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At least 19 recordsLinked to original sources
PubMed2003

Cochlin, a secreted von Willebrand factor type a domain-containing factor, is regulated by leukemia inhibitory factor in the uterus at the time of embryo implantation.

Embryo implantation is a required step in the reproduction of all mammals. In mice, a transient rise in the uterine expression of leukemia inhibitory factor (LIF) occurs on d 4 of pregnancy and is essential for embryo implantation. However, which genes are regulated by LIF in the uterus at implantation has not been determined. We performed a subtractive hybridization assay between luminal epithelial (LE) mRNAs from d 3 and 4 of pregnancy to find genes up-regulated on d 4 and which would be potentially regulated by LIF. One candidate, Coch-5b2, was up-regulated on the day of implantation. Coch mRNA localized to the LE of wild-type mice and was not detected in uteri from Lif-deficient mice. Treatment of LE with LIF, both in vitro and in vivo, resulted in the up-regulation of Coch. Coch is also highly expressed in other tissues, including the spleen and inner ear, but only in the uterus is Coch expression regulated by LIF. Mice were derived in which Coch was either deleted or tagged with a LacZ reporter. In mice carrying the tagged Coch gene, expression of Coch was detected in the LE and also at the site of embryo implantation. However, mice in which the Coch gene was deleted were normal, showing no overt defects in their reproduction. Although loss of Coch expression is not essential to reproduction in mice, it may serve as a useful marker for assessing the state of uterine receptivity in response to LIF at the onset of implantation.

Animals↗
PubMedDate not supplied

The cytokine network during embryo implantation.

Embryo implantation is an essential step in mammalian pregnancy. The molecular events of embryonic attachment to the endometrial epithelium and the subsequent invasion of the stroma have long been of interest. The process involves both the scientific interest of reproductive biologists and clinical interest of physicians that care for infertility couples. Understanding the molecular factors involved in each phase of the implantation process is critical to comprehending the mechanisms that control reproduction, especially as part of a human in vitro fertilization program. This review will focus on the role during early embryonic development and implantation of two distinct cytokines, the interleukin-1 (IL-1) system and interleukin-18 (IL-18) system; it will also examine the role of the matrix metalloproteinases (MMP) and their inhibitors as well as vascular endothelial growth factor (VEGF) system. The possible influence of the cytokines on other systems involved in embryonic implantation, including the embryonic-endometrial dialogue, the subsequent invasion and neoangiogenesis will be discussed. These suggest a role for the two cytokine families in early embryonic development.

Animals↗
PubMed2005

Cochaperone immunophilin FKBP52 is critical to uterine receptivity for embryo implantation.

Embryo implantation in the uterus is a critical step in mammalian reproduction, requiring preparation of the uterus receptive to blastocyst implantation. Uterine receptivity, also known as the window of implantation, lasts for a limited period, and it is during this period blastocysts normally implant. Ovarian steroid hormones estrogen and progesterone (P(4)) are the primary regulators of this process. The immunophilin FKBP52 serves as a cochaperone for steroid hormone nuclear receptors to govern appropriate hormone action in target tissues. Here we show a critical role for FKBP52 in mouse implantation. This immunophilin has unique spatiotemporal expression in the uterus during implantation, and females missing the Fkbp52 gene have complete implantation failure due to lack of attainment of uterine receptivity. The overlapping uterine expression of FKBP52 with nuclear progesterone receptor (PR) in wild-type mice together with reduced P(4) binding to PR, attenuated PR transcriptional activity and down-regulation of several P(4)-regulated genes in uteri of Fkbp52(-/-) mice, establishes this cochaperone as a critical regulator of uterine P(4) function. Interestingly, ovulation, another P(4)-mediated event, remains normal. Collectively, the present investigation provides evidence for an in vivo role for this cochaperone in regulating tissue-specific hormone action and its critical role in uterine receptivity for implantation.

Animals↗
PubMed1998

Mucin and proteoglycan functions in embryo implantation.

