This is a competing renewal of NIH 5 T35 DK072923 which was originally funded for five years with 6 students supported/year. The principal objectives of the Summer Endocrine Research Training Program are to provide research experience for medical students and to stimulate interest among medical students in becoming clinical research scientists. Trainees engage in research activities with faculty members and participate in projects that are germane to the field of endocrinology and the health concerns of this country. Over the past 3 years, we have trained 18 second year medical students who participated in our """"""""Summer Endocrine Research Training Program"""""""" research programs in Endocrinology, Metabolism and Diabetes at University of Louisville School of Medicine and as this application is submitted, 6 new second year medical students will begin their summer research in this program. Approximately 25% of our trainees are members of minority populations and 1/3rd of trainees are female. Our program includes didactic instruction (""""""""Summer Endocrine Research Training Seminar Series"""""""" and """"""""Bench-to-Bedside: Introduction to Clinical Research"""""""") as well as a hands-on-research experience under the direction of a team of experienced basic and clinical research scientists centered on a core of NIDDK-funded investigators and collaborating faculty. Trainees also attend Endocrine-specific seminars and journal clubs in basic and clinical research. The present application addressses 2 Specific Aims:
Aim 1 : To provide hands-on training in basic and clinical Endocrine-based research to medical students in a structured mentored environment.
Aim 2 : To provide an interactive, educational experience that introduces medical students the fundamental skills necessary for basic, translational, and clinical Endocrine-based research. The T35 competing renewal funding will provide stipends for a 10-week summer program for 8-10 second year medical students. Our current T35 grant funds 6 students/year. Given the increase in training faculty mentors and NIDDK-funded research at the University of Louisville School of Medicine, documented within the text, we request funds to increase to 8 students/year in years 6 and 7 (Yr. one and two of the next funding period), 9 in years 8 and 9 (Yr. three and four of the next funding period, and 10 in year 10 (Yr. five of the next funding period).
This competing renewal T35 application directly addresses the NIH's goal of ensuring that a diverse pool of highly trained scientists are available in the field of Endocrinology to address the Nation's biomedical and clinical research needs.
|Ellingwood, Sara S; Cheng, Alan (2018) Biochemical and clinical aspects of glycogen storage diseases. J Endocrinol 238:R131-R141|
|Muluhngwi, Penn; Richardson, Kirsten; Napier, Joshua et al. (2017) Regulation of miR-29b-1/a transcription and identification of target mRNAs in CHO-K1 cells. Mol Cell Endocrinol 444:38-47|
|Muluhngwi, Penn; Krishna, Abirami; Vittitow, Stephany L et al. (2017) Tamoxifen differentially regulates miR-29b-1 and miR-29a expression depending on endocrine-sensitivity in breast cancer cells. Cancer Lett 388:230-238|
|Radde, Brandie N; Ivanova, Margarita M; Mai, Huy Xuan et al. (2016) Nuclear respiratory factor-1 and bioenergetics in tamoxifen-resistant breast cancer cells. Exp Cell Res 347:222-31|
|Kimbrough, Charles W; Lakshmanan, Jaganathan; Matheson, Paul J et al. (2015) Resveratrol decreases nitric oxide production by hepatocytes during inflammation. Surgery 158:1095-101; discussion 1101|
|Zhang, Baochun; Crankshaw, Will; Nesemeier, Ryan et al. (2015) Calcium-mediated signaling and calmodulin-dependent kinase regulate hepatocyte-inducible nitric oxide synthase expression. J Surg Res 193:795-801|
|Winters, Stephen J; Ghooray, Dushan T; Yang, Rong Q et al. (2014) Dopamine-2 receptor activation suppresses PACAP expression in gonadotrophs. Endocrinology 155:2647-57|
|Ivanova, Margarita M; Luken, Kristen H; Zimmer, Amber S et al. (2011) Tamoxifen increases nuclear respiratory factor 1 transcription by activating estrogen receptor beta and AP-1 recruitment to adjacent promoter binding sites. FASEB J 25:1402-16|
|Klinge, Carolyn M; Radde, Brandie N; Imbert-Fernandez, Yoannis et al. (2011) Targeting the intracellular MUC1 C-terminal domain inhibits proliferation and estrogen receptor transcriptional activity in lung adenocarcinoma cells. Mol Cancer Ther 10:2062-71|
|Klinge, Carolyn M; Riggs, Krista A; Wickramasinghe, Nalinie S et al. (2010) Estrogen receptor alpha 46 is reduced in tamoxifen resistant breast cancer cells and re-expression inhibits cell proliferation and estrogen receptor alpha 66-regulated target gene transcription. Mol Cell Endocrinol 323:268-76|