Chronic renal failure is clinical syndrome manifested as hypoactivity of renal function that can be caused by manifold diseases. CRF is difficult to be treated and has bad prognosis. In recent years, according TCM physiological and pathological mechanism, doctors have achieved good effects in preventing and delaying CRF in its early and middle stage by adopting the therapeutic principle of expelling toxin, strengthening body resistance, and promoting blood circulation to dissipating blood stasis.

OBJECTIVE: To probe into the status quo of hospital pharmacy practice in Japan and to provide reference for the further improvement of hospital pharmacy model in China.METHODS: Hospital pharmacy practice in affiliated hospital of Nippon Medical School was introduced,and the development of hospital pharmacy practice in Japan in the past few decades was also investigated.RESULTS & CONCLUSIONS: There is still a certain gap in the level of hospital pharmacy between China and Japan,so it is particularly important to improve hospital pharmacy system in China by the means of defining the pharmacist's responsibility and obligation,etc.

[摘 要] 目的：探讨鼠尾草酸（CA）通过调节CXC基序趋化因子受体7（CXCR7）/CXC基序趋化因子配体（CXCL12）轴对胃癌AGS细胞增殖、迁移和侵袭的影响。方法：用不同浓度（0、5、10、20、40、80 µg/mL））的CA处理胃癌AGS细胞，采用CCK-8法筛选合适的CA浓度；将AGS细胞分为对照组（未经处理的AGS细胞）、CA组（20 µg/mL CA处理）、CA+siCXCR7组（转染siCXCR7+20 µg/mL CA处理）、CA+siNC组（转染siNC+20 µg/mL CA处理）、CA+vectorNC组（转染vectorNC+20 µg/mL CA处理）、CA+vectorCXCR7组（转染vectorCXCR7+20 µg/mL CA处理），采用CCK-8法检测AGS细胞增殖的变化，qPCR法检测细胞中CXCR7、CXCL12 mRNA表达水平的变化，Transwell实验检测细胞侵袭能力的变化，划痕实验检测细胞迁移能力的变化，WB法检测周期蛋白D1、Bcl-2、CXCR7、CXCL12、MMP-2蛋白表达的变化。结果：不同浓度CA均可抑制AGS细胞存活率，且浓度为20 µg/mL时，细胞存活率接近50%，故选择20 µg/mL CA用于后续研究。与对照组相比，CA组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA及蛋白表达显著降低（均P<0.05）；与CA+siNC组相比，CA+siCXCR7组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA及蛋白表达显著降低（均P<0.05）；与CA+vectorNC组相比，CA+vectorCXCR7组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA及蛋白表达显著增加（均P<0.05）。结论：CA可抑制AGS细胞增殖、迁移和侵袭，其机制可能与抑制CXCR7/CXCL12轴有关。

Objective: To investigate the prognostic factors of multi-drug resistant organism (MDRO) infection in patients with infected pancreatic necrosis(IPN). Methods: A retrospective study was performed to assess the MDRO in IPN patients. The clinical data of 104 IPN patients admitted to the Department of Pancreatic and Biliary Surgery, the First Affiliated Hospital of Harbin Medical University from June 2013 to January 2019 were analyzed. Fifty-six patients were allocated in the MDRO group and 48 patients in the non-MDRO group depended on drug sensitivity test. There were 37 males and 19 females in the MDRO group with age of 40 (23) years. The duration time was 3(5) days between onset and admission. In the non-MDRO group, 34 males and 14 females were included with age of (42±14) years. The duration time was 3(4) days between onset and admission. Normally distributed quantitative variables was represented by ±s, non-normally distributed quantitative variables was represented by M(Q_R). Wilcoxon rank-sum test and χ² test were used to analyze the data. Univariate and multivariable Logistic regression analytic model were used to figure out the risk factors associated with MDRO infection. Results: The mean duration of hospital stay was 29.5(31.8) days and hospitalization expenses were CNY 166 991(270 692), which were much higher than those in non-MDRO group (16.5(15.7) days, CNY 56 789(62 354)) (W=1 889, 2 019, both P<0.01). Gram-negative isolates(67.2%, 80/119) were commonly detected in IPN patients.Acinetobacter baumannii was the most common MDRO(27.0%,20/74). Initial use of carbapenem(OR=2.22, 95%CI: 1.02-4.96, P=0.047) and open necrosectomy(OR=10.00, 95%CI: 3.14-44.77, P<0.01) were the potential risk factors for MDRO-induced infections in IPN. Furthermore, the Logistic regression analysis revealed that open necrosectomy was the independent variable for MDRO infections(OR=9.42, 95%CI: 2.92-42.42, P<0.01). Conclusion Open necrosectomy is the independent risk factor for the infection of MDRO.

[摘 要] 目的：探讨多结节非小细胞肺癌（NSCLC）组织中的驱动基因突变情况与临床病理特征的关系，为多结节NSCLC患者治疗提供分子诊断依据。方法：本研究共纳入2018年1月至2023年10月间云南省肿瘤医院分子诊断中心检测的121例多结节NSCLC患者的253个肺结节肿瘤组织标本，以第二代测序（NGS）技术或扩增阻滞突变系统PCR（ARMS-PCR）技术检测多结节NSCLC 组织中驱动基因突变情况，分析其与患者临床病理特征的关系，比较不同结节间肺癌驱动基因的突变异质性。结果：与非“宣威”NSCLC相比，“宣威”多结节NSCLC患者驱动基因突变具有显著的地域特点，表现在“宣威”患者具有较低（20%）的EGFR敏感突变（L858R、19-del）及较高（27.26%）的EGFR少见突变（主要为G719/S768I、G719）；“宣威”多结节NSCLC患者的KRAS突变率（27.27%）亦显著高于非“宣威”患者突变率（12.59%）（P<0.05）。此外，“宣威”多结节NSCLC患者驱动基因突变不一致率高达69.23%，远高于非“宣威”患者驱动基因突变不一致率（55.07%）（P<0.05）。结论：“宣威”多结节NSCLC患者具有较高的EGFR少见突变及KRAS突变率，同一患者不同病灶之间存在更高的驱动基因突变异质性，本研究将为“宣威”多结节NSCLC的诊疗策略提供更多的选择。