Reinforcement ability of mechanical pulp fibres

The objective of this study was to find out the reasons why the long fibres of mechanical pulp do not seem to reinforce paper as effectively as chemical reinforcement pulp. A preliminary laboratory trial showed that artificially increasing the average fibre length of TMP pulp by adding long fibres extracted from the same pulp increased the tear index, but decreased the tensile strength, internal bond strength and the fracture energy. Increasing the average fibre strength with chemical (NBSK) pulp fibres improved all of those properties considerably. In the second trial fibre properties and reinforcement ability of various mechanical pulps were investigated. It was shown that fibre dimensions of mechanical pulp fibres did not differ essentially from chemical pulp fibres. The biggest differences were in the properties characterizing the cell wall structure. This was clearly seen in fibre flexibility and fibre swelling (WRV), for instance. Mechanical pulp fibres are evidently more damaged than chemical pulp fibres which is seen as a much lower fibre strength (zero-span tensile strength). The reinforcement potential, on the grounds of fracture energy, tear strength and tensile strength of handsheets was much lower for mechanical pulp fibres than for chemical pulp. In the third trial, mechanical (MRP) and chemimechanical reinforcement pulp (CMRP) was manufactured from Norway spruce (P.abies) on a pilot scale. The focus was to increase fibre flexibility, bonding ability and maintain the fibre length and strength. The runnability of LWC base paper made from the trial pulps was tested using the KCL AHMA runnability tester. In spite of the good strength properties of the trial pulps, they did not have the same overall reinforcement ability than chemical pulp. The sulphonated trial pulp (CMRP) gave the same tensile stiffness and tensile strength as the chemical pulp. However, the fracture properties and extensibility of the paper was worse with it. The lower average length of the trial pulps did not explain the difference totally. Scaling the fibre length with the zero-span tensile strength improved the explanatory power essentially. It was concluded that the low fibre strength is the basic reason for the poorer reinforcement ability of mechanical pulps fibres over chemical ones

An interaction between NDE1 and high birth weight increases schizophrenia susceptibility

Pre- and perinatal environmental factors have been shown to increase schizophrenia risk particularly when combined with genetic liability. The investigation of specific gene environment interactions in the etiology of psychiatric disorders has gained momentum. We used multivariate GEE regression modeling to investigate the interaction between genes of the DISCI pathway and birth weight, in relation to schizophrenia susceptibility in a Finnish schizophrenia family cohort. The study sample consisted of 457 subjects with both genotype and birth weight information. Gender and place of birth were adjusted for in the models. We found a significant interaction between birth weight and two NDE1 markers in relation to increased schizophrenia risk: a four SNP haplotype spanning NDE1 (b = 1.26, SE= 0.5, p = 0.012) and one of its constituent SNPs rs4781678 (b = 1.33, SE = 0.51, p = 0.010). Specifically, high birth weight (> 4000 g) was associated with increased schizophrenia risk among subjects homozygous for the previously identified risk alleles. The study was based on a family study sample with high genetic loading for schizophrenia and thus our findings cannot directly be generalized as representing the general population. Our results suggest that the functions mediated by NDE1 during the early stages of neurodevelopment are susceptible to the additional disruptive effects of pre- and perinatal environmental factors associated with high birth weight, augmenting schizophrenia susceptibility. (C) 2015 The Authors. Published by Elsevier Ireland Ltd.Peer reviewe

Serum lipopolysaccharide neutralizing capacity in ischemic stroke.

Introduction Periodontitis is associated with increased serum lipopolysaccharide (LPS) activity, which may be one mechanism linking periodontitis with the risk of cardiovascular diseases. As LPS-carrying proteins including lipoproteins modify LPS-activity, we investigated the determinants of serum LPS-neutralizing capacity (LPS-NC) in ischemic stroke. The association of LPS-NC and Aggregatibacter actinomycetemcomitans, a major microbial biomarker in periodontitis, was also investigated. Materials and methods The assay to measure LPS-NC was set up by spiking serum samples with E. coli LPS. The LPS-NC, LPS-binding protein (LBP), soluble CD14 (sCD14), lipoprotein profiles, apo(lipoprotein) A-I, apoB, and phospholipid transfer protein (PLTP) activity, were determined in 98 ischemic stroke patients and 100 age- and sex-matched controls. Serum and saliva immune response to A. actinomycetemcomitans, its concentration in saliva, and serotype-distribution were examined. Results LPS-NC values ranged between 51-83% in the whole population. Although several of the LPS-NC determinants differed significantly between cases and controls (PLTP, sCD14, apoA-I, HDL-cholesterol), the levels did not (p = 0.056). The main determinants of LPS-NC were i) triglycerides (beta = -0.68, p Conclusion Serum LPS-NC comprised low PLTP-activity, triglyceride and LDL cholesterol concentrations, as well as high HDL cholesterol and IgG against A. actinomycetemcomitans. The present findings let us to conclude that LPS-NC did not associate with stroke.Peer reviewe

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms