(C) 2010 Elsevier B.V. All rights reserved.”
“Precise in situ measurements of the high-frequency (f approximate to 560 kHz) shear modulus G of Pd(40)Cu(30)Ni(10)P(20) bulk metallic glass at heating rates 0: 38 <= (over dot)T <= 7.5 K/min have been performed. It has been found that

structural relaxation leads to an increase of G below the glass transition Nepicastat cell line temperature T(g) while decreasing it at T > T(g). A quantitative analysis of this phenomenon within the framework of the interstitialcy theory has shown that structural relaxation below T(g) can be understood as a decrease of the concentration of interstitialcy-like defects frozen-in upon glass production. The relaxation turns into defect multiplication on continued heating above T(g). The beginning of defect multiplication represents the glass transition temperature. An excellent agreement between calculated and experimental T(g) ‘s as a function of the heating rate has been found. (C) 2011 American Institute of Physics. [doi: 10.1063/1.3569749]“
“Understanding

liver development should lead to greater insights into liver diseases and improve therapeutic strategies. In a forward genetic screen for genes regulating liver development in zebrafish, we identified a mutant – oliver – that exhibits liver-specific defects. In oliver mutants, the liver is specified, bile ducts form and hepatocytes differentiate. However, the hepatocytes die shortly after their differentiation, and thus the resulting mutant liver consists mainly of biliary SB525334 concentration tissue. We identified a mutation in the gene encoding translocase of the outer mitochondrial membrane 22 (Tomm22) as responsible for selleck this phenotype. Mutations in tomm genes have been associated with mitochondrial dysfunction, but most studies on the effect of defective mitochondrial protein translocation have been carried out in cultured cells or unicellular organisms. Therefore, the tomm22 mutant represents an important vertebrate genetic model

to study mitochondrial biology and hepatic mitochondrial diseases. We further found that the temporary knockdown of Tomm22 levels by morpholino antisense oligonucleotides causes a specific hepatocyte degeneration phenotype that is reversible: new hepatocytes repopulate the liver as Tomm22 recovers to wild-type levels. The specificity and reversibility of hepatocyte ablation after temporary knockdown of Tomm22 provides an additional model to study liver regeneration, under conditions where most hepatocytes have died. We used this regeneration model to analyze the signaling commonalities between hepatocyte development and regeneration.”
“Background and aims: An increased number of circulating osteoprogenitor cells (OPCs) expressing bone-related proteins and the stem cell marker CD34 have been identified in women with postmenopausal osteoporosis, who also have stiffer arteries than nonosteoporotic subjects.