PubMed Health⌕ Search

Biomedical subjects

M Colin

Publications and source records attributed to M Colin.

33 records · Page 2Linked to original sources
PubMed1980

[Attempt to induce diarrhea in young rabbits with different dietary crude fiber contents (author's transl)].

The influence of five diets containing 14.5, 10, 6.9, 4.6 and 3.3 per cent of crude fiber was studied in 6-week-old rabbits. Two additional groups of animals fed with the rations with 14.5, 6.9 and 3.3 per cent crude fiber were used. The first was inoculated with coccidia, the second was treated with ampicillin. In non-inoculated and untreated rabbits, diarrhea was inconstant, of short duration and low intensity and appeared only for cellulosis rate less than 4.6 per cent. There was no mortality. Decrease in the dietary crude fiber level cannot be considered as directly responsible for digestive ailments, when sanitary conditions are good. In our experimental conditions, it has been shown that a low level of cellulosis in the diet did not increase the pathological phenomena. Inversely pathogenic elements (coccidia) or medicaments used (ampicillin) can change the relations which exist between growth and components of the diet (cellulosis).

Animals↗
PubMedDate not supplied

[Cutaneous lesions of bilharziosis. Report of fourteen cases (author's transl)].

The cutaneous localization of bilharziosis are infrequent. In a country of endemic disease, the Ivory Coast, where about 10 p. 100 of the population suffer from bilharziosis, it has been observed, between 1970 and 1980, 14 cases of cutaneous bilharziosis which have been diagnosed by micropathology. These lesions appear as papules or lichenoid plaques, usually clustering around umbilicus and upper dorsal regions. They require the presence of living eggs which induce the formation of a granuloma called "bilharziosis follicle", within which bilharziosis eggs are discovered. This reaction is explained by delayed hypersensitivity against soluble antigens of the eggs. The treatment is that of bilharziosis.

Adolescent↗
PubMedDate not supplied

Study of sodium orthovanadate as a reverser of multidrug resistance on lymphoblastic leukemic CEM/VLB100 cells.

The occurrence of multidrug resistance (MDR) is the major cause of failure of cancer chemotherapy. Finding a way to circumvent this problem is now a major challenge in oncology. Multidrug resistant CEM/VLB100 cells accumulate 10 times less vinblastine (VLB) after 30 min than their sensitive counterparts (CEM cells). At a non-cytotoxic concentration (1 mM) of sodium orthovanadate (OVN), uptake by CEM/VLB100 cells was increased 4 times while no effect was observed on CEM cells. The action on VLB uptake of OVN and verapamil (VPL), an usual MDR modulator, was additive. In CEM/VLB100 cells, OVN did not alter efflux. Its cellular mechanism of action could involve a transitory stimulation of VLB influx (x3). OVN uptake in CEM and CEM/VLB100 cells was not significantly different and reached saturation after 30 s (180 pmol/10(6) CEM cells and 150 pmol/10(6) CEM/VLB100 cells). This OVN uptake was concentration dependent. IC50 of VLB and doxorubicin were decreased by approximately 43 and 62% after 1 hour's exposure to OVN and 48 hours of culture. Under these conditions, OVN was more efficient than OVN.

Doxorubicin↗
PubMedDate not supplied

Alterations of vinblastine influx in multidrug-resistant lymphoblastic leukaemic CEM cells.

Typical multidrug-resistant (MDR) CEM/VLB100 cells exhibited reduced uptake of vinblastine (VLB) compared to their sensitive CEM counterparts mean results were respectively, 3.19 and 35.4 pmol per 10(6) cells. In CEM cells, the efflux of drug reached a steady state after 10-15 min while in CEM/VLB100 cells, the typical P170-mediated efflux was still efficient after 40 min. Nevertheless, the most striking difference observed in CEM/VLB100 cells was a dramatic decrease in early (30 sec) influx of drug which was 10 times lower than in sensitive cells, a characteristic still observed in the presence of Na azide and absence of glucose. MDR cells without little or no effect on sensitive cells. The Q10 entry of VLB into sensitive cells was 1.2 while it was 2.2 in CEM, suggesting that the mode of entry of VLB into MDR cells differed from that of CEM cells. Verapamil or nigericin, which rapidly increased the accumulation of VLB raised the Q10 to >2. These results suggest that the primary defect in MDR cells would be an inhibition of influx, which might involve interactions with P170 through a reversible process.

Drug Resistance, Multiple↗