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Biomedical subjects

L Barret

Publications and source records attributed to L Barret.

36 records · Page 2Linked to original sources
PubMed1985

Carbon monoxide poisoning, a diagnosis frequently overlooked.

Carbon monoxide (CO) is a common source of poisoning, yet the diagnosis is often overlooked. A study was undertaken to establish the true incidence of missed diagnosis and to assess retrospectively the effects of a campaign of public medical information on this subject. The wrong diagnoses reflected all the unusual clinical presentations that CO could produce. The high initial rate of wrong diagnoses (30% in 1975-1977) was reduced following the campaign (12% in 1978 and 5% in 1980) despite a considerable increase in the rate of admission to hospital of confirmed CO poisoning cases.

Carbon Monoxide Poisoning↗
PubMed1984

Trichloroethylene occupational exposure: elements for better prevention.

One hundred and eighty-eight workers occupationally exposed to trichloroethylene (TRI) were studied by physical examination, exposure parameters (measure of atmospheric TRI and urinary trichloroacetic acid (CA) and evaluation of personal factors (age, alcoholic and tobacco consumption). A statistical comparison (chi 2 test) of the frequency of the symptoms observed in the high- and low-exposure populations with an analysis of nonprofessional factors allowed us to distinguish different classes of symptoms. Those more likely linked with TRI exposure are trigeminal and optic nerve impairment, asthenia, headache and dizziness. An interaction between TRI exposure and alcohol intake on the occurrence of clinical liver impairment and degreaser flush is suggested.

Adult↗
PubMed1984

[Brain stem AEP in toxic comas. Correlation with brain stem reflexes].

24 deep toxic comas with respiratory assistance were studied by brain-stem reflex and BAEP. Laboratory analysis showed several simultaneous toxics (phenobarbital, benzodiazepines, tricyclic antidepressants...). Three groups of patients were defined: Twelve patients with normal BAEP and with relatively preserved brain-stem reflex (oculocephalic and oculovestibular are often disturbed but photomotor is present). Eleven patients with delayed BAEP and with more disturbed brain-stem reflex (photomotor is missing 3 times). In 2 cases (one of which is mentioned above in group B) brain-stem reflex and BAEP disappear and these patients die. Cerebral anoxia is associated here with toxics. Causes of delayed latencies (group B) are discussed (hypothermia, toxics). BAEP seems important in diagnosis and prognosis of toxic coma.

Adult↗
PubMed1983

[Poisoning with chlorine gas. Immediate and late sequelae].

The goal of this study is to appreciate the early and late sequelae caused by Chlorine Gas. 186 exposed patients have been admitted to our unit since 1962-119 had functional respiratory explorations (FRE) with an analysis of blood gases, 79 underwent a study of carbon monoxide transfer. The results are in accordance with the literature for example 25% of the CO transfer test were pathological. 56 occupationally exposed subjects having had at least three acute episodes of exposure have been compared to 197 control subjects (groups were classed in function of age, tobacco intake, and pulmonary antecedent). Chlorine exposure even when frequent has no the influence on the FRE results or the appearance of pulmonary pathology. The pre-existence of a pulmonary disease doesn't affect the prognosis.

Adult↗
PubMed1982

Evoked trigeminal nerve potential in chronic trichloroethylene intoxication.

Results of a study of trigeminal nerve impairment resulting from trichloroethylene intoxication by the somatosensory-evoked potential method reveal three kinds of abnormalities: increased stimulation voltage, excessive latency delay with morphological abnormalities, and excessive graph amplitude. These abnormalities confirm clinical disturbance (hypesthesia of the trigeminal nerve area) and open debate about the real mechanism of trichloroethylene neurotoxicity. Industrial intoxication by solvents, particularly trichloroethylene, is common. We have conducted a study of 188 workers chronically exposed to trichloroethylene and have confirmed the selective neurological disturbances of this intoxication in the trigeminal nerve (20%) [3, 10]. We utilized a new experimental method, developed for studies of chronic intoxications effecting the median nerve [5, 8], of recording the somatosensory evoked potential following stimulation of the trigeminal nerve [4, 6, 7]. The workers in this study were selected following clinical evaluation of their facial sensitivity and trigeminal nerve reflexes. In this paper we present our preliminary results on 11 workers, 9 suffering effects of intoxication and 2 controls.

Environmental Exposure↗
PubMed1982

[Value of the study of trigeminal nerve evoked potentials in chronic trichloroethylene poisoning. Preliminary results].

Results of a study concerning the trigeminal nerve impairment as the one caused by trichlorethylene chronic intoxication by somatosensory evoked potential reveal three kinds of anomalies: increase of the stimulation voltage, excessive latency delay with morphological anomalies and excessive graph amplitude. These anomalies confirm clinical disturbance (hypoesthesia in the trigeminal area) and open a debate about the real mechanism of the trichlorethylene neurotoxicity.

