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Nitrous oxide (N 2 O), nitric oxide (NO), denitrification losses and NO À 3 leaching from an irrigated sward were quantified under Mediterranean conditions. The effect of injected pig slurry (IPS) with and without the nitrification inhibitor dicyandiamide (DCD) was evaluated and also compared with that of a surface pig slurry application (SPS) and a control treatment (Control) without fertiliser. After application, fluxes of NO and N 2 O peaked from SPS (3.06 mg NO-N m )2 d )1 and 108 mg N 2 O-N m )2 d )1 ) and IPS (3.50 mg NO-N m )2 d )1 and 105 mg N 2 O-N m )2 d )1 ). However, when irrigation was applied, N 2 O and NO emissions declined. The total N 2 O and denitrification losses were slightly large from IPS than from SPS, although the differences were not significant (P < 0.05). Emission of NO was not affected by the method of pig slurry application. DCD inhibited nitrification during the first 20-30 days and reduced N 2 O and NO emissions from pig slurry by at least 46% and 37%, respectively. Considering the 215 days following pig slurry application, the emission factor of N 2 O based on N fertiliser was 1.60% (SPS), 2.95% (IPS), and 0.50% (IPS + DCD). The emission factor for NO was 0.14% (SPS), 0.12% (IPS), and 0.02% (IPS + DCD). Environmental conditions of the crop favoured the denitrification process as the most important source of N 2 O during the experimental period. The differences in the denitrification rate between treatments could be explained by the pattern of water soluble carbon (WSC), that was the highest value in injected pig slurry (with and without DCD). Due to low drainage (5% of water applied), leaching losses of NO À 3 were lower than those of denitrification from the upper soil layer (0-10 cm) in all treatments and especially with IPS + DCD, where the nitrification inhibitor was very efficient in reducing leaching losses.

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1. Treatment of rat brain microsomal membranes with a neuraminidase preparation from Clostridium perfringens resulted in an almost complete conversion of polysialogangliosides into monosialogangliosides. 2. Neuraminidase treatment of the membranes did not increase the incorporation of N-[(3)H]acetylneuraminic acid from CMP-N-[(3)H]acetylneuraminic acid into the gangliosidic fraction, indicating that a monosialoganglioside is an acceptor of N-acetylneuraminic acid in these membranes only if, in addition to having the right chemical structure, it is in a proper position, probably in relation to the endogenous sialyltransferases. 3. These experiments also indicated that no independent turnover of the neuraminidase-labile N-acetylneuraminyl groups of gangliosides occurred in vitro. 4. N-[(3)H]Acetylneuraminic acid from endogenous polysialogangliosides labelled in vitro was released by neuraminidase at a slower rate than N-acetylneuraminic acid from unlabelled gangliosides of the same membranes. From this it was concluded that recently synthesized polysialogangliosides (completed in vitro) are in the membranes in a position less accessible to neuraminidase than are those synthesized earlier which were present in the membranes at the start of the labelling experiment.