Introduction: The study investigated the risk factors of phlebitis associated with infusion by peripheral intravenous catheter (PIVC). Methodology: Hospitalized adults (n = 506) were placed with PIVCs by trained nurses. Rates of phlebitis were noted according to PIVC gauge, insertion site, and dwell time; and type and volume of infusion solution. Results: The development of phlebitis appeared to be significantly associated with the size of the outer diameter of the PIVC. The rate of phlebitis among patients given a hypertonic infusion solution was significantly higher; and also associated with infusion volume. There was no difference in phlebitis development among insertion sites, and dwell times among these sites were comparable. Conclusion: The risk of phlebitis increased with the PIVC size and volume of infusion solution, and use of a hypertonic solution. The recognition of risk factors and standardized intervention may reduce the occurrence of phlebitis associated with PIVC use.

A prospective study was performed to investigate the effects of hyperoxia on the expression of small ubiquitin‑related modifier (SUMO) and sirtuin 1 (SIRT1) proteins, and to examine interactions between these proteins in premature neonates with bronchopulmonary dysplasia (BPD). Peripheral blood mononuclear cells (PBMCs) were isolated from residual venous blood samples of 20 premature infants with BPD and 20 gender‑matched premature infants without BPD (non‑BPD group). Expression levels of SUMO and SIRT1 proteins in PBMCs were assessed by western blot analysis, and their interactions in PBMCs were detected using the immunoprecipitation assay. Based on the fraction of inspired oxygen (FiO2) administered, neonates were divided into normoxia, low‑(21%

Adenosine receptors play a key role in cancer progression. This study investigated the effect of the adenosine A2B receptor (ADORA2B) on epithelial–mesenchymal transition (EMT) markers and cell metastasis of gastric cancer (GC) cells. Public databases were used to investigate the specificity of ADORA2B expression in GC tissue. We used immunohistochemistry and immunofluorescence to detect ADORA2B expression in GC tissue, paracancerous tissue, and metastatic greater omental tissue. AGS and HGC-27 GC cells were selected. The effect of ADORA2B on the invasion and migration of GC cells was examined using cell scratch and transwell assays. The effect of ADORA2B on the expression of EMT marker proteins (β-catenin, N-cadherin, and vimentin) in GC cells was measured by cellular immunohistochemistry, immunofluorescence, and Western blot. The effects of an ADORA2B inhibitor combined with cisplatin on EMT markers in GC cells were further explored. The expression levels of ADORA2B in GC tissue, metastatic greater omental tissue, and lymphatic metastasis tissue were significantly higher than those in paracancerous tissue, and ADORA2B was associated with lymph node metastasis and invasion. ADORA2B significantly regulated the invasion and migration ability of GC cells and the expression levels of EMT marker proteins. The combination of an ADORA2B antagonist (PSB-603) and cisplatin had a more significant effect on reversing the expression of EMT marker proteins. ADORA2B was overexpressed in GC tissue, metastatic greater omental tissue, and metastatic lymph node tissue. ADORA2B regulated the expression of EMT marker proteins in GC cells and affected GC cell metastasis. Antagonizing ADORA2B expression increased the efficacy of cisplatin treatment.