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Age as a risk factor for myocardial infarction in Leiden mutation carriers.

https://arctichealth.org/en/permalink/ahliterature204822
Source
Mol Genet Metab. 1998 Jun;64(2):155-7
Publication Type
Article
Date
Jun-1998
Author
S. Baranovskaya
S. Kudinov
E. Fomicheva
V. Vasina
D. Solovieva
V. Khavinson
E. Schwartz
Author Affiliation
Laboratory of Human Molecular Genetics, Petersburg Nuclear Physics Institute, St.Petersburg Area, 188350, Russia.
Source
Mol Genet Metab. 1998 Jun;64(2):155-7
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Aged
Aged, 80 and over
Aging - genetics - pathology
Alleles
Child
Data Interpretation, Statistical
Drug resistance
Factor V - genetics
Gene Frequency
Heterozygote
Homozygote
Humans
Middle Aged
Mutation - genetics
Myocardial Infarction - epidemiology - genetics
Protein C - pharmacology
Risk factors
Russia - epidemiology
Abstract
A single factor V gene G-A mutation (Arg506Gln) underlying activated protein C (APC) resistance is a common risk factor for venous thromboembolism. It is still unclear whether the factor V Leiden predisposes patients to arterial thrombosis and myocardial infarction (MI). To determine a correlation between the factor V Leiden mutation and MI in different age categories, DNA samples from 287 patients with "early" and "late" MI were investigated. As control groups 373 young subjects (mean age 11 years) and 110 elderly ones (mean age 80 years) were studied. We found a significant difference in mutant allele distribution in the "late" MI group compared to the "early" MI group (chi2 = 9.86, OR = 13,7, P
PubMed ID
9705241 View in PubMed
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Age, Gene/Environment Susceptibility-Reykjavik Study: multidisciplinary applied phenomics.

https://arctichealth.org/en/permalink/ahliterature78517
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Publication Type
Article
Date
May-1-2007
Author
Harris Tamara B
Launer Lenore J
Eiriksdottir Gudny
Kjartansson Olafur
Jonsson Palmi V
Sigurdsson Gunnar
Thorgeirsson Gudmundur
Aspelund Thor
Garcia Melissa E
Cotch Mary Frances
Hoffman Howard J
Gudnason Vilmundur
Author Affiliation
Laboratory of Epidemiology, Demography, and Biometry, Intramural Research Program, National Institute on Aging, Bethesda, MD 20892-9205, USA. Harris99@mail.nih.gov
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Date
May-1-2007
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Aging - genetics - pathology
Body Composition
Cardiovascular Diseases - epidemiology - genetics
Chronic Disease
Dementia - epidemiology - genetics
Disease Susceptibility
Environment
Female
Genotype
Geriatrics
Health Status Indicators
Humans
Iceland - epidemiology
Male
Osteoporosis - epidemiology - genetics
Phenotype
Questionnaires
Risk Assessment - methods
Risk factors
Variation (Genetics)
Abstract
In anticipation of the sequencing of the human genome and description of the human proteome, the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik) was initiated in 2002. AGES-Reykjavik was designed to examine risk factors, including genetic susceptibility and gene/environment interaction, in relation to disease and disability in old age. The study is multidisciplinary, providing detailed phenotypes related to the cardiovascular, neurocognitive (including sensory), and musculoskeletal systems, and to body composition and metabolic regulation. Relevant quantitative traits, subclinical indicators of disease, and medical diagnoses are identified by using biomarkers, imaging, and other physiologic indicators. The AGES-Reykjavik sample is drawn from an established population-based cohort, the Reykjavik Study. This cohort of men and women born between 1907 and 1935 has been followed in Iceland since 1967 by the Icelandic Heart Association. The AGES-Reykjavik cohort, with cardiovascular risk factor assessments earlier in life and detailed late-life phenotypes of quantitative traits, will create a comprehensive study of aging nested in a relatively genetically homogeneous older population. This approach should facilitate identification of genetic factors that contribute to healthy aging as well as the chronic conditions common in old age.
PubMed ID
17351290 View in PubMed
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[Age-related and clinical-pathogenetic features of colorectal cancer associated with status of K-ras gene].

