finnilä
Peter Zioupos
Maria Herlin
Hanna M Miettinen
Ulla Simanainen
Helen Håkansson
Juha Tuukkanen
Matti Viluksela
Timo Jämsä
Author Affiliation
Department of Medical Technology, University of Oulu, P.O. Box 5000, 90014 University of Oulu, Finland. mikko.finnila@oulu.fi
Source
J Biomech. 2010 Apr 19;43(6):1097-103
Date
Apr-19-2010
Language
English
Publication Type
Article
Keywords
Animals
Biomechanics
Bone Density - drug effects
Bone Matrix - drug effects - pathology - physiopathology
Female
Nanotechnology
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced - pathology - physiopathology
Rats
Rats, Sprague-Dawley
Stress, mechanical
Tetrachlorodibenzodioxin - administration & dosage - toxicity
Tibia - drug effects - pathology - physiopathology
Abstract
Dioxins are known to decrease bone strength, architecture and density. However, their detailed effects on bone material properties are unknown. Here we used nanoindentation methods to characterize the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on nanomechanical behaviour of bone matrix. Pregnant rats were treated with a single intragastric dose of TCDD (1 microg/kg) or vehicle on gestational day 11. Tibias of female offspring were sampled on postnatal day (PND) 35 or 70, scanned at mid-diaphysis with pQCT, and evaluated by three-point bending and nanoindentation. TCDD treatment decreased bone mineralization (p
PubMed ID
20132933 View in PubMed
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Estrogen metabolism as a regulator of estrogen action in the mammary gland.

https://arctichealth.org/en/permalink/ahliterature17899
Source
J Mammary Gland Biol Neoplasia. 2000 Jul;5(3):259-70
Publication Type
Article
Date
Jul-2000
Author
M. Miettinen
V. Isomaa
H. Peltoketo
D. Ghosh
P. Vihko
Author Affiliation
Biocenter Oulu and WHO Collaborating Centre for Research on Reproductive Health, University of Oulu, Finland.
Source
J Mammary Gland Biol Neoplasia. 2000 Jul;5(3):259-70
Date
Jul-2000
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - metabolism
Breast - metabolism
Breast Neoplasms - metabolism
Dose-Response Relationship, Drug
Estrogens - metabolism
Female
Humans
Mammary Glands, Human - metabolism
Models, Biological
Models, Molecular
Ovary - metabolism
Protein Isoforms
Time Factors
Abstract
Estrogen action in the target cells is dependent on estrogen receptor activity and intracellular estrogen concentration, which, in turn, is affected by the serum concentration and local metabolism in these cells. During the reproductive years the main source of estrogens is the ovarian follicles, but in postmenopausal women most of the estrogens are formed in peripheral tissues. 17Beta-hydroxysteroid dehydrogenases (17HSDs) catalyze the reaction between 17beta-hydroxysteroids and 17-ketosteroids, and several distinct 17HSD isoenzymes have been characterized. 17HSD type 1 catalyzes the reaction from low-activity estrone to high-activity estradiol. The type 2 enzyme has an opposite activity, thereby reducing the exposure of tissues to estrogen action. 17HSD type 1 is expressed both in steroidogenic tissues and in the target tissues of steroid action, such as normal and malignant breast tissue, where it may be responsible for maintaining the high intracellular estradiol concentration seen in breast cancer specimens. Therefore, 17HSD type 1 inhibitors may be useful in the treatment and/or prevention of estrogen-dependent malignancies, such as breast cancer. This article deals mainly with 17HSD types 1 and 2 and their role in estrogen action in breast tissue.
PubMed ID
14973388 View in PubMed
Less detail

Human 17 beta-hydroxysteroid dehydrogenase type 1 and type 2 isoenzymes have opposite activities in cultured cells and characteristic cell- and tissue-specific expression.

https://arctichealth.org/en/permalink/ahliterature22714
Source
Biochem J. 1996 Mar 15;314 ( Pt 3):839-45
Publication Type
Article
Date
Mar-15-1996
Author
M M Miettinen
M V Mustonen
M H Poutanen
V V Isomaa
R K Vihko
Author Affiliation
Biocenter Oulu and Department of Clinical Chemistry, University of Oulu, Finland.
Source
Biochem J. 1996 Mar 15;314 ( Pt 3):839-45
Date
Mar-15-1996
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - biosynthesis - metabolism
Animals
Breast Neoplasms
Cell Line
Cell Membrane - enzymology
Cercopithecus aethiops
Comparative Study
Endometrial Neoplasms
Endometrium - enzymology
Female
Gene Expression
Humans
Isoenzymes - biosynthesis - metabolism
Kidney
Kinetics
Male
Ovarian Neoplasms
Prostatic Neoplasms
RNA, Messenger - analysis - biosynthesis
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
17 beta-Hydroxysteroid dehydrogenase (17HSD) isoenzymes catalyse the interconversion between highly active 17 beta-hydroxy- and low-activity 17-keto-steroids and thereby regulate the biological activity of sex steroids. The present study was carried out to characterize 17HSD activity and the expression of 17HSD type 1 and 2 isoenzymes in several human cell types and tissues. The data indicate that in cultured cells the direction of 17HSD activity is exclusively determined by the expression of these distinct isoenzymes. The intracellular environment could not modulate the direction of the enzyme activities in any of the cell types analysed. 17HSD type 1 acts as a reductase converting oestrone into oestradiol, whereas 17HSD type 2 possesses oxidative activity inactivating oestradiol by converting it into oestrone. The data, furthermore, suggest that of the two 17HSD type 1 mRNAs (1.3 and 2.3 kb), expression of the 1.3 kb mRNA is related to enzyme concentration in all the cell types studied. This mRNA is principally expressed in cells of placental and ovarian origin, but is also present in malignant breast epithelial cells. In contrast, 17HSD type 2 is more widely expressed. It is present in several oestradiol-metabolizing tissues as well as in some target cells of sex steroid action. The opposite reaction directions observed in the cultured cells, together with differences in the distribution of the isoenzymes, suggest that type 1 is involved in oestradiol production in females while type 2 plays a role in the inactivation of this sex steroid in peripheral tissues, both in females and in males. However, some examples exist of simultaneous expression of both enzymes in the same cell type or tissue.
PubMed ID
8615778 View in PubMed
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21 records – page 1 of 3.