Smoothness Improvement of High Speed Recycled Paperboard through Base Coating Formula Optimization

As the trend in printing recycled paperboard shifts toward the rotogravure process, the surface smoothness of the paperboard is becoming increasingly important. Also, as recycled paperboard machine speeds increase, greater demands are being placed on the coating process and formulation to yield superior coating characteristics. The objective of this research project is to determine a base coat formulation that improves the base coating characteristics in high-speed recycled paperboard. This study examines the replacement of a traditional #1 clay with calcined clay and fine particle clay, which through their different properties alter the characteristics of the coating. The bulky calcined particles are more effective at filling the micro-valleys on the surface of the paperboard, while the smaller fine particle clay particles help prevent the coating from becoming dilatent. The less costly fine particle clay also offsets the high cost of the calcined clay. The lab experiments on the Cylindrical Laboratory Coater have shown that at a constant coat weight, 20 parts calcined clay, 32 parts fine particle clay and 48 parts #1 clay provided improved smoothness and brightness while maintaining adequate flow characteristics. Above 20 parts of calcined clay the coating consisting of 10 parts calcined clay, 32 parts fine clay and 58 parts #1 clay provided almost the same smoothness and brightness results, but costs less. This would be the most cost effective coating formulation for improving the surface smoothness and brightness characteristics of recycled paperboard. Because only a relatively small amount of research has been done in this area, this project could be extended into any number of areas including the addition of delaminated clay, effect of coat weight, and pilot/machine trials

Cytokine response patterns, exposure to viruses, and respiratory infections in the first year of life

Keywords: interferon-␥; respiratory syncytial virus; daycare; sibling Viral respiratory illnesses, many of which are contracted through contact with siblings or attendance at daycare, are the most common triggers for wheezing and asthma exacerbations among young children. In both the Tucson Children's Respiratory Study (1, 2) and the Italian Studies of Respiratory Disorders in Childhood and the Environment project (3), daycare attendance was shown to be a risk factor for viral infections and viral-associated wheezing in the first 2 years of life, but protective against viral infections and asthma later in life. Celedon and colleagues found that daycare attendance during the first year of life was associated with lower rates of asthma at 6 years of age, but only among children without a maternal history of asthma (4). Similarly, children with older siblings in the home are more likely to experience viral illnesses and wheezing in the first 2 years of life, but have decreased rates of wheezing, and decreased rates of atopic sensitization later in childhood (2, 3, 5, 6). Despite the convincing evidence linking exposure to other children with rates of respiratory illnesses and wheezing, the effects of increased exposure on specific viral infections have not been ascertained. While exposure is an important determinant of lower respiratory tract illnesses, it does not explain why some children entering daycare experience a dramatic increase in viral infections, while others are relatively healthy. In addition, recent genetic studies suggest that clinical outcomes of viral infections in infancy might also be influenced by polymorphisms in cytokine genes (7-9). These observations suggest the hypotheses that variations and/or subtle defects in the antiviral immune response also affect the clinical expression of viral respiratory infections. Furthermore, stressing the immune system with increased viral exposure may uncover relatively minor immune defects that are not apparent in children with less exposure to viruses. To test these hypotheses, we conducted a prospective birth cohort study to evaluate interactions between exposure to other children, the development patterns of cytokine responses in peripheral blood cells, and the etiology and severity of respiratory viral infections during the first year of life. Other study results pertinent to this cohort have been previously published as both original articles and abstracts (10-13)

Expression quantitative trait locus fine mapping of the 17q12–21 asthma locus in African American children: a genetic association and gene expression study

Background: African ancestry is associated with a higher prevalence and greater severity of asthma than European ancestries, yet genetic studies of the most common locus associated with childhood-onset asthma, 17q12–21, in African Americans have been inconclusive. The aim of this study was to leverage both the phenotyping of the Children's Respiratory and Environmental Workgroup (CREW) birth cohort consortium, and the reduced linkage disequilibrium in African Americans, to fine map the 17q12–21 locus. Methods: We first did a genetic association study and meta-analysis using 17q12–21 tag single-nucleotide polymorphisms (SNPs) for childhood-onset asthma in 1613 European American and 870 African American children from the CREW consortium. Nine tag SNPs were selected based on linkage disequilibrium patterns at 17q12–21 and their association with asthma, considering the effect allele under an additive model (0, 1, or 2 effect alleles). Results were meta-analysed with publicly available summary data from the EVE consortium (on 4303 European American and 3034 African American individuals) for seven of the nine SNPs of interest. Subsequently, we tested for expression quantitative trait loci (eQTLs) among the SNPs associated with childhood-onset asthma and the expression of 17q12–21 genes in resting peripheral blood mononuclear cells (PBMCs) from 85 African American CREW children and in upper airway epithelial cells from 246 African American CREW children; and in lower airway epithelial cells from 44 European American and 72 African American adults from a case-control study of asthma genetic risk in Chicago (IL, USA). Findings: 17q12–21 SNPs were broadly associated with asthma in European Americans. Only two SNPs (rs2305480 in gasdermin-B [GSDMB] and rs8076131 in ORMDL sphingolipid biosynthesis regulator 3 [ORMDL3]) were associated with asthma in African Americans, at a Bonferroni-corrected threshold of p<0·0055 (for rs2305480_G, odds ratio [OR] 1·36 [95% CI 1·12–1·65], p=0·0014; and for rs8076131_A, OR 1·37 [1·13–1·67], p=0·0010). In upper airway epithelial cells from African American children, genotype at rs2305480 was the most significant eQTL for GSDMB (eQTL effect size [β] 1·35 [95% CI 1·25–1·46], p<0·0001), and to a lesser extent showed an eQTL effect for post-GPI attachment to proteins phospholipase 3 (β 1·15 [1·08–1·22], p<0·0001). No SNPs were eQTLs for ORMDL3. By contrast, in PBMCs, the five core SNPs were associated only with expression of GSDMB and ORMDL3. Genotype at rs12936231 (in zona pellucida binding protein 2) showed the strongest associations across both genes (for GSDMB, eQTLβ 1·24 [1·15–1·32], p<0·0001; and for ORMDL3 (β 1·19 [1·12–1·24], p<0·0001). The eQTL effects of rs2305480 on GSDMB expression were replicated in lower airway cells from African American adults (β 1·29 [1·15–1·44], p<0·0001). Interpretation: Our study suggests that SNPs regulating GSDMB expression in airway epithelial cells have a major role in childhood-onset asthma, whereas SNPs regulating the expression levels of 17q12–21 genes in resting blood cells are not central to asthma risk. Our genetic and gene expression data in African Americans and European Americans indicated GSDMB to be the leading candidate gene at this important asthma locus.6 month embargo; published: 01 May 2020This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]