Incorporation of α-aminobutyric acid into ergostine byClaviceps purpurea

Summary Claviceps purpurea 275 F.I. fed with -aminobutyric acid produces ergostine with the corresponding -hydroxy--aminoacid undiluted by endogenous aminoacid. Almost all the -aminobutyric acid not incorporated into the ergostine remains unchanged in the medium. The significance of these results in the biosynthesis of ergot alkaloids is discussed.     

In vivo effects of Escherichia coli endotoxin on sulfobromophthalein clearance in the guinea-pig.

In vivo studies indicated that the primary effects of E. coli endotoxin on hepatic clearance of sulfobromophthalein were at the excretory level. Newborns were more sensitive to the LPS than older animals.     

Effects of ACTH and diabetes on phospholipid metabolism in adrenal mitochondria.

Incorporation of 32P into adrenal mitochondrial phospholipids (PL) incrased in ACTH-treated rats, but it decreased in diabetics, inspite of the fact that these animals showed adrenal overacity. Since diabetics did not show increased 11 beta-hydroxylation. as opposed to ACTH-treated rats, it is suggested that the stimulation of this enzyme activity by exogenous ACTH is related to an increased turnover of PL at the mitochondrial membrane. The process is impaired in diabetics and prevents the stimulation of 11 beta-hydroxylation.     

Effect of aldosterone and methylprednisolone on cardiac NaK-ATPase

Summary Aldosterone (15 g BID) and methylprednisolone (8 mg QD) administration to female guinea-pigs augmented both the total and the specific activity of NaK-ATPase but not the activity of adenylate cyclase in the cardiac sarcolemma. The rise in NaK-ATPase was due to increase in the number of enzyme molecules; catalytic activity and ouabain-sensitivity of individual molecules did not change.Acknowledgments. This work was supported by grant 1 R01 HL16611 from the National Heart and Lung Institute of the National Institutes of Health, United States Public Health Service. I thank Mr Kooil Kang for his excellent technical assistance.     

Early foetal thrombosis induced by Thalidomide in mouse: Possible explanation for teratogenicity

Summary Mouse foetuses were treated by Thalidomide on days 11–12 in order to verify whether the drug would induce blood abnormalities leading to circulatory troubles. About 18% of the treated foetuses showed both severe limb haemorrhages on day 14, and obvious alterations of the nucleated red blood cells of vitelline origin. These blood abnormalities, occurring suddenly during the well-known critical stage of foetal development, could be responsible for circulatory blocks leading to necrosis.     

Changes in ecdysone levels in the spiderPisaura mirabilis nymphs (Araneae,Pisauridae)

Summary RIA of ecdysones are made on nymphal extracts ofPisaura mirabilis during the intermoulting cycle. The hormone level is low during exuviation and the greatest part of the intermoulting period but increases notably before and after ecdysis. The main hormonal peak or pre-ecdysial peak is due to -ecdysone, characterized by combined TLC/RIA.Acknowledgment. We wish to thank Dr M. Hirn for his help during the manipulations and J. Britton who has translated the text into English.     

A centrally induced vasodepressor response after intravenous administration of whole venom ofNaja mossambica pallida in cats

Summary Naja mossambica pallida venom administered i.v. (300 /kg) produces an initial brief fall in blood pressure, due to a direct myocardial depressant effect, and a sustained fall due to central depressant effect.This study was supported by University of Nairobi research grants (670–376). We also thank Mr E. Njogu for photographic assistance.     

Influence of PGA1 on cartilage growth

Summary Using the Fell technique of organ culture of cartilage in a chemically defined medium, it has been shown that prostaglandin A₁ at a concentration of 25 g/ml caused chondrocyte death in chick embryonic limb rudiments. An equimolar concentration of PGE₂ was not toxic to the cells.Acknowledgments. We are grateful for the support of C. J. K. by the Medical Research Council and of D. L. G. by the Arthritis and Rheumatism Council for Research. Our thanks are due to Dame Honor Fell, F. R. S. for invaluable advice and guidance, to Dr J. Pike (Upjohn Co.) for supplies of prostaglandin A₁, and to Dr Sylvia Fitton-Jackson for the gift of culture medium.