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Excess Levels (excess + level)
Selected AbstractsEffect of application form of nitrogen on oxalate accumulation and mineral uptake by napiergrass (Pennisetum purpureum)GRASSLAND SCIENCE, Issue 3 2010Mohammad Mijanur Rahman Abstract Oxalate occurs naturally in forage species, but excess levels of soluble oxalate adversely affect their nutritional quality as animal feed. Although induction of oxalate in plants has been associated with nitrate application, relatively little is known about oxalate in forage grasses. In the present study, we investigated oxalate accumulation and mineral uptake by napiergrass (Pennisetum purpureum, cv. dwarf-late) cultured in complete nutrient solution containing either solely nitrate or mainly ammonium as the main form of nitrogen. Total (shoot and root) yield of plants did not differ significantly between the nitrate and ammonium treatments. By contrast, the nitrogen form significantly affected oxalate accumulation and mineral uptake by plants. Nitrate application resulted in higher concentrations of soluble and insoluble oxalates in the shoot and soluble oxalate in the root than ammonium application. Nitrate application also resulted in higher concentrations of sodium and calcium in the shoot, and higher concentrations of sodium, calcium and magnesium in the root than ammonium application. The results suggest that the application of nitrate fertilizer as the sole source of nitrogen should be avoided in the cultivation of oxalate-rich forages, though further studies are needed under field conditions. [source] Expression of interleukin-1 receptors and their role in interleukin-1 actions in murine microglial cellsJOURNAL OF NEUROCHEMISTRY, Issue 4 2002Emmanuel Pinteaux Abstract Interleukin (IL)-1 is an important mediator of acute brain injury and inflammation, and has been implicated in chronic neurodegeneration. The main source of IL-1 in the CNS is microglial cells, which have also been suggested as targets for its action. However, no data exist demonstrating expression of IL-1 receptors [IL-1 type-I receptor (IL-1RI), IL-1 type-II receptor (IL-1RII) and IL-1 receptor accessory protein (IL-1RAcP)] on microglia. In the present study we investigated whether microglia express IL-1 receptors and whether they present target or modulatory properties for IL-1 actions. RT,PCR analysis demonstrated lower expression of IL-1RI and higher expression of IL-1RII mRNAs in mouse microglial cultures compared with mixed glial or pure astrocyte cultures. Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1,, IL-6 and prostaglandin-E2 (PGE2), and activated nuclear factor ,B (NF-,B) and the mitogen-activated protein kinases (MAPKs) p38, and extracellular signal-regulated protein kinase (ERK1/2), but not c-Jun N-terminal kinase (JNK) in microglial cultures. In comparison, IL-1, induced the release of PGE2, IL-6 and activated NF-,B, p38, JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures. IL-1, also failed to affect LPS-primed microglial cells. Interestingly, a neutralizing antibody to IL-1RII significantly increased the concentration of IL-1, in the medium of LPS-treated microglia and exacerbated the IL-1,-induced IL-6 release in mixed glia, providing the first evidence that microglial IL-1RII regulates IL-1, actions by binding excess levels of this cytokine during brain inflammation. [source] Pulmonary manifestations of light chain deposition diseaseRESPIROLOGY, Issue 5 2009Lisa RHO ABSTRACT Light chain deposition disease (LCDD) is a rare condition characterized by extracellular light chain deposition in tissues. Patients commonly have an underlying plasma cell dyscrasia, and produce excess levels of monoclonal light chains. Renal involvement is the most common clinical manifestation. Rarely, light chains are deposited in the lung. We present the pathologic and radiographic findings of three patients with biopsy-proven pulmonary light chain disease and a review of the literature. [source] Altered localization of gene expression in both ectoderm and mesoderm is associated with a murine strain difference in retinoic acid,induced forelimb ectrodactyly,BIRTH DEFECTS RESEARCH, Issue 6 2007Hirohito Shimizu Abstract BACKGROUND: Defects in digit number or fusion as a teratogenic response are well documented in humans and intensively studied in various mouse models. Maternal exposure to excess levels of all- trans -retinoic acid (RA) at gestational day 9.5 induces postaxial ectrodactyly (digit loss) in the murine C57BL/6N strain but not in the SWV/Fnn strain. METHODS: Whole-mount in situ hybridization was used to examine the differential expression of limb patterning genes at the transcriptional level between the two mouse strains following the maternal exposure to a teratogenic level of RA. The detection of a gene with altered expression was followed by either the evaluation of other genes that were synexpressed or with an assessment of downstream genes. RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Furthermore, although RA caused comparable reductions of Shh expression between the strains in the 12 h after administration, some Shh downstream genes were differentially expressed (e.g., Gli1, Ptc, and Hoxd13), whereas others were not (e.g., Fgf4, Bmp4, and Gremlin). CONCLUSIONS: It is proposed that altered gene expression in both pre-AER and mesoderm is involved in the pathogenesis of postaxial digit loss, and that because the alterations in the pre-AER occur relatively early in the temporal sequence of events, those changes are candidates for an initiating factor in the malformation. Birth Defects Research (Part A) 2007. © 2007 Wiley-Liss, Inc. [source] | ||||||||||