Neonatal admission rate after vaginal breech delivery.

OBJECTIVES: The safest mode of delivery for fetuses in breech presentations is still an ongoing debate. The aim of this study was to analyze neonatal admission rates after vaginal breech delivery and compare it to other modes of delivery in order to counsel pregnant women with breech presentation adequately. METHODS: We performed a retrospective monocentric analysis of all deliveries with singleton pregnancies in breech presentation > 36.0 weeks of gestation between 01/2018-12/2019. Short-term neonatal morbidity data was collected for vaginal delivery and primary as well as secondary cesarean sections from breech presentations. RESULTS: A total of n=41/482 (8.5%) neonates had to be admitted to NICU: vaginal breech delivery n=18/153 (11.8%), primary cesarean section n=9/101 (8.9%, OR 0.73; CI 0.32-1.70; p=0.47), secondary cesarean section n=10/76 (13.2%, OR 1.14; CI 0.50-2.60, p=0.76) and vaginal vertex delivery n=4/152 (2.6%, OR 0.20; CI 0.06-0.51; p=0.005). There was no significant difference in transfer to NICU between all breech position delivery modes. Despite significantly lower pH and 5' APGAR values after vaginal delivery, neonates delivered by primary cesarean section and NICU admission had to be treated there significantly longer (mean 80.9 vs. 174.0 h). No significant difference in terms of ventilation parameters and infections were found between the vaginal delivery, primary and secondary cesarean section from breech presentation. CONCLUSIONS: Vaginal breech delivery does not result in a higher neonatal admission rate in comparison to primary and secondary section. In contrast, there is a shorter NICU duration in case of neonatal admission after vaginal delivery.

ILKAP, ILK and PINCH1 control cell survival of p53-wildtype glioblastoma cells after irradiation.

The prognosis is generally poor for patients suffering from glioblastoma multiforme (GBM) due to radiation and drug resistance. Prosurvival signaling originating from focal adhesion hubs essentially contributes to therapy resistance and tumor aggressiveness. As the underlying molecular mechanisms remain largely elusive, we addressed whether targeting of the focal adhesion proteins particularly interesting new cysteine-histidine-rich 1 (PINCH1), integrin-linked kinase (ILK) and ILK associated phosphatase (ILKAP) modulates GBM cell radioresistance. Intriguingly, PINCH1, ILK and ILKAP depletion sensitized p53-wildtype, but not p53-mutant, GBM cells to radiotherapy. Concomitantly, these cells showed inactivated Glycogen synthase kinase-3ß (GSK3ß) and reduced proliferation. For PINCH1 and ILKAP knockdown, elevated levels of radiation-induced γH2AX/53BP1-positive foci, as a marker for DNA double strand breaks, were observed. Mechanistically, we identified radiation-induced phosphorylation of DNA protein kinase (DNAPK), an important DNA repair protein, to be dependent on ILKAP. This interaction was fundamental to radiation survival of p53-wildtype GBM cells. Conclusively, our data suggest an essential role of PINCH1, ILK and ILKAP for the radioresistance of p53-wildtype GBM cells and provide evidence for DNAPK functioning as a central mediator of ILKAP signaling. Strategies for targeting focal adhesion proteins in combination with radiotherapy might be a promising approach for patients with GBM.