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12-mo intervention of physical exercise improved work ability, especially in subjects with low baseline work ability.

https://arctichealth.org/en/permalink/ahliterature258283
Source
Int J Environ Res Public Health. 2014 Apr;11(4):3859-69
Publication Type
Article
Date
Apr-2014
Author
Oili Kettunen
Timo Vuorimaa
Tommi Vasankari
Author Affiliation
Department of Health and Exercise & Paavo Nurmi Center, University of Turku, 20520 Turku, Finland. oili.kettunen@vierumaki.fi.
Source
Int J Environ Res Public Health. 2014 Apr;11(4):3859-69
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Adult
Exercise
Female
Finland
Humans
Life Style
Male
Middle Aged
Oxygen - metabolism
Physical Fitness
Questionnaires
Work Capacity Evaluation
Young Adult
Abstract
This study's objective was to assess the effects of a 12-month physical exercise intervention on work ability (WAI) and cardiorespiratory fitness (CRF) in healthy working adults.
The study group had 371 participants, of which 338 (212 women and 126 men) were allocated in the exercise group and 33 (17 women and 16 men) in the control group. The exercise group underwent a 12-month exercise program followed by a 12-month follow-up. WAI and CRF were evaluated at baseline, and at 4, 8, 12, and 24 study months, in both exercise and control groups. The exercise group was divided into subgroups according to baseline WAI classifications (poor/moderate, good, excellent).
During the 12-month exercise intervention, the exercise group increased their leisure-time physical activity by 71% (p = 0.016) and improved the mean WAI by 3% and CRF by 7% (p
Notes
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PubMed ID
24714059 View in PubMed
Less detail

17 beta-hydroxysteroid dehydrogenases and cancers.

https://arctichealth.org/en/permalink/ahliterature18539
Source
J Steroid Biochem Mol Biol. 2002 Dec;83(1-5):119-22
Publication Type
Article
Date
Dec-2002
Author
P. Vihko
P. Härkönen
O. Oduwole
S. Törn
R. Kurkela
K. Porvari
A. Pulkka
V. Isomaa
Author Affiliation
Biocenter Oulu and Research Center for Molecular Endocrinology, University of Oulu, P.O. Box 5000, FIN-90014 Oulu, Finland. pvihko@whoccr.oulu.fi
Source
J Steroid Biochem Mol Biol. 2002 Dec;83(1-5):119-22
Date
Dec-2002
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - metabolism
Breast Neoplasms - enzymology
Cell Line
Colonic Neoplasms - enzymology - pathology
Disease Progression
Female
Humans
Male
Neoplasms - enzymology
Oxygen - metabolism
Prostatic Neoplasms - enzymology
Protein Isoforms
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
17 beta-Hydroxysteroid dehydrogenases (17HSDs) catalyze the interconversions between active 17 beta-hydroxysteroids and less-active 17-ketosteroids thereby affecting the availability of biologically active estrogens and androgens in a variety of tissues. The enzymes have different enzymatic properties and characteristic cell-specific expression patterns, suggesting differential physiological functions for the enzymes. Epidemiological and endocrine evidence indicate that estrogens play a key role in the etiology of breast cancer while androgens are involved in mechanisms controlling the growth of prostatic cells, both normal and malignant. Recently, we have developed, using LNCaP prostate cancer cell lines, a cell model to study the progression of prostate cancer. In the model LNCaP cells are transformed in culture condition to more aggressive cells, able to grow in suspension cultures. Our results suggest that substantial changes in androgen and estrogen metabolism occur in the cells during the process. These changes lead to increased production of active estrogens during transformation of the cells. Data from studies of breast cell lines and tissues suggest that the oxidative 17HSD type 2 may predominate in human non-malignant breast epithelial cells, while the reductive 17HSD type 1 activity prevails in malignant cells. Deprivation of an estrogen response by using specific 17HSD type 1 inhibitors is a tempting approach to treat estrogen-dependent breast cancer. Our recent studies demonstrate that in addition to sex hormone target tissues, estrogens may be important in the development of cancer in some other tissues previously not considered as estrogen target tissues such as colon. Our data show that the abundant expression of 17HSD type 2 present in normal colonic mucosa is significantly decreased during colon cancer development.
PubMed ID
12650708 View in PubMed
Less detail

