Our results indicate that among women who have good quality embryos in their first IVF/ICSI, good treatment results can be achieved. They support the idea of changing embryo transfer policy towards one embryo transfer without any remarkable decrease in the success rate, while dizygotic twins can be avoided.

The presence of ≥1 top quality embryo at any step of the freezing and thawing process increases the chance of pregnancy. The data do not support the freezing of all embryos for transfer in order to improve the outcome. A top quality embryo transferred in FET may even have the same potential as in a fresh cycle. On the contrary, LBR in the group with no top quality embryos frozen was quite low (10.4%), raising the question of whether a re-evaluation of freezing criteria is necessary to avoid costly treatments with a low success rate.

The biological activity of certain estrogens and androgens is modulated by enzymes called 17p-hydroxysteroid dehydrogenases (I~P-HSDS), which catalyze the interconversion between less active 17-oxosteroid and more active 17P-hydroxysteroid forms. In the present report, we describe cloning of mouse 17P-HSD type-I cDNA from an ovarian library generated from 4,4'-( 1,2-diethyl-I ,2-ethenediyl)bisphenol-(diethylstiIbestro1)-treated mice, and characterization of the corresponding enzyme. The open reading frame of the mouse 17P-HSD type-1 cDNA encodes a peptide of 344 amino acid residues with a predicted molecular mass of 3678.5 Da. The mouse 17P-HSD type-1 enzyme shares 63 % and 93 % overall identity with human and rat 17P-HSD type-I enzymes, respectively, and the most striking differences between the mouse and human type-1 enzymes are between the amino acid residues 197 and 230 and in the carboxy terminus of the enzymes. Similarly to the human 17P-HSD type-I enzyme, the mouse type-I enzyme primarily catalyzes reductive reactions from 17-0x0 forms to 17P-hydroxy forms in intact cultured cells, but unlike the human type-I enzyme, the mouse enzyme does not prefer phenolic over neutral substrates. Thus, mouse 17P-HSD type 1 catalyzes reduction of androst-4-ene-3,17-dione (androstenedione) to 17P-hydroxyandrost-4-en-3-one (testosterone) as efficiently as 3P-hydroxyestra-l,3,.5(10)-trien-17-one (estrone) to estra-1,3,5(10)-triene-3~,17~-diol (estradiol). 17P-HSD type 1 is predominantly expressed in mouse ovaries, in which it is located in granulosa cells.Keywords: 17-hydroxysteroid dehydrogenases ; cloning ; mouse; estrogen ; B1 repetitive sequence.17P-Hydroxysteroid dehydrogenases (17p-HSDs) catalyze the conversion of neutral and phenolic 17-oxosteroids to 17P-hydroxysteroids and vice versa. Both androgens and estrogens are biologically more active in their l7P-hydroxy configurations, such as 17P-hydroxyandrost-4-en-3-one (testosterone) and estra-1,3,S(10)-triene-3~,17~-diol (estradiol), than in their 17-0x0 configuration. Thus, 17P-HSDs, along with other steroidogenic enzymes such as 3P-hydroxysteroid dehydrogenases and Sa-reductases, modulate the biological activity of the sex steroids.

A high cumulative pregnancy rate per oocyte retrieval can be achieved after eSET in daily clinical practice. The implantation rate of fresh top-quality embryos in the ICSI cycles was significantly higher than in the IVF cycles, possibly due to more successful selection of the embryo for embryo transfer on day 2 after ICSI. In addition, our data suggest that embryo quality is a more important determinant of outcome than the age of the woman.

The inhibitory effects of recombinant porcine interferon-gamma (IFN gamma) on human CG (hCG)-stimulated testosterone production, and on mRNA concentrations of cholesterol side-chain cleavage (P450scc) and 17 alpha-hydroxylase/C17-20lyase (P450c 17) were investigated using porcine primary Leydig cell culture as a model. After preincubation of Leydig cells for 24 h with 1000 pM IFN gamma, hCG-stimulated (10 ng/ml, 2 h) testosterone production was inhibited by 50%, whereas no significant changes were seen in hCG-stimulated cAMP production. Incubation with 10 microM 5-cholestene-3 beta,22(R)-diol or 10 microM 5-cholestene-3 beta,20 alpha-diol together with hCG (10 ng/ml, 2 h) reversed most of the inhibitory effect of IFN gamma, suggesting that IFN gamma inhibits P450scc activity, possibly by inhibiting the substrate (cholesterol) availability for P450scc. Incubation with IFN gamma also decreased basal concentrations of P450scc (45%) and P450c 17 (35%) mRNA, although these changes probably did not contribute to the decreased testosterone production. Long-term treatment with hCG (100 ng/ml, 24 h) increased P450scc mRNA (3- to 4-fold) and P450c 17 mRNA (4- to 5-fold) concentrations. Simultaneous treatment with IFN gamma attenuated these hCG-induced increases in P450scc mRNA (50%) and P450c 17 mRNA (40-100%) concentrations, as well as in testosterone production (77%). This inhibition of testosterone production could only be partly reversed by the hydroxylated cholesterol derivatives. This suggests that in addition to possible suppression of cholesterol availability, decreased P450scc and/or P450c 17 activities (through decreased mRNA concentrations) were also involved in the IFN gamma suppressed steroidogenic capacity of porcine Leydig cells during long-term hCG stimulation.