Resistance of thermo-hygro-mechanically densified wood to colonisation and degradation by brown-rot fungi

Colonisation and wood degradation by three brown-rot fungi, Coniophora puteana, Gloeophyllum trabeum and Poria placenta, were studied in wood of Norway spruce (Picea abies) subjected to three different treatments: hygro-thermal (TH) (160 and 180°C), mechanical densification and thermo-hygro-mechanical (THM) treatment including densification and post-treatment under saturated steam conditions at different temperatures (140, 160 and 180°C). The weight loss induced by all three fungi was lowest in THM-densified wood post-treated at 180°C. Highest weight losses were recorded for controls and TH-treated wood. Fungal colonisation varied in its intensity, depending on the treatment applied to the wood. Hyphal growth in controls and TH-treated wood was abundant, whereas in densified and THM-densified wood it was sparse and confined predominantly to the cell lumina of earlywood tracheids. Also, penetration of large-diameter hyphae and associated degradation in THM-densified wood was impeded by occlusion of the lumina, associated with irreversible compression (loss in shape memory). In contrast to C. puteana and P. placenta, which showed typical brown-rot behaviour, G. trabeum frequently showed hyphal tunnelling within the secondary walls of tracheids and xylem ray parenchyma of controls and thermally treated wood. Such growth was never observed in THM-densified wood post-treated at 180°

Assessment of resonance wood quality by comparing its physical and histological properties

The quality of wood used for music instrument making (resonance wood) is determined by assessing six physical properties: density, modulus of elasticity, sound velocity, radiation ratio, emission ratio, and loudness index. This can easily be done by means of measurements of the resonance frequency and the corresponding damping factor. The method described here is based on vibrational analyses, adapted from standard non-destructive testing of solid material, so as to provide information both for scientific studies and for violin making. The above six properties were assessed in samples of resonance wood of different quality and in normal (control) wood of Norway spruce and sycamore. The differences observed between the samples correlated with anatomical or histological characteristics of the wood. A sample of best-quality Norway spruce resonance wood showed a high radiation ratio in the axial direction, which correlated with the presence of small wood cells with thin cell walls. In "curly maple”, a high sound velocity in the radial direction correlated with the presence of broad xylem rays. The influence of external factors like wood moisture content or the geometry of the system is discussed within the context of the present stud

Aldose Reductase Inhibition Prevents Metaplasia of Airway Epithelial Cells

BACKGROUND: Goblet cell metaplasia that causes mucus hypersecretion and obstruction in the airway lumen could be life threatening in asthma and chronic obstructive pulmonary disease patients. Inflammatory cytokines such as IL-13 mediate the transformation of airway ciliary epithelial cells to mucin-secreting goblet cells in acute as well as chronic airway inflammatory diseases. However, no effective and specific pharmacologic treatment is currently available. Here, we investigated the mechanisms by which aldose reductase (AR) regulates the mucus cell metaplasia in vitro and in vivo. METHODOLOGY/FINDINGS: Metaplasia in primary human small airway epithelial cells (SAEC) was induced by a Th2 cytokine, IL-13, without or with AR inhibitor, fidarestat. After 48 h of incubation with IL-13 a large number of SAEC were transformed into goblet cells as determined by periodic acid-schiff (PAS)-staining and immunohistochemistry using antibodies against Mucin5AC. Further, IL-13 significantly increased the expression of Mucin5AC at mRNA and protein levels. These changes were significantly prevented by treatment of the SAEC with AR inhibitor. AR inhibition also decreased IL-13-induced expression of Muc5AC, Muc5B, and SPDEF, and phosphorylation of JAK-1, ERK1/2 and STAT-6. In a mouse model of ragweed pollen extract (RWE)-induced allergic asthma treatment with fidarestat prevented the expression of IL-13, phosphorylation of STAT-6 and transformation of epithelial cells to goblet cells in the lung. Additionally, while the AR-null mice were resistant, wild-type mice showed goblet cell metaplasia after challenge with RWE. CONCLUSIONS: The results show that exposure of SAEC to IL-13 caused goblet cell metaplasia, which was significantly prevented by AR inhibition. Administration of fidarestat to mice prevented RWE-induced goblet cell metaplasia and AR null mice were largely resistant to allergen induced changes in the lung. Thus our results indicate that AR inhibitors such as fidarestat could be developed as therapeutic agents to prevent goblet cell metaplasia in asthma and related pathologies

Le Grand écho de l'Aisne : organe hebdomadaire d'informations et de défense des intérêts généraux de la région

07 juillet 19261926/07/07 (A8,N569).Appartient à l’ensemble documentaire : Picardi

Assessment of resonance wood quality by comparing its physical and histological properties

ISSN:0043-7719ISSN:1432-522

Genesis of and Trafficking to the Maurer's Clefts of Plasmodium falciparum-Infected Erythrocytes

Malaria parasites export proteins beyond their own plasma membrane to locations in the red blood cells in which they reside. Maurer's clefts are parasite-derived structures within the host cell cytoplasm that are thought to function as a sorting compartment between the parasite and the erythrocyte membrane. However, the genesis of this compartment and the signals directing proteins to the Maurer's clefts are not known. We have generated Plasmodium falciparum-infected erythrocytes expressing green fluorescent protein (GFP) chimeras of a Maurer's cleft resident protein, the membrane-associated histidine-rich protein 1 (MAHRP1). Chimeras of full-length MAHRP1 or fragments containing part of the N-terminal domain and the transmembrane domain are successfully delivered to Maurer's clefts. Other fragments remain trapped within the parasite. Fluorescence photobleaching and time-lapse imaging techniques indicate that MAHRP1-GFP is initially trafficked to isolated subdomains in the parasitophorous vacuole membrane that appear to represent nascent Maurer's clefts. The data suggest that the Maurer's clefts bud from the parasitophorous vacuole membrane and diffuse within the erythrocyte cytoplasm before taking up residence at the cell periphery