Biomedical subjects
J Lavoie
Publications and source records attributed to J Lavoie.
Affinities and densities of high-affinity [3H]muscimol (GABA-A) binding sites and of central benzodiazepine receptors are unchanged in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy.
The integrity of GABA-A receptors and of central benzodiazepine receptors was evaluated in membrane preparations from prefrontal cortex and caudate nuclei obtained at autopsy from nine cirrhotic patients who died in hepatic coma and an equal number of age-matched control subjects. Histopathological studies revealed Alzheimer Type II astrocytosis in all cases in the cirrhotic group; controls were free from neurological, psychiatric or hepatic diseases. Binding to GABA-A receptors was studied using [3H]muscimol as radioligand. The integrity of central benzodiazepine receptors was evaluated using [3H]flunitrazepam and [3H]Ro15-1788. Data from saturation binding assays was analyzed by Scatchard plot. No modifications of either affinities (Kd) or densities (Bmax) of [3H]muscimol of central benzodiazepine binding sites were observed. These findings do not support recent suggestions that alterations of either high-affinity GABA or benzodiazepine receptors play a significant role in the pathogenesis of hepatic encephalopathy.
Ammonia: key factor in the pathogenesis of hepatic encephalopathy.
There is substantial clinical and experimental evidence to suggest that ammonia toxicity is a major factor in the pathogenesis of hepatic encephalopathy associated with subacute and chronic liver disease. Ammonia levels in patients with severe liver disease are frequently found to be elevated both in blood and cerebrospinal fluid (csf). Hepatic encephalopathy results in neuropathological damage of a similar nature (Alzheimer type II astrocytosis) to that found in patients with congenital hyperammonemia resulting from inherited defects of urea cycle enzymes. Following portocaval anastomosis in the rat, blood ammonia concentration is increased 2-fold, and brain ammonia is found to be increased 2-3-fold. Administration of ammonia salts or resins to rats with a portocaval anastomosis results in coma and in Alzheimer type II astrocytosis. Since the CNS is devoid of effective urea cycle activity, ammonia removal by brain relies on glutamine formation. Cerebrospinal fluid and brain glutamine are found to be significantly elevated in cirrhotic patients with encephalopathy and in rats following portocaval anastomosis. In both cases, glutamine is found to be elevated in a region-dependent manner. Several mechanisms have been proposed to explain the neurotoxic action of ammonia. Such mechanisms include: Modification of blood-brain barrier transport; alterations of cerebral energy metabolism; direct actions on the neuronal membrane; and decreased synthesis of releasable glutamate, resulting in impaired glutamatergic neurotransmission.
Cerebral GABA-ergic and glutamatergic function in hepatic encephalopathy.
Measurement of amino acids in brain tissue obtained at autopsy from cirrhotic patients dying in hepatic coma revealed a threefold increase in glutamine and a concomitant decrease in brain glutamate. The GABA levels were found to be unaltered. Studies using an animal model of portal-systemic encephalopathy gave similar results. Glutamic acid decarboxylase (GAD) activities were within normal limits, both in the brains of cirrhotic patients and portocaval-shunted rats. A previous study reported normal [3H]GABA binding to synaptic membrane preparations from cerebral cortex in these animals. Taken together, these findings suggest that cerebral GABA function is not impaired in hepatic encephalopathy associated with chronic liver disease and portal-systemic shunting. On the other hand, there is evidence to suggest that the releasable pool of glutamate may be depleted in brain in hepatic encephalopathy. Data consistent with this hypothesis include: Reduction in the evoked release of endogenous glutamate by superfusion of hippocampal slices with pathophysiological levels of ammonia; ammonia-induced reduction of glutamatergic neurotransmission; and an increase in the number of [3H]glutamate binding sites in synaptic membrane preparations from hyperammonemia rats and from rats with portocaval shunts. Such neurochemical changes may be of pathophysiological significance in hepatic encephalopathy.
Emissions of chemical compounds and bioaerosols during the secondary treatment of paper mill effluents.
This study identified and quantified the main chemical compounds--the substances responsible for the disagreeable odors--and the bioaerosols emitted during the biological treatment of paper mill effluents. It also identified the characteristics of the process that effects the generation or diffusion of these substances. All treatment stages were evaluated. Measuring sites were located as closely as possible to the potential emission sources. Measurements were taken in the summer in 11 paper mills during a 2- to 3-day period in each mill. Chemical compounds were evaluated by direct-reading instruments; bioaerosols were sampled by impaction and counted. Sulfur compounds, emitted into the air when the effluent or the sludge is stirred, had the highest concentrations; their presence was attributable to such things as kraft-type paper pulp. Next in concentration were the carbon and nitrogen oxides, ammonia, and some organic acids, produced by the action of microorganisms. These acids are found mainly in the sludge environment. Terpenes, which come from wood, are present at various locations in paper mills. Odor perception thresholds for most of these substances are much lower than those established to protect the health of workers. Significant concentrations of total bacteria, total molds, and endotoxins were measured at several sites. Gram-negative bacteria were high at only one site, whereas the mold Aspergillus fumigatus was occasionally present at low concentration. No actinomycetes bacteria were detected. The highest concentrations were measured where there was water or dust aerosolization. Emissions are therefore controlled by controlling the operations that lead to the dispersion of water and particles into the air.
[For better political expertise of nurses].
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[The historical analysis of migration: the pertinence of longitudinal analysis based on retrospective histories].
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