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。     

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。     

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。     

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。     

Dynamics of simian immunodeficiency virus populations in blood and cerebrospinal fluid over the full course of infection

BACKGROUND. Human immunodeficiency virus (HIV) replication and compartmentalization in the central nervous system, including in cerebrospinal fluid (CSF), are associated with severe neurological disease and may contribute to viral persistence during antiretroviral therapy. To understand the relationships between viral populations in multiple compartments, we performed a systematic longitudinal characterization of viral populations in blood plasma and CSF obtained at short time intervals over the full course of infection in 3 macaques infected with simian immunodeficiency virus (SIVsm strain E660). METHODS: Complex viral genetic populations in blood plasma and CSF were characterized using a heteroduplex tracking assay targeted to the V1/V2 hypervariable region of env. To identify signs of neurological disease, monocyte chemoattractant protein (MCP)-1 levels in CSF and CD68(+) monocyte/macrophage infiltration in brain tissues were quantified. RESULTS: Two patterns of blood/CSF viral dynamics were apparent as infection progressed: concordant blood/CSF viral evolution and discordant blood/CSF viral evolution. Perivascular CD68(+) cells in autopsy brain tissue and elevated CSF MCP-1 levels accompanied blood/CSF viral population discordance but not concordance. CONCLUSIONS: Two distinct patterns of blood/CSF viral population dynamics can be observed in SIV-infected macaques, and the patterns may be associated with different neurological disease outcomes.     

Retroviral transduction and expression of the human alkyltransferase cDNA provides nitrosourea resistance to hematopoietic cells

Myelosuppression is the dose-limiting toxicity for nitrosourea chemotherapy. This toxicity predominantly involves modification of the O6 position of guanine with an alkyl moiety. The enzyme responsible for repair of O6-alkylguanine adducts, O6-alkylguanine-DNA alkyltransferase (alkyltransferase), is expressed at low levels in bone marrow (BM) cells. High alkyltransferase expression prevents the cytotoxicity and carcinogenicity of nitrosoureas in several transgenic and in vitro gene transfer models. We used gene transfer using a novel myeloproliferative sarcoma virus (MPSV) based retrovirus (vM5MGMT) to express the human alkyltransferase cDNA (MGMT) in human and murine hematopoietic cells. Transduced K562 cells had very high levels of alkyltransferase expression and significantly increased resistance to 1,3-bis (2- chloroethyl) nitrosourea (BCNU) as compared with untransduced K562 cells. Primary murine BM progenitors showed a high transduction efficiency with vM5MGMT and have increased BCNU resistance in vitro. After BM transplantation with vM5MGMT-transduced BM cells and BCNU treatment of these mice, BM, spleen and thymus had a 10- to 40-fold increase in alkyltransferase expression that persisted for at least 23 weeks posttransplantation. Progenitor cells procured from mice expressing high levels of alkyltransferase also had increased resistance to BCNU. Thus, an MPSV-based retroviral vector transduces mouse and human hematopoietic cells at high efficiency and results in high levels of gene expression both in vitro and in vivo. Overexpression of the alkyltransferase protein may protect hematopoietic progenitors from nitrosourea-induced myelosuppression.     

Cleavage of HIV-1 gag polyprotein synthesized in vitro: sequential cleavage by the viral protease

The virally encoded protease of human immunodeficiency virus is responsible for the processing of the gag and gag-pol polyprotein precursors to their mature polypeptides. Since correct processing of the viral polypeptides is essential for the production of infectious virus, HIV protease represents a potential target for therapeutic agents that may prove beneficial in the treatment of AIDS. In this study, full-length gag polyprotein has been synthesized in vitro to serve as a substrate for bacterially expressed HIV-1 protease. Expression of the protease in E. coli from the lac promoter was enhanced approximately five-fold by deletion of a potential hairpin loop upstream from the codon determining the amino terminus of mature protease. Extracts of induced cultures of E. coli harboring a protease-containing plasmid served as the source of protease activity. The gag polyprotein synthesized in vitro was cleaved by such lysates, producing fragments corresponding in size to p17 plus p24 and mature p24. Immunoprecipitations with monoclonal antibodies to p17 and p24 polypeptides suggest that initial cleavage of gag polyprotein occurs near the p24-p15 junction. The proteolysis was inhibited by pepstatin with an IC50 of 0.15 mM for cleavage at the p24-p15 junction and 0.02 mM for cleavage at the p17-p24 junction.     

p16INK4A and p15INK4B gene deletions in primary leukemias

The 9p21 locus has been deleted at a high frequency in a wide variety of tumors. Recently, two genes, p16INK4A and p15INK4B (also called MTS1 and MTS2), have been localized in close proximity at the 9p21 locus, encoding cyclin-dependent kinases 4/6 inhibitors of relative molecular mass 16 kD and 15 kD, respectively and also found to be deleted at a high frequency in tumor cell lines. We analyzed p16INK4A and p15INK4B genes in 178 cases of primary leukemias including 81 cases of chronic lymphocytic leukemia (CLL), seven of hairy cell leukemia (HCL), seven of chronic myelogenous leukemia (CML), 43 of acute myelogenous leukemia (AML), 27 of acute lymphoblastic leukemia (ALL), and 13 of myelodysplastic syndrome (MDS) by Southern blot analyses. The ALL cases showed a relatively high frequency of homozygous deletions (22%, 6 of 27) at the p16INK4A gene locus. Interestingly, of the six cases with p16INK4A homozygous deletions, only three showed homozygous deletions at the p15INK4B gene. In 81 CLL patients, we detected one homozygous and five heterozygous deletions at both the p16INK4A and p15INK4B genes and two heterozygous deletions at the p16INK4A gene alone. Deletion of these two genes in AML cases is relatively low (9%). We did not detect deletions in any of the MDS, HCL, and CML cases examined. Sequence analyses of p16INK4A gene of six CLL cases with heterozygous deletion at this locus showed a 27-bp deletion at the splice acceptor site of intron 1 in one case and changes in the coding sequence in three other cases. The data presented in this report showed that (1) p16INK4A and p15INK4B genes are preferentially deleted homozygously in ALL and heterozygously in CLL cases with frequent mutation in the second allele, and (2) p16INK4A gene appears to be more frequently deleted than p15INK4B gene.