1.
Dahlqvist-Edberg, Ulla, et al.
(författare)
Purification of a Ca2+-activated protease from rat erythrocytes and its possible effect on pyruvate kinase in vivo
1981
Ingår i: Biochimica et Biophysica Acta-Enzymology. - : Elsevier BV. - 0005-2744. ; 660:1, s. 96-101
Tidskriftsartikel (refereegranskat) abstract
A Ca2+-activated protease with [32P]phosphopyruvate kinase as substrate was purified to about 50% from rat erythrocytes. The purification involved chromatography on Sepharose/Sephadex gels, DEAE-cellulose and (NH4)2SO4 precipitation. The protease required 3.3 mM Ca2+ for full activity. When pyruvate kinase (ATP: pyruvate 2-O-phosphotransferase, EC 2.7.1.40) was purified from erythrocytes incubated with [32P]phosphate it contained 0.5 mol [32P]phosphate/mol enzyme subunit. When 3.3 mM Ca2+ were added at hemolysis this incorporation decreased. The possible importance of this Ca2+-activated protease for the regulation of pyruvate kinase in erythrocytes is discussed.
2.
Ekman, Pia, et al.
(författare)
The in vitro modification of phosphorylated pyruvate kinase by a Ca2+-activated protease from rat liver
1980
Ingår i: Acta Chemica Scandinavica. - : Danish Chemical Society. - 0904-213X .- 1902-3103. ; 34:6, s. 419-422
Tidskriftsartikel (refereegranskat) abstract
A Ca/+-activated protease from rat liver cell sap was prepared. It was shown to act on rat liver pyruvate kinase that had been phosphorylated by the catalytic subunit of cyclic AMP-dependent protein kinase, the activity being optimum at neutral pH. The modified pyruvate kinase had the same Vmax as the phosphoenzyme but showed a lower affinity for the substrate phosphoenolpyruvate. The possibility that this proteolytic attack is the step that initiates further degradation in the cell is discussed.
3.
Stubbe, Ingo, et al.
(författare)
In-hospital exercise therapy in patients with severe angina pectoris
1983
Ingår i: Archives of Physical Medicine and Rehabilitation. - 0003-9993. ; 64:9, s. 396-401
Tidskriftsartikel (refereegranskat) abstract
The authors evaluated physiologic, psychologic and metabolic effects of a nine-week in-hospital training program on 14 men with severe disabling angina pectoris. The exercise program consisted of intensive interval training on an ergometer bicycle for two 30 min sessions daily. The physical performance increased by about 40% (p less than 0.001). Plasma insulin levels were reduced and glucose tolerance improved significantly. There was a decrease in plasma triglyceride and low-density lipoprotein (LDL) cholesterol levels, but no change in high-density lipoprotein (HDL) cholesterol, apolipoprotein AI and B concentrations. Plasma triglyceride (p less than 0.05) and LDL cholesterol (p less than 0.05) levels remained low three weeks after completion of the training period and the physical performance remained improved (p less than 0.01) even six months post-training. Four of the patients who had been disabled for at least five months were able to return to work. The authors suggest that comparatively short and intensive in-hospital rehabilitation of patients with coronary heart disease may be an attractive alternative to prolonged training on an outpatient basis, especially in patients with severe angina pectoris.
