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Biomedical subjects

F Oberling

Publications and source records attributed to F Oberling.

At least 145 records · Page 8Linked to original sources
PubMed1978

[Myelosclerosis : pseudo-tumors forms (author's transl)].

Signs of pseudo-tumor growth may be seen in myelosclerosis. Eight personal cases and a review of the literature are discussed in this article. The observations here reported cover pseudo-tumors occurring in ganglia, liver, suprarenals (3), abdomen and pancreas. They are classified as sclerotic haemopoietic tumors. This category has particular characteristics when compared to extra-medullary haemopoiesis, extra-medullary haemopoietic growths, and a fourth category, sarcoma-type malignant tumors in myelosclerosis. The identity of these last three entities is widely discussed in the literature. The main histological and cytological characteristics for pseudo-tumor diagnosis in myelosclerosis are reported here.

Abdominal Neoplasms↗
PubMed1977

Experimental bone marrow fat necrosis.

We have studied serially by light and electronmicroscopy the development of lesions of the adipose tissue of the bone marrow of the rabbit following intravenous injections of saponin. Two types of steatonecrotic lesions were seen: in the femur giant-cell granulomas surrounding necrotic fat cells and in the sternum, small foci of fat necrosis containing calcified deposits. In both cases the lesions were of ischemic origin and secondary to the destruction of the microcirculation of the bone marrow by saponin. These studies suggest that necrosis of the bone marrow fat cells can contribute to the pathogenesis of myelofibrosis. They also suggest that adipose tissue responds differently to ischemia depending on topography. In hematopoietic marrow necrosis of fat cells is followed by calcium deposits, whereas in fatty marrow necrosis leads to resorptive giant cell reaction.

Adipose Tissue↗
PubMed1977

[Comparative study of the regeneration of the microcirculation of rabbit femur bone marrow after curetage and at the time of experimental myelosclerosis].

Destruction and regeneration of the bone marrow microcirculation in rabbit femur have been studied after curetage and experimental myelosclerosis. Different lesions lead to comparable restoration processes such as: installation of supplying vascular networks, appearance of a neovascularisation progressively replaced by neighboring structures of normal interadipocytic networks.

Animals↗
PubMed1977

Normal active rosette-forming-cells in untreated patients with Hodgkin's disease.

The percentage of E-rosettes and active E-rosettes was determined in untreated patients with Hodgkin's disease. All patients had numbers of peripheral blood lymphocytes within the normal range (1,200-5,000 lymphocytes/cu mm). The mean percentage of E-rosettes was significantly lower in the patients (55 +/- 15.7) as compared to normal controls (63 +/- 6.7). No difference in the percentage of active E-rosettes was found (36.6 +/- 8.6 in controls versus 40.3 +/- 10.8 in patients).

Hodgkin Disease↗
PubMed1976

Autophagia in myeloid precursors: an explanation for neutropenia in Chediak-Higashi syndrome?

Neutropenia is an almost constant feature of Chediak-Higashi syndrome (CHS). There is evidence for a central mechanism of neutropenia. Ultrastructural studies of the bone marrow from a child with CHS showed marked autophagic phenomena within myeloid precursor cells and mature neutrophils. Autophagic vacuoles were randomly distributed in the cytoplasm of the cells from the granulocytic series and some of them contained giant granules which thus appeared particularly resistant to the autophagic process. The vital cellular damage through endophagocytosis suggests the possibility of intramedullary destruction as an explanation for neutropenia.

Agranulocytosis↗
PubMed1975

[Acquired C1-esterase inhibitor deficiencies during lymphoid syndromes].

Very marked abnormalities of the complement system were discovered in two patients suffering from a lymphoid syndrome and an IgM 7S dysglobulinaemia. The abnormalities in the complement system were related to a deficiency in C1-estérase (C1 INH). Several findings suggest that such a deficiency is acquired, in particular the absence of any family history of angio-neurotic oedema and, above all, the detection of a marked fall in levels of the C1 fraction which does not exist in the congenital form of deficiency of the inhibitor. The IgM 7S immunoglobulins found in the serum of both patients are probably responsible for the abnormalities in the complement system observed. Such acquired deficiencies in C1 INH are extremely rare since only a few cases have been reported in the literaute, in particular two cases in patients with lymphosarcoma with a serum IgM 7S.

Aged↗
PubMed1975

Lymphosarcoma, cold urticaria, IgG1 monoclonal cryoglobulin and complement abnormalities.

A patient with lymphosarcoma and cold urticaria showed evidence of complement activation by the classical pathway with low levels of the early complement components, normal levels of late acting components, normal functioning of the alternate pathway and reduction of the C1-inhibitor level. The serum contained an IgG1 monoclonal cryoglobulin responsible for the complement activation. In vitro tests demonstrated a high capacity of the serum to activate C1.

Cold Temperature↗