The mediating role of resilience between emotional intelligence and academic procrastination in nursing undergraduates: A cross-sectional study.

AIM: To investigate the relationship among emotional intelligence (EI), resilience and academic procrastination (AP), and provide suggestions for the development of targeted intervention strategies and lowering of AP level of nursing undergraduates. DESIGN: A cross-sectional study. METHODS: Three provincial universities offering nursing courses in China were investigated in this study. A convenience sample of 256 nursing undergraduates from May 2021 to September 2021 were recruited, with a response rate of 91.4%. Data were collected using face-to-face interviews. The survey tools included the General Information Questionnaire, Academic Procrastination Scale, Emotional Intelligence Scale and Resilience Scale. IBM SPSS v19.0 and Amos 22.0 were used for data analysis. RESULTS: The AP of sampled nursing undergraduates was at the middle level (54.4 ± 21.5). The AP of nursing undergraduates was negatively correlated with EI and resilience. Moreover, the analysis on the mediating role of resilience via structural equation model showed a good fit, with χ2/df = 2.34, RMSEA = 0.07, CFI = 0.99, GFI = 0.95, TLI = 0.98. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution.

Clinical study of extrahepatic biliary adenoma.

BACKGROUND: Biliary adenomas that occur in the extrahepatic biliary tree are rare. It is difficult to distinguish it from cholangiocarcinoma or cholangiolithiasis by various imaging examinations, and it is very easy to be misdiagnosed. AIM: To evaluate the cumulative experiences including clinical characteristics and treatments of nine patients diagnosed with extrahepatic biliary adenoma admitted to the First Affiliated Hospital of Xi'an Jiaotong University from 2016 to 2022. METHODS: A total of nine patients were included in our study. The laboratory examinations, disease diagnosis, therapy and pathological characteristics, and follow-up of every patient were evaluated. RESULTS: Our cohort consisted of six females and three males with an average diagnosis age of 65.1 years (range 46-87). Six extrahepatic biliary adenomas were located in the common bile ducts and three in the hepatic duct. On initial presentation, all of the patients have symptom of biliary origin, including obstructive jaundice (4/9, 44.4%), abdominal pain (6/9, 66.7%), and fever (3/9, 33.3%). Preoperative imaging examination considered bile duct carcinoma in 6 cases and bile duct calculi in 3 cases. All the patients received surgical treatment and were confirmed by pathology as biliary adenoma. The symptoms improved significantly in all 9 patients after surgery. Seven of nine patients recovered well at follow-up without tumor recurrence. One patient died 2 mo after the surgery due to heart failure. One patient developed jaundice again 8 mo after surgery, underwent endoscopic retrograde cholangiopancreatography and biliary stent placement. CONCLUSION: Benign extrahepatic biliary tumors are rare and difficult to diagnosis preoperatively. Intraoperative choledochoscopy and timely biopsy may offer great advantages.

Mutant p53 driven-LINC00857, a protein scaffold between FOXM1 and deubiquitinase OTUB1, promotes the metastasis of pancreatic cancer.

Tumour metastasis is the major adverse factor for recurrence and death in pancreatic cancer (PC) patients. P53 mutations are considered to be the second most common type of mutation in PC and significantly promote PC metastasis. However, the molecular mechanisms underlying the effects of p53 mutations, especially the regulatory relationship of the protein with long noncoding RNAs (lncRNAs), remain unclear. In the present study, we demonstrated that the lncRNA LINC00857 exhibits a significantly elevated level in PC and that it is associated with poor prognosis; furthermore, TCGA data showed that LINC00857 expression was significantly upregulated in the mutant p53 group compared with the wild-type p53 group. Gain- and loss-of-function experiments showed that LINC00857 promotes the metastasis of PC cells. We further found that LINC00857 upregulates FOXM1 protein expression and thus accelerates metastasis in vitro and in vivo. Mechanistically, LINC00857 bound simultaneously to FOXM1 and to the deubiquitinase OTUB1, thereby serving as a protein scaffold and enhancing the interaction between FOXM1 and OTUB1, which inhibits FOXM1 degradation through the ubiquitin-proteasome pathway. Interestingly, we found that mutant p53 promotes LINC00857 transcription by binding to its promoter region. Finally, atorvastatin, a commonly prescribe lipid-lowering drug, appeared to inhibit PC metastasis by inhibiting the mutant p53-LINC00857 axis. Taken together, our results provide new insights into the biology driving PC metastasis and indicate that the mutant p53-LINC00857 axis might represent a novel therapeutic target for PC metastasis.

