Etiology of otospongiotic sensorineural losses.

The etiology of otospongiotic-otosclerotic disease is enzymatic; the proteolytic enzymes released by the otospongiotic-otosclerotic foci damage the inner ear and are also the basis of the bony rebuilding of the OW niche leading to stapedial fixation. The trigger may be an autoimmune process due to the reaction of the enchondral otic capsule against the embryonic cartilaginous remnants, genetically determined to be located in the otic capsule and mainly in the fissula antefenestram.

Nasal allergy to fungi in guinea pigs.

Sensitized guinea pigs produced specific IgG and IgE antibodies toward Cladosporium and Alternaria. In presence of fungal extracts, nasal mast cells degranulate. Ultrastructural modifications of the cells during degranulation have been established.

[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.

Convulxin-induced activation of intact and of thrombin-degranulated rabbit platelets: specific crossed desensitisation with collagen.

The aggregation of plasma-free rabbit platelets induced by convulxin (Cx), a glycoprotein extracted from the venom of Crotalus durissus cascavella was accompanied by the secretion of ATP and by the formation of thromboxane A2 (TxA2) and of 'platelet-activating factor' (PAF-acether). Thrombin-induced exhaustion of the pool of releasable ADP, or inactivation of cyclooxygenase with aspirin or with arachidonic acid failed to suppress Cx-induced activation. Electron microscopy studies showed that platelets exposed to Cx could be recovered without damage to the cytoplasmic membrane, whereas dense bodies were depleted.

[Heat inhibition of mastocyte degranulation in the nasal mucosa of the guinea pig].

Heating of Guinea-Pig nasal mucosa fragments during 30 min. at 43 degrees inhibits the degranulation of mast cells and the liberation of histamine. This accounts for the success of the thermotherapy of persistent allergic rhinitis.

Degranulation of rabbit platelets with PAF-acether: a new procedure for unravelling the mode of action of platelet-activating substances.

Aggregation and secretion of ATP induced by thrombin, collagen, the snake venom component convulxin and platelet-activating factor (PAF-acether) were studied after the exposure of rabbit platelets to 1 microM of PAF-acether. This concentration, which is around 6 orders of magnitude above the concentration needed to induce full aggregation, was required to remove most of the releasable ATP from the platelets. The depleted platelets aggregated to PAF-acether, to thrombin and to convulxin under conditions where only very low amounts of ATP were secreted, confirming that these agents do not require the release of dense body components to trigger aggregation.

[Variations in mucociliary drainage of the nasal fossae after sulfoarsenical thermal therapy].

The saccharine test described by Andersen appears as a simple, harmless and reproducible means to measure the rate of the mucociliary clearance mainly in children. The sweet taste is so strong that the answer is always clear cut. This measured clearance is a good estimate of the efficiency of the first line of defence that builds up the mucus ciliary complex against most of the inhaled noxious agents.

Bone resorption in otospongiosis.

"Considerable interest has been raised in recent years concerning the basic mechanisms involved in bone destruction and rebuilding in the otospongiotic focus. Under general bone resorption the osteoclasts play a decisive role, but in otospongiotic tissue electron-microscopic and cytochemical studies have shown that osteoclasts alone are not responsible for the bone resorption. Mononuclear histiocytes found in the marrow spaces and in the surrounding bone of an otospongiotic focus together with osteocytes take active part in the resorption.

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.

[Quantitative cytochemical study of local immunostimulation of the respiratory mucosae by mineral spa water (author's transl)].

After non-specific stimulation (by mineral spa water) of the secretion of IgA by the respiratory tract of rabbits, the animals were killed and a study made of the number of plasmocytes per 500 diameter field by phase contrast microscopy. The number of plasmocytes was markedly increased on the 15th day and remained 5 times higher than in control animals on the 100th day. Immunocytochemical labelling by the secretory anti-IgA Fab fraction confirmed these data electron microscopically.

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.

Sensorineural hearing loss due to cochlear otospongiosis: etiology.

This presentation discusses the most valuable way to correlate specific morphologic changes in cochlear otospongiosis with sensorineural hearing loss. Both biochemical and vascular factors may be responsible for the association of far advanced otospongiosis and histopathologic changes. An enzymatic concept of the disease is proposed on the basis of experimental findings and cytoclinical correlations, and the spread of proteolytic enzymes from the bursting lysosomes in histiocytes of the otospongiotic microfoci of the lateral wall.

Cochlear otospongiosis etiology, diagnosis and therapeutic implications.

First, the authors discuss the most valuable way to correlate specific morphological changes encountered in cochlear otospongiosis with sensorineural hearing loss. They think that biochemical factors may be responsible for this association of cochlear otospongiosis and histopathologic changes, and they explain their enzymatic concept resulting from experimental findings and cyto-clinical relationship. Second, the authors analyze clinical, audiometric and X-Rays investigations enabling the diagnosis of cochlear otospongiosis, in its pure pereceptive form as well as in the perceptive component added to the conductive loss in far-advanced mixed audiometric types in surgical otospongiosis.

[Audiometry and cytological study of the external hair cells of 4 strains of mice].

The auditory apparatus of two strains of mices with normal audition is compared to that of two substrains with genetic auditory impairment. Audiometry by auditory evoked potentials at the inferior collicular level indicates complete deafness for one substrain and a 40-48 dB S.P.

[The genetics of the protease inhibitor system and osteospongiosis. Statistical study in 199 patients].

Since the trypsin activity of the inner ear fluid appears to be essential in the evolution of otosclerosis towards a cochlear deafness it was obvious that the protease inhibitor system which is an excellent genetic marker ought to be studied during the onset and the evolution of otosclerosis. No differences with the statistical data from the normal population was found the origin of the trypsin that destroys the inner ear is to be found locally the histiocytes of the otosclerosis focus.

[Functional and morphological modifications of the respiratory tract ciliated epithelium after local immunization of the rabbit with the influenza virus. I.--A comparison of the migration index of the alveolar macrophages and of the inhibition of the ciliary movement (author's transl)].

Induction of cell mediated immunity in the respiratory tract after intratracheal immunization with live or killed influenza A virus was investigated. Respiratory ciliated epithelium appears to be one of the targets involved in the expression of local cell mediated immunity. The degree of inhibition of ciliary movement registered after contact with the antigen is compared with the degree of the development of cell mediated immunity in the lower respiratory tract as evaluated by macrophage migration inhibitory factor (MIF).

Alpha 1-antitrypsin activity of perilymph. Occurrence during progression of otospongiosis.

Previous studies by the Adams method demonstrated a strong correlation between hydrolytic enzyme activity of perilymph and progression of bone conduction loss two years preceding stapedectomy. Alpha 1-Antitrypsin was chosen since its activity can be very precisely measured by a radical immunodiffusion technique and since it is one of the enzymes identified in perilymph of patients with active otospongiosis. Samples of 3 mul to 5 mul of perilymph removed during 103 stapedectomies and samples of known alpha 1-trypsin activity were placed on slides coated with alpha 1-antitrypsin serum.

[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.

[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.