https://arctichealth.org/en/permalink/ahliterature123353
Source
Adv Gerontol. 2012;25(1):72-8
Publication Type
Article
Date
2012
Author
A V Beliaeva
G A Ianus
E N Suspithyn
O A Zaitseva
O S Iatsuk
A B Moiseenko
A V Guliaev
E N Imianitov
Source
Adv Gerontol. 2012;25(1):72-8
Date
2012
Language
Russian
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Aging - genetics - pathology
Colonic Neoplasms - epidemiology - genetics - pathology
Female
Genes, ras - genetics
Humans
Male
Middle Aged
Mutation
Mutation Rate
Polymerase Chain Reaction
Rectal Neoplasms - epidemiology - genetics - pathology
Russia
Abstract
Activating mutation in K-ras gene is a key event in the pathogenesis of colon carcinoma. This study analyses frequency of this mutation in different age groups of colorectal cancer patients residing in North-Western Russia, and examines its relationship with essential clinical characteristics of tumor disease.
PubMed ID
22708448 View in PubMed
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Age transcended: a semiotic and rhetorical analysis of the discourse of agelessness in North American anti-aging skin care advertisements.

https://arctichealth.org/en/permalink/ahliterature104666
Source
J Aging Stud. 2014 Apr;29:20-31
Publication Type
Article
Date
Apr-2014
Author
Kirsten L Ellison
Author Affiliation
Joint Graduate Program in Communication & Culture, 3013 TEL Centre, 88 Pond Rd., York University, 4700 Keele St., Toronto, ON M3J 1P3, Canada. Electronic address: klelliso@ucalgary.ca.
Source
J Aging Stud. 2014 Apr;29:20-31
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Adult
Advertising as Topic - methods - utilization
Aging - genetics - psychology
Attitude to Health
Beauty Culture - methods
Canada
Consumer Health Information - methods
Data Display
Humans
Middle Aged
Models, Psychological
Mythology - psychology
Self Concept
Skin Aging
Skin Care - methods
United States
Abstract
Drawing from a collection of over 160 North American print advertisements for anti-aging skin care products from January to December of 2009, this paper examines the discourse of agelessness, a vision of esthetic perfection and optimal health that is continually referred to by gerontologists, cultural theorists, and scientific researchers as a state of being to which humankind can aspire. Employing critical discourse analysis through the use of semiotics and visual rhetoric, this paper explores the means through which anti-aging skin care advertisements present to their viewers a particular object of desire, looking, more specifically, at how agelessness is presented as a way out and ultimate transcendence of age. Through the analytical tools of semiotics and visual rhetoric, four visions of agelessness are identified and explored in this paper: Agelessness as Scientific Purity, Agelessness as Genetic Impulse, Agelessness as Nature's Essence, and Agelessness as Myth. Whether found in the heights of scientific purity, the inner core of our genetic impulse, the depths of nature's essence, or whether agelessness itself has reached its own, untouchable, mythic status, the advertisements in this study represent one of the most pervasive vehicles through which our current vision(s) of ageless perfection are reflected, reinforced, and suspended in a drop of cream.
PubMed ID
24655670 View in PubMed
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Alterations of telomere length and DNA methylation in hairdressers: A cross-sectional study.

