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Biomedical subjects

W Hsiao

Publications and source records attributed to W Hsiao.

6 recordsLinked to original sources
PubMed1992

Small-group judgment methods for determining resource-based relative values.

National telephone surveys used in the Resource-Based Relative Value Scale Study produce reliable and valid relative values of work, but phone surveys are expensive and time consuming. We evaluated three small-group processes as alternatives. We compared national survey work estimates for 38 surgical services to those generated by panels of 11 and 19 highly qualified general surgeons using 1) single-round mail survey; 2) Delphi multiple-round ratings; and 3) modified Delphi with face-to-face discussion. Single-round mail-survey ratings were closest to the national survey; average differences were 11.0% and 12.6%. Delphi feedback led to increased differences: typical values differed by 14.6% and 15.2%. Face-to-face discussion led to still further divergence (21.0%). Single-round mail survey of a small number of experts provides relative work values that compare more favorably to those of the national survey than those obtained from Delphi multiple-round ratings or modified Delphi with face-to-face discussion.

Data Collection↗
PubMed1990

Influence of cholesterol oxides on endocytosis of cultured endothelial and smooth muscle cells.

Human umbilical vein endothelial cells and rabbit aortic smooth muscle cells in culture were incubated for intervals up to 24 hrs with varying concentrations of cholesterol, 7-ketocholesterol, 25-hydroxycholesterol, cholestane-3 beta,5 alpha,6 beta-triol or cholesterol-5 alpha, 6 beta-epoxide. Endocytosis, as measured by uptake of horseradish peroxidase (HRP), was inhibited in a dose and time dependent manner in both endothelial and smooth muscle cell cultures by cholestane-3 beta,5 alpha,6 beta-triol and 25-hydroxycholesterol. Inhibition by 7-ketocholesterol in endothelial cells occurred only at higher concentrations, and cholesterol and cholesterol epoxide showed no significant inhibitory effects. The viability of the cells exposed to the cholesterol oxides at the concentrations that inhibited the uptake of HRP was not changed. Cholesterol oxides induce functional endothelial injury, not morphologically apparent, which may be involved in atherogenesis.

Animals↗
PubMed1986

Studies on the mechanism of action of protein kinase C and the isolation of molecular clones encoding the enzyme.

Protein kinase C (PKC) plays an important role in signal transduction and the action of phorbol ester tumor promoters, and it is of interest to isolate the coding sequence of this enzyme. Using a 53-base pair synthetic oligonucleotide probe that corresponds to an 18-amino acid peptide obtained from rat brain PKC, we have isolated rat brain cDNA clones corresponding to PKC. We have also isolated several closely related clones. Partial nucleotide sequence analysis of one of the PKC clones (RP41) identifies a 224-amino acid region with approximately 40% homology to the carboxy terminal and catalytic domains of both the cAMP-dependent and cGMP-dependent protein kinases. The levels of mRNA homologous to RP41 are very high in brain; very low but detectable levels are present in heart and liver. A second cDNA (RP16) was only partially sequenced, and based on its predicted amino acid sequence, it shares 65% homology with the corresponding region of the PKC clone RP41. The levels of mRNA corresponding to RP16 are also highest in rat brain, but they are of a different size than those detected with RP41. These and additional results indicate that the gene for the enzyme PKC shares considerable homology with other protein kinases and that PKC itself may belong to a new multigene family. The availability of these cDNA clones should greatly facilitate further studies on the role of PKC in growth control, differentiation, and multistage carcinogenesis.

Amino Acid Sequence↗
PubMed1985

Mechanisms of multistage chemical carcinogenesis and their relevance to respiratory tract cancer.

The evolution of a fully malignant tumor is a multistep process resulting from the action of multiple factors, both environmental and endogenous, and involves alterations in the function of multiple cellular genes. Chemical carcinogens that initiate this process appear to do so by damaging cellular DNA. In addition to producing simple point mutations, this damage appears to induce the synthesis of a transacting factor that can induce asynchronous DNA replication. This response may result in gene amplification and/or gene rearrangement. This phenomenon may also play a role in synergistic interactions between chemicals and viruses in the causation of certain cancers. The primary target of the tumor promoters TPA, teleocidin, and aplysiatoxin appears to be cell membranes. All three of these agents act, at least in part by, enhancing the activity of the phospholipid-dependent enzyme PKC. We have proposed a stereochemical model to explain the interaction of these amphiphilic compounds with the PKC system. We have found that TPA and teleocidin markedly enhance the transformation of C3H10T1/2 mouse fibroblasts when these cells are transfected with the cloned H-ras human bladder cancer oncogene. Thus, tumor promoters can act synergistically with an activated oncogene to enhance cell transformation. Furthermore, carcinogen-transformed rodent cells display aberrations in the expression of various endogenous retrovirus-related sequences. Activation of some of these sequences may lead to insertion mutations and further aberrations in gene expression. These findings are discussed in terms of a multistep model that involves progressive changes in cellular oncogenes and aberrations in the function of DNA transcription enhancer sequences. It will be of interest to determine to what extent these concepts apply to the etiology of cancers of the respiratory tract.

Animals↗