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Biomedical subjects

C Cywiner-Golenzer

Publications and source records attributed to C Cywiner-Golenzer.

At least 37 records · Page 2Linked to original sources
PubMed1984

Tumoral calcinosis: light and electron microscopic study with electron diffraction and x-ray microanalysis of the mineral deposit.

Samples of deposits taken from sites close to articulations in a young black African suffering from tumoral calcinosis with hyperphosphoraemia were studied by light and electron microscopy techniques. Light microscopy demonstrated lesions of a foreign body granuloma type in contact with calcium salt deposits suggesting that the process was of an active nature. Electron microscopy, and the demonstration of acid phosphatase activity, led to the identification of two cell types: mono or multinuclear macrophage type cells which phagocytose the deposit, and fibroblastic type cells. No signs of damage to the microvessels or the interstitial collagen were noted which could serve as a basis or a physiopathological explanation of the deposition. The deposits were analysed by energy dispersive X-ray microanalysis and by electron diffraction and were considered to be hydroxyapatite.

Acid Phosphatase↗
PubMed1981

Gray platelet syndrome: alpha-granule deficiency. Its influence on platelet function.

The ultrastructure, cytochemistry, biochemistry, and functions of platelets from two patients with the familial gray platelet syndrome are described. Ultrastructural studies showed a lack of alpha-granules in the megakaryocytes in the vicinity of a marrow myelofibrosis and/or in platelets. A normal number of mitochondria and a slight increase of dense bodies was confirmed by labeling the whole patient with mepacrine. Platelet peroxidase (in the dense tubular system) and catalase-positive granules (revealed by the cytochemistry) were present. Platelets from both patients had severe deficiency of beta TG either after tritonization (less than 4% of normal) or thrombin treatment (less than 15% of normal), and the plasma beta TG levels were slightly increased. Functional studies of these platelets showed an uptake of [14C]5HT inhibited by reserpine similar to that in the control platelets. Thromboxane formation was within normal limits in the presence of arachidonic acid, ADP, collagen, or ionophore A23187, indicating that (1) the cyclooxygenase/thromboxane synthetase systems were not altered and (2) the phospholipase activities were not impaired. Although the platelet adhesion to prepolymerized fibrillar type III collagen and the ADP-, arachidonic acid-, and ionophore A23187-mediated aggregations were apparently normal, in every case the release of [14C]5HT was either at the low side of the normal range or decreased. This abnormality was increased when collagen or thrombin was added to either PRP or washed platelets from both patients, where at the same time, the aggregation and the release were markedly reduced. The results suggest that alpha-granules or their content has an influence on not only the platelet aggregation but also the dense bodies involved in the [14C]5HT release reaction.

Adolescent↗
PubMed1981

[Congenital deficiency of platelet alpha-granules and medullary reticulinic fibrosis. Physiopathogenic hypothesis (author's transl)].

Hematological investigations of two propositus from a family with congenital thrombopathia characterised by a moderate thrombopenia and a specific platelet alpha granule deficiency revealed that the thrombopathia was associated with a constitutive reticulinic myelofibrosis, without any sign of evolutivity. This association led us to present an hypothesis to explain the genesis of this myelofibrosis. This hypothesis is based on the potential role of a mitogenic factor(s) synthetized in megakaryocytes and transported normally by platelets in alpha granules, to induce fibroblastic proliferation and increased synthesis of collagen type III by bone marrow. This myelofibrosis is similar to that found in most of myeloproliferative disorders at some step of evolutivity. In these diseases myelofibrosis is associated with qualitative and quantitative abnormalities of platelets and megakaryocytes. These abnormalities give elements to sustain our hypothesis.

Blood Platelet Disorders↗
PubMed1978

[Pulmonary arterial hypertension caused by neoplastic thrombosis of the pulmonary artery].

Neoplastic thrombosis of the pulmonary artery is a rare and little known cause of pulmonary arterial hypertension. The clinical picture is one of acute respiratory failure and progressive right ventricular failure caused by pre-capillary pulmonary hypertension. In the living patient there is no way of distinguishing this condition from that of subacute cor pulmonale due to embolism, especially as the primary tumour is not always found either because it is too small or because it has already regressed by the time it has metastasised. The diagnosis usually rests on histological examination of the lungs, and two pathological types can be distinguished: carcinomatous lymphangitis with secondary invasion and thrombosis of the pulmonary arterioles on the one hand, and the neoplastic arterial emboli of a chorio-epithelioma on the other.

Adult↗
PubMed1977

[Diaphyseal bone tuberculosis].

The authors report a case of diaphyseal bony tuberculosis, in which the diagnosis was not made for a long time as bony tuberculosis is considered exceptional and owing to the presence of a staphylococcus which oriented the diagnosis towards osteomyelitis. Bony tuberculosis certainly affects more easily immigrant patients, in whom one may see multifocal forms, but also affects those who, by their environment, might imagine they are protected, and it is not exceptional to see unifocal forms.

Femur↗
PubMed1976

[Subcutaneous and tendinous nodules in scleroderma. Apropos of 4 anatomo-clinical cases].

The authors have observed 3 cases of pure scleroderma and one case of scleroderma in which tendinous or subcutaneous nodular structures were present. To the author's knowledge, such nodules have never been described previously in cases of scleroderma. Their site and their histology identifies them as "rheumatoid" nodules and at the same time provides other valuable information. Scleroderma is thus, together with rheumatoid polyarthritis and lupus erythematosus, one of the possible causes of nodule formation, and the authors put forward the hypothesis that these nodules might represent one of the first lesions of the Thibierge and Weissenbach syndrome.

Adult↗
PubMed1975

[Muscular disorders of the patient with scleroderma. Clinical study].

In scleroderma, the scapular striated muscles may be affected showing rapid fatigability, and sometimes, muscle wasting with EMG changes. The smooth muscle changes, well known in the esophagus, where they lead to loss of peristalsis, may also be marked in other parts of the digestive tract. They lead to various symptoms, such as cramps, vomiting and diarrhea.

Colic↗
PubMedDate not supplied

[Changes in the bone marrow in cancer patients. 61 bone marrow biopsies].

The authors studied 61 bone marrow biopsies carried out in cancerous patients, presumably suffering from a bone metastasis and before any treatment. They feel that quantitative and qualitative changes in the bone marrow may be considered to be an indirect diagnostic indication of metastatic spread.

Adult↗