PubMed Health⌕ Search

Biomedical subjects

M Cote

Publications and source records attributed to M Cote.

At least 19 recordsLinked to original sources
PubMed1984

[Population distribution in Algeria: inertia and change].

"This study is an attempt to measure the meaning of the inter-regional movements of population in Algeria during a long period of time (1897-1977). As in the whole of the Mediterranean countries, these movements have resulted in rebalancing the differences in density between mountains and plains. Nevertheless, as a result of demographic growth, the population in the mountains is much denser than it was in 1897. And the populations moving from the mountains have not settled equally in the different types of plains: coastal plains, and amongst them chiefly Algiers, received most of it." (summary in ENG, GER)

Africa↗
PubMed1981

Components of alveolar-arterial O2 gradient during rest and exercise at sea level and high altitude.

To determine the effects of exercise and high altitude on the contributions of shunt, ventilation-perfusion (V/Q) nonhomogeneity, and diffusion limitation to the alveolar-arterial O2 gradient (AaDo2), we measured pulmonary exchange of O2, CO2, and six inert gases (SF6, ethane, cyclopropane, halothane, diethyl ether, and acetone) during rest and exercise in unanesthetized dogs at sea level and after acute exposure to an altitude of 6,096 m in a hypobaric chamber. Shunt and dead-space fractions, calculated from inert gas measurements, did not change. High altitude decreased the inert gas partial pressure gradients between mixed alveolar gas and mixed end-capillary blood, indicating that V/Q relationships became more homogeneous. Exercise had no effect on these gradients. At sea level, AaDo2 was mainly due to V/Q nonhomogeneity, with a small portion due to shunt. At high altitude, the contribution of shunt became negligible and that of V/Q nonhomogeneity diminished. These improvements were partially offset, however, by a gradient due to diffusion limitation. Exercise had no effect on AaDo2 or any of its components. At high altitude, estimated pulmonary O2 diffusing capacity averaged 20.8 ml.min-1 at rest and 35.3 ml-min-1.Torr-1 during exercise.

Altitude↗
PubMed1979

Cardiovascular evaluation of obligate heterozygotes in Friedreich's ataxia.

A study of 17 parents (obligate heterozygotes) of children with Friedreich's ataxia was carried out. In addition to medical histories and physical examinations, a standard 12 lead ECG tracing was obtained. In the age group below 50, there was no significant evidence of ischaemic or primary cardiomyopathy. Older subjects had more frequent risk factors for arteriosclerotic heart disease.

Adult↗
PubMed1979

Evolution of cardio-pulmonary involvement in Friedreich's ataxia.

The evolution of 15 patients initially evaluated during Phase One of the Quebec Cooperative Study of Friedreich's ataxia has been studied approximately three years later. It is concluded that the deterioration of cardio-pulmonary function in Friedreich's ataxia is multifactorial. The neuromyopathy (or the underlying metabolic or cellular defect) appears to be the main contributing factor to the deterioration of cardio-pulmonary function, which is exacerbated by the scoliosis and varying severity of the cardiomyopathy.

Adolescent↗
PubMed1978

Oxygen transport in patients with Friedreich's ataxia.

The hypothesis is that an abnormal oxygen-hemoglobin dissociation curve is a primary or a secondary defect in patients with Friedreich's ataxia was investigated in 12 subjects with this disease. Hemoglobin and P50 were measured and compared with age and sex matched controls. The mean hemoglobin concentration was 14.2 g% and the P50 was 26.25 torr for the patients and 13.8 g% and 26.27 torr in the controls. These results indicate that the oxygen transport system is normal in this disease and likely exclude an abnormal oxygen dissociation curve as a primary or a secondary factor in the pathophysiology of the cardiomyopathy and the neuromyopathy found in this disease.

Friedreich Ataxia↗
PubMed1976

Cardiological signs and symptoms in Friedreich's ataxia.

The cardiovascular signs and symptoms were recorded in 36 patients with typical Friedreich's Ataxia (Group Ia, Ib). Seventeen patients were asymptomatic and this did not correlate with the severity of the disease. No pathognomonic clinical constellation was found to reveal the underlying cardiomyopathy.

Adolescent↗
PubMed1976

Electrocardiographic and vectocardiographic findings in Friedreich's ataxia.

Electrocardiographic and vectocardiographic changes are frequent in Friedreich's ataxia. In one of 35 patients both tests were normal. The vectocardiogram is more explicit in demonstrating the severity of the QRS changes with a right ventricular hypertrophy pattern present in 60% of cases. Serial examination of ECG tracings are recommended to monitor the cardiomyopathy in this progressive neurological disorder, in order to detect the onset of congestive heart failure, significant tachyarrythmias, or obstructive cardiomypathy.

Atrial Fibrillation↗
PubMed1976

Hemodynamic findings in Friedreich's ataxia.

Thirteen patients with classical Friedreich's ataxia underwent cardiac catheterization with recordings of retrograde cardiac pressures, measurements of cardiac output and calculation of the left ventricular volumes and mass. The cardiomyopathy in Friedreich's ataxia falls into the hypertrophic group of cardiomyopathies with decreased compliance of ventricular myocardium, varying degrees of concentric and asymmetric hypertrophy and outflow tract obstruction. Although there is no clear parallel between the degree of abnormal hemodynamic findings and the degree of neurological impairment, severely handicapped patients may present a diffusely hypertrophied and hypokinetic left ventricular myocardium.

Adolescent↗
PubMed1976

Cardiac angiographic findings in Friedreich's ataxia.

Angiograms of 12 patients with typical Friedreich's ataxia were analyzed. The results corroborate previous reports and justify the conclusion that the cardiomyopathy is of the hypertrophic type. In 10 of 12 cases, the hypertrophy is concentric, and non obstructive. Less frequently (2 cases), this hypertrophy is accompanied by diffuse hypokinesis and depressed ejection fraction.

Angiocardiography↗
PubMed1976

Pathology of the heart in Friedreich's ataxia: review of the literature and report of one case.

A single case of typical Friedreich's ataxia was analyzed for cardiac changes and compared to the findings from the literature. Macroscopically, there was a cardiomegaly with some degree of ventricular hypertrophy and probable mild dilatation of the auricles. The more important and constant histologic changes were myocardial fibrosis and degeneration of the cardiac muscle cells. Granular deposits of calcium salts and iron were found in the muscle cells. A cardiomyopathy hypertrophic in type and occasionally obstructive appears to be an integral part of Friedreich's ataxia.

Adult↗