OBJECTIVE: To evaluate the effect of serum obtained before and after treatment for endometriosis on in vitro fertilization and development of two cell mouse embryo. Design: Pretreatment and posttreatment comparoson of fertilization of mouse oocyte and embryo development in serum supplement form patients with endometriosis; result were compared using Stuent T-test analysis. METHOD: Infertility Clinic, Department of Obstetrics and Gynecology, Collage of Medicine, Won Kwang university, Korea. Patients was chosed eleven consecutive women with endometriosis. Interventions was all patient underwent laparoscopic or conservative surgery. This was followed by a 6-month course of burserelin acetate 900 microgram/d. Main outcome was measured total number of fertilization and embryo that was fertilization after 24 hours and reached blastocyst stage after 72 hours of incubation were compared before and after treatment. RESULT: Before treatment, 47% of the oocyte were fertilized and 31% of the embryo reached blastocyst stage. After treatment, Significantly more fertilized and Significantly more embryo developed to blastocyst on the stage I and II of endometriosis. CONCLUSION: The fertilization and embryo toxicity of serum samples from patients with endometriosis is lost after treatment.
Animals ; Blastocyst ; Embryonic Development ; Embryonic Structures ; Endometriosis* ; Female ; Fertilization ; Fertilization in Vitro* ; Gynecology ; Humans ; Infertility ; Korea ; Mice* ; Obstetrics ; Oocytes* ; Pregnancy

No abstract available.
Jeollabuk-do* ; Pregnancy* ; Toxoplasma*

The cell cycle is composed of a series of steps which can be negatively or positively regulated by various factors. p53 gene aberrations are common in human malignancies, and recent studies suggest that in cervical carcinoma p53 function is inactivated either by complex formation wilh human papilloma virus (HPV) E6 product or by gene mutation. To study the expression of p53 gene in the cervical cancer and cervical intraepithebal neoplasia, immunohistochemistry for the p53 protein was done in the 47 cases of squamous cell carcinoma, 6 cases of adenocarcinoma and 32 cases of cervical intraepithelial neoplasia. I. The p53 protein was detected in the 31% of cervical intraepithelial neoplasia (10/32 cases). 2. The p53 protein was detected in the 55% of invasive cervical cancer (29/53 cases). 3. By the histologic type of cervieal cancer, the p53 protein was detected in the 57% of squamous cell carcinoma (27/47 cases) and 33% of(2/6 cases) adenocarcinoma. The p53 protein wes more frequently detected in the squamous cell carcinoma than in the adenocarcinoma. 4. By the staging in cervical cancer, the p53 protein was detected in the 31% of stage 0, 50% of Stage Ia, 50% of stage I b, 75% of IIa and 50% of stage II b.
Adenocarcinoma ; Carcinoma, Squamous Cell ; Cell Cycle ; Cervical Intraepithelial Neoplasia ; Genes, p53 ; Humans ; Immunohistochemistry* ; Papilloma ; Uterine Cervical Neoplasms*

A previous report by this laboratory demonstrated that bacterial iron chelator (siderophore) triggers inflammatory signals, including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs). Microarray-based gene expression profiling revealed that iron chelator also induces macrophage inflammatory protein 3 alpha (MIP-3alpha)/ CC chemokine-ligand 20 (CCL20). As CCL20 is chemotactic for the cells involved in host adaptive immunity, this suggests that iron chelator may stimulate IECs to have the capacity to link mucosal innate and adaptive immunity. The basal medium from iron chelator deferoxamine (DFO)-treated HT-29 monolayers was as chemotactic as recombinant human CCL20 at equivalent concentrations to attract CCR6+ cells. The increase of CCL20 protein secretion appeared to correspond to that of CCL20 mRNA levels, as determined by real-time quantitative RT-PCR. The efficacy of DFO at inducing CCL20 mRNA was also observed in human PBMCs and in THP-1 cells, but not in human umbilical vein endothelial cells. Interestingly, unlike other proinflammatory cytokines, such as TNF-alpha and IL-1beta, a time-dependent experiment revealed that DFO slowly induces CCL20, suggesting a novel mechanism of action. A pharmacologic study also revealed that multiple signaling pathways are differentially involved in CCL20 production by DFO, while some of those pathways are not involved in TNF-alpha-induced CCL20 production. Collectively, these results demonstrate that, in addition to some bacterial products known to induce host adaptive immune responses, direct chelation of host iron by infected bacteria may also contribute to the initiation of host adaptive immunity in the intestinal mucosa.
Calcium/metabolism ; Cell Movement/drug effects ; Chemokines, CC/genetics/*metabolism ; Deferoxamine/*pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; HT29 Cells ; Humans ; Immunity, Mucosal/*drug effects ; Intestinal Mucosa/*drug effects/immunology/metabolism ; Iron Chelating Agents/*pharmacology ; Macrophage Inflammatory Proteins/genetics/*metabolism ; NF-kappa B/metabolism ; Phosphoprotein Phosphatase/physiology ; Protein Transport/drug effects ; Protein-Serine-Threonine Kinases/physiology ; RNA, Messenger/genetics/metabolism ; Receptors, Chemokine/metabolism ; Research Support, Non-U.S. Gov't