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Biomedical subjects

E Bertrand

Publications and source records attributed to E Bertrand.

243 records · Page 14Linked to original sources
PubMedDate not supplied

[Heart and schistosomiasis (author's transl)].

The review is based on three studies previously reported and involving the clinical, epidemiological and hemodynamic aspects of this problem. Schistosomasis may give frequently (21.6 p. 100) an arterial pulmonary hyperpressure related to the development of granulomas and arteriolitis. A myocarditis may be suspected but is rarely proved. Anemia and specific treatment are also responsible for myocardial deficiency. The parasitic changes of the urinary tract may give a systemic hypertension. Some very rare cases of acute pulmonary heart insufficiency have been reported and the responsibility of schistosomiasis in constrictive fibrous endomyocarditis is still questionned.

Animals↗
PubMedDate not supplied

[Clinical features of constrictive endomyocardial fibrosis (author's transl)].

Constrictive endomyocardial fibrosis is very frequent in tropical areas with a hot and rainy climate. Young patients and specially male ones are generaly concerned. The onset is gradual and low-giving an adiastolic condition which may prevail on the right or the left heart. Some periods of more acute evolution may be observed. Death is caused by adiastolic disorders, thrombosis or arythmia. Aetiology is still unknown. A surgical treatment may be considered in some cases.

Adolescent↗
PubMedDate not supplied

[Value of indirect immunofluorescence in the diagnosis of "Trypanosoma gambiense" trypanosomiasis. 46 cases (author's translation)].

Several indirect fluorescents reactions were performed on 46 trypanosomepositive specimens which had been confirmed by parasitologic diagnosis. 38 sera analysed before the commencement of treatment were found to have a G.M.R.T. equal to I:I, 350 and the titer of antibody was, in all cases, greater than I:320. In all cases in the first phase, the titer was I:640 or higher. Four cases were followed beyond the second month and their titers decreased slowly, becoming negative in the fifth month. In 12 cases in the second phase, the cerebrospinal fluid demonstrated fluorescent antibodies although 10 cases in the first phase were negative for these antibodies. Three cerebrospinal fluid were faintly positive and these corresponded to the second phase biologically. In the treatment of individuals (using the analysis of cerebrospinal fluid for antibody) the I.F.A.T. permits the classification of the patient into one of the two phases and enables the clinician to follow the course of therapeutic effectiveness. In mass screening, apparently healthy individuals possessing a serum titer of I:640 or higher are shown to need definitive treatment for trypanosomiasis, while those with titers of I:320 are those who may either be treated with Lomidine or tested regularly for change in serum titer.

Antibodies↗
PubMedDate not supplied

[50 cases of acute malaria: symptomatic study, especially cardiac].

The authors have studied 50 records of patients who had presented an acute attack of P. falciparum malaria. Both sexes were equally implied. Young people were predominant. The distribution of cases was about the same in the whole year. The fever decreases on the second day and increases on the third day (300/0). Among the classical signs: relative rarity of hepatomegalia (100/0), splenomegalia (10 0/0), jaundice (140/0), nervous symptoms (100/0). Vomiting is rather frequent (30 0/0). From the cardiovascular point of view a relative bradycardia is observed in 16 0/0 of the cases, and a relative tachycardia in 100/0 of the cases; hypotension in 100/0 of the cases. Electrocardiographic signs are observed in 360/0 of the cases; they are aspecific, concerning mainly ST-T anomalias (22 0/0) and a QT lengthening (200/0). The cardiothoracic ratio is higher than 0.5 in 320/0 of the cases. From the pulmonary point of view the authors have observed symptoms contemporary of the attack: two asthma attacks, three radiologic anomalias reminding of viral pneumopathias. The biological symptoms are mainly transitory functional renal insufficiency in 18 0/0 of the cases. Protection due to AS heterozygosis seems to be confirmed in this study. The efficiency of intravenous quinin treatment is certain.

