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Biomedical subjects

G Brun

Publications and source records attributed to G Brun.

At least 91 records · Page 5Linked to original sources
PubMed1984

An enzyme-linked immunosorbent assay for the detection of complement components on red blood cells.

A new technic using the principle of enzyme-linked immunoassay (ELISA) has been developed for the detection of complement components on red blood cells sensitized in vivo or in vitro. Using a double-antibody technic, anticomplement antisera (anti-C3c or anti-C3c/C3d) produced in rabbits was incubated with the red blood cells, followed by incubation with antirabbit alkaline phosphatase conjugated antiglobulin. The amount of the enzyme fixed was measured spectrophotometrically by the enzymatic hydrolysis of the substrate PNPP. A calibration curve was made from red blood cells on which complement was deposited by the method of Fruitstone . The technic showed a greater sensitivity than the standard antiglobulin tests and allowed simultaneous qualitative and semiquantitative estimates. The technic can be performed in any laboratory equipped with the standard equipment found in a blood bank, including a spectrophotometer. The authors made a modification of Alsever 's solution, which allowed the safe and stable preservation of complement coated red blood cells for 15 days. Significant positive results were obtained clinically using this technic, while negative or weakly positive reactions were obtained by the conventional antiglobulin tests.

Animals↗
PubMed1984

[Mucoid peritonitis. Apropos of 2 case reports. Review of the literature].

From two cases of pseudomyxoma peritonei of ovarian origin, the authors review the subject and emphasize the rarity of this condition. The diagnosis is simple once the decision to operate is made. Treatment, however, is disappointing because of recurrences. The pathogenesis is not well understood, and further studies are warranted of this condition by histochemists and physiologists to better understand the secreting mechanisms causing the ascites and methods to control it. Mortality is principally related to mechanical complications due to ascites and the characteristics of the groups of secretory cells.

Adenocarcinoma, Mucinous↗
PubMed1984

[External genital endometriosis. Endemiologic, diagnostic, therapeutic and prognostic aspects].

189 cases were selected, representing 26 admissions per 1 000. From their analysis of the case files, the authors conclude that the development of endometriosis does not need any specific anatomical or hormonal condition and that it is difficult to determine the role of endometriosis and associated lesions in the production of symptoms. The responsibility of endometriosis in sterility has not been always, even in cases with frank lesions. The treatment is aimed at eradicating the lesions which should be followed up with laparoscopy.

Adolescent↗
PubMed1984

[Swyer syndrome. Apropos of a new case of pure gonadal dysgenesis with Karyotype 46 XY].

The authors describe a case they have personally seen of pure gonadal dysgenesis with caryotype 46 XY (Swyers' syndrome) in which they found absence of HY antigen. They analysed the descriptions in the literature about this syndrome and show how this antigen is responsible for testicular differentiation. They show the place this syndrome has in the group of syndromes of bands and once again draw attention that there is a great risk of gonadoblastoma development when the Y chromosome is present and especially when the HY antigen is present. This means that these dysgenetic gonads should be removed surgically.

Adolescent↗
PubMed1983

Nongenetic complementation in VSV: asymmetric contribution of the L proteins of each parent in the rescue of group I ts mutants.

Complementation group I temperature-sensitive mutants of vesicular stomatitis virus (VSV) are rescued at nonpermissive temperature by UV-irradiated virus. Rescue is a nongenetic process mediated by the structural L protein molecules of the parental irradiated virus. This is shown by action spectra analysis (V. Deutsch, B. Muel, and G. Brun (1977), Virology 77, 294-305), efficiency of rescue at doses high enough to inactivate every gene I, and rescue by irradiated defective-interfering short particles. Viral molecular synthesis at 39.6 degrees using the ts genomes as templates and stimulated by UV-irradiated virus is shown by gel electrophoresis of rescued virion proteins. Parental strain ts 053(I) is thermolabile in vitro while the thermostability of the rescued virions, genetically characterized as ts group I virus, is identical to that of helper wt or ts+ revertant. This suggests that some parental Lwt molecules are reincorporated in the rescued virions, together with newly synthesized Lts molecules. Efficiency variation of the rescue as a function of the multiplicity of infection of the UV-irradiated virions depends on the m.o.i. of the unirradiated ts I mutants. This result suggests that rescue depends on the concentration of the helper L molecules and also of that of the L initially bound to the ts template. That L of both parents contribute to rescue is supported by the observations that (1) rescue by UV-wt is strongly diminished after in vitro heating of thermolabile ts O53(I). (2) Intragenic rescue can be demonstrated: The helper activity of a given UV-ts I mutant is different according to the unirradiated ts I mutant used; the activity of helper L associated with different templates in intragenic heterologous combinations is higher or lower than its activity in the homologous combination (self-rescue control), instead of being equal as expected. (3) Efficiency of rescue by UV-wt also varies according to the ts I mutant. The initially bound Lts seems therefore to play a role important and different from that of the helper L. Contribution of both parent L to rescue seems thus to be qualitatively different.

