Quality of working life and adaptability of returning to work in nurse cancer survivors: a cross-sectional study.

OBJECTIVE: To explore the relationship between quality of working life (QWL) and adaptability of returning to work (RTW) among nurse cancer survivors (NCSs). METHOD: We conducted a cross-sectional study on nurses previously diagnosed with cancer. QWL was quantified using the Quality of Working Life Scale (QWL7-32), and the level of RTW adaptability was assessed using the Adaptability of Returning to Work for Cancer Survivors (ARTW-CS) scale. Multiple linear regression analysis was used to control for confounding factors, and a simple effect analysis was performed on the interaction term. RESULTS: After controlling for sociodemographic, work-related, and health-related factors, the findings indicated a significant correlation between "adaptation and planning" and QWL score (p < 0.05). Further analysis revealed that "RTW gradualness" and "support seeking" had an interaction effect (p = 0.021). The simple effect analysis demonstrated that when the "RTW gradualness" score was ≥ 16 points, nurses with a high "support seeking" score (≥ 7 points) exhibited a significantly better QWL than those with a low "support seeking" score (< 7 points) (p < 0.001). CONCLUSION: The interaction between "RTW gradualness" and "support seeking" in the ARTW-CS scale significantly impacted the QWL of the NCSs, underscoring the importance of implementing a gradual career plan and seeking support to enhance QWL.

Combined Amelioration of Prebiotic Resveratrol and Probiotic Bifidobacteria on Obesity and Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) and obesity are becoming increasingly common globally and characteristic as gut microbiota disturbance. Supplement of probiotics is considered as a promising strategy for NAFLD and obesity treatment. However, this effect varied from each other in clinical trials. We proposed that combination with a prebiotic substrate may improve the effects of probiotics. Thus, in this study, we investigated the separated and combined effects of Bifidobacteria and resveratrol (RSV) against obesity and NAFLD. NAFLD was caused by high-fat diet (HFD) feeding for 8 weeks. HFD-treated mice were orally treated with B. longum (1 × 109 CFU/mouse/day), RSV (100 mg/kg/day), and both of them from the fifth week. HFD feeding caused obesity and NAFLD as indicated by significantly increased body and liver weights, liver steatosis, elevated serum transaminases and lipid profiles, increased inflammation and imbalanced redox status. Based on these physical and biochemical parameters, inflammatory and antioxidant markers, individual administration of B. longum and RSV alleviated obesity and NAFLD, while coadministration of both products further enhanced the efficacy. These data suggested that combined prebiotic RSV and probiotic B. longum would be a potential candidate or adjuvant for the treatment of obesity and NAFLD.

Romidepsin induces G2/M phase arrest via Erk/cdc25C/cdc2/cyclinB pathway and apoptosis induction through JNK/c-Jun/caspase3 pathway in hepatocellular carcinoma cells.

The aim of the study is to demonstrate the effect of Romidepsin in hepatocellular carcinoma (HCC) by inducing G2/M phase arrest via Erk/cdc25C/cdc2/cyclinB pathway and apoptosis through JNK/c-Jun/caspase3 pathway in vitro and in vivo. Human HCC cell lines were cultured with Romidepsin and DMSO (negative control) and 5-fluorouracil (positive control). Then the cells' viability and apoptosis were determined by cell proliferation assay and flow cytometry. Protein concentrations and expression changes were measured by Western blot. Subsequently, Huh7 cells were subcutaneously inoculated into the nude mice, which were employed to further probe the tumor-suppressive effect of Romidepsin in vivo. Romidepsin treatment led to a time- and dose-dependent induction of cell cycle arrest in the G2/M phase and apoptosis. G2/M phase arrest inhibited the proliferation of HCC cells by alterations in p21/cdc25C/cdc2/cyclinB proteins. Increased concentrations of Erk and JNK phosphorylations were observed in a dose-dependent manner in the Romidepsin group, but p38 phosphorylation was not affected. G2/M phase arrest and the apoptosis of HCC cells induced by Romidepsin were mediated by the activation of Erk/MAPK pathways and JNK/MAPK pathways. The tumor size was significantly larger in the negative control group compared to Romidepsin group and no significant loss in body weight was observed in the Romidepsin group. Our findings offer proof-of-concept for use of Romidepsin as a novel class of chemotherapy in the treatment of HCC.

Expression of AQP1 Was Associated with Apoptosis and Survival of Patients in Gastric Adenocarcinoma.

RATIONALE AND OBJECTIVE: Recently, interest in the role of aquaporin 1 (AQP1) in human gastrointestinal carcinogenesis has developed. However, to date no studies have examined relationships between AQP1 expression and specific characteristics of gastric adenocarcinoma. METHODS: We investigated 109 specimens of primary gastric adenocarcinoma and their corresponding normal gastric mucosa using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) to determine AQP1 expression. We then evaluated disease free survival (DFS) and overall survival (OS) in these patients in association with AQP1 expression. RESULTS: Both immunohistochemical and RT-PCR analyses identified increased AQP1 expression in tumors from patients with gastric adenocarcinoma (p < 0.001). The 3-year DFS and OS rates were higher in the AQP1-negative group than in the positive group (DFS: 77.2 vs. 52.8%, p < 0.001; OS: 85.1 vs. 70.7%, p < 0.001). The 5-year DFS and OS rates exhibited a similar trend (p < 0.001). Subgroup analysis of patients with early gastric adenocarcinoma (stages I and II) revealed a total 5-year OS of 90.0%, with 5-year OS being higher in the AQP1-negative group than in the positive group (95.2 vs. 84.2%). Furthermore, incidence of tumor recurrence following surgical treatment was significantly higher in the AQP1-positive group (4/19, 21.1%) compared with the negative group (0/21, 0%). CONCLUSIONS: Our study demonstrates that AQP1 plays an important role in gastric adenocarcinoma and may therefore represent a novel therapeutic target and prognostic marker in this disease.

Clematichinenoside inhibits VCAM-1 and ICAM-1 expression in TNF-α-treated endothelial cells via NADPH oxidase-dependent IκB kinase/NF-κB pathway.

Proinflammatory cytokine TNF-α-induced adhesion of leukocytes to endothelial cells plays a critical role in the early stage of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Thus, compounds that mediate intracellular redox status and regulate transcription factors are of great therapeutic interest. Clematichinenoside (AR), a triterpene saponin isolated from the root of Clematis chinensis Osbeck, was previously demonstrated to have anti-inflammatory and antioxidative properties. However, little is known about the exact mechanism underlying these actions. Thus we performed a detailed study on its effect on leukocytes-endothelial cells adhesion with TNF-α-stimulated human umbilical vein endothelial cells (HUVECs) and cell-free systems. First, we found that AR reduced TNF-α-induced VCAM-1 and ICAM-1 expression and their promoter activity, inhibited translocation of p65 and phosphorylation of IκBα, suppressed IκB kinase-ß (IKK-ß) activity, lowered O2(∙-) and H2O2 levels, tackled p47(phox) translocation, and decreased NOX4 NADPH oxidase expression. Second, we showed that AR exhibited no direct free radical scavenging ability in cell-free systems at concentrations that were used in intact cells. Besides, AR had no direct effect on the activity of IKK-ß that was extracted from TNF-α-stimulated HUVECs. We also found that p47 translocation, NOX4 expression, and reactive oxygen species (ROS) levels were up-regulated before IκB phosphorylation in TNF-α-induced HUVECs. Moreover, TNF-α-enhanced IKK-ß activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-κB pathways in TNF-α-induced HUVECs, which finally suppress monocyte-HUVECs adhesion. This compound is potentially beneficial for early-stage atherosclerosis.