https://arctichealth.org/en/permalink/ahliterature274023
Source
Environ Mol Mutagen. 2016 Mar;57(2):159-67
Publication Type
Article
Date
Mar-2016
Author
Huiqi Li
Gabriella Åkerman
Carola Lidén
Ayman Alhamdow
Tomasz K Wojdacz
Karin Broberg
Maria Albin
Source
Environ Mol Mutagen. 2016 Mar;57(2):159-67
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Adult
Aging - genetics
Case-Control Studies
Cross-Sectional Studies
Cyclin-Dependent Kinase Inhibitor p16 - genetics
DNA Methylation
DNA Modification Methylases - genetics
DNA Repair Enzymes - genetics
Female
Glutathione S-Transferase pi - genetics
Humans
Middle Aged
Nuclear Proteins - genetics
Occupational Diseases - etiology
Occupational Exposure - adverse effects
Sweden
Telomere
Time Factors
Tumor Suppressor Proteins - genetics
Twist Transcription Factor - genetics
Young Adult
Abstract
Working as hairdressers has been associated with increased risk for cancer, particularly bladder cancer. To evaluate if current hairdressers have elevated risks of adverse health effects, we measured several biomarkers related to cancer-related DNA alterations. We enrolled 295 hairdressers and 92 non-hairdressers (all female non-smokers) from Stockholm and southern Sweden. Questionnaire data were collected for each participant, including work tasks for the hairdressers. We measured telomere length in peripheral blood leucocytes using quantitative PCR and DNA methylation status of genes relevant for bladder cancer using methylation sensitive high resolution melting analysis. The hairdressers had shorter telomeres (ß =?-0.069, P = 0.019) compared with non-hairdressers. Shorter telomeres were found in hairdressers up to 32 years old performing hair waving more than once per week as compared with hairdressers in the same age group performing hair waving less often (ß =?-0.12, P = 0.037). Hair waving was associated with less frequent CDKN2A methylation (odds ratio, OR = 0.19, P = 0.033). Shorter telomeres in hairdressers may indicate a genotoxic effect. Performing hair waving was associated with short telomere length, although the effect was only observed in young hairdressers. No clear patterns were discerned with regard to DNA methylation of bladder cancer-related genes. The observed changes of methylation were not all in the expected direction and warrant further investigation.
PubMed ID
26637967 View in PubMed
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An age-associated decrease in the frequency of C4B*Q0 indicates that null alleles of complement may affect health or survival.

https://arctichealth.org/en/permalink/ahliterature181004
Source
Ann N Y Acad Sci. 2003 Dec;1010:496-9
Publication Type
Article
Date
Dec-2003
Author
Gudmundur Jóhann Arason
Sigurdur Bödvarsson
Sigurudr Thor Sigurdarson
Gardar Sigurdsson
Gudmundur Thorgeirsson
Sveinn Gudmundsson
Judit Kramer
Georg Füst
Author Affiliation
Department of Immunology, Institute of Laboratory Medicine and Department of Medicine, Landspítali University Hospital, LSH Hringbraut, 101 Reykjavík, Iceland. garason@landspitali.is
Source
Ann N Y Acad Sci. 2003 Dec;1010:496-9
Date
Dec-2003
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Aging - genetics
Complement C3 - genetics
Complement C4b - genetics
Complement System Proteins - genetics
Gene Frequency
Genetic Variation
HLA-B Antigens - genetics
Health status
Humans
Iceland
Middle Aged
Survivors
Abstract
We studied the distribution of complement C4, C3, and factor B allotypes in 423 healthy Icelandic subjects from 17 to 89 years of age. A marked decrease was observed in the carrier frequency of variant alleles of complement C4B (C4B(*)Q0) and C3 (C3(*)F). These results confirm our previous observations on Hungarian subjects and suggest a negative effect of C4B(*)Q0 on health or survival.
PubMed ID
15033778 View in PubMed
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Anxiety trajectories in the second half of life: Genetic and environmental contributions over age.

