Clinical Care Costing Method for the Clinical Care Classification System™

PURPOSE: To provide a means for calculating the cost of nursing care using the Clinical Care Classification System (CCCS). DATA SOURCES: Three CCCS indicators of care components, actions, and outcomes in conjunction with Clinical Care Pathways (CCPs). DATA SYNTHESIS: The cost of patient care is based on the type of action time multiplied by care components and nursing costs. CONCLUSIONS: The CCCM for the CCCS makes it possible to measure and cost out clinical practice. IMPLICATIONS FOR PRACTICE: The CCCM may be used with CCPs in the electronic patient medical record. The CCPs make it easy to track the clinical nursing care across time, settings, population groups, and geographical locations. Collected data may be used many times, allowing for improved documentation, analysis, and costing out of care.     

医院集中式空调通风系统分区设计与控制院内感染的效应

医院中各种感染源与易感人群同时存在,极易发生医院感染,其中经空气导致的医院感染容易被忽视。分散于空气中的气溶胶与微生物以及运动的微粒是重要的感染传播媒介,而医院集中式空调的通风系统是医院环境中微粒最主要的来源,故此类型通风系统已成为经空气传播医院感染(并非只是呼吸道传染病)的重要传播途径。基于此,认为医院不应设置统一集中的中央空调通风系统,并依据流行病控制原则提出医院空调通风系统“分区”设计,即将医院内的污染区、清洁区、普通区的空调通风系统分别设置,区内根据实际工作需要增设必要的空气过滤设备,以有效控制经空气传播的医院感染发生。     

脑源性神经生长因子促进成年大鼠脑海马神经干细胞定向分化的浓度选择

目的：探讨培养基中表皮生长因子与血清两者浓度一定的条件下，不同浓度的脑源性神经生长因子对成年大鼠脑海马神经干细胞向神经元分化的影响。 方法：实验于2007—08在中国医科大学神经解剖研究室完成。①材料：清洁级雄性成年SD大鼠1只，由中国医科大学实验动物部提供，实验过程中对动物的处置符合动物伦理学标准。实验过程中应用的表皮生长因子、脑源性神经生长因子均由R＆D公司提供：（多实验方法：无菌条件下分离大鼠脑海马组织，剪碎后胰蛋白酶消化，过滤、离心、弃上清，加入含2％B27、20μg／L表皮生长因子、20μg／L碱性成纤维生长因子的DMEM／F12无血清条件培养基体外培养神经干细胞，传至第4代时利用有限稀释法进行单克隆培养，100倍镜下克隆球直径约为200μm时制备单细胞悬液，稀释后滴加于96孔板内，设立两组，全量新鲜培养基组加入刚配置未使用过的DMEM／F12无血清培养基100μL，半量条件培养基组加入上述曾用于神经干细胞培养且含有其代谢产物的1／2DMEM／F12无血清培养基100斗L。（劲实验评估：观察神经干细胞的单克隆培养增殖情况。对克隆球行巢蛋白、神经元特异性烯醇化酶、胶质原纤维酸性蛋白免疫细胞化学染色。按培养基中脑源性神经生长因子终浓度的不同将所培养细胞设立0，50，100，150，200μg／L组，各组均加入20μg／L表皮生长因子和体积分数为0．1的胎牛血清，1周后行神经元特异性烯醇化酶免疫细胞化学染色，检测神经干细胞向神经元分化情况。 结果：①神经干细胞单克隆培养结果：单克隆培养开始时神经干细胞增殖缓慢，半量条件培养基组细胞增殖速度快于全量新鲜培养基组，随着细胞数的增多，两组细胞增殖速度也相应加快，分别在培养后第12天、第15天形成直径为200μm的克隆球。②神经干细胞免疫细胞化学染色结果：单克隆培养后克隆球表达巢蛋白，诱导分化后神经元特异性烯醇化酶、胶质原纤维酸性蛋白均呈阳性表达：③各组神经干细胞分化为神经元的比例：与0μg／L脑源性神经生长因子组比较，50，100μg／L脑源性神经生长因子组的神经干细胞分化为神经元比例均明显增高（t=2．502～5．025，P〈0．05）；而浓度为150，200μg／L时均无明显变化（t=0．420～1．857，P〉0．05）。 结论：向含有B27、表皮生长因子、碱·性成纤维生长因子的DMEM／F12条件培养基中加入20μg／L表皮生长因子和体积分数为0．1胎牛血清的情况下，脑源性神经生长因子促使神经干细胞向神经元分化的较佳浓度为50μg／L。     

