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Biomedical subjects

J C Fournet

Publications and source records attributed to J C Fournet.

40 records · Page 3Linked to original sources

[Bone allografts revascularized by autogenous endosseous flap. Experimentation in rats].

The experimentation was based on the analysis of revascularization phenomenons and reossification of cross allografts of Wistar rat femoral diaphysis firstly canalized with an epigastric subcutaneous intramedullar autogenous flap. An endosteal revascularization has been observed in addition to the periosteal one which is usually the sole characteristic of classic allografts. The bone transplant, quickly vascularized after a short period of creeping substitution, had normal histomechanical properties which were never observed without the addition of a vascular pedicule. The use of such cortical allografts seems to be useful in human surgery.

Animals↗

In vivo evaluation of a retrievable vena cava filter--the Dibie-Musset filter: experimental results.

PURPOSE: To evaluate, in an animal model, the efficacy and safety of a 7 Fr percutaneous vena cava filter for temporary or permanent use. METHODS: The Dibie-Musset (DM) filter is a wire preformed into a double-spiral shape with a spring effect. The experiment was performed in 15 adult sheep and consisted of the insertion of 45 filters, clot trapping tests, and filter retrieval. Follow-up in all sheep consisted of radiologic (abdominal radiograph, inferior vena cavogram, abdominal computed tomography), macroscopic, and microscopic examinations between days 8 and 386 after filter placement. RESULTS: Of the 45 filters implanted in 15 sheep, 29 were retrieved between day 0 and day 15. Filtration efficiency was 100% for clots 4 x 4 x 20 mm. No long-term (1 year) side-effects were detectable. Microscopic examination of the vein wall showed only a dense intimal fibrosis without signs of acute inflammation at 1 year. CONCLUSION: These results support the efficiency and safety of the DM filter in an animal model.

Animals↗

Role of lipid emulsions in cholestasis associated with long-term parenteral nutrition in children.

BACKGROUND: In children who depend on long-term parenteral nutrition (PN), liver disease is a major complication that may lead to end-stage liver failure requiring liver transplantation. METHODS: This retrospective study investigated the influence of lipid emulsions on cholestasis onset in children receiving long-term total parenteral nutrition (TPN) with lipids. Ten children who presented with a total of 23 episodes of cholestasis, associated in 13 cases with thrombocytopenia, were studied. RESULTS: Changes in the lipid delivery preceded these complications in more than half the cases. The temporary decrease in lipid administration led to normalization of bilirubin in 17 episodes. CONCLUSIONS: These data suggest that lipid supply is one of the risk factors for PN-associated cholestasis. The link between cholestasis and the reticuloendothelial system overload needs to be better understood. Prevention of cholestasis might include the decrease in the lipid load. When cholestasis occurs, lipid supply should be temporarily stopped, especially in the case of associated thrombocytopenia.

Adolescent↗

[Clinical, biological and genetic heterogeneity of the inborn errors of pulmonary surfactant metabolism: SP-B deficiency and alveolar proteinosis].

Pulmonary surfactant is a multimolecular complex located at the air-water interface within the alveolus and to which a bulk of functions has been assigned, physical (surface-active properties) as well as immune or depurant. This complex consists of a surface active lipid layer (mainly phospholipids), and of an aqueous subphase. From discrete surfactant sub-fractions, one can isolate very hydrophobic proteins SP-B and SP-C as well as the collectins SP-A and SP-D, which were shown to have structural, metabolic, or defensive properties. Inborn or acquired abnormalities of surfactant, qualitative or quantitative in nature, account for a number human diseases. Beside hyaline membrane disease of the preterm neonate, a cluster of hereditary or acquired lung diseases have been characterized by the storage of periodic acid Schiff-positive material filling the alveoli. From this heterogeneous nosologic bulk, at least two discrete entities presently seem to emerge: 1) SP-B deficiency, in which an essentially proteinaceous material is stored within the alveoli, and which is a bona fide autosomal recessive Mendelian entity linked to the SFTPB gene (MIM 1786640), generally entailing neonatal respiratory distress with rapid fatal outcome, although partial or transient deficiencies have also been observed; 2) alveolar proteinosis, characterized by the storage of a mixed, protein and lipid material, and which constitutes a relatively heterogeneous clinical biological syndrome, with regards to age at onset (from the neonate through to adulthood) as well as the severity of associated signs. Murine models with a targeted mutation of the gene encoding GM-CSF (Csfgm) or the beta subunit of its receptor (Il3rbl) support the hypothesis of an abnormality of surfactant turnover in which the alveolar macrophage would be a key player. Beside SP-B deficiency, in which a near-consensus diagnostic chart can be designed, the ascertainment of other abnormalities of surfactant metabolism is not straightforward. The disentanglement of this disease cluster is however essential, with aim to propose differentiated therapeutic procedure : repeated bronchoalveolar lavages, GM-CSF replacement, bone marrow grafting or lung transplantation.

Amino Acid Metabolism, Inborn Errors↗