Release of homovanillic acid from the brain of children.

Cerebral arterio-venous differences of homovanillic acid (HVA) and cerebral blood flow were measured in 24 patients, 6 adults and 18 children, anaesthetized by different techniques. A statistically significant release of HVA from the brain (p < 0.001) was demonstrated in five children anaesthetized by barbiturate, nitrous oxide and droperidol/fentanyl. The release rate was 509 pmoles HVA/100 g brain tissue/minute - corresponding to approximately 1.3 mg HVA/24 hours from the whole brain.     

Cycloheximide resistance in Chinese hamster cells. II. Induction of Chm resistance in Chinese hamster cells by N-nitrosomethylurea.

Mutant Chinese hamster ovarian (CHO) cells with a resistance to 7-10(-7) and 8-10(-7) M cycloheximide (CHM) were induced at mutation rates of 1.9-5.2-10(-3) and 1.6-1.8-10(-3) respectively after treatment with N-nitrosomethylurea (NMU) at 100 mug/ml. The induced mutation rates differed by two orders of magnitude from the spontaneous rate of mutation to CHM resistance.     

Tryptic peptide analysis on nonstructural and structural precursor proteins from Semliki Forest virus mutant-infected cells.

Analysis of [35S]methionine-labeled tryptic peptides of the large proteins induced by temperature-sensitive mutants of Semliki Forest virus was carried out. The 130,000-molecular-weight protein induced by ts-2 and ts-3 mutants contained the peptides of capsid protein and of both major envelope proteins E1 and E2. The ts-3-induced protein with molecular weight of 97,000 contained peptides of the capsid and envelope protein E2 but not those of E1. Two proteins with molecular weights of 78,000 and 86,000 from ts-1-infected cells did not contain the peptides of the virion structural proteins. They are evidently expressions of the nonstructural part of the 42S RNA genome of Semliki Forest virus.     

Non-random intrachromosomal distribution of chromatid aberrations induced by X-rays,alkylating agents and ethanol in Vicia faba

A reconstructed karyotype of Vicia faba with all chromosomes individually distinguishable was treated with triethylene melamine (TEM), cytostasan (CYT) (a new benzimidazol nitrogen mustard), mitomycin C (MI), ethanol (EA) and X-rays. The distribution within chromosomes of induced chromatid abberations was non-random for all agents. The number of segments involved in aberration clustering corresponded to the number of sites representing constitutive heterochromatin, or the regions immediately adjacent to these, as evidenced by the position of Giemsa marker bands. Which of these potential regions of aberration clustering reacted with preferential involvement in aberrations was, in part at least, dependent upon the inducing agent used. It is argued that this may be due to differences in the base composition and/or molecular conformation of heterochromatic regions. Unexpectedly, the distribution pattern of chromatid aberrations induced by mitomycin C was found to be different from those after treatment with the alkylating agents TEM and cytostasan although mitomycin C is assumed to induce aberrations via alkylation. If mitomycin C-induced aberrations are indeed due to alkylation, this indicates that different alkylating agents do not necessarily result in identical patterns of abberation clustering. The other two alkylating agents and ethanol resulted in similar patterns of preferential distribution of abberations. X-Ray induced chromatid aberrations also showed a non-random intrachromosomal distribution, but the clustering was less pronounced than after treatment with the chemical agents.     

Cyclization of 13beta-ethyl-3-methoxy-17beta-ol-8,14-seco-1,3,5(10),9-gonatetraen-14-one and its 17 acetate derivative.

13beta-Ethyl-3-methoxy-17beta-ol-8,14-seco-1,3,5(10),8-gonatetraen-14-one (IIIa) was isolated and its participation in the well-known acidic cyclization process was established.     

Genlokalisation auf den larvalen speicheldrüsenchromosomen der stechmücke Culex pipiens L.

