omega-3 vs. omega-6 lipid emulsions differentially influence the plasma free fatty acid profile with impact on neutrophil functions. Lipid-based parenteral nutrition in septic patients may thus exert profound influence on sequelae and status of immunocompetence and inflammation.

No abstract

As the main nitrogen source in Malassezia furfur, tryptophan induces the formation of fluorochromes and pigments, which make the yeast less sensitive to UV light. To detect a chemical UV filter, M. furfur (CBS 1878) was incubated at 30 degrees C for 14 days on a pigment-inducing medium and agar extracts were purified by column chromatography, preparative TLC and HPLC. Structural analysis of the pure metabolites was performed by mass spectroscopy and NMR. A yellow compound eluting from the column with 64% acetonitrile was found to be a potential UV filter because of its broad UV absorption (lambda(max) 389, 315, 289, 212 nm). It was an indole derivative (C(20)H(13)N(3)O; pityriacitrin) which had recently been shown to be a potent UV filter in bacteria. Its UV protective properties were confirmed in a yeast model and also in humans. Pityriasis versicolor induced by Malassezia yeasts is characterized by depigmented skin areas showing reduced melanin synthesis but no increased UV sensitivity. This UV protection might be explained by the presence of pityriacitrin which is produced by M. furfur.

Using the interstitial space as a third compartment may introduce an error into the measurement of GFR with the Patlak plot technique. We found that the CT protocol in our study resulted in considerable overestimation of GFR as determined with the Patlak plot in patients with increased interstitial space.

Intraalveolar fibrin formation is a hallmark of many acute and chronic lung inflammatory processes. We investigated the influence of fibrin polymerization on biochemical and biophysical properties of a calf lung surfactant extract (CLSE) used for therapy of neonatal distress syndrome. Thrombin-induced coagulation of human fibrinogen (range, 0.04 to 4 mg/ml) in the presence of CLSE (2 mg/ml phospholipids) resulted in progressive loss of surface tension-lowering properties and adsorption facilities of this surfactant preparation; the CLSE-inhibitory capacity of desAABB-fibrin surpassed that of fibrinogen by more than two orders of magnitude. In parallel with the loss of surface activity, association of the predominant surfactant phospholipid dipalmitoylphosphatidylcholine (DPPC) (14C-labeled, admixed to 2 mg/ml CLSE) with polymerizing desAABB-fibrin occurred. A volume of 0.3 mg/ml insoluble fibrin effected a approximately 50% loss, and 0.6 mg/ml a > 90% loss, of DPPC from the aqueous phase. Dioleoylphosphatidylcholine, dipalmitoylphosphatidic acid, stearic acid, palmitic acid, and arachidonic acid, admixed to CLSE as labeled compounds, as well as total CLSE phospholipids were retained in polymerizing desAABB-fibrin with dose-effect curves superimposable to that of DPPC; no fibrin association was noted for 14C-glycerol-3-phosphate. Polymerizing desAA-fibrin, generated by incubation of CLSE-fibrinogen mixtures with arvin, captured DPPC and resulted in loss of surface properties at even lower concentrations, compared with desAABB-fibrin. In contrast, CLSE incubation with preformed desAABB- and desAA-fibrin polymers did not cause substantial phospholipid coupling with the clot material or loss of surface properties. Microtiter plate-immobilized fibrinogen and desAABB- and desAA-fibrinomonomers did not bind CLSE phospholipids enriched with 14C-DPPC.(ABSTRACT TRUNCATED AT 250 WORDS)