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M Schardt

Publications and source records attributed to M Schardt.

26 records · Page 2Linked to original sources
PubMed1979

Cancer progression and monocyte inflammatory dysfunction: relationship to tumour excision and metastasis.

In a longitudinal study performed before and after surgical resection of a chemically-induced, transplanted rat tumour we found that a monocytosis- and tumour-induced anti-inflammatory effect directed against macrophages was promptly corrected by tumour excision but recurred with metastasis. These observations indicate that the monocyte abnormalities are acquired and related to cancer progression. The anti-inflammatory effect required relatively large primary or metastatic tumour burdens. Our findings support the clinical impression that monocyte abnormalities are associated with a poor prognosis.

Animals↗
PubMed1979

Anti-inflammatory consequences of transplanted tumors.

Rats and mice bearing transplanted chemically induced neoplasms have defective macrophage infiltration of inflammatory sites distant to the tumor. The defect limits concurrently accumulation of macrophages within the tumor, raising dramatically the tumor to macrophage cell ratio. The defect may not compromise host surveillance because it requires relatively large numbers of tumor cells. The abnormality does not appear to result from circulating monocyte depletion, defective monocyte chemotaxis, or the traffic of monocytes into the tumor.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Anti-inflammatory effect of spontaneous lymphoma in SJL/J mice.

Histiocytic lymphomas develop spontaneously in about 80% of SJL/J mice between the ages of 8 and 14 months. These animals were used for the determination of whether spontaneously arising cancers compromise monocyte function similar to the monocyte defects described during growth of transplanted tumors. SJL/J mice with tumors accumulated significantly fewer macrophages than did age-matched animals without tumors either on sc implanted filters or in peritoneal exudates induced by phytohemagglutinin. There was no corresponding defect in polymorphonuclear neutrophil responses. Whereas no apparent correlation existed between tumor size and degree of inhibition, animals without demonstrable tumors had no inflammatory defects. Aging did not alter the inflammatory response to implanted filters but increased both the resident peritoneal macrophage population and the total macrophage yield to phytohemagglutinin provocation. When given transplants of histiocytic lymphomas, young SJL/J mice developed similar inflammatory defects. This study represents the first demonstration that spontaneous tumors, in addition to transplanted tumors, produce abnormalities in monocyte inflammatory responses.

Animals↗
PubMed1977

Hormonal control of neutrophil chemotactic activity in the rat vagina.

A sexual-hormone-dependent neutrophil chemotactic factor(s), operative under physiological conditions, is described. Rat vaginal washouts were shown to be both chemotactic and chemokinetic for rat neutrophils in vitro, whereas macrophages were not attracted. Peak activity was observed at the end of estrus and preceded maximal neutrophil infiltration in the vagina. In order to mimic these events, gonadectomized animals were treated with estradiol for a week. They showed a similar peak of chemotactic activity 30-36 h after estradiol withdrawal, accompanied by a massive neutrophil accumulation. These data suggest that a decrease in estradiol level permits the expression of the chemotactic signal. There was no evidence for chemotaxis and/or migration inhibitors before and during estrus or during long-term estradiol treatment of gonadectomized rats. Induced neutrophil accumulation in the peritoneal cavity and chemotactic responsiveness of these cells in vitro were similar in all stages during the estrus cycle. Estradiol, progesterone, testosterone, and hydrocortisone neither promoted nor significantly inhibited the neutrophil migratory behavior over a wide range of concentrations. Our experiments suggest that the periodic neutrophil accumulation in the rat vagina after estrus is triggered by locally expressed chemotactic mechanisms that are controlled by sexual hormones. The data provide the first evidence that hormonal changes can control chemotactic factors and thus indirectly control cell migration.

Animals↗