ImportanceWomen with interstitial cystitis/bladder pain syndrome (ICBPS) face isolation and treatment challenges. Group medical visits using Centering models have successfully treated other conditions but have not been explored in ICBPS.ObjectiveThis study aimed to describe ICBPS pain and symptom control comparing standard treatment alone versus standard treatment augmented with Centering visits.Study DesignThis prospective cohort study recruited women with ICBPS receiving standard care (control) or standard care augmented with group Centering. We administered validated questionnaires at baseline and monthly for 12 months. The primary outcome was change in the pain numerical rating scale, with Patient-Reported Outcomes Measurement Information System Pain Interference Scale and Bladder Pain/Interstitial Cystitis Symptom Score change as secondary measures.ResultsWe enrolled 45 women (20 Centering, 25 controls). Centering had significantly better numerical rating scale pain scores at 1 month (mean difference [diff], −3.45) and 2 months (mean diff, −3.58), better Patient-Reported Outcomes Measurement Information System Pain Interference Scale scores at 1 month (mean diff, −10.62) and 2 months (mean diff, −9.63), and better Bladder Pain/Interstitial Cystitis Symptom Score scores at 2 months (mean diff, −13.19), and 3 months (mean diff, −12.3) compared with controls. In modeling, treatment group (Centering or control) and educational levels were both associated with all the outcomes of interest. Beyond 6 months, there were too few participants for meaningful analyses.ConclusionsWomen with ICBPS participating in a Centering group have, in the short term, less pain, pain interference, and ICBPS-specific symptoms than patients with usual care alone. Larger studies with more follow-up are needed to determine if this treatment effect extends over time.

No abstract

No abstract

Previous investigations have indicated that c-Jun N-terminal kinase (JNK) regulates the maturation and aging of oocytes produced by deuterostome animals. In order to assess the roles of this kinase in a protostome, oocytes of the marine nemertean worm Cerebratulus were stimulated to mature and subsequently aged before being probed with phospho-specific antibodies against active forms of JNK and maturation-promoting factor (MPF). Based on blots of maturing oocytes, a 40-kD putative JNK is normally activated during germinal vesicle breakdown (GVBD), which begins at 30 min post-stimulation with seawater, whereas treating immature oocytes with JNK inhibitors downregulates both the 40-kD JNK signal and GVBD, collectively suggesting a 40-kD JNK may facilitate oocyte maturation. Along with this JNK activity, mature oocytes also exhibit high levels of MPF at 2 h post-stimulation. However, by ~6-8 h post-GVBD, mature oocytes lose the 40-kD JNK signal, and at ~20-30 h of aging, an ~48-kD phospho-JNK band arises as oocytes deactivate MPF and begin to lyse during a necroptotic-like mode of death. Accordingly, JNK inhibitors reduce the aging-related 48-kD JNK phosphorylation while maintaining MPF activity and retarding oocyte degradation. Such findings suggest that a 48-kD JNK may help deactivate MPF and trigger death. Possible mechanisms by which JNK activation either together with, or independently of, protein neosynthesis might stimulate oocyte degradation are discussed.

No abstract