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Abstract: Among various coating processes, slot die coating belongs to a class of pre-metered coating, in which the coating film thickness can be predetermined. In the past, most research works on slot die coating have focused mainly on polymer solutions; very little information is available using suspensions as coating fluids. In this study, the effect of adding TiO2 and SiO2 in aqueous polyvinyl alcohol (PVA) solutions on slot die coating is investigated. It was found that the stable coating window was enlarged with the addition of particles, and its size increased with solids concentration. This is due to the strong interaction between polymer and particles, resulting in a higher viscosity and surface tension. As a result, the upstream coating bead is more stable and the maximum coating speed is extended to a high value, hence the coating window becomes larger. Although both viscosity and surface tension appear to contribute to the stability of coating flow, the effect of surface tension is more dominant. The surface tension of a suspension with porous particles was higher than one with hard solid particles. Consequently, the coating window obtained with the former was significantly larger than the latter. Flow visualization revealed that under the same operating conditions, the upstream dynamic contact angle for the suspension was smaller than for the aqueous polymer solution. This observation could be related to the stability of the upstream coating bead, and hence the coating window. The experimental flow fields were verified numerically with the aid of a numerical simulation package (Flow-3D). [Copyright &y& Elsevier]

Abstract: Biocontrol efficiency of various Bacillus preparations (BB11 and FH17 strains, and a mixture of both strains (BF) at a 1:1 ratio by concentration) and different application methods against Phytophthora blight of bell pepper were studied. The application methods included (A) mixing (mixing BF with rapeseed residue and then immediately applying in the field), (B) composting (mixing BF with rapeseed residue and made compost before application), (C) spraying (spraying diluted BF into field or rhizosphere of plants), and (D) watering (watering diluted BF into field or rhizosphere of plants). In greenhouse experiments, the addition of BF increased biocontrol efficiency (60.3%), and yield increase (200%) was better than with BB11 (55.8 and 80.6%, respectively) or FH17 (37.1 and 50.0%, respectively). In field trials at Huai’an in 2001, the best dosages of BF mixture (1010 cfu/ml) with the four above-mentioned application methods were 15, 7.5, 15, and 22.5L/ha, respectively. When preparations were applied at the best dosage in the same field, the BF mixture provided superior biocontrol efficiency and greater yield increase with treatment B than those with treatment A or C. Combining the field trial results from 2002 to 2003 at Huai’an and Wu’han, the total average control efficiencies and yield increases for treatments A, B, and C reached 81.0, 88.0, and 79.1% and 33.1, 44.3, and 29.1%, respectively, with their best dosages. However, method B, composting, provided better disease control and greater yield increases than all other methods, and did so at a lower application rate. [Copyright &y& Elsevier]

A novel member of the human UDP-N-acetyl-d-galactosamine:polypeptide N-acetylgalactosaminyltransferase (pp-GalNAc-T) gene family was cloned and designated pp-GalNAc-T14. This type II membrane protein contains all motifs that are conserved in the pp-GalNAc-T family proteins and forms a subfamily with pp-GalNAc-T2 on the phylogenetic tree. Quantitative real time PCR analysis revealed significantly high expression of the pp-GalNAc-T14 transcript in kidney, although the transcripts were ubiquitously expressed in all tissues examined. Furthermore, the recombinant pp-GalNAc-T14 transferred GalNAc to a panel of mucin-derived peptide substrates such as Muc2, Muc5AC, Muc7, and Muc13 (-58). Our results provide evidence that pp-GalNAc-T14 is a new member of the pp-GalNAc-T family and suggest that pp-GalNAc-T14 may be involved in the O-glycosylation in kidney. [Copyright &y& Elsevier]

• A statistical hypothesis testing scheme is presented for structural damage detection. • The RSE constructed by the MSR is selected as a damage-sensitive feature. • The sensitivity formula of the test statistic with respect to damage is derived. • The MSR that only includes translational DoFs is sufficient for detecting damage. • Both numerically simulated and field test data indicate the effectiveness of the method. A statistical hypothesis testing scheme is presented for damage detection considering environmental variations, in which the presence of damage is identified via Welch's t-test by comparing the means of two groups of residual strain energy (RSE) samples from healthy and inspected structures. The RSE, as a damage indication feature, is determined from the mode shape residual (MSR), and the corresponding effects of environmental variations are eliminated via the PCA method. To further improve the damage sensitivity of RSE samples, an MSR selection strategy is proposed to examine the sensitivity of the available MSR matrices to damage and select the most effective MSR matrix. The sensitivity formula of the test statistic with respect to damage is derived and defined as the sensitivity index. Moreover, the mode shape expansion process is not required because an MSR that only includes x - or y -translational degrees of freedom (DoFs) at the measured points is sufficient for detecting damage. The effects of the location and extent of damage, incomplete measurements, and the critical value of the t-test on the performance of the proposed scheme are discussed by numerically analyzing an offshore platform. The results indicate that the scheme can simultaneously limit the probability of committing Type I and Type II errors under temperature variations and noise contamination. An analysis of field test data for a real-world wind turbine also indicates that this approach can avoid Type I error in a real marine environment. [ABSTRACT FROM AUTHOR]

