Transvaginal cervical cerclage - How well do surgeons assess their own procedures?

Introduction: In women with cervical incompetence, transvaginal cerclage may help prevent preterm birth. However, training for this procedure poses challenges due to the low number of cases and difficulties in visualizing the operative field. Furthermore, the objective criteria for a successful cerclage procedure are not well-described.

EHD2 regulates plasma membrane integrity and downstream insulin receptor signaling events.

Adipocyte dysfunction is a crucial driver of insulin resistance and type 2 diabetes. We identified EH domain-containing protein 2 (EHD2) as one of the most highly upregulated genes at the early stage of adipose-tissue expansion. EHD2 is a dynamin-related ATPase influencing several cellular processes, including membrane recycling, caveolae dynamics, and lipid metabolism.

Cervical cerclage technique: what do experts actually achieve?

Background: Cervical cerclage is a recognized intervention in the management of women at risk of preterm birth and midtrimester loss. The mechanism of action of cerclage is unclear, and the technique has been poorly researched.

Objective: This study aimed to evaluate cerclage technique among experienced obstetricians, using a previously developed and evaluated cerclage simulator.

Cervical cerclage training: Development and assessment of a simulator.

Background: Cervical cerclage is a mainstay intervention for the prevention of spontaneous preterm birth in high-risk women. Simulation training facilitates high-level skill transfer in a low-consequence environment, and is being integrated into obstetrics and gynecology training.

Objective: This study aimed to develop a simulator for cervical cerclage, determine its validity as a simulator, and identify parameters suitable as proxy markers for performance.

EFR3 and phosphatidylinositol 4-kinase IIIα regulate insulin-stimulated glucose transport and GLUT4 dispersal in 3T3-L1 adipocytes.

Insulin stimulates glucose transport in muscle and adipocytes. This is achieved by regulated delivery of intracellular glucose transporter (GLUT4)-containing vesicles to the plasma membrane where they dock and fuse, resulting in increased cell surface GLUT4 levels. Recent work identified a potential further regulatory step, in which insulin increases the dispersal of GLUT4 in the plasma membrane away from the sites of vesicle fusion.