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One of the peptide fragments obtained in a preceding study of the cyanogen bromide hydrolysate of S-sulfo-pepsin has been investigated in more detail. The peptide was purified by ion-exchange chromatography and obtained in homogeneous form. It contains 158 amino acid residues, among their number the only histidine residue of pepsin and two half-cystine residues. Evidence was obtained that the peptide is derived from the N-terminal region of the molecule of hog pepsin. The peptide was reduced by 2-mercaptoethanol and converted into its S-(β -amino-ethyl)-cysteinyl derivative. From the tryptic digest of this derivative a 105-residue peptide containing N-terminal isoleucine was isolated which represents the N-terminal segment of the pepsin molecule.

A Table of amino acid replacements based on one-point mutations is presented. For each amino acid replacement the number of mutations of various codons resulting in this mutation is recorded.

Partially purified enzyme fraction from rat kidney possessing high uridine kinase and phosphomonoesterase activity was insolubilized by means of zinc precipitation without substantial loss of the activity. While uridine kinase in a soluble and Zn-precipitated form was inhibited by low concentrations (0.5–1.0 mM) of Zn 2+ -ions, phosphomonoesterase was fully active. In contrast to the soluble fraction, the two enzymes in zinc-precipitated and lyophilized preparations were stable on heating at 100°C. Metal complexed proteins catalyze the dephosphorylation of 5′-UMP, 6-AzaUMP as well as of 2′(3′)-UMP or 2,4-dinitrophenyl phosphate indicating thus the presence of several phosphomonoesterases in the complex.

The preparation and the juvenilization effect of some derivatives of 3,7-dimethyl-9-(5-methyl-2-oxolanyl)-2,6-nonadenoic, 3,7-dimethyl-9-(5-methyl-2-oxolanyl)-2-nonenoic (methyl, ethyl and isopropyl ester, monomethyl and dimethylamide) and 3,7-dimethyl-9-(-methyl-2-oxolanyl)-2,4-nonadenoic acid (methyl, ethyl and isopropyl ester) have been described.

In the literature, numerous morphogenetically active mixed ethers have been reported, containing phenyl and epoxidated terpenoid groupings1'2. In view of the juvenile activity of those juvenile hormone analogues in which the oxirane ring of the parent hormone is replaced by the more stable oxolane ring3'4, attention has been now paid to the preparation** of some alkyl aryl ethers containing an oxolane ring in the aliphatic portion of the molecule instead of the oxirane ring. Some of these ethers have been so far reported in a Czechoslovak Patent Application only5. The present bioanalogues have been prepared by alkylation of 4-chloropheno l (I), 4-methylphenol {II), 4-ethylphenol (ill) or 4-methoxycarb onylphenol (IV) with 1 -bromo-3-methyl-5-(2-oxolanyl)pentane3 (V), l-bromo-3-methyl-5-(2-oxolanyl)-2-pentene3 (VI) or 2-bromo-4-(2- oxolanyl)butane4 (VII).

3-Hydroxy-(I, X = β- and α-OH; Y = H) and 2 β-senecioyloxy-(I, X = H; Y = OCOCH=CMe2) eremophilenolides were synthesized stereoselectively starting from ethylenedioxy octalone derivative (II, X = H2). The present synthetic study demonstrates unequivocally that the positions of ester groups of petasitolides should be located at C2- rather than C3- exposition.

Resistance to 5-azacytidine, a potent inhibitor of the growth of mouse lympaoid leukemia cells in vivo, was achieved in an inbred strain of AKR mice in the third transplant period. The incorporation of orotic acid into the livers of such resistant mice was more than six times lower than in animals carrying the 5-azacytidine-sensitive parent strain of leukemia. The incorporation of orotic acid by 5-azacytidine-sensitive mice was inhibited by 5-azacytidine twice as much as in 5-azacytidine-resistant animals. The incorporation of uridine, cytidine, thymidine, deoxycytidine, and of guanosine into nucleic acids was also significantly depressed in 5-azacytidine-resistant leukemic cells. Uridine kinase activity was decreased by 20%, while uridine phosphorylase activity was diminished by 31–50%. The resistant leukemic mice were cross-resistant to 5-fluorouracil; in contrast, however, their sensitivity to aminopterin was increased significantly. Une resistance a l'aza-5 cytidine, puissant inhibiteur de croissance des celluks de la leuremie lyniphoide de la souris in vivo, a ete obtenue dans une souche endogame de souris AKR a la troisienie periode de transplantation. L'incorporation d'acide orotique dans le foie de ces souris resistantes etait plus de six fois inferieure a re qu'elle etait chez les animaux porteurs de la souche parentale, sensible a l'aza-5 cytidine, de cellulrs Ieucemiques. Chez les souris sensibles a l'aza-5 cytidine, l'incorporation de l'acide orotique ktait deux fois plus inhibee par I'aza-5 cytidine que chez les souris resistantes. L'incorporation d'uridine, de cytidine, de thymidine, de desoxycytidine et de guanosine dans les acides nucleiques etait aussi abaissee dans une mesure significative dans la cellules leucemiques resistantes a l'aza-5 cytidine. L'activite uridine kinasique etait abaissee de 20 pour cent et celle de I'uridine phosphorylase de 31 a 50 pour cent. Les souris Ieucemiques resistantes presentaient une resistance croisee avec le fiuoro-5 uracile; en revanche, leur sensibilite a I'aminopterine etait significativement augmentee.