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Search Results: 1 - 10 of 225972 matches for " James L. Searcy "
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Impact of Age on the Cerebrovascular Proteomes of Wild-Type and Tg-SwDI Mice
James L. Searcy, Thierry Le Bihan, Natalia Salvadores, James McCulloch, Karen Horsburgh
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089970
Abstract: The structural integrity of cerebral vessels is compromised during ageing. Abnormal amyloid (Aβ) deposition in the vasculature can accelerate age-related pathologies. The cerebrovascular response associated with ageing and microvascular Aβ deposition was defined using quantitative label-free shotgun proteomic analysis. Over 650 proteins were quantified in vessel-enriched fractions from the brains of 3 and 9 month-old wild-type (WT) and Tg-SwDI mice. Sixty-five proteins were significantly increased in older WT animals and included several basement membrane proteins (nidogen-1, basement membrane-specific heparan sulfate proteoglycan core protein, laminin subunit gamma-1 precursor and collagen alpha-2(IV) chain preproprotein). Twenty-four proteins were increased and twenty-one decreased in older Tg-SwDI mice. Of these, increases in Apolipoprotein E (APOE) and high temperature requirement serine protease-1 (HTRA1) and decreases in spliceosome and RNA-binding proteins were the most prominent. Only six shared proteins were altered in both 9-month old WT and Tg-SwDI animals. The age-related proteomic response in the cerebrovasculature was distinctly different in the presence of microvascular Aβ deposition. Proteins found differentially expressed within the WT and Tg-SwDI animals give greater insight to the mechanisms behind age-related cerebrovascular dysfunction and pathologies and may provide novel therapeutic targets.
Deep Sleep and Parietal Cortex Gene Expression Changes Are Related to Cognitive Deficits with Age
Heather M. Buechel,Jelena Popovic,James L. Searcy,Nada M. Porter,Olivier Thibault,Eric M. Blalock
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018387
Abstract: Age-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption's well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep's relationship to cognitive aging.
Reversal of Glial and Neurovascular Markers of Unhealthy Brain Aging by Exercise in Middle-Aged Female Mice
Caitlin S. Latimer, James L. Searcy, Michael T. Bridges, Lawrence D. Brewer, Jelena Popovi?, Eric M. Blalock, Philip W. Landfield, Olivier Thibault, Nada M. Porter
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026812
Abstract: Healthy brain aging and cognitive function are promoted by exercise. The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance neurogenesis, neuronal morphology and/or neurotrophin release. However, the brain is also composed of glial and vascular elements, and comparatively less is known regarding the effects of exercise on these components in the aging brain. Here, we show that aerobic exercise at mid-age decreased markers of unhealthy brain aging including astrocyte hypertrophy, a hallmark of brain aging. Middle-aged female mice were assigned to a sedentary group or provided a running wheel for six weeks. Exercise decreased hippocampal astrocyte and myelin markers of aging but increased VEGF, a marker of angiogenesis. Brain vascular casts revealed exercise-induced structural modifications associated with improved endothelial function in the periphery. Our results suggest that age-related astrocyte hypertrophy/reactivity and myelin dysregulation are aggravated by a sedentary lifestyle and accompanying reductions in vascular function. However, these effects appear reversible with exercise initiated at mid-age. As this period of the lifespan coincides with the appearance of multiple markers of brain aging, including initial signs of cognitive decline, it may represent a window of opportunity for intervention as the brain appears to still possess significant vascular plasticity. These results may also have particular implications for aging females who are more susceptible than males to certain risk factors which contribute to vascular aging.
Effects of Long-Term Pioglitazone Treatment on Peripheral and Central Markers of Aging
Eric M. Blalock,Jeremiah T. Phelps,Tristano Pancani,James L. Searcy,Katie L. Anderson,John C. Gant,Jelena Popovic,Margarita G. Avdiushko,Don A. Cohen,Kuey-Chu Chen,Nada M. Porter,Olivier Thibault
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010405
Abstract: Thiazolidinediones (TZDs) activate peroxisome proliferator-activated receptor gamma (PPARγ) and are used clinically to help restore peripheral insulin sensitivity in Type 2 diabetes (T2DM). Interestingly, long-term treatment of mouse models of Alzheimer's disease (AD) with TZDs also has been shown to reduce several well-established brain biomarkers of AD including inflammation, oxidative stress and Aβ accumulation. While TZD's actions in AD models help to elucidate the mechanisms underlying their potentially beneficial effects in AD patients, little is known about the functional consequences of TZDs in animal models of normal aging. Because aging is a common risk factor for both AD and T2DM, we investigated whether the TZD, pioglitazone could alter brain aging under non-pathological conditions.
