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Age trajectories of physiological indices in relation to healthy life course.

https://arctichealth.org/en/permalink/ahliterature101888
Source
Mech Ageing Dev. 2011 Mar;132(3):93-102
Publication Type
Article
Date
Mar-2011
Author
Konstantin G Arbeev
Svetlana V Ukraintseva
Igor Akushevich
Alexander M Kulminski
Liubov S Arbeeva
Lucy Akushevich
Irina V Culminskaya
Anatoliy I Yashin
Author Affiliation
Centre for Population Health and Aging, Duke University, Department of Sociology, Durham, NC 27708-0408, USA. konstantin.arbeev@duke.edu
Source
Mech Ageing Dev. 2011 Mar;132(3):93-102
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
Adult
Aging
Blood pressure
Cohort Studies
Female
Hematocrit
Humans
Life Style
Male
Middle Aged
Models, Biological
Sex Factors
Stress, Physiological
Abstract
We analysed relationship between the risk of onset of "unhealthy life" (defined as the onset of cancer, cardiovascular diseases, or diabetes) and longitudinal changes in body mass index, diastolic blood pressure, hematocrit, pulse pressure, pulse rate, and serum cholesterol in the Framingham Heart Study (Original Cohort) using the stochastic process model of human mortality and aging. The analyses demonstrate how decline in resistance to stresses and adaptive capacity accompanying human aging can be evaluated from longitudinal data. We showed how these components of the aging process, as well as deviation of the trajectories of physiological indices from those minimising the risk at respective ages, can lead to an increase in the risk of onset of unhealthy life with age. The results indicate the presence of substantial gender difference in aging related decline in stress resistance and adaptive capacity, which can contribute to differences in the shape of the sex-specific patterns of incidence rates of aging related diseases.
PubMed ID
21262255 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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Beta2-adrenergic receptor gene polymorphisms as systemic determinants of healthy aging in an evolutionary context.

https://arctichealth.org/en/permalink/ahliterature97315
Source
Mech Ageing Dev. 2010 May;131(5):338-45
Publication Type
Article
Date
May-2010
Author
Alexander M Kulminski
Irina Culminskaya
Svetlana V Ukraintseva
Konstantin G Arbeev
Kenneth C Land
Anatoli I Yashin
Author Affiliation
Center for Population Health and Aging, Duke University Population Research Institute, Durham, NC 27708, USA. ander.Kulminski@duke.edu
Source
Mech Ageing Dev. 2010 May;131(5):338-45
Date
May-2010
Language
English
Publication Type
Article
Abstract
The Gln(27)Glu polymorphism but not the Arg(16)Gly polymorphism of the beta2-adrenergic receptor (ADRB2) gene appears to be associated with a broad range of aging-associated phenotypes, including cancers at different sites, myocardial infarction (MI), intermittent claudication (IC), and overall/healthy longevity in the Framingham Heart Study Offspring cohort. The Gln(27)Gln genotype increases risks of cancer, MI and IC, whereas the Glu(27) allele or, equivalently, the Gly(16)Glu(27) haplotype tends to be protective against these diseases. Genetic associations with longevity are of opposite nature at young-old and oldest-old ages highlighting the phenomenon of antagonistic pleiotropy. The mechanism of antagonistic pleiotropy is associated with an evolutionary-driven advantage of carriers of a derived Gln(27) allele at younger ages and their survival disadvantage at older ages as a result of increased risks of cancer, MI and IC. The ADRB2 gene can play an important systemic role in healthy aging in evolutionary context that warrants exploration in other populations.
PubMed ID
20399803 View in PubMed
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Source
Ann N Y Acad Sci. 2004 Jun;1019:200-5
Publication Type
Article
Date
Jun-2004
Author
Svetlana V Ukraintseva
Anatoly I Yashina
Author Affiliation
Max Planck Institute for Demographic Research, Rostock, Germany. ukraintseva@cds.duke.edu
Source
Ann N Y Acad Sci. 2004 Jun;1019:200-5
Date
Jun-2004
Language
English
Publication Type
Article
Keywords
Aging
Animals
Apoptosis
Cell Aging
Down-Regulation
Genes, Tumor Suppressor
Humans
Neoplasms - metabolism - pathology
Oncogenes
Phenotype
Signal Transduction
Abstract
Comparative analysis of malignant and senescent cells shows that their phenotypic features are in many instances contrary. Cancer cells do not "age"; their metabolic and growth characteristics are opposite to those observed with cellular aging (both replicative and functional). In many such characteristics, cancer cells resemble embryonic cells. One can say that cancer manifests itself as a local uncontrolled "rejuvenation" in an organism. Available evidence from human and animal studies suggests that the opposite phenotypic features of aging and cancer arise from the opposite regulation of common genes, such as those participating in apoptosis/growth arrest or in growth signal transduction pathways in the cell. For instance, in aging cells and organisms, proto-oncogenes are often downregulated, while tumor suppressors are permanently expressed. In cancer cells the situation is just the opposite: the proto-oncogenes are commonly overexpressed, while tumor suppressors are downregulated. This fact may have various applications for the development of new antiaging and anticancer treatments. First, genes that are oppositely regulated in cancer and aging could be candidate targets for antiaging interventions. Their "cancerlike" regulation, if strictly controlled, might help to rejuvenate the aging organism. Recent evidence from human and animal studies in support of this view is discussed. Second, the fact that cancer cells do not "age" implies that these cells may have a survival advantage in the surrounding of senescent cells. This could be a partial reason for an increase in the risk of cancer with age, because the proportion of senescent cells increases in an organism with age, too. In such a situation, the rejuvenation of normal cells surrounding the tumor might be a perspective anticancer treatment. For instance, a controlled activation of oncogenes in normal host cells or the grafting of young proliferating cells (such as embryonic stem cells) in the area near a malignant tumor might help to supplant cancer cells rather than to kill them.
PubMed ID
15247014 View in PubMed
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Cancer in rodents: does it tell us about cancer in humans?

