Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of six BALB/c mice each were intravenously inoculated with lethal doses of Ba-P210 (B210) or 12B1 cells and examined by autopsy, histology, special staining methods, enzyme histochemistry and immunohistochemistry. Clinical symptoms related to neoplasia consisted of a poor nutritional state, anaemia, mild to moderate dehydration and apathy. Paresis was apparent in three mice inoculated with 12B1 cells. Necropsy revealed splenomegaly in all animals. Sporadic haemorrhages in the lungs and enlargement of some lymph nodes were seen in some of the animals. Histological examination showed neoplastic cells in the spleen, in the bone marrow of the sternum, in the lung interstitium and in sinusoids of the liver in all mice. In six of nine brains examined, mild to moderate infiltration by neoplastic cells was observed. In all but two mice mild infiltration of the kidneys was found. The enlargement of lymph nodes was caused by an accumulation of neoplastic cells. The paresis was due to neoplastic infiltration of the vertebra, epidural space and spinal roots. Staining with Sudan black revealed cytoplasmic granules in neoplastic cells; however, the peroxidase reaction was negative. Numerous neoplastic cells disseminated in the red pulp of the spleen were reactive with CD3, CD79beta, CD11b and with neutrophil antibodies. We classified the disease induced by both of the cell lines as acute myeloid undifferentiated leukaemia (AML MO).
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PMID:Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice. 1618 May 44

During the resolution phase of inflammation, apoptotic leukocytes are efferocytosed by macrophages in a nonphlogistic fashion that results in diminished responses to bacterial moieties and production of anti-inflammatory cytokines. Complement receptor 3 and pro-resolving lipid mediators promote the engulfment of apoptotic leukocytes by macrophages. Here, we present evidence for the emergence of pro-resolving, CD11b(low) macrophages in vivo during the resolution of murine peritonitis. These macrophages are distinct from the majority of peritoneal macrophages in terms of their functional protein expression profile, as well as pro-resolving properties, such as apoptotic leukocyte engulfment, indifference to TLR ligands, and emigration to lymphoid organs. Notably, we also found macrophages convert from the CD11b(high) to the CD11b(low) phenotype upon interaction with apoptotic cells ex vivo. In addition, we found that the pro-resolving lipid mediators resolvin E1 and D1, and the glucocorticoid dexamethasone regulated pro-resolving macrophage functions in vivo. This regulation culminated in a novel pro-resolving function, namely reducing the apoptotic leukocyte ingestion requirement for CD11b(low) macrophage generation. These new phenotype and molecular pathway markers define the new satiated macrophage. Thus, we suggest that satisfying efferocytosis generates CD11b(low) macrophages that are essential for complete nonphlogistic containment of inflammatory agents and the termination of acute inflammation.
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PMID:Saturated-efferocytosis generates pro-resolving CD11b low macrophages: modulation by resolvins and glucocorticoids. 2126 7