17 beta-hydroxysteroid dehydrogenases--their role in pathophysiology.

https://arctichealth.org/en/permalink/ahliterature17852
Source
Mol Cell Endocrinol. 2004 Feb 27;215(1-2):83-8
Publication Type
Article
Date
Feb-27-2004
Author
P. Vihko
P. Härkönen
P. Soronen
S. Törn
A. Herrala
R. Kurkela
A. Pulkka
O. Oduwole
V. Isomaa
Author Affiliation
Biocenter Oulu and Research Center for Molecular Endocrinology, University of Oulu, P.O. Box 5000, FIN-90014, Oulu, Finland. pvihko@whoccr.oulu.fi
Source
Mol Cell Endocrinol. 2004 Feb 27;215(1-2):83-8
Date
Feb-27-2004
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - metabolism
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Gonadal Steroid Hormones - metabolism
Humans
Neoplasms - enzymology
Oxygen - metabolism
Research Support, Non-U.S. Gov't
Abstract
17 beta-Hydroxysteroid dehydrogenases (17HSDs) regulate the biological activity of sex steroid hormones in a variety of tissues by catalyzing the interconversions between highly active steroid hormones, e.g. estradiol and testosterone, and corresponding less active hormones, estrone and androstenedione. Epidemiological and endocrine evidence indicates that estrogens play a role in the etiology of breast cancer, while androgens are involved in mechanisms controlling the growth of normal and malignant prostatic cells. Using LNCaP prostate cancer cell lines, we have developed a cell model to study the progression of prostate cancer. In the model LNCaP cells are transformed in culture condition into more aggressive cells. Our data suggest that substantial changes in androgen and estrogen metabolism occur in the cells, leading to increased production of active estrogens during the process. In breast cancer, the reductive 17HSD type 1 activity is predominant in malignant cells, while the oxidative 17HSD type 2 mainly seems to be present in non-malignant breast epithelial cells. Deprivation of an estrogen response by using specific 17HSD type 1 inhibitors is a tempting approach in treating estrogen-dependent breast cancer. Our recent studies demonstrate that in addition to sex hormone target tissues, estrogens may be important in the development of cancer in some other tissues previously not considered to be estrogen target tissues, such as the gastrointestinal tract.
PubMed ID
15026178 View in PubMed
Less detail

Abnormal control of ventilation in high-altitude pulmonary edema.

https://arctichealth.org/en/permalink/ahliterature3383
Source
J Appl Physiol. 1988 Mar;64(3):1268-72
Publication Type
Article
Date
Mar-1988
Author
P H Hackett
R C Roach
R B Schoene
G L Harrison
W J Mills
Author Affiliation
Denali Medical Research Project, Center for High Latitude Health Research, University of Alaska, Anchorage 99508.
Source
J Appl Physiol. 1988 Mar;64(3):1268-72
Date
Mar-1988
Language
English
Publication Type
Article
Keywords
Adult
Altitude
Anoxemia - physiopathology
Anoxia - physiopathology
Female
Humans
Male
Oxygen - metabolism
Oxygen Inhalation Therapy
Pulmonary Edema - physiopathology - therapy
Respiration
Abstract
We wished to determine the role of hypoxic chemosensitivity in high-altitude pulmonary edema (HAPE) by studying persons when ill and upon recovery. We studied seven males with HAPE and seventeen controls at 4,400 m on Mt. McKinley. We measured ventilatory responses to both O2 breathing and progressive poikilocapnic hypoxia. Hypoxic ventilatory response (HVR) was described by the slope relating minute ventilation to percent arterial O2 saturation (delta VE/delta SaO2%). HAPE subjects were quite hypoxemic (SaO2% 59 +/- 6 vs. 85 +/- 1, P less than 0.01) and showed a high-frequency, low-tidal-volume pattern of breathing. O2 decreased ventilation in controls (-20%, P less than 0.01) but not in HAPE subjects. The HAPE group had low HVR values (0.15 +/- 0.07 vs. 0.54 +/- 0.08, P less than 0.01), although six controls had values in the same range. The three HAPE subjects with the lowest HVR values were the most hypoxemic and had a paradoxical increase in ventilation when breathing O2. We conclude that a low HVR plays a permissive rather than causative role in the pathogenesis of HAPE and that the combination of extreme hypoxemia and low HVR may result in hypoxic depression of ventilation.
PubMed ID
3366741 View in PubMed
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Abnormality of energy metabolism in the skeletal muscle of patients with liver cirrhosis and changes under administration of glucose and branched-chain amino acids.

