Feasibility and acceptability of a culturally adapted psychological first aid training intervention (Preparing Me) to support the mental health and well-being of front-line healthcare workers in China: a feasibility randomized controlled trial.

Background: Psychological first aid (PFA) training helps to prepare healthcare workers (HCWs) to manage trauma and stress during healthcare emergencies, yet evidence regarding its effectiveness and implementation is lacking.Method: A two-arm feasibility randomized controlled trial design was conducted in a Chinese tertiary hospital. Participants were randomly allocated to receive either a culturally adapted PFA training (the intervention arm) or psychoeducation (the control arm). Feasibility indicators and selected outcomes were collected.Results: In total, 215 workers who expressed an interest in participating in the trial were screened for eligibility, resulting in 96 eligible participants being randomly allocated to the intervention arm (n = 48) and control arm (n = 48). There was a higher retention rate for the face-to-face PFA training session than for the four online group PFA sessions. Participants rated the PFA training as very helpful (86%), with a satisfaction rate of 74.25%, and 47% reported being able to apply their PFA skills in responding to public health emergencies or providing front-line clinical care. Positive outcome changes were observed in PFA knowledge, skills, attitudes, resilience, self-efficacy, compassion satisfaction, and post-traumatic growth. Their scores on depression, anxiety, stress, and burnout measures all declined. Most of these changes were sustained over 3 months (p < .05). Repeated measures analysis of variance found statistically significant interaction effects on depression (F2,232 = 2.874, p = .046, ηp2 = .031) and burnout (F2,211 = 3.729, p = .018, ηp2 = .037), indicating a greater reduction in symptoms of depression and burnout with PFA compared to psychoeducation training.Conclusion: This culturally adapted PFA training intervention was highly acceptable among Chinese HCWs and was feasible in a front-line care setting. Preliminary findings indicated positive changes for the PFA training intervention on knowledge, skills, attitudes, resilience, self-efficacy, compassion satisfaction, and post-traumatic growth, especially a reduction of depression and burnout. Further modifications are recommended and a fully powered evaluation of PFA training is warranted.

Psychological first aid (PFA) training was culturally adapted and evaluated to help prepare healthcare workers to manage trauma and stress during healthcare emergencies.This culturally adapted PFA training was highly acceptable among Chinese healthcare workers and was feasible in a front-line care setting.Preliminary findings show positive changes for the PFA training intervention on knowledge, skills, attitudes, resilience, self-efficacy, compassion satisfaction, and post-traumatic growth, especially a reduction of depression and burnout.

The RNF26/CBX7 axis modulates the TNF pathway to promote cell proliferation and regulate sensitivity to TKIs in ccRCC.

Clear cell renal cell carcinoma (ccRCC) accounts for 85% of all malignant renal tumors. Currently, the pathogenesis of ccRCC is not fully understood. Chromobox (CBX) family proteins are the major subunits of PcG complexes and are implicated in regulating mammalian development. The CBX family consists of eight members, namely, CBX1-8. Numerous studies have highlighted that each CBX protein exhibits distinct functions and prognostic roles in specific cancer types. In this study, in silico analysis indicated that CBX7 was downregulated in ccRCC and correlated with favorable prognosis in a ccRCC cohort. Subsequent studies showed that CBX7 inhibited cancer cell proliferation and invasion. Then, we showed that CBX7 downregulated ETS1 to inactivate the tumor necrosis factor (TNF) signaling pathway, which inhibited tumor proliferation and enhanced the sensitivity of ccRCC cells to tyrosine kinase inhibitors (TKIs). Moreover, we found that CBX7 was a bona fide substrate of RNF26. RNF26 promoted the degradation of CBX7 and enhanced ccRCC tumor growth. Therefore, our results revealed a novel RNF26/CBX7 axis that modulates the TNF signaling pathway in ccRCC.

MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity.

Tumor cells utilize the overexpression of the programmed death-1 ligand 1(PD-L1) to escape T-cell controlled immune-surveillance. The clinical therapy that dilapidates PD1 or PD-L1-mediated cancer tolerance has pushed out the need to uncover the molecular regulation of PD-L1 overexpression in the tumor cell. In this study, we identify histone methyltransferase mixed-lineage leukemia protein 3 (MLL3) as a critical regulator of PD-L1 in prostate cancer cells. MLL3 and PD-L1 were highly expressed in the metastatic cancer tissues, compared to the primary cancer tissues. Furthermore, their expressions were highly correlated in the cancer tissues in the databases of TCGA and Xiangya Hospital. We found that MLL3 bound to the enhancer of PD-L1. Depletion of MLL3 decreased the binding level of H3K4me1 in the enhancer of PD-L1 and Pol II Ser-5p in the promoter of PD-L1. Importantly, MLL3 depletion impaired the mouse xenograft growth and decreased the response to PD-L1 antibody treatment in mice. The findings extend the understanding of the biology regulation of PD-L1 transcription and identify the histone writer MLL3 in an important immune checkpoint, and give prominence to a hidden therapeutic target to conquer immune evasion by tumor cells.

