A systematic review of amniopatch

The objective of this review is to evaluate the safety and effectiveness of the amniopatch procedure for the treatment ofpreterm premature rupture of the membranes. The searches were conducted via electronic databases including Ovid-MEDLINE, Ovid-Embase, the Cochrane Library, and eight Korean databases. In the study design, in addition to randomized controlled trials, case report studies in which patients underwent the amniopatch procedure were included. Two reviewers independently selected data in standardized form and assessed the methodological quality. Quality evaluation was performed by the SIGN (Scottish Intercollegiate Guideline Network) method. A total of 11 studies (2 cohort studies, 1 case series, and 8 case reports) were included. There were no serious maternal or fetal complications. It was reported that there were lower rates of maternal chorioamnionitis after the amniopatch relative to conservative treatment (control). The mean gestational age at delivery was 27.7 weeks (a total of 70 cases in 10 studies; spontaneous group, 27.6 weeks; iatrogenic group, 27.8 weeks). The amniopatch was successful in 46.6% of cases (33/71 cases in 11 studies). The overall neonatal survival rate was 55.3% (52/94 cases in 11 studies). Neonatal morbidity was 23.4% (11/47 cases in 7 studies). Although this systematic review, did not find clear evidence of the safety and effectiveness, the amniopatch procedure is a viable treatment option to prolong a pregnancy with previable premature rupture of membranes.

GSK3beta Inhibitor Peptide Protects Mice from LPS-induced Endotoxin Shock

BACKGROUND: Glycogen synthase kinase 3beta (GSK3beta) is a ubiquitous serine/threonine kinase that is regulated by serine phosphorylation at 9. Recent studies have reported the beneficial effects of a number of the pharmacological GSK3beta inhibitors in rodent models of septic shock. Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. METHODS: Based on the unique phosphorylation motif of GSK3beta, we designed and generated a novel class of GSK3beta inhibitor (GSK3i) peptides. In addition, we investigated the effects of a GSK3i peptide on lipopolysaccharide (LPS)-stimulated cytokine production and septic shock. Mice were intraperitoneally injected with GSK3i peptide and monitored over a 7-day period for survival. RESULTS: We first demonstrate its effects on LPS-stimulated pro-inflammatory cytokine production including interleukin (IL)-6 and IL-12p40. LPS-induced IL-6 and IL-12p40 production in macrophages was suppressed when macrophages were treated with the GSKi peptide. Administration of the GSK3i peptide potently suppressed LPS-mediated endotoxin shock. CONCLUSION: Collectively, we present a rational strategy for the development of a therapeutic GSK3i peptide. This peptide may serve as a novel template for the design of non-ATP competitive GSK3 inhibitors.