RESUMEN
Objective To evaluate the effects of a self-designed multi-function anti-reflux drainage connector on preventing catheter-associated urinary infection in patients with long-term indwelling catheters.Methods A total of 100 elderly males with indwelling catheters from 10 nursing homes in our city were selected and randomly divided into the control group (n=50) and the experimental group (n=50) from January 2013 to December 2015.The patients in the control group were indwelled with Foley catheters and connected with an ordinary disposable drainage bags;the patients in the experimental group were indwelled the same catheters and connected to disposable drainage bags with an multi-function anti-reflux drainage connector.Patients' urine in catheters and drainage bags from two groups were collected for urine culture on 7th,14th,21st,28th days.The cases of catheter plugging on the 7th,14th,21st,28th days and the cases of catheter encrustation on 28th day in two groups were recorded.Results The cases of bacteriuria on the 7th,14th,21st,28th days in the experimental group were significantly less than those in the control group (P＜0.05),and were also significantly less than those in the drainage bags in the same group (P＜0.05).The cases of catheter plugging on the 7th,14th,21st,28th days were not significantly different between two groups(P＞0.05).The cases of catheter encrustation on the 28th day in the experimental group were significantly less than those in the control group (P＜0.05).Conclusion Multi-function anti-reflux drainage connector can safely and effectively prevent catheter-associated urinary infection,reducing bacteria ascending with reflux of urine as well as catheter encrustation.
RESUMEN
The molecular mechanism of DNA damage induced by hydroquinone (HQ) remains unclear. Poly(ADP-ribose) polymerase-1 (PARP-1) usually works as a DNA damage sensor, and hence, it is possible that PARP-1 is involved in the DNA damage response induced by HQ. In TK6 cells treated with HQ, PARP activity as well as the expression of apoptosis antagonizing transcription factor (AATF), PARP-1, and phosphorylated H2AX (γ-H2AX) were maximum at 0.5 h, 6 h, 3 h, and 3 h, respectively. To explore the detailed mechanisms underlying the prompt DNA repair reaction, the above indicators were investigated in PARP-1-silenced cells. PARP activity and expression of AATF and PARP-1 decreased to 36%, 32%, and 33%, respectively, in the cells; however, γ-H2AX expression increased to 265%. Co-immunoprecipitation (co-IP) assays were employed to determine whether PARP-1 and AATF formed protein complexes. The interaction between these proteins together with the results from IP assays and confocal microscopy indicated that poly(ADP-ribosyl)ation (PARylation) regulated AATF expression. In conclusion, PARP-1 was involved in the DNA damage repair induced by HQ via increasing the accumulation of AATF through PARylation.