Impact of supportive interventions on resilience and self-assessed psychopathology symptoms of 92 nurses in isolation ward during the COVID-19 pandemic was evaluated. Resilience and psychopathological symptoms of nurses in the isolation ward was assessed by Connor-Davidson Resilience Scale (CD-RISC) and the Symptom Checklist 90 (SCL-90). A total resilience score was 87.04 ± 22.78. The SCL-90 score was 160-to 281 (202.5 ± 40.79). Only 8.70% of the nurses (n = 8) had a total SCL-90 score >160, suggesting positive symptoms. The majority of nurses had 0 to 90 positive self-assessment items (median 14); 19.57% (n = 18) had > 43 positive items. Interpersonal sensitivity, depression, hostility, and paranoid ideation scores were below national averages (p=0.000, 0.040, 0.002, 0.004, respectively). SCL-90 items reflecting diet and sleep conditions were higher(P = 0.009), and somatization, obsessive-compulsive, anxiety, phobic anxiety, and psychoticism domains and scores were similar to national averages (P>0.3). With exception of somatization and other domains, the mean resilience score was negatively associated with the scores of other SCL-90 domains. High resilience promotes physical and mental health, and may be improved by training, psychological interventions and full use of hospital resources ARTICLE HISTORY

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Circulating histones increased significantly in necrotizing pancreatitis due to extensive pancreatic acinar cell death. Levels of circulating histones may have translational potential as a biomarker of disease severity.

COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.

Background: CD4 + T cells are critical effectors of anti-tumor immunity, but how tumor cells influence CD4 + T cell effector function is not fully understood. Tumor cell-released autophagosomes (TRAPs) are being recognized as critical modulators of host anti-tumor immunity during tumor progression. Here, we explored the mechanistic aspects of TRAPs in the modulation of CD4 + T cells in the tumor microenvironment. Methods: TRAPs isolated from tumor cell lines and pleural effusions or ascites of cancer patients were incubated with CD4 + T cells to examine the function and mechanism of TRAPs in CD4 + T cell differentiation and function. TRAPs-elicited CD4 + T cells were tested for their suppression of effector T cell function, induction of regulatory B cells, and promotion of tumorigenesis and metastasis in a mouse model. Results: Heat shock protein 90α (HSP90α) on the surface of TRAPs from malignant effusions of cancer patients and tumor cell lines stimulated CD4 + T cell production of IL-6 via a TLR2-MyD88-NF-κB signal cascade. TRAPs-induced autocrine IL-6 further promoted CD4 + T cells secretion of IL-10 and IL-21 via STAT3. Notably, TRAPs-elicited CD4 + T cells inhibited CD4 + and CD8 + effector T cell function in an IL-6-and IL-10-dependent manner and induced IL-10producing regulatory B cells (Bregs) via IL-6, IL-10 and IL-21, thereby promoting tumor growth and metastasis. Consistently, inhibition of tumor autophagosome formation or IL-6 secretion by CD4 + T cells markedly retarded tumor growth. Furthermore, B cell or CD4 + T cell depletion impeded tumor growth by increasing effector T cell function. Conclusions: HSP90α on the surface of TRAPs programs the immunosuppressive functions of CD4 + T cells to promote tumor growth and metastasis. TRAPs or their membrane-bound HSP90α represent important therapeutic targets to reverse cancer-associated immunosuppression and improve immunotherapy.

AIM:To evaluate the effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in the tissues of premalignant gastric lesions. METHODS:Thirty-eight patients, with premalignant gastric lesions including 18 colonic-type intestinal metaplasia (IM) and 20 mild or moderate dysplasia, were randomly divided into a treatment group (n = 19) receiving folic acid 10 mg thrice daily and a control group (n = 19) receiving sucralfate 1 000 mg thrice daily for 3 mo. All patients underwent endoscopies and four biopsies were taken prior to treatment and repeated after concluding therapy. Folate concentrations in gastric mucosa were measured with chemiluminescent enzyme immunoassay. Epithelial apoptosis and the expression of Bcl-2 and p53 protein in gastric mucosa were detected with flow cytometric assay. RESULTS:The mean of folate concentration in gastric mucosa was 9.03±3.37 g/g wet wt in the folic acid treatment group, which was significantly higher than 6.83±3.02 g/g wet wt in the control group. Both the epithelial apoptosis rate and the tumor suppressor p53 expression in gastric mucosa significantly increased after folic acid treatment. In contrast, the expression of Bcl-2 oncogene protein decreased after folic acid therapy. CONCLUSION:These data indicate that folic acid may play an important role in the chemoprevention of gastric carcinogenesis by enhancing gastric epithelial apoptosis in the patients with premalignant lesions.