https://arctichealth.org/en/permalink/ahliterature5271
Source
Tokai J Exp Clin Med. 2004 Dec;29(4):191-8
Publication Type
Article
Date
Dec-2004
Author
Jun Doi
Koichi Shiraishi
Munetaka Haida
Shohei Matsuzaki
Author Affiliation
Department of Gastroenterology, Tokai University Hachioji Hospital, Hachioji, Tokyo 192-0032, Japan.
Source
Tokai J Exp Clin Med. 2004 Dec;29(4):191-8
Date
Dec-2004
Language
English
Publication Type
Article
Keywords
Aged
Amino Acids, Branched-Chain - administration & dosage
Case-Control Studies
Citric Acid Cycle
Comparative Study
Energy Metabolism
Exercise
Fasting
Female
Glucose - administration & dosage - metabolism
Humans
Hydrogen-Ion Concentration
Liver Cirrhosis - metabolism
Magnetic Resonance Spectroscopy
Male
Middle Aged
Muscle, Skeletal - metabolism
Oxygen - metabolism
Phosphocreatine - metabolism
Spectroscopy, Near-Infrared
Abstract
We assessed changes in skeletal muscle energy metabolism by 31P-magnetic resonance spectroscopy (31P-MRS) and oxygen supply by near-infrared spectroscopy (NIR), after exercise and after administration of glucose and a branched-chain amino acids (BCAA), in healthy volunteers and patients with liver cirrhosis. As for the patients with liver cirrhosis, 4 were classified in Child-Pugh Grade A and the other 4 in Grade B. In patients with liver cirrhosis, the intramuscular pH and PCr index (PCr/PCr + Pi) were lower than in healthy subjects after exercise in the fasting state; the deltapH and deltaPCr index were statistically siginificant (p
PubMed ID
15717491 View in PubMed
Less detail

Aerobic growth at nanomolar oxygen concentrations.

https://arctichealth.org/en/permalink/ahliterature100200
Source
Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18755-60
Publication Type
Article
Date
Nov-2-2010
Author
Daniel A Stolper
Niels Peter Revsbech
Donald E Canfield
Author Affiliation
Nordic Center for Earth Evolution and Institute of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark.
Source
Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18755-60
Date
Nov-2-2010
Language
English
Publication Type
Article
Keywords
Aerobiosis - physiology
Escherichia coli K12 - physiology
Models, Biological
Oxygen - metabolism
Abstract
Molecular oxygen (O(2)) is the second most abundant gas in the Earth's atmosphere, but in many natural environments, its concentration is reduced to low or even undetectable levels. Although low-oxygen-adapted organisms define the ecology of low-oxygen environments, their capabilities are not fully known. These capabilities also provide a framework for reconstructing a critical period in the history of life, because low, but not negligible, atmospheric oxygen levels could have persisted before the "Great Oxidation" of the Earth's surface about 2.3 to 2.4 billion years ago. Here, we show that Escherichia coli K-12, chosen for its well-understood biochemistry, rapid growth rate, and low-oxygen-affinity terminal oxidase, grows at oxygen levels of = 3 nM, two to three orders of magnitude lower than previously observed for aerobes. Our study expands both the environmental range and temporal history of aerobic organisms.
PubMed ID
20974919 View in PubMed
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The air we breathe: three vital respiratory gases and the red blood cell: oxygen, nitric oxide, and carbon dioxide.

