A rare case of basilar-middle meningeal arterial anastomosis is reported. Pertinent literature is reviewed and an embryological explanation of this anastomosis is discussed.

Basilar Artery↗

PubMed1978

Metabolism of fatty acids and the levels of ketone bodies in the livers of pyridoxine-deficient rats.

Lipid metabolism was examined in rats fed a high-protein pyridoxine-deficient diet, and their livers were found to contain large amounts of lipids, mainly in the forms of triglycerides and cholesteryl ester. The contents of ketone bodies in the livers of pyridoxine-deficient and the control rats were similar. Their NAD+/NADH ratios, calculated from the amounts of ketone bodies, were also similar in pyridoxine-deficient and control groups when the animals were fed, but the ratio in pyridoxine-deficient rats was lower than that of control rats when the animals were starved. After injection of 14C-linoleic acid, the amounts of expired 14CO2 in pyridoxine-deficient and control rats were similar. The pattern of incorporations of 14C-linoleic acid into various lipid components of the livers were examined; incorporation into the phospho-lipid fraction was similar in control and deficient rats, but the incorporation into the triglyceride fraction was slower, and the incorporation into cholesterol was faster in deficient animals than in controls.

Animals↗

PubMed1978

Carcinogenicity of 4-nitrosoquinoline 1-oxide and its possible role in carcinogenesis by 4-nitroquinoline 1-oxide.

4-Nitrosoquinoline 1-oxide induced malignant tumors at the subcutaneous site of injection in mice. It affected Escherichia coli to induce the so-called UV-type lesion in cellular DNA. DNA base-quinoline adducts produced by the treatment of mammalian cellular DNA with this carcinogen were proved to be identical with those obtained by the action of 4-nitroquinoline 1-oxide. Although this carcinogen was reactive enough to modify DNA chemically by itself, a different DNA modification took place in a chemical process from thos obtained in the in vivo process.

4-Nitroquinoline-1-oxide↗

PubMed1978

LPS-or 8Br-cyclic AMP-induced production of T cell-activating factor(s) in macrophage tumor cell line J774.1.

The macrophage tumor cell line J774.1 replaced the function of normal macrophages in the induction of polyclonal killer T cells with 2-mercaptoethanol. J774.1 does not normally release soluble factor(s) which we have shown to be responsible for the differentiation of T cells to killer T cells. However, stimulation of J774.1 with LPS induced soluble factor(s) for T cell activation. An optimum concentration of LPS for the production of soluble factor(s) was 1 to 10 microgram/ml, which completely inhibited growth of the tumor cells. The production of soluble factor(s) was observed within 6 hr after LPS stimulation and reached its maximum level at 24 hr. Incubation of the cell line with 8Br-cyclic AMP and theophylline induced soluble factor(s), suggesting that LPS stimulation induced an increase in intracellular cyclic AMP which leads to the synthesis of soluble factor(s).

Animals↗

PubMed1978