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Abstract: In the chip refining process used for mechanical pulp production, wood fibers are treated in a narrow gap between rotating plates. The process is energy consuming and much of the electrical energy supplied to the refiner is transferred to the fiber material through friction forces. Even though the importance of friction has been discussed frequently, little has been proven due to the complexity of the process and the process conditions. This paper presents a new apparatus for studying the frictional properties of wood, in lab-scale, under conditions which are aimed at simulating those prevalent in a chip refiner. Tests can be performed in saturated steam at high temperature/pressure with sliding velocities as high as 150m/s. Studies at room temperature showed that the friction coefficient between spruce wood and smooth steel increased with the moisture content of the specimens. Impregnation by wood extractives lowered the friction coefficient for dry wood sliding at high speed. When tests were performed in a saturated steam environment, the frictional properties were affected and varied by the temperature of the surroundings. This is interesting in view of the fact that the friction coefficient is usually considered constant in analytical and numerical models of the process. [Copyright &y& Elsevier]

Summary: Angiogenesis, the process by which new blood vessels arise from preexisting ones, is critical for embryonic development and is an integral part of many disease processes. Recent studies have provided detailed information on how angiogenic sprouts initiate, elongate, and branch, but less is known about how these processes cease. Here, we show that S1PR1, a receptor for the blood-borne bioactive lipid sphingosine-1-phosphate (S1P), is critical for inhibition of angiogenesis and acquisition of vascular stability. Loss of S1PR1 leads to increased endothelial cell sprouting and the formation of ectopic vessel branches. Conversely, S1PR1 signaling inhibits angiogenic sprouting and enhances cell-to-cell adhesion. This correlates with inhibition of vascular endothelial growth factor-A (VEGF-A)-induced signaling and stabilization of vascular endothelial (VE)-cadherin localization at endothelial junctions. Our data suggest that S1PR1 signaling acts as a vascular-intrinsic stabilization mechanism, protecting developing blood vessels against aberrant angiogenic responses. [Copyright &y& Elsevier]

Abstract: We have previously shown that angiomotin (Amot) plays an important role in growth factor-induced migration of endothelial cells in vitro. Genetic knock-down of Amot in zebrafish also results in inhibition of migration of intersegmental vessels in vivo. Amot is expressed as two different isoforms, p80-Amot and p130-Amot. Here we have analyzed the expression of the two Amot isoforms during retinal angiogenesis in vivo and demonstrate that p80-Amot is expressed during the migratory phase. In contrast, p130-Amot is expressed during the period of blood vessel stabilization and maturation. We also show that the N-terminal domain of p130-Amot serves as a targeting domain responsible for localization of p130-Amot to actin and tight junctions. We further show that the relative expression levels of p80-Amot and p130-Amot regulate a switch between a migratory and a non-migratory cell phenotype where the migratory function of p80-Amot is dominant over the stabilization and maturation function of p130-Amot. Our data indicates that homo-oligomerization of p80-Amot and hetero-oligomerization of both isoforms are critical for this regulation. [Copyright &y& Elsevier]