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In current work, the interaction between representative CFAS deposit (33CaO-10FeO 1.5 -13AlO 1.5 -44SiO 2) and Yb 4 Hf 3 O 12 ceramics at 1400 °C was investigated. Results indicated that the Yb 4 Hf 3 O 12 ceramics are of high resistance to infiltration of CFAS melt. Microstructure characterization revealed that Yb 4 Hf 3 O 12 reacted with CFAS to form a continuous reaction layer mainly composed of Yb-Ca-Si apatite, which inhibits CFAS further infiltration. Before the formation of the reaction layer, CFAS melts underwent a crystallization process at high temperatures, precipitating CaYbFeAlSi-garnet, which raised the viscosity of CFAS and thus inhibited the fluidity of CFAS. [ABSTRACT FROM AUTHOR]

In this work, Yb 4 Hf 3 O 12 ceramic, a typical rare-earth hafnate, was exposed to water vapor with Al(OH) 3 impurities at 1400 ℃, and microstructural evolution and corrosion mechanisms were investigated. The long-term corrosion can be divided into initial hydration and gasification of Hf4+ and steady-state corrosion after the formation of Al 5 Yb 3 O 12. In the initial stage, Hf4+ and the surrounding O2- tend to be hydrated and then volatilized in the form of Hf(OH) 4 , causing a metastable state of Yb 4 Hf 3 O 12 on the surface. Besides, the preferential corrosion of small grains, grain boundary, and specific crystal plane on the surface and sintered and densified grains result in varied corrosion behavior from the early linear law to the later parabolic law. In the steady-state corrosion stage, due to the consumption of Hf4+, more vacancies promote bonding and diffusion of Al3+ to form corrosion product (Al 5 Yb 3 O 12), and during this stage, regrowth and shedding of the corrosion layer reach a dynamic balance. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.11.003 Byline: Min Deng (a), Ling Pan (a), Xiaoling Xie (a), Lin Gan (a)(b)(c) Keywords: LIM; LMO; LMO4; Otic vesicle; Otocyst; Vestibular morphogenesis; Inner ear development; Transcription factor Abstract: During development, compartmentalization of an early embryonic structure produces blocks of cells with distinct properties and developmental potentials. The auditory and vestibular components of vertebrate inner ears are derived from defined compartments within the otocyst during embryogenesis. The vestibular apparatus, including three semicircular canals, saccule, utricle, and their associated sensory organs, detects angular and linear acceleration of the head and relays the information through vestibular neurons to vestibular nuclei in the brainstem. How the early developmental events manifest vestibular structures at the molecular level is largely unknown. Here, we show that LMO4, a LIM-domain-only transcriptional regulator, is required for the formation of semicircular canals and their associated sensory cristae. Targeted disruption of Lmo4 resulted in the dysmorphogenesis of the vestibule and in the absence of three semicircular canals, anterior and posterior cristae. In Lmo4-null otocysts, canal outpouches failed to form and cell proliferation was reduced in the dorsolateral region. Expression analysis of the known otic markers showed that Lmo4 is essential for the normal expression of Bmp4, Fgf10, Msx1, Isl1, Gata3, and Dlx5 in the dorsolateral domain of the otocyst, whereas the initial compartmentalization of the otocyst remains unaffected. Our results demonstrate that Lmo4 controls the development of the dorsolateral otocyst into semicircular canals and cristae through two distinct mechanisms: regulating the expression of otic specific genes and stimulating the proliferation of the dorsolateral part of the otocyst. Author Affiliation: (a) University of Rochester Flaum Eye Institute, University of Rochester, Rochester, NY 14642, USA (b) Center for Neural Development and Disease, University of Rochester, Rochester, NY 14642, USA (c) Department of Neurobiology and Anatomy, University of Rochester, Rochester, NY 14642, USA Article History: Received 26 November 2008; Revised 4 November 2009; Accepted 4 November 2009

The effects and underlying mechanisms of metformin which can improve glucose homeostasis of fish have rarely been explored. This experiment aimed to explore the influence of metformin on growth performance, body composition, liver health, hepatic glucolipid metabolic capacity and IR/PI 3 K/AKT pathway in grass carp (Ctenopharyngodon idella) fed high-carbohydrate diets. A normal diet (Control) and high carbohydrate diets with metformin supplementation (0.00 %, 0.20 %, 0.40 %, 0.60 % and 0.80 %) were configured. Six groups of healthy fish were fed with the experimental diet for eight weeks. The results showed that the growth performance of grass carp was impaired in high carbohydrate diet. Impairment of IR/PI 3 K/AKT signalling pathway reduced insulin sensitivity, while hepatic oxidative stress damage and decreased immunity affected liver metabolic function. The glycolysis and lipolysis decrease while the gluconeogenesis and fat synthesis increase, which triggers hyperglycaemia and lipid deposition in the body. Metformin supplementation restored the growth performance of grass carp. Metformin improved IR/PI 3 K/AKT pathway signalling and alleviated insulin resistance, while liver antioxidant capacity and immunity were enhanced resulting in the restoration of liver health. The elevation of glycolysis and lipolysis maintains glycaemic homeostasis and reduces lipid deposition, respectively. These results suggest that metformin supplementation restores liver health and activates the IR/PI 3 K/AKT signalling pathway, ameliorating insulin resistance and glucose-lipid metabolism disorders caused by a high-carbohydrate diet. As judged by HOMA-IR, the optimum supplementation level of metformin in grass carp (C. idella) fed a high-carbohydrate diet is 0.67 %. [Display omitted] • Metformin returns HOMA-IR to normal levels in grass carp. • Metformin repairs liver injury and improves antioxidant capacity in grass carp. • Metformin improves lipid metabolism and reduces body lipid deposition in grass carp. • Metformin activates the IR/PI 3 K/AKT pathway to improve glycolipid metabolism. • The optimum level of metformin in high carbohydrate diet for grass carp was 0.67 %. [ABSTRACT FROM AUTHOR]

In mice, all of the six retinal neuron types are generated from common multipotent retinal progenitors, and their differentiation from progenitors is regulated by both extrinsic and intrinsic factors. Previously, we showed that targeted deletion of the atonal (ato) homologue math5 blocked the differentiation of most retinal ganglion cells (RGCs), revealing an essential role for math5 in RGC differentiation. In this study, we used the Cre-loxP recombination system to trace the fate of math5-expressing cells in retina. Our results demonstrated that math5 expression was associated with the differentiation of multiple retinal neuron types, including RGCs, photoreceptor, horizontal, and amacrine cells, implying that math5 expression alone is not sufficient to determine the RGC fate. Math5 expression was restricted to postmitotic cells in developing retina, suggesting that cell fate commitment of retinal neurons occurs after the terminal mitosis. The insufficiency of and requirement for math5 in RGC differentiation indicates that, like ato in the development of Drosophila R8 photoreceptors, math5 plays a role in determining the RGC competence state of retinal progenitors and that additional positive and negative factors are required in determining RGC fate. Furthermore, we show that loss of Math5 function severely reduced the RGC expression of the transcription factors Brn-3b, Gfi-1, Isl-1, Isl-2, Nscl-1, Nscl-2, and RPF-1, suggesting that Math5 expression is required to activate a comprehensive transcription network of RGC differentiation. Keywords: math5; Retina; Cell lineage; Neurogenesis; Retinal ganglion cells; Basic helix-loop-helix (bHLH)