Objective To explore the effect of multimodal interventions in improving the compliance rate of core infection control measures on reducing the incidence rate of vessel catheter associated infection (VCAI). Methods Inpatients with intravascular catheters in 5 departments with high rates of vascular catheterization and infection of Dongguan People’s Hospital between January 2021 and December 2022 were selected. According to the hospital stay, patients were divided into a pre-intervention group (January to December 2021) and a post-intervention group (January to December 2022). The core infection control measures assessment pass rates of medical staff between the two periods and the differences in the incidence rate of VCAI, average catheterization days, and catheterization rate before and after intervention in both groups were compared. Results A total of 8174 patients were included. Among them, there were 3915 patients in the pre-intervention group and 4259 patients in the post-intervention group. In the pre-intervention group, the total length of hospital stay was 122885 days, the total number of catheterization days was 48028 days, and 28 cases of VCAI occurred. In the post-intervention group, the total length of hospital stay was 126966 days, the total number of catheterization days was 51253 days, and 12 cases of VCAI occurred. After intervention, the compliance rate of VCAI core infection control measures was improved [69.21% (2907/4200) vs. 91.24% (3832/4200); χ2=642.090, P＜0.001], the pass rate of medical staff’s core infection control measures assessment was improved [53.33% (128/240) vs. 91.67% (220/240); χ2=88.443, P＜0.001], the catheterization rate was increased [39.08% (48028/122885) vs. 40.37% (51253/126966); χ2=42.979, P<0.001], and the incidence rate of VCAI was reduced [0.58‰ (28/48028) vs. 0.23‰ (12/51253); incidence-rate ratios =0.40, 95% confidence interval (0.20, 0.79), P=0.008]. Conclusions Improving the compliance rate of VCAI core infection control measures through multimodal interventions can significantly improve the passing rates of core infection control measures of medical staffs. This will help to reduce the incidence of VCAI and ensuring patient safety, provide evidence-based support for the prevention and control of VCAI.
Objective To investigate the role and mechanism of S100 calcium binding protein B (S100B) in osteoarthritis (OA) cartilage damage repair. Methods Twenty New Zealand rabbits were randomly divided into control group and model group, with 10 rabbits in each group. Rabbits in the model group were injured by the right knee joint immobilization method to make the artilage injury model, while the control group did not deal with any injury. After 4 weeks, the levels of interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in synovial fluid were detected by ELISA method; the mRNA and protein expressions of S100B, fibroblast growth factor 2 (FGF-2), and FGF receptor 1 (FGFR1) in cartilage tissue were examined by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot assay. Human synovial fibroblasts (SF) were isolated and cultured in vitro. The effects of S100B overexpression and knockdown on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Moreover, the effects of FGFR1 knockdown in above S100 overexpression system on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Results ELISA detection showed that the expressions of IL-1β and TNF-α in the synovial fluid of the model group were significantly higher than those of the control group (P<0.05); qRT-PCR and Western blot detection showed that the mRNA and protein expressions of S100B, FGF-2, and FGFR1 in cartilage tissue were significantly higher than those of the control group (P<0.05). Overexpression and knockdown S100 could respectively significantly increase and decrease lipopolysaccharides (LPS) induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 (P<0.05); whereas FGFR1 knockdown could significantly decrease LPS induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 (P<0.05). Conclusion S100B protein can regulate the inflammatory response of SF and may affect the repair of cartilage damage in OA, and the mechanism may be related to the activation of FGF-2/FGFR1 signaling pathway.