Profile: Linda Searcy Howard
Linda Searcy Howard
Partnership : the Canadian Journal of Library and Information Practice and Research , 2011,
Planning Office and Community Influence on Land-Use Decisions Intended to Benefit the Low-Income: Welcome to Chicago
Yan Dominic Searcy
Urban Studies Research , 2014, DOI: 10.1155/2014/146390
Abstract: This study explores urban planning office and community influence on land-use decision making in two poverty-stricken but redeveloping neighborhood areas in Chicago. The Department of Planning and Development in this study had marginal impact on land-use decisions due to administrative limitations. Community influence is moderated by the degree to which low-income housing advocates can act directly as developers and produce housing units. The research findings indicate that land-use decisions intended to benefit the low-income resulted not from community-based political conflict but more so from community organization cooperation with political actors. 1. Purpose of the Study Much of the literature on poverty focuses on federal level initiatives as a response to urban poverty, seeming to ignore local level political processes. Researchers have tended to accept Peterson’s [1] contention that cities will not redistribute their own resources and that actual redistribution, utilizing monies from taxes from upper income groups to support initiatives that benefit lower income groups, can only occur with federal assistance [2, 3]. As a result, scarce attention has been given to policy efforts that utilize local resources that are intended to address urban poverty. A few researchers, mainly urban planners, suggested that it is possible to address poverty at the local level but offered little substantiation of what could be done or what was done [4–7]. Urban planning researchers Mayer [4], Pierre [5], and Wong [6] suggest that planning offices and community involvement can influence local policy decisions so that they benefit low-income urban residents. The researchers also suggest political conditions which may allow for policy innovations that can be couched in technical and bureaucratic processes that may yield potential benefits for low-income residents. However, missing from the literature are examinations of instances of planning office and community influence on the use of local resources to address urban poverty. Broadly, this study explores a local policy effort that utilized land as a local resource with the stated intention to address urban and neighborhood-based poverty. Specifically, the study (1) examines to what degree and under what conditions the Chicago Department of Urban Planning and communities influenced decision making regarding land use for low-income residents through an analysis of two neighborhood areas in Chicago from 1990–1997. The hypothesis proffered is that community-based political conflict would be the factor that influenced the
The Discrete Agglomeration Model: Equivalent Problems  [PDF]
James L. Moseley
Applied Mathematics (AM) , 2012, DOI: 10.4236/am.2012.311236
Abstract: In this paper we develop equivalent problems for the Discrete Agglomeration Model in the continuous context.
Uptake of Cystatin by Melanoma Cells in Culture  [PDF]
Lauren Deady, James L. Cox
CellBio (CellBio) , 2013, DOI: 10.4236/cellbio.2013.22008

The cystatins are a super family of cysteine protease inhibitors which are ubiquitous in their biologic occurrence. Cystatin C, a type II cystatin, is primarily a secreted protein found in most biological fluids. Besides acting as inhibitors of cathepsin, the cystatins have been found to have some non-inhibitor related functions and multiple physiological roles. Much interest has been generated for the cystatins as metastasissuppressor-like proteins, as they have been shown to inhibit metastasis for multiple cancer types. The sites and actions of the cystatins related to tumor suppressor actions are still unclear, however. In this work, we have examined the uptake of cystatin by metastatic melanoma cells in culture. Our results indicate cystatin uptake is mediated by a non-canonical endocytotic pathway in B16 murine melanoma cells.

In-Vitro Effect of Sex Steroids on Mouse Melanoma (B16F10) Cell Growth  [PDF]
Pandurangan Ramaraj, James L. Cox
CellBio (CellBio) , 2014, DOI: 10.4236/cellbio.2014.32007
A battery of sex steroids were used to check their effect on mouse melanoma (B16F10) cell growth in-vitro. Progesterone and its synthetic receptor antagonist RU-486 showed maximum inhibition on in-vitro melanoma cell growth [1]. Further research work showed that the inhibition by progesterone was not a toxic, spurious or non-specific effect on mouse melanoma cell growth and the inhibition by progesterone was not mediated through progesterone receptor.
In-Vitro Determination of Biological and Anabolic Functions of Weak Androgen Dehydroepiandrosterone (DHEA) Using a Variety of Cell Lines  [PDF]
James L. Cox, Yingzi Chang, Pandurangan Ramaraj
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2015, DOI: 10.4236/ojemd.2015.58014
Abstract: Dehydroepiandrosterone (DHEA) is a weak androgen and is shown to have anti-cancer, anti-atherogenic, anti-adipogenic and anti-inflammatory effects on mouse, rat and rabbit models. However, human clinical trials data did not support animal findings and were inconclusive. These systemic differences in biological actions between rodents and humans were attributed to the low level of DHEA in rodents. In order to further understand the differences in biological functions between rodents and humans, we resorted to an in-vitroapproach involving mouse, rat and human cell lines to assess DHEA biological and anabolic functions separately and independently without systemic influence. Results indicated that DHEA was effective on mouse and rat cell lines but not on human cell lines, as observed in in-vivo studies. In addition, our in-vitrostudy showed that DHEA was able to induce myogenesis in mouse mesenchymal cells revealing its anabolic function, even though DHEA was considered as a weak androgen. This observation lent credence to the ban on DHEA by IOC medical commission, citing DHEA as an anabolic steroid. These in-vitro experiments suggested that the differences in biological actions of DHEA between rodents and humans existed not only in-vivo
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