ABSTRACT
Objective To investigate the relationship between nasal colonization of Staphylococcus aureus(SA) and nosocomial infection in intensive care unit(ICU), and observe the therapeutic effect of Anerdian III in nasal decolonizaion. Methods Bacterial cultures were made by means of nasal swabs among inpatients whom the occurrence of nosocomial infection were observed.Patients with SA colonization were randomly divided into two groups:control and treatment.Control group were given regular treatment, and treatment group were administered Anerdian III in addition to regular treatment.Then the clearance rate of SA and the occurrence of nosocomial infection of two groups were observed. Results A total of 751 patients were enrolled, of whom 108(14.4%) were with nosocomial infection and 85(11.3%) with SA nasal colonization. Methicillin resistant Staphylococcus aureus ( MRSA ) was detected in 33 patients (4.4%).The nosocomial infection rate of patients with MRSA colonization was 51.5%, which was significantly higher than those in patients with other bacterial colonization(P<0.05).The SA clearance rate in treatment group was significantly higher than that in control group(81.4% vs.42.8%,P<0.05).The nosocomial infection rate in treatment group was significantly lower than that in control group ( 16 .3% vs. 40.5%,P <0.05).After decolonization treatment,the nosocomial infection rate of patients with MRSA colonization was significantly lower than that in control group(25.0% vs.76.5%,P <0.05). Conclusion The incidence rate of nosocomial infection in patients with MRSA nasal colonization is markedly increased in ICU, and the decolonization treatment by Anerdian III increases the clearance rate of nasal SA and decreases the incidence rate of nosocomial infection.
ABSTRACT
Objective] To discuss comprehensive intervention effect on the control of hospital in-fections in the intensive care unit ( ICU ) of a hospital by monitoring Staphylococcus aureus infections and their drug resistance . [ Methods] Comparative analysis was done retrospectively in separation results of Staphylococcus aureus between 2011 and 2012 in ICU patients of a hospital . [ Results] Between 2011 and 2012, there was no obvious difference found in relevance ratio of Staphylococcus aureus(P>0.05), but that of methicillin resistant Staphylococcus aureus was on the decline significantly (P<0.05).The drug re-sistance rates of Staphylococcus aureus to oxacillin, ciprofloxacin, levofloxacin were on the decline signifi-cantly(P <0.05).The drug susceptibility rates of Staphylococcus aureus to vancomycin, teicoplanin, linezolid , nitrofurantoin and primaquine slave tianeptine/dafoe tianeptine were the highest , reaching up to 100.00%. [ Conclusion] By comprehensive intervention , Staphylococcus aureus infections in ICU have been improved and drug resistance rates on the decline as a whole .
ABSTRACT
Emerging data indicated that HCV subverts the antiviral activity of interferon (IF); however,whether HCV core protein contributes to the process remains controversial. In the present study, we examined the effect of HCV core protein on interferon-induced antiviral gene expression and whether the effect is involved in the activation and negative regulation of the Jak/STAT signaling pathway. Our results showed that, following treatment with IFN-α, the transcription of PKR, MxA and 2'-5'OAS were down-regulated in HepG2 cells expressing the core protein. In the presence of HCV core protein,ISRE-dependent luciferase activity also decreased. Further study indicated that the core protein could inhibit the tyrosine phosphorylation of STAT1, whereas the level of STAT1 expression was unchanged.Accordingly, SOCS3, the negative regulator of the Jak/STAT pathway, was induced by HCV core protein. These results suggests that HCV core protein may interfere with the expression of some interferon-induced antiviral genes by inhibiting STAT1 phosphorylation and induction of SOCS3.
ABSTRACT
To study the effect of HCV core protein on the interferon-induced antiviral genes expression and its mechanisms. Methods HepG2 cells were transiently transfected with HCV core protein expression plasmid and the blank plasmid respectively. RT-PCR was used to analyze the effect of HCV core protein on PKR and 2'-5'OAS expression. The effect of HCV core protein on ISRE-medicated gene expression was detected by luciferase activity assay. Western-blot assay was performed to observe the change of mRNA and protein levels of SOCS3, STAT1 and p-STAT1 following HCV core expression. In the presence of HCV core protein, the transcription of PKR and 2'-5' OAS are down-regulated. ISRE-medicated reporter gene expression and STAT1 phosphorylation were inhibited. The transcription and expression of SOCS3 were induced compared with blank plasmid-transfected group. In HepG2 cells, HCV core protein can down-regulate the expression of some interferon-induced antiviral genes, which involves the induction of SOCS3 and the inhibition of STAT1 phosphorylation.