我院静脉用药集中调配中心自动化智能建设与实践

目的:探讨我院静脉用药集中调配中心(PIVAS)的自动化智能建设及效果。方法:介绍我院PIVAS自动化智能建设的主要情况,收集我院PIVAS自动化智能建设前(2016年7-9月)、后(2016年10-12月)相关工作环节的用时和差错率,评价建设效果。结果:我院在PIVAS的摆药、贴签、分拣以及配送环节进行了自动化智能建设,并进行了相关的制度和流程建设。自动化智能建设后,每张医嘱摆药用时由建设前的(6.78±0.87)s缩短至(2.65±0.71)s,贴签用时由(3.24±0.71)s缩短至(1.41±0.55)s,分拣每袋输液成品用时由(13.37±2.84)s缩短至(5.33±1.72)s,配送相同数量的输液用时由(35.64±4.33)min缩短至(18.12±3.57)min(P<0.05);摆药差错率由(2.35±0.59)‰降至(0.26±0.21)‰,贴签差错率由(1.51±0.45)‰降至(0.22±0.10)‰,分错病区差错率由(3.47±1.02)‰降至(0.17±0.10)‰,配送差错率由(1.33±0.55)‰降至(0.13±0.11)‰(P<0.05)。结论:我院PIVAS自动化智能建设后工作效率提高、差错率降低,降低了潜在的用药风险,提升了PIVAS管理水平。     

某三甲医院静脉用药集中调配中心智能化、信息化、均质化建设的实践

目的：探讨静脉用药集中调配中心（PIVAS）流程智能化、信息闭环化、模式均质化的实践效果。方法：收集某院PIVAS在2017年3-6月和2017年7-10月的各项报表数据，对比评估PIVAS信息化改造和智能设备引入前后各运行指标的变化，包括每日排药时间、贴签时间、分拣时间，输液存储量以及各个环节中的人力分配、差错发生率等；基于PIVAS流程整体设计，评价PIVAS工作新模式的价值。结果：在经过智能化、信息化改造后，PIVAS的工作效率显著提高，差错率大幅下降，其中贴签环节每张标签贴签、核对、排筐用时（7.81±1.66）s下降至（5.34±0.64）s，差错率由（1.38±0.40）‰下降至（0.15±0.05）‰；排药环节每张标签用时（5.37±0.97）s下降至（3.38±0.27）s，差错率由（1.91±0.41）‰下降至（0.44±0.18）‰；分拣环节每袋输液分拣用时（4.57±1.30）s下降至（1.49±0.19）s，差错率由（2.87±0.34）‰下降至（0.29±0.11）‰，PIVAS人员工作模式达到均质化要求。结论：该院智能化、信息化、均质化改造后，PIVAS人员工作效率显著提高、差错率大幅下降，在质量管控方面成效卓著。     

静脉用药集中调配中心智能一体化设备设计与应用

目的 介绍静脉用药集中调配中心(PIVAS)智能一体化设备设计思路及应用情况,评价其在降低人力成本、减少差错发生及提升工作效率等方面的实践效果。方法 针对PIVAS工作环节中的输液出入库、贴标签、发筐、针剂摆药及成品输液分拣进行模块化硬件设计,通过医院内部局域网对各模块可编程逻辑控制器进行互通控制及数据交互,实现PIVAS智能输液出入库、智能贴标签、智能发筐、智能针剂摆药、智能分拣及数据追溯等功能,比较使用该设备前后工作指标,评估其应用价值。结果 应用该设备后,PIVAS贴签及摆药人数由每天4人降至1人;单个医嘱贴签及摆药平均耗时由(7.01±0.56) s缩短至(6.54±0.44) s;应用前后人工贴签与智能贴签均未发生差错,单月医嘱针剂摆药差错由6件降低至1件,单月成品输液分拣差错由12件降低至2件;成品输液分拣时间由(1.22±0.08) h缩短至(0.91±0.06) h,平均每袋分拣时间由(4.24±0.34) s缩短至(2.92±0.21) s,均差异有统计学意义(P<0.01)。结论 PIVAS智能一体化设备降低了医院人力资源投入及差错发生率,提高了工作效率并减轻...     

智能化系统在某院PIVAS的应用效果分析

目的 探讨本院静脉药物调配中心的智能化水平，为PIVAS的发展提供参考。方法 利用回顾性分析，介绍目前本院PIVAS智能化系统组成和实际应用，收集本院智能化系统使用前后贴签、分拣环节工作耗时和产生差错件数，通过比较加以评价智能化系统对本院静脉用药调配工作的影响。结果 本院PIVAS使用智能贴签系统后，贴签环节的工作人员从4人减至2人，每袋溶媒平均贴签时间降低76.33%,差错率减少87.48%(P<0.05);使用自动分拣系统后，分拣环节的工作人员由7人减至4人，降低42.86%,每袋输液平均分拣时间用时减少63.66%,差错率减少81.22%(P<0.05)。结论 智能化设备在本院的投入使用提高了PIVAS工作效率、降低贴签和分拣环节差错发生率、实现减轻静脉用药调配中心工作人员的劳动强度、提升药学服务质量的目标，推动了本院PIVAS工作流程的升级，促进PIVAS的发展。     

