Microstructure and Fabric Transitions in Calcite Tectonites from the Sierra Alhamilla

A suite of marble specimens from the Sierra Alhamilla (Spain), deformed to large strains under natural conditions at about 300° C shows distinct variations in microstructure and fabrics. It can be demonstrated that the development of crystallographic preferred orientations and grain shape fabrics are strongly dependent on recrystallized grain size. This is interpreted to reflect the relative importance of various deformational mechanisms. Superplasticity seems to have a sharp upper grain size limit at 10–15 /smm. Within the power law creep regime, deformation in fine grained aggregates is probably dominated by diffusional, in coarser ones by dislocation mechanisms. The transition is a gradual one, and may span a grain size range of 30 /sm

Is HFE involved in increased hepcidin expression and hypoferremia in inflammation and anemia of chronic disease?

Inflammation influences iron balance in the whole organism. A common clinical manifestation of these changes is anemia of chronic disease (ACD; also called anemia of inflammation). Inflammation reduces duodenal iron absorption and increases macrophage iron retention, resulting in low serum iron concentrations (hyposideremia). Despite the protection hyposideremia provides against proliferating microorganisms, this ?iron withholding? reduces the iron available to maturing red blood cells and eventually contributes to the development of anemia. Hepcidin antimicrobial peptide (Hamp) is a hepatic defensin-like peptide hormone that inhibits duodenal iron absorption and macrophage iron release. Hamp is part of the type II acute phase response and is thought to have a crucial regulatory role in sequestering iron in the context of ACD. Mice with deficiencies in the hemochromatosis gene product, Hfe, mounted a general inflammatory response after injection of lipopolysaccharide but lacked appropriate Hamp expression and did not develop hyposideremia. These data suggest a previously unidentified role for Hfe in innate immunity and ACD

Enzymatic versus Electrocatalytic Oxidation of NADH at Carbon-Nanotube Electrodes Modified with Glucose Dehydrogenases: Application in a Bucky-Paper-Based Glucose Enzymatic Fuel Cell

International audienc

IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin

Hypoferremia is a common response to systemic infections or generalized inflammatory disorders. In mouse models, the development of hypoferremia during inflammation requires hepcidin, an iron regulatory peptide hormone produced in the liver, but the inflammatory signals that regulate hepcidin are largely unknown. Our studies in human liver cell cultures, mice, and human volunteers indicate that IL-6 is the necessary and sufficient cytokine for the induction of hepcidin during inflammation and that the IL-6–hepcidin axis is responsible for the hypoferremia of inflammation

Molecular cloning of a cDNA encoding calmodulin from <i>Neurospora crassa</i>

A full-length cDNA encoding Neurospora crassa calmodulin was isolated from λZAP II cDNA expression library. The open reading frame encodes a protein of 148 amino acid residues with a calculated Mr, of 16,865 Da. Using site-directed mutagenesis, the complete cDNA was ligated into a trc promoter-regulated bacterial expression vector to allow expression of N. crassa calmodulin in E. coli. The expressed protein was found to be identical to the native protein on the basis of some of its biochemical properties. Finally, Southern analysis of restriction digests of genomic DNA indicates that calmodulin is encoded by a single-copy gene

Bone morphogenetic proteins 2, 4, and 9 stimulate murine hepcidin 1 expression independently of Hfe, transferrin receptor 2 (Tfr2), and IL-6

Recently, it has been suggested that hepcidin, a peptide involved in iron homeostasis, is regulated by bone morphogenetic proteins (BMPs), apparently by binding to hemojuvelin (Hjv) as a coreceptor and signaling through Smad4. We investigate the role of Hfe, Tfr2 (transferrin receptor 2), and IL-6 in BMP2-, BMP4-, and BMP9-stimulated up-regulation of murine hepcidin, because these molecules, like Hjv, are known to be involved in hepcidin signaling. We show that the BMP signaling pathway acts independently of Hfe, Tfr2, and IL-6: The response to BMP2, BMP4, and BMP9 is similar in isolated hepatocytes of wild-type, Hfe(−/−), IL-6(−/−), and Tfr2(m) mutant mice. The potency of different human BMPs in stimulating hepcidin transcription by murine primary hepatocytes is BMP9 > BMP4 > BMP2. However, in human HepG2 cells, BMP4 and BMP9 are equally potent, whereas BMP2 requires a higher dose to become an effective hepcidin activator. Moreover, all of the tested BMPs are more potent regulators of hepcidin than IL-6 and thus are the most potent known stimulators of hepcidin transcription