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In order to realize the optimize design of the 6-degree-of-freedom (6-DF) accelerometer according to its cross-coupling degree, the analysis mathematical modeling of the accelerometer′s cross-coupling must be carried out. In this work, the working principle and structure characteristics of the six-wafer piezoelectric 6-DF-accelerometer are analyzed. According to the mechanical analysis of the sensing element, the 6-DF component force equation of the accelerometer and the composite formula of the six-wafer are deduced. Analytical mathematical model and cross-coupling graph model of cross-coupling degree are derived by analyzing the static structure and coupling mechanism. The numerical simulation experiment is carried out using ANSYS software. An experimental prototype of the 6-DF-accelerometer is fabricated. The vibrator is used as a loading source for calibration. The experimental results show that the Pearson correlation index of the multiple parameter model about the cross-coupling degree, the numerical simulation model, and calibration experiment is 0.9881. The results of the cross-coupling research of the three models are consistent, which verifies the effectiveness of the analytical mathematical model. Coupling direction and coupling number were obtained based on the cross-coupling graph model. The results of this work provide the theoretical basis for further research on the active optimization design method of 6-DF-accelerometer based on cross-coupling.

For tissue engineering, pore structure is an essential element in the development of scaffolds. In this paper, we obtained highly porous cross-linked partially hydrolyzed poly (vinyl alcohol) (PVA) hydrogels by templating concentrated CO2-in-water (C/W) emulsions, which avoid the use of traditional organic solvents and additional surfactants. This method is very convenient for the formation of biocompatible PVA hydrogels, because redundant crosslinking agent and catalyst could be easily removed by washing with the absence of organic solvent and surfactants, and would have widespread applications due to the biocompatibility of the resulting materials. These PVA hydrogels were further evaluated for cellular growth and proliferation to demonstrate their applications in tissue engineering.

Cyclins are a family of diverse proteins that play fundamental roles in regulating cell cycle progression in Eukaryotes. Cyclins have been identified from protists to higher Eukaryotes, while its evolution remains vague and the findings turn out controversial. Current classification of cyclins is mainly based on their functions, which may not be appropriate for the systematic evolutionary analysis. In this work, we performed comparative and phylogenetic analysis of cyclins to investigate their classification, origin and evolution. Cyclins originated in early Eukaryotes and evolved from protists to plants, fungi and animals. Based on the phylogenetic tree, cyclins can be divided into three major groups designated as the group I, II and III with different functions and features. Group I plays key roles in cell cycle, group II varied in actions are kingdom (plant, fungi and animal) specific, and group III functions in transcription regulation. Our results showed that the dominating cyclins (group I) diverged from protists to plants, fungi and animals, while divergence of the other cyclins (groups II and III) has occurred in protists. We also discussed the evolutionary relationships between cyclins and cyclin-dependent kinases (CDKs) and found that the cyclins have undergone divergence in protists before the divergence of animal CDKs. This reclassification and evolutionary analysis of cyclins might facilitate understanding eukaryotic cell cycle control.

Heat shock factor protein 4 (HSF4) is expressed exclusively in the ocular lens and plays a critical role in the lens formation and differentiation. Mutations in the HSF4 gene lead to congenital and senile cataract. However, the molecular mechanisms causing this disease have not been well characterized. DNA damage in lens is a crucial risk factor in senile cataract formation, and its timely repair is essential for maintaining the lens' transparency. Our study firstly found evidence that HSF4 contributes to the repair of DNA strand breaks. Yet, this does not occur with cataract causative mutations in HSF4. We verify that DNA damage repair is mediated by the binding of HSF4 to a heat shock element in the Rad51 promoter, a gene which assists in the homologous recombination (HR) repair of DNA strand breaks. HSF4 up-regulates Rad51 expression while mutations in HSF4 fail, and DNA does not get repaired. Camptothecin, which interrupts the regulation of Rad51 by HSF4, also affects DNA damage repair. Additionally, with HSF4 knockdown in the lens of Zebrafish, DNA damage was observed and the protein level of Rad51 was significantly lower. Our study presents the first evidence demonstrating that HSF4 plays a role in DNA damage repair and may contribute a better understanding of congenital cataract formation. (C) 2012 Elsevier B.V. All rights reserved.

Bacteria infecting eukaryotic hosts often encounter therapeutic antimicrobial and DNA damaging agents and respond by forming biofilms. While mechanisms of biofilm response are incompletely understood, they seem to involve bacterial second messenger bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP) signaling. We hypothesized that DNA replication inhibition induces bacterial biofilm formation via c-di-GMP signaling. Evidently, we found that Pseudomonas aeruginosa mounted a biofilm response to the subinhibitory DNA replication inhibitors hydroxyurea and nalidixic acid, but planktonic proliferation was inhibited. The biofilm response was suppressed either genetically by mutations causing planktonic resistance or biochemically by reversal of replication inhibition. Biofilms were induced by a mechanism of stimulated adhesion of planktonic filaments having impaired DNA replication, as examined under fluorescence microscopy. Induction was suppressed by either inhibition or mutation of Arr-a c-di-GMP phosphodiesterase. These results suggest that P. aeruginosa, under DNA replication stress, tends to form biofilms via Arr. The profound implications of the SOS response, planktonic-sessile and bacteria-cancer relationships are discussed.

Initiation of eukaryotic DNA replication requires many proteins that interact with one another and with replicators. Using a yeast genetic screen, we have identified Noc3p (nucleolar complex-associated protein) as a novel replication-initiation protein. Noc3p interacts with MCM proteins and ORC and binds to chromatin and replicators throughout the cell cycle. It functions as a critical link between ORC and other initiation proteins to effect chromatin association of Cdc6p and MCM proteins for the establishment and maintenance of prereplication complexes. Noc3p is highly conserved in eukaryotes and is the first identified bHLH (basic helix-loop-helix) protein required for replication initiation. As Noc3p is also required for pre-rRNA processing, Noc3p is a multifunctional protein that plays essential roles in two vital cellular processes.

The transient receptor potential vanilloid receptor 1 (TRPV1) channel is a nonselective cation channel activated by a variety of exogenous and endogenous physical and chemical stimuli, such as temperature (≥42 °C), capsaicin, a pungent compound in hot chili peppers, and allyl isothiocyanate. Large-conductance calcium- and voltage-activated potassium (BK) channels regulate the electric activities and neurotransmitter releases in excitable cells, responding to changes in membrane potentials and elevation of cytosolic calcium ions (Ca(2+)). However, it is unknown whether the TRPV1 channels are coupled with the BK channels. Using patch-clamp recording combined with an infrared laser device, we found that BK channels could be activated at 0 mV by a Ca(2+) influx through TRPV1 channels not the intracellular calcium stores in submilliseconds. The local calcium concentration around BK is estimated over 10 μM. The crosstalk could be affected by 10 mM BAPTA, whereas 5 mM EGTA was ineffectual. Fluorescence and co-immunoprecipitation experiments also showed that BK and TRPV1 were able to form a TRPV1-BK complex. Furthermore, we demonstrated that the TRPV1-BK coupling also occurs in dosal root ganglion (DRG) cells, which plays a critical physiological role in regulating the "pain" signal transduction pathway in the peripheral nervous system.