https://arctichealth.org/en/permalink/ahliterature16721
Source
Nat Rev Cancer. 2005 Oct;5(10):807-19
Publication Type
Article
Date
Oct-2005
Author
Vladimir N Anisimov
Svetlana V Ukraintseva
Anatoly I Yashin
Author Affiliation
Department of Carcinogenesis and Oncogerontology, N.N. Petrov Research Institute of Oncology, Pesochny-2, St. Petersburg 197758, Russia. aging@mail.ru
Source
Nat Rev Cancer. 2005 Oct;5(10):807-19
Date
Oct-2005
Language
English
Publication Type
Article
Keywords
Age Factors
Animals
Carcinogens - toxicity
Female
Humans
Incidence
Male
Mice
Neoplasm Regression, Spontaneous
Neoplasms - epidemiology - mortality - veterinary
Rats
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Rodent Diseases - epidemiology - mortality
Sex Characteristics
Species Specificity
Abstract
Information obtained from animal models (mostly mice and rats) has contributed substantially to the development of treatments for human cancers. However, important interspecies differences have to be taken into account when considering the mechanisms of cancer development and extrapolating the results from mice to humans. Comparative studies of cancer in humans and animal models mostly focus on genetic factors. This review discusses the bio-epidemiological aspects of cancer manifestation in humans and rodents that have been underrepresented in the literature.
PubMed ID
16195752 View in PubMed
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Dynamic determinants of longevity and exceptional health.

https://arctichealth.org/en/permalink/ahliterature100264
Source
Curr Gerontol Geriatr Res. 2010;
Publication Type
Article
Date
2010
Author
Anatoli I Yashin
Konstantin G Arbeev
Igor Akushevich
Liubov Arbeeva
Julia Kravchenko
Dora Il'yasova
Alexander Kulminski
Lucy Akushevich
Irina Culminskaya
Deqing Wu
Svetlana V Ukraintseva
Author Affiliation
Center for Population Health and Aging, Duke University, Durham, NC 27708, USA.
Source
Curr Gerontol Geriatr Res. 2010;
Date
2010
Language
English
Publication Type
Article
Abstract
It is well known from epidemiology that values of indices describing physiological state in a given age may influence human morbidity and mortality risks. Studies of connection between aging and life span suggest a possibility that dynamic properties of age trajectories of the physiological indices could also be important contributors to morbidity and mortality risks. In this paper we use data on longitudinal changes in body mass index, diastolic blood pressure, pulse pressure, pulse rate, blood glucose, hematocrit, and serum cholesterol in the Framingham Heart Study participants, to investigate this possibility in depth. We found that some of the variables describing individual dynamics of the age-associated changes in physiological indices influence human longevity and exceptional health more substantially than the variables describing physiological state. These newly identified variables are promising targets for prevention aiming to postpone onsets of common elderly diseases and increase longevity.
PubMed ID
20953403 View in PubMed
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Early hematopoiesis inhibition under chronic radiation exposure in humans.

