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Spatial and temporal variations in vegetation dielectric properties strongly influence the microwave backscatter characteristics of forested landscapes. This paper examines the relationship between xylem tissue dielectric constant, xylem sap flux density, and xylem sap chemical composition as measured in the stems of two Norway Spruce (Picea abies [L.] Karst.) trees in the Fichtelgebirge region of Northern Bavaria, Germany. Dielectric constant and xylem sap flux were monitored continuously from June through October 1995, at several heights along the tree trunks. At the end of the measurement series, each tree was harvested, and its xylem sap extracted and analyzed to determine the concentrations of amino acids and cations. Results show that the sap flux density was correlated with vapor pressure deficit (VPD) at all heights in the stem. In contrast, the xylem tissue dielectric constant is influenced by VPD but can exhibit a significant temporal lag relative to changes in VPD. This lag varies with position along the tree trunk. The temporal variability of the dielectric constant is compared with both trees at several positions along the tree trunks. Results of xylem sap chemical analysis are presented. We show that spatial and temporal variability in the xylem tissue dielectric constant is influenced not only by water content, but by variations in xylem sap chemistry as well. This has important implications for microwave remote sensing of forested landscapes, as useful information may be acquired regarding stand physiology and water relations and where variations in dielectric properties within individual trees and across geographic areas can be significant error sources for forest inventory mapping.  相似文献   
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Glucose levels in rats with hyperglycemia induced by streptozotocin were determined after i.p. administration of marsupsin (1), pterosupin (2), and pterostilbene (3), three important phenolic constituents of the heartwood of Pterocarpus marsupium. Marsupsin and pterostilbene significantly lowered the blood glucose level of hyperglycemic rats, and the effect was comparable to that of 1,1-dimethylbiguanide (metformin).  相似文献   
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Nitric oxide (NO) is reported to cause neuronal damage through various mechanisms. The present study tests the hypothesis that NO synthase inhibition by N(omega)-nitro-L-arginine (NNLA) will result in decreased oxygen-derived free radical production leading to the preservation of cell membrane structure and function during cerebral hypoxia. Ten newborn piglets were pretreated with NNLA (40 mg/kg); five were subjected to hypoxia, whereas the other five were maintained with normoxia. An additional 10 piglets without NNLA treatment underwent the same conditions. Hypoxia was induced with a lowered FiO2 and documented biochemically by decreased cerebral ATP and phosphocreatine levels. Free radicals were detected by using electron spin resonance spectroscopy with a spin trapping technique. Results demonstrated that free radicals, corresponding to alkoxyl radicals, were induced by hypoxia but were inhibited by pretreatment with NNLA before inducing hypoxia. NNLA also inhibited hypoxia-induced generation of conjugated dienes, products of lipid peroxidation. Na+,K+-ATPase activity, an index of cellular membrane function, decreased following hypoxia but was preserved by pretreatment with NNLA. These data demonstrate that during hypoxia NO generates free radicals via peroxynitrite production, presumably causing lipid peroxidation and membrane dysfunction. These results suggest that NO is a potentially limiting factor in the peroxynitrite-mediated lipid peroxidation resulting in membrane injury.  相似文献   
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