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71.
A competitive enzyme-linked immunoadsorbent assay (ELISA) technique has been developed to facilitate quantitative analysis of the earliest step in the initiation of the extrinsic pathway of coagulation, i.e., complex formation of factor VII/VIIa with tissue factor. The ELISA measures the binding of biotinylated human plasma factor VII to relipidated recombinant human tissue factor. Quantitation of the relative affinity (expressed as IC50) of any factor VII molecular population or structural analogue for tissue factor can be determined by competitive binding. Subnanomolar concentrations of both wild-type recombinant human factor VII (rFVII) and rFVII(R152Q), a mutation at the FVII activation site, competed effectively with biotinylated plasma-derived factor VII in binding to tissue factor. In contrast, the affinity of rFVII(R79Q), a mutation in the first epidermal growth factor-like domain, was 12-fold lower. Following activation of rFVII(R79Q), its affinity for tissue factor and enzymatic activity increased 4-fold and 6-fold, respectively. For wild-type rFVII, enzymatic activity rose significantly following activation. However, its affinity for tissue factor was unchanged. We conclude that both the activation state of factor VII and the mutation of amino-acid residues within the first epidermal growth factor-like domain may alter the affinity of factor VII for tissue factor. 相似文献
72.
Memory reallocation is used to construct a run-time data structure for fast/efficient storage of information during collection and analysis. The data structure presented uses dynamic memory but does not require the use of pointers to link nodes of information together. It allows for simple and efficient access to data via array indexing rather than through the use of lists or tree structures and it provides flexibility for competing storage requirements that are determined dynamically. The data structure is developed in the C programming language and a suite of ANSI standard C subroutines that make up a run-time data structure management system is provided. 相似文献
73.
Davidson J.D. Wager J.F. Khormaei R.I. King C.N. Williams R. 《Electron Devices, IEEE Transactions on》1992,39(5):1122-1128
Electrical characterization of evaporated ZnS:Mn alternating-current thin-film electroluminescent (ACTFEL) devices is accomplished by capacitance-voltage (C -V ) analysis. Interpretation of these C -V characteristics is aided by SPICE modeling and by electrical characterization of an ideal ACTFEL device constructed from discrete components, based on a simple equivalent circuit for the ACTFEL device. Various features of the C -V curve are ascribed to equivalent circuit parameters and associated device physics parameters 相似文献
74.
A Williams 《Canadian Metallurgical Quarterly》1996,92(14):40-41
This article examines factors that may contribute to errors in drug administration. These can range from the omission of a single dose of a non-essential drug to a major overdose resulting in serious harm to a patient. It concludes that a combination of being observant and well-informed can help to prevent errors. 相似文献
75.
76.
An extremely large database describes genotypes associated with the human cancer phenotype and genotypes of human populations with genetic predisposition to cancer. Aspects of this database are examined from the perspective of risk analysis, and the following conclusions and hypotheses are proposed: (1) The genotypes of human cancer cells are characterized by multiple mutated genes. Each type of cancer is characterized by a set of mutated genes, a subset from a total of more than 80 genes, that varies between tissue types and between different tumors from the same tissue. No single cancer-associated gene nor carcinogenic pathway appears suitable as an overall indicator whose induction serves as a quantitative marker for risk analysis. (2) Genetic defects that predispose human populations to cancer are numerous and diverse, and provide a model for associating cancer rates with induced genetic changes. As these syndromes contribute significantly to the overall cancer rate, risk analysis should include an estimation of the effect of putative carcinogens on individuals with genetic predisposition. (3) Gene activation and inactivation events are observed in the cancer genotype at different frequencies, and the potency of carcinogens to induce these events varies significantly. There is a paradox between the observed frequency for induction of single mutational events in test systems and the frequency of multiple events in a single cancer cell, suggesting events are not independent. Quantitative prediction of cancer risk will depend on identifying rate-limiting events in carcinogenesis. Hyperproliferation and hypermutation may be such events. (4) Four sets of data suggest that hypermutation may be an important carcinogenic process. Current mechanisms of risk analysis do not properly evaluate the potency of putative carcinogens to induce the hypermutable state or to increase mutation in hypermutable cells. (5) High-dose exposure to carcinogens in model systems changes patterns of gene expression and may induce protective effects through delay in cell progression and other processes that affect mutagenesis and toxicity. Paradigms in risk analysis that require extrapolation over wide ranges of exposure levels may be flawed mechanistically and may underestimate carcinogenic effects of test agents at environmental levels. Characteristics of the human cancer genotype suggest that approaches to risk analysis must be broadened to consider the multiplicity of carcinogenic pathways and the relative roles of hyperproliferation and hypermutation. Further, estimation of risk to general human populations must consider effects on hypersusceptible individuals. The extrapolation of effects over wide exposure levels is an imprecise process. 相似文献
77.
The long‐term consequences of the sale of public sector dwellings to sitting tenants are under‐researched; in particular, the experience of tenant purchasers in the housing market subsequent to purchase is little known. This paper reports research designed to fill this gap in knowledge. Over 200 tenants who had bought their dwelling from the Scottish Special Housing Association and subsequently resold on the open market were traced using the Register fo Sasines and the Land Register and interviewed. Most had made considerable capital gains on resale and had used some of the realised capital to trade up in the housing market. They were, on average, slightly more affluent and younger than sitting tenant purchasers generally; they represented a group of households who were privileged within the public sector through living as tenants in the best stock and who were enabled by the Right to Buy to convert that good luck into hard cash and move into mainstream owner occupation. This good luck compounded the advantaged position vis‐à‐vis other tenants that they enjoyed in the labour market. 相似文献
78.
79.
Arylalkynes such as 4-phenyl-1-butyne (PBY), 5-phenyl-1-pentyne (PPY) and 2-ethynylnaphthalene (2-EN) are suicide inhibitors of cytochrome P450 enzymes. Arylalkyl isothiocyanates such as 6-phenylhexyl isothiocyanate (PHITC) are structurally related to arylalkynes and are known to inhibit the cytochrome P450 mediated metabolic activation and tumorigenicity of a tobacco-specific lung carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In this study, we compared the ability of PBY, PPY, 2-EN and PHITC to inhibit A/J mouse lung tumorigenesis by NNK. Groups of 20 female mice were gavaged with 5 mumol of arylalkyne or PHITC in corn oil. Two hours later they were given a single i.p. injection of 10 mumol NNK. The mice were killed 16 weeks later. PPY and PHITC were both potent inhibitors of tumorigenesis by NNK, reducing lung tumor multiplicity from 8.35 tumors per mouse to 0.40 and 0.35 respectively. PBY and 2-EN also significantly inhibited tumor multiplicity. The results of this study demonstrate that arylalkynes and PHITC are potent inhibitors of NNK induced lung tumorigenesis in A/J mice, consistent with the hypothesis that inhibition of specific cytochrome P450 enzymes is involved in inhibition of tumorigenesis. 相似文献
80.