Publications by authors named "Jennifer E Phillips"

Background: Diabetes impacts 1 in 4 patients in the Veterans Health Administration and is associated with serious negative health consequences in addition to high health care system utilization and cost. The Cincinnati Veterans Affairs Medical Center developed Diabetes Basic Training, a 9-week intervention that blends medical consultation with group support and training in self-management strategies for enhancing patient motivation and empowerment.

Observations: Diabetes Basic Training combined 3 monthly shared medical appointments and 6 Diabetes Self-Management Program sessions led in part by trained peers with diabetes.

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The aim of this study is to examine existing research on social cognitive factors that may, in part, mediate the relationship between socioeconomic status (SES) and coronary heart disease (CHD). We focus on how social status is 'carried' in the mental systems of individuals, and how these systems differentially affect CHD risk and associated behaviors. To this end, literatures documenting the association of various social cognitive factors (e.

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Injuries to the growth plate remain a significant clinical challenge. The need to better understand mechanisms of growth disruption following transphyseal injuries and evaluate new therapeutic approaches to growth restoration motivates development of a well characterized model of growth plate injury. The goals of this study were to develop a growth plate defect model in the rat and to use microcomputed tomography (micro-CT) imaging to detect and quantify associated changes in growth plate morphology and mineralization over time following injury and in response to treatment.

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Objective: Objective indices of socioeconomic status (SES) predict diverse sources of morbidity and mortality as well as numerous biological and behavioral risk factors for disease. Here we examine whether subjective measures of SES may be similarly associated with measured risk factors including the metabolic syndrome and its components of elevated blood pressure, high fasting glucose, dyslipidemia, and central adiposity.

Methods: Observations were based on a community sample of 981 adults (30-54 years of age; 52% female; 84% white, 16% African American).

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Human mesenchymal stem cells (hMSCs) have tremendous potential as a cell source for regenerative medicine due to their capacity for differentiation into a wide range of connective tissue cell types. Although significant progress has been made in the identification of defined growth factor conditions to induce lineage commitment, the effect of underlying biomaterial properties on functional differentiation is far less understood. Here we conduct a systematic assessment of the role for surface chemistry on cell growth, morphology, gene expression and function during hMSC commitment along osteogenic, chondrogenic and adipogenic lineages.

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CTCF is a highly conserved zinc finger protein implicated in diverse regulatory functions, including transcriptional activation/repression, insulation, imprinting, and X chromosome inactivation. Here we re-evaluate data supporting these roles in the context of mechanistic insights provided by recent genome-wide studies and highlight evidence for CTCF-mediated intra- and interchromosomal contacts at several developmentally regulated genomic loci. These analyses support a primary role for CTCF in the global organization of chromatin architecture and suggest that CTCF may be a heritable component of an epigenetic system regulating the interplay between DNA methylation, higher-order chromatin structure, and lineage-specific gene expression.

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Growing evidence suggests that socioeconomic attributes of both childhood and adulthood confer risk for cardiovascular morbidity and mortality. In this study, we examine the association of both parental and individual educational attainment with C-reactive protein (CRP), an inflammatory mediator relevant to cardiovascular pathophysiology, in a mid-life community sample. Subjects were 811 men and women (394 men/417 women; 87% European-American/13% African-American), 30-54 years of age.

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Interfacial zones between tissues provide specialized, transitional junctions central to normal tissue function. Regenerative medicine strategies focused on multiple cell types and/or bi/tri-layered scaffolds do not provide continuously graded interfaces, severely limiting the integration and biological performance of engineered tissue substitutes. Inspired by the bone-soft tissue interface, we describe a biomaterial-mediated gene transfer strategy for spatially regulated genetic modification and differentiation of primary dermal fibroblasts within tissue-engineered constructs.

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Bone tissue engineering has emerged as a promising strategy for the repair of critical-sized skeletal fractures. However, the clinical application of this approach has been limited by the availability of a robust mineralizing cell source. Non-osteogenic cells, such as skin fibroblasts, are an attractive cell-source alternative because they are easy to harvest from autologous donor skin biopsies and display a high capacity for in vitro expansion.

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Cell-based bone tissue engineering strategies have been effectively applied toward the development of grafting templates for skeletal repair and regeneration, but remain limited by inadequate availability of a robust mineralizing cell source. Dermal fibroblasts have emerged as a particularly promising cell alternative because they are harvested from autologous donors through minimally invasive skin biopsy and display a high capacity for in vitro expansion. In the present study, we investigated retroviral gene delivery of the osteogenic transcription factor Runx2 as a mineralization induction strategy in primary dermal fibroblasts.

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The clinical challenges of skeletal regenerative medicine have motivated significant advances in cellular and tissue engineering in recent years. In particular, advances in molecular biology have provided the tools necessary for the design of gene-based strategies for skeletal tissue repair. Consequently, genetic engineering has emerged as a promising method to address the need for sustained and robust cellular differentiation and extracellular matrix production.

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Gene therapy has emerged as a promising strategy for the repair and regeneration of damaged musculoskeletal tissues. Application of this paradigm to bone healing has shown enhanced efficacy in preclinical animal studies compared to conventional bone grafting approaches. This review discusses current and emerging virus-based genetic engineering strategies for the delivery of therapeutic molecules which promote skeletal regeneration.

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Development of tissue-engineered constructs for skeletal regeneration of large critical-sized defects requires the identification of a sustained mineralizing cell source and careful optimization of scaffold architecture and surface properties. We have recently reported that Runx2-genetically engineered primary dermal fibroblasts express a mineralizing phenotype in monolayer culture, highlighting their potential as an autologous osteoblastic cell source which can be easily obtained in large quantities. The objective of the present study was to evaluate the osteogenic potential of Runx2-expressing fibroblasts when cultured in vitro on three commercially available scaffolds with divergent properties: fused deposition-modeled polycaprolactone (PCL), gas-foamed polylactide-co-glycolide (PLGA), and fibrous collagen disks.

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Glucocorticoid hormones have complex stimulatory and inhibitory effects on skeletal metabolism. Endogenous glucocorticoid signaling is required for normal bone formation in vivo, and synthetic glucocorticoids, such as dexamethasone, promote osteoblastic differentiation in several in vitro model systems. The mechanism by which these hormones induce osteogenesis remains poorly understood.

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