海洋中CO2引起的pH降低对紫海胆亚氏提灯附属肌肉生理机能的影响

研究了高浓度CO2(1 000μL/L,3 000μL/L)引起的海洋环境pH降低对紫海胆亚氏提灯附属肌肉的呼吸耗氧、总ATP含量、乙酰胆碱含量以及肌肉收缩力的影响。140 d处理后,结果显示肌肉呼吸在3 000μL/L组中仅为对照组(380μL/L)的40%。总ATP含量未见显著差异。乙酰胆碱脂酶含量在高浓度CO2组有降低的趋势,但不显著。肌肉收缩力在高浓度组低于对照组。综上所述,海洋中CO2引起的pH降低对紫海胆亚氏提灯附属肌肉的生理会造成一定的影响。     

Effects of air injection on properties of particleboard manufactured using a radio-frequency hot press

The effectiveness of air injection for preventing the blowout of particleboards manufactured using a radio-frequency hot press was investigated by evaluating the board properties under artificially created conditions that were conducive to blowout. For evaluation, 10-mm-thick boards with densities of 0.7 and 0.8 g/cm³ and 20-mm-thick boards with a density of 0.7 g/cm³ were manufactured. Pressing times for the 10-mm-thick boards were 2, 4, 6, and 8 min, and those for the 20-mm-thick boards were 4, 6, 8, and 10 min. Without air injection, blowout occurred in all manufactured boards. With air injection, however, blowout did not occur in the 10-mm-thick boards with a density of 0.7 g/cm³. Moreover, air injection prevented blowout even when the board density and board thickness were increased to 0.8 g/cm³ (for 10-mm-thick boards) and 20 mm (the density was kept at 0.7 g/cm³), respectively. Air-injection radio-frequency pressing reduced the pressing time from 4 to 2 min for 10-mm-thick boards, and from 6 to 4 min for 20-mm-thick boards. Moreover, this reduction in the pressing time was achieved without a large reduction in the internal bond strength of the boards.     

Properties of particleboard manufactured using an air-injection radio-frequency hot press

A hot press was used to manufacture particleboards (H boards). A radio-frequency hot press (for RH boards) and an air-injection radio-frequency hot press (for ARH board) were also used, and the effects of air injection on preventing blowout and board properties were analyzed. The thicknesses and densities of manufactured boards were 10 and 30 mm, and 0.6, 0.7, and 0.8 g/cm³, respectively. The investigation ascertained the effects of air injection in preventing blowout when a radio-frequency hot press is used. The increasing order of temperature was ARH board > RH board > H board during the final pressing stage. For the 30-mm-thick boards, the temperature of H board increased to 100 °C and remained constant at 100 °C even when the pressing time was extended. The temperature of the RH board increased to 100 °C more quickly than in the case of the H board and remained constant at 110–118 °C. The temperature of the ARH board increased linearly to 130–142 °C. For both the 10- and 30-mm-thick boards, the internal bond strength of the RH board was almost the same as that of the ARH board at densities of 0.6 and 0.7 g/cm³. In contrast, the internal bond strength of the RH board was lower than that of the ARH board at a density of 0.8 g/cm³. For the 10-mm-thick boards, the thickness swelling in the RH board was almost the same as that in the ARH board irrespective of the density. However, for the 30-mm-thick boards, the thickness swelling in the RH board was higher than that in the ARH board. The low plasticization of particles due to air injection presumably results in a high degree of thickness swelling.     

Comparison of histological responses and tissue damage expansion between resistant and susceptible Pinus thunbergii infected with pine wood nematode Bursaphelenchus xylophilus

Pine wilt disease caused by the pine wood nematode (PWN), Bursaphelenchus xylophilus, has been epidemic and has had disastrous impacts on pine forests and forest ecosystems in eastern Asia. Many pine species in this area are susceptible to this disease. Pinus thunbergii is particularly susceptible. In Japan, tree breeders have selected surviving trees from severely damaged forests as resistant candidates, and have finally established several resistant varieties of P. thunbergii. However, this breeding procedure requires much time and effort due to the lack of physiological and phenotypical information about resistance. To investigate the resistance mechanisms of selected P. thunbergii, we compared histochemical responses, tissue damage expansion, and PWN distribution in resistant and susceptible clones of P. thunbergii after PWN inoculation. The results suggested that the mechanisms of resistance are as follows: damage expansion in the cortex, cambium, and xylem axial resin canals are retarded in resistant trees soon after inoculation, probably due to the induction of wall protein-based defenses. Suppression of PWN reproduction was particularly caused by inhibition of damage expansion in the cambium. The slow expansion of damage in each tissue provides time for the host to complete the biosynthesis of lignin in the walls of cells that surround the damaged regions. This lignification of cell walls is assumed to effectively inhibit the migration and reproduction of the PWNs. The mechanism of initial damage retardation is presumed to be a key for resistance.     

Identification of fructo- and malto-oligosaccharides in cured tobacco leaves (Nicotiana tabacum)

Fructo-oligosaccharides (FOSs) and malto-oligosaccharides (MOSs) in cured tobacco leaves ( Nicotiana tabacum ) were detected and quantified using high-performance liquid chromatography (HPLC) coupled with electrospray ionization (ESI) tandem mass spectrometry (MS/MS). These oligosaccharides were present in several tobacco materials including flue-cured tobacco, sun/air-cured tobacco, and cut filler of commercially available tobacco products, but were not detected in air-cured tobacco. The changes in these oligosaccharides during storage were also investigated. The results revealed that MOSs simply decreased under a warm atmosphere and FOSs increased. In addition, the formation of FOSs in cured tobacco leaves occurred in the presence of sucrose. With regard to FOSs, it has been reported that green tobacco leaves do not contain FOSs such as kestose, nystose, and fructosyl-nystose. The results of a model test suggested that the changes in FOS amount were caused by enzymatic reactions.     

Foot rot disease of sweet potato in Japan caused by Diaporthe destruens: first report,pathogenicity and taxonomy

Journal of General Plant Pathology - Foot rot, also known as stem rot or tuber-root rot syndrome, on sweet potato occurs in sweet potato fields in Okinawa, Japan. Isolates of one fungal species...     

Essential cytoplasmic translocation of a cytokine receptor-assembled signaling complex

Cytokine signaling is thought to require assembly of multicomponent signaling complexes at cytoplasmic segments of membrane-embedded receptors, in which receptor-proximal protein kinases are activated. Indeed, CD40, a tumor necrosis factor receptor (TNFR) family member, forms a complex containing adaptor molecules TRAF2 and TRAF3, ubiquitin-conjugating enzyme Ubc13, cellular inhibitor of apoptosis proteins 1 and 2 (c-IAP1/2), IkappaB kinase regulatory subunit IKKgamma (also called NEMO), and mitogen-activated protein kinase (MAPK) kinase kinase MEKK1 upon ligation. TRAF2, Ubc13, and IKKgamma were required for complex assembly and activation of MEKK1 and MAPK cascades. However, these kinases were not activated unless the multicomponent signaling complex translocated from CD40 to the cytosol upon c-IAP1/2-induced degradation of TRAF3. This two-stage signaling mechanism may apply to other innate immune receptors, accounting for spatial and temporal separation of MAPK and IKK signaling.