National Institute on Aging

Baltimore, Maryland, United States

Departments View all

Laboratory of Clinical Investigation (LCI)
509
Total Impact Points
11
Members
Laboratory of Molecular Biology and Immunology (LMBI)
314
Total Impact Points
10
Members
Laboratory of Molecular Gerontology (LMG)
1,675
Total Impact Points
9
Members

Publication History View all

  • Source
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    ABSTRACT: Despite the advances in cancer medicine and the resultant 20% decline in cancer death rates for Americans since 1991, there remain distinct cancer health disparities among African Americans, Hispanics, Native Americans, and the those living in poverty. Minorities and the poor continue to bear the disproportionate burden of cancer, especially in terms of stage at diagnosis, incidence, and mortality. Cancer health disparities are persistent reminders that state-of-the-art cancer prevention, diagnosis, and treatment are not equally effective for and accessible to all Americans. The cancer prevention model must take into account the phenotype of accelerated aging associated with health disparities as well as the important interplay of biological and sociocultural factors that lead to disparate health outcomes. The building blocks of this prevention model will include interdisciplinary prevention modalities that encourage partnerships across medical and nonmedical entities, community-based participatory research, development of ethnically and racially diverse research cohorts, and full actualization of the prevention benefits outlined in the 2010 Patient Protection and Affordable Care Act. However, the most essential facet should be a thoughtful integration of cancer prevention and screening into prevention, screening, and disease management activities for hypertension and diabetes mellitus because these chronic medical illnesses have a substantial prevalence in populations at risk for cancer disparities and cause considerable comorbidity and likely complicate effective treatment and contribute to disproportionate cancer death rates.
    American journal of preventive medicine 03/2014; 46(3 Suppl 1):S87-97.
  • [show abstract] [hide abstract]
    ABSTRACT: Background: Accelerometers have emerged as a useful tool for measuring free-living physical activity in epidemiological studies. Validity of activity estimates depends on the assumption that measurements are equivalent for males and females while performing activities of the same intensity. The primary purpose of this study was to compare accelerometer count values in males and females undergoing a standardized 6-minute walk test. Methods: The study population was older adults (78.6 ± 4.1 years) from the AGES-Reykjavik Study (N = 319). Participants performed a 6-minute walk test at a self-selected fast pace while wearing an ActiGraph GT3X at the hip. Vertical axis counts·s-1 was the primary outcome. Covariates included walking speed, height, weight, BMI, waist circumference, femur length, and step length. Results: On average, males walked 7.2% faster than females (1.31 vs. 1.22 m·s-1, P < .001) and had 32.3% greater vertical axis counts·s-1 (54.6 vs. 39.4 counts·s-1, P < .001). Accounting for walking speed reduced the sex difference to 19.2% and accounting for step length further reduced the difference to 13.4% (P < .001). Conclusion: Vertical axis counts·s-1 were disproportionally greater in males even after adjustment for walking speed. This difference could confound free-living activity estimates.
    Journal of Physical Activity and Health 03/2014; 11(3):626-37.
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    ABSTRACT: Alzheimer's disease (AD) is a senile dementia with increased incidence in older subjects (age >65 years). One of the earliest markers of AD is oxidative DNA damage. Recently, it has been reported that preclinical AD patient brains show elevated levels of oxidative damage in both nuclear and mitochondrial nucleic acids. Moreover, different oxidative lesions in mitochondrial DNA are between 5- and 10-fold higher than in nuclear DNA in both control and AD postmortem brains. We previously showed that there is a significant loss of base excision repair (BER) components in whole tissue extracts of AD and mild cognitive impairment subjects relative to matched control subjects. However, comprehensive analysis of specific steps in BER levels in mitochondrial extracts of AD patient brains is not available. In this study, we mainly investigated various components of BER in mitochondrial extracts of AD and matched control postmortem brain samples. We found that the 5-hydroxyuracil incision and ligase activities are significantly lower in AD brains, whereas the uracil incision, abasic site cleavage, and deoxyribonucleotide triphosphate incorporation activities are normal in these samples.
    Neurobiology of aging 01/2014;

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    Baltimore, Maryland, United States
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Top publications last week by downloads

 
NeuroMolecular Medicine 02/2008; 10(2):128-40.
21 Downloads
 
Neurobiology of aging 12/2011; 32(12):2279-86.
20 Downloads

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