Based on the high self-renewal ability and osteoblastic differentiation capacity, dental pulp stem cells (DPSCs) are suggested to be promising cell source for osteogenesis. Therefore, illustrating the mechanism of osteoblastic differentiation of DPSCs is required. This current study aims to illustrate the role and mechanism of Sp1 in regulating osteoblastic differentiation of DPSCs. In this study, we downregulated Sp1 in DPSCs and evaluated the osteoblastic differentiation by measuring Runx2 and OCN expression with Western blot analysis and by Alizarin red staining. Furthermore, we investigated the mechanism of Sp1 regulating noggin with Firefly luciferase reporter gene assay and ChIP assay, and correspondingly evaluated the function of noggin in Sp1-regulated osteoblastic differentiation of DPSCs. We found that knockdown of Sp1 inhibits the expression of ALP, Runx2, COL1A1 and OCN, and decreases ALP staining, Alizarin red staining. Sp1 binds to noggin promoter and inhibits noggin expression, thus correspondingly regulates DPSCs osteoblastic differentiation. In conclusion, our study revealed that Sp1 regulates DPSCs osteoblastic differentiation through noggin and that Sp1/noggin can provide new perspective for enhancing DPSCs osteogenesis. • Sp1 promotes osteoblastic differentiation of DPSCs. • Sp1 regulates osteoblastic differentiation of DPSCs by downregulating noggin. • Sp1 regulating noggin through modulating noggin promoter activity. [ABSTRACT FROM AUTHOR]

Schematic diagram of the proposed molecular targets and mechanisms of celastrol in induction of autophagic cell death and inhibition of P-glycoprotein. Multidrug resistance (MDR) represents an obstacle in anti-cancer therapy. MDR is caused by multiple mechanisms, involving ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp), which reduces intracellular drug levels to sub-therapeutic concentrations. Therefore, sensitizing agents retaining effectiveness against apoptosis- or drug-resistant cancers are desired for the treatment of MDR cancers. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump is an emerging target to overcome MDR, because of its continuous expression and because the calcium transport function is crucial to the survival of tumor cells. Previous studies showed that SERCA inhibitors exhibit anti-cancer effects in Bax-Bak-deficient, apoptosis-resistant and MDR cancers, whereas specific P-gp inhibitors reverse the MDR phenotype of cancer cells by blocking efflux of chemotherapeutic agents. Here, we unraveled SERCA and P-gp as double targets of the triterpenoid, celastrol to reverse MDR. Celastrol inhibited both SERCA and P-gp to stimulate calcium-mediated autophagy and ATP depletion, thereby induced collateral sensitivity in MDR cancer cells. In vivo studies further confirmed that celastrol suppressed tumor growth and metastasis by SERCA-mediated calcium mobilization. To the best of our knowledge, our findings demonstrate collateral sensitivity in MDR cancer cells by simultaneous inhibition of SERCA and P-gp for the first time. [ABSTRACT FROM AUTHOR]

Three layered compounds CsLiCoS 2 , CsAgCoS 2 and CsLiFeS 2 have been synthesized by conventional solid-state reaction method. All of three compounds exhibit semiconducting behavior in electrical transport with small thermal activation energy gap. The crystal structure of CsLiCoS 2 is isostructural to ThCr 2 Si 2 -type CsCo 2 S 2 with random mixture of Li+ and Co2+. The latter two compounds exhibit √2 ​× ​√2 ​× ​1 superstructure of ThCr 2 Si 2 -type because the monovalent Ag+/Li+ and divalent Co2+/Fe2+ independently occupy inequivalent sites in [AMS 2 ]- layer. Through comprehensive investigation of the crystallographic lattice in CsAMS 2 , a phase boundary between disorder and ordered phases may be identified, which highlights the importance of the atomic size and lattice mismatch in determining the crystal structure. Image 1 • Three layered sulfides CsAMS 2 (A ​= ​Li, Ag; M ​= ​Co, Fe) are synthesized by solid state reaction method. • Introducing monovalent Li+/Ag+ could significantly change the structure and property of Co-based sulfides. • A phase boundary between random and ordered occupation in the [AMS 2 ]- layers is determined by the atomic size difference. [ABSTRACT FROM AUTHOR]

Mastitis, as the main disease to affect the dry dairy cow with the characterized by increasing number of somatic cells in milk and reducing milk production, has been known as one of the most serious expensive disease for the dairy industry. Escherichia coli (E.coli), a gram negative bacterial, have normally been considered to be an opportunistic pathogen that can invade the mammary gland sometimes to cause inflammatory diseases. Lippolysacchride (LPS), as the co-cell wall component of the Escherichia coli (E.coli), is the main virulence factors to induce acute inflammation. Itaconate is an endogenous metabolite which has recently been reported to regulate the macrophage function and has the ability to reduce the secretion of pro-inflammatory cytokines, such as IL-6 and IL-12. Here, the aim of this study is to investigate the protective role of dimethyl itaconate (DI)-the membranepermeable derivative of itaconate, on LPS-induced mastitis in mice. To establish the model of mastitis, mice 5–7 day after delivery were utilized by nipple duct injection of LPS, while DI was treated 24h intraperitoneally before LPS injection. Further, the hematoxylin-eosin (H&E) staining was used to evaluate the pathological changes of the mammary gland, the inflammatory cytokines of TNF-α and IL-1β and the myeloperoxidase (MPO) activity were also measured respectively by enzyme-linked immunosorbent assay (ELISA) and MPO assay kit. To clarify the underling mechanisms of the protective role of DI on mastitis, the MAPKs, NF-κB and Nrf2 signaling pathways were detected via western blotting. The results demonstrated that DI markedly decreased the pathological injury of mammary, and considerably reduced the production of TNF-α and IL-1β, as well as up-regulated the Nrf2, HO-1, phosphorylation of p38 and ERK, but down-regulated TLR4 and phosphorylation of p65 NF-κB. Our research recommended that DI ameliorated LPS-induced mastitis which highlights itaconate may as a potential candidate to protect against mastitis. Image 1 • DI has protective effects against LPS-induced mastitis in mice. • DI significantly decreases the secretion of TNF-α and IL-1β. • DI inhibits LPS-induced TLR4 expression and NF-κB activation. • DI up-regulated the MAPKs and Nrf2 actiation. [ABSTRACT FROM AUTHOR]