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Chinese fir (Cunninghamia lanceolata (Lamb.) Hook.) has been an important afforestation species in northeast China. It has obvious defects of buckling and cracking easily, which are caused by its chemical components. Trametes versicolor (L.) Lloyd, a white-rot fungus, can decompose the cellulose, hemicellulose, and lignin in the wood. White-rot fungus was used to biologically degrade Chinese fir wood. The effects of different degradation time on the Chinese fir wood's mechanical properties, micromorphology, chemical components, and crystallinity were studied. The results showed that the heartwood of Chinese fir was more durable than the sapwood and the durability class of Chinese fir was III. Trametes versicolor (L.) Lloyd had a greater influence on the mechanical properties (especially with respect to the modulus of elasticity (MOE)) for the sapwood. Trametes versicolor (L.) Lloyd degraded Chinese fir and colonized the lumen of various wood cell types in Chinese fir, penetrated cell walls via pits, caused erosion troughs and bore holes, and removed all cell layers. The ability of white-rot fungus to change the chemical composition mass fraction for Chinese fir was: hemicellulose > lignin > cellulose. The durability of the chemical compositions was: lignin > cellulose > hemicellulose. The crystallinity of the cellulose decreased and the mean size of the ordered (crystalline) domains increased after being treated by white-rot fungus. [ABSTRACT FROM AUTHOR]

The effects of a three-layer structure and age on the mechanical properties of moso bamboo were investigated. The ages of 1-, 3-, and 5-year-old bamboo were chosen to make test samples, and specimens from each age of moso bamboo were divided into three groups (raw bamboo, bamboo removed from outer layer, and bamboo removed from inner layer) for evaluation of modulus of rupture and parallel-to-grain compressive strength. The regression analysis was completed to evaluate the relationship between mechanical properties and bamboo age. The results showed that the age of moso bamboo was positively correlated with the flexural and parallel-to-grain compressive strengths. The mechanical strength of moso bamboo increased with the increased age of moso bamboo. For the moso bamboo with same age, the flexural and parallel-to-grain compressive strengths decreased for the samples without bamboo outer layer. However, for the samples without bamboo inner layer, the parallel-to-grain compressive strength remained unchanged, but the flexural strength increased. The outer layer of bamboo with high toughness and flexibility played an important role during bending. However, the inner layer of bamboo is relatively brittle, which has negative effects on its flexural strength. These results provide an important basis for the bamboo used in engineering. [ABSTRACT FROM AUTHOR]

The article offers information on a study that explores the deacetylation-phosphorylation regulation of SIRT2-SMC1A axis as a mechanism of antimitotic catastrophe in early tumorigenesis. It mentions that regulation of the SIRT2-SMC1A axis through deacetylation-phosphorylation permits escape from mitotic catastrophe.

MutS protein homolog 2 (MSH2) is a key DNA mismatch repair protein. It forms the MSH2-MSH6 (MutSα) and MSH2-MSH3 (MutSβ) heterodimers, which help to ensure genomic integrity. MutSα not only recognizes and repairs mismatched nucleotides but also recognizes DNA adducts induced by DNA-damaging agents, and triggers cell-cycle arrest and apoptosis. Loss or depletion of MutSα from cells leads to microsatellite instability (MSI) and resistance to DNA damage. Although the level of MutSα can be reduced by the ubiquitin-proteasome pathway, the detailed mechanisms of this regulation remain elusive. Here we report that histone deacetylase 6 (HDAC6) sequentially deacetylates and ubiquitinates MSH2, leading to MSH2 degradation. In addition, HDAC6 significantly reduces cellular sensitivity to DNA-damaging agents and decreases cellular DNA mismatch repair activities by downregulation of MSH2. Overall, these findings reveal a mechanism by which proper levels of MutSα are maintained. [ABSTRACT FROM AUTHOR]