Oncogenic non-coding RNA NEAT1 promotes the prostate cancer cell growth through the SRC3/IGF1R/AKT pathway.

Steroid receptor co-activator3 (SRC3) has been known to severe as an androgen receptor (AR) coactivator and is involved in the prostate cancer progression. Non-coding RNA (ncRNA) plays an important role in the cancer progression. However, the mechanism underlying the relationship between ncRNA and AR coactivators is still unclear. Here, we found a ncRNA, Nuclear Enriched Abundant Transcript 1 (NEAT1), was able to interact with SRC3 in the prostate cancer cell lines. NEAT1 can upregulate the AKT phosphorylation via a SRC3/IGF1R pathway. In function, NEAT1 promoted the prostate cancer cell growth through IGF1R/AKT signaling pathway. The NEAT1, SRC3, and IGF1R were highly expressed in the patients' samples of prostate cancer. Therefore, we found a novel SRC3 binding ncRNA that can promote the prostate cancer cell growth through SRC3/IGF1R/AKT pathway.

Association of nonsteroidal anti-inflammatory drugs and aspirin use and the risk of head and neck cancers: a meta-analysis of observational studies.

PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have emerged as the potential chemopreventive agents for a number of cancer types, however, previous studies of head and neck cancers (HNC) have yielded inconclusive results. We performed a meta-analysis of observational studies to quantitatively assess the association between NSAIDs use and the risk for HNC. METHODS: We searched Pubmed, Embase, Google scholar, and Cochrane library for relevant studies that were published in any language, from January 1980 to April 2016. We pooled the odds ratio (OR) from individual studies and performed subgroup, heterogeneity, and publication bias analyses. RESULTS: A total of eleven studies (eight case-control studies and three cohort studies), involving 370,000 participants and 10,673 HNC cases contributed to this meta-analysis. The results of these studies suggested that neither use of overall NSAIDs (OR=0.95; 95% CI, 0.81-1.11), aspirin (OR=0.93; 95% CI, 0.79-1.10), nor nonsteroidal NSAIDs (OR=0.92; 95% CI, 0.76-1.10) were associated with HNC risk. Similar nonsteroidal results were observed when stratified by HNC sites, study design, sample size, and varied adjustment factors. However, we found significant protective effect of ibuprofen (OR=0.85; 95% CI, 0.72-0.99) and long-term aspirin use (≧5years) (OR=0.75; 95% CI, 0.65-0.85) on HNC risk, with low heterogeneity and publication bias. CONCLUSIONS: Our meta-analysis results do not support the hypothesis that overall use of NSAIDs significant reduces the risk of HNC. Whereas, we cannot rule out a modest reduction in HNC risk associated with ibuprofen and long-term aspirin use.

Nonsteroidal anti-inflammatory drug use and the risk of melanoma: a meta-analysis.

Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have emerged as potential chemopreventive agents for melanoma. However, the clinical studies have provided contradictory results as to whether NSAIDs reduce the risk of melanoma. Our aim was to assess this association through a detailed meta-analysis of the studies on the subject published in the peer-reviewed literature. Relevant studies were identified by searching PubMed, EMBASE and Web of Science electronic databases up to July 2012. Reference lists from retrieved articles were also reviewed. Pooled relative risk (RR) estimates and corresponding 95% confidence intervals (CIs) were calculated using the fixed-effects or the random-effects models on the basis of heterogeneity analysis. Subgroup analyses were carried out where data were available. Ten studies involving 490 322 participants contributed to the meta-analysis. The summary RR estimate on the basis of all studies did not indicate that overall NSAIDs use significantly decreases the risk of melanoma (RR=0.94; 95% CI, 0.86-1.03). The use of neither aspirin (RR=0.96; 95% CI, 0.89-1.03) nor nonaspirin NSAIDs (RR=1.05; 95% CI, 0.96-1.14) was associated with the risk of melanoma. Similar results were obtained in the subgroup analyses of cohort studies (RR=1.03; 95% CI, 0.95-1.13), high-intensity NSAID use (the highest dose of NSAID use reported by included studies, RR=1.05; 95% CI, 0.79-1.40), and long-term NSAID use (longest duration of NSAID use reported by included studies, RR=0.87; 95% CI, 0.66-1.14). However, a slight reduction in the risk of melanoma by taking NSAIDs was observed in case-control studies (RR=0.86; 95% CI, 0.80-0.93). In conclusion, the results of our meta-analysis did not indicate that the use of NSAIDs or aspirin is associated with the risk of melanoma. More and in-depth research should focus on those problems in the future.