医疗过程质量实时监控系统研究

传统的医疗质量管理主要方法是终末病历检查,数据来自人工提取或二次录入,缺乏准确性和时效性。分析了医疗质量管理的现状与存在的问题,阐述了医疗过程质量实时监控的内容与方法,对实时监控系统的架构和功能进行了设计,并指出了实现医疗质量实时监控需解决的一些关键问题。

     

Quality Control of Pharmaceuticals

Quality control is an essential operation of the pharmaceutical industry. Drugs must be marketed as safe and therapeutically active formulations whose performance is consistent and predictable. New and better medicinal agents are being produced at an accelerated rate. At the same time more exacting and sophisticated analytical methods are being developed for their evaluation. Requirements governing the quality control of pharmaceuticals in accordance with the Canadian Food and Drugs Act are cited and discussed.     

蛇伤药酒的质量控制

目的　建立蛇伤药酒的质量控制方法。　方法　用薄层色谱法对蛇伤药酒制剂中黄连、黄柏、大黄进行定性鉴别 ;用紫外分光光度法测定黄连、黄柏中有效成分小檗碱的含量。测定波长为 ( 2 64± 1 ) nm。　结果　定性鉴别色谱特征明显 ,易于区别 ;盐酸小檗碱的含量测定线性范围在 1 .42～ 7.1 0 μg,r=0 .9996,平均回收率为 99.1 4% ,RSD为 1 .3 4%。　结论　该方法可有效的控制蛇伤药酒的质量。     

Mieap与线粒体的质量控制

线粒体在细胞能量代谢和细胞凋亡中起着至关重要的作用.质量控制是线粒体在细胞中维持正常状态的关键机制.2011年Miyamoto等发现Mieap参与线粒体质量控制的两个新机制.Mieap诱导的溶酶体样细胞器,进入线粒体内,并在线粒体积累,能通过特异性的清除氧化的线粒体蛋白来修复异常线粒体,使得线粒体维持在正常状态.Mieap诱导的通过细胞膜内吞机制形成的囊泡,识别异常线粒体,并对其特异性的清除.Mieap诱导的这两个过程参与了线粒体质量控制,并决定线粒体的命运.     

Quality Control of Membraneless Organelles

The formation of membraneless organelles (MLOs) by phase separation has emerged as a new way of organizing the cytoplasm and nucleoplasm of cells. Examples of MLOs forming via phase separation are nucleoli in the nucleus and stress granules in the cytoplasm. The main components of these MLOs are macromolecules such as RNAs and proteins. In order to assemble by phase separation, these proteins and RNAs have to undergo many cooperative interactions. These cooperative interactions are supported by specific molecular features within phase-separating proteins, such as multivalency and the presence of disordered domains that promote weak and transient interactions. However, these features also predispose phase-separating proteins to aberrant behavior. Indeed, evidence is emerging for a strong link between phase-separating proteins, MLOs, and age-related diseases. In this review, we discuss recent progress in understanding the formation, properties, and functions of MLOs. We pay special attention to the emerging link between MLOs and age-related diseases, and we explain how changes in the composition and physical properties of MLOs promote their conversion into an aberrant state. Furthermore, we discuss the key role of the protein quality control machinery in regulating the properties and functions of MLOs and thus in preventing age-related diseases.     

