对承受疲劳载荷的海洋平台K型管节点首先进行了静力测试,确定了沿着焊缝的热应力区的应力分布及热应力区最大应力点的位置,从而判断裂纹产生的位置;然后通过专用测试设备提供循环疲劳载荷,用ACPD(Alternating Current Potential Drop,...对承受疲劳载荷的海洋平台K型管节点首先进行了静力测试,确定了沿着焊缝的热应力区的应力分布及热应力区最大应力点的位置,从而判断裂纹产生的位置;然后通过专用测试设备提供循环疲劳载荷,用ACPD(Alternating Current Potential Drop,即交流电流势能落差法)技术检测裂纹的产生和增长过程,得到裂纹最深点,用S-N曲线估算其疲劳寿命。对已有裂纹的K型管节点,用应力强度因子估计其剩余寿命。同时用测试的结果验证了S-N的准确性和可靠性。展开更多
The effects of glutamate and its agonists and antagonists on the swelling of cultured astrocytes were studied. Swelling of astrocytes was measured by [3H]-O-methyl-D-glucose uptake. Glutamate at 0.5, 1 and 10mmol/L an...The effects of glutamate and its agonists and antagonists on the swelling of cultured astrocytes were studied. Swelling of astrocytes was measured by [3H]-O-methyl-D-glucose uptake. Glutamate at 0.5, 1 and 10mmol/L and irons-l-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD), a metabotropic glutamate receptor (mGluR) agonist, at 1 mmol/L caused a significant increase in astrocytic volume, whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) was not effective. L-2-amino-3-phosphonopropionic acid (L-AP3), an antagonist of mGluR, blocked the astrocytic swelling induced by trans-ACPD or glutamate. In Ca2+-free condition, glutamate was no longer effective. Swelling of astrocytes induced by glutamate was not blocked by CdCl2 at 20 μmol/L, but significantly reduced by CdCl2 at 300 μmol/L and dantrolene at 30 μmol/L. These findings indicate that mGluR activation results in astrocytic swelling and both extracellular calcium and internal calcium stores play important roles in the展开更多
文摘对承受疲劳载荷的海洋平台K型管节点首先进行了静力测试,确定了沿着焊缝的热应力区的应力分布及热应力区最大应力点的位置,从而判断裂纹产生的位置;然后通过专用测试设备提供循环疲劳载荷,用ACPD(Alternating Current Potential Drop,即交流电流势能落差法)技术检测裂纹的产生和增长过程,得到裂纹最深点,用S-N曲线估算其疲劳寿命。对已有裂纹的K型管节点,用应力强度因子估计其剩余寿命。同时用测试的结果验证了S-N的准确性和可靠性。
文摘The effects of glutamate and its agonists and antagonists on the swelling of cultured astrocytes were studied. Swelling of astrocytes was measured by [3H]-O-methyl-D-glucose uptake. Glutamate at 0.5, 1 and 10mmol/L and irons-l-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD), a metabotropic glutamate receptor (mGluR) agonist, at 1 mmol/L caused a significant increase in astrocytic volume, whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) was not effective. L-2-amino-3-phosphonopropionic acid (L-AP3), an antagonist of mGluR, blocked the astrocytic swelling induced by trans-ACPD or glutamate. In Ca2+-free condition, glutamate was no longer effective. Swelling of astrocytes induced by glutamate was not blocked by CdCl2 at 20 μmol/L, but significantly reduced by CdCl2 at 300 μmol/L and dantrolene at 30 μmol/L. These findings indicate that mGluR activation results in astrocytic swelling and both extracellular calcium and internal calcium stores play important roles in the