Animals↗
PubMed1983

Interrelationships in mice of antipyrine half-life, hepatic monooxygenase activities and liver S9-mediated mutagenicity of aflatoxin B1, benzo[alpha]pyrene 7,8-dihydrodiol, 2-acetylaminofluorene and N-nitrosomorpholine.

To evaluate the predictive value of serum antipyrine half-life AP(T1/2) as an index of hepatic carcinogen metabolism, groups of C57BL/6 and DBA/2 mice were treated with various inducers and inhibitors of cytochrome P-450-dependent monooxygenases (pregnenolone-16 alpha-carbonitrile (PCN), phenobarbital (PB), 5,6-benzoflavone (5,6-BF), 3-methylcholanthrene (MC), disulfiram (DIS), 7,8-BF). Groups of mice were also given ethanol (3% in drinking water) for 12 days. Within each group, mean serum AP-(T1/2) was compared with (i) the in vitro activity of hepatic microsomal benzo[alpha]pyrene (BP) 3-hydroxylase, 2-acetylaminofluorene (AAF)-N-hydroxylase and aldrin monooxygenase, and (ii) the liver S9-mediated mutagenicity of aflatoxin B1 (AFB), trans-7,8-dihydro-7,8-dihydroxybenzo[alpha]pyrene (BP 7,8-diol), 2-acetylaminofluorene and N-nitrosomorpholine (NMOR) in Salmonella typhimurium strains. Serum AP(T1/2) was only correlated negatively with the activity of BP 3-hydroxylase (P less than 0.001) and aldrin monooxygenase (P less than 0.001). No statistically significant correlation was found between serum AP(T1/2) and liver S9-mediated mutagenicity for any of the four carcinogens. On the basis of these results, we conclude that serum AP(T1/2) may not be a reliable index of the capacity of liver to convert carcinogens into reactive intermediates.

2-Acetylaminofluorene↗
PubMed1983

Quantitative comparison of carcinogenicity, mutagenicity and electrophilicity of 10 direct-acting alkylating agents and of the initial O6:7-alkylguanine ratio in DNA with carcinogenic potency in rodents.

The quantitative relationship between carcinogenicity in rodents and mutagenicity in Salmonella typhimurium was examined, by using 10 monofunctional alkylating agents, including N-nitrosamides, alkyl methanesulfonates, epoxides, beta-propiolactone and 1,3-propane sultone. The compounds were assayed for mutagenicity in two S. typhimurium strains (TA1535 and TA100) and in plate and liquid assays. The mutagenic activity of the agents was compared with their alkylating activity towards 4-(4'-nitrobenzyl)pyridine and with their half-lives (solvolysis constants) in an aqueous medium. No correlations between these variables were found, nor was mutagenic activity correlated with estimates of carcinogenicity in rodents. There was a positive relationship between carcinogenicity and the initial ratios of 7-:O6-alkylguanine formed or expected after their reaction with double-stranded DNA in vitro. The results suggest that alkylation of guanine at position O6 (or at other O atoms of DNA bases) may be a critical DNA-base modification that determines the overall carcinogenicity of these alkylating agents in rodents.

Alkylating Agents↗
PubMed1983

Hydroxylation and nitroreduction are required to activate dimethylnitramine into alkylating and mutagenic agents.

Dimethylnitramine (DMNO) was shown to undergo hydroxylation in the presence of 9000 g supernatant from rat liver (S9) to yield hydroxymethyl-methylnitramine (OH-MNO). OH-MNO displayed a 100-fold higher mutagenic activity in Salmonella typhimurium TA100 strain than DMNO, when compared on a molar basis. The mutagenicity of DMNO in TA100 strain in the presence of S9 paralleled the production of OH-MNO. Acetoxymethyl-methylnitramine (Ac-MNO) and methylnitramine (MNO), two synthetic derivatives of DMNO, were also investigated. Ac-MNO was found to be mutagenic in TA100 strain only in the presence of S9, probably through the release of OH-MNO catalysed by esterase(s); under similar conditions, MNO showed no mutagenicity or toxicity to TA100 strain. OH-MNO showed no alkylating activity towards nicotinamide. These findings implicate OH-MNO as a proximate mutagenic metabolite of DMNO. DMNO and Ac-MNO were found to be more mutagenic in a nitroreductase(s)-proficient (TA100) than in a deficient (TA100 NR) strain. After reduction of OH-MNO with Zn/NH4Cl, it yielded an agent(s) which alkylated nicotinamide. The latter results imply a reduction of the nitro group in OH-MNO to yield a hydroxylamino derivative as the ultimate (or penultimate) mutagenic metabolite. The enzymes and reactive intermediates that may be involved in the activation of DMNO are discussed.