双能X射线骨密度仪测量不同个体腰椎椎骨骨面积、骨矿含量的精度差异

目的：对不同个体椎骨短期精度进行观察,发现骨质疏松的严重程度不同其短期精度不同。分析DPX-MD双能X射线骨密度仪测量不同个体椎骨骨面积、骨矿含量、椎体宽、椎体高的短期精密度,了解上述指标对骨矿含量或骨密度测定的影响,以便为骨矿含量或骨密度检测质量控制和减少误差提供依据。 方法：实验于2004-05/2006-12在川北医学院人体解剖实验室与川北医学院附属医院内分泌科骨密度室完成。①对象：铝体模;3个活体椎体（38岁骨密度正常男性;40岁骨质疏松症男性;62岁轻微骨量减少女性）;1个带软组织的死体椎体（由川北医学院人体解剖实验室提供）。②方法及评估：采用美国Lunar公司生产的DPX-MD双能X射线骨密度仪测量各椎体的椎骨面积、骨矿含量、椎体宽、椎体高及骨矿含量/椎体宽。3次/d,连续测定5d。铝体模和死体椎体两端均用小木块固定在6.5cm的高度,放在15cm的水浴中,为减少误差由一人操作。由不同椎骨面积、骨矿含量、椎体宽、椎体高及骨矿含量/椎体宽可得到各自的变异系数。 结果：①腰椎各椎体和L2～4的骨矿含量的变异系数：各椎体或L2～4骨矿含量变异系数从正常男性椎体、骨质疏松症男性椎体、轻微骨量减少女性椎体与死体椎体呈依次增大。②各椎体和L2～4的椎骨面积、椎体宽、椎体高的变异系数：椎骨面积、椎体宽的值从铝体模、正常男性椎体、骨质疏松症男性椎体、轻微骨量减少女性椎体与死体椎体呈依次增大,尤其是轻微骨量减少女性椎体与死体椎体较大;椎体高的变异系数以骨质疏松症男性椎体与轻微骨量减少女性椎体较大,尤其是轻微骨量减少女性椎体的变异系数最大。 结论：不同个体椎骨骨面积、骨矿含量、椎体宽、椎体高的精度不同,对骨密度测定的影响不同。椎间隙欠清楚者由于椎体分椎线难于确定,椎体高度的测定对骨密度测定影响较椎间隙清楚者大;有骨质增生和骨质疏松越严重者由于椎体边缘线难于确定,椎体宽度的测定对骨密度测定影响较无骨质增生和骨密度正常者大;有骨质增生存在和骨质疏松越严重,骨面积的测定对骨密度测定影响越大;骨质疏松越严重,骨矿含量测定对骨密度测定影响越大。     

重庆居民与流动人口结核病就诊及诊断的延迟因素：隐蔽性调查分析

目的:调查重庆居民及流动人口结核病就诊及诊断延迟情况,探索在其过程中存在的问题,分析问题产生的原因。方法:在重庆市主城区按照经济发展水平的不同选取了两个区Y和J,采用方便抽样的方法在Y区抽取了一家综合性医院的呼吸科门诊R,在J区抽取了一家综合性医院的一般基层门诊P,于2005-10-10/14和2005-10-17/21,采用隐蔽性观察法对门诊情况进行了观察,主要观察医生和患者的相关语言、行为,了解结核病就诊及诊断延迟情况。实验得到了利物浦大学热带医学院伦理委员会的许可,并通过了重庆市卫生局的批准。资料分析采用主题框架分析法。结果:重庆居民和流动人口都存在结核病就诊延迟的情况,主要与患者的经济状况、健康意识和社会支持等因素有关;医院在结核病的诊断方面具备基本的技术和条件,诊断延迟则主要与医务人员对结核病的意识和责任心有关;另外患者自身在诊疗过程中的中途退出现象不容忽视,也是导致延迟的一个重要因素。结论:一方面综合医院缺乏对结核病患者的管理措施和意识,对结核患者重治轻管,另一方面特殊人群的患者卫生保健支付能力差,缺乏相关结核病防控知识,应依据目前的形势对相关领域进行政策倾斜和调控,积极开展对人群行之有效的健康教育。     

