Clinical epidemiology and outcomes of emergency department-acute kidney injury: A systematic review.

Background: Over half of all community-acquired acute kidney injury (CA-AKI) initially presented to emergency department (ED), but emergency department acute kidney injury (ED-AKI) is poorly characterised, poorly understood with no systematic review, often under-recognized and under-managed. Objective: To review the incidence, risk factors, and outcomes of ED-AKI, and risk factors of post-ED-AKI mortality globally. Methods: We included published prospective or retrospective observational studies, controlled trials, and systematic reviews reporting AKI in adult ED attendees within 24 h of ED admission. Iatrogenic causes of AKI from medical interventions were excluded. We used PubMed to identify articles from 1996 to August 14, 2021, and adopted the National Heart, Lung, and Blood Institute (NHLBI) Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies to assess risk of bias. We used a Forest plot to present pooled ED-AKI incidence rates and I2 statistics. Other parameters were summarized narratively. Results: Using 24 h from ED admission as the definition for ED-AKI we identified six articles from 2005 to 2018 in high-income settings and one article with a 48-h timeframe. The pooled incidence of ED-AKI was 20 per 1000 adult ED attendances. Risk factors for ED-AKI included increasing age, nursing home residence, previous hospital admission within 30 days, discharge diagnosis of diabetes, obstructive uropathy, sepsis, gastrointestinal medical conditions, high serum creatinine, bilirubin, C-reactive protein, white blood cell, alanine aminotransferase, low serum sodium or albumin on admission, poor premorbid renal function, antibiotic use, active malignancy, lung disease, hyperlipidaemia, and infection. Crude, all-cause 24-h mortality rate was 4.56 % and the one-year mortality rate was 35.04 %. Increasing age and comorbidities including cardiovascular disease and malignancy were associated with higher mortality rates. Conclusion: The review reveals a paucity of relevant literature which calls for further research, increased vigilance, red flag identification, and standardized management protocols for ED-AKI.

Suicide ideation in older people: a qualitative review and Meta-aggregation of Asian studies.

Aims: To appraise and synthesize qualitative studies examining older Asian people's experiences of suicidal ideation. Design: Qualitative review and meta-aggregation. Data sources: Four databases were accessed to retrieve papers published between 1990 and 2022 including the grey literature, hand-searching of reference lists of retrieved papers and key journals. The phenomenon of interest included participants older than 60 years old, must have experienced a form of suicidal ideation and/or an unsuccessful attempt, had actively thought about harming themselves and be of Asian ethnicity. Review methods: This review was conducted according to Consolidated Criteria for Reporting Qualitative Research and the Joanna Briggs Institute's System for the Unified Management of the Assessment and Review of Information. Results: Of the 289 potential studies, seven papers met the inclusion criteria. Two synthesized findings resulted from this review-The Suffering Situation: A Life without Meaning in Older Age and The Healing Situation: A Life Worth Living. The experiences of older Asian people varied from feelings of loneliness, despair and isolation to wanting to live a fruitful life into old age. Conclusion: Suicidal ideation in the older person is a growing concern especially with the rise in suicide in this age group. Rising health care costs and erosion of traditional family values means that the older person views themselves as a burden. However, because of the limited number of qualitative studies from an Asian perspective it is difficult to ascertain the full extent of the issues surrounding suicide in older people.

Perfluorooctanoate suppresses spheroid attachment on endometrial epithelial cells through peroxisome proliferator-activated receptor alpha and down-regulation of Wnt signaling.

Exposure of animals to perfluorooctanoic acid (PFOA), a surfactant used in emulsion polymerization processes causes early pregnancy loss, delayed growth and development of fetuses. The mechanisms of action are largely unknown. We studied the effect of PFOA on implantation using an in vitro spheroid-endometrial cell co-culture model. PFOA (10-100µM) significantly reduced Jeg-3 spheroid attachment on RL95-2 endometrial cells. PFOA also suppressed ß-catenin expression in Jeg-3 cells. The Wnt agonist Wnt3a stimulated ß-catenin expression in Jeg-3 cells and reversed the PFOA suppression of the spheroid attachment. The putative PFOA receptors (PPARα, ß, γ) present in both cell lines were not affected by PFOA (0.01-100µM). The PPARα antagonist MK886 restored the ß-catenin and E-cadherin expression levels in Jeg-3 cells and reversed the suppression of the spheroid attachment caused by PFOA. Taken together, PFOA suppresses spheroid attachment through PPARα and Wnt signaling pathways via down-regulation of ß-catenin and E-cadherin expression.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway.

The environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects embryo development, implantation and fertility in humans. The underlying molecular mechanism by which TCDD suppresses implantation remains largely unknown. We used the trophoblastic spheroids (embryo surrogate)-endometrial cells co-culture assay to study the attachment of trophoblastic spheroids (BeWo and Jeg-3) onto the endometrial epithelial (RL95-2 and Ishikawa) cells. TCDD dose-dependently induced cytochrome P450 1A1 (Cyp1A1) expression in trophoblastic and endometrial epithelial cells. Moreover, TCDD at 1 and 10 nM suppressed ß-catenin (a Wnt-signaling molecule) and E-cadherin expression, as well as spheroids attachment onto endometrial cells. Interestingly, activation of the canonical Wnt-signaling pathway via Wnt3a or lithium chloride reverted the suppressive effect of TCDD on ß-catenin and E-cadherin expressions in the BeWo and RL95-2 cells, and restored the spheroids attachment rate to be comparable to the untreated controls. Taken together, TCDD induces Cyp1A1 expression, modulates the Wnt-signaling pathway and suppresses spheroids attachment onto endometrial cells.