Biomedical subjects
C J Epstein
Publications and source records attributed to C J Epstein.
Spectral studies on the denaturation of myoglobin.
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An approach to the problem of conformational isozymes.
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Mitochondrial malate dehydrogenase: reversible denaturation studies.
The malate dehydrogenase isoenzymes from the mitochondria of chicken hearts have been partially resolved into separate pools. Reversible denaturation, in concentrated guanidine hydrochloride, does not change the isoenzyme distribution in each pool. This result suggests that the electrophoretic differences among the isoenzymes are not solely conformational in origin.
A convenient method of preparing polyacrylamide gels for liquid scintillation spectrometry.
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Hereditary dysplasia of bone with kyphoscoliosis, contractures, and abnormally shaped ears.
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The role of calcium in the reactivation of reduced Taka-amylase.
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Non-randomness of amino-acid changes in the evolution of homologous proteins.
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Nuclear ploidy in mammalian parenchymal liver cells.
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The incorporation of [3H]leucine into protein by tetraphenylboron- and citrate-dispersed rat liver parenchymal cells.
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A structural analysis of hepatomegaly induced by a hormone-secreting tumor.
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Cell size, nuclear content, and the development of polyploidy in the Mammalian liver.
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Social aspects of medical genetics.
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Role of the amino-acid "code" and of selection for conformation in the evolution of proteins.
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Werner's syndrome a review of its symptomatology, natural history, pathologic features, genetics and relationship to the natural aging process.
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Evolutionary origins of human proteins.
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Werner's syndrome; caricature of aging. A genetic model for the study of degenerative diseases.
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Neurotoxicity, drugs and abuse, and the CuZn-superoxide dismutase transgenic mice.
Administration of methamphetamine (METH) to animals causes loss of DA terminals in the brain. The manner by which METH causes these changes in neurotoxicity is not known. We have tested the effects of this drug in copper/zinc (CuZn)-superoxide dismutase transgenic (SOD Tg) mice, which express the human CuZnSOD gene. In nontransgenic (non-Tg) mice, acute METH administration causes significant decreases in DA and dihydroxyphenylacetic acid (DOPAC) in the striata of non-Tg mice. In contrast, there were on significant decreases in striatal DA in the METH administration caused decreases in striatal DA and DOPAC in the non-Tg mice, but not in the SOD-Tg mice. Similar studies were carried out with 1-methyl-1,2,3,6-tetrahydropyridine (MPTP), which also causes striatal DA and DOPAC depletion. As in the case of METH, MPTP causes marked depletion of DA and DOPAC in the non-Tg mice, but not in the SOD Tg mice. These results suggest that the mechanisms of toxicity of both METH and MPTP involved superoxide radical formation.