Bladder neck mobility in continent nulliparous women

To evaluate the mobility of the vesical neck during coughing and valsalva in healthy nulliparous volunteers and to test the reliability of the technique applied. Design Clinical observational study. Setting Department of Obstetrics and Gynaecology, Cantonal Hospital Lucerne, Switzerland. Population Thirty-nine nulliparous volunteers. Methods Vesical neck motion was assessed with perineal ultrasound. Intra–abdominal pressure was controlled for with an intrarectal probe. Intra-rater reliability was evaluated. Results Vesical neck mobility was significantly lower during coughing (8 mm, SD 4 mm) than during valsalva (15 mm, SD 10 mm) ( P < 0.005 ). Between individuals mobility varied from 4 mm to 32 mm during coughing and from 2 mm to 31 mm during valsalva. Test-retest-studies showed a maximum difference between to tests during coughing of 4 mm and during valsalva of 5 mm. Conclusion The bladder neck is mobile in normal continent women and bladder neck mobility is lower during coughing than during Valsalva.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74987/1/j.1471-0528.2001.00066.x.pd

IKKα Regulates Mitogenic Signaling through Transcriptional Induction of Cyclin D1 via Tcf

The Wnt/β-catenin/Tcf and IκB/NF-κB cascades are independent pathways involved in cell cycle control, cellular differentiation, and inflammation. Constitutive Wnt/β-catenin signaling occurs in certain cancers from mutation of components of the pathway and from activating growth factor receptors, including RON and MET. The resulting accumulation of cytoplasmic and nuclear β-catenin interacts with the Tcf/LEF transcription factors to induce target genes. The IκB kinase complex (IKK) that phosphorylates IκB contains IKKα, IKKβ, and IKKγ. Here we show that the cyclin D1 gene functions as a point of convergence between the Wnt/β-catenin and IκB pathways in mitogenic signaling. Mitogenic induction of G(1)-S phase progression and cyclin D1 expression was PI3K dependent, and cyclin D1(−/−) cells showed reduced PI3K-dependent S-phase entry. PI3K-dependent induction of cyclin D1 was blocked by inhibitors of PI3K/Akt/IκB/IKKα or β-catenin signaling. A single Tcf site in the cyclin D1 promoter was required for induction by PI3K or IKKα. In IKKα(−/−) cells, mitogen-induced DNA synthesis, and expression of Tcf-responsive genes was reduced. Reintroduction of IKKα restored normal mitogen induction of cyclin D1 through a Tcf site. In IKKα(−/−) cells, β-catenin phosphorylation was decreased and purified IKKα was sufficient for phosphorylation of β-catenin through its N-terminus in vitro. Because IKKα but not IKKβ induced cyclin D1 expression through Tcf activity, these studies indicate that the relative levels of IKKα and IKKβ may alter their substrate and signaling specificities to regulate mitogen-induced DNA synthesis through distinct mechanisms