Phosphofructokinases from Lactobacteriaceae. II. Purification and properties of phosphofructokinase from Streptococcus thermophilus

Phosphofructokinase (ATP : D-fructose-6-phosphate 1-phosphotransferase, EC 2.7.1.11) from Streptococcus thermophilus has been purified. It is a tetramer composed of identical subunits of molecular weight 36 000 and exhibits Michaelis-Menten kinetics. Compared to the phosphofructokinases from taxonomically related bacteria, the enzyme from S. thermophilus is more stable at high temperatures. In addition, it has been demonstrated that the phosphofructokinases from lactobacteria and also from Bacillus stearothermophilus show immunologic cross-reaction. In spite of the significantly different kinetic properties and the different thermostability of these enzymes, this finding indicates great structural resemblance.     

Oxalate accumulation from citrate by Aspergillus niger. I. Biosynthesis of oxalate from its ultimate precursor.

Carbon-14 was incorporated from citrate-1,5-14C, glyoxylate-14C(U), or glyoxylate-1-14C into oxalate by cultures of Aspergillus niger pregrown on a medium with glucose as the sole source of carbon. Glyoxylate-14C(U) was superior to glyoxylate-1-14C and citrate-1,5-14C as a source of incorporation. By addition of a great amount of citrate the accumulation of oxalate was accelerated and its maximum yield increased. In a cell-free extract from mycelium forming oxalate from citrate the enzyme oxaloacetate hydrolase (EC3.7.1.1) was identified. Its in vitro activity per flask exceeded the rate of in vivo accumulation of oxalate. Glyoxylate oxidizing enzymes (glycolate oxidase, EC1.1.3.1; glyoxylate oxidase, EC1.2.3.5;NAD(P)-dependent glyoxylate dehydrogenase; glyoxylate dehydrogenase, CoA-oxalylating, EC1.2.1.7) could not be detected in cell-free extracts. It is concluded that in cultures accumulating oxalate from citrate after pregrowth on glucose, oxalate arises by hydrolytic cleavage of oxaloacetate but not by oxidation of glyoxylate.     

Death from asthma.

The factors associated with the deaths of 31 asthma patients were examined. The subjects, whose deaths occurred in the period 1967 through 1979, had all received some care at the Hospital for Sick Children in Toronto, but only nine died there. The greatest single cause of death was the inappropriate use of beta-agonists, with or without the concurrent use of epinephrine. In seven patients an asthma attack that occurred outside hospital progressed so rapidly that there was insufficient time for them to obtain adequate therapy. In five cases the assessment of the patient''s condition or the therapy recommended by the attending physician appeared to have been inadequate. Two patients suffered an acute attack in hopital and did not respond to treatment that appeared to have been adequate. In six cases the available information was insufficient to indicate the cause of death. Over half (18) of the deaths occurred in teenagers. Various ways of preventing death from asthma are discussed, including better education of physicians and patients, adequate management of factors that provoke bronchospasm, sufficient follow-up -- especially in teenagers -- and the use of approaches with teenagers that encourage better compliance.