Embryo implantation is a complex series of events that involves changes in pattern of expression of embryonic as well as uterine cell surface components. In the case of the embryo, these changes are driven by the developmental program. In the case of the uterus, these changes are triggered by both maternal hormonal influences as well as embryo-derived factors. Aspects of the implantation process vary among species; however, interaction between the external surface of the embryonic trophectoderm and the apical surface of the lumenal uterine epithelium is a common event. Progress is being made in defining the molecular players in these cell surface interactions. Large-molecular-weight mucin glycoproteins such as MUC1 are present at the apical surface of the uterine epithelium under most conditions. Under most circumstances, these mucins appear to protect the mucosal surface from infection and the action of degradative enzymes. These mucins are antiadhesive and also appear to represent a barrier to embryo attachment. Consistent with this model, reduction of mucin expression is observed in uterine lumenal epithelia in many species. Nonetheless, mucin expression persists in the human uterus during the proposed receptive phase. It is possible that mucin loss is localized to implantation sites in humans. Alternatively, mucins may function differently within the context of human implantation than in other species. Studies primarily performed in mice indicate that heparan sulfate proteoglycans, in particular, perlecan, appears on the exterior trophectodermal surface coincident with the acquisition of attachment competence. Various in vitro studies indicate that heparan sulfate proteoglycans support embryo attachment activity that may represent an early event in embryo-uterine interaction. Uterine epithelia cells express several complementary heparan sulfate-binding proteins that may participate in these attachment processes. Use of molecular genetic approaches in mouse models, as well as careful studies of the expression and function of these molecules in the context of implantation in various species are beginning to shed light on the key molecular events of implantation.

Animals↗
PubMed2000

Where does the embryo implant after embryo transfer in humans?

OBJECTIVE: To investigate where human embryos implant after ET. DESIGN: Prospective analysis. SETTING: University hospital. PATIENT(S): Sixty infertile women without uterine fibroids, a major uterine anomaly, or a history of cesarean section. INTERVENTION(S): Transabdominal and transvaginal three-dimensional ultrasound examinations. MAIN OUTCOME MEASURE(S): The location of ET-associated air bubbles in the uterine cavity and the location of the resultant gestational sac. RESULT(S): Sixty ETs resulted in 22 pregnancies, and 32 gestational sacs were located. Twenty-six of the 32 embryos were within or between the area in which the catheter tip was situated and the area over which air bubbles had spread immediately after ET. CONCLUSION(S): In cases of pregnancy achieved through ET, approximately 80% of embryos implant in areas to which they initially are transferred and approximately 20% implant in other areas.

Adult↗
PubMed2000

Embryo implantation and GnRH antagonists: embryo implantation: the Rubicon for GnRH antagonists.

When gonadotrophin-releasing hormone (GnRH) was discovered, the agonist and antagonist of GnRH were developed to control the release of FSH and LH by the gonadotrophs. More than 10 years of research were needed to develop a GnRH antagonist free of histamine release. Recent studies have shown that these GnRH antagonists are effective in preventing a rise in LH during ovarian stimulation in IVF. However, a decrease in ongoing pregnancies seems to suggest that implantation rates per transferred embryo are reduced in GnRH antagonist-stimulated cycles. In my opinion, these data highlight an area less well known to clinicians: the role of the GnRH antagonist at the cellular level in extrapituitary tissues. There are sufficient data in the literature suggesting that GnRH antagonist is an inhibitor of the cell cycle by decreasing the synthesis of growth factors. Given that, for folliculogenesis, blastomere formation and endometrium development, mitosis is everything; the interaction between the GnRH antagonist and the GnRH receptor (present in all these cells and tissues) may compromise the mitotic programme of these cells. This is the Rubicon for the GnRH antagonist: to demonstrate irrevocably that, at the minimal doses necessary to suppress LH release, it does not affect processes such as implantation, embryo development and folliculogenesis.

Animals↗
PubMed1989

Plasminogen activators in tissue remodeling and invasion: mRNA localization in mouse ovaries and implanting embryos.

To assess in vivo the postulated participation of urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators in processes involving tissue remodeling and cell migration, we have studied the cellular distribution of u-PA and t-PA mRNAs during mouse oogenesis and embryo implantation. By in situ hybridizations, we detected t-PA mRNA in oocytes and u-PA mRNA in granulosa and thecal cells from preovulatory follicles. These findings are compatible with a role for plasminogen activators in oogenesis and follicular disruption. We demonstrated the presence of u-PA mRNA in the invasive and migrating trophoblast cells of 5.5- and 6.5-d-old embryos. At 7.5 days, u-PA mRNA was predominantly localized to trophoblast cells that had reached the deep layers of the uterine wall, while the peripheral trophoblast cells surrounding the presomite stage embryo were devoid of specific signal. In 8.5-d-old embryos abundant u-PA mRNA expression resumed transiently in the giant trophoblast cells at the periphery of the embryo and in the trophoblast cells of the ectoplacental cone, to become undetectable in 10.5-d-old embryos. These observations establish the in vivo expression of the u-PA gene by invading and migrating trophoblast cells in a biphasic time pattern; they are in agreement with the proposed involvement of the enzyme in the extracellular proteolysis accompanying embryo implantation.

