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Biomedical subjects

L G Chevance

Publications and source records attributed to L G Chevance.

At least 55 records · Page 3Linked to original sources
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[A biochemical and cytological explanation of cochlear otospongiosis].

In a study of 250 otosclerotic perilymphatic fluids, it was found statistically that in the presence of developing inner ear deafness, 90% of cases will demonstrate increased trypsin activity. Conversely, elevated antitrypsin levels are found in the absence of developing inner ear deafness.

Histocytochemistry↗
PubMedDate not supplied

[A biochemical and cytological explanation of cochlear otospongiosis].

Carrying on their study about the enzymatic activity of the otospongiotic micro-foci and the hydrolytic activity of the perilymph, the authors present their work concerning the value of trypsin and alpha-1-anti-trypsin in the perilymph of otospongiotic patients operated on by stapedectomy. They describe the method used and give the obtained results which permit to believe that the values of trypsin, and a contrario of anti-trypsin, appear to constitute an index of the severity of the progression. Moreover, the authors have investigated the eventual toxic action of various trypsin concentrations on the hair cells of the Corti organ in the guinea-pig. This study has been carried through successfully by means of the electron microscopic scanning method which allows to obtain an "electron cochleogramme in situ". They explain the method and come to the conclusion that the intensity and extension of the Corti hair cells alterations in a cochlea receiving a perfusion with trypsin solutions, are tightly related to the trypsin concentration. However, they do not pretend so far that these results reflect exactly the anatomo-pathologic reality during the slow progression of otospongiosis towards cochlear deterioration. These two series of experimentation appear to confirm their enzymatic concept of otospongiosis: the long, slow and extremely capricious progression of the disease is the duplicate of its cytologic progression, the contact between hydroltic enzymes and Corti cells having the same capricious character. These findings perfectly corroborate the previus ones they made in this field, as well as the correlations they have established between hydrolytic activity of the perilymph and audiometric progression. Consequently, they believe that the mechanism of the otospongiotic disease is provoked by the rupture of the balance trypsin/anti-trypsin in the otospongiotic micro-foci and thus in the inner ear fluids.

Animals↗
PubMedDate not supplied

[A peptide (a magnesium salt of N-acetyl (alpha, beta)-aspartyl-glutamic acid). Demonstration of the protection against local cellular destruction induced by in situ complement activation].

A peptide of simple chemical structure has demonstrated its efficiency in preventing the large cellular destruction that locally activated complement produced on the ciliary epithelium of the respiratory tract. Previously (1980), it was demonstrated by the authors that these cellular destructions after sensitization of the epithelium was due to the local activation of the complement (alternate pathway) by immune complexes with secretory IgA. The cellular protection afforded by Naaga was demonstrated by the persistance of a normal ciliary beating when the sensitized mucosa is in contact with the antigen; by electron microscopic studies both in transmission and scanning E.M. contrasting with the complete cellular destructions of the epithelium which appear obvious. The protection appear complete when Naaga (56 mM) is present in the testing solution (or instillated before the test). By in vitro human complement studies; study of the cytolytic sequence inhibition for the classical pathway 1,5.10(-3) M of Naaga produces a 50% inhibition of 1 H50 hemolytic unit. For the alternate pathway, the same inhibition is observed with 1,75.10(-3) M of Naaga; by two-dimensions immuno-electrophoresis: a dilution of 1/2 of C3 in Naaga reduced to 1/10 of its normal value the C3b profile; the "Rockets" technique demonstrated that the same 1/2 dilution of Naaga in complement prevents the clivage of factor B and that this peptide acts by inhibition of the alternate C3 convertase formation (see illustrations). If we consider the subject of this study i.e. the upper respiratory tract mucosa and knowing the physiopathological importance of the muco ciliary complex in preventing dust, microbs and other particulate foreign materiel to penetrate the epithelium, the therapeutic importance of such a simple non toxic and unharmful chemical compound must be stressed.

Animals↗
PubMedDate not supplied

Scanning and transmission electron microscopy study of ferret respiratory mucosa infected with influenza A virus.

The use of both SEM and TEM techniques in studying the alterations of the columnar ciliated epithelium of the whole respiratory tract of ferrets enables the authors to find a significant discrepancy between tracheal and nasal mucosa destructions. This discrepancy is not a function of the anatomical location of virus instillation. Theoretical and pratical meanings are discussed.

Animals↗
PubMedDate not supplied

Complement activation and cyto-immunological alterations of the respiratory mucosa.

The action of activated complement on the upper respiratory tract was studied using the registration of ciliary beating and the transmission and scanning electron microscopy of ciliated cell lesions. The alternative pathway of activation was done using (1) non-specific activators, i. e. zymosan, dextran sulfate and polymerised sIgA, and (2) specific activators, i. e. "Ag-sIgA" immune complexes on normal mucosa and contact between an antigen and the tracheal mucosa of an immunized animal. In all cases, a quick alteration of the ciliary beating rythm was registered as well as more or less extensive cytological destruction. Such results were obtained with or without adjunction of complement; this suggested the existence of complement locally. A new method to demonstrate the occurrence of complement was developed, and the results showed that complement was present in the trachea. The above results were corroborated (1) by EDTA inhibition of the two complement pathways which prevented stopping of the ciliary beating and eliminated most of the cytological lesions, whilst EGTA left the alternative pathway operative with consequent alterations, and (2) by using C6-deficient rabbits in which no alterations were found. This study demonstrated that under certain conditions, local sIgA may activate the complement, and this fact explains many aspects of these immunological reactions of the respiratory epithelium.

Animals↗