Habitat management: a tool to modify ecosystem impacts of nitrogen deposition?

Atmospheric nitrogen deposition has been shown to affect both the structure and the function of heathland ecosystems. Heathlands are semi-natural habitats and, as such, undergo regular management by mowing or burning. Different forms of management remove more or less nutrients from the system, so habitat management has the potential to mitigate some of the effects of atmospheric deposition. Data from a dynamic vegetation model and two field experiments are presented. The first involves nitrogen addition following different forms of habitat management. The second tests the use of habitat management to promote heathland recovery after a reduction in nitrogen deposition. Both modelling and experimental approaches suggest that plant and microbial response to nitrogen is affected by management. Shoot growth and rates of decomposition were lowest in plots managed using more intensive techniques, including mowing with litter removal and a high temperature burn. Field data also indicate that ecosystem recovery from prolonged elevated inputs of nitrogen may take many years, or even decades, even after the removal of plant and litter nitrogen stores which accompanies the more intensive forms of habitat management.

GM1 gangliosidosis (type 1) in a cat.

A kitten with clinical and morphological symptoms of a neurovisceral lysosomal-storage disease has been shown to have a marked deficiency of acidic beta-D-galactosidase in the brain, kidney and spleen. Chromatography on concanavalin A-Sepharose and inhibition studies with 2,5-dihydroxymethyl-3,4-dihydroxypyrrolidine, a selective inhibitor of the neutral broad-specificity beta-D-galactosidase, have shown that the residual beta-D-galactosidase at pH 4.0 in the tissues of the affected cat is due to the neutral beta-D-galactosidase and that there is a complete deficiency of the acidic (lysosomal) beta-D-galactosidase. There is marked accumulation in all tissues and excretion in the urine of neutral oligosaccharides. Analysis of these oligosaccharides by fast-atom-bombardment mass spectrometry and g.l.c. suggests that they arise from the incomplete catabolism of N-glycans of glycoproteins. The ganglioside content of all the tissues is elevated, and it has been shown by t.l.c. that the concentration of a ganglioside fraction with a mobility similar to that of GM1 ganglioside is particularly increased. There is also some evidence of accumulation of glycosaminoglycans in the brain. The clinical symptoms, the complete deficiency of acidic beta-D-galactosidase and the storage products in visceral organs all suggest that this is a case of feline GM1-type gangliosidosis comparable with the severe infantile (Type 1) form of the disease in humans.