MODIFICATION OF PAPERMAKING GRADE FILLERS: A BRIEF REVIEW

The use of fillers in paper products can provide cost and energy savings, improved paper properties, increased productivities, and specifically desired paper functionalities. There are many problems associated with the use of fillers, such as unsuitability of calcium carbonate fillers in acid papermaking, negative effects of filler loading on paper strength, sizing, and retention, and tendencies of fillers to cause abrasion and dusting. In order to solve these problems and to make better use of fillers, many methods have been proposed, among which filler modification has been a hot topic. The available technologies of filler modification mainly include modification with inorganic substances, modification with natural polymers or their derivatives, modification with water-soluble synthetic polymers, modification with surfactants, modification with polymer latexes, hydrophobic modification, cationic modification, surface nano-structuring, physical modification by compressing, calcination or grinding, and modification for use in functional papers. The methods of filler modification can provide improved acid tolerant and optical properties of fillers, enhanced fiber-filler bonding, improved filler retention and filler sizabilities, alleviated filler abrasiveness, improved filler dispersability, and functionalization of filled papers. Filler modification has been an indispensable way to accelerate the development of high filler technology in papermaking, which is likely to create additional benefits to papermaking industry in the future

MODIFICATION OF PRECIPITATED CALCIUM CARBONATE FILLER USING SODIUM SILICATE/ZINC CHLORIDE BASED MODIFIERS TO IMPROVE ACID-RESISTANCE AND USE OF THE MODIFIED FILLER IN PAPERMAKING

In order to improve the acid-resistant property of papermaking grade precipitated calcium carbonate filler and to obtain modified filler in powder form, sodium silicate/zinc chloride based modifiers were used in filler modification, and the use of modified filler in papermaking of deinked pulp derived from recycled newspaper was also preliminarily investigated. Under the preliminarily optimized experimental conditions, when sodium silicate, zinc chloride, sodium hexametaphosphate, and phosphoric acid with dosages of 10 wt%, 3 wt%, 1 wt% and 0.2 wt%, respectively, were used as modifiers, and when the temperature, aging time, and PCC concentration during the filler modification process was 70 oC, 7 h and 9.1 wt%, respectively, the acid-resistant property of filler was significantly improved after modification, as evaluated using alum consumption and pH methods. The use of modified precipitated calcium carbonate filler prepared under the optimized conditions provided considerably more brightness and light scattering improvement in comparison to unmodified filler, and filler modification was found to have only negligible influence on tensile and burst strength of the paper, air permeability of the paper, and retention performance of the filler. Surface analysis of the modified filler using XPS and SEM confirmed the occurring of surface encapsulation and modification of precipitated calcium carbonate filler when the relevant modifiers were used in filler modification. The encapsulating effect of modifiers on filler was thought to be favorable to improvement in acid-resistant property, and optical properties of the filled paper

Increased creditor protection in bankruptcy and trade credit: Evidence from the 2005 BAPCPA

We examine whether the increased creditor protection under the 2005 Bankruptcy Abuse Prevention and Consumer Protection Act (BAPCPA) affects suppliers’ provision of trade credit to their customers with high default risk. Employing a difference-in-differences analysis for a sample of U.S. public firms during 2002-2008, we find that suppliers whose customers have high default risk extend more trade credit after BAPCPA. We also find that this relation exists when suppliers have stronger reliance on their customers and when customers exhibit fewer risk characteristics. Overall, our results indicate that the increased creditor protection in bankruptcy induces suppliers to offer more trade credit to customers with high default risk during the ordinary course of business. Our findings have policy implications given the heated debate on the BAPCPA’s effect on Chapter 11 bankruptcy process

Proteomic analysis of the biomass hydrolytic potentials of Penicillium oxalicum lignocellulolytic enzyme system

Additional file 2: Table S1. The functional annotations of proteins identified in the proteome of SP. Mass spectrometry-based proteomics study was performed to comprehensively dissect the lignocellulolytic enzyme profile of SP. Accession, Protein name, PSM, Calc. MW, CBM, Calc. pI and CAZy family of identified proteins were shown

