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M D Sans

Publications and source records attributed to M D Sans.

8 recordsLinked to original sources
PubMed1997

Chloroquine stabilizes pancreatic lysosomes and improves survival of mice with diet-induced acute pancreatitis.

Activation of digestive zymogens by lysosomal enzymes has been suggested as a triggering event in acute pancreatitis (AP). chloroquine (CQ), a weak base that accumulates in the lysosomes and increases their pH, can inhibit the activity of lysosomal enzymes. In the present study, we examined the effect of CQ on choline-deficient, ethionine-supplemented (CDE) diet-induced AP. CQ-diphosphate (15-50 mg.kg-1) or vehicle was given intraperitoneally at 0, 24, and 48 h to female CD1 mice that were fed with either normal diet or CDE diet. For mortality studies, animals were observed for 168 h. Serum and pancreas samples were collected from animals sacrificed 56 h after the start of the CDE diet. Treatment with CQ at 50 mg.kg-1 significantly (p < 0.05) improved the survival of mice with CDE diet-induced AP. In the normal pancreas, CQ decreased the specific activity of lysosomal enzymes cathepsin B1, beta-hexosaminidase, beta-glucuronidase, and acid phosphatase. In the pancreas with AP, CQ did not modify the activity of cathepsin B1, whereas it increased the latency of all enzymes. In conclusion, our results confirm the beneficial effect of CQ on survival of mice with CDE diet-induced AP and suggest that this effect of CQ may be due to its stabilizing action on lysosomes.

Acid Phosphatase↗
PubMed1996

[Activity and subcellular distribution of lysosomal enzymes in acute pancreatitis induced by CDE diet in mice].

The aim of the present study was to analyze the activity and subcellular distribution of the lisosomal enzymes and the stability of the lisosomes in acute pancreatitis induced by CDE diet in mice. The activity and the latency of the catepsin-B1 enzymes, acid phosphatase, beta-hexosaminidase and beta-glucuronidase in normal pancreas and in pancreatitis induced by CDE diet were determined. The distribution of the acid phosphatase lisosomal marker was determined in subcellular fractions obtained by differential centrifugation. The activity of the catepsin-B1 enzyme increased 47% in the pancreas of mice with pancreatitis induced by CDE diet. The acid phosphatase activity was not modified and the beta-hexosaminidase and beta-glucuronidase was decreased. The specific activity of the acid phosphatase lisosomal marker also increased in the subcellular fraction containing the zimogene granules and decreased the latency (parameter indicative of lisosome stability) of all the lisosomal enzymes analyzed in the pancreatic homogenate. These results suggest that the lisosomal enzymes, specially the catepsin-B1, and the decrease in the stability of the lisosomes may play a role in the pathogenesis of acute pancreatitis.

Acid Phosphatase↗
PubMed1975

Bacterial studies of Clindamycin-associated colitis. A preliminary report.

The cause of pseudomembraneous colitis is not known but has been attributed to an alteration in the microbial flora of the colon. To test this hypothesis, a blind, prospective study was undertaken in which fecal samples were cultured quantitatively for aerobic and anaerobic organisms. The patients from which these samples were taken were all receiving clindamycin and had diarrhea secondary to the use of the drug. We were able to show definite differences in the colonic microflora which correlated with the presence of pseudomembranes on biopsy. Those patients who had diarrhea and pseudomembranous colitis showed a striking decrease, both quantitatively and qualitatively, in the number of anaerobes present. Those patients who had diarrhea but no pseudomembranes had large numbers of anaerobes which qualitatively approximated normal fecal cultures but quantitatively were fewer in number. A third group of patients, which had resolving pseudomembranous colitis, and were no longer symptomatic, had large numbers of anaerobic organisms which approximated those found in normal fecal cultures. There were no differences among the three groups with regard to facultative anaerobic microflora. Thus, the presence of pseudomembranous colitis correlated directly with a striking quantitative and qualitative decrease in the anaerobic microflora of the colon. The symptom of diarrhea alone appeared to have no meaning with regard to changes in the bacterial flora. Resolution of pseudomembranous colitis was associated with a return of the anaerobic microflora.

Bacteroides↗
PubMed1968

Cryptococcus neoformans. 3. Inhibition of phagocytosis.

Isolated nonhydrolyzed cryptococcal polysaccharide is a rather specific potent inhibitor of the phagocytosis of Cryptococcus neoformans by human leukocytes in vitro. When an encapsulated strain of C. neoformans was cultured in the nonencapsulated state, the rate of phagocytosis was three times greater than when the encapsulated form was used. Our theory that capsular material plays a role in the pathogenesis of cryptococcosis requires (i) that C. neoformans exist in soil in a nonencapsulated state and (ii) that human phagocytes be capable of killing the organisms.

Candida↗
PubMed1967

Cryptococcus neoformans. I. Nonencapsulated mutants.

Seven nonencapsulated mutants of Cryptococcus neoformans were isolated from an encapsulated strain of human origin. Initially, the mutants were avirulent for mice. After several months of subculturing, six of the seven isolates reverted to the encapsulated state and possessed varying degrees of virulence. The results of these experiments suggest that a strong correlation exists between the presence of a capsule and the virulence of C. neoformans.

Animals↗
PubMed1967

Cryptococcus neoformans. II. Phagocytosis by human leukocytes.

Twenty-four per cent of the leukocytes from healthy human subjects phagocytized an encapsulated strain of Cryptococcus neoformans. Phagocytosis was approximately three times more effective with nonencapsulated mutants of C. neoformans. When the mutants reverted to the encapsulated state, the percentages of phagocytosis decreased. These data indicate that cryptococcal polysaccharide inhibits the phagocytosis of C. neoformans by human leukocytes.

Cryptococcus↗