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124 results on '"McGehee, Robert E."'

1. Outcomes of the UAMS Summer Undergraduate Research Program to Increase Diversity in Research and Health Professions

Author

Prince, Latrina Y., Williams, Tremaine B., Allen, Antino R., McGehee, Robert E., and Thomas, Billy R.

Abstract

The University of Arkansas for Medical Sciences (UAMS) Summer Undergraduate Research Program (SURP) aims to increase diversity in research and health-related careers. The SURP provides underrepresented minority (URM) and disadvantaged students with research, mentoring, and networking experiences; real-life surgical observations; and simulated cardiovascular demonstrations. A postprogram survey was developed to assess program outcomes and explore ways of improving the program to stimulate URM and disadvantaged students' interest in research and health-related careers. This is a report of those postprogram survey findings. Using a survey research design, an online survey was emailed to participants (n = 88). Data were collected for 6 weeks beginning March 2020. There were 37 multiple-choice and open-ended questions regarding education, career choices, and program experiences. Responses were downloaded to statistical software for analyses. Quantitative data were analyzed using descriptive statistics. Major themes were identified for qualitative data. Responses were received from 44.3% (n = 39) of former SURP participants. Overall, 59% stated that the SURP influenced their career goals. When asked about mentor-mentee relationships, 69.3% responded that their interactions were excellent or good; 61.5% maintained contact with their mentor after the SURP. Finally, 79% indicated their SURP experience was excellent or good, and 84.6% would recommend the SURP to others. The SURP has been successful at providing URM and disadvantaged students with positive research experiences and long-term mentor-mentee relationships and has influenced educational and/or career goals. Programs that expose URM and disadvantaged students to basic, clinical, and/or translational research are beneficial for stimulating interest in research and health-related careers.

Published
2023
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5. Muscle inflammatory response and insulin resistance: synergistic interaction between macrophages and fatty acids leads to impaired insulin action

Author

Varma, Vijayalakshmi, Yao-Borengasser, Aiwei, Rasouli, Neda, Nolen, Greg T., Phanavanh, Bounleut, Starks, Tasha, Gurley, Cathy, Simpson, Pippa, McGehee, Robert E., Jr., Kern, Philip A., and Peterson, Charlotte A.

Subjects
Fatty acids -- Physiological aspects, Fatty acids -- Research, Macrophages -- Physiological aspects, Macrophages -- Research, Insulin resistance -- Research, Biological sciences
Abstract

Obesity is characterized by adipose tissue expansion as well as macrophage infiltration of adipose tissue. This results in an increase in circulating inflammatory cytokines and nonesterified fatty acids, factors that cause skeletal muscle insulin resistance. Whether obesity also results in skeletal muscle inflammation is not known. In this study, we quantified macrophages immunohistochemically in vastus lateralis biopsies from eight obese and eight lean subjects. Our study demonstrates that macrophages infiltrate skeletal muscle in obesity, and we developed an in vitro system to study this mechanistically. Myoblasts were isolated from vastus lateralis biopsies and differentiated in culture. Coculture of differentiated human myotubes with macrophages in the presence of palmitic acid, to mimic an obese environment, revealed that macrophages in the presence of palmitic acid synergistically augment cytokine and chemokine expression in myotubes, decrease I[kappa]B-[alpha] protein expression, increase phosphorylated JNK, decrease phosphorylated Akt, and increase markers of muscle atrophy. These results suggest that macrophages alter the inflammatory state of muscle cells in an obese milieu, inhibiting insulin signaling. Thus in obesity both adipose tissue and skeletal muscle inflammation may contribute to insulin resistance. muscle cells; inflammation

Published
2009

21. Regulation of Small Ubiquitin-Like Modifier-1, Nuclear Receptor Coreceptor, Histone Deacetylase 3, and Peroxisome Proliferator-Activated Receptor-γ in Human Adipose Tissue

Author

Finlin, Brian S., primary, Bodles-Brakhop, Angela M., additional, Yao-Borengasser, Aiwei, additional, Zhu, Beibei, additional, Starnes, Catherine P., additional, McGehee, Robert E., additional, Peterson, Charlotte A., additional, Kern, Philip A., additional, and Rasouli, Neda, additional

Published
2012
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25. Human Visfatin Expression: Relationship to Insulin Sensitivity, Intramyocellular Lipids, and Inflammation

Author

Varma, Vijayalakshmi, primary, Yao-Borengasser, Aiwei, additional, Rasouli, Neda, additional, Bodles, Angela M., additional, Phanavanh, Bounleut, additional, Lee, Mi-Jeong, additional, Starks, Tasha, additional, Kern, Leslie M., additional, Spencer, Horace J., additional, McGehee, Robert E., additional, Fried, Susan K., additional, and Kern, Philip A., additional

Published
2006
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47. Lipin expression is attenuated in adipose tissue of insulin-resistant human subjects and increases with peroxisome proliferator-activated receptor gamma activation.

Author

Yao-Borengasser A, Rasouli N, Varma V, Miles LM, Phanavanh B, Starks TN, Phan J, Spencer HJ 3rd, McGehee RE Jr, Reue K, Kern PA, Yao-Borengasser, Aiwei, Rasouli, Neda, Varma, Vijayalakshmi, Miles, Leslie M, Phanavanh, Bounleut, Starks, Tasha N, Phan, Jack, Spencer, Horace J 3rd, and McGehee, Robert E Jr

Subjects
PROTEIN metabolism, ADIPOSE tissues, INSULIN resistance, OBESITY, PROTEINS, RESEARCH funding, GLUCOSE intolerance, SKELETAL muscle, THIAZOLIDINEDIONES, PHARMACODYNAMICS
Abstract

Lipin-alpha and -beta are the alternatively spliced gene products of the Lpin1 gene, whose product lipin is required for adipocyte differentiation. Lipin deficiency causes lipodystrophy, fatty liver, and insulin resistance in mice, whereas adipose tissue lipin overexpression results in increased adiposity but improved insulin sensitivity. To assess lipin expression and its relation to insulin resistance in humans, we examined lipin-alpha and -beta mRNA levels in subjects with normal or impaired glucose tolerance. We found higher expression levels of both lipin isoforms in lean, insulin-sensitive subjects. When compared with normal glucose-tolerant subjects, individuals with impaired glucose tolerance were more insulin resistant, demonstrated higher levels of intramyocellular lipids (IMCLs), and expressed approximately 50% lower levels of lipin-alpha and -beta. In addition, there was a strong inverse correlation between adipose tissue lipin expression and muscle IMCLs but no evidence for an increase in muscle lipid oxidation. After treatment of the impaired glucose-tolerant subjects with insulin sensitizers for 10 weeks, pioglitazone (but not metformin) resulted in a 60% increase in the insulin sensitivity index (Si) and a 32% decrease in IMCLs (both P < 0.01), along with an increase in lipin-beta (but not lipin-alpha) expression by 200% (P < 0.005). Lipin expression in skeletal muscle, however, was not related to obesity or insulin resistance. Hence, high adipose tissue lipin expression is found in insulin-sensitive subjects, and lipin-beta expression increases following treatment with pioglitazone. These results suggest that increased adipogenesis and/or lipogenesis in subcutaneous fat, mediated by the LPIN1 gene, may prevent lipotoxicity in muscle, leading to improved insulin sensitivity. [ABSTRACT FROM AUTHOR]

Published
2006
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