Correlation Between Basal Metabolic Rate and Clinical Outcomes in Gastric Cancer Patients: A Retrospective Study.

OBJECTIVES: Hypermetabolism is associated with clinical prognosis of cancer patients. The aim of this study was to explore the association between basal metabolic rate (BMR) and postoperative clinical outcomes in gastric cancer patients. METHODS: We collected data of 958 gastric cancer patients admitted at our center from June 2014 to December 2018. The optimal cutoff value of BMR (BMR ≤1149 kcal/day) was obtained using the X-tile plot. Logistic and Cox regression analyses were then performed to evaluate the relevant influencing factors of clinical outcomes. Finally, R software was utilized to construct the nomogram. RESULTS: A total of 213 patients were defined as having a lower basal metabolic rate (LBMR). Univariate and multivariate analyses showed that gastric cancer patients with LBMR were more prone to postoperative complications and had poor long-term overall survival (OS). The established nomogram had good predictive power to assess the risk of OS in gastric cancer patients after radical gastrectomy (c-index was 0.764). CONCLUSIONS: Overall, LBMR on admission is associated with the occurrence of postoperative complications in gastric cancer patients, and this population has a poorer long-term survival. Therefore, there should be more focus on the perioperative management of patients with this risk factor before surgery.

C1q/tumor necrosis factor-related protein-3 (CTRP3) activated by forkhead box O4 (FOXO4) down-regulation protects retinal pericytes against high glucose-induced oxidative damage through nuclear factor erythroid 2-related factor 2 (Nrf2)/Nuclear factor-kappaB (NF-κB) signaling.

Diabetic retinopathy (DR) remains a major cause of blindness among diabetes mellitus patients. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a novel adipokine which is associated with multiple types of metabolism. Nevertheless, little is known about the role of CTRP3 in high glucose (HG)-induced human retinal pericytes (HRPs). This study set out to assess the influence of CTRP3 on HG-induced HRPs and elucidate the latent regulatory mechanism. RT-qPCR and Western blot were to analyze CTRP3 and forkhead box O4 (FOXO4) expression. Western blot was also utilized to detect the protein levels of apoptosis-related factors and nuclear factor erythroid 2-related factor 2 (Nrf2)/Nuclear factor-kappaB (NF-κB) signaling-related factors. CCK-8 was to measure cell proliferation while TUNEL assay was to estimate cell apoptosis. Levels of oxidative stress biomarkers including manganese (MnSOD), catalase (CAT) and malonedialdehyde (MDA) were evaluated by the corresponding kits. JASPAR database, ChIP and luciferase reporter assay were to verify the interaction between FOXO4 and CTRP3 promoter. The experimental results uncovered that CTRP3 expression was decreased in HG-stimulated HRPs. Moreover, CTRP3 overexpression strengthened the viability while abrogated the apoptosis and oxidative stress of HG-induced HRPs. Furthermore. FOXO4 was up-regulated in HG-induced HRPs. Besides, FOXO4 bond to CTRP3 promoter and inhibited CTRP3 transcription to modulate the Nrf2/NF-κB signaling pathway. FOXO4 up-regulation reversed the influence of CTRP3 elevation on the proliferation, apoptosis and oxidative stress of HG-induced HRPs. To be summarized, CTRP3 negatively modulated by FOXO4 prevented HG-induced oxidative damage in DR via modulation of Nrf2/NF-κB signaling.

LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9.

INTRODUCTION: Diabetic nephropathy (DN) is one of the major complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. MicroRNA (miR)-106a is predicated to be a target of long noncoding RNA (lncRNA) SNHG16 and has been identified as a therapeutic biomarker for diabetic kidney diseases. However, the role of SNHG16/miR-106a axis in DN has not been illustrated. This study aimed to investigate whether SNHG16 could regulate podocyte injury via miR-106a in DN and uncover the underlying mechanism. METHODS: MPC5 podocytes were treated with control or high glucose (HG) medium, and then miR-106a level was measured. MPC5 cells that exposed to HG were overexpressed with miR-106a or not, following by overexpression with or without KLF9 or SNHG16. Then, cell viability, apoptosis, reactive oxygen species and the protein expression of synaptopodin and podocin were evaluated. RESULTS: MiR-106a was down-regulated in the serum of DN patients and HG-induced MPC5 podocytes. Overexpression of miR-106a suppressed HG-induced decrease in cell viability, Bcl-2, synaptopodin and podocin expression, increase in ROS, apoptotic cells, Bax and cleaved-caspase 3 expression. MiR-106a could bind to both KLF9 and lncRNA SNHG16, which were up-regulated in the serum of DN patients and HG-induced MPC5 podocytes. The level of miR-106a was decreased by SNHG16 overexpression and miR-106a overexpression reduced KLF9 expression. Furthermore, overexpression of KLF9 or SNHG16 blunted the protective effects of miR-106a on HG-induced MPC5 injury. DISCUSSION: LncRNA SNHG16 could promote HG-stimulated podocytes injury via targeting miR-106a to enhance KLF9 expression. The intervention of SNHG16/miR-106a/KLF9 may be a therapeutic treatment for DN.

Fluorescence sensing of chromium (VI) and ascorbic acid using graphitic carbon nitride nanosheets as a fluorescent "switch".

Using graphitic carbon nitride (g-C3N4) nanosheets, an effective and facile fluorescence sensing approach for the label-free and selective determination of chromium (VI) (Cr(VI)) was developed. The fluorescence of the solution of g-C3N4 nanosheets was quenched effectively by Cr(VI) via the inner filter effect. Under optimal conditions, a wide detection linear range for Cr(VI) was found to be from 0.6 µM to 300 µM with a limit of detection (LOD) of 0.15 µM. In addition, the fluorescence of the solution of g-C3N4 nanosheets-Cr(VI) could be sensitively turned on in the presence of a reductant such as ascorbic acid (AA) via an "on-off-on" fluorescence response through the oxidation-reduction between Cr(VI) and AA. And a wide detection linear range for AA was found to be from 0.5 µM to 200 µM with an LOD of 0.13 µM. Furthermore, the proposed method has the potential application for detection of Cr(VI) in lake waters and AA in biological fluids.