Zusammenfassung Die Austauschhäufigkeiten zwischen cytologisch bekannten Bruchkontaktpunkten in den larvalen Speicheldrüsenchromosomen und Mutationen erlauben bei der Stechmücke Culex pipiens L. erstmals die Zuordnung von Genorten zu chromosomalen Strukturen oder Abschnitten. Die vorliegenden Kreuzungsergebnisse stimmen mit der bereits bekannten Zuordnung der drei Koppelungsgruppen zu den cytologisch sichtbaren Chromosomen überein.Um Kreuzungsergebnisse innerhalb eines Chromosoms jedoch sicher miteinander in Bezug setzen zu können, mußte das Problem der unterschiedlichen Austauschhäufigkeiten geklärt werden. Gründe dafür sind weder Alter noch Geschlecht, noch kleine chromosomale Aberrationen der heterozygoten Individuen. Die Höhe des Austausches zwischen zwei Faktoren ist jeweils eine Stamm-spezifische Eigenschaft, die vermutlich faktoriell bedingt ist. Dies konnte durch den Vergleich einer allelen Mutation in zwei Stämmen erarbeitet werden. Es sind deshalb nur solche Austauschwerte vergleichbar, die in ein und demselben Stamm gewonnen wurden, oder bei verschiedenen Stämmen, wenn diese in einen festen Bezug gebracht werden können.Im kleinen Chromosom I ist die Zuordnung des Geschlechts-bestimmenden Allelenpaares M bzw. m zu der heteromorphen Bande 10 C 3 in Arm I L durch Austausch-Analyse mit Bruchkontaktpunkten geschlechtsgekoppelter Translokationen bestätigt. Der Locus der Augenfarbmutation w liegt in unmittelbarer Nähe davon. Der Genort der Augenfarbmutation r ist in Arm I R, in Abschnitt 3 B/C gelegen.Im mittellangen Chromosom II werden zwei Genorte eingegrenzt: die Larvenfarbmutation d ist am distalen Ende des Armes II L gelegen; die Augenfarbmutation ru im zentralen Teil des Armes II R, zwischen den Abschnitten 29 A-21 A. Im langen Chromosom III ist der Genort der Männchen-begrenzten Palpenmutation kps dem Arm III L zugeordnet worden.Eine Zuordnung zu einer distinkten Bande oder Struktur war nur für den Geschlechtsfaktor möglich. Mit den vorliegenden Werten wird für Culex pipiens erstmals eine grobe cytologische Genkarte erstellt.

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Gene mapping on the salivary gland chromosomes of the mosquito Culex pipiens L.

Summary Crossing experiments were done with several mutations and aberrant lines of the mosquito Culex pipiens L. Gene loci and chromosomal structure could be correlated by comparing crossover rates of mutations with breakage points of chromosomal aberrations in the larval salivary gland chromosomes. This confirms linkage groups and their correlated chromosomes.Before comparing crossover rates in one chromosome in different experiments, the problem of different crossover rates between two distinct factors should be solved. The reason for these different rates is not sex, age or small chromosomal aberrations in the heterozygous individuals. It could be interstrain behaviour, characteristic for each strain. This was shown by comparing crossover rates of an allelomorph mutation in two different laboratory strains. Therefore, only results within one pure strain or between two strains with known correlation can be compared. In the small chromosome I, the correlation of the sex-determining allelomorphs M and m with the heteromorphic band 10 C 3 in arm I L was confirmed. This was done by crossover analysis of breakpoints in sex-linked aberrations. The locus of the eye colour mutation w is situated near this band. The eye colour mutation r is located in the segment 3 B/C in arm I R.In chromosome II, two gene loci are narrowed down: the larval colour mutation d is situated on the distal end of arm II L, the eye colour mutation ru in the central part of arm II R. In chromosome III, the male-limited mutation kps is located in arm III L.Hitherto only the sex-factor could be correlated which a distinct structure, i.e. the heteromorphic band 10 C 3 in arm I L. The results of the described experiments made it possible for the first time to establish a cytological gene map of Culex pipiens.