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer.

As one of the best-studied long noncoding RNAs, nuclear paraspeckle assembly transcript 1 (NEAT1) plays a pivotal role in the progression of cancers. NEAT1, especially its isoform NEAT1-1, facilitates the growth and metastasis of various cancers, excluding acute promyelocytic leukemia. NEAT1 can be elevated via transcriptional activation or stability alteration in cancers changing the aggressive phenotype of cancer cells. NEAT1 can also be secreted from other cells and be delivered to cancer cells through exosomes. Hence, elucidating the molecular interaction of NEAT1 may shed light on the future treatment of cancer. Herein, we review the molecular function of NEAT1 in cancer progression, and explain how NEAT1 interacts with RNAs, proteins, and DNA promoter regions to upregulate tumorigenic factors.

Resveratrol inhibits the expression of RYR2 and is a potential treatment for pancreatic cancer.

Resveratrol is a polyphonous natural compound that has cardioprotective, anticancer, and anti-inflammatory properties. Studies have proved that resveratrol (RES) inhibits cancer cell proliferation, migration, and invasion and promotes apoptosis. Elevated expression of ryanodine receptor type 2 (RYR2) may participate in the pathway responsible for calcium metabolism as well as anti-apoptosis and anti-autophagy events in malignant tumor cells. However, the underlying molecular mechanisms of RES anticancer effects with RYR2 are not completely understood in pancreatic cancer. The aim of the present study was tantamount to study the effect of RES in human pancreatic cancer and investigate the underlying mechanisms of RES. We found that RES inhibits proliferation, migration, and invasion and suppresses RYR2 expression in pancreatic cancer cells. In addition, RYR2 knockdown impedes the proliferation, migration, and invasiveness of pancreatic cancer cells. RYR2 knockdown can also increase PTEN expression, while increased RYR2 expression can inhibit PTEN expression. Moreover, RES can upregulate PTEN expression. Taken together, these results indicate that RES could play an antitumor role by decreasing RYR2 expression.

Transforming growth factor-ß1 and inducible nitric oxide synthase signaling were involved in effects of prostaglandin E2 on progression of lower limb varicose veins.

OBJECTIVE: The vital pathogenesis of varicose veins includes remodeling of the extracellular matrix and decreased vascular tone. Prostaglandin E2 (PGE2), a small molecule substance and inflammatory medium that belongs to the arachidonic acid derivatives, has the capacity to influence the expression of metalloproteinase and the vascular tone of the venous wall. The purpose of the present study was to investigate the role of PGE2 in the development of varicose veins in lower limbs. METHODS: The collected venous specimens were analyzed using hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining. Transforming growth factor (TGF)-ß1, PGE2, CD31, and α-smooth muscle actin antibody were used to detect the expression and distribution of these proteins. The effect of PGE2 on the proliferation, migration, and tube formation capacity of human umbilical vein endothelial cells (HUVECs) was detected in vitro. The effect of TGF-ß1 on the expression of PGE2 and matrix metalloproteinases (MMPs) was assessed using Western blotting. Quantitative reverse transcription polymerase chain reaction was used to evaluate the effect of PGE2 on the expression of nitric oxide synthase (NOS) and other genes. RESULTS: The expression of PGE2 and TGF-ß1 in varicose veins was upregulated in the media tunica and intima tunica, and a strong positive correlation was found between PGE2 and TGF-ß1 expression in both varicose veins (95% confidence interval, 0.5207-0.9582; R = 0.848; P = .0005) and normal veins (95% confidence interval, 0.2530-0.8532; R = 0.643; P = .003). PGE2 promoted the migration and tube formation ability of HUVECs. Moreover, PGE2 also upregulated the expression of MMP-1 and TGF-ß1 in HUVECs and increased the mRNA level of inducible NOS. CONCLUSIONS: PGE2 can affect the remodeling of the extracellular matrix and reduce the elasticity of the vascular walls by promoting the synthesis of TGF-ß1 and MMP-1. PGE2 can also reduce the tension of the great saphenous vein by promoting the expression of inducible NOS, thus aggravating the blood stasis.