Quality Control of Mitochondrial Proteostasis

A decline in mitochondrial activity has been associated with aging and is a hallmark of many neurological diseases. Surveillance mechanisms acting at the molecular, organellar, and cellular level monitor mitochondrial integrity and ensure the maintenance of mitochondrial proteostasis. Here we will review the central role of mitochondrial chaperones and proteases, the cytosolic ubiquitin-proteasome system, and the mitochondrial unfolded response in this interconnected quality control network, highlighting the dual function of some proteases in protein quality control within the organelle and for the regulation of mitochondrial fusion and mitophagy.In all cellular compartments, correct protein folding is critical to maintain cellular homeostasis. In cases where proteins become misfolded or damaged, it is imperative that they are turned over and removed to prevent the formation of toxic folding intermediates or the accumulation of aggregates to levels that can be deleterious for the cell. Several neurodegenerative diseases share a common pathogenic mechanism, which involves the formation of fibrillar aggregates of a particular protein that can accumulate in the cytosol, the nucleus, or the mitochondria. Examples of this include accumulation of the amyloid-β peptide in Alzheimer’s disease (Kayed et al. 2003; Tanzi and Bertram 2005), accumulation of α-synuclein in Parkinson’s disease (Spillantini et al. 1997; Zarranz et al. 2004), and aggregation of a mutant form of the huntingtin protein caused by extended polyglutamine stretches in Huntington’s disease (DiFiglia et al. 1997). Although the exact mechanism of pathogenesis for these diseases remains unresolved, mitochondrial dysfunction is implicated in their progression, which may in turn be responsible for the loss of neurological cell populations because of their sensitivity and requirement for functional mitochondria (Rodolfo et al. 2010).The evolution of mitochondria began approximately 1.5 billion years ago after an α-proteobacterium was engulfed by a preeukaryotic cell (Gray et al. 1999). Since that time, mitochondria have retained two phospholipid bilayers that segregate two aqueous compartments, the mitochondrial intermembrane space (IMS) and the mitochondrial matrix (Palade 1953). Mitochondria are found in essentially all eukaryotic cells and play integral roles in a number of the cell''s metabolic pathways. For example, mitochondria are the key players in cellular ATP production through an elaborate respiratory chain network found in the organelles inner membrane (IM) (Mitchell 1961; Leonard and Schapira 2000). Mitochondria are also required for the β-oxidation of fatty acids, Fe-S biosynthesis, and Ca²⁺ homeostasis (Pinton et al. 1998; Rizzuto et al. 2000; Lill 2009; Modre-Osprian et al. 2009). Moreover, mitochondria are key regulators of programmed cell death and they participate in developmental processes as well as aging (Singh 2004; Green 2005).In contrast to early depictions of mitochondria as singular kidney bean shaped entities, it is now well established that mitochondria form elaborate, reticular networks in many tissues (Bereiter-Hahn 1990). The ability of mitochondria to form such networks arises from two major factors: (1) Specialized machineries in the mitochondrial outer membrane (OM) and the IM allow mitochondria to fuse and divide and (2) mitochondria are able to be shuttled along cytoskeletal elements (Anesti and Scorrano 2006; Hoppins et al. 2007). This plasticity of mitochondria ensures that they are able to respond to different cellular cues, which is potentially important for their numerous functions. In different cell types, mitochondria adopt varying morphologies (Kuznetsov et al. 2009). For example, in cultured fibroblasts mitochondria form extensive reticular networks, whereas in neuronal cells, mitochondria can be found enriched at areas of high-energy demand, including presynaptic termini, axon initial segments, and growth cones. Furthermore, in muscle cells, mitochondria adopt a very uniform intermyofibrillar conformation (Vendelin et al. 2005). The dynamic nature of mitochondria provides an explanation as to how they adopt varying organizations in different cell populations. The importance of mitochondrial networks is highlighted by the fact that mutations in components involved in maintaining mitochondrial dynamics results in neurodegenerative diseases (Chan 2006; Olichon et al. 2006; Knott et al. 2008; Martinelli and Rugarli 2010; Winklhofer and Haass 2010).     

三级综合医院护理质量实时监控方法探讨

传统的护理质量管理以终末质量控制为主,简单的事后检查和评比,缺乏可靠性和科学性,难以保证护理质量。文章通过对护理质量关键环节监控内容的分析,建立护理质量实时监控指标体系,并探讨了护理过程质量实时监控的方法,包括组件库、规则库的构建,监控信息实时获取,以及护理过程质量实时监测与预警。     

前馈控制在ICU护理质量控制中的应用

目的 探讨ICU实施前馈控制的方法和效果,以提高护理质量。方法 在ICU病区建立质量控制架构（三级质控网）,采用前馈质控方法,对ICU护理工作进行全面质量控制管理。结果 实施前馈质控后,病房护理管理质量、消毒隔离质量、护理文件书写质量、教学质量、家属满意度、护士工作满意度等各项指标评分都有明显提高,不良事件发生率明显下降,差异有统计学意义(P<0.01)。结论 前馈控制方法整体上提高了ICU风险管理能力、护理管理效率和护理质量。     

基于开题报告的品管圈活动质量管理实践

自2015年年初起对全院品管圈项目进行基于开题报告的质量管理,包括在品管圈前期开展开题报告及评审、举办“圈长论坛”交流平台等多种形式的品管技巧培训,中期进行评估及实地查访,后期成果汇报管理等措施,有效提升了品管圈活动的质量和结题率。

     

Quality Control: Proteins and Organelles

This review summarizes materials on the mechanisms of intracellular degradation of proteins whose topogenesis is disturbed at one stage or another. Chaperone and proteolytic systems involved in this process in the endoplasmic reticulum, mitochondria, and chloroplasts of eucaryotic cells as well as those in distinct subcellular compartments of procaryotic cells are considered. The available data suggest that living cells contain numerous systems keeping under control both folding of newly synthesized and newly imported polypeptide chains and their incorporation into heterooligomeric complexes. The point of view is elaborated that organelle formation is controlled not only at the level of individual protein molecules but also at the supermolecular level when whole organelles incapable of carrying out their integral key functions become targets for partial or total elimination. This type of control is realized through an autophagic mechanism involving lysosomes/vacuoles.     