N-WASP Is Essential for the Negative Regulation of B Cell Receptor Signaling

Negative regulation of receptor signaling is essential for controlling cell activation and differentiation. In B-lymphocytes, the down-regulation of B-cell antigen receptor (BCR) signaling is critical for suppressing the activation of self-reactive B cells; however, the mechanism underlying the negative regulation of signaling remains elusive. Using genetically manipulated mouse models and total internal reflection fluorescence microscopy, we demonstrate that neuronal Wiskott–Aldrich syndrome protein (N-WASP), which is coexpressed with WASP in all immune cells, is a critical negative regulator of B-cell signaling. B-cell–specific N-WASP gene deletion causes enhanced and prolonged BCR signaling and elevated levels of autoantibodies in the mouse serum. The increased signaling in N-WASP knockout B cells is concurrent with increased accumulation of F-actin at the B-cell surface, enhanced B-cell spreading on the antigen-presenting membrane, delayed B-cell contraction, inhibition in the merger of signaling active BCR microclusters into signaling inactive central clusters, and a blockage of BCR internalization. Upon BCR activation, WASP is activated first, followed by N-WASP in mouse and human primary B cells. The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced WASP activation, and is restored by the activation of SH2 domain-containing inositol 5-phosphatase that inhibits WASP activation. Our results reveal a new mechanism for the negative regulation of BCR signaling and broadly suggest an actin-mediated mechanism for signaling down-regulation

5. Innenpolitik/Aussenpolitik

5.1. Aussenpolitik der Schweiz Herausragendes Ereignis im Jahr 2000 war zweifellos die Präsentation der aussenpolitischen Ziele des Bundesrats und insbesondere des neuen Aussenpolitischen Berichts der Landesregierung. Im Laufe der 90er Jahre war eine Reihe von Berichten veröffentlicht worden, welche den Rahmen der schweizerischen Aussenpolitik für die ersten zehn Jahre des neuen Jahrtausends absteckten. Im Bericht über die Legislaturplanung 1999-2003 werden die Prioritäten für die kommenden v..

WASP family proteins regulate the mobility of the B cell receptor during signaling activation.

Regulation of membrane receptor mobility tunes cellular response to external signals, such as in binding of B cell receptors (BCR) to antigen, which initiates signaling. However, whether BCR signaling is regulated by BCR mobility, and what factors mediate this regulation, are not well understood. Here we use single molecule imaging to examine BCR movement during signaling activation and a novel machine learning method to classify BCR trajectories into distinct diffusive states. Inhibition of actin dynamics downstream of the actin nucleating factors, Arp2/3 and formin, decreases BCR mobility. Constitutive loss or acute inhibition of the Arp2/3 regulator, N-WASP, which is associated with enhanced signaling, increases the proportion of BCR trajectories with lower diffusivity. Furthermore, loss of N-WASP reduces the diffusivity of CD19, a stimulatory co-receptor, but not that of FcγRIIB, an inhibitory co-receptor. Our results implicate a dynamic actin network in fine-tuning receptor mobility and receptor-ligand interactions for modulating B cell signaling

Macrophage CGI-58 Deficiency Activates ROS-Inflammasome Pathway to Promote Insulin Resistance in Mice

SummaryOvernutrition activates a proinflammatory program in macrophages to induce insulin resistance (IR), but its molecular mechanisms remain incompletely understood. Here, we show that saturated fatty acid and lipopolysaccharide, two factors implicated in high-fat diet (HFD)-induced IR, suppress macrophage CGI-58 expression. Macrophage-specific CGI-58 knockout (MaKO) in mice aggravates HFD-induced glucose intolerance and IR, which is associated with augmented systemic/tissue inflammation and proinflammatory activation of adipose tissue macrophages. CGI-58-deficient macrophages exhibit mitochondrial dysfunction due to defective peroxisome proliferator-activated receptor (PPAR)γ signaling. Consequently, they overproduce reactive oxygen species (ROS) to potentiate secretion of proinflammatory cytokines by activating NLRP3 inflammasome. Anti-ROS treatment or NLRP3 silencing prevents CGI-58-deficient macrophages from oversecreting proinflammatory cytokines and from inducing proinflammatory signaling and IR in the cocultured fat slices. Anti-ROS treatment also prevents exacerbation of inflammation and IR in HFD-fed MaKO mice. Our data thus establish CGI-58 as a suppressor of overnutrition-induced NLRP3 inflammasome activation in macrophages