https://arctichealth.org/en/permalink/ahliterature97559
Source
Radiat Environ Biophys. 2010 May;49(2):281-91
Publication Type
Article
Date
May-2010
Author
Alexander V Akleyev
Igor V Akushevich
Georgy P Dimov
Galina A Veremeyeva
Tatyana A Varfolomeyeva
Svetlana V Ukraintseva
Anatoly I Yashin
Author Affiliation
Clinical Department, Urals Research Center for Radiation Medicine, Chelyabinsk, Russia.
Source
Radiat Environ Biophys. 2010 May;49(2):281-91
Date
May-2010
Language
English
Publication Type
Article
Keywords
Blood Cell Count
Bone Marrow - physiology - radiation effects
Cell Line
Dose-Response Relationship, Radiation
Environmental Exposure - adverse effects
Female
Hematopoiesis - radiation effects
Humans
Leukocytes, Mononuclear - physiology - radiation effects
Male
Middle Aged
Radiation Dosage
Retrospective Studies
Time Factors
Abstract
The major goal of this study was to identify and quantitatively describe the association between the characteristics of chronic (low-dose rate) exposure to (low LET) ionizing radiation and cellularity of peripheral blood cell lines. About 3,200 hemograms (i.e., spectra of blood counts) obtained over the years of maximal exposure to ionizing radiation (1950-1956) for inhabitants of the Techa River were used in analyses. The mean cumulative red bone marrow dose (with standard errors), calculated using Techa River Dosimetry System-2000, was 333.6 +/- 4.6 mGy (SD = 259.9 mGy, max = 1151 mGy) to the year 1956. The statistical approach included both empirical methods for estimating frequencies of cytopenic states of the investigated blood cell lines (e.g. neutrophile, platelets, erythrocyte, etc.), and regression methods, including generalized linear models and logistic regressions which allowed taking into account confounding factors (e.g., attained age, age at maximal exposure, presence of concomitant diseases, and demographic characteristics). The results of the analyses demonstrated hematopoiesis inhibition manifested by a decrease in peripheral blood cellularity and an increase in the frequency of cytopenia in all blood cell lines (leukocytes, including lymphocytes, monocytes, neutrophiles, as well as platelets and erythrocytes). The intensity of hematopoiesis inhibition in the period of maximal exposures is determined by the combined influence of the dose rate and cumulative dose. The contribution of specific confounding factors was quantified and shown to be much less important than dose characteristics. The best predictor among dose characteristics was identified for each blood cell line. A 2-fold increase in dose rate is assumed to be a characteristic of radiosensitivity and a quantitative characteristic of the effect.
PubMed ID
20340030 View in PubMed
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Early hematopoietic effects of chronic radiation exposure in humans.

https://arctichealth.org/en/permalink/ahliterature99269
Source
Health Phys. 2010 Sep;99(3):330-6
Publication Type
Article
Date
Sep-2010
Author
Alexander V Akleyev
Igor V Akushevich
Georgy P Dimov
Galina A Veremeyeva
Tatyana A Varfolomeyeva
Svetlana V Ukraintseva
Anatoly I Yashin
Author Affiliation
Urals Research Center for Radiation Medicine (URCRM), 68-a Vorovsky Street, 454076, Chelyabinsk, Russia.
Source
Health Phys. 2010 Sep;99(3):330-6
Date
Sep-2010
Language
English
Publication Type
Article
Abstract
The major goal of this study is to investigate and quantitatively describe the nature of the relationship between the characteristics of chronic exposure to ionizing radiation and specific patterns of hematopoiesis reduction. The study is based on about 3,200 hemograms taken for inhabitants of the Techa riverside villages over the years 1951-1956, i.e., the period characterized by a gradual decrease in dose rates. The mean cumulative red bone marrow dose was 333.6 + or - 4.6 mGy. The approach to statistical analyses involved both empirical methods and modeling (generalized linear models and logistic regressions). The results of the analyses highlighted a gradual increase in the frequency of cytopenias with dose rate. The impact of exposure on hematopoiesis reduction patterns was found to be more substantial than that of age and health status. Dose rates resulting in a two-fold increase in the frequency of cytopenias have been estimated.
PubMed ID
20699694 View in PubMed
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Effects of phentermine and phenformin on biomarkers of aging in rats.

