Fluoride evaporation and crystallization behavior of CaF2–CaO–Al2O3–(TiO2) slag for electroslag remelting of Ti-containing steels

To elucidate the behavior of slag films in an electroslag remelting process, the fluoride evaporation and crystallization of CaF₂–CaO–Al₂O₃–(TiO₂) slags were studied using the single hot thermocouple technique. The crystallization mechanism of TiO₂-bearing slag was identified based on kinetic analysis. The fluoride evaporation and incubation time of crystallization in TiO₂-free slag are found to considerably decrease with decreasing isothermal temperature down to 1503 K. Fish-bone and flower-like CaO crystals precipitate in TiO₂-free slag melt, which is accompanied by CaF₂ evaporation from slag melt above 1503 K. Below 1503 K, only near-spherical CaF₂ crystals form with an incubation time of less than 1 s, and the crystallization is completed within 1 s. The addition of 8.1wt% TiO₂ largely prevents the fluoride evaporation from slag melt and promotes the slag crystallization. TiO₂ addition leads to the precipitation of needle-like perovskite (CaTiO₃) crystals instead of CaO crystals in the slag. The crystallization of perovskite (CaTiO₃) occurs by bulk nucleation and diffusion-controlled one-dimensional growth.     

混合基底记法的无失真图像信息隐藏技术的改进及实验研究

无失真信息隐藏技术,可以使一个原始图像在经过藏入、取出秘密信息之后依然完整存储,为了进一步改进压缩域图像信息隐藏方法,文中提出了一种基于混合基底记法的无失真图像信息隐藏技术,主要做了以下工作：给出了应用的VQ编码、SMVQ编码的理论基础;完成了基于混合基底记法的信息隐藏的设计;应用6张512×512像素的灰度图片完成了实验结果验证。实验结果表明：新方法与传统的基于边缘匹配矢量量化编码方法相比,减少了秘密信息嵌入时间,提高了秘密信息嵌入容量。     

Basic amino-acid side chains regulate transmembrane integrin signalling

Side chains of Lys/Arg near transmembrane domain (TMD) membrane-water interfaces can 'snorkel', placing their positive charge near negatively charged phospholipid head groups; however, snorkelling's functional effects are obscure. Integrin β TMDs have such conserved basic amino acids. Here we use NMR spectroscopy to show that integrin β(3)(Lys?716) helps determine β(3) TMD topography. The α(ΙΙb)β(3) TMD structure indicates that precise β(3) TMD crossing angles enable the assembly of outer and inner membrane 'clasps' that hold the αβ TMD together to limit transmembrane signalling. Mutation of β(3)(Lys?716) caused dissociation of α(ΙΙb)β(3) TMDs and integrin activation. To confirm that altered topography of β(3)(Lys?716) mutants activated α(ΙΙb)β(3), we used directed evolution of β(3)(K716A) to identify substitutions restoring default state. Introduction of Pro(711) at the midpoint of β(3) TMD (A711P) increased α(ΙΙb)β(3) TMD association and inactivated integrin α(ΙΙb)β(3)(A711P,K716A). β(3)(Pro?711) introduced a TMD kink of 30?±?1° precisely at the border of the outer and inner membrane clasps, thereby decoupling the tilt between these segments. Thus, widely occurring snorkelling residues in TMDs can help maintain TMD topography and membrane-embedding, thereby regulating transmembrane signalling.     

DESIGNING THE OPTIMUM CONFIGURATIONS OF CIRCULAR AND SPHERICAL PRODUCT SPECIFICATIONS FOR MULTIPLE QUALITY CHARACTERISTICS

1. Introduction The problem of determining an optimal tolerance is equivalent to the problem of determining optimal specification limits, since the term tolerance refers to the distance between its lower and upper specification limits. Functional performance and economic considerations are the two primary factors affecting the design of tolerances. A tighttolerance usually implies high manufacturing cost due to additional manufacturing operations, slow processing rates, additional care on part…     

