RESUMO
OBJECTIVE To observe the efficacy and safety of ceftazidime and avibactam sodium （CAZ/AVI） in the treatment of carbapenem-resistant organism （CRO） infection. METHODS The information of patients with CRO infection admitted to the Second Affiliated Hospital of Soochow University from September 2019 to March 2022 was collected， and the patients were retrospectively divided into observation group （48 cases） and control group （48 cases） according to the treatment plan. The control group was given Polycolistin B sulfate for injection intravenously at a dose of 500 000 U every 12 hours； no dose adjustment was performed in patients with renal insufficiency or receiving continuous renal replacement therapy （CRRT）. The observation group was given continuous micropump of CAZ/AVI for injection intravenously at a dose of 2.5 g every 8 hours for 2 continous hours； among them， the patients with renal insufficiency received an adjusted dose based on creatinine clearance， and no dose adjustment was performed in patients receiving CRRT. The clinical efficacy and microbiological efficacy as well as body temperature， white blood cell （WBC）， C-reactive protein （CRP） and procalcitonin （PCT） before and after treatment were compared between 2 groups. The prognosis and the occurrence of adverse drug reactions were recorded. The factors influencing the clinical efficacy were screened by Logistic regression analysis. RESULTS The effective rate and microbial clearance rate of the observation group were significantly higher than the control group （P＜0.05）. After treatment， body temperature， PCT and CRP of 2 groups were significantly lower than before treatment， and CRP of the observation group was significantly lower than the control （No.SDFEYJLC2105） group （P＜0.05）. There was no statistically significant differencebetween the two groups in terms of rehabilitation discharge rate， the proportion of patients transferred to general wards，the proportion of dead patients， and the total incidence ofadverse drug reactions （P＞0.05）. CAZ/AVI and prolonging therapy duration were more likely to achieve clinical benefits （odds ratios of 1.146， 7.707，P＜0.05）， while lung infection and CRRT may be independent risk factors for treatment failure （odds ratios of 0.182， 0.236， P＜0.05）. CONCLUSIONS CAZ/AVI has good efficacy and safety in the treatment of CRO infection， the appropriate extension of antibacterial treatment time can achieve a higher clinical response rate， while lung infection or CRRT may lead to treatment failure.
RESUMO
Objective To test the effects of Vitamin D (VitD) on endothelial nitric oxide(NO) production and to study the signal pathway leading to NO release.Methods In vitro cultured human umbilical vein endothelial cells (HUVEC) were treated with various concentrations of VitD(0 mmol/L,0.01 mmol/L,0.10 mmol/L,1.00 mmol/L,10.00 mmol/L) for 60 min,and VitD at concentration of 1.00 mmol/L at different time points (30 min,60 min,90 min,120 min).The effect of VitD on NO production in presence of VitD receptor(VDR) agonist(ZK191784) or antagonist(ZK159222) for 60 min were examined in cell culture supernatant with kit for the detection of nitric oxide fluorescent probe(DAF-FM DA).HUVEC was cultured with VitD in presence of VDR agonist or antagonist for 60 min,and the effect of VitD on NO production with DAF-FM DA and the protein expression and phosphorylation of Caveolin-1 and endothelial nitric oxide synthase(eNOS) were detected by Western blot,respectively.Results VitD caused a concentration-dependent increase in NO production.The maximum effect was observed at a concentration of 1.0 mmol/L and the optimal time of stimulation was 60 min.Effects induced by VitD were enhanced by VDR agonist,and abolished by antagonist.VitD and VDR agonist maintained the expression of Caveolin-1 at the same low phosphorylation level the same as normal,increased the phosphorylated level of eNOS.However,VDR antagonist increased the phosphorylation of caveolin-l,but reduced the level of eNOS phosphorylation,respectively.Conclusions VitD can induce a significant increase in endothelial NO production through VDR.VitD interaction with VDR causes the low phosphorylation of caveolin-1 leading to eNOS activation and NO production.