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Biomedical subjects

V Bourdon

Publications and source records attributed to V Bourdon.

52 records · Page 3Linked to original sources
PubMed1976

[Noradrenaline clearance in human urine].

The urinary clearance for DL-[3H] noradrenaline has been measured in four human subjects. The mean ratio of noradrenaline clearance over glomerular filtration rate was 0.93, the confidence limit for the mean at the 5% level being 0.81-1.06. These results are in perfect agreement with those obtained in dogs with the same experimental procedure. It is concluded that the urinary excretion of noradrenaline is strictly proportional to the glomerular filtration rate.

Female↗
PubMedDate not supplied

Deletion screening by fluorescence in situ hybridization in Rett syndrome patients.

Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene have been found to be a cause of Rett syndrome (RTT). Mutation screening was based on various techniques including denaturing gradient gel electrophoresis, single-strand conformation polymorphism analysis, heteroduplex analysis, DNA sequencing and recently Southern Blot analysis. Mutation detection was achieved in 80% of typical RTT with a high prevalence of recurrent mutations. In order to provide further insights into the spectrum of MECP2 rearrangements in patients without any point mutation or small deletion/insertion in the coding region MECP2 gene, we screened 25 classical RTT females using fluorescence in situ hybridization analysis. No deletion were found in our group, suggesting that MECP2 gross rearrangements are a rare cause of Rett syndrome.

Chromosomal Proteins, Non-Histone↗
PubMedDate not supplied

Purification and characterization of plasma T-kininogen from Wistar and brown Norway rats.

A rapid and convenient three-step purification scheme has been developed for the purification of T-kininogen (alpha 1-cysteine proteinase inhibitor) from rat plasma. The purification process includes chromatography on hydroxyapatite, immunoaffinity chromatography and gel filtration. This procedure is applied to plasma from the brown Norway rat which is known to be deficient in high and low molecular weight kininogens. The method furnished large amounts of T-kininogen from turpentine-treated Wistar rats as well as from untreated and turpentine-treated deficient brown Norway rats. The amino acid and hexose content of the three T-kininogens has been determined. While the composition of the molecules isolated from both injured rats was similar, the neutral sugar content of T-kininogen purified from untreated brown Norway rats was lower and its amino acid composition showed slight differences. The three molecules have identical behaviour and similar physicochemical and immunological properties when analysed by SDS electrophoresis, isoelectrofocusing and two-dimensional immunoelectrophoresis.

Amino Acids↗
PubMedDate not supplied

The release of glandular kallikrein from submaxillary glands of rats exposed to heat.

The salivary flow elicited by phenylephrine was reduced in kininogen-deficient rats or by pretreatment of normal Wistar rats with HOE 140, a bradykinin antagonist. Salivary flow induced by substance P was similar in normal and kininogen-deficient rats. Phenylephrine released large amounts of kallikrein in saliva. Isoproterenol was less active while pilocarpine and substance P induced a small secretion of kallikrein. The saliva produced by anaesthetized rats in response to heat stress contained low levels of kallikrein. However a large depletion of the kallikrein content of submaxillary glands was observed in awake animals exposed to 36 degrees C and 40 degrees C for one hour. This depletion was suppressed by prazosin administered with a beta-adrenergic antagonist. Administered alone, these drugs had no effect, whereas atropine increased the depletion. The presence of kallikrein was observed in the oedema fluid which developed around the submaxillary glands in rats pretreated with atropine or exposed to 40 degrees C. A consumption of plasma kininogens occurred during heat exposure. The reflex-induced release of kallikrein during heat exposure is mainly controlled by sympathetic nerves through activation of both alpha and beta-adrenoreceptors. This release induces the formation of kinins which participate to the thermolytic salivation.

Animals↗