英国价值定价理念对我国医保药品报销政策的启示

本文在梳理英国医保药品报销政策的基础上,通过对价值定价理念的深入研究和理解,系统探讨其在报销政策制定过程中对药品目录遴选、价值测算、支付标准确定、医保基金平衡和报销效益评估的作用机制,并深入思考通过价值定价理念建立起的药物警戒体系与药品报销政策间的衔接机制。在此基础上总结价值定价理念的特点、应用阶段和具体操作方法,以期为我国提供借鉴。     

工作分解结构法在手术室血管造影机移机项目中的应用

目的:探讨工作分解结构法应用于手术室血管造影机移机项目中的可行性。方法:应用鱼骨图分析导致血管造影机移机失败的风险因素,再应用工作分解结构法按照既定的逻辑顺序将移机项目分解为8个操作性强的子项目,并分配给相应的责任科室在规定时间内完成。结果:各责任科室相互协作,在规定时间内完成了血管造影机移机,保障了移机后的血管造影机各项功能均正常。结论:应用工作分解结构法能有效地调配医院各相关科室的人、财、物资源,保证血管造影机的顺利移机。     

DRG支付方式改革下医院财务管理应对策略

通过探讨DRG支付方式改革下医院财务管理的应对策略,可以有效地降低医疗支付方式改革对医院财务管理的负面影响,促使医院财务管理在"危"与"机"的转换中抢抓机遇,促进医院财务管理提质增效。     

ATC/DDD体系指标用于质子泵抑制剂使用管理效果评价

目的为质子泵抑制剂(PPI)的临床规范使用提供参考。方法采用ATC/DDD体系的分类法查询并计算各PPI的限定日剂量(DDD)值,回顾性分析医院2015年至2017年使用PPI的品种、消耗数量、科室分布、用药频度(DDDs)、使用强度(AUD)及使用率等相关指标。结果医院PPI的DDDs、AUD及使用率,各科室PPI的DDDs、AUD及使用率排名相对稳定;住院患者PPI的DDDs呈上升趋势,PPI销售金额排前10名的科室波动不大,PPI使用率总体略有下降,但仍较高。结论以ATC/DDD评价系统为基础制订各临床科室PPI使用指标具有可行性,可为医疗机构规范PPI的临床应用提供参考。     

血必净注射液对EICU脓毒症患者炎症应激反应和心肌功能的影响

目的:探讨血必净注射液治疗急诊重症监护室(EICU)脓毒症患者的疗效,以及对机体炎症应激反应和心肌功能的影响。方法:采用随机数字表法将190例脓毒症分为常规组和血必净组,每组均95例。两组均严格按照脓毒症治疗指南(2016年版)给予常规抗脓毒症集束化治疗,血必净组在常规治疗基础上给予血必净注射液治疗,常规组给予等量的0.9%氯化钠注射液。观察两组治疗前和治疗7 d后急性和慢性健康状况评分系统Ⅱ(APACHE Ⅱ)评分,检测并比较治疗前后血清炎性因子肿瘤坏死因子-α(TNF-α)、超敏C-反应蛋白(hs-CRP)、降钙素原(PCT)、白介素-6(IL-6)和心肌损伤标志物血肌钙蛋白I(cTn I)、肌酸激酶同工酶(CK-MB)水平,统计两组EICU住院时间和28 d死亡率。结果:两组治疗7 d后血清TNF-α、hs-CRP、PCT、IL-6和cTn I、CK-MB水平均明显下降(P<0.05),且治疗组治疗7 d后上述炎性因子和心肌功能指标水平显著低于常规组,差异有统计学意义(P<0.05)。治疗组治疗7 d后APACHEⅡ评分明显低于常规组,EICU住院时间较常规组明显缩短,差异有统计学意义(P<0.05),两组28 d病死率比较差异无统计学意义(P>0.05)。结论:常规对症治疗联合血必净注射液能有效减轻脓毒症患者机体炎症应激反应和保护心肌功能,对改善病情程度和缩短EICU住院时间有一定价值。     

光强对野菊生理生化特性的影响

通过分析光强对野菊生长及生理生化特性的影响,揭示适于野菊生长的光照强度,为野菊种植提供参考依据。分别在100%,80%,60%,40%,20%全自然光强水平下种植野菊,生长旺盛期测定野菊相关生长,光合色素含量、光合参数、荧光参数等光合生理及保护酶系统指标,采取透射电镜技术观察叶绿体超微结构。结果表明:野菊叶片在80%以上全自然光强下出现不同程度发黄现象,株高和茎粗在60%全自然光强达到最大值,60%以上全自然光强下野菊分枝数显著增加;光合色素含量和净光合速率均与光强负相关,光合参数与叶绿素荧光参数则随光强下降呈先上升后下降趋势,60%全自然光强下野菊气孔导度、胞间CO2浓度、蒸腾速率、水分利用效率及PSⅡ实际光化学量子产量等生理指标均处于最高水平;60%~80%全自然光强下野菊叶绿体结构无明显异常,全自然光强下基质片层破碎,20%~40%全自然光强下叶绿体数量、淀粉粒数量与体积均明显降低;随光强下降,SOD与CAT活性呈下降趋势,POD活性呈先上升后下降趋势,MDA含量呈上升趋势。综上,野菊在20%~100%全自然光强下均能生长,但在60%全自然光强下生长最佳。     