https://arctichealth.org/en/permalink/ahliterature135250
Source
Transfusion. 2011 Apr;51(4):676-85
Publication Type
Article
Date
Apr-2011
Author
Walter H Dzik
Author Affiliation
Blood Transfusion Service, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. sdzik@partners.org
Source
Transfusion. 2011 Apr;51(4):676-85
Date
Apr-2011
Language
English
Publication Type
Article
Keywords
2,3-Diphosphoglycerate - metabolism
Air
Carbon Dioxide - metabolism
Erythrocytes - metabolism
Humans
Nitric Oxide - metabolism
Oxygen - metabolism
Abstract
Three vital respiratory gases-oxygen (O(2)), nitric oxide (NO), and carbon dioxide (CO(2))-intersect at the level of the human red blood cell (RBC). In addition to hemoglobin (Hb)'s central role in O(2) transport, interaction of Hb with the Band 3 metabolon balances RBC energy flow. 2,3-Diphosphoglycerate enhances O(2) transport across the placenta and plays an important role in regulating RBC plasticity. NO is a key mediator of hypoxic vasodilation, but the precise role of RBC Hb remains controversial. In addition to established theories that depend on RBC uptake, delivery, and discharge of NO or its metabolites, an alternative hypothesis based on RBC permeability is suggested. NO depletion by free Hb may account for several clinical features seen during intravascular hemolysis or during deliberate infusion of Hb solutions used as RBC substitutes. CO(2) released by tissues triggers oxygen release through a series of well-coordinated reactions centered on the Band 3 metabolon. While RBC carbonic anhydrase and the Band 3 anion exchanger are central to this process, there is surprisingly little research on the kinetics of CO(2) clearance by transfusion. The three RBC gases are directly related to the three principal gases of Earth's atmosphere. Human fossil fuel consumption dumps 90 million metric tons of carbon into the atmosphere annually. Increasing CO(2) levels are linked to global warming, melting Arctic ice, rising sea levels, and climate instability. Just as individual cells depend on balance of the three vital gases, so too will their balance determine survival of life on Earth.
PubMed ID
21496039 View in PubMed
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Antiaging treatments have been legally prescribed for approximately thirty years.

https://arctichealth.org/en/permalink/ahliterature49664
Source
Ann N Y Acad Sci. 2004 Jun;1019:64-9
Publication Type
Article
Date
Jun-2004
Author
Svetlana V Ukraintseva
Konstantin G Arbeev
Anatoly I Michalsky
Anatoly I Yashin
Author Affiliation
Max Planck Institute for Demographic Research, 18057 Rostock, Germany. ukraintseva@cds.duke.edu
Source
Ann N Y Acad Sci. 2004 Jun;1019:64-9
Date
Jun-2004
Language
English
Publication Type
Article
Keywords
Aging
Brain - drug effects - pathology
Cognition
Humans
Longevity
Oxygen - metabolism
Prescriptions, Drug
gamma-Aminobutyric Acid - metabolism
Abstract
There is an interesting divergence between the achievements of geriatrics and gerontology. On the one hand, during the last 30 years physicians in many developed countries have successfully prescribed several medicines to cure various symptoms of senescence. On the other hand, the influence of such medicines on human life span practically has not been studied. The most common of the relevant medicines are nootropic piracetam, gamma-aminobutyric acid (GABA), selegiline, Ginkgo biloba, pentoxifylline, cerebrolysin, solcoseryl, ergoloid, vinpocetin, sertraline, and estrogens, among others. Available data from human clinical practices and experimental animal studies indicate that treatments with these drugs improve learning, memory, brain metabolism, and capacity. Some of these drugs increase tolerance to various stresses such as oxygen deficit and exercise, stimulate the regeneration of neurons in the old brain, and speed up the performance of mental and physical tasks. This means that modern medicine already has "antiaging" treatments at its disposal. However, the influence of such treatments on the mean and maximal life span of humans, and on the age trajectory of a human survival curve has been poorly studied. The increase in human life expectancy at birth in the second half of the last century was mostly caused by the better survival at the old and oldest old rather than at the young ages. In parallel, the consumption of brain protective and regenerative drugs has been expanding in the elderly population. We provide evidence in support of the idea that the consumption of medicines exerting antiaging properties may contribute to the increase in human longevity.
PubMed ID
15246996 View in PubMed
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Applicability of biological time temperature integrators as quality and safety indicators for meat products.

