The impact of a carbohydrate-electrolyte solution with sodium alginate and pectin for hydrogel formation (CES-HGel), was compared to a standard CES with otherwise matched ingredients (CES-Std), for blood glucose, substrate oxidation, gastrointestinal symptoms (GIS; nausea, belching, bloating, pain, regurgitation, flatulence, urge to defecate, and diarrhea), and exercise performance. Nine trained male endurance runners completed 3 hr of steady-state running (SS) at 60% , consuming 90 g/hr of carbohydrate from CES-HGel or CES-Std (53 g/hr maltodextrin, 37 g/hr fructose, 16% w/v solution) in a randomized crossover design, followed by an incremental time to exhaustion (TTE) test. Blood glucose and substrate oxidation were measured every 30 min during SS and oxidation throughout TTE. Breath hydrogen (H2) was measured every 30 min during exercise and every 15 min for 2 hr postexercise. GIS were recorded every 15 min throughout SS, immediately after and every 15-min post-TTE. No differences in blood glucose (incremental area under the curve [mean ± SD]: CES-HGel 1,100 ± 96 mmol·L−1·150 min−1 and CES-Std 1,076 ± 58 mmol·L−1·150 min−1; p = .266) were observed during SS. There were no differences in substrate oxidation during SS (carbohydrate: p = .650; fat: p = .765) or TTE (carbohydrate: p = .466; fat: p = .633) and no effect of trial on GIS incidence (100% in both trials) or severity (summative rating score: CES-HGel 29.1 ± 32.6 and CES-Std 34.8 ± 34.8; p = .262). Breath hydrogen was not different between trials (p = .347), nor was TTE performance (CES-HGel 722 ± 182 s and CES-Std: 756 ± 187 s; p = .08). In conclusion, sodium alginate and pectin added to a CES consumed during endurance running does not alter the blood glucose responses, carbohydrate malabsorption, substrate oxidation, GIS, or TTE beyond those of a CES with otherwise matched ingredients.

No abstract

Prostate cancer (PCa) exhibits a high incidence among men, but there is no effective and non-invasive biomarker for the diagnosis of PCa, and the pathogenesis of PCa remains unclear. The present study identified that miR-27a was significantly overexpressed in the tumor tissues and sera of patients with PCa. In addition, high serum levels of miR-27a were correlated with poor survival in patients with PCa. Receiver-operating characteristic curves analysis demonstrated that the serum levels of miR-27a exhibited a high area under the curve value. Furthermore, miR-27a mimics or inhibitors significantly promoted or repressed the proliferation of PCa cells, respectively. In addition, it was identified that the expression of Sprouty2 (SPRY2) was inversely correlated with the expression of miR-27a in PCa tissues. The knockdown or overexpression of SPRY2 promoted or suppressed the proliferation of PCa cells, respectively, and the overexpression of SPRY2 inhibited the increased proliferation and cell cycle distribution of PCa cells mediated by miR-27a mimics. Taken together, these data indicated that the serum levels of miR-27a may be a novel and non-invasive biomarker for the diagnosis and prognosis of patients with PCa, and miR-27a/SPRY2 may be a therapeutic target for the treatment of PCa.

Background/Aims: Renal cell carcinoma (RCC) is currently the ninth most common cancer in men. Interleukin (IL)-33 expression has previously been associated with a number of cancers; however, its biological role in RCC is poorly understood. In this study, we sought to elucidate the role of IL-33 in RCC. Methods: Serum IL-33 levels were measured by ELISA. IL-33 expression in clinical RCC samples was examined by immunocytochemistry. The proliferation and apoptosis rate of RCC were determined by CCK8 and flow cytometry. Mcl1 and Bcl-2 expression were measured by quantitative real-time PCR and western blotting. JNK expression were measured by western blotting and flow cytometry. The in vivo role of IL-33 in RCC tumorigenesis was examined by animal models. Results: We found that increased expression of IL-33 in RCC was associated with tumor-lymph node-metastasis (TNM) stage and inversely correlated with prognosis. IL-33 enhances RCC cell growth in vivo and stimulates RCC cell proliferation and prevents chemotherapy-induced tumor apoptosis in vitro. Furthermore, we demonstrated that IL-33 promotes RCC cell proliferation and chemotherapy resistance via its receptor ST2 and the JNK signaling activation in tumor cells. Conclusion: Our findings suggest that targeting IL-33/ST2 and JNK signaling may have potential value in the treatment of RCC.

Recent studies have shown that circular RNA circFLNA is abnormally expressed in a variety of malignant tumors, but its role and mechanism in bladder carcinoma (BCa) are still unclear. The present paper aims to contribute to research on the effects and mechanism of circFLNA on the malignant phenotype of BCa. In this study, the expressions of circFLNA, miR-216a-3p and BTG2 in BCa and BCa cells (EJ, T24, 5637, TCC-SUP) were detected by qRT-PCR. EdU staining, colony formation, Transwell assay, wound healing assays, and sphere formation assay were used to measure the cell proliferation, viability, invasion, migration, and cell stemness of BCa cells after circFLNA overexpression. In addition, the correlation existed between miR-216a-3p and circFLNA or BTG2 was confirmed by Dual-Luciferase Reporter assay and RNA pull-down. Western blot was utilized to determine the expression of BTG2, MMP2, epithelial-mesenchymal transition (EMT)-related proteins (vimentin, E-cadherin) and stem cell-specific proteins (CD34, OCT4, SOX2). Our study confirmed that downregulated circFLNA and BTG2 expression and upregulated miR-216a-3p were found in both BCa tissues and cell lines. Meanwhile, upregulated circFLNA inhibited proliferation, invasion and migration, EMT and stemness of BCa cells. MiR-216a-3p was a target gene of circFLNA and could target BTG2. Further analysis finally demonstrated that circFLNA sponged miR-216a-3p and indirectly promoted BTG2 expression, ultimately regulating proliferation, migration, invasion and EMT of BCa cells. In conclusion, circFLNA inhibits the malignant phenotype of BCa cells and their stemness through miR-216a-3p/BTG2, thus suppressing BCa progression.