ROLE OF FUNGAL LACCASE AND LOW MOLECULAR MEDIATORS ON DECOLOURIZATION OF AROMATIC DYES IN PAPER MILL EFFLUENTS

INTRODUCTIONFungal laccases (benzenediol:oxygen oxidoreductases, EC 1.10.3.2) are multicopper oxidases, capable of reducing oxygen to water and simultaneously involved in oxidation of aromatic hydrogen donors. These enzymes and very similar polyphenol oxidases can be used as free or immobilized type both in water or in some organic solvents for improving several biotechnological processes (Burton etal. 1995; Luterek etal. 1998; Milstein etal. 1993). Of possible applications, the enzyme i…     

Quantification of actinide alpha-radiation damage in minerals and ceramics

There are large amounts of heavy alpha-emitters in nuclear waste and nuclear materials inventories stored in various sites around the world. These include plutonium and minor actinides such as americium and curium. In preparation for geological disposal there is consensus that actinides that have been separated from spent nuclear fuel should be immobilized within mineral-based ceramics rather than glass because of their superior aqueous durability and lower risk of accidental criticality. However, in the long term, the alpha-decay taking place in these ceramics will severely disrupt their crystalline structure and reduce their durability. A fundamental property in predicting cumulative radiation damage is the number of atoms permanently displaced per alpha-decay. At present, this number is estimated to be 1,000-2,000 atoms/alpha in zircon. Here we report nuclear magnetic resonance, spin-counting experiments that measure close to 5,000 atoms/alpha in radiation-damaged natural zircons. New radiological nuclear magnetic resonance measurements on highly radioactive, 239Pu zircon show damage similar to that caused by 238U and 232Th in mineral zircons at the same dose, indicating no significant effect of half-life or loading levels (dose rate). On the basis of these measurements, the initially crystalline structure of a 10 weight per cent 239Pu zircon would be amorphous after only 1,400 years in a geological repository (desired immobilization timescales are of the order of 250,000 years). These measurements establish a basis for assessing the long-term structural durability of actinide-containing ceramics in terms of an atomistic understanding of the fundamental damage event.     

A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva

Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder of skeletal malformations and progressive extraskeletal ossification. We mapped FOP to chromosome 2q23-24 by linkage analysis and identified an identical heterozygous mutation (617G --> A; R206H) in the glycine-serine (GS) activation domain of ACVR1, a BMP type I receptor, in all affected individuals examined. Protein modeling predicts destabilization of the GS domain, consistent with constitutive activation of ACVR1 as the underlying cause of the ectopic chondrogenesis, osteogenesis and joint fusions seen in FOP.     

Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus

We carried out a multistage genome-wide association study of type 2 diabetes mellitus in Japanese individuals, with a total of 1,612 cases and 1,424 controls and 100,000 SNPs. The most significant association was obtained with SNPs in KCNQ1, and dense mapping within the gene revealed that rs2237892 in intron 15 showed the lowest Pvalue (6.7 x 10(-13), odds ratio (OR) = 1.49). The association of KCNQ1 with type 2 diabetes was replicated in populations of Korean, Chinese and European ancestry as well as in two independent Japanese populations, and meta-analysis with a total of 19,930 individuals (9,569 cases and 10,361 controls) yielded a P value of 1.7 x 10(-42) (OR = 1.40; 95% CI = 1.34-1.47) for rs2237892. Among control subjects, the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of beta-cell function or the corrected insulin response. Our data thus implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries.     

Mitochondrial dynamics in cell death and neurodegeneration

Mitochondria are highly dynamic organelles that continuously undergo two opposite processes, fission and fusion. Mitochondrial dynamics influence not only mitochondrial morphology, but also mitochondrial biogenesis, mitochondrial distribution within the cell, cell bioenergetics, and cell injury or death. Drp1 mediates mitochondrial fission, whereas Mfn1/2 and Opa1 control mitochondrial fusion. Neurons require large amounts of energy to carry out their highly specialized functions. Thus, mitochondrial dysfunction is a prominent feature in a variety of neurodegenerative diseases. Mutations of Mfn2 and Opa1 lead to neuropathies such as Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy. Moreover, both Aβ peptide and mutant huntingtin protein induce mitochondrial fragmentation and neuronal cell death. In addition, mutants of Parkinson’s disease-related genes also show abnormal mitochondrial morphology. This review highlights our current understanding of abnormal mitochondrial dynamics relevant to neuronal synaptic loss and cell death in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.