The Influence of PRO-SELF Cancer Pain Control Programme on Patients' Self-Management Ability.

Objective: Recently, cancer patients have challenges with self-management. This study aims to improve symptoms of chronic pain, and anxiety and depression associated with cancer by PRO-SELF nursing intervention. Methods: Sixty-four patients were randomly assigned to an intervention and a control group from Jan 2016 to Dec 2019, 34 usable cases in the intervention group and 30 cases in the control group were collected. The control group received a routine cancer pain nursing intervention, whereas the intervention group received a PRO-SELF based multidisciplinary collaborative cancer pain nursing intervention. After three months of intervention, the Numeric Rating Scale (NRS), Medication Compliance Questionnaire (MCQ), Social Support Rating Scale (SSRS), Self-rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), Quality of Life Scale (FACT-G Chinese version) and Chronic Pain Self-efficacy Scale were resent to compare the differences in the observation indicators included evaluation of patients' social support degree, anxiety and depression score, quality of life scores and self-efficacy scores between two groups. The t-test and rank-sum test were used for statistic analysis. Results: No significant differences were found between groups for pain and medication compliance (P > 0.05). However, significant differences were found between groups in social support, life quality, chronic pain self-efficacy, and self-rating anxiety and depression index scores (P < 0.001). The intervention group report more social support, pain self-efficacy and less anxiety and depression (P < 0.001). Conclusion: The PRO-SELF pain symptoms in patients with a cancer pain management programme improved degree of social support, life quality, self-efficacy, anxiety, depression which is worthy of clinical application.

Surgical methods influence on the risk of anastomotic fistula after pancreaticoduodenectomy: a systematic review and network meta-analysis.

BACKGROUND: Pancreaticoduodenectomy is the first choice surgical intervention for the radical treatment of pancreatic tumors. However, an anastomotic fistula is a common complication after pancreaticoduodenectomy with a high mortality rate. With the development of minimally invasive surgery, open pancreaticoduodenectomy (OPD), laparoscopic pancreaticoduodenectomy (LPD), and robotic pancreaticoduodenectomy (RPD) are gaining interest. But the impact of these surgical methods on the risk of anastomosis has not been confirmed. Therefore, we aimed to integrate relevant clinical studies and explore the effects of these three surgical methods on the occurrence of anastomotic fistula after pancreaticoduodenectomy. METHODS: A systematic literature search was conducted for studies reporting the RPD, LPD, and OPD. Network meta-analysis of postoperative anastomotic fistula (Pancreatic fistula, biliary leakage, gastrointestinal fistula) was performed. RESULTS: Sixty-five studies including 10,026 patients were included in the network meta-analysis. The rank of risk probability of pancreatic fistula for RPD (0.00) was better than LPD (0.37) and OPD (0.62). Thus, the analysis suggests the rank of risk of the postoperative pancreatic fistula for RPD, LPD, and OPD. The rank of risk probability for biliary leakage was similar for RPD (0.15) and LPD (0.15), and both were better than OPD (0.68). CONCLUSIONS: This network meta-analysis provided ranking for three different types of pancreaticoduodenectomy. The RPD and LPD can effectively improve the quality of surgery and are safe as well as feasible for OPD.

Acinar ATP8b1/LPC pathway promotes macrophage efferocytosis and clearance of inflammation during chronic pancreatitis development.

Noninflammatory clearance of dying cells by professional phagocytes, termed efferocytosis, is fundamental in both homeostasis and inflammatory fibrosis disease but has not been confirmed to occur in chronic pancreatitis (CP). Here, we investigated whether efferocytosis constitutes a novel regulatory target in CP and its mechanisms. PRSS1 transgenic (PRSS1Tg) mice were treated with caerulein to mimic CP development. Phospholipid metabolite profiling and epigenetic assays were performed with PRSS1Tg CP models. The potential functions of Atp8b1 in CP model were clarified using Atp8b1-overexpressing adeno-associated virus, immunofluorescence, enzyme-linked immunosorbent assay(ELISA), and lipid metabolomic approaches. ATAC-seq combined with RNA-seq was then used to identify transcription factors binding to the Atp8b1 promoter, and ChIP-qPCR and luciferase assays were used to confirm that the identified transcription factor bound to the Atp8b1 promoter, and to identify the specific binding site. Flow cytometry was performed to analyze the proportion of pancreatic macrophages. Decreased efferocytosis with aggravated inflammation was identified in CP. The lysophosphatidylcholine (LPC) pathway was the most obviously dysregulated phospholipid pathway, and LPC and Atp8b1 expression gradually decreased during CP development. H3K27me3 ChIP-seq showed that increased Atp8b1 promoter methylation led to transcriptional inhibition. Atp8b1 complementation substantially increased the LPC concentration and improved CP outcomes. Bhlha15 was identified as a transcription factor that binds to the Atp8b1 promoter and regulates phospholipid metabolism. Our study indicates that the acinar Atp8b1/LPC pathway acts as an important "find-me" signal for macrophages and plays a protective role in CP, with Atp8b1 transcription promoted by the acinar cell-specific transcription factor Bhlha15. Bhlha15, Atp8b1, and LPC could be clinically translated into valuable therapeutic targets to overcome the limitations of current CP therapies.