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Biomedical subjects

J Emerit

Publications and source records attributed to J Emerit.

At least 37 records · Page 2Linked to original sources
PubMed1988

[Prolonged delta antigen in the blood without occurrence of anti-delta antibodies in 2 immunosuppressed patients].

Delta coinfection or superinfection in a patient with chronic hepatitis B is characterized by a very transient delta antigenemia and an early seroconversion of IgM to IgG anti-delta. The persistent expression of delta antigen in the liver can be associated with acute, severe, or chronic hepatitis. In our two patients, delta antigenemia persisted respectively 10 weeks and 14 months with aggravation of liver histopathologic lesions without seroconversion. Such a serologic profile during delta infection does not seem to have been reported previously. These two cases concerned two patients with an important immunosuppression, one by a major immunosuppressive therapy and HIV superinfection, the other by an acquired immunodeficiency syndrome. The cytotoxic effect of delta virus in such circumstances is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1986

[Study of a marker of free radical activity in myocardial infarction and in the prodromal syndrome].

Myocardial ischemia is accompanied by a release of free radicals (FR) derived from oxygen, elements having an important cytotoxic activity. These FR react with unsaturated lipids from the membrane fatty acids, leading possibly to a lysis of the membrane. This lipidic peroxidation of the fatty acids generates, in fact, endoperoxides, unstable lipid by-products and also with a cytotoxic activity. At the end of these reactions, cyclical compound and aldehydes are formed, and it is possible to titrate one of them, the malondialdehyde (MDA) which represents a marker of the aggression of the radicals on the membranes. We have therefore studied the appearance of MDA in the systemic venous blood and compared 10 patients with a threat syndrome (group I) to 8 other patients with acute myocardial infarction (group II). The plasma MDA level is measured upon admission (D1), on the 5th day (D2) and on the 12th day (D3) of the evolution. We have therefore found a significant elevation of MDA in the two groups of patients at D1 and D2, in comparison with the results obtained in a reference group of 15 normal patients (p less than 0.01). In the infarction group, the level of MDA on the 12th day (189 +/- 41 ng/ml) drops significantly as compared to the highest level noted upon admission and on the 5th day, called MDA peak (258 +/- 62 ng/ml, p less than 0.01). The MDA drop is less marked in group I of the threat syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

[Study of lipid peroxidation by the assay of malondialdehyde in human and experimental atheroma].

Malondialdehyde is a marker for the oxidation of membrane unsaturated fatty acids. This biochemical process, called lipid peroxidation, occurs in the biosynthesis of leukotrienes, prostaglandins and other cytotoxic and chemotactic lipid peroxides. It may play a part in the genesis of atheroma from lipids stored in the arterial wall. Plasma malondialdehyde levels were found to be different in hyperlipidemic subjects with or without arterial lesions, and in rabbits under an atherogenic diet with or without added silicon. The same positive correlation was found in rabbit aorta between atheromatous lesions and high levels of malondialdehyde. These data would support the hypothesis that lipid peroxidation plays a role in atherogenesis.

Animals↗
PubMed1986

[Membrane lipid peroxidation in coronary insufficiency].

Malondialdehyde (MDA) as lipid peroxidation marker was studied in 27 patients with acute coronary insufficiency. Significantly elevated plasma levels as compared with controls were found in patients with myocardial necrosis and with preinfarction syndrome. No correlation was found between MDA and creatine phosphokinase, and a significant MDA decrease was observed at day 12: plasma MDA reached normal levels in the myocardial necrosis group. The MDA decrease was also significant in the preinfarction group, but the MDA level remained high in 4 patients with unstable angina. MDA is not a prognostic index. No correlation was found between MDA and plasma lipid levels or patients' ages. These data confirm that myocardial ischemia is associated with abnormal production of oxygen-derived free radicals which react with the membrane unsaturated fatty acids, resulting in toxic endoperoxides. This is thought to be one of the physio-pathological pathways which aggravate ischemic myocardial tissue damage.

Animals↗
PubMed1986

[Free radicals derived from oxygen and lipid peroxidation. Role in cellular biology and physiopathology].

Lipid peroxidation results from the attack of membrane phospholipids by free radicals derived from oxygen. It plays a major role in normal cell life processes. Under physiological conditions, this attack is modulated by an enzymatic system (superoxide dismutase, catalase, glutathione peroxidase) and by a non-enzymatic system (vitamin E and others). Many pathological processes might be explained by a deficient protection system or by an imbalance between attack and protection. Lipid peroxidation is difficult to detect and measure, and the methods available still have low sensitivity.

Animals↗
PubMed1986

[Free radical toxicity in coronary insufficiency].

