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Biomedical subjects

G Chabot

Publications and source records attributed to G Chabot.

16 recordsLinked to original sources
PubMed1991

[Parental knowledge about their asthmatic children].

A questionnaire was administered to parents of 171 asthmatic children, and their knowledge of asthma was evaluated using a quantitative score. The mean age of children was 5 yr and the mean duration of their asthma was 3 yr. Each sign of the classical triad "noisy breathing, cough, indrawing" was mentioned by two-thirds of parents. Inhaled agents perceived as triggers of asthma were: animal hair (73.7%), dust (69.6%), pollen (60.2%), tobacco (44.4%), molds (14.6%). Other triggering agents mentioned were: stress (51.5%), infections (38%), exercise (13.5%). Mothers with college or university education knew more clinical signs of an attack (P less than 0.01) and more triggering factors (P less than 0.005). Parents satisfied with previous teaching knew more threatening signs of an attack (P less than 0.01). About 80% of those that used theophylline and 49.4% of those that used inhaled beta-2-agonists knew the correct mode of administration. Parents satisfied with previous teaching had better knowledge of the side-effects of theophylline (P less than 0.005) and beta-2-agonists (P less than 0.02). 58.5% of those that used cromolyn sodium did not know the mean duration of a therapeutic trial and 15% did not use it as prophylaxis. 57.1% of those that used oral corticosteroids did not know any side-effects of the drug. About half of the parents indicated that they would like to receive more information about the causes and the appropriate treatment of asthma. It was concluded that parental teaching should focus more on environmental and therapeutic issues.

Asthma↗
PubMed1986

Schedule-dependent potentiation of lomustine cytotoxicity by amphotericin B in mice.

The sensitivity of leukemia cells of AKR/J mice to subsequent lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU)] exposure was found to vary with time following the ip administration of a single dose or multiple doses of amphotericin B (AmB) (0.5 mg/mouse/dose). Following 1 dose of AmB, leukemia cell sensitivity to CCNU, as measured by a spleen colony assay, reached a maximum by 24 hours with a tenfold increase in cell killing noted over cell killing with CCNU alone (0.15 mg/mouse). Two pretreatments with AmB separated by 24 hours led to a hundredfold increase in cell killing, whereas 4 pretreatments, each separated by 24 hours, gave more than a thousandfold increase in cytotoxicity by 8 hours, gave more than a thousandfold increase in cytotoxicity by 8 hours. Increasing the AmB dose, given as a single injection 24 hours before CCNU, resulted in increased potentiation of CCNU cytotoxicity, which reached a maximum at 0.5 mg/mouse. The kinetics of cell killing following either CCNU alone or the combination of AmB and CCNU were similar, although the extent of cell killing was greater with the combination. The AmB plasma pharmacokinetics for single doses showed a dose-dependent serum peak level and a half-life of about 24 hours for doses up to 1 mg/mouse. Nonlinearity was noted at the dose level of 2 mg/mouse because of saturation of absorption from the peritoneal cavity. These data are of importance for the optimal sequencing and dosing of these drugs for future clinical trials.

Amphotericin B↗
PubMed1984

[Septicemia associated with urinary infection in infants. Apropos of 36 cases].

While studying 213 cases of septicemia among children less than one year of age, we found 36 cases of septicemia with bacteriuria. Among these 213 septicemic children, urinary tract infection (UTI) was second only to meningitis as an associated focus of infection. A radiological investigation was done in 27 cases; the pyelography or the cystography was abnormal in 14 instances, and 6 of these 14 patients needed to be surgically corrected.

Bacteriuria↗
PubMed1982

Relationship between plasma corticosterone and adrenal epinephrine after diazepam treatment in rats.

Following recent observations that diazepam treatment increases adrenal epinephrine in rats, we were interested in studying the possible mechanisms of this action of diazepam on rat adrenal glands. All diazepam treatments studied (1-25 mg . kg-1.day-1 for 10 days) led to an increase in adrenal epinephrine following a linear dose-effect relationship. Since epinephrine synthesis is under neuronal and humoral controls, we investigated their respective importance in the effect of diazepam on the adrenal gland. The denervation of the adrenal gland did not prevent the increase in adrenal epinephrine by diazepam treatment. On the hand, diazepam treatment was shown to cause an increase in plasma corticosterone in parallel with an increase in adrenal epinephrine. Administration of dexamethasone (a synthetic corticoid) and hypophysectomy prevented the increase in adrenal epinephrine and plasma corticosterone resulting from diazepam treatment. We thus conclude that the increase in adrenal epinephrine seen after diazepam treatment is parallel to the increase in plasma corticosterone. Moreover, since the action of diazepam on adrenal epinephrine is prevented by dexamethasone or hypophysectomy, we hypothesize that diazepam is acting on the adrenal cortex via the release of adrenocorticotropic hormone (ACTH). ACTH and corticosterone would be responsible for the increased activity of epinephrine-synthesizing enzymes in adrenal medulla.

Adrenal Glands↗
PubMed1976

[Critical analysis of the arteriography of primary malignant tumors of the bones, on the occasion of 19 unedited cases].

From the analysis of a series of 62 unedited cases of arteriography of osseous tumors including 19 primary malignant tumors, it was confirmed that the majority of angiographic signs described as being characteristic of malignant tumors of the bones are not significant. They are found in benign tumors and in ordinary inflammatory phenomena: several cases of osteoid osteoma, myeloplax tumor or simply of osseous reconstruction permit one to make criticisms. On the other hand, one must endeavour to demonstrate, by means of a technique whose main elements are recalled, vascular abnormalities which are the only typical ones and which furthermore are found in "silent" tumors such as chondrosarcomas or fibrosarcomas. These vascular abnormalities are given in detail, and several examples of them are given.

Adolescent↗