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Biomedical subjects

J Guilbaud

Publications and source records attributed to J Guilbaud.

11 recordsLinked to original sources

European comparative clinical study of Inerpan: a new wound dressing in treatment of partial skin thickness burns.

Eleven European burns centres in five countries (Belgium, England, Germany, Italy, Switzerland) participated in a prospective, randomized clinical trial comparing a new wound dressing Inerpan with conventional dressings such as petroleum jelly gauze, petroleum jelly gauze with antibiotics and silver sulphadiazine cream. The indication was partial skin thickness burns and 62 patients were included. In each patient, two similar lesions (with respect to depth and surface area) were compared, one being treated with Inerpan, the other one with a control dressing. The following parameters were studied: healing time, quality of healing, intensity of pain, local tolerance and frequency of dressing changes. Analysis of the results showed that Inerpan-treated sites healed faster than conventional ones, and were associated with a highly significant reduction of pain. The frequency of dressing changes was greatly reduced and the local tolerance was good.

Adolescent

Effect of platelet-activating factor on tumor necrosis factor-induced superoxide generation from human neutrophils. Possible involvement of G proteins.

The effect of platelet-activating factor (PAF) and of two specific PAF antagonists on tumor necrosis factor (TNF) induced superoxide production by human polymorphonuclear neutrophils (PMN) was examined. PAF alone (0.1 pM to 0.1 nM) failed to evoke superoxide production; however, when PAF was added for 10 min to cells upon prior incubation with 10 ng/mL TNF for 50 min, superoxide production was significantly enhanced as compared to that induced by TNF alone. Maximum amplification (+30%) was obtained with 10 pM PAF; however, the effect was completely abolished by two structurally unrelated PAF antagonists, BN 52021 and BN 52111. The antagonists also decreased by 25% the superoxide production elicited solely by TNF, implicating the involvement of endogenous PAF in this process. Pretreatment of the PMN with either pertussis or cholera toxin attenuated the PAF amplified superoxide production in TNF stimulated cells, suggesting that G proteins sensitive to these toxins may be involved in the mechanisms controlling amplification.

Cholera Toxin

Biochemical and pharmacological properties of a neurotoxic protein isolated from the blood serum of heavily burned patients.

Blood serum of heavily burned patients contains neurotoxic substances which are not present in normal control sera. In the present paper, we describe the purification by gel filtration and ultracentrifugation of such a neurotoxic factor. The purified factor appeared to be a high molecular weight (2 to 3.10(6) daltons) lipoprotein. This factor was present in all the sera of patients with more than 35 per cent of the body surface burned. When injected into rabbits the lipoprotein caused a flattening of the EEG tracing, then trembling and convulsions with bursts of spikes on the EEG. The activity of this neurotoxic substance was enhanced when the permeability of the blood-brain barrier was increased by previous intraventricular injection of collagenase. The presence of such a neurotoxic factor in the blood serum of burned patients, together with the increased serum collagenase activity they exhibit may explain the neurotoxic symptoms observed in them.

Animals

Biochemical and pharmacological properties of a cardiotoxic factor isolated from the blood serum of burned patients.

Blood serum of severely burned patients contains several substances which are not present in normal sera. One of these substances, a small protein of an approximate molecular weight of 12 to 14,000 daltons displayed a toxic action on the circulatory system. This cardiotoxic factor was obtained in a purified form by alcohol precipitation followed by gel filtration and carboxymethyl cellulose chromatography. The purified preparation seems to be a low molecular weight protein of about 8000 daltons. The biological effects of this substance consist essentially of alterations of the ECG pattern, indicating decreased cardiac output and ischaemia of the cardial muscle. The blood pressure decreases and respiratory function is also altered. The presence of such a toxic factor in sufficient concentration in the blood serum may explain the cardiovascular complications observed in some burned patients.

Animals

Serum elastase and its inhibitors in the blood of heavily burnt patients.

Serum elastase and its inhibitors were determined in the sera of heavily burnt patients. Serum elastase levels were elevated at two to eight days after a severe burn-accident and returned towards normal values from the 10th day on. Both alpha1-antitrypsin and alpha2-macroglobulin levels were also elevated in the sera of heavily burnt patients. alpha1-Antitrypsin showed a parallel evolution to the elastase level but alpha2-macroglobulin followed a somewhat different time curve. Plasminogen and antithrombin were not elevated significantly. It is suggested that serum elastase may play a role in tissue degradation in burnt patients.

Antithrombin III

[Evolution of serum and erythrocyte magnesium levels in burn patients (author's transl)].

The study of the evolution of serum and erythrocyte magnesium in burn patients shows there exists, immediately after the thermic aggression, a reduction in the concentration of this cation. The hypomagnesemia is generally moderate and short; return to values considered normal is usually registered from the third day. Variations of the serum level are similar to those induced after a surgical operation. The hypothesis according to which there could exist a link between hypomagnesemia and a number of neuropsychiatric manifestations met simultaneously in the same patient cannot be excluded.

Adolescent

[Demonstration and partial characterization of cardiotoxic and neutrotoxic substances in the serum of burnt patients (author's transl)].

Cardio-circulatory and neurological complications may appear between the second and seventh day of treatment of severely burnt (greater than 30% of body surface, 3rd degree) patients between the 2nd and 7th day, even if their lesions follow an apparently favorable course. The purpose of the present work was to isolate substances from the sera of such patients which would be responsible for the toxic effects. The sera of several patients were fractionated by Cohn's method n degree 6 and the fractions were tested in vivo in rabbits, rats and mice for their toxic effects. We could demonstrate in some of the fractions (II + III, IV and VI) toxic activity on the central nervous system, on the cardiocirculatory and respiratory systems. An acute toxic activity was also present as well as a substance increasing the permeability of the blood-brain barrier. All these factors together may be involved in the production of the above-mentioned clinical symptoms. Their appearance may depend on the concentration of toxic substances in the blood and on the resistance of the patients.

Animals

Creatine kinase activity in suicide by burning.

In the course of a systematic study of serum enzymes activities from muscular tissues, applied to fifty six burnt patients taken at random, the authors have observed a significant and isolated raised of serum CPK in six burnt people when they were admitted to hospital. There were no known causes of raised CPK essentially due to muscular isozyme. The only common point between those six persons is that they all attempted to commit suicide by burning.

Burns

[Evolution of serum copper and zinc levels in burn patients (author's transl)].

The study of copper and zinc in 35 patients, over periods of up to 21 days following thermal injury, is marked by an important and early fall in serum copper and zinc levels. The maximum intensity of the biological disturbance appears about two days after the injury. Reversion to near normal values coincides with recovery from the large part of the lesions. The comparison of the evolution of serum levels does not permit any definite relationship to be established between copper and zinc metabolism.

Burns