【摘要】 目的 分析成都市近年一线抗结核药的耐药状况，为耐药结核病预防控制提供依据。 方法 对成都市2007年1月-2009年12月就诊的结核患者，临床分离株培养鉴定为结核分枝杆菌的菌株采用绝对浓度法进行一线抗结核药:链霉素（SM）、异烟肼（INH）、利福平（RF）、乙胺丁醇（EMB）耐药性检测，分析结核分枝杆菌的耐药情况。 结果 1 235例结核患者中，总耐药率和总耐多药率分别为28.83%、14.01%，初始耐药率和获得性耐药率分别为12.82%、61.27%。近3年耐多药率有下降趋势，但获得性耐药率呈逐年上升趋势。 结论 成都市结核耐药状况仍然比较严重，进一步加强耐药结核的监测和控制非常重要。【Abstract】 Objective To analyze the drug resistant treating mycobacterium tuberculosis (MTB) in Chengdu in recent three years, and to provide the evidence for tuberculosis controlling. Methods The patients with MTB diagnosed from January 2007 to December 2009 in Chengdu were enrolled. Absolute concentration method was used to test the drug-resistance of streptomycin (SM), isoniazide (INH), rifampicin (RFP), and ethambutol (EMB). Results The total rate of drug resistance and multi-drug resistance were 28.83% and 14.01% respectively. The rates of initial drug resistance and the acquired drug resistance were 12.88% and 61.27% respectively. Multi-drug resistance rate showed a downward trend, but the rate of acquired drug resistance increased gradually. Conclusion The situation of drug resistance of tuberculosis in Chengdu is still serious, and it′s very important to further monitor and control the drug resistance treating tuberculosis.
【Abstract】 Objective To detect the expression of lung resistance protein (LRP) and investigate its significance in pancreatic carcinoma cell lines (SW1990, PCT-2, PCT-3, PCT-4, Aspc-1, Capan-1, Mia-PaCa-2 and Panc-1). Methods Reverse transcription PCR (RT-PCR) and immunocytochemistry (ICC) were carried out to investigate the expression of LRP. Results LRP mRNA was absent in PCT-2 cell line by RT-PCR. Mild to moderate expression level was found in other pancreatic carcinoma cell lines. PCT-4, Aspc-1 and Panc-1 presented the highest LRP mRNA expression level, in contrast, SW1990, PCT-3, Capan-1 and Mia-PaCa-2 showed moderate LRP mRNA expression. The median value was 0.56±0.33. LRP was further validated by ICC. Absent to weak protein expression of LRP was found in PCT-2 and PCT-3. Overexpressed LRP was present in SW1990, Capan-1 and Aspc-1, furthermore, the highest expression of LRP was found in Panc-1, Mia-PaCa-2 and PCT-4 cell lines. Conclusion All these data showed that LRP might play an important role in multidrug resistance of pancreatic carcinoma.
ObjectiveTo investigate the value of serum soluble CD146 (sCD146) in determining acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance in lung adenocarcinoma.MethodsA total of 144 lung adenocarcinoma EGFR sensitive patients in People’s Hospital of Zhengzhou University diagnosed from January 2016 to December 2016 were recruited in the study. According to the different time of taking drugs, the patients were divided into a non-medication group (31 cases), a 1 to 3 month treatment group (25 cases), a 4 to 6 month treatment group (19 cases), a 7 to 12 month treatment group (25 cases), a drug-resistant group (24 cases), and a nonresistant group up to 1 year of treatment (20 cases). The serum levels of sCD146, carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE) were measured by ELISA and chemiluminescence and compared between different period of medication. The relationship of serum sCD146 with tumor markers (CEA, NSE) and tumor related clinical parameters (age, gender, tumor stage, metastasis, tumor diameter, number of the lesions) were analyzed.ResultsThe serum sCD146 level was minimum in the non-medication group that did not receive pioglitazone treatment, highest in the 1 to 3 month treatment group (early treatment period), and declined with duration of medication until resistance occurred without significant difference (P>0.05). The level of sCD146 of the drug-resistant group was significantly lower than that of all nonresistant groups, with significant difference (allP<0.05), but still higher than that of the non-medication group (P<0.05). The serum sCD146 levels in the nonresistant patients with medication over 1 year and within 1 year were similar (P>0.05), and significantly higher than the non-medication group and drug-resistance group (allP<0.05). The serum CEA levels did not differ significantly between 6 groups (P>0.05). The serum NSE level of the 4 to 6 month treatment group was lower than that of the 7 to 12 month treatment group (P<0.05), but both in the normal reference range. The NSE levels did not differ in any other groups (P>0.05). Serum sCD146 was associated with metastasis (P<0.05), but not associated with serum CEA or NSE, nor with sex, age, tumor staging, tumor diameter or lesion number (allP>0.05).ConclusionsCD146 may be involved in the mechanism of TKI killing tumor cells and the mechanism of TKI resistance, and may be a serological marker for monitoring the efficacy of TKI and judging the resistance of TKI.