[Changes in myocardial metabolism in patients with angina and normal coronary arteries].
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Biomedical subjects
Publications and source records attributed to P David.
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Heparinized human placental arteries (internal diameter less than or equal to 1 mm) were cross-linked with glutaraldehyde and implanted in infrarenal aortas in rats (n = 78). At three months and one year following aortic replacement, the neo-intimal hyperplasia covering the patent conduits and the host intima media were excised. Glycosaminoglycans (GAGs) and elastin were metabolically labelled in vitro with radioactive glucosamine and valine, respectively. The incorporation of 3H glucosamine into GAGs decreased sixfold in both neo-intima and host intima media from three months to one year. At three months, the 3H label of hyaluronic acid accounted for 66 per cent and 43 per cent of the 3H GAGs in the neo-intima and host aorta, respectively. At one year, 55 per cent of the 3H GAG label were identified as 3H heparan sulphate in the neo-intima and host intima media. From three months to one year, the ratio of chondroitin 4 sulphate (CS 4) to chondroitin 6 sulphate (CS 6) decreased from 6 to 1.5 in the neo-intima, whilst the ratio of CS 4 to CS 6 (0.6) was constant in the host aorta during the experimental period. At one year, the neo-intima contained elastin. The radioactive incorporation pattern of GAGs and the biosynthetic label of valylproline dipeptides indicated a decrease in biosynthetic activity in neo-intimal and the host aortic cells with progressing time in vivo.
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The authors report 43 observations of pulmonary or extra-pulmonary tuberculosis, bacteriologically proved, in which liver biopsies revealed more or less complete granulomatous lesions. The culture of 29 liver fragments on Löwenstein and Colestos medium enabled the identification of the tuberculous bacillum in only one case. In the other cases the hepatic lesion has only been related to the tuberculosis because of the clinical and bacteriological context. Therefore, besides exceptional cases where Koch bacillum is revealed in the liver parenchyma, it seems that granulomatosis can be considered a control for the delayed hypersensitivity reaction to the tuberculous antigens, and not to the tuberculous infection localized to liver.
The coexistence of gastroesophageal reflux (GER) and respiratory diseases has led us to raise three questions : 1) how frequent is GER in patients with chronic bronchitis?, 2) is the respiratory function in patients with chronic bronchitis different when they have a GER and when they do not?, 3) is the GER different in patients with chronic bronchitis and in subjects not suffering with chronic bronchitis? The study of esophageal pH after a test meal showed there was a GER in 29 out of the 47 patients studied. The measurements of lung volume, air flow, pulmonary compliance, as well as the alveolo-capillary transfer of carbon monoxide, showed that there was no difference in the lung function of bronchitics whether they had a reflux or not. On the other hand, refluxes are less frequent but longer in patients having bronchitis and a GER, than in those having a GER but not having bronchitis. This must be linked to a low esophageal clearance which could be related to the attack of bronchitis. Only a well carried out prospective study of the treatment of GER in patients will reveal if the reflux increases bronchitic symptoms.
In a group of 34 chronic alcohol addicts with neuropsychic manifestations--alcoholic encephalopathy (AE)--and 9 subjects with chronic non-alcoholic liver diseases, biochemical (ammonemia, pyruvicemia, lactacidemia), enzymatic (gamma-glutamyltranspeptidase (gamma-GPT)) and morphological assays were carried out comparatively with conventional liver investigations. Alcoholic liver disease was found present in 16 patients (47%). A peculiar biochemical profile was observed in subjects with hepato-alcoholic encephalopathy: ammonemia 191.3 +/- 70.3 gamma %, pyruvicemia 2.7 +/- 0.82 mg %, lactacidemia 15.76 mg % and gamma-GPT 80.5 U/l, as compared with ammonemia 121 +/- 33.5 gamma %, pyruvicemia 2.74 +/- 1.2 mg %, lactacidemia 16.65 mg % and gamma-GPT 42.6 U/l in AE without hepatic disease, and in non-alcoholic liver diseases in which ammonemia was 88.6 gamma % (in chronic hepatitis) and 126.3 gamma % (in hepatic cirrhosis). Thus, coexisting involvement of the liver and presence of portal-systemic shunts in AE can be estimated by the assay of certain biochemical and enzymatic parameters.
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