Exploring predictors of mesh exposure after vaginal prolapse repair.

Objectives: To evaluate clinical, demographic, and surgical factors that may be associated with mesh exposure after vaginal repair of pelvic organ prolapse (POP).

Methods: Records of women who underwent POP repair with Elevate or Prolift were retrospectively reviewed. Body mass index (BMI), prolapse grade, smoking history, diabetes, steroid and estrogen use, parity, compartment repaired, concurrent hysterectomy, operative time, postoperative pain, change in hemoglobin (ΔHgb) and other characteristics were evaluated for associations with mesh exposure.

Apremilast in the Treatment of Chronic Prostatitis/Chronic Pelvic Pain Syndrome: A Pilot Study.

Objective: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a disease with an uncertain cause and limited effective treatments. Apremilast (Celgene Corporation, Summit, NJ, USA) is a selective phosphodiesterase type 4 (PDE4) inhibitor that modulates the immune system. An open-label, one-arm, pilot study was conducted to explore its potential for improving CP/CPPS symptoms.

Perioperative experience of pelvic organ prolapse repair with the Prolift and Elevate vaginal mesh procedures.

Introduction And Hypothesis: We compared the operative and immediate postoperative experience of the trocar-based Prolift and non-trocar-based Elevate techniques used to repair vaginal prolapse.

Methods: A retrospective review of Prolift and Elevate repairs was performed. Baseline characteristics and operative and postoperative variables evaluated included compartment(s) repaired, adjacent organ injury, operative time (OT), change in hemoglobin (ΔH), pain score, narcotic use, length of stay (LOS), and short-term complications.

Inhibition of EGF-induced ERK/MAP kinase-mediated astrocyte proliferation by mu opioids: integration of G protein and beta-arrestin 2-dependent pathways.

Although micro, kappa, and delta opioids activate extracellular signal-regulated kinase (ERK)/mitogen-activated protein (MAP) kinase, the mechanisms involved in their signaling pathways and the cellular responses that ensue differ. Here we focused on the mechanisms by which micro opioids rapidly (min) activate ERK and their slower (h) actions to inhibit epidermal growth factor (EGF)-induced ERK-mediated astrocyte proliferation. The micro-opioid agonists ([d-ala(2), mephe(4), gly-ol(5)] enkephalin and morphine) promoted the phosphorylation of ERK/MAP kinase within 5 min via G(i/o) protein, calmodulin (CaM), and beta-arrestin2-dependent signaling pathways in immortalized and primary astrocytes.

Kappa opioids promote the proliferation of astrocytes via Gbetagamma and beta-arrestin 2-dependent MAPK-mediated pathways.

GTP binding regulatory protein (G protein)-coupled receptors can activate MAPK pathways via G protein-dependent and -independent mechanisms. However, the physiological outcomes correlated with the cellular signaling events are not as well characterized. In this study, we examine the involvement of G protein and beta-arrestin 2 pathways in kappa opioid receptor-induced, extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated proliferation of both immortalized and primary astrocyte cultures.