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Biomedical subjects

M Clement

Publications and source records attributed to M Clement.

At least 37 records · Page 2Linked to original sources

HIV-1 V3 domain variation in brain and spleen of children with AIDS: tissue-specific evolution within host-determined quasispecies.

DNA coding for the principal neutralization epitope of HIV-1 (the V3 domain of the envelope glycoprotein gp120) was amplified by polymerase chain reaction from postmortem brain and spleen tissue of three perinatally infected children who died of AIDS with progressive encephalopathy. Sequences obtained directly (without cloning) from this DNA were compared with sequences of 52 molecular clones made from this DNA. Cluster analysis showed that V3 domain sequences from two of the three children were similar to sequences from the American MN/SC isolates, while those from one child were more closely similar to the Caribbean RF isolate. Comparison of sequences obtained directly with consensus sequences derived from cloned DNA showed that V3 sequences are characteristic for an individual host. In one child, the V3 sequence determined directly from brain DNA was very distant from the consensus brain clone sequence and from the spleen sequences, suggesting a diverging quasispecies distribution. Site-directed hybridization demonstrated that brain-specific sequences present in 33% of brain-derived clones were absent from clones derived from spleen. The evidence suggests that brain- and spleen-specific variants evolve independently within each host-delimited quasispecies.

Acquired Immunodeficiency Syndrome↗

Kinetics of rat peripheral nerve, forebrain and cerebellum alpha-tocopherol depletion: comparison with different organs.

Forty-two 60-d-old rats were fed a vitamin E-deficient diet for up to 8 wk and the kinetics of alpha-tocopherol depletion were measured in nervous tissue and various organs. In most tissues examined, including the sciatic nerve but not the cerebellum, the disappearance was biphasic, suggesting the existence of two pools of vitamin E. In forebrain the disappearance was poorly biphasic. After an 8-wk period of vitamin E deprivation, forebrain, cerebellum, sciatic nerve endoneurium, liver, heart, muscle, testes and serum vitamin E concentrations were 51, 64, 65, 10, 20, 20, 40, and 19%, respectively, of initial values.

Animals↗

Rapid characterization of oral and nonoral pigmented Bacteroides species with the ATB Anaerobes ID system.

The ATB Anaerobes ID system (API SYSTEM, La Balme Les Grottes, France) was evaluated for its ability to differentiate between species of the pigmented Bacteroides group. This identification system is based on the degradation of chromogenic substrates in combination with sugar fermentation reactions. The results showed that the ATB system can be useful for differentiation between the 10 pigmented Bacteroides species. However, additional tests may be necessary.

Bacteriological Techniques↗

Brain alterations induced by vitamin E deficiency and intoxication with methyl ethyl ketone peroxide.

Rats fed a vitamin E-deficient diet from age 3-10 weeks were either maintained on a vitamin E-deficient diet or fed a vitamin E-enriched diet for 8 subsequent weeks. The content of vitamin E, endoperoxide-derived malonaldehyde, lipofluorescent material and polyunsaturated fatty acids, and the activities of catalase, glutathione reductase, and glutathione peroxidase were then measured in cerebral tissues, with or without intoxication with methyl ethyl ketone peroxide (MEKP). For this purpose, one half of the animals in each vitamin E group received an ip injection of 5 mg MEKP per kg of body weight, which was followed 44 hours later, i.e., 4 hours before sample collection, by a second ip injection of 15 mg MEKP per kg of body weight. Despite the fact that the vitamin E concentration was 12-times lower in the brain of vitamin E-deficient rats, no significant change in other cerebral parameters was found between the two groups of animals. In contrast, the activity of selenium-glutathione peroxidase was markedly decreased in the liver of 10-week old vitamin E-deficient rats. Unexpectedly, acute systemic intoxication with MEKP caused only a small, albeit significant, decrease in glutathione reductase activity in the brain of vitamin E-sufficient rats, while no significant change in other cerebral parameters was observed in either group of animals. These results suggest that the central nervous system (CNS) is still substantially protected when its vitamin E content has been decreased to 3 micrograms/g fresh weight, and that systemic intoxication with MEKP may not cause lipid peroxidation in the CNS.

Animals↗

Alteration of the alpha-tocopherol content in the brain and peripheral nervous tissue of dysmyelinating mutants.

In the brain of quaking and shiverer mutants, vitamin E content was normal when related to both wet weight and dry weight. When related to lipid extract, phosphorus, and polyunsaturated fatty acids, vitamin E was slightly increased only in the quaking mutant. In the sciatic nerve from trembler mutants, vitamin E was 134% of control values in the dry material, but normal in relation to wet weight. It was 260% in the lipid extract and 716% based on phosphorus. In relation to total fatty acids, there was a threefold increase in trembler mutants. Interestingly, it was increased approximately three times when related to 18:2 n-6, 20:4 n-6, and 20:5 n-3, and seven times when related to 22:6 n-3. The fact that the amount of vitamin E in fresh weight was normal, suggests that vitamin E plays a role in some nonmembrane material, such as the extracellular matrix or the basal lamina.

Animals↗

Fatty acid composition of rat liver mitochondrial phospholipids during ethanol inhalation.

Male Sprague-Dawley rats were exposed to increasing concentrations (15-22 mg/l) of ethanol vapor over a 4-day period. Phospholipids were analyzed in liver mitochondria isolated from ethanol-treated and pair-weighted control animals. After a 2-day inhalation period, the proportion of monoenoic acids in total phospholipids increased, whereas that of arachidonic acid decreased. These changes were more striking in phosphatidylcholine (PC) than in phosphatidylethanolamine (PE). The decrease in 20:4 may be related to increased lipid peroxidation. After a 4-day inhalation period, quite different changes in phospholipid fatty acids were found. They consisted in a trend towards a more unsaturated system, the proportion of 20:4 being increased in PC and that of 22:6 in PE. This increase in polyunsaturated acids might be related to a direct ethanol effect on lipid structure and/or metabolism that would be linked to the high blood alcohol level present at this stage of ethanol intoxication.

Animals↗

The effect on epidermal DNA synthesis of a combination of topical steroid with either dithranol or tar as used for psoriasis.

The hairless mouse was used to investigate the effects of a combination of glucocorticosteroid with either dithranol or tar on epidermal DNA synthesis, in order to determine whether such combinations reduce epidermal DNA synthesis more effectively than the single agents. Dithranol alone produced a significant local inhibition of DNA synthesis at concentrations of 0.1% and 0.05% but not at lower concentrations. Dose-response data for dilutions of clobetasol propionate and betamethasone 17-valerate showed progressive diminution of both local and systemic effects with decreasing concentrations. An additive effect was found from combining clobetasol propionate with dithranol and from combining betamethasone 17-valerate with liquor picis carbonis. These combined preparations were tested again after storage for 6 months and 2 months respectively and showed no loss of efficacy. These results lend justification to the use of these combined preparations in the treatment of psoriasis.

Animals↗

Sunscreens.

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Animals↗