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Because of the complexity of procedure interface and working conditions, the further improvement of steel strip quality and production efficiency is limited. Realizing the optimization of product quality and production process in multi-process, system-level through intelligent key technology is one of the strategic directions in steel strip production. (1) Collaborative intelligent optimization and dynamic scheduling technology for steel manufacturing supply chain oriented to customized production, reducing the cost of raw material purchase and production operations and improving production efficiency and precision service ability; (2) Online monitoring, diagnosis and optimization technology of product quality. Getting through the process information flow of product, the correlation analysis of process quality parameters, the tracing of quality anomalies, the reverse optimization of process parameters and the optimization of process route will be realized; (3) Multi-process coordination optimization and quality control based on CPS architecture. The precise control technology of process quality parameters will be developed; the structure of multi-process coordination optimization system is established and optimization of key quality parameters in the through process will be realized; and (4) Microstructure and mechanical property optimization and surface quality intelligent control technology in the hot strip rolling process. Intelligent prediction of microstructure and mechanical properties, rapid dynamic design and steel grade merging technology will be formed and green process design technology of oxide scale will be developed.

A novel blast wave mitigation device was investigated experimentally in this paper. The device consists of a piston-cylinder assembly. A shock wave is induced within the cylinder when a blast wave impacts on the piston. The shock wave propagates inside the device and is reflected repeatedly. The shock wave propagation process inside the device lengthens the duration of the force on the base of the device to several orders of magnitude of the duration of the blast wave, while it decreases the maximum pressure over an order of magnitude. Two types of experiments were carried out to study the blast wave mitigation device. The first type of experiments was done with honeycomb structures protected by the blast wave mitigation device. Experimental results show that the device can adequately protect the honeycomb structure. A second type of experiments was done using a Hopkinson bar to measure the pressure transmitted through the blast wave mitigation device. The experimental results agree well with results from a theoretical model.

Voltage-dependent L-type calcium channels that permit cellular calcium influx are essential in calcium-mediated modulation of cellular signaling. Although the regulation of voltage-dependent L-type calcium channels is linked to many factors including cAMP-dependent protein kinase A (PKA) activity and actin cytoskeleton, little is known about the detailed mechanisms underlying the regulation in osteoblasts. Our present study investigated the modulation of L-type calcium channel activities through the effects of forskolin on actin reorganization and on its functional interaction with actin binding protein actinin 4. The results showed that forskolin did not significantly affect the trafficking of pore forming α1c subunit and its interaction with actin binding protein actinin 4, whereas it significantly increased the expression of β3 subunit and its interaction with actinin 4 in osteoblast cells as assessed by co-immunoprecipitation, pull-down assay, and immunostaining. Further mapping showed that the ABD and EF domains of actinin 4 were interaction sites. This interaction is independent of PKA phosphorylation. Knockdown of actinin 4 significantly decreased the activities of L-type calcium channels. Our study revealed a new aspect of the mechanisms by which the forskolin activation of adenylyl cyclase - cAMP cascade regulates the L-type calcium channel in osteoblast cells, besides the PKA mediated phosphorylation of the channel subunits. These data provide insight into the important role of interconnection among adenylyl cyclase, cAMP, PKA, the actin cytoskeleton, and the channel proteins in the regulation of voltage-dependent L-type calcium channels in osteoblast cells.

Large conductance Ca2+-activated potassium channels (BK) are targets for research that explores therapeutic means to various diseases, owing to the roles of the channels in mediating multiple physiological processes in various cells and tissues. We investigated the pharmacological effects of curcumin, a compound isolated from the herb Curcuma longa, on BK channels. As recorded by whole-cell patch-clamp, curcumin increased BK (α) and BK (α+β1) currents in transfected HEK293 cells as well as the current density of BK in A7r5 smooth muscle cells in a dose-dependent manner. By incubating with curcumin for 24 hours, the current density of exogenous BK (α) in HEK293 cells and the endogenous BK in A7r5 cells were both enhanced notably, though the steady-state activation of the channels did not shift significantly, except for BK (α+β1). Curcumin up-regulated the BK protein expression without changing its mRNA level in A7r5 cells. The surface expression and the half-life of BK channels were also increased by curcumin in HEK293 cells. These effects of curcumin were abolished by MG-132, a proteasome inhibitor. Curcumin also increased ERK 1/2 phosphorylation, while inhibiting ERK by U0126 attenuated the curcumin-induced up-regulation of BK protein expression. We also observed that the curcumin-induced relaxation in the isolated rat aortic rings was significantly attenuated by paxilline, a BK channel specific blocker. These results show that curcumin enhances the activity of the BK channels by interacting with BK directly as well as enhancing BK protein expression through inhibiting proteasomal degradation and activating ERK signaling pathway. The findings suggest that curcumin is a potential BK channel activator and provide novel insight into its complicated pharmacological effects and the underlying mechanisms.

