Biomedical subjects

J Salles

Publications and source records attributed to J Salles.

9 recordsLinked to original sources

PubMed2005

Environmental tobacco smoke exposure in public places of European cities.

BACKGROUND: Exposure to environmental tobacco smoke (ETS) has important public health implications. The results of the first European multi-centre study that measured ETS exposure in a range of public places (transport, educational settings, and leisure facilities such as bars and restaurants) are presented. METHOD: Nicotine vapour phase was measured using ETS passive samplers containing a filter treated with sodium bisulfate. RESULTS: Bars and discos are the places with the highest concentrations of nicotine from ETS, median ranging from 19 to 122 microg/m(3). Restaurants had the next highest values. Concentrations of nicotine generally range from 0.1-5 microg/m(3) in airports, and from 0.5-10 microg/m(3) in train stations. Nicotine was also found in schools and universities, yet schools tended to have the lowest concentrations compared to all the other public places sampled. In hospitals levels were generally below 5 microg/m(3). CONCLUSIONS: Although there is some variability between cities, this study shows that tobacco smoke is present in most of the studied public places. The study also showed that in areas where smoking is prohibited, concentrations of nicotine are lower than in areas where smoking is allowed but they are not zero. The results of this study indicate that policies should be implemented that would effectively reduce levels of tobacco smoke in public areas.

Air Pollutants↗

PubMed2001

The homeotic protein dlk is expressed during peripheral nerve development.

To investigate the molecular events controlling myelination of the peripheral nervous system, we compared gene expression of normal mouse sciatic nerves to that of the trembler mouse, whose Schwann cells are blocked in a pre-myelinating phenotype. Using cDNA array, we assessed expression levels of 1176 genes, and we found that delta-like protein (dlk), an epidermal growth factor-like homeotic protein, was expressed in the normal developing nerves, but at a low level in the dysmyelinating mutant trembler. Moreover, dlk expression was down-regulated when myelin protein expression was up-regulated, and no expression was observed in the developing brain. These results suggest that dlk expression is required for Schwann cell acquisition of the myelinating phenotype.

Animals↗

PubMed2000

Peroxisomal beta-oxidation enzyme gene expression in the developing mouse brain.

Using the northern blot technique, the steady-state levels for the mRNAs encoding acyl-CoA oxidase, pristanoyl-CoA oxidase, trans2, 3enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase multifunctional enzyme type 2, 3-ketoacyl-CoA thiolase and sterol-carrier-protein x during postnatal brain development were measured. The developmental patterns obtained for each mRNA species studied were similar, with an increase in the mRNA level between birth and postnatal day 5, followed by a gradual decrease to 34-55% of the maximal value at postnatal day 30. These results are in agreement with a coordinately controlled expression of the genes involved in VLCFA beta-oxidation during brain development. Moreover, comparison of these developmental profiles with that obtained for ceramide galactosyltransferase showed that the set-up of the very-long-chain fatty acids beta-oxidation system is independent of the myelinating signal in the central nervous system.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1999

Gene expression of peroxisomal beta-oxidation enzymes in rat brain.

Despite increasing insight into peroxisomal beta-oxidation, it is still not clear which enzymes catalyze very-long-chain fatty acid degradation. Using the northern blot and RT-PCR techniques, a brain-specific expression is demonstrated for acyl-CoA oxidase 3II mRNA, thiolase-A and trans2,3enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase multifunctional enzyme type 2.

17-Hydroxysteroid Dehydrogenases↗

PubMed1999

High metabolism and subsequent elongation of 3-hydroxyeicosanoyl-CoA in very-long-chain fatty acid deficient PNS of Trembler mice.

The developmental patterns of the overall fatty acid elongation and of the last two partial activities of microsomal elongase (dehydration and reduction of 3-hydroxyacyl-CoA) were investigated in the PNS of normal and Trembler mice. Unexpectedly, Trembler microsomes synthesized normal C22-CoA amounts from 3-hydroxyeicosanoyl-CoA (3-OHC20-CoA), a C18-CoA elongation intermediate. Hydroxy- acyl-CoA dehydrase and enoyl-CoA reductase activities were found to be higher in the mutant than in the control, whatever the stage of development. Moreover, C20-CoA elongation led to normal C22-CoA and C24-CoA formation in the mutant whereas C20-CoA formation from C18-CoA was always far lower in Trembler than in control. C18-CoA condensing enzyme emerges as the only elongation step involved in the VLCFA deficit evidenced in Trembler PNS.

Acyl Coenzyme A↗

PubMed1999

Trembler as a mouse model of CMT1A?

