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J Yin

Publications and source records attributed to J Yin.

186 records · Page 11Linked to original sources
PubMed1982

Specific, saturable binding and uptake of rat chylomicron remnants by rat skin fibroblasts.

To investigate the possible contribution of chylomicron remnants to the accumulation of cholesterol in non-hepatic tissues, rat chylomicron remnants were incubated with rat skin fibroblasts. The binding of remnants was saturable and specific. Native, undegraded chylomicrons were almost as effective as unlabeled remnants in displacing the uptake of labeled remnants. Rat low density and high density lipoproteins were relatively ineffective in displacing the uptake of labeled remnants. Accumulation of radioactive unesterified fatty acids occurred in proportion to the uptake of labeled remnants, indicating probable internalization and degradation of the particles after binding. The incorporation of added [14C]acetate into cell non-saponifiable lipids was not significantly suppressed by added remnants, indicating an apparent lack of feedback regulation of cholesterol biosynthesis after remnant uptake. Our results show that the physiological mechanism underlying uptake of remnants by hepatic parenchymal cells might not be accounted for by tissue or cellular specificity, but may perhaps arise because of the lower capillary permeability of extra-hepatic sites compared with the hepatic sinusoid.

Animals↗
PubMedDate not supplied

Quantifying viral propagation in vitro: toward a method for characterization of complex phenotypes.

For a eukaryotic virus to successfully infect and propagate in cultured cells several events must occur: the virion must identify and bind to its cellular receptor, become internalized, uncoat, synthesize viral proteins, replicate its genome, assemble progeny virions, and exit the host cell. While these events are taking place, intrinsic host defenses activate in order to defeat the virus, e.g., activation of the interferon system, induction of apoptosis, and attempted elicitation of immune responses via chemokine and cytokine production. As a first step in developing an imaging methodology to facilitate direct observation of such complex host/virus dynamics, we have designed an immunofluorescence-based system that extends the traditional plaque assay, permitting simultaneous quantification of the rate of viral spread, as indicated by the presence of a labeled viral protein, and cell death in vitro, as indicated by cell loss. We propose that our propagation and cell death profiles serve as phenotypic read-outs, complementing genetic analysis of viral strains. As our virus/host system we used vesicular stomatitis virus (VSV) propagating in hamster kidney epithelial (BHK-21) and murine astrocytoma (DBT) cell lines. Viral propagation and death profiles were strikingly different in these two cell lines, displaying both very different initial titer and cell age effects. The rate of viral spread and cell death tracked reliably in both cell lines. In BHK-21 cells, the rate of viral propagation, as well as maximal spread, was relatively insensitive to initial titer and was roughly linear over several days. In contrast, viral plaque expansion in DBT cells was contained early in the infections with high titers, while low titer infections spread in a manner similar to the BHK-21 cells. The effect of cell age on infection spread was negligible in BHK-21 cells but not in DBTs. Neither of these effects was clearly observed by plaque assay.

Animals↗
PubMedDate not supplied

A comparison of solid sampler methods for the determination of hexamethylene-based isocyanates in spray-painting operations.

A polyurethane foam sponge impregnated with 1-(2-methoxyphenyl) piperazine in dimethylsulfoxide was mounted in both cassette and inhalable organic monitor samplers and these were then compared with a dual-filter cassette. The samplers were used for the collection of hexamethylene diisocyanate (HDI) monomer and oligomers during actual spray-painting operations. The dual filter cassettes were positioned on a mannequin. The polyurethane foam cassette (PUF CAS) and polyurethane foam inhalable organic monitor (PUF IOM) samplers were positioned on a cart in the same maximum overspray area. Data from this pilot study suggest that there is no significant difference (P < 0.05, n = 6) in the amount of HDI monomer obtained with the PUF IOM sampler when compared with the amount obtained from the dual filter cassette. The data also suggest that the PUF IOM sampler yields a higher amount of HDI oligomer than either the dual filter cassette or the PUF CAS sampler, neither of which exhibited a significant difference (P < 0.05, n = 6) from each other.

Air Pollutants, Occupational↗
PubMedDate not supplied

Growth suppression of esophageal cancer cells by p16INK4 and p15INK4B in vitro.

PURPOSE: We investigate whether p16INK4 and p15INK4B inhibit cellular proliferation and exert a growth suppressive effect on esophageal cancer cells. MATERIALS AND METHODS: The growth suppressive effects of p16INK4 and p15INK4B were evaluated by transfecting vectors containing the p16INK4 cDNA or the p15INK4B cDNA, or both, constitutively driven by a cytomegalovirus promoter, into two human esophageal cancer cell lines containing or lacking endogenous p16INK4 and/or p15INK4B. RESULTS: These experiments demonstrated that in both cells lines tested, the numbers of cells surviving dramatically decreased in p16INK4-transfected and p15INK4B-transfected cells compared with control vector-transfected cells. There was no significant difference in the degree of growth inhibition between p16INK4-transfected and pI5INK4B-transfected cell lines. CONCLUSIONS: These results suggest that p16INK4 and p15INK4B play important roles in the initiation or promotion of esophageal cancer. The inactivation of p16INK4 and p15INK4B may contribute to uncontrolled growth in human cancer.

Carcinoma, Squamous Cell↗