Browsing by Subject "arthritis"
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Item Arthritis impact on the physical function, disability, and health-related quality of life among older Mexican-Americans(2009-03-02) Saad M. Bindawas; Elizabeth J. Protas, P.T., Ph.D.; Yong-fang Kuo, Ph.D.; Soham Al Snih, M.D., Ph.D.; Kenneth J. Ottenbacher, O.T.R., Ph.D.; Dennis L. Hart, P.T., Ph.D.; Anita C. Mercado, M.D.Background and Purpose: Arthritis is a major cause of disability with a sizable impact on health-related quality of life (HRQoL) in older adults, especially among older non-Hispanic white subjects. The purpose of this study is to examine the relation between arthritis and its effects on the physical function, disability, and health-related quality of life, over time, among older Mexican-Americans, the fastest growing subset of the older population. \r\nDesign: A six-year prospective cohort study (2000 to 2006). Setting: Five Southwestern states: Texas, New Mexico, Colorado, Arizona, and California. \r\nParticipants: A population-based sample of 621 non-institutionalized Mexican-Americans aged 65 or older from wave four of the Hispanic Established Population for Epidemiologic Studies of the Elderly (Hispanic EPESE). \r\nMeasurements: Included sociodemographic variables, self-reported of: arthritis, pain on weight-bearing, activities of daily living (ADL), instrumental activities of daily living (IADL), physical and mental HRQoL, medical conditions, cognitive function and depressive symptoms. Lower and upper extremity muscles strength, lower body function test and body mass index (BMI) were also obtained. General linear mixed models and generalized estimating equations (GEE) were used to examine the time effect on: 1) each stage of the disablement process and 2) physical and mental HRQoL over three points of time (2000-2001, 2001-2002, and 2006). This study conforms to STROBE (STrengthening the Reporting of OBservational studies in Epidemiology) guidelines for cohort studies. \r\nResults: The results indicate 1) a significant association between arthritis and greater impairment (pain and poor muscle strength), functional limitation, disability (ADL and IADL), and physical HRQoL across time; and 2) a significant association between impairment, functional limitation, and IADL limitation with physical and mental HRQoL across time. Conclusions: In older Mexican-Americans, arthritis is a highly prevalent medical condition which significantly impacts physical function, daily activities, and physical HRQoL over time. In this cohort, impairment, functional limitation, and disability were associated with poorer physical and mental HRQoL. These findings could guide efforts in reaching the goals of the National Arthritis Action Plan, as well as the Healthy People 2010 initiative goals of increasing quality of life and eliminating health disparities in this segment of the older U.S. population.Item Effect of n-3 PUFAs on markers of inflammation in arthritic horses(2009-05-15) Manhart, Denise RaeSixteen horses with at least one arthritic joint were randomly divided into two groups. The control group (n=8) was fed a control ration at 1% BW in grain. The treatment group (n=8) was fed an isocaloric diet similar to the control diet with additional n-3 polyunsaturated fatty acids (PUFAs) in the form of two pelleted supplements. Coastal hay was fed free choice, and both groups consumed their respective diet for 90 days. On d 0, 30, 60, and 90 synovial fluid was collected from one arthritic joint on each horse, and blood samples were collected every 15 days. Synovial fluid was analyzed for Tumor Necrosis Factor-?, Interleukin-1, and white blood cell concentration, and plasma was analyzed for fibrinogen and Prostaglandin E2. Force plate analysis was used to determine changes in weight distribution throughout the trial. Fatty acid analysis revealed the main n3 supplied by the supplements was docosahexaenoic acid (C22:6n3). Treatment horses consumed 9.3 g docosahexaenoic acid daily, while control horses consumed only 0.42 g daily. A reduction in concentrate intake also allowed treatment horses to consume 25.45 g less of linoleic acid (C18:2n6)per day. Excluding hay, the n6:n3 ratio of the treatment diet was 5:1 compared to the control diet with a ratio of 11:1. Analysis of plasma fatty acid profiles revealed treatment horses experienced an increase in plasma docosahexaenoic acid, along with a decrease in linoleic acid (C18:2n6). Total plasma n6:n3 ratio of treatment horses was 23:1, as opposed to 27:1 in the control horses. Treatment horses had significantly lower synovial fluid white blood cell concentration and plasma Prostaglandin E2 (P < 0.05). A trend towards decreased fibrinogen (P = 0.076) was also seen in the treatment horses. Synovial fluid TNF-? and IL-1 concentrations were not obtained due to problems with the assay kits or procedures. Force plate data from seven horses was analyzed. No significant increase in weight placed on arthritic limbs (P = 0.12) was seen. This data provides further evidence that a decrease in the n6:n3 ratio of the diet and plasma can lead to a decrease in the production of inflammatory compounds in arthritic joints.Item Role of CGRP in the amygdala in pain-related synaptic plasticity and behavior(2005-11-02) Jeong Seok Han; Volker Neugebuaer, M.D, Ph.D.; William D. Willis, M.D., Ph.D.; Robert W. Gereau IV, Ph.D.; Melvyn S. Soloff, Ph.D.; Karin W. High, Ph.D.; Haring J.W Nauta, M.D., Ph.D.Pain has a strong emotional component. In particular, arthritic pain is closely related to affective disorders such as anxiety and depression. A key player in the emotional evaluation of sensory stimuli, the amygdala has been suggested as a neural substrate of the reciprocal relationship between pain and affect. Nociceptive information reaches the central nucleus of the amygdala (CeA) through the spino-parabrachio-amygdaloid pain pathway and spino-amygdaloid connections. Highly processed polymodal information from thalamo-cortical areas is transmitted to the CeA through the lateral and basolateral amygdaloid nuclei. Previous studies have shown that CeA neurons undergo significant neuroplastic changes in a model of arthritic pain. \r\nImportantly, high levels of calcitonin gene-related peptide (CGRP) are present in the CeA, most notably in the latero-capsular part (CeLC), which is now defined as the \"nociceptive amygdala\". The parabrachio-amygdaloid connection is essentially the exclusive source of CGRP in the CeA. The role of CGRP in pain processing has been studied mainly in peripheral tissues and in the spinal cord. However, information about CGRP function in the brain is still limited. Moreover, the role of neuropeptides in synaptic plasticity is less well understood than that of classical transmitters such as glutamate. \r\nThe present study determined the role of CGRP in the amygdala at the cellular and systems levels, using an integrative approach that combines patch-clamp recordings in brain slices in vitro and analysis of spinally (withdrawal reflexes) and supraspinally (vocalizations) organized behavior in awake animals. A well-established preclinical animal model of arthritic pain induced by kaolin and carrageenan was used. Our results show that selective CGRP1 receptor antagonists (CGRP8-37 and BIBN4096NS) in the CeLC reverse arthritis pain-related plasticity and behavior through a PKA-dependent postsynaptic mechanism that involves NMDA receptors. In addition, exogenous CGRP application in the CeLC in naive animals mimics pain-related synaptic plasticity and behavior. Selective inhibitors of PKA and MEK (ERK1/2), but not PKC, inhibit pain-related synaptic plasticity and behavior in arthritic animals and CGRP-induced synaptic plasticity and behavior in naive animals. \r\nThis work shows for the first time the importance of CGRP as a critical link between amygdala plasticity and pain behavior. The results provide direct evidence that CGRP receptor activation in the amygdala contributes to pain-related synaptic plasticity in the amygdala through a postsynaptic mechanism that involves PKA, ERK1/2 and NMDA receptors. This plasticity results in spinally and supraspinally organized pain behavior.\r\n