Super-selective arterial embolization in the control of acute lower gastrointestinal hemorrhage.

BACKGROUND: Acute gastrointestinal bleeding is an emergency condition that can lead to significant morbidity and mortality. Embolization is considered the preferred therapy in the treatment of lower gastrointestinal bleeding when it is unrealistic to perform the surgery or vasopressin infusion in this population. Treatment of acute lower gastrointestinal (GI) bleeding (any site below the ligament of Treitz) using this technique has not reached a consensus, because of the belief that the risk of intestinal infarction in this condition is extremely high. The purpose of the study is to evaluate the effectiveness and safety of this technique in a retrospective group of patients who underwent embolization for acute lower GI bleeding. AIM: To evaluate the efficacy and safety of super-selective arterial embolization in the management of acute lower GI bleeding. METHODS: A series of 31 consecutive patients with angiographically demonstrated small intestinal or colonic bleeding was retrospectively reviewed. The success rate and complication rate of super-selective embolization were recorded. RESULTS: Five out of thirty-one patients (16.1%) could not achieve sufficiently selective catheterization to permit embolization. Initial control of bleeding was achieved in 26 patients (100%), and relapsed GI bleeding occurred in 1 of them at 1 wk after the operation. No clinically apparent bowel infarctions were observed in patients undergoing embolization. CONCLUSION: Super-selective embolization is a safe therapeutic method for acute lower GI bleeding, and it is suitable and effective for many patients suffering this disease. Importantly, careful technique and suitable embolic agent are essential to the successful operation.

PlGF signaling and macrophage repolarization contribute to the anti-neoplastic effect of metformin.

Placental growth factor (PlGF) related signaling pathway has been shown to have close relationship with the progression of cancers. Metformin has been reported to have an inhibitory effect on PlGF expression in a breast cancer model. However, little is known about whether the anti-neoplastic activity of metformin is contributed by its inhibitory effect on PlGF expression. Protein, mRNA and secretion levels of PlGF were tested and the proliferation of cancer cells was determined. After treatment of metformin, BALB/c mice bearing 4T1 tumors were sacrificed and immunohistochemistry staining of the tumor sections was obtained. Baseline expression of autocrine PlGF varied between different breast cancer cell lines, while the expression of vascular endothelial growth factor receptor-1 (VEGFR-1) was comparable between cell lines. Other clinical data showed that the expression of PlGF other than VEGFR-1 had a prognostic value for patients with breast cancers. Metformin significantly decreased the secretion and mRNA levels of PlGF, which greatly contributed to its inhibitory effect on the proliferation of breast cancer cells with high P1GF expression. The unresponsiveness of tumor cells with low PlGF expression to genetic silencing was reversed by the supplementation of exogenous PlGF. Systemic metformin administration apparently inhibited the in vivo growth of 4T1 carcinoma, which was accompanied by the repolarization of macrophages from M2 to M1. These findings indicated that both autocrine and paracrine PlGF signaling and macrophage repolarization are involved in the progression of breast cancer, which could be targeted by metformin.