Comparison of two trocar-guided trans-vaginal mesh systems for repair of pelvic organ prolapse: a retrospective cohort study

Contains fulltext : 127290.pdf (publisher's version ) (Closed access)INTRODUCTION AND HYPOTHESIS: The aim of this study was to compare failure and complication rates in patients who underwent a trocar-guided vaginal mesh repair with either a non-absorbable or a partially absorbable mesh. METHODS: Retrospective analysis of prospectively collected data from consecutive women undergoing either non-absorbable or partially absorbable mesh for symptomatic stage 2 prolapse or higher were evaluated at 12 months. Outcome measures included objective and subjective failure rates, patient's satisfaction, complications and perioperative outcomes. RESULTS: Five hundred and sixty-nine women (347 with non-absorbable mesh, 222 with partially absorbable mesh) were included. Failure rates were similar in the two groups; the re-operation rate in the untreated compartments was higher in the non-absorbable mesh group compared with the partially absorbable mesh group (5 % vs 1 %). Mesh exposure rate in the non-absorbable mesh group was 12 % and in the partially absorbable mesh group it was 5 %. Other complication and patient satisfaction rates were similar. CONCLUSIONS: Non-absorbable and partially absorbable mesh demonstrated similar outcome rates at 12 months. The risk of reoperation was lower for partially absorbable mesh. The mesh exposure rate was significantly lower for the partially absorbable mesh group compared with the non-absorbable mesh group

In the presence of L-NAME SERCA blockade induces endothelium-dependent contraction of mouse aorta through activation of smooth muscle prostaglandin H2/thromboxane A2 receptors

1. The mechanism of transient contractions induced by the sarcoplasmic–endoplasmic reticulum calcium ATPase (SERCA) blocker cyclopiazonic acid (CPA) in the presence of L-NAME was investigated in mouse aorta. 2. The contractions elicited by 10 μM CPA required an intact endothelium, were dependent upon external Ca(2+) and were prevented by 10 μM indomethacin, the inhibitor of prostaglandin synthesis, or 1 μM SQ29548, the specific prostaglandin H2/thromboxane A2 (PGH2/TXA2) receptor blocker. 3. A blocker of receptor/store operated Ca(2+) channels and voltage gated calcium channels (VGCC), SK&F 96365 (10 μM), completely abolished the contractions, while a specific blocker of VGCC nifedipine (1 μM) inhibited them by one third. 4. Dichlorobenzamyl hydrochloride, a blocker of Na(+)/Ca(2+) exchange effectively prevented return of tension to baseline value. 5. At higher concentrations (30–100 μM) CPA induced indomethacin-resistant tonic contractions of mouse aorta. The CPA dose response curve for tonic contractions is shifted to the right compared to the transient contractions suggesting that smooth muscle is less sensitive to CPA than endothelium. 6. PGH2/TXA2 receptors in mouse aorta are highly sensitive to the thromboxane analogue U46619 (EC(50) : 1.93 nM). This compound stimulates contractions even in the absence of external Ca(2+), which are abolished by the Rho-kinase inhibitor HA-1077. 7. The results suggest that 10 μM CPA induced capacitive Ca(2+) entry in endothelial cells stimulating the release of PGH2/TXA2, which subsequently caused smooth muscle contraction dependent on Ca(2+) influx and myofilament sensitization by Rho-kinase. Higher concentrations of CPA (30–100 μM) directly induced contraction of mouse aortic smooth muscle

Connexin 30 sets synaptic strength by controlling astroglial synapse invasion.

Astrocytes play active roles in brain physiology by dynamic interactions with neurons. Connexin 30, one of the two main astroglial gap-junction subunits, is thought to be involved in behavioral and basic cognitive processes. However, the underlying cellular and molecular mechanisms are unknown. We show here in mice that connexin 30 controls hippocampal excitatory synaptic transmission through modulation of astroglial glutamate transport, which directly alters synaptic glutamate levels. Unexpectedly, we found that connexin 30 regulated cell adhesion and migration and that connexin 30 modulation of glutamate transport, occurring independently of its channel function, was mediated by morphological changes controlling insertion of astroglial processes into synaptic clefts. By setting excitatory synaptic strength, connexin 30 plays an important role in long-term synaptic plasticity and in hippocampus-based contextual memory. Taken together, these results establish connexin 30 as a critical regulator of synaptic strength by controlling the synaptic location of astroglial processes