Strictly ergodic distal models and a new approach to the Host-Kra factors

Cocycles are a key object in Antol\'{i}n Camarena and Szegedy's (topological) theory of nilspaces. We introduce measurable counterparts, named nilcycles, enabling us to give conditions which guarantee that an ergodic group extension of a strictly ergodic distal system admits a strictly ergodic distal topological model, revisiting a problem studied by Lindenstrauss. In particular we show that if the base space is a dynamical nilspace then a dynamical nilspace topological model may be chosen for the extension. This approach combined with a structure theorem of Gutman, Manners and Varj\'{u} applied to the ergodic group extensions between successive Host-Kra characteristic factors gives a new proof that these factors are inverse limit of nilsystems

Maximal pronilfactors and a topological Wiener-Wintner theorem

For strictly ergodic systems, we introduce the class of CF-Nil($k$) systems: systems for which the maximal measurable and maximal topological $k$-step pronilfactors coincide as measure-preserving systems. Weiss' theorem implies that such systems are abundant in a precise sense. We show that the CF-Nil($k$) systems are precisely the class of minimal systems for which the $k$-step nilsequence version of the Wiener-Wintner average converges everywhere. As part of the proof we establish that pronilsystems are $coalescent$. In addition, we characterize a CF-Nil($k$) system in terms of its $(k+1)$-$th\ dynamical\ cubespace$. In particular, for$k=1$, this provides for strictly ergodic systems a new condition equivalent to the property that every measurable eigenfunction has a continuous version

c-Lysozyme promotes proliferation of chicken embryonic fibroblast through bFGF pathway

The egg white (EW) contains the majority of bioactive components which maintain embryo growth and differentiation. The discovery of new growth promoting factor in egg white will provide vital clue to understand the developmental regulation of early chicken embryo. The egg white heated with different temperatures (63.5, 70 and 95°C) underwent testing on its growth-promoting effect on chicken fibroblast in vitro. The purified c-lysozyme and the expression of related genes in basic fibroblast growth factor (bFGF) pathway were analyzed to ascertain its growth-promoting mechanism. 13 h after egg white treatment, more fibroblast synchronized with serum starvation transited into S phrase from G0/G1 in EW group than in the control group (CM) and reached the phase of peak proliferation at 15 h after treatment. It was found that c-lysozyme had the function of promoting cells growth and was decided by gradient heat inactivation of egg white. The addition of more than 0.25 mg/ml c-lysozyme produced significant increase in the cellular proliferation during 48 to 72 h of culture. At 13 h after c-lysozyme treatment, the bFGF, cyclin D, cyclin A and CDK2 were up-regulated significantly and promoted the transition from G0/G1 into S phrase and the accurate completion of S phrase. C-Lysozyme contains a growth-activating domain to promote the cell proliferation besides its anti-microbe domain.Key words: c-Lysozyme, fibroblast, fibroblast growth factor receptor (FGFR), cell cycle

Construction of a 7-fold BAC library and cytogenetic mapping of 10 genes in the giant panda (Ailuropoda melanoleuca)

BACKGROUND: The giant panda, one of the most primitive carnivores, is an endangered animal. Although it has been the subject of many interesting studies during recent years, little is known about its genome. In order to promote research on this genome, a bacterial artificial chromosome (BAC) library of the giant panda was constructed in this study. RESULTS: This BAC library contains 198,844 clones with an average insert size of 108 kb, which represents approximately seven equivalents of the giant panda haploid genome. Screening the library with 15 genes and 8 microsatellite markers demonstrates that it is representative and has good genome coverage. Furthermore, ten BAC clones harbouring AGXT, GHR, FSHR, IRBP, SOX14, TTR, BDNF, NT-4, LH and ZFX1 were mapped to 8 pairs of giant panda chromosomes by fluorescence in situ hybridization (FISH). CONCLUSION: This is the first large-insert genomic DNA library for the giant panda, and will contribute to understanding this endangered species in the areas of genome sequencing, physical mapping, gene cloning and comparative genomic studies. We also identified the physical locations of ten genes on their relative chromosomes by FISH, providing a preliminary framework for further development of a high resolution cytogenetic map of the giant panda

Toll-Like Receptor 4 Reduces Oxidative Injury via Glutathione Activity in Sheep

Toll-like receptor 4 (TLR4) is an important sensor of Gram-negative bacteria and can trigger activation of the innate immune system. Increased activation of TLR4 can lead to the induction of oxidative stress. Herein, the pathway whereby TLR4 affects antioxidant activity was studied. In TLR4-overexpressing sheep, TLR4 expression was found to be related to the integration copy number when monocytes were challenged with lipopolysaccharide (LPS). Consequently, production of malondialdehyde (MDA) was increased, which could increase the activation of prooxidative stress enzymes. Meanwhile, activation of an antioxidative enzyme, glutathione peroxidase (GSH-Px), was increased. Real-time PCR showed that expression of activating protein-1 (AP-1) and the antioxidative-related genes was increased. By contrast, the expression levels of superoxide dismutase 1 (SOD1) and catalase (CAT) were reduced. In transgenic sheep, glutathione (GSH) levels were dramatically reduced. Furthermore, transgenic sheep were intradermally injected with LPS in each ear. The amounts of inflammatory infiltrates were correlated with the number of TLR4 copies that were integrated in the genome. Additionally, the translation of γ-glutamylcysteine synthetase (γ-GCS) was increased. Our findings indicated that overexpression of TLR4 in sheep could ameliorate oxidative injury through GSH secretion that was induced by LPS stimulation. Furthermore, TLR4 promoted γ-GCS translation through the AP-1 pathway, which was essential for GSH synthesis