改变中心药房摆药模式提高医院药学服务水平

通过改变中心药房摆药模式,从原来手工摆药转变成全自动口服片剂摆药机的使用,促进中心药房摆药自动化,提高摆药效率及药学服务水平。全自动口服片剂摆药机的使用提高摆药速度和准确性,改善卫生状况,减少药品污染机会,节约人员,提高效率,能更好地为临床进行药学服务。     

我院住院药房全自动片剂摆药机应用体会

目的促进药房摆药自动化,提高调剂效率及药学服务质量。方法介绍全自动片剂摆药机应用优缺点。结果与结论全自动片剂摆药机可提高摆药的速度和准确性,减少摆药人数,缩短护士领药时间,减少药品污染,改善卫生状况,提高工作效率,从而提升药学服务质量与水平。     

全自动片剂摆药机对药品拆零管理的利与弊

目的 通过综合分析我院使用全自动片剂摆药机3年来的情况,讨论建立科学、可控的质量管理体系,加强医院拆零药品的质量管理.方法 从5个方面分析我院中心药房拆零药品质量管理中存在的问题,探讨应用全自动片剂摆药机加强拆零药品管理的优点与缺点.结果与结论 摆药机应用于拆零药品的质量管理,可减少人为污染,避免交叉感染,有利于提高拆零药品管理水平.虽然在使用过程中也存在着资源浪费、药师工作量加大、药房运营成本增加等问题,但总体上配备片剂摆药机仍是值得推广的方法.     

全自动片剂摆药机在本院住院药房的应用体会

目的:为医院药房应用摆药机提供参考。方法:考查全自动片剂摆药机(DIH-AP336FS)在本院住院药房的工作流程和应用情况,总结其优缺点及应用过程中发现的问题及解决办法。结果:全自动片剂摆药机具有提高摆药效率及准确率、确保用药安全的优点,但相关费用高;应用过程中出现药盒卡药、药片多摆或少摆等问题,得到了较好的解决。结论:应用全自动片剂摆药机有助于提高医院药学服务水平,是医院药房的发展趋势。     

全自动片剂摆药机在住院药房的实施与评价

目的:评价住院药房中全自动片剂摆药机的工作效率与价值。方法:介绍全自动片剂摆药机(YS-CS-260FDSⅡ)系统的主要结构、功能、工作流程及使用情况,并通过实践检验,探讨其优势及不足。结果:自动摆药机的应用,可以加快摆药速度、提高摆药准确度、降低人员成本、减少药品污染的机会、方便患者服药等,但也存在新的机器误差、成本提高等问题。结论:全自动摆药机提高了医院自动化水平和药学服务水平,为患者的用药安全提供了保障。     

全自动片剂摆药机在我院住院药房的应用

目的:从实践中探索单剂量全自动片剂摆药机在住院药房应用的可行性,优化摆药工作模式,为其推广应用提供参考。方法:介绍全自动片剂摆药机在我院的使用情况,描述常见的差错类型并提出解决方法,全面分析摆药机使用效果。结果与结论:摆药机常见的差错类型有药片窜包、手动放药单元不漏药等,解决方法包括设置合适的包药速度、定期清洁药片托盘等。摆药机的使用完善了摆药工作流程、避免了药品污染和交叉感染、提高了患者用药依从性和药品管理水平、转变了药师的工作模式等,给药房带来了调剂模式和管理的变革,更符合新形势下药房管理的需求。     

住院药房全自动口服摆药机应用分析

目的分析全自动口服摆药机应用情况,为医院病房口服药品的分包使用及管理提供参考。方法统计口服摆药药房的药品种类、剂型、分劈药片及临床口服摆药医嘱情况,对常见问题进行分析,并提出解决办法。结果我院目前常摆药品289种,占口服药品的77.69%,其中分劈药品156种,占口服摆药品种的53.98%,分劈药品摆药品种仍以普通片剂和胶囊为主,缓控释制剂品种相对少。结论我院住院药房全自动口服摆药机应用普及较广,品种配置合理,分劈药品的共性问题仍存在。     

充分利用全自动片剂摆药机,提升药学服务水平

目的 实现住院药房中心摆药的自动化.方法 介绍我院全自动片剂摆药机的主要构造、运行环境、工作原理、调剂流程及流程改善环节,并与传统手工摆药模式相比较.结果 全自动片剂摆药机的应用可提高药师摆药、发药的速度和准确性,改善卫生状况,避免病人二次感染,缩短护士的取药时间,提高病人的用药依从性.结论 全自动片剂摆药机适合住院药房使用,可提升药房的药学服务水平.     