医院静脉用药调配中心自动化智能建设与实践

目的 为医院静脉用药调配中心（PIVAS）自动化智能建设提供参考。方法 引进智能贴签机和自动化分拣机，并接入医院信息系统。统计医院PIVAS自动化系统启用前、后3个月相关工作环节的用时和差错数等信息并比较。结果 自动化系统启用后，每日贴签用时由启用前的（0.67±0.15）h减至（0.42±0.12）h，每日贴签差错数由（9.20±1.86）件减至（0.20±0.13）件，每日分拣成品输液用时由（1.12±0.21）h减至（0.58±0.16）h，每日分拣差错数由（21.03±2.58）件减至（0.13±0.06）件。结论 医院PIVAS自动化系统的应用提高了工作效率、降低了差错率，减轻了工作人员的劳动强度。     

我院静脉用药集中调配中心信息管理系统的改进及优化实践

目的:通过对静脉用药集中调配中心(PIVAS)信息管理系统改进优化,提高PIVAS的工作质量和效率。方法:比较PIVAS信息管理系统优化前后(2016年8-12月和2017年4-8月)系统审核率、不合理医嘱漏审率、排批耗时、打印耗时、贴签耗时、配置扫描耗时,以评价PIVAS信息管理系统改进优化后的效果。结果:PIVAS信息管理系统改进及优化后,医嘱审核效率明显提升,不合理医嘱漏审率由2.6%降至0.88%;排批、打印、贴签时间较优化前均有明显缩短;配置扫描耗时由每袋1 100 ms降至每袋10 ms,提高了配置效率。结论:信息管理系统的优化可明显提高PIVAS各环节工作效率。     

我院静脉用药调配中心差错分析及防范措施

目的:减少静脉用药调配中心(PIVAS)运行中差错的发生,提高静脉用药调配质量,保证临床用药安全、有效。方法:对我院PIVAS 2013年1-4月工作流程中各个环节出现的差错进行原因分析,并制订防范措施,比较改进前、后(2013年5-8月)差错率。结果:通过改进和细化工作流程,分别针对审方、分签、贴签、排药、配制、退药、复核及打包等各环节制定了相应的防范措施并进行了改进。与改进前比较,差错率显著降低,由0.079%下降至0.037%。结论:通过分析差错发生原因并制定相关防范措施可减少差错发生,提高临床用药安全。     

医院静脉用药调配中心的自动化系统建设与实践

目的：探讨某院静脉用药调配中心（PIVAS）的自动化和信息化水平，为PIVAS的发展提供参考。方法：介绍该院PIVAS自动化系统建设和实践的主要情况，收集该院PIVAS自动化系统启用前、后相关工作环节的用时和差错件数等数据信息，进行比较以评价其应用效果。结果：该院PIVAS的自动化系统由智能贴签系统、智能退药模式、智能配液系统、智能责任追溯系统、智能分拣系统组成。自动化系统使用后，每日贴标签的用时由（1.97±0.19）h缩短至（1.15±0.17）h；每日贴签差错由（6.51±1.24）件降低至（0.53±0.30）件；每日配液用时由（1.73±0.20）h缩短至（1.41±0.62）h；每日分拣成品输液的内部差错由（3.52±1.68）件降低至（0.03±0.16）件。结论：该院PIVAS自动化系统的应用使工作效率提高、差错率降低、减轻了工作人员的劳动强度，在提高PIVAS工作效率和防范差错方面起到了重要作用。     

静脉用药调配中心调剂差错与防范措施分析

目的 分析静脉用药调配中心（PIVAS）调剂差错发生的原因，降低医院调剂差错率。方法 根据层次任务分析（HTA）-人为差错模式（HET）理论分解PIVAS调剂流程，确定调剂差错类型，构建HTA-HET数据统计表；分析2020年7月至12月（整改前）的调剂差错，并制订防范措施，与2021年1月至6月（整改后）的调剂差错进行比较。结果 共收集整改前的医嘱127 262条，调剂差错512条；整改后的医嘱132 983条，调剂差错392条。整改前，各项子流程调剂差错排名前3的分别为摆放主药、溶剂贴签、加药混合调配，占比分别为26.17%,21.48%,16.80%；主要调剂差错类型分别为品种差错、规格差错、数量差错，分别占26.76%,25.00%,18.95%。整改后，摆放主药差错率由0.105%降至0.074%，溶剂贴签差错率由0.086%降至0.053%，加药混合调配差错率由0.068%降至0.043%，成品输液核对差错率由0.020%降至0.008%，差异显著（P <0.05）；品种差错率由0.108%降至0.082%，规格差错率由0.101%降至0.067%，数量差错率由0.0...     

我院PIVAS的自动化建设与实践

目的:为静脉用药集中调配中心(PIVAS)的信息化、自动化管理建设提供参考。方法:介绍我院开发的PIVAS自动化管理系统的组成和实践应用情况,并对其应用前、后的不合格医嘱率、摆药效率、差错件数等进行比较以评价其应用效果。结果与结论:通过对相应的工作流程进行智能优化,我院开发的PIVAS自动化管理系统由自动审方系统、智能摆药系统、智能配液系统、自动分拣系统以及自动运送系统等组成。该系统应用后分别实现了用药医嘱的自动审核、智能化摆药与贴签、调配全过程的责任追溯、静脉输液的智能化混合调配、成品输液的自动分拣以及自动运送;不合格医嘱率由应用前的2.07%下降为1.73%,摆药贴签用时由每日(3.15±0.53)h缩短至(1.55±0.27)h,每日调配内差由(0.26±0.78)件降低至(0.06±0.13)件,每日成品输液打包分拣差错由(6.57±1.76)件降低至(0.07±0.17)件。该系统的建设实现了PIVAS主要工作的信息化和自动化,提高了PIVAS的管理水平。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.