Alkylating Agents↗
PubMed1983

Studies on the efficiency of the Salmonella/rat hepatocyte assay for the detection of carcinogens as mutagens: activation of 1,2-dimethyl-hydrazine and procarbazine into bacterial mutagens.

Aflatoxin B1, benzo[a]pyrene, N-nitrosomorpholine, procarbazine (PC) and 1,2-dimethylhydrazine (DMH) were used to investigate the efficiency of the Salmonella/rat hepatocyte assay for detecting carcinogens as mutagens. In this assay, bacteria and the test compound were co-incubated with freshly isolated rat hepatocytes and then plated onto minimal glucose agar. Factors for optimal mutagenicity, including the number of hepatocytes and the number of bacteria, the type of assay medium and the length of incubation in liquid medium were investigated. All the compounds were metabolized into bacterial mutagens. Mediation of the mutagenicity of PC and DMH by rat hepatocytes indicates that freshly isolated cells of this type are a useful alternative metabolic activation system for use in screening chemicals found to be non-mutagenic in the Salmonella/microsome assay.

1,2-Dimethylhydrazine↗
PubMed1982

Quantitative comparisons between carcinogenicity, mutagenicity and electrophilicity of direct-acting N-nitroso compounds and other alkylating agents.

The quantitative relationship between carcinogenicity in rodents and mutagenicity in S. typhimurium was examined using 10 monofunctional alkylating agents, including N-nitrosamides, alkylmethane sulfonates and epoxides. The compounds were assayed for mutagenicity in two S. typhimurium strains (TA1535, TA100) and in plate and liquid assays. Mutagenic activity was compared with alkylating activity, half-life (solvolysis constant) and carcinogenic activity in rodents (TD50). No correlations between these variables were found. However, there was a good positive relationship between the TD50 values of the carcinogens and the initial ratios of N-7-alkylguanine to 0(6)-alkylguanine formed after reaction with double-stranded DNA in vitro (r = 0.88, p less than 0.01; n = 9). From these results, it is concluded that the N-7/0(6)-alkylguanine ratio is quantitatively related to the carcinogenic activity for this class of compounds and it may therefore be used to predict the carcinogenic potency of new compounds within this class.

Alkylating Agents↗
PubMed1982

Inhibition by specific antibodies of the mutagenicity of aflatoxin B1 in bacteria.

Two anti-aflatoxin B1 antisera, antiserum 'O' and antiserum 'C', were raised against conjugates in which the bovine serum albumin protein carrier was coupled to aflatoxin B1 derivatives at carbon 1 or 8. Their action was investigated in Salmonella thyphimurium assays using a fortified 9000 x g supernatant (S9) of rat liver homogenate or using rat hepatocytes as the metabolic activation system. In all cases, a substantial reduction in mutagenicity was observed: the mutagenicity caused by 12.5 ng aflatoxin B1 was inhibited by 50% with 2 microliters of antiserum 'O' and with 12 microliters of antiserum 'C' when activation was catalysed by rat liver supernatant; the mutagenicity of 3.31 micrograms aflatoxin B1 was inhibited by 50% with 25 microliters of antiserum 'O' in experiments using hepatocytes as the metabolic activation system. Several lines of evidence indicate that the inhibition is caused by specific antibodies. The molar ratios of aflatoxin B2 or aflatoxin G2 to aflatoxin B1 required to reduce by 50% the effect of antisera on aflatoxin B1 mutagenicity were 2.9-76-fold higher than those required to reduce by 50% the tracer antibody binding in radioimmunoassay. Possible mechanisms by which anti-aflatoxin B1 antisera inhibit aflatoxin B1 mutagenicity are discussed.

Aflatoxin B1↗
PubMed1982

Mutagenic and alkylating activities of 3-methyl-1-phenyltriazenes and their possible role as carcinogenic metabolites of the parent dimethyl compounds.

