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Biomedical subjects

L Reik

Publications and source records attributed to L Reik.

24 records · Page 2Linked to original sources
PubMed1981

Administration of 3-methylcholanthrene to rats increases the specific hybridizable mRNA coding for cytochrome P-450c.

Poly(A)+-RNA obtained from the livers of 3-methylcholanthrene (3MC)-treated rats was translated into cytochrome P-450c in a cell-free reticulocyte system. In this translational system, no precursor cytochrome P-450c was observed. The mRNA responsible for the synthesis of this cytochrome was isolated by immunoprecipitation of liver polyribosomes obtained at 15 hr after 3MC treatment, and a cDNA was constructed by the reverse transcriptase reaction. The cDNA was further purified by hybridizing at a high R0t (product of RNA concentration and incubation time) to poly(A)+-RNA isolated from control rat liver, and the nonhybridized, single-stranded cDNA was isolated by hydroxylapatite chromatography. This cDNAp-450c was employed in hybridization reactions with poly(A)+-RNA isolated from the livers of rats treated with 3MC for various times. These studies indicated a maximal induction of mRNAp-450c at about 15 hr after 3MC injection, although levels of this mRNA were significantly increased by 7 hr. The mRNAp-450c concentration had diminished by 24 hr but remained higher than control levels for at least 48 hr. These studies establish an effect of 3MC upon the accumulation of mRNAp-450c in rat liver.

Animals↗
PubMed1981

Pernicious anemia seen initially as orthostatic hypotension.

A 69-year-old man complaining of syncope was found to have pernicious anemia and orthostatic hypotension due to autonomic neuropathy. Following vitamin B12 replacement with cyanocobalamin, the blood pressure became normal. To our knowledge, this is the first reported case of neurogenic orthostatic hypotension as the initial feature of vitamin B12 deficiency.

Aged↗
PubMed1980

Disseminated vasculomyelinopathy: an immune complex disease.

The numerous nervous system abnormalities which follow antecedent infections and immunization appear to share a common pathogenesis involving the immune system. Pathologically, a small vessel vasculopathy involving arterioles and capillaries as well as venules in both gray and white matter is the earliest and most consistent change. Perivascular demyelination appears to develop subsequently. Delayed hypersensitivity to myelin basic protein may not adequately account for these changes. Humoral immunity may be involved instead. I postulate that antigen-antibody complexes, formed following the introduction of foreign antigen by infection or inoculation, cause vascular injury with secondary damage to myelin. There is considerable evidence that circulating immune complexes are present in some postinfectious nervous system disorders, as are associated systemic features which suggest immune complex disease. Similar clinical and pathological nervous system changes occur in a variety of disorders in which circulating immune complexes are thought to cause vascular injury.

Antigen-Antibody Complex↗
PubMed1970

Hormone-sensitive adenyl cyclase: cytochemical localization in rat liver.

An electron microscopic procedure has been developed, using rat liver, for the localization of hormone-sensitive adenyl cyclase. Isoproterenol-sensitive adenyl cyclase is located almost exclusively in the parenchymal cells. In contrast, glucagon-sensitive adenyl cyclase is located primarily in the reticulo-endothelial cells but is also present in parenchymal cells. Sodium fluoride-sensitive adenyl cyclase is found in both cell types.

Adenine Nucleotides↗