Animals↗
PubMed2000

Effect of 32/67 kDa laminin-binding protein antibody on mouse embryo implantation.

Mouse embryo implantation depends on the complex interaction between the embryo trophoblast cells and the uterine environment, which deposits an extracellular matrix with abundant amounts of laminin. Intrauterine injection and blastocyst or ectoplacental cone culture models were used to study the effect of 32/67 kDa laminin-binding protein antibody on mouse embryo implantation in vivo and in vitro. Intrauterine injection of 32/67 kDa laminin-binding protein antibody (0.4 mg in 1 ml Ham's F-10 medium, 5 microl per mouse) into the left uterine horns of mice (n = 22) on day 3 of pregnancy inhibited embryo implantation significantly (P < 0.001) compared with the contralateral horns that had been injected with normal rabbit IgG. A continuous section study on day 5 after injection showed that the embryos in the control uteri implanted normally and developed healthily, but there were no embryos or the remaining embryos had disintegrated in the uteri injected with 32/67 kDa laminin-binding protein antibody. Blastocysts or ectoplacental cones were cultured in media containing 32/67 kDa laminin-binding protein antibody (0.2 mg ml(-1)) on laminin-coated dishes with normal rabbit IgG at the same concentration as in the controls. The 32/67 kDa laminin-binding protein had no effect on blastocyst or ectoplacental cone attachment, but prohibited the blastocyst or ectoplacental cone outgrowth and primary or secondary trophoblast giant cell migration. These results indicate that 32/67 kDa laminin-binding protein antibody blocked mouse embryo implantation by preventing embryo trophoblast cell invasion and migration through the uterine decidual basement membrane-like extracellular matrix which has a high laminin content.

Analysis of Variance↗
PubMed2006

Uterine (CD56+) natural killer cells recruitment: association with decidual reaction rather than embryo implantation.

PROBLEM: Whether decidual leukocyte recruitment and/or increase is primarily hormonally regulated or induced mainly by blastocyst implantation is a matter of debate. Thus, this study investigated the number and distribution of leukocyte populations, with emphasis on natural killer (NK) cells of uterine and peripheral type, within decidual tissue from women with decidualized endometrium both related and unrelated to pregnancy and those with ectopic decidua associated with intrauterine pregnancy, as well as in tubal implantation sites. METHOD OF STUDY: Immunohistochemical characterization of immune cells using antibodies to CD3, CD4, CD8, CD20, CD68, CD16, CD56, CD57, in formalin-fixed, paraffin-embedded tissue, and a quantitative analysis of these subpopulations was conducted in tissue blocks from four groups of patients: (i) 20 women with decidualized endometrium due to progestin therapy (i.e. not associated with gestation) (group Prog-D); (ii) 20 women with intrauterine pregnancy-associated ectopic decidua (seven in the Fallopian tube, five in the ovary, five in the uterine cervix, and three in the omentum) (group Ect-D); (iii) 20 women with spontaneous abortion who had an histologic sample of the decidua at the uterine implantation site (group Uter-D); and (iv) 20 consecutive patients who had had an ectopic tubal pregnancy (group Tub-Preg). Twenty gynecologic specimens with marked inflammatory reaction were used as controls (group Con). RESULTS: CD3+, CD4+, CD8+, CD68+ cells were detected in all tissue samples investigated. In contrast, CD20+ cells were detected in all samples in group Con, but only in 75%, 25%, 55% and 70% of groups Prog-D, Ect-D, Uter-D and Tub-Preg, respectively. In all tissue samples investigated, CD57+ and CD16+ cells were detected. Conversely, CD56+ cells were completely absent in 15 of 40 cases (37.5%) lacking decidual reaction (group Tub-Preg, 7/20; group Con, 8/20) but were present in all cases showing decidual reaction. In contrast with CD56+ cells, CD57+ NK cells were more abundant in group Con than in the four study groups. CONCLUSIONS: CD56+ NK cells are closely related to decidua irrespective of its eutopic or ectopic location rather than to the implantation site. This suggests that the recruitment and/or increase of uterine NK cells into the uterus is not dependent on the physical presence of an implanting embryo but instead is controlled hormonally.