3-Methyl-1-phenyltriazene and a series of ring-substituted derivatives (4-methylphenyl, 4-chlorophenyl, and 2,4,6-trichlorophenyl), structurally related benzenediazonium fluoborates and phenyl azides, as well as the recently isolated [1-methyl-3-(2,4,6-trichlorophenyl)-2-triazeno]methyl-beta-D-glucopyranoside uronic acid, were studied for their mutagenic activity in Salmonella typhimurium strains. Of these compounds, the 3-methyl-1-phenyltriazene derivatives and 2,4,6-trichlorobenzenediazonium fluoborate were found to be direct-acting mutagens; the glucuronide was active in strain TA 1530 only after deconjugation with beta-glucuronidase. The half-lives of the monomethylphenyltriazenes in vitro were determined and compared with their methylating activity towards 4-(4-nitrobenzyl)pyridine and their mutagenicity. The results are discussed in relation to the possible mechanism of action of the N,N-dimethylphenyltriazenes and their monomethyl derivatives as mutagens and organ-specific carcinogens.

Alkylating Agents↗
PubMed1982

C3b inactivator deficiency with immune complex manifestations.

We report a complete C3b inactivator deficiency in a 28-year-old patient referred for bronchiectasis and recurrent pneumonia. In addition to these recurrent infections, previously described with this deficiency, he also had several immune complex manifestations (rheumatoid factor, circulating immune complexes and one episode of serum sickness). The consequences of C3b inactivator deficiency on complement activation, chemotaxis and opsonization, clearance of immune complexes, and on red blood cell sensitization are discussed. The study of the parents showed an autosomal dominant transmission.

Adult↗
PubMed1981

Effect of glutathione and uridine 5'-diphosphoglucuronic acid on mutagenesis by benzo[a]pyrene and aflatoxin B1 in the Salmonella/microsome assay.

In the Salmonella/microsome plate or liquid assay, the addition of glutathione (GSH) and uridine 5'-diphosphoglucuronic acid (UDPGA), both cofactors for GSH-S-transferases or UDPGA-transferases, altered the rat-liver microsome-mediated mutagenesis of benzo[a]pyrene (BP) and aflatoxin B1 (AFB). With either BP or AFB, an increased, unchanged or decreased number of revertant colonies of S. typhimurium was observed, depending on the substrate concentration, the source of rat-liver 9000 X g supernatant (S9), the time of incubation and the type of mutagenicity test (liquid or plate assay). Several factors responsible for quantitative changes in the pattern of BP and AFB metabolites under various assay conditions in vitro, which alter the overall mutagenic activity of the parent compound, are discussed.

Aflatoxins↗
PubMed1981

DNA topoisomerase I from mitochondria of Xenopus laevis oocytes.

Activity of DNA topoisomerase I has been characterized in extracts of mitochondria purified from Xenopus laevis oocytes. Several lines of evidence have been obtained for the intramitochondrial localization of the enzyme. The mitochondria-associated of DNA topoisomerase I represents 1% of the activity recovered from a total ovary population of oocytes. The enzymes has been purified by DEAE-cellulose, phosphocellulose and double-stranded DNA cellulose chromatography and its properties compared to those of its nuclear-cytosolic counterpart purified by the same purification steps. Both enzymes appear to possess very similar if not identical physico-chemical and catalytic properties. Neither enzyme shows DNA gyrase activity and they are both equally sensitive towards trypanocide drugs such as ethidium bromide and berenil. The mitochondrial enzyme is able to remove positive superhelical turns and possibly acts as a swivelase during replication of mitochondrial DNA. These results confirm the pioneering work of Fairfield et al. (1979, J Biol. Chem. 254, 9354) on the presence of a DNA topoisomerase I in mitochondria. However our results support the conclusion that in Xenopus laevis oocytes the mitochondrial and nuclear cytosolic DNA topoisomerase I are in all likelihood one and the same enzyme.

Animals↗
PubMed1981

Child psychiatric advice to legal authorities concerning custody and post-divorce visiting rights. Results of collaboration of lawyers and child psychiatrists over a 2-year period.

The need of the judicial system for psychiatric and psychological examination of parents and children prior to decisions concerning custody and visiting rights is illustrated. Further, the possibility of establishing collaboration with legal authorities is discussed. Most child psychiatric and child psychological clinics in Denmark declared themselves willing to take part in the investigation carried out during 1975 and 1976. Within this period the legal authorities referred 232 cases. The indication for expert advice is discussed. Our suspicion that the parties in these selected cases often were suffering from serious mental disorders was confirmed. The difficulties of evaluating the child's views are described. The authors conclude that it is impossible to fix a lower limit for the age at which children are to be heard in court. The legal decision usually accorded with the conclusion drawn from the statement. The investigation resulted in the establishment of a more permanent collaboration of lawyers and psychiatric examiners with regard to custody and visiting rights.

Adolescent↗