Fe—Mn—Si系形状记忆合金中热诱发ε马氏体的形成机制

通过透射电镜观察和热力学分析,定性地讨论了热诱发γ→ε马氏体相变机制．电镜观察结果表明,层错可以在降温过程中持续形成,并通过堆垛形成马氏体相．热力学分析表明,对于低层错能的合金,热诱发马氏体的形核及长大过程来自于不断地形成新的层错并消耗母相结构,而并非由极轴机制所控制．     

A frame-shift mutation in the cystic fibrosis gene.

Cystic fibrosis (CF) is a common recessive lethal genetic disorder, affecting 1 in 1,600 Caucasians. The disease causes defective regulation of chloride-ion transport in exocrine cells. Although in all CF families the disease is linked to a locus on chromosome 7q31, there is clinical heterogeneity in the severity of the disease and the age at which it is diagnosed. CF is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. A three-nucleotide deletion (delta F508) causing the loss of a phenylalanine residue in the tenth exon of the CFTR gene has been found on 70% of CF chromosomes. We have now characterized a CF family in which neither parent of the affected individual carries the common mutation, and identified a two-nucleotide insertion in the CF allele of the mother. The mutation introduces a termination codon in exon 13 of the CFTR gene at residue 821, and is predicted to result in the production of a severely truncated nonfunctional protein.     

Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells

Adult skeletal muscle robustly regenerates throughout an organism's life, but as the muscle ages, its ability to repair diminishes and eventually fails. Previous work suggests that the regenerative potential of muscle stem cells (satellite cells) is not triggered in the old muscle because of a decline in Notch activation, and that it can be rejuvenated by forced local activation of Notch. Here we report that, in addition to the loss of Notch activation, old muscle produces excessive transforming growth factor (TGF)-beta (but not myostatin), which induces unusually high levels of TGF-beta pSmad3 in resident satellite cells and interferes with their regenerative capacity. Importantly, endogenous Notch and pSmad3 antagonize each other in the control of satellite-cell proliferation, such that activation of Notch blocks the TGF-beta-dependent upregulation of the cyclin-dependent kinase (CDK) inhibitors p15, p16, p21 and p27, whereas inhibition of Notch induces them. Furthermore, in muscle stem cells, Notch activity determines the binding of pSmad3 to the promoters of these negative regulators of cell-cycle progression. Attenuation of TGF-beta/pSmad3 in old, injured muscle restores regeneration to satellite cells in vivo. Thus a balance between endogenous pSmad3 and active Notch controls the regenerative competence of muscle stem cells, and deregulation of this balance in the old muscle microniche interferes with regeneration.     

Progesterone inhibits human endothelial cell proliferation through a p53-dependent pathway

Previous studies have shown that progesterone inhibits endothelial cell proliferation through a nuclear receptor-mediated mechanism. Here, we further demonstrate that progesterone at physiologic levels (5 – 500 nM) dose- and time-dependently inhibited DNA synthesis of cultured human umbilical vein endothelial cells (HUVEC). The mRNA and protein levels of p21, p27, and p53 in HUVEC were increased by progesterone. The formation of CDK2-p21 and CDK2-p27 were increased and the CDK2 activity was decreased in the progesterone-treated HUVEC. The progesterone-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Transfection of HUVEC with dominant negative p53 cDNA prevented the progesterone-induced increases in p21 and p27 promoter activity and protein level, decreases in thymidine incorporation, and capillary-like tube formation. Matrigel angiogenesis assay in mice demonstrated the antiangiogenic effect of progesterone in vivo. These findings demonstrate for the first time that progesterone inhibited endothelial cell proliferation through a p53-dependent pathway. Received 28 July 2008; received after revision 25 September 2008; accepted 26 September 2008     

Immobilization of cross-linked In-doped Mo(O,S)2 on cellulose nanofiber for effective organic-compound degradation under visible light illumination