Adult↗
PubMedDate not supplied

Electron spin resonance study of free radicals produced from ethanol and acetaldehyde after exposure to a Fenton system or to brain and liver microsomes.

Free radical formation from ethanol and acetaldehyde was studied in the presence of a spin-trap and a NADPH generating system with a chemical model, Fenton's reagent, or by enzymatic oxidation of these solvents by rat liver and brain microsomes. The free radicals were detected by electron spin resonance spectroscopy (E.S.R.), using the spin-trapping agent, alpha-(4-pyridyl l-oxide)-N-tertbutyl-nitrone (POBN). Under such conditions, the hydroxyethyl radical derived from ethanol was obtained after both incubation in liver and brain microsomes as well as after exposure to the Fenton system. Enzymatic inhibition and activation showed that the mixed function oxidase system plays an important role in the generation of such a radical, even in the brain. Under all the experimental conditions acetaldehyde could also generate a free radical deriving directly from the parent molecule and modified by enzymatic activation or inhibition. A second, longer lasting radical was also observed in the presence of acetaldehyde. On the basis of a comparative study to a known process causing lipoperoxidation, its lipidic origin was suggested.

Acetaldehyde↗
PubMedDate not supplied

There is not simple method to maintain a constant ethanol concentration in long-term cell culture: keys to a solution applied to the survey of astrocytic ethanol absorption.

Ethanol evaporation from the culture medium is a potential source of misinterpretation of long-term exposure of cells. Different methods have been proposed to prevent this evaporation, the most effective being the saturation of the atmosphere over the culture medium with ethanol. Unfortunately, no simple predictive method has been devised to determine the appropriate concentration of ethanol in the system avoiding either evaporation or contamination of the culture medium. We present some keys to a solution adapted to the culture of astrocytes, which allow for the first time a direct evaluation of ethanol absorption by these cells. The system described remains compatible with normal growth and viability.

Absorption↗
PubMedDate not supplied

Chronic trichloroethylene intoxication: a new approach by trigeminal-evoked potentials?

Trigeminal nerve impairment is frequently seen in chronic trichlorethylene intoxication (TRI). A total of 104 occupationally exposed subjects were selected for study because they were employed at a highly exposed workplace. They were studied by clinical examination and by trigeminal somatosensory evoked potentials (TSEP). Normal values for TSEP were obtained from the study of 52 healthy nonexposed subjects. Facial hypoesthesia, when present, was global and predominant in the mandibular and maxillary nerve areas, associated or not with absent reflexes. A disturbed TSEP was found in 40 subjects which was predictable from their clinical symptoms. Correlation with exposure parameters (duration of exposure, trichlorethanol, and trichloracetic acid urinary rates) was mainly observed in subjects presenting both clinical and electrical alterations. Electrical alterations alone were less predictive. An abnormal TSEP may thus provide objective determination of risk assessment in the absence of clinical signs.

Adult↗
PubMedDate not supplied

Acute exposure of cultured neurones to ethanol results in reversible DNA single-strand breaks; whereas chronic exposure causes loss of cell viability.

AIMS: Ethanol can create progressive neuropathological and functional alterations of neurones. However, the influence of exposure duration is still debated. It is difficult to specify the level of alcohol consumption leading to alcohol-induced brain damage. Moreover, the mechanism of toxicity is assumed to combine direct and metabolically induced effects, although numerous uncertainties remain. Finally, the genotoxic power of ethanol has not fully been investigated in the brain. In the experiment reported herein, primary cultures of neurones were exposed either chronically or acutely to doses of ethanol within the range of blood alcohol levels in intoxicated humans. The impact on the integrity of neurones was assessed by cytotoxicity tests and DNA alterations by single-cell gel electrophoresis (Comet assay) and flow cytometry. Chronic ethanol exposure, even at a low dose, was more harmful to neurones than acute exposure. Both significant reductions in cell viability and DNA alterations were observed in this condition. On the other hand, DNA repair capacities seemed to be preserved as long as the viability measured by specific tests was not affected. Instead, neurones entered a death cell process compatible with apoptosis.

Analysis of Variance↗
PubMedDate not supplied

[Digitalis poisoning in children. Treatment with anti-digoxin Fab antibody fragments. Apropos of a case and a discussion of therapeutic indications].

We report one case of Digoxin intoxication in a child treated with Fab Fragments of Digoxin-Specific antibodies (Fabad), although there was no evidence of early life threatening complications. The efficacy of this treatment, which prevents further complications as well as its safety, represent strong arguments to treat children at the early stage of the intoxication in order to avoid temporary cardiac pacing.

Antibodies↗