https://arctichealth.org/en/permalink/ahliterature278402
Source
Psychol Aging. 2016 Feb;31(1):101-13
Publication Type
Article
Date
Feb-2016
Author
Lewina O Lee
Margaret Gatz
Nancy L Pedersen
Carol A Prescott
Source
Psychol Aging. 2016 Feb;31(1):101-13
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Aging - genetics - psychology
Anxiety - epidemiology - etiology - genetics
Anxiety Disorders - epidemiology - etiology - genetics
Biometry
Cohort Studies
Death
Environment
Female
Gene-Environment Interaction
Humans
Individuality
Life Change Events
Male
Middle Aged
Social Environment
Sweden - epidemiology
Twin Studies as Topic
Twins - genetics - psychology - statistics & numerical data
Abstract
Clinically significant anxiety symptoms are prevalent among the elderly, yet knowledge about the longitudinal course of anxiety symptoms in later life remains scarce. The goals of this study were to (a) characterize age trajectories of state anxiety symptoms in the second half of life, and (b) estimate genetic and environmental contributions to individual differences in the age trajectory of state anxiety. This study was based on data from 1,482 participants in the Swedish Adoption/Twin Study of Aging who were aged 50 and older at their first occasion (512 complete twin pairs, 458 singletons) and had up to 6 measurement occasions spanning 11 years. Consistent with life span developmental theories of age-related emotional change, anxiety symptom levels declined during the transition from midlife to the mid-60s, followed by a mild increase that gradually plateaued in the 80s. There were substantial individual differences in the age trajectory of anxiety. After accounting for effects of sex, cohort, mode of testing, and proximity to death, this longitudinal variation was partitioned into biometric sources. Nonshared environmental variance was highest in the late 60s and declined thereafter, whereas genetic variance increased at an accelerated pace from approximately age 60 onward. There was no evidence for effects of rearing or other shared environment on anxiety symptoms in later life. These findings highlight how the etiology of anxiety symptoms changes from midlife to old age.
Notes
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PubMed ID
26751006 View in PubMed
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APOE and cognitive decline in preclinical Alzheimer disease and non-demented aging.

https://arctichealth.org/en/permalink/ahliterature178421
Source
Neurology. 2004 Sep 14;63(5):816-21
Publication Type
Article
Date
Sep-14-2004
Author
D. Bunce
L. Fratiglioni
B J Small
B. Winblad
L. Bäckman
Author Affiliation
Department of Psychology, Goldsmiths College, University of London, London SE14 6NW, UK. d.bunce@gold.ac.uk
Source
Neurology. 2004 Sep 14;63(5):816-21
Date
Sep-14-2004
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - genetics - psychology
Alleles
Alzheimer Disease - epidemiology - genetics
Apolipoprotein E4
Apolipoproteins E - genetics - physiology
Cognition Disorders - epidemiology - genetics
Disease Progression
Female
Follow-Up Studies
Genetic Predisposition to Disease
Genotype
Humans
Male
Mental Status Schedule
Neurologic Examination
Neuropsychological Tests
Risk factors
Sampling Studies
Single-Blind Method
Sweden - epidemiology
Abstract
To investigate whether presence of the APOE epsilon4 allele is related to the pathologic progression of preclinical Alzheimer disease (AD), as reflected by change in Mini-Mental State Examination (MMSE) scores among persons in the preclinical phase of AD, and cognitively intact adults confirmed as dementia-free during the 6-year assessment period.
In a population-based sample, participants were stratified according to APOE genotype (epsilon4 or non-epsilon4) and whether they received a diagnosis of AD at the end of either a 3- or 6-year assessment period. Participants were aged 75 years and older, and were nondemented at baseline. At the end of the 3-year period, 17.2% of non-epsilon4 and 26.7% of epsilon4 carriers became demented. For the 6-year period those percentages were 11.2% for non-epsilon4 carriers and 16.9% for epsilon4-carriers.
Individuals in the preclinical phase of AD showed greater decline on the MMSE as compared to nondemented adults. However, the decline was most marked in the 3 years prior to clinical diagnosis. Further, APOE-epsilon4 genotype did not modify the rate of decline among to-be-demented participants, as well as individuals who would remain free of AD.
Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period. Further, in the absence of preclinical dementia, APOE did not influence global cognitive change in nondemented persons.
PubMed ID
15365129 View in PubMed
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124 records – page 1 of 13.