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Robert S Kern,
Roberto Zarate,
Shirley M Glynn,
Luana R Turner, Kellie M Smith,
Sharon S Mitchell,
Deborah R Becker,
Robert E Drake,
Alex Kopelowicz,
Wendi Tovey,
Robert P Liberman
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ABSTRACT: Objective: The present demonstration project involved development of a training program designed to teach recovering consumers employed as peer advocates how to provide evidence-based supported employment services to consumers with severe mental illness. Methods: A training curriculum was developed to teach the core competencies of the Individual Placement and Support (IPS) model of supported employment. Three peers participated in training and provided work outcome data from their caseloads. Assessments were conducted of peers' competence in implementing IPS and effectiveness in promoting job placements. Peer competency was assessed by the following: (a) a formal IPS fidelity review performed by two external reviewers to evaluate service implementation, and (b) the Kansas Employment Specialist Job Performance Evaluation, an objective measure of employment specialist attitudes and skills. Program efficacy was assessed by examining the number of job placements and corresponding tenure. Results: The fidelity review revealed that peers met IPS standards of implementation on 7 of 14 items assessing service delivery. The Kansas scale results revealed attitudes to be a relative strength and job performance competency ratings fell in the average to above average range across skill areas assessed (e.g., vocational assessment, job development). Thirty-three percent of consumers from the peers' caseloads got competitive jobs; mean tenure was 26.1 weeks. Conclusions and Implications for Practice: This demonstration project provides a starting point for future efforts aimed at expanding the role of peers as providers of evidence-based mental health services and provides a measured degree of optimism that this is a realistic, attainable goal. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
Psychiatric Rehabilitation Journal 06/2013; 36(2):99-107. · 0.75 Impact Factor
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Craig S Nunemaker,
Meng Chen,
Hong Pei,
Sarah D Kimble,
Susanna R Keller,
Jeffrey D Carter,
Zandong Yang, Kellie M Smith,
Runpei Wu,
Melissa H Bevard,
James C Garmey,
Jerry L Nadler
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ABSTRACT: Inflammation is a key pathological process in the progression of atherosclerosis and type 2 diabetes. 12/15-lipoxygenase (12-LO), an enzyme involved in fatty acid metabolism, may contribute to inflammatory damage triggered by stressors such as obesity and insulin resistance. We hypothesized that mice lacking 12-LO are protected against inflammatory-mediated damage associated with a "western" diet. To test this hypothesis, age-matched male 12-LO knockout (12-LOKO) and wild-type C57BL/6 (B6) mice were fed either a standard chow or western diet and assessed for several inflammatory markers. Western-fed B6 mice showed expected reductions in glucose and insulin tolerance compared with chow-fed mice. In contrast, western-fed 12-LOKO mice maintained glucose and insulin tolerance similar to chow-fed mice. Circulating proinflammatory cytokines, tumor necrosis factor-alpha and interleukin-6, were increased in western B6 mice but not 12-LOKO mice, whereas the reported protective adipokine, adiponectin, was decreased only in western B6 mice. 12-LO activity was significantly elevated by western diet in islets from B6 mice. Islets from 12-LOKO mice did not show western-diet-induced islet hyperplasia or increases in caspase-3 apoptotic staining observed in western-fed B6 mice. Islets from 12-LOKO mice were also protected from reduced glucose-stimulated insulin secretion observed in islets from western-fed B6 mice. In visceral fat, macrophage numbers and monocyte chemoattractant protein-1 expression were elevated in western B6 mice but not 12-LOKO mice. These data suggest that 12-LO activation plays a role in western-diet-induced damage in visceral fat and islets. Inhibiting 12-LO may provide a new therapeutic approach to prevent inflammation-mediated metabolic consequences of excess fat intake.
AJP Endocrinology and Metabolism 10/2008; 295(5):E1065-75. · 4.75 Impact Factor
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ABSTRACT: Protection of transplanted pancreatic islet grafts in recipients with autoimmune diabetes depends on the suppression of autoimmune recurrence and allogeneic rejection. The aim of this study was to investigate the efficiency of viral IL-10 gene delivery in the prevention of autoimmune recurrence following islet transplantation. We evaluated the effectiveness of a systemically delivered adeno-associated viral vector (AAV vIL-10) carrying viral IL-10 in protecting islet engraftment. We observed significant prolongation of graft survival after treatment with AAV vIL-10 when using islets from donors lacking autoimmunity. We found that the mechanism of vIL-10-mediated protection was associated with suppression of T cell activation and that donor immune cells that were simultaneously transferred with the islet grafts could induce autoimmune recurrence. AAV vIL-10 gene transfer suppressed previously activated T cells and protected grafted islets from autoimmune-mediated destruction. We conclude that vIL-10 can regulate autoimmune activity and that transfer of its gene may have potential for therapeutic islet transplantation.
Molecular Therapy 09/2005; 12(2):360-8. · 6.87 Impact Factor
