Dr. Ana A. Murphy is a professor in Gynecology and Obstetrics and Director of the Division of Reproductive Endocrinology and Infertility at Emory University School of Medicine. Dr. Murphy initiated, designed and implemented the Reproductive Endocrinology and Infertility Fellowship at Emory University that is currently approved by the American board of Obstetrics and Gynecology, Inc. Dr. Murphy became first Director in1997 and accepted her first fellow in 1998. The goal is to help the mentee became published and recognized and to achieve independent research support. The successful mentor must provide instruction on development of hypotheses that are original and worthwhile, the experimental tools to test the hypotheses, help the mentee identify a worthwhile field of investigation, and to remain focused. The line of research used to train the mentees will be the study of the pathophysiology of endometriosis and leiomyoma. She has demonstrated continued commitment to mentoring and training in patient-orientated research. The main focus of Dr. Murphy's research has been endometriosis, its pathophysiology as well as its surgical/medical treatment. Our hypothesis focuses on oxidative stress as the inciting agent that results in peritoneal fluid changes and activation of macrophages that mediate the infertility and pain seen in these patients. In the first year we have accumulated significant basic and clinical data in support of our hypothesis that a significant oxidative stress occurs in women with endometriosis. Recruitment for Aim 1 is complete and the data is being analyzed. Recruitment is underway for Aims 2,3. We have used RU486 as a biologic probe to study the in vivo regulation of endometrium and leiomyoma seen with low dose, in vivo. Preliminary data, has shown that leiomyoma and myometrium immunostain for glycodelin. In turn, glycodelin has been shown to decrease natural killer cell (NK cell) activity which is also decreased in women with leiomyoma. We hypothesize that RU486 has direct antiproliferative effect mediated by its antioxidant activity and an indirect immunomodulatory effect by decreasing glycodelin levels. Glycodelin may increase NK cell activity thus decreasing tumor growth.
|Park, John K; Song, MingQing; Dominguez, Celia E et al. (2006) Glycodelin mediates the increase in vascular endothelial growth factor in response to oxidative stress in the endometrium. Am J Obstet Gynecol 195:1772-7|
|Hayes, Ellen C; Dominguez, Celia E; Voelkel, Steven et al. (2006) Effect of glycodelin on the production of vascular endothelial growth factor in cumulus cells. Fertil Steril 85:1553-6|
|Ramachandran, Sumathi; Song, Ming Qing; Lowe, Erin et al. (2005) RU486 inhibits expression of lysophosphatidic acid induced glycodelin. Am J Obstet Gynecol 192:1285-93; discussion 1293-4|
|Richlin, Spencer S; Ramachandran, Sumathi; Shanti, Aida et al. (2002) Glycodelin levels in uterine flushings and in plasma of patients with leiomyomas and polyps: implications for implantation. Hum Reprod 17:2742-7|