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Biomedical subjects

J Briere

Publications and source records attributed to J Briere.

124 records · Page 7Linked to original sources

[Hyperthyroidism by autonomous metastasis of thyroid carcinoma (author's transl)].

Nine years after surgical ablation of a trabeculo-vesicular carcinoma of the tyroid, a patient developped bone and liver metastasis. She had clinical signs of thyrotoxicosis, clear increase of blood T3 and sligh increase of T4. The TSH secretion was blocked. Exogenous TSH increased iodine uptake in the thyroid and not in the metastasis. After 2 doses of 120 mCi of 131I, she became hypothyroid, the liver was normal and the scan revealed the disappearance of uptake in thyroid and in metastasis. Such a clinical course was previously found in only 10 cases despite the frequent funcitonal differenciation of the metastasis of thyroid carcinomas.

Adenocarcinoma↗

[Prognostic factors in idiopathic myeloid splenomegaly].

The study of the evolution of 168 cases of idiopathic myeloid splenomegaly allowed to point out the prognostic value of the clinical, hematologic, isotopic and radiological parameters. The correlation of these data with the histological type of the osteomedullary lesions at the time of the diagnosis, allows to confirm the long survival of the hyperplastic formes (type I), and the more reserved prognosis in advanced myelofibroses (type II and type III together) without it being possible to bring out a significant difference between the average presumption of survival of type II and type III considered each separately. Indeed, average survival is of 82 months for type I, and 60 months for type II and type III together. The regrouping of these two types seems to be justified and allows to individualize two anatomoclinical forms. One is characterized by hyperplastic marrow with reticulinic fibrosis, usually associated with enlarged spleen and sometimes even with polyglobulia but without radiological bone lesions. The other form is characterized by a marrow of middle importance or frankly hypoplastic, fibrous, with or without osteosclerosis, and shows moderate or marked radiological changes (respectively 16,9 p. 100 of the cases, and, as a rule, pancytopenia.

Adolescent↗

Increased fibroblast colony stimulating activity (F-CSA) in serum of myeloproliferative disorders.

Sera of patients with primary myelofibrosis (PMF), primary thrombocythemia (PT), polycythaemia vera (PV) and chronic myeloid leukemia (CML) contained a significantly increased F-CSA (or F-CSAs) compared to those of normal subjects and patients with secondary thrombocytosis (ST). This F-CSA was heat sensitive and had the capacity to promote both proliferation and maturation of normal marrow fibroblast colony-forming cells (CFU-F). This F-CSA seemed to be different from human platelet derived growth factor (PDGF), tumor necrosis factor (TNF) and fibroblast growth factor (FGF) from bovine brain. This F-CSA might be of importance in the pathogenesis of bone marrow fibrosis in myeloproliferative disorders.

Animals↗

Effects of recombinant human interferon alpha on human megakaryocyte and fibroblast colony formation.

Effects of recombinant human interferon alpha (HuIFN-alpha) on human megakaryocyte (CFU-MK) and fibroblast (CFU-F) colony-forming cell growth were studied. Concentration-dependent inhibition of both CFU-MK and CFU-F by HuIFN-alpha was demonstrated. Statistically significant suppression of both CFU-MK and CFU-F was seen at a HuIFN-alpha concentration of 1000 U/ml or greater. No significant difference was found between HuIFN-alpha treated cultures and controls for the distribution of CFU-MK types and for the size and cell morphology of CFU-F. When a concentration of 1000 u/ml HuIFN-alpha was added at varying time points during the marrow cultures, decreased numbers of megakaryocyte and fibroblast colonies only appeared at the early days of cultures. When bone marrow cells were incubated with HuIFN-alpha for different periods of time prior to initiation of cultures, a reduction of megakaryocyte colony formation also occurred. These studies demonstrate a suppressive effect of HuIFN-alpha on human CFU-MK and CFU-F growth. This effect seems to occur at the initial stages of CFU-MK and CFU-F development.

Cells, Cultured↗