BackgroundPancreatic cancer is currently one of the leading causes of cancer deaths without any effective therapies. Mir-145 has been found to be tumor-suppressive in various types of cancers. The aim of this study is to investigate the role of miR-145 in pancreatic cancer cells and explore its underlying mechanism.MethodsQuantitative real time PCR was used to determine the expression level of miR-145 and angiopoietin-2 (Ang-2) mNRA, and the expression level of Ang-2 protein was measured by western blotting. The anti-cancer activities of miR-145 were tested both in in vitro by using cell invasion and colony formation assay and in vivo by using xenograft assay. The direct action of miR-145 on Ang-2 was predicted by TargetScan and confirmed by luciferase report assay. The vascularization of xenografts were performed by immunohistochemical analysis.ResultsThe expression level of miR-145 was significantly lower and the expression levels of Ang-2 mRNA and protein was significantly higher in the more aggressive pancreatic cancer cells (MiaPaCa-2 and Panc-1) when compared to that in BxPC3 cells. Overexpression of miR-145 in the BxPC3, MiaPaCa-2 and Panc-1 cells suppressed the cell invasion and colony formation ability, and the expression level of Ang-2 protein in MiaPaCa-2 and Panc-1 cells was also suppressed after pre-miR-145 transfection. Intratumoral delivery of miR-145 inhibited the growth of pancreatic cancer xenografts and angiogenesis in vivo, and also suppressed the expression level of angiopoietin-2 protein. Luciferase report assay showed that Ang-2 is a direct target of miR-145, and down-regulation of angiopoietin-2 by treatment with Ang-2 siRNA in the BxPC3, MiaPaCa-2 and Panc-1 cells suppressed cell invasion and colony formation ability. The reverse transcription PCR results also showed that Tie1 and Tie2 were expressed in BxPC3, MiaPaCa-2 and Panc-1 cells.ConclusionMiR-145 functions as a tumor suppressor in pancreatic cancer cells by targeting Ang-2 for translation repression and thus suppresses pancreatic cancer cell invasion and growth, which suggests that restoring of miR-145 may be a potential therapeutic target for pancreatic cancer.

Long noncoding RNAs (lncRNAs) serve important functions in many crucial biological processes; however, the effects of lncRNAs in early gastric cancer (EGC) are not entirely clear. The present study aimed to demonstrate the potential of lncRNAs to be used as biomarkers in EGC. Reverse transcription‑quantitative polymerase chain reaction was used to measure the expression levels of lncRNAs, including X inactive‑specific transcript (XIST), Yiya, brain cytoplasmic RNA 1 (BCYRN1), ribosomal RNA processing 1B (RRP1B), KCNQ1 opposite transcript 1 (KCNQ1OT1) and testes development related 1 (TDRG1), in EGC tissues compared with normal adjacent tissues (NATs). XIST, BCYRN1, RRP1B and TDRG1 were identified as differentially expressed in EGC tissues compared with NATs. The specificity and sensitivity of XIST, BCYRN1, RRP1B and TDRG1 were determined by receiver operating characteristic curve analysis. In addition, RRP1B expression was revealed to be significantly correlated with distal metastasis (P=0.020) and tumor‑node‑metastasis staging (P=0.018), and TDRG1 expression was significantly correlated with lymph node metastasis (P=0.001). Furthermore, BCYRN1, RRP1B and TDRG1 expression levels were compared between EGC tissues and plasma, and the results indicated that there were significant positive correlations of XIST, BCYRN1, RRP1B and TDRG1 expression levels between the EGC tissues and plasma. Therefore, the present study suggested that XIST, BCYRN1, RRP1B and TDRG1 may be served as potential diagnostic biomarkers for EGC.