聚乙二醇化重组蛋白药物的质量控制

重组蛋白经聚乙二醇(PEG)化修饰在优化药物代谢动力学和药效学性质的同时,使药物的结构和质量属性变得更为复杂,修饰后的重组蛋白在结构、理化性质和生物学活性等方面与未修饰的重组蛋白相比有较大差异,对其质量控制的研究必须结合品种自身独特的质量属性。现从蛋白质药物质量控制的角度,对PEG化蛋白质药物的重要质量属性的质控难点和相应检测方法进行综述,以期对工艺开发和生产上的实际工作有所帮助。     

SAQC: SNP Array Quality Control

Background  

Genome-wide single-nucleotide polymorphism (SNP) arrays containing hundreds of thousands of SNPs from the human genome have proven useful for studying important human genome questions. Data quality of SNP arrays plays a key role in the accuracy and precision of downstream data analyses. However, good indices for assessing data quality of SNP arrays have not yet been developed.     

Quality Control Test for Sequence-Phenotype Assignments

Relating a gene mutation to a phenotype is a common task in different disciplines such as protein biochemistry. In this endeavour, it is common to find false relationships arising from mutations introduced by cells that may be depurated using a phenotypic assay; yet, such phenotypic assays may introduce additional false relationships arising from experimental errors. Here we introduce the use of high-throughput DNA sequencers and statistical analysis aimed to identify incorrect DNA sequence-phenotype assignments and observed that 10–20% of these false assignments are expected in large screenings aimed to identify critical residues for protein function. We further show that this level of incorrect DNA sequence-phenotype assignments may significantly alter our understanding about the structure-function relationship of proteins. We have made available an implementation of our method at http://bis.ifc.unam.mx/en/software/chispas.     

含非竞争性内标四重荧光RT-PCR方法检测手足口肠道病毒方法的研究

旨在了解手足口病的流行和感染情况,并进行快速准确的检测。建立了含非竞争性内标的同时检测肠道病毒通用型、肠道病毒EV71型及柯萨奇病毒CA16型的四重荧光RT-PCR方法,对该方法的特异性、灵敏度等进行评价,并对多份临床样本进行应用检测。结果表明,该检测方法特异性强,对肠道病毒及其他人类非肠道病毒进行检测,显示了良好的特异性;该检测方法对EV71型和CA16型的检测灵敏度分别达到31.25 TCID50和1.25×102TCID50;将浓度为1×104TCID50及5×102TCID50的EV71样本进行重复性试验,其变异系数均小于1.5%;将浓度为5×102-5×105TCID50的EV71和CA16样本进行线性试验,其相关系数R2值在0.982-0.998之间。采用本研究建立的方法检测40份疑似临床样本,最后检出31份肠道病毒阳性样本,其中8例EV71型阳性,13例CA16阳性。另外,试验数据表明,内标对监控PCR抑制物的存在具有重要作用。本方法能同时快速检测所有肠道病毒并进行EV71型及CA16型的分型,并且灵敏度高、特异性好、扩增效率高,由于加入了内标,能有效地监控假阴性的出现,适合于手足口病的临床检测。     

浅谈电解质分析仪的质量控制

介绍了XD683电解质分析仪的质量控制,它涉及仪器本身、所用的试剂、分析过程的各个环节及仪器维护和检查校准等。     

GFP质控芯片的初步研究

目的：建立一种质量控制芯片来监测样品标记、杂交和检测过程中的失误。方法：针对GFP基因设计的4条60mer寡核苷酸探针和1条阳性对照探针polv（U）与流感寡核苷酸探针一起打印在DAKO玻片上,并构建了GFP基因的克隆载体和体外表达载体,将从这两种重组载体上获得的绿色荧光蛋白（Green Fluorescent Protein,GFP）基因的ILNA、DNA片段和人的全血样品中的DNA用限制性显示技术（Restriction Display technology,RD）扩增标记,将标记的样品和荧光标记的通用引物U分别与芯片杂交、检测,并对扫描的结果进行统计分析。结果：GFP探针与相应的样品杂交时出现阳性信号,阳性对照探针在所有的杂交中均出现阳性信号,而空白对照则未检测荧光信号。结论：建立的质控芯片具有较好的敏感性和特异性,可以用于基因芯片中的质量监控。     

线粒体蛋白质组及蛋白质量控制

线粒体是哺乳动物细胞内重要细胞器,不仅通过氧化磷酸化产生ATP为细胞提供能量,也参与调节钙离子稳态、活性氧(reactive oxygen species,ROS)的产生、细胞应激反应和细胞死亡等过程,其功能障碍不仅导致多种人类疾病的发生,而且也能降低动物卵母细胞质量和早期胚胎发育能力。大量证据表明,线粒体的功能依赖于线粒体蛋白质组完整性和稳态。基于此,该文综述了线粒体蛋白组、线粒体蛋白转运,聚焦蛋白酶、分子伴侣、线粒体囊泡、线粒体自噬和线粒体未折叠蛋白反应在帮助正确的蛋白质折叠,去除错误折叠或聚集的蛋白质和清除功能失调的线粒体方面的作用,为调控线粒体蛋白质量,从而维持线粒体健康、降低疾病发生提供理论依据。