Adult↗
PubMed1994

The immunolocalization of basic fibroblast growth factor in the mouse uterus during the initial stages of embryo implantation.

Mammalian embryo implantation involves a series of complex interactions between maternal and embryonic cells. Uterine polypeptide growth factors may play critical roles in these cell interactions. Basic fibroblast growth factor (basic FGF) is a member of a family of growth factors. This growth factor may be potentially important for the process of embryo implantation because it (a) is stored within the extracellular matrix and is thus easily available during embryo invasion, (b) is a potent modulator of cell proliferation and differentiation and (c) stimulates angiogenesis. The immunolocalization of basic FGF in the uterus during the peri-implantation period of pregnancy is presented in this study. Uterine tissue samples were obtained on days 6-9 of pregnancy with day 1 of pregnancy being the day of a vaginal copulatory plug. Uterine samples were fixed in Bouin's fluid for no longer than 18 h. Following fixation and paraffin embedding, sections were exposed to primary antisera made in rabbits against either (a) human recombinant basic FGF or (b) 1-24 synthetic fragment of bovine basic FGF. The primary antibody was followed by biotinylated goat anti-rabbit IgG and a biotin-avidin-peroxidase complex. There were no differences in the immunolocalization of basic FGF using either source of primary antibody. Our results demonstrated both temporal and spatial changes in the localization of immunoreactive basic FGF within the implantation chamber during days 6-9 of pregnancy. Inter-implantation sites resembled the non-pregnant uterus with basic FGF present in extracellular matrices including basal laminae. On day 6 of pregnancy, decidual cells within the primary decidual zone lacked both intracellular and pericellular basic FGF while non-decidualized uterine stroma resembled inter-implantation sites. By days 7-8 of pregnancy, the secondary decidual zone had formed and was characterized by the distinct pericellular localization of basic FGF around individual decidual cells. By day 9 of pregnancy, the mesometrial region was forming and contained cords of decidual cells and a labyrinth of maternal blood vessels. The decidual cells contained diffuse intracellular basic FGF. Trophoblast cells were devoid of basic FGF at all times examined. These results indicate that basic FGF is present within the implantation chamber on days 6-9 of pregnancy and may be involved in the decidual cell response, trophoblast cell invasion and angiogenesis.

Animals↗
PubMed2004

Leptin serves as an upstream activator of an obligatory signaling cascade in the embryo-implantation process.

Leptin is essential for mouse reproduction, but the exact roles it serves are yet to be determined. Treatment of cultured endometrial cells with leptin increases the level of beta3-integrin, IL-1, leukemia inhibitory factor, and their corresponding receptors. These leptin-induced effects are eliminated by inhibitors of leptin receptor (OB-R) signaling. Herein the impact of blocking leptin/OB-R signaling in the mouse endometrium was assessed. Intrauterine injection of either leptin peptide antagonists (LPA-1 or -2) or OB-R antibody on d 3 of pregnancy impaired mouse implantation in comparison to intrauterine injection of scrambled peptides (LPA-Sc) or species-matched IgGs. Significant reduction in the number of implantation sites and uterine horns with implanted embryos was found after intrauterine injection of LPA-1 (1 of 22) vs. LPA-1Sc (11 of 15) and LPA-2 (3 of 17) vs. LPA-2Sc (14 of 16). The impact of disruption of leptin signaling on the endometrial expression of several molecules in pregnant mice was assessed by Western blot, immunohistochemistry, and confocal microscopy. Disruption of leptin signaling resulted in a significant reduction of IL-1 receptor type I, leukemia inhibitory factor, vascular endothelial growth factor receptor 2, and beta3-integrin levels. The levels of colony stimulating factor-1 receptor and OB-R were unaltered after treatment with LPAs compared with controls. Expression of OB-R protein was pregnancy dependent and found only in glandular epithelium after implantation occurred. Our findings support previous observations that leptin signaling is critical to the implantation process and suggest that molecules downstream of leptin-activated receptor may serve obligatory roles in endometrial receptivity and successful implantation.

Animals↗
PubMed2006

Endometrial receptivity markers, the journey to successful embryo implantation.