神经胶质瘤生物治疗的研究现状与进展

脑胶质瘤是颅内最常见的肿瘤。近年来关于神经胶质瘤的生物学研究取得了一定进展。首先是脑肿瘤干细胞的发现,其次是开展了肿瘤全基因组测序,这对于发现新的分子标记物是非常有用的,这些标记物(如IDH1基因突变)的发现甚至导致了基于分化和间质转化状况对神经胶质瘤的重新分类。此外,利用1p/19q标记及O6-甲基鸟嘌呤-DNA甲基转移酶基因(MGMT)是否被甲基化能为胶质瘤患者选择疗法和进行个性化药物治疗提供有意义的指导。作为治疗策略,替莫唑胺几年前已被确定为治疗脑胶质瘤的标准药物。最近在临床上贝伐单抗已开始用于脑胶质瘤的治疗。其他一些疗法目前还处于临床前开发和临床试验阶段,比如癌症疫苗、溶瘤腺病毒的研究等,这些潜在的疗法将来有可能成为胶质瘤治疗的手段或辅助手段。这些研究不仅揭示了神经胶质瘤的细胞起源,也为胶质瘤的诊断、治疗和预后判断提供了有用的信息和参考。     

银杏叶提取物改善反复脑缺血再灌注小鼠血液流变学的作用

目的：研究银杏叶提取物（ＥＧＢ）改善反复脑缺血再灌注小鼠血液流这的作用。方法：采用反复脑缺血再注模型鼠,应用毛细管微量热沉法和毛细管微量法分别检测血纤维蛋白原含量和红细胞压积数值,并将结果输入全自动血液流变仪得出血浆粘度、血液粘度、血细胞聚集系数,血栓形成系数及微循环滞留时间（ＭＳＴ）。结果：ＥＢＧ２５￣１００ｍｇ／ｋｇ均可不同程度地降低Ｆｉｂ、ＨＣＴ、降低ηｂ、ηｐ、ηｈ,缩小ＶＡＬ及ＴＷＥＬ,     

宁国贝母生物碱的分离和结构鉴定

从贝母新种——宁国贝母(Fritillaria ningguoensis S. C. Chen et S. F. Yin)鳞茎中分离出五个生物碱,其中碱V是一种新的生物碱,命名为宁贝新(ningpeisine),根据理化常数和光谱解析以及衍生物制备,测定其结构为N-methyl-3β-hydroxy-5α-veratranine-6-one。其余四种生物碱鉴定为浙贝甲素(peimine,verticine,Ⅰ),浙贝乙素(peiminine,verticinone,Ⅱ),异浙贝甲素(isoverticine,Ⅲ)和贝母辛(peimisine,Ⅳ)。     

Clastogenic and aneugenic effects of tamoxifen and some of its analogues in hepatocytes from dosed rats and in human lymphoblastoid cells transfected with human P450 cDNAs (MCL-5 cells)

