G. Gabbiani
Université de Montréal
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by G. Gabbiani.
Cell and Tissue Research | 1969
G. Gabbiani; Guido Majno
SummaryIn the Gasserian ganglion and testis of the rat the endothelium of the small blood vessels has a singular appearance due to the presence of a high number of microvillous processes. These arise from the luminal surface, either individually, or in small groups. The significance of this structure is not known. It is pointed out that these vessels are particularly sensitive to cadmium intoxication.
Experimental Biology and Medicine | 1963
G. Gabbiani; Kai Nielsen
Summary A technic is described for the study of mast cells on such “natural tissue spreads” as the external periosteum of the calvarium and the dura mater of small laboratory rodents. These membranes can be fixed as flat sheets, while still attached to their normal osseous base, without the use of the customary traumatic procedures incident to the preparation of artificial tissue mounts.
The American Journal of Clinical Nutrition | 1963
Beatriz Tuchweber; G. Gabbiani
SUMMARY Experiments on the rat indicate that the progenia-like syndrome induced by chronic intoxication with dihydnotachystenol can be prevented by concurrent d-ci-tocophenyl ace- tate treatment. Methyltestosterone is equally effective, but no synergism could be demonstrated between vitamin E and the anabolic androgen. REFERENCES 1. SELYE, H., STREBEL, R. and MIKULAJ, L. A pro- geria-like syndrome produced by dihydrotachys- terol and its prevention by methyltestosterone and ferric dextran. J. .1 in. Geriatrics Soc., 11:1, 1962. 2. SELYE, H., GOLDIE, I. and STREHEL, R. Effect of anabolic hormones and ferric dextran upon theprogeria-like syndrome produced by dihydrotac-hysterol. Gerontologia, 7 : 2, 1963. 3. SELYE, H. and STREBEL, R. Prevention by calci-phylaxis of the progeria-Iike syndrome induced by chronic dihydrotachysterol overdosage. Proc.Soc. Exper. Biol. & Med., 110: 673, 1962. 4. SELYE, H. Calciphylaxis. Chicago, 1962. The Uni-versity of Chicago Press. 5. CANTIN, M., DIEUDONN,
Experimental Biology and Medicine | 1965
G. Gabbiani; Beatriz Tuchweber
Summary Experiments on rats have shown that pretreatment with calcium acetate prevents the skin calcification elicited by means of calcergy and aggravates the cutaneous and renal lesions induced by calciphylaxis. This observation suggests a difference in the mechanisms of the two phenomena.
Journal of the American Geriatrics Society | 1963
G. Gabbiani
Calciphylaxis is a condition of induced systemic hypersensitivity in which tissues respond to appropriate challenging agents with calcification (1). The components of this phenomenon are a systemic calcifying agent or sensitizer [parathyroid hormone, vitamin-D compounds, dihydrotachysterol (DHT)] and an inorganic or organic challenger [e.g., CrC13, serotonin]. The challenger is administered during a very specific time interval (“critical period”) after the sensitizer. We distinguish 1) topical calciphylaxis, in which the challenger is applied directly to the target, from 2) systemic calciphylaxis, in which the challenger is injected parenterally and acts selectively on certain organs. However, under given circumstances, calciphylaxis can also exert a considerable prophylactic effect against certain toxic compounds. Thus,a fatal generalized soft-tissue calcinosis, normally induced by acute overdosage with DHT, fails to occur if a calciphylactic challenger is brought into contact with a large connective-tissue surface. Chronic DHT-intoxication causes no generalized soft-tissue calcinosis, but a syndrome reminiscent of progeria. Among the changes characteristic of this “progeria-like syndrome” are : a Monckeberg type of generalized arteriosclerosis with calcification in the cartilaginous portions of the ribs, trachea and larynx. Concurrently, there is loss of body weight and atrophy of the sex organs, liver, kidney, thymicolymphatic apparatus, fat and connective tissue. The skin loses its elasticity and exhibits many wrinkles. Dental anomalies, similar to those seen in senile rats, develop and the life span is greatly shortened. Cataracts are rarely observed but pretreatment with DHT sensitizes the rat for the production of cataracts by other agents. Whereas these changes are reminiscent of senility, the associated skeletal lesions are not : osteosclerosis is seen rather than osteoporosis, although the newly formed bone tissue is brittle. The question arose whether calciphylaxis could also protect against this progeria-like syndrome and, if so, whether such a prophylactic effect could be accomplished without any massive calcium deposition in a directly challenged area. For this purpose we used a preparation of iron hydroxide with dextran (FeDex), which is readily diffusible throughout the entire body (2, 3). The intraperitoneally injected iron, administered in the form of Fe-Dex, prevented all the changes resembling progeria and did not cause any selective massive challenge and calcium fixation at the injection site; it formed innumerable minute iron deposits fairly evenly distributed throughout the body, but none of these was apparently so much larger than the others as to compete with them successfully by attracting unabsorbable massive deposits of calcium salts.
Calcified Tissue International | 1968
G. Gabbiani; Beatriz Tuchweber; Gaston Côté
Thyroxine does not prevent either the metastatic calcifications seen after bilateral nephrectomy or the lesions produced by Ptr-H overdosage if the animals have been prevlousiy nephrectomlzed. Hence, the presence of the kidney is necessary for the anti-parathyrold action of thyroxine. Finally~ in young animals (100 g) thyroxine prevents hypercalcemia produced by Ptr-H whereas in older rats (250 g) it is not active in this respect; it still retains, however, the property of inhibiting the metastatic calcificatlons induced by Ptr-H overdosage. It would appear that this action of thyroxine is independent of the level of blood calcium and that the interaction between Ptr-H Qnd thyroxine depends on the age of the animals.
Journal of Atherosclerosis Research | 1965
Beatriz Tuchweber; G. Gabbiani
Summary Unilateral nephrectomy combined with an excess of NaCl intake, not only aggravates the usual soft-tissue calcifying effect of DHT, vitamin D 2 , vitamin D 3 , parathyroid extract and calcium acetate, but can even qualitatively alter the vascular and renal actions of such calcifying agents in the rat. This was particularly evident in animals treated with comparatively small doses of DHT, vitamin D 2 and vitamin D 3 . Here, mural thrombi developed in the renal veins with hyalinization of the glomerular capillaries, generalized hydrops and urinary calculi following conditioning by unilateral nephrectomy and an excess NaCl intake.
Endocrinology | 1962
G. Gabbiani; Ralph Strebel
Journal of Vascular Research | 1965
G. Gabbiani; Beatriz Tuchweber
British journal of pharmacology and chemotherapy | 1966
G. Gabbiani; M. L. Jacqmin; R. M. Richard