Modelling the spatial distribution of ammonia emissions from seabirds in the UK.

Knowledge of the sources and distribution of ammonia (NH3) emissions underpins our understanding of the nitrogen budget. Research has focused on quantifying NH3 emissions from anthropogenic sources, whilst those from natural sources have received little attention internationally. Seabirds excrete large quantities of nitrogen, making seabird colonies a major natural source of NH3. Ammonia emissions from each UK seabird species were estimated and combined with population distribution data to model their spatial distribution. Total NH3 emissions from UK seabirds were estimated at 2.7 kt per year. Seabird emissions are concentrated in remote parts of the UK where anthropogenic emissions are small, so that seabirds often represent the main source of NH3 emissions in these areas. Seabird NH3 emissions were found to have increased by 34% since the 1970s. This corresponds to population changes which may be influenced by human activities, showing that even this natural source can be anthropogenically modified.

Pharmacokinetics and pharmacodynamics of methylprednisolone in obesity.

Methylprednisolone pharmacokinetics and its directly suppressive effects on plasma cortisol, blood histamine (basophils), and circulating helper T cells were evaluated in six obese (at least 35% above ideal body weight) men and six nonobese male volunteers. Methylprednisolone doses of 0.6 mg/kg total body weight were administered as the 21-succinate sodium salt. Absolute clearance (in liters per hour) of methylprednisolone was 40% less in the obese subjects. Total volume of distribution (Vss) of methylprednisolone was unchanged (about 120 L), but when normalized for total body weight, Vss per kilogram was less in obesity. The patterns of cortisol, blood histamine, and helper T cell responses after methylprednisolone administration were similar in both groups, but more profound effects were observed in the obese subjects. Pharmacodynamic models were applied for these immediate effects of methylprednisolone based on the premise that receptor interactions of steroids are followed by rapid suppression of the circadian rhythm of cortisol and recirculation of basophils and helper T cells, which persist until inhibitory concentrations (IC50) of methylprednisolone disappear. Similar IC50 values for the three effects were obtained in both groups, indicating no intrinsic pharmacodynamic differences in sensitivity to these methylprednisolone effects in obesity. However, methylprednisolone should be administered on the basis of ideal body weight, and the dosing interval should be potentially lengthened because of decreased methylprednisolone clearance in obesity.