1.Analysis of Clinical Etiology,Serum Type and Drug Resistance of Lung Cancer Complicated with Pulmo-nary Haemophilus influenzae Infection
China Pharmacy 2017;28(17):2346-2350
OBJECTIVE:To investigate the clinical etiology,serum type and drug resistance of lung cancer complicated with pulmonary Haemophilus influenzae (Hi) infection,in order to provide reference for infection prevention and rational drug use. METHODS:Clinical data of 8025 inpatients with lung cancer complicated with pulmonary infection in our hospital from Jan. 2009 to Jun. 2016 were collected,and the clinical etiology of pulmonary Hi infection was analyzed. The slide agglutination method was used for serotyping,nitrocefin slip method was used to detect β-lactamase,K-B method was used for drug sensitivity test,WHO-NET 5.6 software was used to deal with the results of drug sensitivity test. RESULTS:Eleven factors as age,clinical classifica-tion,invasive operation,surgery,radiotherapy and chemotherapy,hospitalization time,use of broad-spectrum antibiotics or hor-mones and other were closely related to pulmonary Hi infection in lung cancer patients(P<0.05 or P<0.01). Among 8025 speci-mens,104 strains of Hi were detected with detection rate of 1.30%. Serum type NTHi accounted for 44.23%. Separable strains were mainly b type(22.12%),followed by f type(17.31%)and a type(11.54%). Among 104 strains of Hi,56 strains of β-lac-tamase were detected with enzyme-producing rate of 53.85%. Drug resistance of 104 strains of Hi to ampicillin,amoxicillin,com-pound sulfamethoxazole and chloramphenicol were all higher than 35%;drug resistance of Hi toβ-lactamase inhibitors,cephalospo-rins,carbapenems,azithromycin and other antibiotics were all lower than 20%. Drug resistance of β-lactamase producing stains to ampicillin,amoxicillin,compound sulfamethoxazole and chloramphenicol were all higher than those of non-producing strains,with statistical significance (P<0.01). There was no statistical significance in drug resistance to other antibiotics between producing stains and non-producing strains(P>0.05). CONCLUSIONS:The clinical etiology of pulmonary Hi infection in patients with lung cancer is complicated. The serum type of the isolate is mainly NTHi;enzyme production situation is not optimistic,but Hi keeps a low rate of drug resistance to most antibiotics. β-lactamase inhibitors,cephalosporins,carbapenems and azithromycin are first choice for the treatment of Hi infections.
2.Effect of Chinese gentian on the proliferation of, apoptosis and phosphorylation of epidermal growth factor receptor in HaCaT cells
Yinfei LOU ; Lili MA ; Mingjing ZHENG ; Hui ZHOU ; Yimiao FANG
Chinese Journal of Dermatology 2014;47(8):593-595
Objective To evaluate the effect of Chinese gentian extracts on the proliferation of,apoptosis and phosphorylation of epidermal growth factor receptor (EGFR) in HaCaT cells induced by epidermal growth factor (EGF).Methods Methyl thiazolyl tetrazolium (MTT) assay was performed to evaluate the proliferation of HaCaT cells pretreated with EGF of 20 μg/L for 24 hours followed by 24 hours of treatment with various concentrations of Chinese gentian extracts.Flow cytometry was carried out to detect apoptosis in HaCaT cells pretreated with EGF of 20 μg/L for 24 hours followed by 4 hours of treatment with different concentrations of Chinese gentian extracts.Western blot was conducted to measure the level of phosphorylated EGFR in HaCaT cells treated with different concentrations of Chinese gentian extracts for 24 hours followed by treatment with EGF of 20 μg/L for 10 minutes.Results Chinese gentian extracts inhibited the proliferation (r =-0.991,P < 0.01),but promoted the apoptosis (r =0.996,P < 0.05) of HaCaT cells induced by EGF in a dose-dependent manner.At the same time,the extracts suppressed the phosphorylation of EGFR in HaCaT cells induced by EGF,and the suppressing effect increased with the rise in the concentration of the extracts.Conclusions Chinese gentian may inhibit the proliferation,but promote the apoptosis of keratinocytes by decreasing EGFR phosphorylation and blocking relevant intracellular signaling pathways.