Higher temperature reduces the effects of litter quality on decomposition by aquatic fungi

1. We investigated the effects of riparian plant diversity (species number and identity) and temperature on microbially mediated leaf decomposition by assessing fungal biodiversity, fungal reproduction and leaf mass loss. 2. Leaves of five riparian plant species were first immersed in a stream to allow microbial colonisation and were then exposed, alone or in all possible combinations, at 16 or 24 °C in laboratory microcosms. 3. Fungal biodiversity was reduced by temperature but was not affected by litter diversity. Temperature altered fungal community composition with species of warmer climate, such as Lunulospora curvula, becoming dominant. 4. Fungal reproduction was affected by litter diversity, but not by temperature. Fungal reproduction in leaf mixtures did not differ or was lower than that expected from the weighted sum of fungal sporulation on individual leaf species. At the higher temperature, the negative effect of litter diversity on fungal reproduction decreased with the number of leaf species. 5. Leaf mass loss was affected by the identity of leaf mixtures (i.e. litter quality), but not by leaf species number. This was mainly explained by the negative correlation between leaf decomposition and initial lignin concentration of leaves. 6. At 24 °C, the negative effects of lignin on microbially mediated leaf decomposition diminished, suggesting that higher temperatures may weaken the effects of litter quality on plant litter decomposition in streams. 7. The reduction in the negative effects of lignin at the higher temperature resulted in an increased microbially mediated litter decomposition, which may favour invertebrate‐mediated litter decomposition leading to a depletion of litter stocks in streams.     

Competitive NMDA receptor antagonists raise electrically kindled generalized seizure thresholds

A sensitive method of estimation of generalized seizure thresholds (GSTs) was used to estimate the relative anticonvulsant potencies of four competitive NMDA antagonists against fully amygdala-kindled seizures. All of the antagonists tested showed potent, dose-dependent anticonvulsant activity following focal administration at doses causing no, or only minimal, overt behavioural abnormalities. These doses were similar to those which have previously been shown to inhibit the development of the kindling process i.e. which show antiepileptogenic activity. Two novel, competitive NMDA antagonists, CGP 37849 and CGP 39551, both unsaturated analogues of the NMDA antagonist AP5, showed by far the greatest anticonvulsant potencies (211-fold and 33-fold greater activity than the parent molecule, respectively). Recent reports of oral anticonvulsant activity of these two compounds in both rodent and primate models of epilepsy (12, 13) make them leading candidates for clinical testing as novel antiepileptic agents in man. Previous reports of weak or non-existent anticonvulsant activity of competitive NMDA antagonists in the kindling model of epilepsy most likely result from the use of experimental protocols which are inherently insensitive in detecting drug-induced changes in seizure thresholds.Special issue dedicated to Dr. Morris H. Aprison.     

Tissue distribution of a plasmid DNA encoding Hsp65 gene is dependent on the dose administered through intramuscular delivery

In order to assess a new strategy of DNA vaccine for a more complete understanding of its action in immune response, it is important to determine the in vivo biodistribution fate and antigen expression. In previous studies, our group focused on the prophylactic and therapeutic use of a plasmid DNA encoding the Mycobacterium leprae 65-kDa heat shock protein (Hsp65) and achieved an efficient immune response induction as well as protection against virulent M. tuberculosis challenge. In the present study, we examined in vivo tissue distribution of naked DNA-Hsp65 vaccine, the Hsp65 message, genome integration and methylation status of plasmid DNA. The DNA-Hsp65 was detectable in several tissue types, indicating that DNA-Hsp65 disseminates widely throughout the body. The biodistribution was dose-dependent. In contrast, RT-PCR detected the Hsp65 message for at least 15 days in muscle or liver tissue from immunized mice. We also analyzed the methylation status and integration of the injected plasmid DNA into the host cellular genome. The bacterial methylation pattern persisted for at least 6 months, indicating that the plasmid DNA-Hsp65 does not replicate in mammalian tissue, and Southern blot analysis showed that plasmid DNA was not integrated. These results have important implications for the use of DNA-Hsp65 vaccine in a clinical setting and open new perspectives for DNA vaccines and new considerations about the inoculation site and delivery system.