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Nitrification, a microbial process, is a key component and integral part of the nitrogen (N) cycle. Soil N is in a constant state of flux, moving and changing chemical forms. During nitrification, a relatively immobile N-form (NH 4 +) is converted into highly mobile nitrate-N (NO 3 ?). The nitrate formed is susceptible to losses via leaching and conversion to gaseous forms via denitrification. Often less than 30% of the applied N fertilizer is recovered in intensive agricultural systems, largely due to losses associated with and following nitrification. Nitrogen-use efficiency (NUE) is defined as the biomass produced per unit of assimilated N and is a conservative function in most biological systems. A better alternative is to define NUE as the dry matter produced per unit N applied and strive for improvements in agronomic yields through N recovery. Suppressing nitrification along with its associated N losses is potentially a key part in any strategy to improve N recovery and agronomic NUE. In many mature N-limited ecosystems, nitrification is reduced to a relatively minor flux. In such systems there is a high degree of internal N cycling with minimal loss of N. In contrast, in most high-production agricultural systems nitrification is a major process in N cycling with the resulting N losses and inefficiencies. This review presents the current state of knowledge on nitrification and associated N losses, and discusses strategies for controlling nitrification in agricultural systems. Limitations of the currently available nitrification inhibitors are highlighted. The concept of biological nitrification inhibition (BNI) is proposed for controlling nitrification in agricultural systems utilizing traits found in natural ecosystems. It is emphasized that suppression of nitrification in agricultural systems is a critical step required for improving agronomic NUE and maintaining environmental quality.  相似文献   

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Light scattering from fibrin structures, obtained by exposure of fibrinogen to thrombin, Batroxobin (Reptilase) or coagulant fraction extracted from Contortrix venom at 20 and and 37°C, show in every case that rod-like intermediates are formed in the beginning of the aggregation process. The fibrils differ in the extent of branching and in lateral aggregation. Contortrix enzyme causes the highest branching density but the lowest lateral aggregation. Thrombin and Batroxobin give almost identical results. A change of temperature from 20 to 37°C yields an increase in branching density and lateral aggregation for the fibrin structures induced by the two snake venoms. With thrombin, however, the branching density decreases with the elevated temperature while the lateral aggregation strongly increases. Mostly opaque clots are obtained, with the exception of the clots induced by thrombin at 37°C, where a fine or traslucent gel is obtained. A very low extent of branching and translucent gels are also found with thrombin at 20°C and pH 7.3 but at pH 9.5 no correlation between a preferential cleavange of fibrinopeptide B and the lateral aggregation could be detected. The opacity is discussed as being the result of inhomogeneity in both branching and lateral aggregation. A quantitative analysis of the angular dependence of the scattered light indicates that non-activated human fibrinogen exists at least in the two conformations of a long rod, L = 95 ± 5 nm, and a short rod of 47.5 ± 5 nm, with mass fractions of ~ 70 and 30%, respectively. Only the long rod conformation of the monomer is built in the fibril. The model of a pure end-to-end aggregation is shown to be unlikely and the possibility of an overlapping of the monomeric rods over a region of ~ 8 nm is discussed.  相似文献   

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