TCM AP is superior to sham AP and verum CHM in reducing menopausal symptoms, whereas verum CHM shows no significant improvements when compared with placebo CHM.

Follicle flushing has been proved to be ineffective in polyfollicular in vitro fertilization. To analyze the effect of flushing in monofollicular in vitro fertilization we aspirated and then flushed the follicles in 164 cycles. Total oocyte yield/aspiration was 44.5% in the aspirate, 20.7% in the 1st flush, 10.4% in the 2nd flush and 4.3% in the 3rd flush. By flushing, the total oocyte yield increased (p < 0.01) by 80.9%, from 44.5 to 80.5%. The total transfer rate increased (p < 0.01) by 91.0%, from 20.1 to 38.4%. The results indicate that the oocyte yield and the number of transferable embryos can be increased significantly by flushing.

Inactivation of the tumor-suppressor gene p16 (MTS1/ CDKN2/INK4a) has been described in various human malignancies. Although p16 deletion has been found in various ovarian tumor cell lines, p16 inactivation by homozygous deletion or mutation has been reported only sporadically in primary ovarian carcinomas. In a comprehensive study, we analyzed p16 protein expression by immuno-histochemistry (IHC) on paraffin sections of 94 primary ovarian carcinomas of different histological subtype. Loss of expression was detected in 19 primary tumors (20%), mainly mucinous and endometrioid carcinomas. To reveal the cause of suppressed expression, we performed (i) analysis of homozygous deletions by comparative PCR after micro-dissection, (ii) mutation analysis by single-strand conformation polymorphism analysis and subsequent direct sequencing and (iii) methylation-specific PCR to determine the methylation status of 5Ј-CpG islands. Loss of or weak p16 expression was caused by hyper-methylation (12/19 IHC-negative cases), somatic mutation (10 tumors) or homozygous deletion (1 case). Aberrant p16 results by one of these methods were detected in 71-79% of endometrioid and mucinous, but in only 10% of serous-papillary, carcinomas. Our data suggest that p16 inactivation is a typical feature of certain subtypes of ovarian carcinoma. Int. J. Cancer (Pred. Oncol.) 75:61-65, 1998. Wiley-Liss, Inc.Deregulation and acceleration of the normal cell cycle is one of the main features of malignant tumor growth. Progression through the cell cycle is regulated by several cyclin-dependent kinases (cdks) and their associated cyclin cofactors. Via phosphorylation, cdks modulate the activity of important transcription factors, among them the retinoblastoma protein RB, while they themselves are regulated by binding of cdk inhibitors (CKIs), among them MTS1/p16.Mice deficient in p16 develop various spontaneous tumors at an early age and are highly sensitive to carcinogenic treatments (Serrano et al., 1996). In humans, inactivation of p16 by deletion or mutation has been described in various tumor cell lines and in a small fraction of primary tumors, predominantly cancer of the pancreas, bladder or esophagus, as well as in glioblastomas and familial melanomas (Cairns et al., 1994;Shapiro and Rollins, 1996). Hyper-methylation of CpG islands in the 5Ј-region leading to reduced expression has been found in several tumors as an additional way of p16 inactivation (Herman et al., 1995). In ovarian carcinomas studied so far, homozygous deletion was detected in 0-14% of tumors, whereas somatic mutations were not found (Campbell et al., 1995;Rodabaugh et al., 1995;Schultz et al., 1995;Schuyer et al., 1996). In the present study, we analyzed p16 protein expression in ovarian carcinomas by immuno-histochemistry (IHC). Our results clearly show that loss of expression is mainly a feature of mucinous and endometrioid histological types, whereas the major group of serous-papillary carcinomas is generally p16-positive. To reveal the mechanism of p16 inactivation, mu...

In-vitro-Fertilisation Zusammenfassung Das Risiko für das Auftreten einer Adnextorsion nach einer IVF-Behandlung wird auf ca. 0,1% geschätzt. Aufgrund der Seltenheit und des initial oft unauffälligen sonographischen Befundes wird eine Adnextorsion oft fehldiagnostiziert und die Behandlung verzögert. Die einzige effektive Therapie ist eine sofortige Laparoskopie, Retorsion und Verkleinerung des Ovars.

Die hormonelle Umstellung in den Wechseljahren kann zu subjektiv sehr belastenden Verände-rungen von Haut und Haaren führen. Einigen Zeichen der Hautalterung kann eine topische Ös-trogentherapie entgegenwirken, eine systemische Hormontherapie ist jedoch nicht indiziert. Von den zahlreichen Haarerkrankungen in der Dermatologie sind für die Gynäkologie mit Schwerpunkt Wechseljahre v. a. die androgenetische Alopezie und der Hirsutismus relevant. Die androgenetische Alopezie der Frau ist klinisch nach dem Ludwig-Schema einteilbar, der Hirsutismus nach dem Ferriman-Gallwey-Index. Die Labordiagnostik ist 3-stufig. Zur Differenzialdiagnose der Alopezie ist ein Trichogramm hilfreich. Die Therapie der androgenetischen Alopezie erfolgt primär lokal mit 2% Minoxidil-Lösung und Alfatradiol. Die Therapie des Hirsutismus umfasst topisches Eflornithin, systemisch kommen steroidale und nichtsteroidale DHT-Rezeptor-Blocker sowie 5α-Reduktase-Blocker zur Anwendung. SchlüsselwörterWechseljahre · Hautalterung · Alopezie · Hirsutismus · Topische und systemische Therapie Effect of the menopause on skin and hair AbstractHormonal changes due to the menopause may induce troublesome alterations of skin and hair. Some effects of skin ageing can be counteracted by local estrogen therapy. However, due to insufficient data systemic hormone therapy is not recommended for this indication. There are various hair diseases in dermatology. This report focuses on those relevant for the gynaecological practice at menopause. Androgenetical alopecia in women may be clinically evaluated by the Ludwig scale and hirsutism by the Ferriman-Gallwey index. Furthermore a 3-step laboratory testing and trichogram for alopecia are recommended. Androgenetical alopecia should be treated locally (2% minoxidil solution, alfatradiol). Hirsutism treatment involves topical (eflornithine) and systemic options (steroidal and non-steroidal DHT receptor inhibitors, 5α-reductase inhibitor).