Biomedical subjects

Laurent Corsois

Publications and source records attributed to Laurent Corsois.

3 recordsLinked to original sources

PubMed2004

[Synaptophysin expression abnormalities in Hirschsprung's disease].

Hirschsprung's disease is defined by the congenital absence of ganglion cells in enteric plexuses. Immunostaining of synaptophysin after formalin fixation may be used to identify hyperplasia of nerve fibers and rarefaction of neuromuscular junctions in Hirschsprung's disease. The aim of the study was to evaluate semi-quantitatively the expression of synaptophysin in Hirschsprung's disease, in correlation with morphologic features. This retrospective study included 3 controls, 42 surgical rectal biopsies performed for suspicion of Hirschsprung's disease in children presenting with lower digestive occlusion or severe chronic constipation, including 18 Hirschsprung's disease, and 23 surgical specimens of Hirschsprung's disease. In the absence of Hirschsprung's disease, synaptophysin-positive fibers were numerous but thin in the muscularis mucosae, thin and scarce in the mucosa and submucosa. Neuromuscular junctions were thin and numerous in the muscularis propria. In Hirschsprung's disease, synaptophysin-positive fibers were coarse, and increased in number on each side of the muscularis mucosae. Plexuses were enlarged, weakly stained, and associated in the connective tissue of the muscularis propria with coarse and intensely stained fibers. In conclusion, staining for synaptophysin could be useful to demonstrate abnormalities of enteric innervation in rectal biopsies performed for suspected Hirschsprung's disease in the absence of acetylcholinesterase staining on frozen sections, in transmural biopsies performed for guiding surgery in Hirschsprung's disease, and in cases of extensive Hirschsprung's disease.

Acetylcholinesterase↗

PubMed2004

[Hirschsprung's disease: practical considerations].

Hirschsprung's disease (1/5000 live births) is defined by the congenital absence of neuronal cells in the nervous plexuses in the distal part of the digestive tract. The disease affects the rectum and sigmoid colon in 80% of cases, or is more extensive. Hirschsprung's disease is suspected in cases of low gastrointestinal obstruction in the neonatal period, or in cases of chronic severe constipation in childhood. It is diagnosed by pathological examination of rectal biopsies that include the submucosa. After standard staining, multiple sections are scrutinized for neuronal cells. Acetylcholinesterase staining is performed on a frozen fragment to demonstrate the hyperplasia of cholinergic fibers that is very suggestive of Hirschsprung's disease. This hyperplasia decreases from the rectum to the splenic flexure of the colon. Hyperplasia of extrinsic nerve fibers and rarefaction of neuromuscular junctions in Hirschsprung's disease may be demonstrated immunohistochemically. Differential diagnosis includes chronic intestinal pseudo-obstructions. The treatment for Hirschsprung's disease is, most often, anastomosis of the normally innervated gut to the anal canal. Peri- or pre-operative biopsies assist surgery, but their interpretation is difficult in the transitional zone. The examination of the surgical specimen allows measurement of the aganglionic segment and transitional zone. Different genes (RET, most often) may be involved in sporadic or familial Hirschsprung's disease. Hirschsprung's disease is associated with other digestive or extra-digestive abnormalities in 5 to 30% of patients. Associated abnormalities may delay the diagnosis and treatment of Hirschsprung's disease.

Biopsy↗

PubMed2002

Association of a new c-Cbl related protein with the very first stages of apoptosis induction.

This study investigates the involvement of the c-cbl proto-oncogene during the first stages of the apoptotic process. We have already shown that a c-Cbl aptotosis-related protein of 90 kDa (CARP 90) is detected very rapidly in the cytoplasm as well as in the nucleus of murine thymocytes after hydrocortisone (HC) treatment. We report here that this protein appeared as well after in vivo treatment of mice by gamma-irradiation or injection of anti-CD3 monoclonal antibody, two potent thymic apoptosis inductors, providing a close relationship between the occurrence of apoptosis and the appearance of CARP 90. We showed that CARP 90 and p120(cbl) share numerous epitopes strikingly suggesting that CARP 90 is coded by c-cbl. In addition, KO mice do not sustain CARP 90 appearance. We finally showed that CARP 90 contains N- and C-terminal end epitopes of p120(cbl), which suggests that CARP 90 is an alternative spliced form of c-cbl. This protein was also observed under gamma-irradiation in tissues of different origin, which enlarges the physiological significance of this phenomenon. The very rapid CARP 90 appearance under apoptotic conditions in the nucleus of cells originating in different tissues makes this protein if not a possible new actor of the apoptotic process, at least an interesting marker of this process.

Animals↗