The Trembler mouse suffers from a dominantly inherited autosomal mutation that results in an abnormal myelination of the peripheral nervous system. Biochemical studies have shown that dysmyelination is the primary event, demyelination being a late-occurring process. The expression of myelin protein genes has been studied. The steady-state levels for PMP22 mRNA represent 10 and 5% of normal values in the nerves of heterozygous and homozygous Trembler, respectively. This is due to a reduced expression of the specific transcript driven by the promoter 1 of the PMP22 gene. Collective results indicate that Trembler dysmyelination is not necessarily the consequence of a large accumulation of the mutated PMP22 protein. Moreover, it appears that the situation in the Trembler is different from that encountered in most CMT1A patients, where an increased PMP22 gene dosage is responsible for the disease. Therefore, the Trembler mutant is perhaps not an ideal model for this human neuropathy.

Animals↗

PubMed1999

Hydroxyacyl-CoA dehydrase and trans-2,3-enoyl-CoA reductase activities are consistent with long-chain fatty acid accumulation during rat brain development.

The developmental changes of microsomal 3-hydroxyacyl-CoA dehydrase and trans-2,3-enoyl-CoA reductase activities were analyzed and compared to very-long-chain fatty acid content and biosynthesis in rat brain. Contrary to the elongation rate of eicosanoyl-CoA and 3-hydroxyeicosanoyl-CoA, which paralleled myelination during brain maturation, the two partial activities of fatty acid elongation were already present at the earliest stages of development. One day after birth, 3-hydroxyacyl-CoA dehydrase and trans-2,3-enoyl-CoA reductase specific activities already represented 54.8% and 49.6% of the adult values, respectively. As a contribution to the quantitative estimation of the brain's ability to form its own VLCFA, it is shown that dehydrase and reductase activities are sufficient to allow the biosynthesis of all rat brain VLCFA at any age.

Acyl-CoA Dehydrogenases↗

PubMed1996

The prevalence of anthelmintic resistance in nematode parasites of sheep in southern Latin America: Uruguay.

This survey was conducted on 252 farms randomly distributed over all the sheep raising areas in Uruguay. The study involved farms with more than 600 sheep, which represented 80% of the total sheep population of the country. Three anthelmintic groups were assessed, namely, benzimidazoles, levamisole and avermectins. Overall, the results showed 80% of sheep flocks had benzimidazole resistance, 71% had resistance to levamisole, and 1.2% of flocks showed resistance to avermectins. Approximately 28% of farms had resistance to one anthelmintic group, 64% to two anthelmintic groups, and 1% resistance to all three groups. Only 7.5% of farms had no detectable levels of anthelmintic resistance. More than 80% of farms had Trichostrongylus populations resistant to both benzimidazoles and levamisole. Resistance was recorded in all three anthelmintic groups for Haemonchus and resistance also occurred to benzimidazoles and levamisole in Ostertagia.

Agriculture↗

PubMedDate not supplied

Triclabendazole biotransformation and comparative diffusion of the parent drug and its oxidized metabolites into Fasciola hepatica.

Triclabendazole (TCBZ) is an halogenated trematodicidal benzimidazole compound extensively used in veterinary medicine. It is active against immature and adult stages of the liver fluke Fasciola hepatica. Free and conjugated TCBZ metabolites have been identified in the bile of treated sheep. The experimental aims were to characterize the in vitro patterns of TCBZ biotransformation both in the animal host (sheep liver microsomes) and target parasite (F. hepatica microsomal preparation); and to compare the ex vivo diffusion of TCBZ parent drug and its oxidized metabolites (TCBZ sulphoxide [TCBZSO], TCBZ sulphone [TCBZSO2], and TCBZ-hydroxy derivatives) into F. hepatica. Additionally, the octanol-water partition coefficients for TCBZ and all its metabolites were estimated as an indicator of the relationship between drug lipophilicity and diffusion into the target parasite. Drug/metabolites concentrations were quantified by HPLC after sample clean up and a solvent-mediated chemical extraction. Sheep liver microsomes metabolized TCBZ into its sulphoxide and sulphone metabolites after 30 min of incubation. The rate of TCBZ sulphoxidation in the liver was significantly greater (p < 0.01) than that observed for the sulphonation of TCBZSO. The trematode parasite oxidized TCBZ into its sulphoxide metabolite after 60 min of incubation at a metabolic rate of 0.09 nmol min(-1) mg protein(-1). TCBZ and all its oxidized metabolic products were recovered from F. hepatica as early as 15 min after their ex vivo incubation in a Kreb's Ringer Tris buffer. However, the diffusion of the hydroxy-derivatives into the fluke was lower than that observed for TCBZ, TCBZSO and TCBZSO2. There was a high correlation (r=0.82) between drug lipophilicity (expressed as octanol-water partition coefficients) and drug availability measured within the parasite. Unlike the uptake pattern previously observed for albendazole, the parent TCBZ and its sulphoxide and sulphone metabolites showed a similar ability to penetrate into the trematode parasite. Understanding the relationship between TCBZ metabolism, the relative pharmacological potency of its metabolic products and their ability to reach the target parasite may be critical to optimize its flukicidal activity, particularly when TCBZ resistant flukes have been already isolated in the field.

Animals↗