Increased uterine vascular permeability and angiogenesis are hallmarks of implantation and placentation. These events are profoundly influenced by vascular endothelial growth factor (VEGF). Although VEGF and its receptor Flk-1 are primarily important for uterine vascular permeability and angiogenesis before and during the attachment phase of the implantation process, VEGF together with the angiopoietins and their receptor Tie-2 directs angiogenesis during decidualization after implantation. Upstream of VEGF, estrogen promotes uterine vascular permeability but inhibits angiogenesis, whereas progesterone stimulates angiogenesis with little effect on vascular permeability. Furthermore, COX-2-derived prostaglandins participate in uterine vascular permeability and angiogenesis during implantation and decidualization.

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Growth of preantral follicles is mainly controled by gonadotropins. Activin stimulates synthesis of FSH at the pituitary gland, and on the other hand inhibin which is secreted by antral follicles is transferred to the pituitary gland, and the complex of inhibin and TGFβ-receptor type III ihibites the function of Actibin receptors, resulting in a decrease of pituitary FSH secretion. In folliculiogenesis, a strong expression of activin mRNA is observed from the preantral follicle stage and Activin induces expression of FSH-R mRNA on granulosa cells of preantral follicles. Thereafter the follicles grow in a FSH-dependent manner. As the follicles grow larger, the activin-rich follicular environment changes to inhibin/follistatin-rich. The inhibin/follistatin-rich environment with decreases of FSH- and Activin- requirement on development of larger follicles would suppress development of smaller follicles in ovary through suppression of FSH secretion. Activin, inhibin and follistatin possibly play an important role in regulating physiolosical follicular development.

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The aim of this study is to investigate whether a natural cycle intrauterine insemination (NC-IUI) monitored with ultrasonography and serum estradiol level can improve the pregnancy rate (PR) of NC-IUI. A total of 311 cycles of 135 cases was treated with a NC-IUI using a ultrasonographic monitor for follicular development (Group A). And a total of 308 cycles of 131 cases underwent a NC-IUI monitored baseline ovarian cysts, follicular development and ovulation using ultrasonography and serum estradiol level (Group B). Forty-two cycles (12.0%) were cancelled due to baseline ovarian cysts and 20 cycles (6.1%) were excluded from group B because of a luteinized unruptured follicle. In group A and B, 16 pregnancies (5.1% per cycle) and 32 pregnancies (10.4% per cycle) were obtained respectively. The differences between the PRs of the two groups attained statistical significance (P<0.05). Our data indicated that a NC-IUI monitored with ultrasonography and serum estradiol level may improve the PR of NC-IUI.

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The purpose of this study was to evaluate the effectiveness of buserelin acetate (BA) for triggering endogenous LH surge before oocyte retrieval in clomiphene citrate (CC) or CC+hMG cycles. Patients were divided into two groups: a buserelin group, which consisted of patients treated with BA for 73 cycles 34-36 hours before oocyte retrieval, and an hCG group, which consisted of patients treated with hCG for 89 cycles 34-36 hours before oocyte retrieval. Rate of oocyte retrieval, ratio of metaphase II oocytes, fertilization rate in ICSI, fertilization rate in IVF, ratio of good cleaved embryos, rate of blastocyst development and pregnancy rate were 59.1%, 74.3%, 78.8%, 78.4%, 64.6%, 50.0% and 8.3%, respectively in the buserelin group and 63.2%, 71.3%, 80.6%, 67.6%, 58.6%, 66.7% and 12.5%, respectively, in the hCG group. There were no significant differences in those results between the groups. In conclusion, BA is present terse should be used for a conclusion effective for triggering LH surge before oocytes retrieval in CC or CC+hMG cycles.

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