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J Bailly

Publications and source records attributed to J Bailly.

At least 37 records · Page 2Linked to original sources
PubMed1991

D19S51 is closely linked with and maps distal to the myotonic dystrophy locus on 19q.

Recent genetic linkage studies have mapped the myotonic dystrophy (DM) locus to 19q13.3. All closely linked DM markers identified to date have been located on the centromeric side of the disease locus, with a relatively large genetic interval (9 cM) observed between the nearest distal marker and DM. We show here that the recently described marker p134C is tightly linked to DM (peak lod score 35.8 at peak recombination fraction .006) and confirm the previous suggestion that the p134C locus, D19S51 maps distal to the disease locus. D19S51 and the closest proximal flanking loci, ERCC1 and D19S115 (pE0.8), define a small genetic interval of less than 2 cM that contains the DM locus.

Chromosome Mapping↗
PubMed1990

Differentiation of F9 embryonal carcinoma cells by synthetic retinoids: amplitude of plasminogen activator production does not depend on retinoid potency or affinity for F9 nuclear retinoic acid receptors.

Retinoic acid and analogues (retinoids) are able to induce the differentiation of F9 murine embryonal carcinoma stem cells into endoderm-like cells. The secretion of plasminogen activator (PA) which accompanies this differentiation is a good index of the biological response of F9 cells to retinoids. We have previously reported that the potency of a series of natural and synthetic retinoids, evaluated by the concentration which provokes half-maximal induction of PA, correlates well with the affinity of these compounds for the endogenous F9 nuclear retinoic acid receptors, but not for the cytosolic retinoic acid binding protein, CRABP. In this paper we show that various retinoids differ, not only in terms of potency, i.e. the dilution at which they are active, but also in terms of the amount of PA that they induce. This parameter, called amplitude, is used to quantify the extent of PA induction by a given retinoid relative to retinoic acid. The amplitude parameters of synthetic retinoids are found to vary over a wide range and are independent of both potency and binding affinity for F9 retinoic acid receptors. It is proposed that the amplitude of the biological response to a given retinoid is the resultant of three factors: (i) the total or partial agonist character of the retinoid; (ii) the binding spectrum of the retinoid for the various types of retinoic acid receptors; (iii) the chemical and metabolic stability of the retinoid in the test system.

Animals↗
PubMed1990

The human ryanodine receptor gene: its mapping to 19q13.1, placement in a chromosome 19 linkage group, and exclusion as the gene causing myotonic dystrophy.

The recent cloning of cDNA encoding the Ca++ release channel (ryanodine receptor) of human sarcoplasmic reticulum has enabled us to use somatic cell hybrids to localize the ryanodine receptor gene (RYR) to the proximal long arm of human chromosome 19. Studies with additional hybrids containing deletions or translocations in chromosome 19 enabled us to localize RYR to 19q13.1 in a region distal to GPI/MAG and proximal to D19S18/DNF11. On the basis that the myotonic dystrophy (DM) locus maps near this region and that myotonia could result from a defect in the ryanodine receptor, we examined the linkage between the DM locus and RYR. Our results, showing several DM-RYR recombinants, rule out an RYR defect as the cause of DM. However, localization of RYR to a region of human chromosome 19 which is syntenic to an area of pig chromosome 6 containing the HAL gene responsible for porcine malignant hyperthermia supports the candidacy of RYR for this disorder.

Blotting, Southern↗
PubMed1988

Effect of diterpene esters on actin cytoskeleton of SV40-transformed keratinocytes is not reproduced by diacylglycerols.

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a disorganization of the actin cytoskeleton and its redistribution at the periphery of the cells in SV40-transformed human keratinocytes. This phenomenon is induced by other diterpene esters, such as 4-O-methyl TPA, 12-O-ethacrynylphorbol-13-acetate (EPA), 12-O-retinoylphorbol-13-acetate (RPA) and mezerein, which exert either convertogenic or promoting effects in skin tumor development in vivo. Two diacylglycerols: oleyl-acetyl glycerol (OAG) and dioctanoyl-glycerol (DOG) do not induce the disorganization of actin. Thus, the effects of these compounds, as they are found in SV40-transformed human keratinocytes, do not exhibit clear-cut correlations to either their protein kinase C activating abilities, or their effects on different stages of multistage carcinogenesis in mouse skin in vivo.

Actins↗
PubMed1988

Effect of CO(2) Concentration on Protein Biosynthesis and Carbonic Anhydrase Expression in Chlamydomonas reinhardtii.