全自动口服药品摆药机在我院药房的应用及体会

目的:为医院药房应用全自动口服药品摆药机摆药提供参考。方法:介绍我院全自动口服药品摆药(TR-200FDS)系统的主要结构,简述摆药机的工作流程及使用情况,并讨论其优势及不足。结果:应用摆药机摆口服药具有方便、卫生、快捷、准确等优势,但相关费用较高。结论:药房应用全自动口服药品摆药机提高了医院药学服务水平,是医院药房的发展趋势。     

应用全自动片剂摆药机，建设现代化药房

本文就近年来我院全自动片剂摆药机的使用经验进行总结,分析了应用摆药机进行口服药品调剂的利弊,并就引进自动化设备对于建设现代化药房的作用进行了阐述。     

全自动药品单剂量分包机在我院药房的应用情况调查与分析

目的:为进一步在医院药房推广应用全自动药品单剂量分包机(下简称自动分包机)提供参考。方法:介绍自动分包机应用前的准备工作及其工作程序,分析其使用优点、差错原因及相关应用问题。结果:自动分包机的应用提高了工作效率,改善了药品的卫生状况,确保了安全用药,完善了药品管理,但有时也会出现医疗差错。本次调查医嘱49059条,出现差错236条,差错率为0.48%。结论:自动分包机具有很高的应用价值,符合药房自动化的趋势,但仍需进一步完善。     

全自动药品单剂量分包机的差错分析及对策

目的：分析评价全自动药品单剂量分包机的常见差错,并制定对策。方法：随机抽取调整前后两个时期（调整前：2007年8月15日-2007年10月15日,调整后：2008年1月1日-2月28日）同一病区的摆药医嘱,并统计分析调整前后的差错情况。结果：全自动药品单剂量分包机的差错率由调整前的4.81‰下降到调整后的1.66‰,通过差错调整措施,差错率显著降低（P〈0.05）。结论：全自动药品单剂量分包机具有很高的实用价值,虽然在使用过程中会出现一定的差错,但通过制定对策,差错率可显著降低。     

ATM蛋白在神经退行性病变中的作用及机制研究进展

ATM蛋白缺失是运动失调性毛细血管扩张症(ataxia telangiectasia,AT),是这种罕见的常染色体隐性遗传病的发病基础,其病变的一个重要特征就是神经退行性病变.本文主要从氧化应激、DNA损伤及修复和细胞自噬等角度对ATM蛋白在神经退行性病变中的作用及相关机制做一综述,以此阐明ATM蛋白作为神经退行性病变治疗药物靶点的可能性.     

Therapeutic role of Artemether in the prevention of hepatic steatosis through miR-34a-5p/PPARα pathway

Artemether (ATM) is a natural antimalarial drug that can also regulate glucose and lipid metabolism. However, little is known regarding its pharmacological action in metabolic dysfunction-associated fatty liver disease (MAFLD), and the underlying mechanisms remain undetermined. The aim of this study was to explore the therapeutic effects of ATM against hepatic steatosis and the possible mechanisms. ATM significantly decreased blood glucose levels, improved glucose tolerance, reduced inflammatory response, and alleviated hepatic steatosis in the ob/ob mouse model as well as the high-fat diet-fed mice. ATM also inhibited lipid accumulation in murine hepatocytes in vitro. Using RNA sequencing, miR-34a-5p and peroxisome proliferator-activated receptor-α (PPARα) were identified as important regulators during ATM treatment. ATM administration downregulated miR-34a-5p expression and miR-34a-5p abrogated the inhibitory effects of ATM on PO (palmitate + oleate)-induced lipid accumulation as well as triglycerides levels in murine hepatocytes. Furthermore, the expression of PPARα, a target gene of miR-34a-5p, was upregulated by ATM and PPARα inhibitor MK-886 abolished the positive effect of ATM. Consequently, PPARα agonist fenofibrate reversed the decreased mitochondrial fatty acid β-oxidation induced by miR-34a-5p mimics after ATM treatment, thereby leading to attenuation of intracellular lipid accumulation. Taken together, ATM is a promising therapeutic agent against MAFLD that reduces lipid deposition by suppressing miR-34a-5p and upregulating PPARα.     

