目的评估Bio-Gide在引导种植体周围骨组织再生的临床疗效。方法选择2004年2月到2005年11月来我院就诊种植区存在骨缺损的患者56例,其中男性患者35例,女性21例;可通过GBR(Guided Bone Regeneration)技术同期植入种植体,共植入种植体81枚...目的评估Bio-Gide在引导种植体周围骨组织再生的临床疗效。方法选择2004年2月到2005年11月来我院就诊种植区存在骨缺损的患者56例,其中男性患者35例,女性21例;可通过GBR(Guided Bone Regeneration)技术同期植入种植体,共植入种植体81枚。生物膜均采用可吸收性的Bio-Gide生物膜,移植物采用自体骨与Bio-oss骨粉1∶1或2∶1的混合物。结果术后6个月,x线片观察到所有种植体骨结合良好,行二期修复术。结论Bio-Gide生物膜在引导骨再生中种植体骨结合成功率为100%。展开更多
Here, we report the identification of GIDE, a mitochondrially located E3 ubiquitin ligase. GIDE contains a C-terminal RING finger domain, which is mostly conserved with those of the lAP family members and is required ...Here, we report the identification of GIDE, a mitochondrially located E3 ubiquitin ligase. GIDE contains a C-terminal RING finger domain, which is mostly conserved with those of the lAP family members and is required for GIDE＇s E3 ligase activity. Overexpression of GIDE induces apoptosis via a pathway involving activation of caspases, since caspase inhibitors, XIAP and an inactive mutant of caspase-9 block GIDE-induced apoptosis. GIDE also activates JNK, and blockage of JNK activation inhibits GIDE-induced release of cytochrome c and Smac as well as apoptosis, suggesting that JNK activation precedes release of cytochrome c and Smac and is required for GIDE- induced apoptosis. These pro-apoptotic properties of GIDE require its E3 ligase activity. When somewhat over-or underexpressed, GIDE slows or accelerates cell growth, respectively. These pro-apoptotic or growth inhibition effects of GIDE may account for its absence in tumor cells.展开更多
文摘目的评估Bio-Gide在引导种植体周围骨组织再生的临床疗效。方法选择2004年2月到2005年11月来我院就诊种植区存在骨缺损的患者56例,其中男性患者35例,女性21例;可通过GBR(Guided Bone Regeneration)技术同期植入种植体,共植入种植体81枚。生物膜均采用可吸收性的Bio-Gide生物膜,移植物采用自体骨与Bio-oss骨粉1∶1或2∶1的混合物。结果术后6个月,x线片观察到所有种植体骨结合良好,行二期修复术。结论Bio-Gide生物膜在引导骨再生中种植体骨结合成功率为100%。
文摘Here, we report the identification of GIDE, a mitochondrially located E3 ubiquitin ligase. GIDE contains a C-terminal RING finger domain, which is mostly conserved with those of the lAP family members and is required for GIDE＇s E3 ligase activity. Overexpression of GIDE induces apoptosis via a pathway involving activation of caspases, since caspase inhibitors, XIAP and an inactive mutant of caspase-9 block GIDE-induced apoptosis. GIDE also activates JNK, and blockage of JNK activation inhibits GIDE-induced release of cytochrome c and Smac as well as apoptosis, suggesting that JNK activation precedes release of cytochrome c and Smac and is required for GIDE- induced apoptosis. These pro-apoptotic properties of GIDE require its E3 ligase activity. When somewhat over-or underexpressed, GIDE slows or accelerates cell growth, respectively. These pro-apoptotic or growth inhibition effects of GIDE may account for its absence in tumor cells.