Berberine ameliorates non-steroidal anti-inflammatory drugs-induced intestinal injury by the repair of enteric nervous system

The study was to detect the role of GDNF, PGP9.5 (a neuronal marker), and GFAP (EGCs’ marker) in the mechanism of non-steroidal anti-inflammatory drugs (NSAIDs) related to intestinal injury and to clarify the protective effect of berberine in the treatment of NSAID-induced small intestinal disease. Forty male SD rats were divided randomly into five groups (A–E): Group A: control group; Group B: model group received diclofenac sodium 7.5 mg/(kg*day) for 5 days; Group C–E: berberine low, medium and high dose groups were treated by 7.5 mg/(kg*day) diclofenac sodium for 5 days then received berberine 25 mg/(kg*day), 50 mg/(kg*day), and 75 mg/(kg*day), respectively, between the sixth and eighth day. Intestinal mucosa was taken on the ninth day to observe the general, histological injuries, and to measure the intestinal epithelial thickness. Then, immunohistochemistry was performed to detect the expression of PGP9.5 and GFAP, and Western blot was performed to detect GDNF expression. The histological score and the general score in the model group were, respectively, 5.75 ± 1.04 and 4.83 ± 0.92. Scores in berberine medium and high berberine group were lower compared with the model group (P < 0.05). The intestinal epithelial thickness in the model group was lower than in the control group and the berberine groups (P < 0.05). PGP9.5, GFAP, and GDNF content in the model group and the three berberine groups were significantly lower than in the control groups (P < 0.05). PGP9.5, GFAP, and GDNF content in the control group and the three berberine groups were higher compared with the model groups (P < 0.05). Berberine can protect the intestinal mucosa of NSAID users, and the mechanism is associated with the reparation of the enteric nervous system via upregulating the expression of PGP9.5, GFAP, and GDNF.     

Proteasome inhibitors and Smac mimetics cooperate to induce cell death in diffuse large B-cell lymphoma by stabilizing NOXA and triggering mitochondrial apoptosis

Copy number gains and increased expression levels of cellular Inhibitor of Apoptosis protein (cIAP)1 and cIAP2 have been identified in primary diffuse large B-cell lymphoma (DLBCL) tissues. Second mitochondria-derived activator of caspases (Smac) mimetics were designed to antagonize IAP proteins. However, since their effect as single agents is limited, combination treatment represents a strategy for their clinical development. Therefore, we investigated the Smac mimetic BV6 in combination with proteasome inhibitors and analyzed the molecular mechanisms of action. We discovered that BV6 treatment sensitizes DLBCL cells to proteasome inhibition. We show a synergistic decrease in cell viability and induction of apoptosis by BV6/Carfilzomib (CFZ) treatment, which was confirmed by calculation of combination index (CI) and Bliss score. BV6 and CFZ acted together to trigger activation of BAX and BAK, which facilitated cell death, as knockdown of BAX and BAK significantly reduced BV6/CFZ-mediated cell death. Activation of BAX and BAK was accompanied by loss of mitochondrial membrane potential (MMP) and activation of caspases. Pretreatment with the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk) rescued BV6/CFZ-induced cell death, confirming caspase dependency. Treatment with CFZ alone or in combination with BV6 caused accumulation of NOXA, which was required for cell death, as gene silencing by siRNA or Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9-mediated NOXA inactivation inhibited BV6/CFZ-induced cell death. Together, these experiments indicate that BV6 and CFZ cooperatively induce apoptotic cell death via the mitochondrial pathway. These findings emphasize the role of Smac mimetics for sensitizing DLBCL cells to proteasome inhibition with important implications for further (pre)clinical studies.     

大鼠急性经口1,1-二氨基-2,2-二硝基乙烯的毒代动力学研究

建立大鼠血液中1,1-二氨基-2,2-二硝基乙烯(FOX-7)的检测方法，将30只健康SPF级SD大鼠随机分为空白对照组、200和500mg/kgFOX-7染毒组，每组10只。采用一次性经口灌胃方式染毒，染毒容量为ImL/lOOg。于染毒后第0.5、1、2、4、8、12、24h对大鼠进行眼眶后静脉丛采血，使用紫外可见分光光度计检测血中FOX-7浓度。使用PhoenixWinNonlin6.1软件进行血药浓度-时间数据分析与毒代参数计算。大鼠单次灌胃FOX-7200和500mg/kg后，药-时曲线下面积AUC(0-24)分别为(27.01±L94)^g/(h?L)和(29.26±3.31)^^(h-L),AUC(0-?>分别为(42.。1±2.18)阿/(h-L)和(4L51±3.66)Mg/(h?L)；达峰浓度Cmax分别为(1.82±0,12)Mg/ml和(2.33±0,20)阿/ml,达峰时间y.为2h；半衰期知2分别为(10.83±2,77)h和(8.66±3,01)h。本研究为FOX-7毒代动力学模型的完善提供了科学依据。