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Biomedical subjects

L Unger

Publications and source records attributed to L Unger.

61 records · Page 4Linked to original sources

Action of a proline analogue, l-thiazolidine-4-carboxylic acid, in Escherichia coli.

Unger, Leon (University of Illinois, Urbana), and R. D. DeMoss. Action of a proline analogue, l-thiazolidine-4-carboxylic acid, in Escherichia coli. J. Bacteriol. 91:1556-1563. 1966.-The effect of the proline analogue, l-thiazolidine-4-carboxylic acid (thioproline), on growth, and its relation to the metabolic function of proline in protein synthesis in Escherichia coli K-12, has been studied. Thioproline causes linear growth in E. coli within one generation. The inhibition is specifically reversed by the simultaneous addition of l-proline. Thioproline, or a closely related metabolic derivative, is incorporated into bacterial proteins. Proline antagonizes the incorporation of "thioproline" into protein. The analogue specifically inhibits the rate and extent of prolyl-ribonucleic acid formation. The effectiveness of thioproline as a proline analogue is attributed to its ability to interfere with the utilization of proline for protein synthesis and to mimic proline in its function of being incorporated into proteins. The effect of the incorporation of thioproline on protein structure and enzyme activity is discussed.

Antimetabolites↗

Metabolism of a proline analogue, l-thiazolidine-4-carboxylic acid, by Escherichia coli.

Unger, Leon (University of Illinois, Urbana), and R. D. DeMoss. Metabolism of a proline analogue, l-thiazolidine-4-carboxylic acid, by Escherichia coli. J. Bacteriol. 91:1564-1569. 1966.-Resting cells of Escherichia coli K-12, pregrown in a proline- and thioproline-free medium, oxidize the proline analogue, l-thiazolidine-4-carboxylic acid (l-thioproline), without a lag with the consumption of 1 atom of oxygen per mole of thioproline. The organism also oxidizes cysteine and formaldehyde, the chemical precursors of thioproline. The total oxygen consumed is the same whether the substrate is thioproline, cysteine, formaldehyde, or an equimolar mixture of cysteine and formaldehyde. The results suggest that neither cysteine nor formaldehyde are free intermediates in the oxidative pathway. Thioproline is available as a metabolic carbon source for the synthesis of the ribonucleic acid bases, guanine and uracil.

Carbon Isotopes↗

Two step cardiomyoplasty with vascular delay: effect of stimulation of latissimus dorsi muscle on diastolic function.

A common concern in cardiomyoplasty is whether latissimus dorsi muscle (LDM) stimulation impairs diastolic function. This study determined the time course of left ventricular (LV) contraction and relaxation and their relationship to the diastolic function. Ten mongrel dogs underwent vascular delay of the left latissimus dorsi muscle 2 weeks before cardiomyoplasty. Fourteen to 18 days later, the effects of LDM stimulation were evaluated. Our study demonstrated that LDM stimulation significantly increased peak LV systolic pressure (131.3 +/- 7.5 to 152.0 +/- 7.5* mm Hg), +dP/dt (1585 +/- 151 to 2088 +/- 176 x mm Hg/s), stroke volume (10.8 +/- 1.5 to 13.8 +/- 1.9* ml), stroke work (17.2 +/- 2.7 to 25.6 +/- 3.8* gm x m), and peak aortic flow (4751 +/- 698 to 6712 +/- 926* ml/min), and significantly decreased the pre-ejection time (113.9 +/- 12.6 to 92.3 +/- 7.8* ms) and total systolic time (366.0 +/- 26.9 to 333.6 +/- 21.3* ms) (*p < 0.05). As for diastolic function, LDM stimulation decreased -dP/dt (-1462 +/- 116 to -1781 +/-116* mm Hg/s) and tau (64.0 +/- 6.1 to 52.1 +/- 2.9* ms). The diastolic filling time (Tdf) was significantly longer (177.9 +/- 17.6 to 213.7 +/- 18.7* ms) during the beat immediately after LDM stimulation. These changes reflected an overall stronger contraction and faster relaxation. Our results imply that with vascular delay, stimulation of LDM not only assists systolic function but also improves diastolic function in cardiomyoplasty.

Animals↗