Autoradiographic demonstration of the antagonism of anthramycin and diazepam against cholecystokinin in the mouse brain using the [14C]-2-deoxyglucose method

Effects of diazepam (DZP), a synthetic benzodiazepine drug, and anthramycin (ATM), a benzodiazepine antitumor antibiotic produced by a certain species of streptomyces, on the uptake of 2-deoxy-D-[14C]-glucose (2-DG) in mouse brain neurons with or without cholecystokinin were examined. 2-DG uptake in neurons was evaluated by using an autoradiographic technique. The sulfated octapeptide CCK (CCK8) was injected intracisternally; DZP and ATM, intraperitoneally; and 2-DG, intravenously to mice. Autoradiograms prepared from the slices of the brain were converted to false color images. CCK8 (1 microgram/mouse) markedly stimulated the 2-DG uptake in neurons in the various regions of the brain, but the stimulative effects of CCK8 was almost completely suppressed after an intraperitoneal administration of 1.0 mg/kg of DZP or 0.5 mg/kg of ATM. Since it has been previously shown that these doses of DZP and ATM almost completely reversed the antinociception produced by 1 microgram/mouse of CCK8, the present results on the 2-DG uptake in the mouse brain are considered to further support the antagonism between CCK8 and DZP or ATM in the central nervous system.     

Impact of goal-oriented and model-based clinical pharmacokinetic dosing of aminoglycosides on clinical outcome: a cost-effectiveness analysis

The benefits of a pharmacy-based, active therapeutic drug monitoring (TDM) service (ATM) on outcomes were examined in a prospective study at four hospitals. ATM involved pharmacokinetic dosage optimization at the start of treatment, subsequent Bayesian adaptive control, and frequent patient evaluation. Cost-effectiveness was calculated based on real costs. The ATM group comprised 105 patients and 127 patients with nonguided TDM who were followed up as controls. Forty-eight of the ATM and 62 of the nonguided TDM patients had an infection on admission. Peak concentrations in ATM patients were significantly higher (10.6+/-2.9 mg/L; nonguided TDM, 7.6+/-2.2 mg/L; p < 0.01). Trough levels in the ATM group were significantly lower (p < 0.01). There was a trend toward lower mortality in the ATM group (nine of 105 versus 18 of 127; p = 0.26) that was significant for patients with an infection on admission (one of the 48 ATM patients died versus nine of the 62 nonguided TDM patients; p = 0.023). ATM reduced the length of hospital stay for all patients in the study (20.0+/-1.4 days; nonguided TDM, 26.3+/-2.9 days; p = 0.045) and for patients admitted with an infection (12.6+/-0.8 days; nonguided TDM, 18.0+/-1.4; p < 0.001). The incidence of nephrotoxicity was reduced from 13.4% (nonguided TDM) to 2.9% (p < 0.01). With ATM, total costs were lower for all patients (Dutch guilders [DFL], 13,125+/-9,267; nonguided TDM, DFL 16,862+/-17,721; p < 0.05) and for patients admitted with an infection (DFL 8,883+/-3,778; nonguided TDM, DFL 11,743+/-7,437; p < 0.01). Goal-oriented, model-based dosing of aminoglycosides resulted in higher antibiotic efficacy, shorter hospitalization, and reduced incidence of nephrotoxicity. By combining efficacy with savings, ATM offered a significant alternative to usual care.     

某基层医院大肠埃希菌的耐药性及其分布

目的 了解医院四个临床科室分离的大肠埃希菌对临床常用抗菌药物的耐药性及分布,为临床经验用药提供理论依据.方法 采用WHONET5.6对2016年1月至2016年12月本院儿内科病房、内一科病房、泌尿外科病房及新生儿科病房分离的大肠埃希菌对临床常用的12种抗菌药物的耐药性及分布进行分析.结果 儿内科病房、内一科病房、泌尿外科病房和新生儿科病房、分别分离86株、10株、60株和7株大肠埃希菌,对哌拉西林/他唑巴坦、阿米卡星、头孢西丁、美洛培南和头孢他啶的耐药率较低,为0％ ～ 26.7％;对其他7种抗菌药的耐药率相对较高,为34.9％～89.5％,由于送检率不同,不同临床科室之间耐药情况存在一定程度上的差异.标本主要来源于尿液、痰液、血液及分泌物.结论 大肠埃希菌存在比较严重的耐药现象,临床应加强对病原菌的分布及耐药性进行检测,并根据药敏试验结果选用抗菌药物.     

