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M Dumas

Publications and source records attributed to M Dumas.

408 records · Page 23Linked to original sources
PubMedDate not supplied

[Nutritional lipidic factors of enzymatic phenobarbital induction in the rat. Effects of quantitative and qualitative composition of dietary lipids (author's transl)].

Diets containing increasing amounts of corn oil (0%, 1,5%, 3%, 4,5%, 6%), diets containing a same quantity (6%) of differents fats (corn oil, coconut oil, fish oil) and one free fat diet containing squalen (1,5%) were fed to rats. The UDP glucuronosyl transferase (UDPGT) activity of hepatic homogenate and cytochrome P 450 concentration of hepatic microsomal fractions were measured without or after phenobarbital treatment. 1. Presence of dietary lipids generally gives a moderate increase of these parameters, but the effect of fish oil is higher than of other fats. 2. With the phenobarbital treatment the induction of hepatic cyt P 450 and UDPGT is higher in the animals fed dietary fats than in animals fed free fat diets. However this difference is more important in the rats fed fish oil, less important with coconut oil and the lowest with corn oil. 3. The addition of squalen in the diet did not give variations of cyt P 450 hepatic concentration and UDPGT hepatic activity. The inducting effect of phenobarbital on microsomal cyt P 450 is unchanged but significantly enhanced in the case of hepatic UDPGT.

Animals↗
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[HIV-1 cognitive and motor syndrome].

The central nervous system (CNS) is often affected by HIV-1 infection. Over 40% of AIDS cases present with neurological symptoms and CNS lesion are detected by anatomical and pathological studies in 80 to 90% of AIDS cases. There may be infections and tumors secondary to the immunodeficiency and pathologies may occur directly due to the neurotropism of the virus. Neurological problems associated with HIV-infection include encephalopathies, myelopathies, neuropathies and myopathies. HIV-1-induced encephalopathy may develop at any stages of HIV-1 infection and affects all risk groups equally. Its frequency worldwide is between 4 and 65% among individuals seropositive for HIV-1. The frequencies reported differ between studies due to differences in sampling methods, geographical factors, diagnostic criteria and investigative methods used. The pathogenesis of HIV-1-associated encephalopathy is not understood, but there are several hypotheses. The involvement of HIV-1 infected macrophages and microglial cells has been demonstrated. Indirect mechanisms such as release of lymphokines (tumor necrosis factor-TNF alpha- and interleukin-1) and neurotoxicity of the HIV envelope protein, gp 120, have also been suggested. This disorder is known as HIV-1-associated cognitive and motor syndrome. It presents clinically as a form of sub-cortical dementia with cognitive problems, motor deficits and behavioral disorders depending on the type and stage of HIV infection. The diagnosis can only be made after all other infections and tumors common in HIV-1 patients have been ruled out by appropriate investigations such as cerebrospinal fluid analysis, cerebral scan and magnetic resonance imaging. Electrophysiological studies, such as evoked responses and electroencephalograms, are particularly useful in its diagnosis. Anatomical examination shows diffuse paleness of the white matter, multi-nucleated giant cells and microglial nodes. Neuropsychological studies could be of value in diagnosis and in assessing the response to anti-retroviral treatment. There is currently no specific therapy for HIV-1-associated cognitive and motor syndrome. The use of new nucleoside analogue drugs in combination with existing drugs may provide new approaches to managing these patients.

AIDS Dementia Complex↗