A number of experimental models have shown abnormally high concentrations of cytotoxic oxygen derived free radicals (FR), and decreased concentrations of protecting anti-oxidising enzymes during myocardial ischaemia. These FR react with the unsaturated lipids of the cell membrane, a phenomenon known as membrane lipidoperoxidation (MLP) to produce very cytotoxic endoperoxides. We studied an intermediary product of MLP, malondialdehyde (MDA) in 10 patients with a preinfarction syndrome (Group 1) and 8 patients in the acute phase of myocardial infarction (Group 2). Plasma MDA was measured on admission (P2) and 12th day (P3). There was a significant elevation of MDA in both groups at P1 and P2 (p less than 0.01) compared with results obtained in 15 normal control subjects of the same age. The MDA concentration on the 12th day in the infarct group was significantly lower (189 +/- 41 ng/ml, p less than 0.01) compared with the highest value observed either on admission or on the 5th day (peak MDA 258 +/- 62 ng/ml). The difference between MDA concentrations on the 12th day and peak MDA was less striking in Group 1. None of the patients in Group 2 had a recurrence of chest pain after the initial phase of infarction and the residuals MDA concentration (P3) was similar to control values (181 +/- 27 ng/ml). On the other hand, in the preinfarction syndrome group, 4 patients had persistent unstable angina on the 12th day and their MDA concentrations remained high (250 +/- 42 ng/ml). This was interpreted as reflecting continuing MLP in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

[Lipid peroxidation and free radicals. Role in cellular biology and pathology].

Membrane phospholipids attack by oxygen free radicals, i.e. lipidoperoxidation, occurs in normal cellular life. This free radicals attack is controlled by a protective system, both enzymatic (superoxide dismutase, catalase, glutahione peroxidase) and non enzymatic (vitamine E). Imbalance between attack and defense can explain many pathological events. In these events, the oxidation products of unsaturated fatty acids are of fundamental importance, in particular those derived from arachidonic acid (prostaglandins, prostacyclins, thromboxanes and leukotrienes).

Animals↗
PubMed1984

[Fatty acids and lipid peroxidation in experimental atheroma in the rabbit. Role played by silicon].

Free fatty acids (FFA) and esterified fatty acids (EFA), lipid peroxidation were analysed in experimental atheroma. Among rabbits receiving cholesterol (formula; see text) compared with controls group in FFA and EFA on plasma and aortas: arachidonic acid in plasma and malonaldehyde (MDA) in plasma and aorta are increased with atheroma and there is a positive correlation between arachidonic acid, MDA, and arterial injury; organo silicic compounds when added to atherogenic diet, had a favorable action about these variations, organic silicon having an antiatheromatous action. Therefore it seems possible that unsaturated fatty acid's peroxidation had an injurious action on arteries in atheroma by discharging toxic endoperoxides; arachidonic acid is probably involved in thromboxane's generation, and consequently in aggregability of blood platelets.

Animals↗
PubMed1983

[Fatty acid and lipid peroxidation in human atherosclerosis].

Plasma fatty acids and lipid peroxidation were studied in human atherosclerosis. Analysis of fatty acids in 16 controls and 32 hyperlipidemic patients showed, in the latter, a decrease in saturated fatty acids, especially palmitic and stearic acids, and an increase in unsaturated fatty acids, especially arachidonic acid. Compared to hyperlipidemic patients without arterial injury, patients with arterial injury exhibit a significant increase in malonaldehyde (MDA). In the former, MDA concentrations are significantly increased compared to controls. Therefore, peroxidation of unsaturated fatty acids may have a deleterious effect on arteries in atheroma, through the release of toxic endoperoxydes and the metabolization of arachidonic acid into thromboxane, which is a platelet aggregator. Lipid peroxidation can also be demonstrated in other diseases: we found very high MDA concentration in 11 alcoholic patients (alcoholic hepatitis, cirrhosis) and 6 patients with inflammatory conditions such as Crohn disease.

Adult↗
PubMed1983

[Superoxide dismutase treatment of 2 cases of radiation-induced sclerosis].

Two patients with severe radio-induced necrosis were treated with bovine copper superoxide dismutase encapsulated in lysosomes (SOD). Two milligrams were injected subcutaneously every other day. This therapy was apparently effective on radio-induced inflammation and fibrosis. These are preliminary results that need confirmation. They suggest that SOD is useful, not only before radiation exposure, as a preventive, but also after exposure, as curative treatment for radiation injury.

Aged↗
PubMed1982

[Free radicals in medicine and biology].

Free radicals have long been well known by physicists but have only interested biologists since 1969 when Fridovich showed that O2 was produced during an enzymatic oxidation. O2 and related radicals are highly toxic. This implies that, in all aerobic cells, mechanisms exist which inactivate free radicals as soon as they are produced by oxidative metabolism. O2 radicals are eliminated by a family of enzymes called superoxide dismutases (SOD). These SOD are present in the cytosol (CuSOD) and in the mitochondria (MnSOD). Overproduction of free radicals, originating in molecular oxygen, may explain the lesions which result from inflammation, ischemia, and radiation exposure. Free radicals can cause damage to membranes, macromolecules, and DNA. Whether free radical production is mainly intracellular or extracellular may determine to a degree which kind of damage will occur.

Animals↗
PubMed1982

[Recent data on the epidemiology and etiology of Crohn's disease].

The disease described by Crohn and co-workers fifty years ago escapes precise definition as it involves not only the ileum but the whole digestive tract. When restricted to the colon, it cannot easily be differentiated from that other inflammatory disease of the large bowel: ulcerative colitis. Meanwhile, Crohn's disease seems to be increasingly frequent, spreading from north to south, with a higher incidence among Jews and relatives of patients presenting with the condition. This would suggest interaction between a specific genetic factor and an as yet undetermined environmental agent which becomes pathogenic in the digestive tract. The lesions of Crohn's disease point to an immune conflict but so far, no definite disorder of the immunoregulation system has been demonstrated.

Crohn Disease↗