The F-box protein gene COI1 from Arabidopsis plays a fundamental role in response to jasmonates, which regulate plant root growth, pollen fertility, wounding and healing, and defense against pathogens and insects. Null mutations in COI1 were previously found to abolish all the jasmonate responses, and the Arabidopsis coi1-1 mutant is male sterile and susceptible to pathogen infection. In this study, we isolated an F-box protein gene from soybean, which shares significant homology with the Arabidopsis COI1 and similarly contains an F-box motif and leucine rich repeats (LRR), here designated GmCOI1 (Glycine max L. (Merr.) COI1). To test whether the sequence homology and structural similarity are indicative of functional conservation, we expressed GmCOI1 in the Arabidopsis coi1-1 mutant. The transgenic coi1-1 plants with expression of the GmCOI1 gene were found to exhibit normal jasmonate responses, including jasmonate-regulated plant defense and fertility. In addition, the chimerical proteins with swapped domain of the F-box motif or LRR between GmCOI1 and COI1 were shown to functionally complement the coi1-1 mutation. Furthermore, GmCOI1 was found to assemble into the Skp1-Cullin-F-box (SCF) complexes, similar to the formation of the Arabidopsis SCFCOI1. These data demonstrate the soybean F-box protein gene GmCOI1 is able to mediate jasmonate-regulated plant defense and fertility in Arabidopsis, which implies a generic jasmonate pathway with conserved signal components in different plant species.

A simple emergency risk prediction tool should be developed for clinicians to quickly identify the prognosis of patients with acute aortic dissection.We enrolled 280 patients with acute aortic dissection admitted to emergency department between May 2010 and February 2013. Multivariate logistic regression analysis was performed to identify independent predictors of in-hospital death.The in-hospital mortality of our patients with acute aortic dissection was 32.5%, in-hospital deaths with surgery less than the survived (34.1% VS 54.5%). Multivariate analysis identified that age (≥65 years old), Type A, blood pressure (mean systolic blood pressure ≤ 90 mmHg), neutrophil percentage (≥ 80%) and serum D-dimer (≥ 5.0 mg/L) were significant predictors of death. With the simple emergency risk prediction tool, scores of all in-hospital deaths were ≥ 3, whereas almost all of the survivors (97.9%) had scores < 15. A score of 10 offered the best threshold value, with the highest sensitivity (81.3%) and specificity (86.8%).The in-hospital mortality rate of patients with acute aortic dissection is high and can be predicted. Early surgery would be beneficial for in-hospital survive. This tool should be available for clinicians in the emergency department to quickly identify the prognosis of patients with acute aortic dissection.

Tubulointerstitial fibrosis (TIF) is the final common pathway in the end-stage renal disease. Epithelial-to-mesenchymal transition (EMT) is considered a major contributor to the TIF by increasing the number of myofibroblasts. Curcumin, a polyphenolic compound derived from rhizomes of Curcuma, has been shown to possess potent anti-fibrotic properties but the mechanism remains elusive. We found that curcumin inhibited the EMT as assessed by reduced expression of α-SMA and PAI-1, and increased E-cadherin in TGF-β1 treated proximal tubular epithelial cell HK-2 cells. Both of the conventional TGF-β1/Smad pathway and non-Smad pathway were investigated. Curcumin reduced TGF-β receptor type I (TβR-I) and TGF-β receptor type II (TβR II), but had no effect on phosphorylation of Smad2 and Smad3. On the other hand, in non-Smad pathway curcumin reduced TGF-β1-induced ERK phosphorylation and PPARγ phosphorylation, and promoted nuclear translocation of PPARγ. Further, the effect of curcumin on α-SMA, PAI-1, E-cadherin, TβR I and TβR II were reversed by ERK inhibitor U0126 or PPARγ inhibitor BADGE, or PPARγ shRNA. Blocking PPARγ signaling pathway by inhibitor BADGE or shRNA had no effect on the phosphorylation of ERK whereas the suppression of ERK signaling pathway inhibited the phosphorylation of PPARγ. We conclude that curcumin counteracted TGF-β1-induced EMT in renal tubular epithelial cells via ERK-dependent and then PPARγ-dependent pathway.

Photoperiod and temperature are two important environmental factors that influence the heading-date of rice. Although the influence of the photoperiod on heading has been extensively reported in rice, the molecular mechanism for the temperature control of heading remains unknown. This study reports an early heading mutant derived from tissue culture lines of rice and investigates the heading-date of wild type and mutant in different photoperiod and temperature treatments. The linkage analysis showed that the mutant phenotype cosegregated with the Hd1 locus. Sequencing analysis found that the mutant contained two insertions and several single-base substitutions that caused a dramatic reduction in Hd1mRNA levels compared with wild type. The expression patterns of Hd1 and Hd3a were also analyzed in different photoperiod and temperature conditions, revealing that Hd1 mRNA levels displayed similar expression patterns for different photoperiod and temperature treatments, with high expression levels at night and reduced levels in the daytime. In addition, Hd1 displayed a slightly higher expression level under long-day and low temperature conditions. Hd3a mRNA was present at a very low level under low temperature conditions regardless of the day-length. This result suggests that suppression of Hd3a expression is a principle cause of late heading under low temperature and long-day conditions.