Impact of retained embryos on the outcome of assisted reproductive technologies.

OBJECTIVE: To assess the impact of embryo retention in the embryo transfer catheter followed by "immediate" retransfer on pregnancy outcome in women undergoing assisted reproduction. DESIGN: Retrospective analysis of embryo transfer following in vitro fertilization. SETTING: Assisted reproductive technology practice in a university in vitro fertilization program. PATIENT(S): In vitro fertilization charts for 1,812 embryo transfer cycles representing 1,139 patients between January 1997 and March 2002 were reviewed. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Pregnancy rate, implantation rate, delivery rate. RESULT(S): Three embryo transfer cycles were excluded from analysis because of missing data, leaving 1,364 embryo transfers during oocyte recovery cycles and 445 embryo transfer cycles using thawed embryos. Seventy-one embryo transfers (3.9% of all transfers) were complicated by finding retained embryos after the initial embryo transfer-all retained embryos were immediately retransferred. There was no difference in the frequency of retained embryos during oocyte retrieval versus thawed embryo cycles. The pregnancy, implantation, and delivery rates per embryo transfer were not negatively affected by embryo(s) retained in the transfer catheter. Age, fresh versus frozen embryo, use of ultrasound during the procedure, or transferring physician did not influence pregnancy outcome. CONCLUSION(S): Immediate retransfer of embryos retained in the catheter following the initial transfer attempt did not have an adverse effect on pregnancy outcome.

Identification of mammalian Sds3 as an integral component of the Sin3/histone deacetylase corepressor complex.

Silencing of gene transcription involves local chromatin modification achieved through the local recruitment of large multiprotein complexes containing histone deacetylase (HDAC) activity. The mammalian corepressors mSin3A and mSin3B have been shown to play a key role in this process by tethering HDACs 1 and 2 to promoter-bound transcription factors. Similar mechanisms appear to be operative in yeast, in which epistasis experiments have established that the mSin3 and HDAC orthologs (SIN3 and RPD3), along with a novel protein, SDS3, function in the same repressor pathway. Here, we report the identification of a component of the mSin3-HDAC complex that bears homology to yeast SDS3, physically associates with mSin3 proteins in vivo, represses transcription in a manner that is partially dependent on HDAC activity, and enables HDAC1 catalytic activity in vivo. That key physical and functional properties are also shared by yeast SDS3 underscores the central role of the Sin3-HDAC-Sds3 complex in eukaryotic cell biology, and the discovery of mSds3 in mammalian cells provides a new avenue for modulating the activity of this complex in human disease.