Decay resistance variability of European wood species thermally modified by industrial process

Thermal modification is now considered as a new ecofriendly industrial wood modification process improving mainly the material decay resistance and its dimensional stability. Most industrial thermal treatment processes use convection heat transfer which induces sometimes heterogeneous treatment temperature propagation within the oven and lead to the heterogeneity in treatment efficiency. Thus, it is common that treatment is not completely effective on several stack boards, in a same batch. The aim of this paper was to study the decay resistance variability of various European wood species thermally modified. Thermal modifications were performed around 240°C during 4h, on about 10 m3 of 27 x 152 x 2000 mm3 wood planks placed in an industrial oven having a volume of 20 m3, on the following wood species: spruce, ash, beech and poplar. All of the tests concerning the decay resistance were carried out in the laboratory using untreated beech and pine woods as reference materials. An agar block test was used to determine the resistance of thermally modified woods, leached beforehand according to EN 84 standard or not, to brown-rot and white-rot fungi, according to XP CEN/TS 15083-1. A large selection of treated wood samples was tested in order to estimate the variability of treatment efficiency. Thermal treatment increased the biological durability of all leached and un-leached modified wood samples, compared with native wood species. The treatment temperature of 240°C used in this study is sufficient to reach durability classes ''durable'' or ''very durable'' for the four wood species. However, the dispersion of weight loss values, due to the fungal attacks was very important and showed a large variability of the durability of wood which has been treated in a single batch. These results showed that there is a substantial need to develop process control and² indicator in order to insure that the quality of treated timber is properly evaluated with a view to putting this modified timber on the market under a chain of custody. (Résumé d'auteur

New Insights into Human Nondisjunction of Chromosome 21 in Oocytes

Nondisjunction of chromosome 21 is the leading cause of Down syndrome. Two risk factors for maternal nondisjunction of chromosome 21 are increased maternal age and altered recombination. In order to provide further insight on mechanisms underlying nondisjunction, we examined the association between these two well established risk factors for chromosome 21 nondisjunction. In our approach, short tandem repeat markers along chromosome 21 were genotyped in DNA collected from individuals with free trisomy 21 and their parents. This information was used to determine the origin of the nondisjunction error and the maternal recombination profile. We analyzed 615 maternal meiosis I and 253 maternal meiosis II cases stratified by maternal age. The examination of meiosis II errors, the first of its type, suggests that the presence of a single exchange within the pericentromeric region of 21q interacts with maternal age-related risk factors. This observation could be explained in two general ways: 1) a pericentromeric exchange initiates or exacerbates the susceptibility to maternal age risk factors or 2) a pericentromeric exchange protects the bivalent against age-related risk factors allowing proper segregation of homologues at meiosis I, but not segregation of sisters at meiosis II. In contrast, analysis of maternal meiosis I errors indicates that a single telomeric exchange imposes the same risk for nondisjunction, irrespective of the age of the oocyte. Our results emphasize the fact that human nondisjunction is a multifactorial trait that must be dissected into its component parts to identify specific associated risk factors

Human aneuploidy: mechanisms and new insights into an age-old problem

Trisomic and monosomic (aneuploid) embryos account for at least 10% of human pregnancies and, for women nearing the end of their reproductive lifespan, the incidence may exceed 50%. The errors that lead to aneuploidy almost always occur in the oocyte but, despite intensive investigation, the underlying molecular basis has remained elusive. Recent studies of humans and model organisms have shed new light on the complexity of meiotic defects, providing evidence that the age-related increase in errors in the human female is not attributable to a single factor but to an interplay between unique features of oogenesis and a host of endogenous and exogenous factors