The purpose of this study is to determine features of uterine leiomyoma on Magnetic Resonance Imaging (MRI) that identify predictors of response to Uterine Arterial Embolization (UAE). MRI images were obtained before and after UAE in 35 women. These images were analyzed for uterine and fibroid size changes along with fibroid border characteristics and location for a total of 73 fibroids. Fibroids were classified as either smooth or lobulated based on border appearance on MR imaging to determine any differences in mean fibroid volume reduction post-embolization. The mean decrease in fibroid volume from pre-embolization to post-embolization was 48.1% ± 28.6 % (SD) (P < 0.001). No statistical difference was detected in the mean volume reduction between lobulated and smooth fibroids, 40.6% ± 23.1% (SD) and 50.9% ± 30.2% (SD) respectively, with a confidence interval [-25.1, 4.6, SEM 7.5, Df 71], single factor ANOVA (F[1,71]=1.88, Fcrit=3.98, p=0.17). However, some difference was detected in the failure rate of lobulated versus smooth fibroids to embolization, 5% and 9.4% respectively, ANOVA (F [1, 71]= 0.37, Fcrit= 3.98, p > 0.1), albeit at low statistical power. Also no difference was detected in mean fibroid volume reduction between intramural, submucosal, and subserosal fibroids. Thus, we introduced a novel characteristic by which to classify uterine fibroids based upon border appearance on MR imaging.

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 286-298).

No description available.

Transient uterine Natural Killer (uNK) cells are the predominant leukocytes of early gestational human and murine uteri. Murine uNK cells promote changes in endometrial structure including initiation of perivascular smooth muscle reduction in spiral arteries. Less is known about human uNK cell functions due to sampling constraints. Xenogeneic engraftment of human lymphocyte progenitors to alymphoid mice has been useful in understanding human lymphocyte functions in vivo. Irradiation of recipients is required to create a niche for successful humanization of the mice but renders recipient mice sterile. The goal of my thesis was to develop a protocol enabling engraftment of human hematopoietic stem cells in alymphoid mice that would permit differentiation of functional human uNK cells. I then planned to evaluate human uNK cell functions and their regulation in vivo. Neonatal Rag2-/-Il2rg-/- mice, which lack T cells, B cells and NK cells were preconditioned with 5-fluorouracil and inoculated with syngeneic mouse bone marrow cells. As adults, inoculated female mice conceived and differentiated functional mouse uNK cells. In contrast, neonatally-preconditioned Rag2-/-Il2rg-/- mice inoculated with human cord blood hematopoietic stem cells conceived but differentiated non-lymphoid cells in sites normally occupied by uNK cells. Weekly injections of human IL-15, which is required for NK cell differentiation, proliferation and survival, did not promote uNK cell differentiation. Rather, treatment with IL-15 altered gestational uteri, even in mice receiving neither preconditioning nor hematopoietic stem cells. I was successful in developing a protocol that enables hematopoietic stem cell engraftment in neonatal mice without compromising mouse fertility. However, this model is apparently not suitable for in vivo studies of human uNK cell functions. / Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2010-08-30 16:27:07.522

No description available.

No description available.

Thesis (Doctoral).--Université de Montpellier, 1908, no. 28.

Thesis (M.S.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains v, 46 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 37-45).

Thesis (M.S.)--Georgia State University, 2007. / Title from title page. Yu-sheng Hsu, committee chair; Xu Zhang, Jia-wei Liu, committee members. Electronic text (44 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Oct. 10, 2007. Includes bibliographical references (p. 35-36).

E–cadherin (CDH1) is a cell–cell adhesion molecule expressed in the epithelium to coordinate key morphogenetic processes, establish cell polarity, and regulate epithelial differentiation and proliferation. CDH1 forms adherens junctions that mediate intercellular adhesion through dynamic interactions with β–catenin (CTNNB1). To determine the role of CDH1 in the mouse uterus, Cdh1 was conditionally ablated by crossing Pgr–Cre and Cdh1–flox mice. Animals with the resulting genotype of Pgrcre/+Cdh1f/f had Cdh1 conditionally ablated in the Pgr expressing tissue, which includes the uterus (referred to as Cdh1d/d). We characterized the phenotype and found that loss of Cdh1 in the neonatal uterus results in a disorganized cellular structure of the epithelium and ablation of endometrial glands. Cdh1d/d mice lost adherens junction (CTNNB1 and CTNNA1) and tight junction (claudin, occludin and ZO–1) in the neonatal uterus leading to loss of epithelial cell–cell interaction. Ablation of Cdh1 induced abnormal epithelial proliferation and massive apoptosis, and disrupted Wnt and Hox gene expression in the neonatal uterus. Although the uteri of Cdh1d/d mice did not show any defect of myometrium, ablation of Cdh1 inhibited stromal (CD10) markers. In addition, a conditional knockout of Ctnnb1 in the uterus and a double conditional knockout of Cdh1&Ctnnb1 in the uterus were created to determine if the uterine defects were caused by an alteration in CDH1, CTNNB1, or a combination of both. Ctnnb1 and Cdh1&Ctnnb1 were conditionally ablated in the uterus by crossing Pgr–Cre and Ctnnb1–flox mice or Cdh1&Ctnnb1–flox mice. The Ctnnb1d/d mice maintained adhesive epithelial characteristics and did not lose adherens junction or tight junction proteins; however ablation of Ctnnb1 induced epithelial hyperplasia and disrupted Wnt and Hox gene expression in the neonatal uterus. The Cdh1d/dCtnnb1d/d mice carried a similar phenotype to the Cdh1d/d mice. Adult Cdh1d/d mice were infertile due to defects during implantation and decidualization. Collectively, these findings suggest that CDH1 has an important role in structural and functional development of the uterus as well as adult uterine function. CDH1 has a capacity to control cell fate by altering directional cell proliferation and apoptosis.