https://arctichealth.org/en/permalink/ahliterature146076
Source
Int J Food Microbiol. 2010 Mar 31;138(1-2):119-29
Publication Type
Article
Date
Mar-31-2010
Author
M. Ellouze
J-C Augustin
Author Affiliation
CRYOLOG SA Département R&D. 58, Nantes, France. mellouze@vet-alfort.fr
Source
Int J Food Microbiol. 2010 Mar 31;138(1-2):119-29
Date
Mar-31-2010
Language
English
Publication Type
Article
Keywords
Animals
Colony Count, Microbial
Consumer Product Safety
Food Contamination - analysis - prevention & control
Food Microbiology
Food Packaging - methods
Food Preservation - methods
Humans
Listeria monocytogenes - growth & development
Meat Products - microbiology - standards
Oxygen - metabolism
Poultry Products - microbiology - standards
Salmonella - growth & development
Staphylococcus aureus - growth & development
Temperature
Time Factors
Abstract
The objective of this study was to evaluate (eO), a biological time temperature integrator (TTI) as a quality and safety indicator for ground beef packed under modified atmosphere and spiced cooked chicken slices packed under modified atmosphere. Storage trials and challenge tests were thus performed on several batches of the studied food to monitor and model the behavior of Listeria monocytogenes, Salmonella, Staphylococcus aureus and the indigenous food flora. Then, two different prototypes of the TTI (eO) were set and manufactured according to the studied products shelf lives. The TTI evolution with time at static and dynamic temperatures was monitored and modeled. Finally, exposure assessment models were set and used under several realistic storage profiles to assess the distributions of the concentration of the indigenous food flora and the distributions of the increase in the pathogens populations obtained at the end of the product shelf life or at the end point of the TTI, taking into account the TTIs batch variability. Results showed that in case of poor storage conditions, TTI can reduce the consumer exposure to altered or hazardous foods.
PubMed ID
20074826 View in PubMed
Less detail

Arctic ground squirrel resist peroxynitrite-mediated cell death in response to oxygen glucose deprivation.

https://arctichealth.org/en/permalink/ahliterature294918
Source
Free Radic Biol Med. 2017 12; 113:203-211
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Date
12-2017
Author
Saurav Bhowmick
Kelly L Drew
Author Affiliation
Department of Chemistry and Biochemistry, University of Alaska Fairbanks, Fairbanks, AK, USA; Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK, USA.
Source
Free Radic Biol Med. 2017 12; 113:203-211
Date
12-2017
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Keywords
Animals
Brain Injuries - etiology - metabolism - physiopathology
Cell Death
Disease Models, Animal
Female
Food Deprivation
Glucose - metabolism
Hippocampus - metabolism - physiopathology
Hypoxia-Ischemia, Brain - metabolism - physiopathology
Male
Nitrosative Stress
Oxidative Stress
Oxygen - metabolism
Peroxynitrous Acid - toxicity
Rats
Rats, Sprague-Dawley
Reperfusion Injury - complications
Sciuridae
Abstract
Cerebral ischemia-reperfusion (I/R) injury initiates a cascade of events, generating nitric oxide (NO) and superoxide(O2•-) to form peroxynitrite (ONOO-), a potent oxidant. Arctic ground squirrels (AGS; Urocitellus parryii) show high tolerance to I/R injury. However, the underlying mechanism remains elusive. We hypothesize that tolerance to I/R modeled in an acute hippocampal slice preparation in AGS is modulated by reduced oxidative and nitrative stress. Hippocampal slices (400µm) from rat and AGS were subjected to oxygen glucose deprivation (OGD) using a novel microperfusion technique. Slices were exposed to NO, O2.- donors with and without OGD; pretreatment with inhibitors of NO, O2.- and ONOO- followed by OGD. Perfusates collected every 15min were analyzed for LDH release, a marker of cell death. 3-nitrotyrosine (3NT) and 4-hydroxynonenal (4HNE) were measured to assess oxidative and nitrative stress. Results show that NO/O2.- alone is not sufficient to cause ischemic-like cell death, but with OGD enhances cell death more in rat than in AGS. A NOS inhibitor, SOD mimetic and ONOO- inhibitor attenuates OGD injury in rat but has no effect in AGS. Rats also show a higher level of 3NT and 4HNE with OGD than AGS suggesting the greater level of injury in rat is via formation of ONOO-.
Notes
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