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Biomedical subjects

A B Glover

Publications and source records attributed to A B Glover.

7 recordsLinked to original sources
PubMed1987

Biochemistry of azacitidine: a review.

Azacitidine is a pyrimidine ring analog of cytidine that is incorporated into RNA causing alteration in RNA synthesis and processing and resulting in inhibition of protein synthesis. Azacitidine as the deoxynucleotide is also incorporated into DNA inhibiting its synthesis and blocking cytosine methylation by noncompetitive inhibition of DNA methyltransferase. The resulting hypomethylation of DNA is thought to induce gene activation and expression and cell differentiation. This may be an underlying factor in azacitidine's antileukemic activity and also contributes to its carcinogenic and tumor-promoting properties in experimental models.

Animals↗
PubMed1975

Modulation by acetylcholine of adrenergic transmission in the rabbit ear artery.

1. Low concentrations of acetylcholine (4 times 10(-11) and 1 times 10(-10) M) increase the vasoconstrictor response of the isolated ear artery of the rabbit to stimulation of the periarterial sympathetic nerves. Higher concentrations (4 times 10(-8) M and greater) decrease the response. 2. Low concentrations of acetylcholine (1 times 10(-11) and 1 times 10(-10) M) increase the stimulation-induced efflux of radioactivity from artery segments previously incubated with [3H]-noradrenaline. Higher ocncentrations (3 times 10(-8) M and greater) decrease the efflux. 3. Neither atropine nor hexamethonium affects the facilitatory action of low concentrations of acetylcholine on adrenergic transmission in the rabbit ear artery. 4. Atropine antagonizes the inhibitory effect of higher concentrations of acetylcholine on adrenergic transmission.

Acetylcholine↗
PubMedDate not supplied

Azacitidine: 10 years later.

Azacitidine has been undergoing clinical trials for almost 20 years and is internationally considered to have a useful place in the treatment of acute nonlymphocytic leukemia. However, its role in the various combinations for induction, intensification, maintenance, or relapse regimens has not yet been clearly defined. This review outlines the last 10 years' clinical experience with the drug in acute nonlymphocytic leukemia, analyzes what critical information has yet to be obtained, and suggests what phase III trials may still be feasible to gather that information.

Acute Disease↗