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您的检索式：作者名="Kefeng Luo"
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| 1 | Poly(methyl methacrylate) bone cement composited with mineralized collagen for osteoporotic vertebral compression fractures in extremely old patients显示文摘To examine the clinical effects of a new bone cement composed of poly(methyl methacrylate)(PMMA)and mineralized collagen(MC)compared with pure PMMA bone cement in treating osteoporotic vertebral compression fractures(OVCFs)in patients aged over 80.In all,32 cases using pure PMMA bone cement and 31 cases using MC-modified PMMA(MC-PMMA)bone cement for OVCFs between June 2014 and March 2016 were screened as PMMA group and MC-PMMA group,respectively,with an average age of over 80.The operation duration,intraoperative blood loss,hospital stay,oswestry disability index(ODI),visual analogue scale(VAS),anterior vertebral height(AVH),intermediate vertebral height(IVH)and posterior vertebral height(PVH)of injured vertebrae,vertebral computed tomography value,re-fracture rate of adjacent vertebrae,correction rate of spinal kyphotic angle and wedge-shaped vertebra angle and surgical complications were compared between the two groups.In the early post-operative period,the VAS,ODI,AVH and IVH in MC-PMMA group were comparable to those in the traditional PMMA group.Moreover,the MC-PMMA group showed better effects compared with the PMMA group 12months after surgery.Thus,this new bone cement has superior clinic effects in the long term. | Kefeng Luo Guoqiang Jiang Jinjin Zhu Bin Lu Jiye Lu Kai Zhang Xiumei Wang Fu-Zhai Cui | 2020 | Regenerative Biomaterials2020，7，1： | 8 |
| 2 | CKIP-1 regulates macrophage proliferation by inhibiting TRAF6-mediated Akt activation显示文摘巨噬细胞在开发,动态平衡,织物修理和免疫起枢轴的作用。巨噬细胞增长被刺激殖民地的因素(M-CSF ) 导致了 Akt 发信号的巨噬细胞支持;然而,这个过程怎么被终止,仍然保持不清楚。这里,我们作为巨噬细胞增长的一个新奇禁止者识别酷蛋白 kinase 2-interacting protein-1 (CKIP-1 ) 。在放松巨噬细胞, CKIP-1 是在由组成地活跃的 GSK3β 的丝氨酸 342 点的 phosphorylated;, Akt 的下游的目标。这 phosphorylation 触发 CKIP-1 的 polyubiquitination 和 proteasomal 降级。在 M-CSF 刺激之上, Akt 被 CSF-1R-PI3K 激活然后使 GSK3β 失去活性;,导致 CKIP-1 和 β 的稳定; -catenin 蛋白质。β -catenin 包括 cyclin D 和 c-Myc 支持增长基因的表示。CKIP-1 与 TRAF6,为连接 K63 的 ubiquitination 要求的 ubiquitin ligase 和 Akt 的血浆膜招募交往,并且终止调停 TRAF6 的 Akt 激活。由这个工具, CKIP-1 在 M-CSF 刺激以后在迟了的阶段明确地禁止巨噬细胞增长。而且, CKIP-1 缺乏在老鼠自发地开发的 vitro 和 CKIP-1 −/− 导致增加的增长和巨噬细胞的减少的 apoptosis 巨噬细胞主导的脾大和 myeloproliferation。一起,这些数据证明 CKIP-1 由禁止调停 TRAF6 的 Akt 激活在巨噬细胞动态平衡的规定起一个关键作用。 | Luo Zhang Yiwu Wang Fengjun Xiao Shaoxia Wang Guichun Xing Yang Li Xiushan Yin Kefeng Lu Rongfei Wei Jiao Fan Yuhan Chen Tao Li Ping Xie Lin Yuan Lei Song Lanzhi Ma Lujing Ding Fuchu He Lingqiang Zhang | 2014 | Cell Research2014，24，6： | 7 |
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