N-methyl-N'-nitro-N-nitrosoguanidine activates cell-cycle arrest through distinct mechanisms activated in a dose-dependent manner

S(N)1-alkylating agents, such as the mutagenic and cytotoxic drug N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), robustly activate the DNA damage-responsive G(2) checkpoint. Establishment of this checkpoint is dependent on a functional mismatch repair (MMR) system; however, exposure to high doses of MNNG overrides the requirement for MMR to trigger G(2) arrest. In addition, unlike moderate-dose exposure, in which the G(2) checkpoint is attenuated in ataxia-telangiectasia, mutated (ATM)-deficient cells, high-dose MNNG treatment activates G(2) arrest through an ATM-independent mechanism. We document that this arrest is sensitive to the pharmacological agents caffeine and 7-hydroxystaurosporine (UCN-01) that inhibit the checkpoint kinases ATM/ATM and Rad-3-related (ATR) and Chk1/Chk2, respectively. Furthermore, these agents block inactivation of the cell-cycle regulatory molecules Cdc25C and Cdc2, establishing the downstream mechanism through which high-dose MNNG establishes G(2) arrest. Activation of both Chk2 and Chk1 was independent of ATM and MMR in response to high-dose MNNG, unlike the response to moderate doses of this drug. Chk2 was found to be dispensable for cell-cycle arrest in response to high-dose MNNG treatment; however, ATR deficiency and decreased Chk1 expression forced by RNA interference resulted in diminished checkpoint response. These results indicate that MNNG activates the G(2) checkpoint through different mechanisms activated in a dose-dependent fashion.     

Activation of DNA damage response pathways as a consequence of anthracycline-DNA adduct formation

The cytotoxicity of doxorubicin, a clinically used anti-neoplastic drug, can be enhanced by formaldehyde (either endogenous or exogenous) to promote the formation of doxorubicin-DNA adducts. Formaldehyde supplies the carbon required for the covalent linkage of doxorubicin to one strand of DNA, with hydrogen bonds stabilising the doxorubicin mono-adduct to the other strand of DNA, to act much like an interstrand crosslink. Interstrand crosslinks present a major challenge for cellular repair processes, requiring the activation of numerous DNA damage response proteins for resolution of the resulting DNA intermediates and damage. This work investigates DNA damage response proteins activated by doxorubicin-DNA adducts. Although p53 was phosphorylated at Serine 15 in response to adducts, long term growth inhibition of mammalian cells was not affected by p53 status. Using siRNA technology and kinase inhibitors we observed enhanced cellular sensitivity to doxorubicin-DNA adducts when the activity of the signalling protein kinases ATM and ATR were lost. Cells synchronised using a double thymidine block were sensitised to adduct-initiated cell death upon ATR knockdown, but relatively unaffected by ATM knockdown. Loss of ATR was associated with abrogation of a drug-induced G(2)/M block and induction of mitotic catastrophe, while loss of ATM was associated with drug-induced apoptosis in non-synchronised cells. These proteins may therefore be potential drug targets to achieve synergistic cytotoxic responses to doxorubicin-DNA adduct forming therapies. The analysis of these protein kinases with respect to cell cycle progression indicates that ATR is required for G(2)/M checkpoint responses while ATM appears to function in G(1) mediated responses to anthracycline adducts.     

氨曲南联合头孢他啶/阿维巴坦对产金属β-内酰胺酶肠杆菌目细菌的体外协同作用初探

摘要：目的 探讨氨曲南(aztreonam,ATM)与头孢他啶/阿维巴坦(ceftazidime averbatan,CAZ/AVI)联合使用对产金属β-内 酰胺酶(metallo-β-lactamases, MBLs)肠杆菌目细菌的体外协同作用。方法 收集四川大学华西医院2019年11月—2020年4月临床 分离的32株产MBLs且同时满足对ATM及CAZ/AVI耐药;采用PCR扩增技术进行基因型检测,采用微量肉汤稀释法测定ATM及 CAZ/AVI的MIC及棋盘稀释法检测ATM联合CAZ/AVI对产MBLs的肠杆菌目细菌的协同作用。结果 32株产MBLs的菌株中,产 NDM-1型金属酶19株,产NDM-5型金属酶12株及产IMP型金属酶1株;ATM联合CAZ/AVI对其中26株产MBLs的菌株有体外协 同作用,占比81.3%;未出现无关和拮抗作用。结论 ATM联合CAZ/AVI对产NDM金属酶菌株体外有协同抗菌作用的可能性较 高,因此有条件情况下,如果临床治疗需要最好做联合药敏试验以更好的指导临床用药。