Human embryo implantation is a three-stage process (apposition, adhesion and invasion) involving synchronized crosstalk between a receptive endometrium and a functional blastocyst. This ovarian steroid-dependent phenomenon can only take place during the window of implantation, a self-limited period of endometrial receptivity spanning between days 20 and 24 of the menstrual cycle. Implantation involves a complex sequence of signalling events, consisting in the acquisition of adhesion ligands together with the loss of inhibitory components, which are crucial to the establishment of pregnancy. Histological evaluation, now considered to add little clinically significant information, should be replaced by functional assessment of endometrial receptivity. A large number of molecular mediators have been identified to date, including adhesion molecules, cytokines, growth factors, lipids and others. Thus, endometrial biopsy samples can be used to identify molecules associated with uterine receptivity to obtain a better insight into human implantation. In addition, development of functional in vitro systems to study embryo-uterine interactions will lead to better definition of the interactions existing between the molecules involved in this process. The purpose of this review was not only to describe the different players of the implantation process but also to try to portray the relationship between these factors and their timing in the process of uterine receptivity.

Animals↗
PubMed2000

Embryo implantation and GnRH antagonists: GnRH antagonists in ART: lower embryo implantation?

Recently, concerns have been raised regarding possible adverse effects of gonadotrophin-releasing hormone (GnRH) antagonists on extra-pituitary reproductive cells and organs, i.e. ovarian cells, oocyte, embryo, endometrium. These concerns are based on numerous in-vitro studies suggesting decreased biosynthesis of growth factors caused by local action of GnRH antagonists. Clinically, it has been shown that the use of high doses (< or =1 mg daily) of GnRH antagonists is associated with low implantation rates in IVF. Although such direct adverse effect of GnRH antagonists cannot be ruled out at this time, so far clinical experience points to profound LH suppression as the major caveat associated with the use of high doses of GnRH antagonists. Very low LH concentrations are associated with aberrant concentrations of oestradiol during ovarian stimulation, which may in turn adversely effect implantation potential. The clinical data available thus far on the use of GnRH antagonists originate from protocols designed for clinical studies. It is predicted that as more clinical experience is gained, and with protocol modifications to suit individual patient response, GnRH antagonists will be comparable with the agonists in terms of cycle outcome.

Embryo Implantation↗
PubMed1998

[A study on the relationship between serum anticardiolipin antibody and embryo implantation in an in vitro fertilization and embryo transfer program].

OBJECTIVE: To study the role of serum anticardiolipin antibody in embryo implantation in an in-vitro fertilization and embryo transfer program. METHODS: 150 in vitro fertilization and embryo transfer (IVF-ET) treatment cycles from Nov. 1994 to May, 1996 were studied. Serum anticardiolipin antibody was measured by enzyme-linked immunosorbent assay (ELISA), and the clinical pregnancy outcome observed. RESULTS: Lower pregnancy rate 9.5% was found in 21 cycles of anticardiolipin antibody seropositive women compared with 26.3% in 129 cycles of anticardiolipin antibody seronegative women (P < 0.05). Patients with biochemical pregnancy and no pregnancy had seropositive anticardiolipin antibody in 20.0% and 16.2% compared with 5.6% in the patients with clinical pregnancy (P < 0.05). CONCLUSIONS: Failure of embryo implantation is associated with many factors. Our study demonstrated the serum anticardiolipin antibody in patients may play a part in embryo implantation and very early postimplantation loss.

Antibodies, Anticardiolipin↗
PubMed2006

MRI analysis of angiogenesis during mouse embryo implantation.

Uterine receptivity and embryo implantation depend on local induction of angiogenesis and vascular permeability. Poor uterine receptivity has been implicated in implantation failure; however, relatively little is known about the mechanism that underlies endometrial vascular hyperpermeability in implantation sites. Here we show that contrast-enhanced (CE)-MRI and fluorescence microscopy using biotin-BSA-GdDTPA allowed high-resolution detection and quantitative assessment of mouse embryo implantation sites as early as embryonic day 4.5 (E4.5), and subsequent vascular expansion at E5.5. Vessel permeability, but not blood volume, was significantly elevated in E4.5 implantation sites relative to nonimplanted uterus, showing that elevation of vascular permeability is a very early response preceding E4.5. A significantly increased blood volume was detected by MRI and fluorescence microscopy in implantation sites between E4.5 and E5.5. On the other hand, despite the increase in blood volume, implantation sites showed only a small nonsignificant further increase in vascular permeability during these 2 days, demonstrating the rapid dynamics of vascular remodeling during the early days of pregnancy. Functional imaging by MRI, as reported here, allows multiparametric measurement of angiogenesis during normal mouse implantation and would facilitate the application of MRI to evaluate involvement of the vasculature in mouse models of impaired implantation.