Tamoxifen and its analogues 4-hydroxytamoxifen, toremifene, 4- hydroxytoremifene, clomifene and droloxifene were tested for clastogenic effects in a human lymphoblastoid cell line (MCL-5) expressing elevated native CYP1A1 and containing transfected CYP1A2, CYP2A6, CYP2E1 and CYP3A4 and epoxide hydrolase and in a cell line containing only the viral vector (Ho1). MCL-5 or Ho1 cells were incubated with 4-hydroxytamoxifen, 4-hydroxytoremifene, clomifene or droloxifene and the incidence of micronuclei estimated. With MCL-5 cells there was an increase in micronuclei with 4-hydroxytamoxifen, 4- hydroxytoremifene and clomifene but not with droloxifene. With Ho1 cells only 4-hydroxytamoxifen and 4-hydroxytoremifene caused an increase in micronuclei. MCL-5 cells were incubated with tamoxifen, 4- hydroxytamoxifen, toremifene, droloxifene, clomifene or diethylstilbestrol (0.25-10 microg/ml) for 48 h and subjected to 3 h treatment with vinblastine (0.25 microg/ml) to arrest cells in metaphase. The incidence of cells with chromosomal numerical aberrations (aneuploidy) was increased in cells treated with tamoxifen, 4-hydroxytamoxifen, toremifene, clomifene and diethylstilbestrol but not droloxifene. The frequency of cells with structural abnormalities (excluding gaps) was increased in cells treated with tamoxifen and toremifene but not 4-hydroxytamoxifen, clomifene, droloxifene or diethylstilbestrol. The clastogenic activities of tamoxifen (35 mg/kg), toremifene (36.3 mg/kg), droloxifene (35.2 mg/kg) and diethylstilbestrol (25 mg/kg) were compared in groups of four female Wistar rats. Each chemical was dissolved in glycerol formal, administered as a single dose by gavage and hepatocytes isolated by collagenase perfusion 24 h later. The cells were cultured in the presence of epidermal growth factor (40 ng/ml) for 48 h, colchicine (10 microg/ml) being added for the final 3 h of incubation. At least 100 chromosomal spreads were examined from each animal for the presence of numerical and structural abnormalities. The incidences of aneuploidy following treatment were: tamoxifen 81%, toremifene 46%, droloxifene 9.6%, diethylstilbestrol 45.7%, vehicle control 5.3%. The incidences of chromosomal structural abnormalities excluding gaps were: tamoxifen 4.3%, toremifene 0.8%, droloxifene 0.5%, diethylstilbestrol 0.8%, control 0.5%. The incidence of chromosomal structural aberrations excluding gaps in the treated animals was not statistically significantly different from controls except in the tamoxifen-treated group. Tamoxifen (35 mg/kg per os) and toremifene (36.3 mg/kg per os) were dosed to rats for 4 weeks and chromosomal spreads made from hepatocytes. The incidences of aneuploidy were: tamoxifen 94%, toremifene 57%, control 6.5%. The incidences of chromosomal aberrations excluding gaps were: tamoxifen 12%, toremifene 1%, control 0.5%. The incidence of tamoxifen-induced chromosomal structural abnormalities was significantly elevated compared with control levels. The results demonstrate that tamoxifen and toremifene are the only two drugs tested in the study that cause chromosomal structural and numerical aberrations in vitro and tamoxifen is the only drug that induces both these effects in rat liver cells stimulated to divide in culture following oral dosing. Since chromosomal mutations require cell division for their manifestation and tamoxifen is the only compound of those tested that causes hyperplasia in the rat liver, chromosomal aberrations and aneuploidy in the rat liver would only be expected to occur following treatment with tamoxifen alone, although aneuploidy could be induced by toremifene in conjunction with a promoter such as phenobarbitone.      

Ki-ras mutations are an early event and correlate with tumor stage in transplacentally-induced murine lung tumors

A previous study from this laboratory demonstrated that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring at 1 year after birth, the incidence of which correlated with fetal inducibility of Cyp1a1. Analysis by PCR amplification and allele- specific hybridization (ASO) of paraffin-embedded tumors generated from that study revealed the presence of point mutations in exon 1 of the Ki- ras gene. This work has now been expanded by PCR amplification and ASO analysis of 31 additional lesions. Point mutations were found in 37 of the 47 (79%) lesions analyzed in this and the previous study, the majority of which were G-->T transversions in the first or second base of codon 12. The mutational spectrum appeared to be dependent on the relative stage of differentiation of the lesion, as both the incidence of mutation and type of mutation produced correlated with malignant progression. Mutations occurred in 60% of the hyperplasias, 80% of the adenomas and 100% of the adenocarcinomas. In the lesions with mutations, GLY12-->CYS12 transversions occurred in 100% of the hyperplasias, 42% of the adenomas and 14% of the adenocarcinomas. The GLY12-->VAL12 transversions occurred in none of the hyperplasias, 42% of the adenomas and 57% of the adenocarcinomas. The remaining mutations, which consisted of ASP12 transitions and ARG13 transversions, occurred only in adenomas (17%) and adenocarcinomas (29%). Between this study and our previous analyses, the identity of the mutations obtained by ASO were confirmed by sequence analysis of eight of the 37 lesions that harbored mutations at the Ki-ras gene locus. There were no differences in the type or incidence of mutations relative to the metabolic phenotype or sex of the mice. These data suggest that mutational activation of the Ki-ras gene locus is an early event in transplacental lung tumorigenesis, and that the type of mutations produced by exposure to chemical carcinogens can influence the carcinogenic potential of the tumor. This may have prognostic significance in determining the malignant progression of the neoplasm.