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Biomedical subjects

L G Chevance

Publications and source records attributed to L G Chevance.

At least 19 recordsLinked to original sources
PubMed1989

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.

Antibody Formation↗
PubMed1988

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. The ciliary epithelium and the ciliary beating are not affected by fungal allergens.

Alternaria↗
PubMed1983

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. Convulxin-treated platelets aggregated in response to ADP, to arachidonic acid and to thrombin, but failed to aggregate in response to Cx itself as well as to collagen. Crossed desensitisation between Cx and collagen was also observed when platelets were exposed to Cx in the presence of prostaglandin E1, which prevented granule depletion, demonstrating that desensitisation was not due to the inability of Cx-treated platelets to secrete ADP in response to collagen. Formation of PAF-acether by thrombin-treated platelets was impaired when thrombin was used as a second stimulus but was maintained when Cx was used as such. The formation of TxA2 by Cx-treated platelets stimulated with arachidonic acid or with thrombin was preserved of only slightly reduced whereas these platelets failed to synthesize TxA2 when stimulated with Cx or with collagen, showing that crossed desensitization between Cx and collagen was not restricted to aggregation, but extended to stimulation of arachidonate metabolism as well. Convulxin is a powerful platelet-stimulating agent which operates through mechanisms which may involve PAF-acether, and which interacts with sites related with those of collagen at an unknown level.

Adenosine Triphosphate↗
PubMed1982

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. Furthermore, when exposure to PAF-acether was associated to inactivation of platelet cyclooxygenase with aspirin, aggregation to thrombin persisted, validating the claim that thrombin induces aggregation by a third pathway unrelated to ADP and to thromboxane A2. Aggregation by collagen was markedly reduced by exposure of the platelets to PAF-acether or to aspirin; when both procedures were associated, aggregation was suppressed. Failure to desensitize the rabbit platelets to PAF-acether upon exposure to high amounts of it indicates the absence of irreversible membrane changes due to PAF-acether, and allows its use as a depleting procedure for the dense body materials, which does not affect platelet membrane components as is the case for thrombin.

Adenosine Triphosphate↗
PubMed1982

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. Cytochemical studies of acid phosphatase activity have shown that hydrolases in the lysosomes are expelled into the surrounding tissue, resulting in its resorption.

Acid Phosphatase↗
PubMed1982

[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. In measuring the rate of the clearance in 83 children before and after the Spa treatment (Saint Honoré les Bains), each subject being its own control, the Authors demonstrate a slowing of the clearance speed in 62,1% of the patients, immediately after the end of the Spa period. This percentage is almost reversed 19 days later at the end of the post Spa period. At this time, in 52.2%, an accelerated clearance is measured. This study demonstrates both the efficiency of the Spa treatment, and the necessity, too often overlooked, of 20 days of post Spa medical care.

Arsenamide↗
PubMed1978

[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.

Animals↗
PubMed1978

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. In addition, according to Ruedi's vascular concept, abnormal vascular connections called "shunts", provoked by active foci breakiny oxygen. Such extensive otospongiotic bone transformation breaking the endosteum of the cochlear is much less frequent than the progressive cochlear component encountered by otologic surgeons in far advanced otospongiosis. It is for this reason that the authors believe that their enzymatic concept of otospongiosis may explain the most important part of the sensorineural impairment in cochlear otospongiosis.

Adult↗
PubMed1977

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. They present two typical cases of cochlear otospongiosis: one combines clinical history, audiometric test and post mortem investigations;-the other shows the passage from a pure cochlear otospongiosis to a secondary stapedial fixation, ten years later, thus confirming by audiometric data and by stapedectomy the otospongiotic etiology of this previous pure sensorineural loss. Finally, they insist upon the great interest of establishing an early diagnosis in cochlear otospongiosis on account of its therapeutic implication, particularly from the enzymatic point of view.

Adult↗
PubMed1977

[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.L. hearing loss at all frequencies for the other. Scanning and transmission electron microscopy demonstrate hair impairment of the external hair cells and degeneration of the chondriosome for the two deaf substrains.

Animals↗
PubMed1976

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. The zone of diffusion was stained and measured after 38 hours of incubation. Antitrypsin values were lowest in 24 cases, two with no preoperative bone conduction progression, three with moderate progression of 10 to 15 dB, and 19 with rapid progression of more than 20 dB. They were highest in 36 cases with no progression, and in one case with moderate progression. This study confirms previous reports on the enzymatic activity in otospongiotic disease.

Humans↗
PubMed1976

[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.

Ear, Middle↗
PubMed1975

Influenza virus and ciliary beating of the respiratory epithelium in sensitized animals.

Normally, under good survival conditions, the ciliary beating can be observed and recorded during hours after dissection of the respiratory epithelium. When laboratory animals have been immunized locally against influenza virus (under delayed type hypersensitivity conditions) the ciliary beating stops within 3 to 6 minutes when the same virus is put in contact with the sensitized mucosa. The specificity and the immunological conditions of this stopping have been analyed and the practical importance of this new test in cellular immunology is discussed.

Animals↗