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Biomedical subjects

R Le Menn

Publications and source records attributed to R Le Menn.

7 recordsLinked to original sources
PubMed1979

[Ultrastructural study on the effect of an inhibitor of platelet aggregation (author's transl)].

10-Methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) is introduced into human platelet-rich plasma at different stages of collagen-, ADP- or epinephrine-induced aggregation. Ultrastructural fixation is processed while aggregation on the same plasma sample is recorded. If introduced before the aggregating agent, nicergoline completely neutralises its action and the platelets become spherical. The microtubule marginal bundle is disorganized and both open and dense canalicular systems are modified. If intoduced after the aggregating agent, nicergoline immediately stops the aggregation and disaggregation follows, with complete separation of the platelets. Morphology of microtubules and canalicular systems depend on the time before application of nicergoline. Nicergoline stops the induction of aggregation as well as ADP release. Disaggregation is an active process involving the microtubules.

Blood Platelets↗
PubMed1978

[Platelet volume in essential thrombopenia].

The electronic method for measuring platelet volume using the Coulter Z BI Counter coupled with a Channelyser C 1000 has been standardized. The distribution of platelet volumes was studied in 28 cases of idiopathic thrombocytopenic purpura (ITP) and in 59 cases of thrombocytopenia attributed to a failure of platelet production. Results showed that the volumetric distribution curve of platelet rich plasma (PRP) was altered in 40 cases, by the presence of small particles interfering with platelets of small volume and/or by residual red cells modifying its terminal segment. These abnormalities seem linked to the degree of thrombopenia, but independent of its central or peripheral origin. A method of isolation and concentration of platelets in an albumin gradient allowed the restoration of the classical volume distribution in 24 cases out of 40. Simulated thrombopenias obtained by dilution of platelets in their own platelet poor plasma (PPP) showed that the abnormalities in the small volume range could be reproduced in vitro by modifying the proportion of platelets and of small residual elements in the PRP. When the albumin gradient method was used, the classical distribution of platelet volumes was found. Preliminary electron-microscopy studies show that the small elements in the PRP of thrombopenic subjects could be formed by red cell fragments. Cytoenzymologic studies should be able to confirm this. Volumetric parameters were determined from the asymmetric and unimodual distribution of platelets, either directly on PRP or after concentration and separation of platelets in an albumin gradient. They showed that platelet volumes were very often increased in ITP but also occasionnally in thrombopenia of attributed to a failure of production.

Blood Platelets↗
PubMed1976

[Megakaryocytes and platelets in congenital thrombopathies].

Different HT have been studied with the electron microscope and the findings compared to those in the literature. Five patients with thrombasthenia and three with Willebrand's diseases showed various disorders, usually anisocytosis and hypertrophic open canalicular system, in relation to regenerative states. Thirteen young children with 21-trisomy (2 with leukemia) and 13/15 trisomy (1 case) had enlarged platelets with abnormalities of membranes and vacuoles indicating some metabolic disorders and necrotic lesions. One child with Cooley's anemia showed a few granules and necrotic lesions. All these symptoms were related to regenerative or primitive megakaryocytopathias. The lesion of these latter cell appears in other HT: aberrations of membranes in giant platelets syndroms (J. Bernard and J. P. Soulier syndrome), disorders in membranes and/or granules in thrombopenic thrombopathias, the short platelet life span in May-Hegglin anomaly, storage pool disease in Hermansky-Pudlak syndrome. Finally the ultrastructural abnormalities of the platelets mainly help to distinguish several diseases of megakaryocytes.

Blood Platelet Disorders↗
PubMed1976

[Ultrastructural study of 11 cases of obstructive myocardiography of the left ventricle].

A fragment of septum was removed for biopsy in 11 patients with obstructive cardiomyopathy who were undergoing surgery. Electron microscopi revealed an increase in the numbers of mitochondria, deposits of glycogen, and deforming fibrosis. As far as the components of muscle fibres are concerned, both lysis and synthesis of neosarcomeres are to be found, together with abnormalities of the Z band and disorientation of the myofibrils. The number and severity of these abnormalities were found to vary from patient to patient and also in different sections. Although these features are virtually constant in cases of obstructive cardiomyopathy, they are not specific for this condition; they are also found in cases of non-obstructive hypertrophic cardiomyopathy.

Cardiomyopathy, Hypertrophic↗
PubMed1975

[Ultrastructure of the blood platelets in the newborn infant and in the young mongolian child. Study of 13 cases].

Blood platelets from infant and new born mongolians were examined and compared taking into consideration existing or non existing haematologic anomalies, such as transitory leucoblastosis with or without hyperthrombocytosis and acute leucosis without thrombopenia. These abnormalities were correlated with the analysis of control samples from haematologically normal new-born and premature children as well as samples from adult mongolian, patients with other chromosomal alterations (13-15, phi) and new-born or adults with thrombocytosis. The presence of dysmorphic platelets could be observed in variable degrees and numbers in all the mongolian samples. The characters of the morphologic abnormalities, constantly observed with variations due to pathological causes, denote either metabolic or structural thrombopathy.

Acute Disease↗