https://arctichealth.org/en/permalink/ahliterature61509
Source
Gerontology. 2005 Jan-Feb;51(1):19-28
Publication Type
Article
Author
Vladimir N Anisimov
Svetlana V Ukraintseva
Ivan V Anikin
Irina G Popovich
Mark A Zabezhinski
Lev M Bertsein
Alexander V Arutjunyan
Donald K Ingram
Mark A Lane
George S Roth
Author Affiliation
N.N. Petrov Research Institute of Oncology, D.O. Ott Research Institute of Obstetrics and Gynecology, St. Petersburg, Russia. aging@mail.ru
Source
Gerontology. 2005 Jan-Feb;51(1):19-28
Language
English
Publication Type
Article
Keywords
Aging - metabolism
Animals
Appetite Depressants - pharmacology
Body Temperature - drug effects - physiology
Body Weight - drug effects
Brain - drug effects - metabolism
Caloric Restriction
Comparative Study
Drinking - drug effects - physiology
Energy Intake - drug effects
Female
Hypoglycemic Agents - pharmacology
Liver - drug effects - metabolism
Models, Animal
Phenformin - pharmacology
Phentermine - pharmacology
Random Allocation
Rats
Rats, Wistar
Abstract
BACKGROUND: Caloric restriction (CR) is the only treatment known to substantially prolong both average and maximal life span in experimental animals. Interventions that mimic certain effects of CR could be potential anti-aging treatments in humans. Drugs which reduce appetite (anorexiants) represent one class of candidate treatments. Agents that reduce the glucose utilization by the organism could also represent another class of candidate CR mimetics. OBJECTIVE: In our study, we addressed the following questions: (1) Does treatment with an anorexiant reduce caloric intake and body weight of experimental animals comparable to that caused by CR? (2) Does treatment with an antidiabetic agent influence caloric intake and body weight? (3) Does treatment with any of these drugs affect metabolic parameters of an organism in the way similar to that observed with CR? Methods: One hundred and twenty 6-month-old female Wistar-derived LIO rats were randomly subdivided into four groups and exposed to: (1) ad libitum feeding with placebo (controls); (2) the antidiabetic drug phenformin (2 mg/kg); (3) the anorectic drug phentermine (1 mg/kg), and (4) the same amount of food as the group with the least food intake during the previous week (pair-fed controls). Food and water intake, body weight, and rectal temperature were measured weekly during 16 weeks. At the end of the 16th week of the experiment, serum levels of glucose, total beta-lipoprotein and pre-beta-lipoprotein fractions, cholesterol, triglycerides, insulin, total triiodothyronine, and free thyroxine were estimated. The contents of diene conjugates and Schiff's bases, total antioxidant activity, the activities of Cu/Zn superoxide dismutase, glutathione S-transferase, and glutathione peroxidase, and the generation of reactive oxygen species (ROS) were studied in brain and liver homogenates and in the serum. RESULTS: The controls exposed to pair feeding had a significantly reduced food consumption (about 20%) as compared with the ad libitum fed controls and thus exhibited a moderate CR. Treatment with phentermine reduced the caloric intake by about 12% as compared with the ad libitum fed controls. Body weight and water intake in this group were only slightly decreased (by about 2 and 5%, respectively) as compared with the controls. The mean rectal temperature in the phentermine group (38 degrees C) was significantly higher than in the ad libitum fed (37.8 degrees C) and pair-fed (37.6 degrees C) controls. Treatment with phentermine also resulted in significantly reduced ROS levels in all tissues studied, while the highest ROS production was found in ad libitum (blood serum) and pair-fed (brain) controls. Treatment with phenformin did not significantly influence food and water consumption, body weight, and temperature when compared with the ad libitum fed controls. Rats treated with this antidiabetic drug showed intermediate values of ROS generation. Differences among the groups in total antioxidant activity were not obvious. CONCLUSIONS: Treatment with phentermine reduces caloric intake slightly less than is commonly observed in CR studies. CR due to forcibly reduced feeding and CR due to substance-suppressed appetite appear to act through different metabolic mechanisms and thus may affect aging and longevity in different ways.
PubMed ID
15591752 View in PubMed
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Evaluation of genotype-specific survival using joint analysis of genetic and non-genetic subsamples of longitudinal data.

https://arctichealth.org/en/permalink/ahliterature99755
Source
Biogerontology. 2010 Dec 31;
Publication Type
Article
Date
Dec-31-2010
Author
Konstantin G Arbeev
Svetlana V Ukraintseva
Liubov S Arbeeva
Igor Akushevich
Alexander M Kulminski
Anatoliy I Yashin
Author Affiliation
Center for Population Health and Aging, Duke University, Trent Hall, Room 002, Box 90408, Durham, NC, 27708-0408, USA, konstantin.arbeev@duke.edu.
Source
Biogerontology. 2010 Dec 31;
Date
Dec-31-2010
Language
English
Publication Type
Article
Abstract
Small sample size of genetic data is often a limiting factor for desirable accuracy of estimated genetic effects on age-specific risks and survival. Longitudinal non-genetic data containing information on survival or disease onsets of study participants for whom the genetic data were not collected may provide an additional "reserve" for increasing the accuracy of respective estimates. We present a novel method for joint analyses of "genetic" (covering individuals for whom both genetic information and mortality/morbidity data are available) and "non-genetic" (covering individuals for whom only mortality/morbidity data were collected) subsamples of longitudinal data. Our simulation studies show substantial increase in the accuracy of estimates in such joint analyses compared to analyses based on genetic subsample alone. Application of this method to analysis of the effect of common apolipoprotein E (APOE) polymorphism on survival using combined genetic and non-genetic subsamples of the Framingham Heart Study original cohort data showed that female, but not male, carriers of the APOE e4 allele have significantly worse survival than non-carriers, whereas empirical analyses did not produce any significant results for either sex.
PubMed ID
21193960 View in PubMed
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18 records – page 1 of 2.