Properties and toughening of silica nanoparticle- and carbon nanotube-modified epoxy polymers

The present work investigates the material properties of a thermosetting epoxy polymer modified with various reinforcements of micron-sized glass beads and rubber particles, and nano-sized silica particles and carbon nanotubes. The Young’s modulus of the modified epoxies with rigid additives was significantly increased, especially for the nanocomposites containing high contents of nanosilica or nanotubes. The fracture testing showed that the combination of the soft rubber particles and carbon nanotubes provided the best way to improve the toughness and fatigue performance, because a synergistic effect on the fracture behaviour was obtained in the hybrid-modified epoxies. Fractography showed various mechanisms caused by the addition of the toughening particles, and the main toughening mechanisms are dependent on the modifiers used. Nanotubes operated the debonding, pull-out and void growth mechanisms improve the toughness and fatigue performance of their composites. The inclusion of the rigid spherical particles into the epoxy increased the toughness and fatigue performance via mechanisms of shear band yield and plastic void growth. Rubber cavitation was considered to be the main toughening mechanism in the rubber-modified materials. Several dispersion methods were examined for the multi-walled carbon nanotubes, and the best way to get well-dispersed nanotubes without significant damage was identified. The level of the nanotube dispersion was assessed using a greyscale analysis and transmission optical microscopy. Finally, a sonication process using an ultrasonic probe was chosen to prepare the nanotube-modified epoxies. Modelling work was carried out to predict the toughening contribution from the nanosilica and nanotubes. There was a good agreement between the predictions and the experimental results for the toughness. The modified Halpin-Tsai equation was used to calculate the increased modulus caused by the addition of the nanotubes, and the predicted modulus can fit well with the measured values, even at high nanotube contents which resulted in serious agglomeration

Three-dimensional Folding of Eukaryotic Genomes

Chromatin packages eukaryotic genomes via a hierarchical series of folding steps, encrypting multiple layers of epigenetic information, which are capable of regulating nuclear transactions in response to complex signals in environment. Besides the 1-dimensinal chromatin landscape such as nucleosome positioning and histone modifications, little is known about the secondary chromatin structures and their functional consequences related to transcriptional regulation and DNA replication. The family of chromosomal conformation capture (3C) assays has revolutionized our understanding of large-scale chromosome folding with the ability to measure relative interaction probability between genomic loci in vivo. However, the suboptimal resolution of the typical 3C techniques leaves the levels of nucleosome interactions or 30 nm structures inaccessible, and also restricts their applicability to study gene level of chromatin folding in small genome organisms such as yeasts, worm, and plants. To uncover the “blind spot” of chromatin organization, I developed an innovative method called Micro-C and an improved protocol, Micro-C XL, which enable to map chromatin structures at all range of scale from single nucleosome to the entire genome. Several fine-scale aspects of chromatin folding in budding and fission yeasts have been identified by Micro-C, including histone tail-mediated tri-/tetra-nucleosome stackings, gene crumples/globules, and chromosomally-interacting domains (CIDs). CIDs are spatially demarcated by the boundaries, which are colocalized with the promoters of actively transcribed genes and histone marks for active transcription or turnover. The levels of chromatin compaction are regulated via transcription-dependent or transcription-independent manner – either the perturbations of transcription or the mutations of chromatin regulators strongly affect the global chromatin folding. Taken together, Micro-C further reveals chromatin folding behaviors below the sub-kilobase scale and opens an avenue to study chromatin organization in many biological systems

Transfer RNA Genes Affect Chromosome Structure and Function via Local Effects

The genome is packaged and organized in an ordered, non-random manner and specific chromatin segments contact nuclear substructures to mediate this organization. Transfer RNA genes (tDNAs) are binding sites for transcription factors and architectural proteins and are thought to play an important role in the organization of the genome. In this study, we investigate the role of tDNAs in genomic organization and chromosome function by editing a chromosome so that it lacks any tDNAs. Surprisingly our analyses of this tDNA-less chromosome show that loss of tDNAs does not grossly affect chromatin architecture or chromosome tethering and mobility. However, loss of tDNAs affects local nucleosome positioning and the binding of SMC proteins at these loci. The absence of tDNAs also leads to changes in centromere clustering and a reduction in the frequency of long-range HML-HMR heterochromatin clustering with concomitant effects on gene silencing. We propose that the tDNAs primarily affect local chromatin structure that result in effects on long-range chromosome architecture

A Linux PC cluster for lattice QCD with exact chiral symmetry

A computational system for lattice QCD with exact chiral symmetry is described. The platform is a home-made Linux PC cluster, built with off-the-shelf components. At present this system constitutes of 64 nodes, with each node consisting of one Pentium 4 processor (1.6/2.0/2.5 GHz), one Gbyte of PC800/PC1066 RDRAM, one 40/80/120 Gbyte hard disk, and a network card. The computationally intensive parts of our program are written in SSE2 codes. The speed of this system is estimated to be 70 Gflops, and its price/performance is better than $1.0/Mflops for 64-bit (double precision) computations in quenched QCD. We discuss how to optimize its hardware and software for computing quark propagators via the overlap Dirac operator.Comment: 24 pages, LaTeX, 2 eps figures, v2:a note and references added, the version published in Int. J. Mod. Phys.

Regulation of CLC-1 chloride channel biosynthesis by FKBP8 and Hsp90β.

Mutations in human CLC-1 chloride channel are associated with the skeletal muscle disorder myotonia congenita. The disease-causing mutant A531V manifests enhanced proteasomal degradation of CLC-1. We recently found that CLC-1 degradation is mediated by cullin 4 ubiquitin ligase complex. It is currently unclear how quality control and protein degradation systems coordinate with each other to process the biosynthesis of CLC-1. Herein we aim to ascertain the molecular nature of the protein quality control system for CLC-1. We identified three CLC-1-interacting proteins that are well-known heat shock protein 90 (Hsp90)-associated co-chaperones: FK506-binding protein 8 (FKBP8), activator of Hsp90 ATPase homolog 1 (Aha1), and Hsp70/Hsp90 organizing protein (HOP). These co-chaperones promote both the protein level and the functional expression of CLC-1 wild-type and A531V mutant. CLC-1 biosynthesis is also facilitated by the molecular chaperones Hsc70 and Hsp90β. The protein stability of CLC-1 is notably increased by FKBP8 and the Hsp90β inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) that substantially suppresses cullin 4 expression. We further confirmed that cullin 4 may interact with Hsp90β and FKBP8. Our data are consistent with the idea that FKBP8 and Hsp90β play an essential role in the late phase of CLC-1 quality control by dynamically coordinating protein folding and degradation