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Many states have invested significant resources to identify components of their Phosphorus (P) Index that reliably estimate the relative risk of P loss and incentivize conservation management. However, differences in management recommendations and manure application guidelines for similar field conditions among state P Indices, coupled with minimal reductions in the extent of P-impaired surface waters and soil test P (STP) levels, led the U.S. Natural Resources Conservation Service (NRCS) to revise the 590 Nutrient Management Standard. In preparation for this revision, NRCS requested that a review of the scientific underpinnings and accuracy of current P Indices be undertaken. They also sought to standardize the interpretation and management implications of P Indices, including establishment of ratings above which P applications should be curtailed. Although some states have initiated STP thresholds above which no application of P is allowed, STP alone cannot define a site's risk of P loss. Phosphorus Indices are intended to account for all of the major factors leading to P loss. A rigorous evaluation of P Indices is needed to determine if they are directionally and magnitudinally correct. Although use of observed P loss data under various management scenarios is ideal, such data are spatially and temporally limited. Alternatively, the use of a locally validated water quality model that has been shown to provide accurate estimates of P loss may be the most expedient option to conduct Index assessments in the short time required by the newly revised 590 Standard., (Copyright © by the American Society of Agronomy, Crop Science Society of America, and Soil Science Society of America, Inc.)

The maturation of malarial parasites in red blood cells produces major alterations in the composition and properties of the host cell surfaces. Existing surface-exposed proteins are modified and new antigenic glycoproteins are synthesized by the parasite and inserted into the membrane. Some of the neoproteins are associated with surface excrescences on the host cells and in some cases these foster adhesion of those cells to capillary endothelium. The erythrocyte endoskeleton is degraded and in association the infected cells become deformed and lose pliability. An increase in intracellular Ca2+ may contribute to the changes in host cells surfaces.

Throughout its erythrocytic cycle the plasmodial parasite modifies the plasma membrane of its host cell. Some changes derive from parasite metabolism. Intraerythrocytic forms use glucose at more than 10-fold normal red cell rates. The H+ accompanying the lactate end-product is exported into the host cell cytoplasm by an electrogenic proton pump in the parasite membrane. This maintains a pH greater than 7.0 in the parasite cytoplasm, but lowers erythrocyte cytoplasmic pH from approximately 7.2 to 6.5. Ca2+ transport across parasite membranes is coupled to the proton pump, possibly a Ca2+/H+ antiporter. The Ca2+, Mg2+-ATPase and Na+,K+-ATPase activities of erythrocyte membranes from schizont-infected erythrocytes have been studied. Under optimal assay conditions (pH = 7.0; [ATP] = 1 mM; +/- calmodulin) membranes from infected cells showed a 30% reduction in Ca2+,Mg2+-ATPase activity but no difference from normal in Na+,K+-ATPase activity. The calmodulin levels of infected cells were depressed by about 30%. The [ATP] in the cytoplasm of infected erythrocytes was only 0.2 mM (as against 1.3 mM in normals) and at this ATP concentration the activities of both ATPases are only 30% of normal. Shifting the pH from 7.0 to 6.5 decreases Na+,K+-ATPase activity by an additional 50% but is without effect on the Ca2+,Mg2+-ATPase. The results provide a partial explanation for the increased Ca2+ permeability and altered Na+/K+ content of plasmodia-infected erythrocytes.