This survey study aims to examine the quality of planned oocyte cryopreservation (POC) decision-making in the domains of decision change, decision difficulty, decision regret and informed choice.

Of the 224 women who completed at least one POC cycle between 2012 and 2018 at a Canadian academic IVF centre, 198 were reachable by email for anonymous survey participation.

Ninety-eight questionnaires were returned (response rate 49.5%). Of these, 86 fully completed questionnaires were analyzed for this study. Eighty-eight percent of respondents stated that it was a ‘good decision’ to cryopreserve oocytes, in retrospect. Despite this, 31% found the decision-making process to be ‘difficult’. Three in five (61%) would have made ‘exactly the same’ decision without any change, yet slightly over a third (35%) would have made a ‘similar’ decision, but with option-related changes and process-related changes. A negative correlation between ‘decision regret’ and ‘informed choice’ was found (p < .005). Those who stated that they would have made exactly the ‘same’ POC decision were found to have a significantly higher ‘informed choice’ score compared to others who would have made a ‘similar’ or ‘completely different’ decision, in retrospect (p < .001). Respondents with lesser ‘decision regret’ were significantly more likely to appraise their decision as a well-informed choice (p < .001).

Our findings show that high-quality POC decision-making is accompanied by the perception of being able to make an informed choice, which can be achieved by providing patients with adequate information and individualized counselling to help patients set realistic expectations of cycle outcomes.

Our findings show that high-quality POC decision-making is accompanied by the perception of being able to make an informed choice, which can be achieved by providing patients with adequate information and individualized counselling to help patients set realistic expectations of cycle outcomes.

Previous research on the association between proton pump inhibitor (PPI) use and the risk of progression to high-grade dysplasia (HGD)/esophageal adenocarcinoma (EAC) in Barrett’s Esophagus (BE) patients has generated inconsistent findings. This meta-analysis was performed to clarify the association.

We performed a comprehensive search strategy to select relevant studies up to September 2020. Heterogeneity was assessed using the I-squared statistic. Odds ratios (OR) and 95% confidence intervals (CI) were calculated through either fixed-effects or random-effects model. Selleckchem BAY 2402234 Duration-response was also performed to assess the gain effects of different PPI intake duration. Sensitivity analysis, subgroup analyses, and tests for publication bias or other small-study effects were conducted.

Twelve studies with 155,769 subjects were included. The PPI use was associated with the reduced risk of BE progression to HGD/EAC (OR = 0.47, 95% CI = 0.32-0.71). In the duration-response analysis, the estimated OR for decreased risk of HGD/EAC with PPI intake duration of 12months was 0.81 (95% CI = 0.71-0.91). Sensitivity analysis suggested the results of this meta-analysis were stable. No publication bias was detected.

PPI use is associated with a decreased risk of HGD/EAC in patients with BE. For further investigation, that more well-designed studies are still needed to elucidate the protective effect of PPI usage on BE patients to prevent HGD/EAC.

PPI use is associated with a decreased risk of HGD/EAC in patients with BE. For further investigation, that more well-designed studies are still needed to elucidate the protective effect of PPI usage on BE patients to prevent HGD/EAC.Corticosteroids (CS), first-line therapeutics for Crohn’s disease (CD) with moderate or severe disease activity, were found to restore intestinal permeability in CD patients, whereas the underlying molecular events are still largely unknown. This study aimed to investigate the effect and mechanisms of CS prednisolone on epithelial barrier using CD patient-derived intestinal organoids. 3D intestinal organoids were generated from colon biopsies of inactive CD patients. To mimic the inflammatory microenvironment, a mixture of cytokines containing TNF-α, IFN-γ, and IL-1β were added to the organoid culture with or without pre-incubation of prednisolone or mifepristone. Epithelial permeability of the organoids was assessed by FITC-D4 flux from the basal to luminal compartment using confocal microscopy. Expression of junctional components were analyzed by qRT-PCR, immunofluorescence staining, and western blot. Activity of signaling pathways were analyzed using western blot. Exposure of the cytokines significantly disrupted epithelial barrier of the intestinal organoids, which was partially restored by prednisolone. On the molecular level, the cytokine mixture resulted in a significant reduction in E-cadherin and ILDR-1, an increase in CLDN-2, MLCK, and STAT1 phosphorylation, whereas prednisolone ameliorated the abovementioned effects induced by the cytokine mixture. This study demonstrates that prednisolone confers a direct effect in tightening the epithelial barrier, identifies novel junctional targets regulated by prednisolone, and underscores intestinal barrier restoration as a potential mechanism that contributes to the clinical efficacy of prednisolone in CD patients. KEY MESSAGES Prednisolone confers a direct preventive effect against cytokine-induced barrier dysfunction. Prednisolone regulates the expression of CLDN-2, E-cadherin, and ILDR-1. The effect of prednisolone is GR-, MLCK-, and STAT1-dependent.Age-related macular degeneration (AMD) is mainly characterized by the progressive accumulation of drusen deposits and loss of photoreceptors and retinal pigment epithelial (RPE) cells. Because amyloid β (Aβ) is the main component of drusen, Aβ-induced activated microglia most likely lead to neuroinflammation and play a critical role in the pathogenesis of AMD. However, the relationship between activated microglia-mediated neuroinflammatory cytokines and photoreceptor death has not been clarified. By subretinal injection of Aβ42 in mice, we mimicked an inflammatory milieu of AMD to better understand how activated microglia-induced neuroinflammatory cytokines lead to photoreceptor apoptosis in the AMD progression. We demonstrated that subretinal injection of Aβ42 induces microglial activation and increases inflammatory cytokine release, which gives rise to photoreceptor apoptosis in mice. Our results were verified in vitro by co-culture of Aβ42 activated primary microglia and the photoreceptor cell line 661W. We also demonstrated that the p38 mitogen-activated protein kinase (MAPK) signaling pathway was involved in Aβ42-induced microglial activation and inflammatory cytokine release.