Animals↗
PubMed1995

The correlation of the embryo implantation rate with uterine arterial impedance in in vitro fertilization and embryo transfer.

The influence of uterine blood flow impedance on embryo implantation rate was investigated by transvaginal color Doppler sonography examination before embryo transfer. A total of 108 women undergoing in vitro fertilization (IVF) procedures and who had at least one good quality embryo for transfer to the uterus received Doppler evaluation before embryo transfer. Color flow imaging with blood flow waveform analysis from bilateral uterine arteries was obtained to calculate the mean pulsatility index (PI). The correlations between mean PI with the pregnancy rate and the embryo implantation rate (number of embryos implanted/number of embryos transferred) were analyzed. Patients were grouped according to the mean PI value, and the pregnancy rate and embryo implantation rate were 25% (5/20) and 10.7% (9/84), respectively, with a PI < 2.0 (n = 20); 27.5% (14/51) and 12.2% (12/109), respectively, with a PI = 2.00-2.49 (n = 51); 9.5% (2/21) and 3.5% (2/57), respectively, with a PI = 2.50-2.99 (n = 21); and 6.3% (1/16) and 4.3% (2/47), respectively, with a PI [symbol: see text] 3.0 (n = 16). There were no significant differences in either pregnancy rate or embryo implantation rate between the groups with mean PI values less than 2.00 and between 2.00 and 2.49. If a mean PI value of 2.50 was used as the cut-off value, both the pregnancy rate and embryo implantation rate were significantly higher in patients with a mean PI less than 2.50 (p < 0.05). The uterine arterial impedance measured by the Doppler sonographic examination is a non-invasive method for evaluating the endometrial response and a mean uterine PI value of 2.5 can be used as a cut-off value to identify optimal uterine receptivity before embryo transfer.

Adult↗
PubMed2004

Uterine expression of implantation serine proteinase 2 during the implantation period and in vivo inhibitory effect of its antibody on embryo implantation in mice.

The aim of the present study was to examine the uterine expression pattern of implantation serine proteinase 2 (ISP2) protein during early pregnancy in mice and the effects of anti-ISP2 antibody on embryo implantation. Expression of ISP2 protein was found to be specifically up-regulated in mouse uterine endometrial glands following the initiation of embryo implantation. Similarly, ISP2 protein expression was observed during pseudopregnancy, indicating that its expression is not embryo dependent. In other experiments, rabbit anti-ISP2 IgG was infused into the mouse uterine lumen on Day 3 or 4 of pregnancy to examine its effects on embryo implantation, whereas vehicle (saline) or unspecific rabbit IgG served as controls. The mean number of implanted embryos from anti-ISP2-IgG-treated mice was significantly lower than that from control mice. These results suggest that ISP2 may play an important role during embryo implantation.

Animals↗
PubMed1992

Factors promoting embryo implantation in in vitro fertilization and embryo transfer.

The low implantation rate after embryo transfer (ET) is the most important problem to be solved in in vitro fertilization and embryo transfer (IVF-ET). Various factors which may affect embryo implantation in the endometrium have been examined. In this study, the influence of the timing of luteinization on the establishment of pregnancy was investigated. Follicle stimulation was performed by luteinizing hormone-releasing hormone agonist, human menopausal gonadotropin and human chorionic gonadotropin (hCG). hCG was injected on the day when the mean diameter of two follicles exceeded 16 mm, and 36 h after the injection the oocyte was retrieved. Progesterone (P4) supplement was started on the day of ovum retrieval (50 mg), followed by 30 mg for 14 days. The patients were divided into three groups: (1) the pregnant patients (n = 20: group Pre); (2) the nonpregnant patients without bleeding during P4 injection (n = 35; group N), and (3) the nonpregnant patients with bleeding during P4 injection (n = 30; group B). The number of follicles that developed, endometrial thickness, the day of operation, the number of oocytes harvested, the number of good quality oocytes, the number of oocytes fertilized, the number of embryos transferred, estradiol (E2) and P4 levels, and the E2/P4 ratio were examined. The endometrial thickness of group Pre (10.9 +/- 0.6 mm; mean +/- SEM) on the day of hCG injection was significantly (p less than 0.05) greater than that of groups N (9.0 +/- 0.4 mm) and B (9.2 +/- 0.3 mm).(ABSTRACT TRUNCATED AT 250 WORDS)

Buserelin↗