Adolescent↗
PubMedDate not supplied

[Morphometric assessment of lesions in the dopaminergic nigrostriatal system in Parkinson disease].

The qualitative changes in substantia nigra were analysed in the material of 25 cases of Parkinson's disease. A morphometric quantitative study of depletion of pigmented dopaminergic cells of substantia nigra was performed in six long-term cases of the disease. In addition, the number of melanin nodules was assessed as a marker of cell disintegration. The results obtained were compared with the morphometric evaluation of neuronal depletion in the mesocorticolimbic system (ventral tegmental area-VTA). The qualitative study indicated that melanin depletion in dopaminergic cells of substantia nigra in Parkinson's disease is diffuse and it is located mainly in the lateral alfa layer. Neuronal depletion with concomitant numerous extracellular neuromelanin nodules and granules was observed. A slight astrocytic gliosis free of macrophages accompanied cellular changes. The qualitative changes in substantia nigra are similar to those observed in VTA. The morphometric evaluation revealed that depletion of dopaminergic neurons in substantia nigra in Parkinson's disease is 73%, on average, while in VTA it remains under 5%. Hence, depletion in substantia nigra is much more intense. The analysis of the relationship between the number of neurons in substantia nigra and the age of subjects in the control group indicated that the number of neurons decreased proportionally to the age. In the group under study no significant relationship between neurons depletion and duration of disease or patients age was found. In the studied group of patients with Parkinson's disease, the number of melanin nodules in substantia nigra was significantly higher than in controls.

Corpus Striatum↗
PubMedDate not supplied

[Current views on the mechanisms of dopaminergic neuron death of the nigrostriatal system in Parkinson's disease].

Current views on the pathogenesis of Parkinson's disease are presented. Studies, particularly those carried out during the last decade, highlight the significance of endogenic processes responsible for a cumulative production of neurotoxic substances, especially free oxygen radicals which exert chronic effect on neurons. In Parkinson's disease, overproduction of free radicals and concomitant failure of protective mechanisms are most likely. An excess of free radicals is cytotoxic because of their very high chemical activity and uncontrolled chain reactions with numerous organic compounds, especially those which are mostly responsible for vital functions of cells. Oxidative stress disturbs metabolism of the cell what finally leads to its death most probably due to damage of cell membrane. That results in increased plasma membrane permeability for calcium ions which activate several subcellular mechanisms and initiate the final phase of cell death. Nonprotein-bound "free" iron ions are the strongest and most dangerous generators of free oxygen radicals. It is thought that ferric (Fe-3+" iron bound to neuromelanin may play a profound role in the overproduction of especially cytotoxic hydroxyl radicals, derivatives of molecular oxygen. Both, oxygen stress inducing factor and the sequence of related biochemical disorders remain still unknown. However, the synergy of the excess of reactive oxygen metabolites (mainly free radicals), nitric oxide, "free" iron ions and neuromelanin may contribute considerably to the generation of oxygen stress.

Brain↗
PubMedDate not supplied

[Modern views on the pathogenesis of Wilson's disease].

Wilson's disease is a rare, multiorganic genetically coded disorder, induced by impaired copper transport. The recent identification of the disease gene and the discovery of gene product--copper transporting P-type ATPase that is integrate membranous protein has contributed greatly to better understanding of the pathogenesis. This protein is probably essential for incorporation of copper into ceruloplasmin and for its biliary excretion. Multiple mutations of Wilson's disease gene are responsible for the excess of so called "free" copper which is toxic to tissues. Copper toxicity involves first of all, functional disorders of many enzymatic systems, particularly those of respiratory chain enzymes. In the central nervous system, a special kind of copper toxicity is medicated by astroglia, so that a direct, harmful effect of both copper and ammonia on the brain is observed. The authors present a current review on biochemical mechanisms of copper toxicity and physiopathological significance of the CNS astroglia in Wilson's disease.

Hepatolenticular Degeneration↗