The effect of external inorganic carbon (C(i)) concentrations on protein biosynthesis and carbonic anhydrase (CA) mRNA abundance were examined in the eukaryotic alga Chlamydomonas reinhardtii. Transfer of high CO(2) (5%) grown algae to air levels of CO(2) resulted in the transitory synthesis of two polypeptides of approximately 49,000 and 52,000 daltons as well as prolonged synthesis and accumulation of the 37,000 dalton CA monomer and an unidentified 20,000 dalton polypeptide. The gene coding for carbonic anhydrase was isolated from a genomic expression library and subjected to restriction endonuclease analysis. Southern blot analysis of chromosomal DNA indicates that only a single copy of the gene is present. The 2.5 kilobase DNA fragment hybridizes specifically to a 1.4 kilobase transcript in RNA isolated from air-grown cells and from cells grown on 5% CO(2) that have been exposed to air levels of CO(2). Maximum mRNA abundance was observed after 1 to 3 hours of exposure to air. Transfer of air-grown cells to a high CO(2) environment resulted in the elimination of the CA transcript after 60 minutes of exposure. Changes in CA transcript abundance in response to external C(i) concentrations occurred in the presence or absence of light.

Journal Article↗
PubMed1987

Effects of antiinflammatory agents on edema and DNA synthesis induced by 12-O-tetradecanoylphorbol-13-acetate in the guinea pig.

Inflammation and hyperplasia are frequently associated in skin diseases. In order to verify this relationship, we studied the antagonistic effect of different classes of antiinflammatory agents on the inflammatory and hyperplasiogenic responses elicited by one topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) to the ear of the guinea-pig. Edema and DNA synthesis were chosen as relevant parameters. All antiinflammatory agents tested significantly inhibited DNA synthesis induced by TPA. Moreover, all compounds except quinacrine and phenylbutazone also inhibited edema formation. In conclusion, our results demonstrate that while edema and hyperplasia are frequently associated, this is not always the case.

Animals↗
PubMed1986

Transformation of human keratinocytes by SV40 virus alters their response to the tumor promoter TPA.

Recently, we have shown that transformation of human keratinocytes by SV40 virus induces the re-expression of characters found in fetal epidermis and monostratified epithelia. In the present study, TPA was found to alter some features of the human keratinocyte phenotype in a similar manner to SV40 transformation. Indeed, 12-O-tetradecanoyl-13-phorbol acetate (TPA) treatment induced the expression of cytokeratin no. 8, recognized by the monoclonal antibody TROMA-1, which is present in fetal epidermis and/or monostratified epithelia only, and fibronectin expression. However, TPA and SV40 transformation had specific non-overlapping effects. For example, TPA did not prevent terminal differentiation and stratification, as SV40-transformation did, but stimulated these processes. Moreover, TPA was found to induce additional changes in SV40-transformed keratinocytes. In particular it provoked the individualization of cells within the colonies. This effect was seen as little as 1 h after treatment and was reversible. This cellular alteration was accompanied by the reorganization of actin and by a decrease in the number of desmosomes; these changes were not observed after treatment of normal keratinocytes with TPA. These observations lead to the conclusion that TPA is able to trigger cellular responses which cannot be induced by SV40 products alone, but that TPA and some SV40 products can cooperate to elicit new responses, which could reflect a higher state of malignancy.

Actins↗
PubMed1985

[Congenital superior mesenteric arteriovenous malformations].

An arteriovenous aneurysm in the region supplied by the superior mesenteric artery was detected fortuitously during abdominal arteriography. The absence of a previous history of injury or operation suggested a congenital origin for this infrequently observed lesion. Logical therapy whenever possible is resection of mesentery and the neighbouring intestine.

Arteriovenous Malformations↗
PubMed1984

A keratin of fetal skin is reexpressed in human keratinocytes transformed by SV40 virus or treated with the tumor promoter TPA.

SV40-transformation as well as treatment with tumor promoters produce alterations in morphology, differentiation and keratinization of human keratinocytes. Two cell lines of SV40-transformed keratinocytes and primary cultures of keratinocytes treated with the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) were found to contain an additional protein of 52.5 kD molecular weight (MW). This protein was identified by its reactivity with the monoclonal antibody TROMA-I as being keratin no. 8, a keratin normally present only in simple epithelia. Since this keratin is present in fetal epidermis but disappears gradually when fetal skin becomes multilayered after week 13 of development (Moll et al., Differentiation 23 (1982) 170. [23]), it suggests that SV40 virus and TPA are able to induce in human keratinocytes the reexpression of fetal characters.

Cell Line↗