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Biomedical subjects

J Timsit

Publications and source records attributed to J Timsit.

At least 145 records · Page 8Linked to original sources
PubMed1982

[Diffuse normolipemic xanthomatosis and IgG monoclonal dysglobulinemia].

A 56-year-old man with diffuse cutaneous xanthomatosis had neither mucosal lesions nor diabetes insipidus. Cutaneous lesions were characterised by dermal histiocytic infiltration, without X bodies, associated with Touton's cells and abundant iron deposits. Plasma lipid levels were normal. A lambda G monoclonal dysglobulinemia was present without Bence-Jones proteinuria or myeloma, except for a moderate increase in medullary plasmocytic cell elements. The diagnosis of disseminated xanthomatosis was established, the differential diagnosis from other histiocytic proliferations, particularly diffuse plane xanthoma, being sometimes difficult. The relation between normolipaemic xanthomatosis and dysglobulinemia certainly exists, but no satisfactory pathogenic explanation was possible in this case, in the absence of cryoglobulin, paraprotein antilipoprotein activity, and cutaneous deposits of lipoprotein-paraprotein complexes.

Dysgammaglobulinemia↗
PubMed1980

Influence of some irritating or immunostimulating substances on experimental pleurisy in the rat.

Irritating substances, such as turpentine, carrageenan and a reticulo-endothelial system-activating immunostimulant (crude cell walls of Mycobacterium smegmatis), when administered parenterally, inhibit various types of experimental pleurisies. These anti-inflammatory properties may be related to the increase which they induce in serum and pleural exudate levels of haptoglobin and of oxidative activity towards paraphenylenediamine.

Adjuvants, Immunologic↗
PubMed1978

The influence of anti-inflammatory compounds on some effects of BCG in the rat.

In the rat, intravenous injection of BCG induced an increase in complement activity, oxidative activity towards paraphenylenediamine and serum haptoglobin level. A strong correlation was shown between oxidative activity and haptoglobin level. These increases were inhibited by glucocorticoids (cortisone, dexamethasone, methylprednisolone) but not by two non-steroidal anti-inflammatory drugs (indometacin, phenylbutazone). It is suggested that these BCG effects are related to the release of macrophage constituents and that this is inhibited by glucocorticoids.

Animals↗
PubMed1976

Induction of DNA synthesis in rat peritoneal macrophages in culture by a pleural inflammatory exudate.

Peritoneal macrophages in culture are blocked in the G0 phase of the cell cycle, but retain many of their functional characteristics such as phagocytic ability. Peritoneal macrophages have been thought to be a terminal cell type. It has been investigated whether such properties could be modified by a substance released in acute inflammatory exudates. For this purpose a pleural exudate obtained from rats injected with dextran (40,000) 4 hours before, was centrifuged to eliminate cells, sterilized by filtration on Millipore filter 0.22 mum and diluted 50% with 199 medium culture. This medium was used to treat normal and activated peritoneal macrophages in culture. The effects were observed 24, 48, 72, 96 hours after the beginning of treatment. An enhancement of spreading and capacity of phagocytosis was observed 24 hours after the beginning of treatment. After 48 hours, the number of cells incorporating tritiated thymidine increased and became highest 4 days later. These phenomena were also obtained with pleural exudate of inbred rats (Lewis, Wag) treating macrophages of the same strain and with rat pleural exudate treating mouse macrophages. No effects were observed with dextran alone. The chemical nature of the stimulatory factor remains to be elucidated.

Animals↗
PubMed1975

[The effect of prostaglandins E1 and A2 on the proliferation and phagocytosis of mouse peritoneal macrophages in culture].

The action of prostaglandins E1 and A2 was studied on the proliferation and the phagocytosis of mouse peritoneal macrophages in culture. The proliferation was not stimulated by prostaglandins E1 and A2, but the phagocytosis was increased by prostaglandin A2 and decreased by prostaglandin E1. These actions could be correlated with the regulatory role of prostaglandins.

Animals↗