Relatively small amounts of In-doped Mo(O,S)₂ (IMS) catalysts (10%, 20%, and 30%) were deposited on cellulose nanofiber (CNF) by cross-linking them with functional groups of siloxane and epoxy to form CNF-IMS hybrid composites. The as-prepared hybrid composites were characterized and tested their performances toward the photo degradations of cationic (MB and RhB) and anionic (MO) dyes. As indium was doped into Mo(O,S)₂ lattice to form solid-solution, the charge transfer and photocarrier separation during the catalytic reaction were simultaneously enhanced as probed with electrochemical impedance spectroscopy and photoluminescence measurements, respectively. To ensure the catalyst on CNF was well deposited and recyclable, the hybrid composite was evaluated with a reusability experiment to show the stability performance in degrading organic dyes. It was found the environmentally friendly CNF-IMS hybrid composite was relatively stable during the reusability experiment, indicating no catalyst powder was leached out during the photocatalytic reaction. The photoreaction mechanism was convinced by radical-scavenging experiments to show that hydroxyl and superoxide played essential roles for the organic dye degradations in visible-light illuminated conditions. The cross-linked organic/inorganic hybrid catalyst showed a prospective visible light active material not only to solve the environmental issue due to the leaching of nanoparticles but also to lower the post-treatment/recycling cost of photocatalyst in industrial application.     

Evaluation of the going-concern status for companies: An ensemble framework-based model

Issuing a going-concern opinion is a difficult and complex task for auditors. The auditors have to take into account different critical factors in order to make the right decision based on information obtained from the auditing process. This study adopts the so-called “random forest” approach (based on the ensemble method) to assist auditors in making such a decision. To investigate the corresponding effect of the proposed approach, we conduct a series of experiments and a performance comparison. The results show that the random forest method outperforms the baseline methods in terms of the accuracy rate, ROC area, kappa value, type II error, precision, and recall rate. The proposed approach is proven to be more accurate and stable than previous methods.     

Road surface mirage： A bunch of hot air？

The inferior mirage from road surfaces is a common phenomenon, which can be easily seen in everyday life. It has been recognized in the literature as a light refraction phenomenon due to the refractive index gradient caused by the temperature gradient in the air strata above the road surfaces. However, it was also suggested that the mirage is just a phenomenon of specular reflection at grazing incidence. Because of the lack of reasonable and quantitative evidence, the generally accepted light refraction theory has not yet been refuted. Here we show some mirror-like reflection images captured from a road surface stretch in Yujiashan North Road, Wuhan, China, when there was no obvious temperature gradient on or above the road, measured on a winter day in December 2009. This provided direct evidence to doubt the temperature induced light refraction mechanism of the inferior mirage. Furthermore, the critical grazing angle of about 0.2° to the road plane where the mirror-like reflection appears could not make the rough surface scatter incident light as a smooth surface according to the Rayleigh criterion. Therefore the phenomenon is a mirrorlike observation effect of scattering from the surface, which cannot be entirely explained by light refraction via air strata. The results demonstrate that the image-formation mechanism and the observer-based-analysis method shown here potentially offer a means of understanding a wide range of scattering phenomena from rough surfaces at grazing angle; for example, the superior mirages of unusual brightness occasionally observed over frozen lakes and the off-specular reflection phenomenon.     

Zebrafish rgs4 is essential for motility and axonogenesis mediated by Akt signaling

The schizophrenia susceptibility gene, Rgs4, is one of the most intensively studied regulators of G-protein signaling members, well known to be fundamental in regulating neurotransmission. However, little is known about its role in the developing nervous system. We have isolated zebrafish rgs4 and shown that it is transcribed in the developing nervous system. Rgs4 knockdown did not affect neuron number and patterning but resulted in locomotion defects and aberrant development of axons. This was confirmed using a selective Rgs4 inhibitor, CCG-4986. Rgs4 knockdown also attenuated the level of phosphorylated-Akt1, and injection of constitutively-activated AKT1 rescued the motility defects and axonal phenotypes in the spinal cord but not in the hindbrain and trigeminal neurons. Our in vivo analysis reveals a novel role for Rgs4 in regulating axonogenesis during embryogenesis, which is mediated by another schizophrenia-associated gene, Akt1, in a region-specific manner.     

The pattern of esterase variation in the Mimulus glabratus complex (Scrophulariaceae)

Disc gel electrophoretic assays of Mimulus plants showed young stems to contain at least 15 esterase bands. The 6 bands in the center of the gels were highly reproducible. Eighty-one populations representative of all the cytotaxonomic groups and of the Western Hemisphere geographic range of the Mimulus glabratus complex were assayed for those 6 bands. There was no apparent correlation between the distribution of the esterase bands and important environmental parameters such as elevation and latitude. Hence, their distribution did not appear to reflect environmental adaptive values. Each population was monophonic for its particular combination and intensity of esterase bands which is consistent with our previous suggestion that genetic drift is a strong component of the evolutionary pattern of the complex.