Publications by authors named "HEBERT E"

Some reactive textile dyes are used for years as biomimetic ligands in protein purification. The reluctance to use these performant systems in large scale for therapeutically applicable proteins is related with the possible dye leakage and consequently with problems of contamination. Therefore, toxicology data are necessary to quantify the level of danger in association with sensitive assays.

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The increase in galectin-3 lectin content observed in tumours or in in vitro transformed cells suggests that this lectin is important in the transformation process. In the present study, we investigated the mRNA expression level of the galectin-3, galectin-1 and macrophage mannose receptor in normal and ras-transformed NIH 3T3 cells in relation to their transformation state. The galectin-3 mRNA content in ras-transformed cells is increased in fully transformed cells, with a maximum in ras-transformed cells that have lost their growth anchorage-dependence.

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Phospholipids of optic nerve (n = 30) from 5.6-kg rabbits were analyzed by 31P nuclear magnetic resonance (NMR) spectroscopy. Phospholipid metabolites detected were as follows (mol %): phosphatidylcholine (PC; 25.

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It is now well established that malignant transformation of eucaryotic cells is concomitant with typical alterations of glycosylation and the expression pattern of endogenous lectins. In parallel, oncogene transfection studies revealed a correlation between the expression of some of these genes, the transformed state and perhaps metastasis. These observations lead to the idea that oncogenes may control the expression of enzymes involved in the biosynthetic pathway of cell membrane glycoconjugates and the expression of endogenous lectins.

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Foci of transformed NIH3T3 cells were observed after transfection of plasmids containing the c-Ha-ras-1 protooncogene modified in vitro either with the 3-N,N-acetoxyacetyl derivative (N-AcO-AGlu-P-3) of the mutagenic L-glutamic acid pyrolysis product 3-amino-4,6-dimethyldipyrido-[1,2-a:3',2'-d]imidazole (Glu-P-3) or with 1'-acetoxysafrole (AcO-S), a reactive derivative of the carcinogen safrole. DNA isolated from these foci were used in a second round of transfection, and the DNA obtained from the secondary transformants was analysed to determine the nature of mutations responsible for activating the protooncogene. The polymerase chain reaction method was used to amplify sequences of the gene likely to contain activating mutations, and these regions were then subjected to selective hybridization with specific oligonucleotides to locate and identify the point mutations.

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Improvements in technology have dramatically increased the survival of children with spinal dysraphism. Because this complex condition affects multiple organ systems as well as the psychosocial functioning of the child and family, these children require care from a host of specialists in order to achieve optimum functioning. This article reviews the pathophysiology and discusses the current management of the medical and psychosocial effects of spinal dysraphism.

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The mutation frequency and mutation spectrum resulting from 3-N-acetylamino-4,6-dimethyldipyrido[1,2-a:3',2'-d]imidazole (AGluP3) DNA adducts using a previously developed forward mutation assay were established. AGluP3-induced mutagenesis requires the umuC gene product(s) and exhibits similar amounts of base pair substitution and frameshift mutation. Comparison between these results and those obtained with the isosteric amine 2-N-acetylaminofluorene suggests the involvement of deacetylated adduct in the molecular mechanisms of AGluP3-induced mutagenesis.

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The reactivity of nucleic acids in various conformations and two isosteric chemical carcinogens 2-N,N-acetoxyacetylaminofluorene (N-AcO-AAF) and 3-N,N-acetoxyacetylamino-4,6-dimethyldipyrido [1,2-a:3',2'-d] imidazole (N-AcO-AGlu-P-3) have been studied. Both carcinogens bind covalently to poly(dG-dC).poly(dG-dC) (B form) and to poly(dG-br5C).

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Both the initial velocity and the overall methylation of DNA modified by acetylamino-4,6-dimethyldipyrido(1,2-a:3',2'-d)imidazole (A-Glu-P-3) by rat liver DNA-(cytosine-5-)-methyltransferase are decreased as compared to native DNA. A-Glu-P-3 bound to guanine residues may block the movement of the enzyme along the helix. The modified DNA does not inhibit the enzymatic methylation of native DNA.

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Antibodies to N-(guanosin-8-yl)-3-N-acetylamino-4,6-dimethyldipyrido(1,2-a :3',2'-d)imidazole were elicited in rabbits by immunization with a conjugate formed between this compound and bovine serum albumin. The specificity of the antibodies was studied by radioimmunoassay. These antibodies were used to titrate the adducts formed in liver DNA of rats treated with 3-N-acetyl-hydroxyamino-4,6-dimethyldipyrido(1,2-a:3',2'-d)imidazo le,p6 a supposed metabolite of the mutagenic amine 3-amino-4,6-dimethyldipyrido(1,2-a:3',2'-d)imidazole (Glu-P-3).

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3-Amino-4,6-dimethyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-3), an analog amine of the potent genotoxic Glu-P-1 isolated from a glutamic acid pyrolysate, has been chemically synthesized. Glu-P-3 was found much more mutagenic than Glu-P-1 to S. typhimurium TA 98 and TA 100 with S-9 mix.

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The conformation of synthetic or natural DNAs modified in vitro by covalent binding of N-AcO-A-Glu-P-3 was investigated by fluorescence and circular dichroism. In all cases, substitution occurs mainly on the C8 of guanine residues. In modified poly(dG-dC).

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The study of the recovery cycle of the H reflex of the soleus, in constant pool, was made on 88 normal men of different ages. The recurrent inhibition has been demonstrated in most of the adults and elderly subjects. In young children, there were powerful inhibitory mechanisms, among which the Renshaw inhibition can be isolated.

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