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F Arnault

Publications and source records attributed to F Arnault.

7 recordsLinked to original sources
PubMed1998

Cloning, sequencing and structural analysis of 976 base pairs of the promoter sequence for the rat lipoprotein lipase gene. Comparison with the mouse and human sequences.

We cloned and sequenced the -976bp promoter of the rat lipoprotein lipase LPL gene. The sequence was compared with the mouse and human sequences. The homology between the rat and mouse LPL nucleotide sequences was not quite as strong in the promoter sequence as in the coding sequence. Among the 976nt promoter there were 118 divergences, i.e. 11.8%, compared to only 5.6% for the LPL coding region. However, within the 200nt immediately 5' to the transcriptional start site (proximal promoter), the divergence was only 4%. New potential cis-elements (such as CACCC, GATA, GC and GA boxes, IRS, Krox, MEF 2, E-box, CCArGG and 1/2 VDRE) were identified in the rat, mouse or human LPL gene.

Animals↗
PubMed1996

Human lipoprotein lipase last exon is not translated, in contrast to lower vertebrates.

We have sequenced the first fish (zebrafish, Brachydanio rerio) lipoprotein lipase (LPL) cDNA clone. Similarities were found in mammalian LPL cDNA, but the codon spanning the last two exons (which is thus split by the last intron) is AGA (Arg) as opposed to TGA in mammals. Exon 10 is thus partially translated. These results were confirmed with rainbow trout (Oncorhynchus mykiss). We also investigated whether mammal TGA coded for selenocystein (SeCys), the 21st amino acid, but found that this was not the case: TGA does not encode SeCys but is a stop codon. It thus appears that the sense codon AGA (fish) has been transformed into a stop codon TGA (human) during the course of evolution. It remains to be determined if the "loss" of the C-terminal end of mammalian LPL protein has conferred an advantage in terms of LPL activity or, on the contrary, a disadvantage (e.g., susceptibility to diabetes or atherosclerosis).

Animals↗
PubMed1995

Comparison of the cDNA and amino acid sequences of lipoprotein lipase in eight species.

By aligning nucleotide and amino acid sequences of lipoprotein lipase in eight species (man, pig, cow, sheep, mouse, rat, guinea-pig and chicken), we found that the main domains (catalytic, N-glycosylation and putative heparin binding sites) are well conserved. The longest identical amino acid chain was encoded by a sequence between the end of exon 2 and the beginning of exon 3, emphasizing the importance of this region which encodes the beta 5-loop of the active site, among other domains. Exon 10 is entirely untranslated in the seven mammals studied here and contains species-characteristic deletions, insertions or elements rich in A or A + T. In chicken, the beginning of exon 10 is translated. These eight previously unreported alignments could be a useful tool for further studies on LPL function.

Amino Acid Sequence↗
PubMed1995

Homozygous deletion of exon 9 causes lipoprotein lipase deficiency: possible intron-Alu recombination.

We studied a homozygous deletion in the lipoprotein lipase gene at the molecular level. Comprising the end of intron 8, the whole of exon 9, and about two-thirds of intron 9, this 2.136-kb deletion caused complete lipoprotein lipase deficiency and severe hypertriglyceridemia (type I hyperlipoproteinemia). Intron 9 of a normal control subject was also sequenced in order to define the exact borders of the deletion. Up to now, only the first 0.721 kb of intron 9 had been sequenced. Thus the complete sequence of intron 9 (3.090 kb) is now available. Three Alu sequences were characterized in the normal intron 9, while the proband had only the third complete Alu sequence. The first Alu sequence was located in the deleted region, and only the left arm of the second was present, as the deletion began near its center. A stem-loop structure involving a 14-nt region towards the end of intron 8 and an Alu sequence in intron 9 might have led to the deletion. Sequence analysis showed that the three Alu sequences belonged to the 40-million-year-old Alu-Sa subclass.

Adult↗
PubMedDate not supplied

[Acetabuloplasty by pedicled transfer of the iliac crest apophysis in the dog].

Appositional incremental acetabuloplasty using a self growing iliac crest graft pedicle on its epipyseal vessels was performed in 54 puppies 3 months old. Remodeling an adaptation to the shape of the acetabulum is excellent in most of the cases, issuing into a spherical composite cavity. Persistance of a hyaline cartilage is noted until the end of the first years, but long term morphological transmission electronmicroscopy studies demonstrate a progressive transformation into fibrocartilage. This experimental study demonstrates the possibility to use remodeling and growth properties of a pedicled iliac crest, transplanted as an iland flap on the extraarticular acetabular roof. This new surgical technique can be proposed for the care of difficult dysplastic hips in children.

Acetabulum↗
PubMedDate not supplied

[Syncope].

Syncopes related to cerebral or cardio-vascular lesions, or resulting from a reflex or from a mixed origin should remain exceptional. Adequate knowledge of their possible etiology and of the curative and preventive measures to use, are very important. To avoid an irreversible issue every practitioner should master the resuscitation technics. Each office should have an adequate equipment for resuscitation and CPR courses should be taken every year.

Dental Offices↗