目的:总结外侧半月板前角-前体部损伤的临床分型及相应手术策略并评估治疗效果。方法:回顾性分析2020年1月至2020年12月收治的87例外侧半月板前角-前体部损伤患者病例资料,总结撕裂类型和手术策略,根据术前和末次随访的国际膝关节评分...目的:总结外侧半月板前角-前体部损伤的临床分型及相应手术策略并评估治疗效果。方法:回顾性分析2020年1月至2020年12月收治的87例外侧半月板前角-前体部损伤患者病例资料,总结撕裂类型和手术策略,根据术前和末次随访的国际膝关节评分委员会(IKDC)评分和Lysholm膝关节评分评估治疗效果。结果:前角-前体部损伤占所有外侧半月板损伤的10.8%。依据撕裂类型将外侧半月板前角-前体部损伤分为5型,其中Ⅰ型为复合撕裂,表现为水平撕裂合并某一层垂直撕裂,并根据垂直撕裂的部位分为Ⅰa、Ⅰb、Ⅰc三种亚型;Ⅱ型为水平撕裂;Ⅲ型为垂直撕裂,并根据移位情况和形态分为Ⅲa、Ⅲb、Ⅲc三种亚型;Ⅳ型为松散型,发生在前角;Ⅴ型为缺失型,半月板前角-前体部消磨殆尽。对于常规手术入路无法处理的Ⅰb型和Ⅱ型损伤,附加外下入路进行操作并视情况进行Outside-in缝合。87例患者均获得随访,平均随访25.1±5.7月(19~31月)。末次随访时IKDC评分和Lysholm评分均显著高于术前(分别为64.5±7.4 vs 84.3±6.9和73.3±5.1 vs 90.1±5.0,均P<0.05)。结论:基于不同分型采取相应手术策略是治疗外侧半月板前角-前体部损伤的有效方法。展开更多
Androgen receptor （AR） is able to promote stress-induced cell death independently of its transcription activity in androgen-independent prostate cancer cells. Yet, the underlying mechanism is incompletely understood...Androgen receptor （AR） is able to promote stress-induced cell death independently of its transcription activity in androgen-independent prostate cancer cells. Yet, the underlying mechanism is incompletely understood. Here, we report that stress-induced proteasomal degradation of AR contributes to its pro-death activity. Upon exposure to ul- traviolet fight and staurosporine, AR underwent proteasomal degradation. Blockade of AR degradation significantly suppressed stress-induced apoptosis in androgen-independent prostate cancer cells. Ectopic expression of the AR N-terminal （AR-N） domain, which lacks DNA- and ligand-binding abilities, led to cell death without any additional death stimuli. Truncation analysis revealed that AR-N domain contains several sub-domains that regulate the pro- death activity of AR, specifically the first 105 amino acids, which function as a minimal pro-death domain acting upstream of caspases. The pro-apoptotic activity of AR N-terminal fragments was suppressed by ectopic expression of Bcl-2 or selected caspase inhibitors. Thus, our results reveal a novel mechanism by which AR promotes stressinduced cell death in androgen-independent prostate cancer cells.展开更多
文摘目的:总结外侧半月板前角-前体部损伤的临床分型及相应手术策略并评估治疗效果。方法:回顾性分析2020年1月至2020年12月收治的87例外侧半月板前角-前体部损伤患者病例资料,总结撕裂类型和手术策略,根据术前和末次随访的国际膝关节评分委员会(IKDC)评分和Lysholm膝关节评分评估治疗效果。结果:前角-前体部损伤占所有外侧半月板损伤的10.8%。依据撕裂类型将外侧半月板前角-前体部损伤分为5型,其中Ⅰ型为复合撕裂,表现为水平撕裂合并某一层垂直撕裂,并根据垂直撕裂的部位分为Ⅰa、Ⅰb、Ⅰc三种亚型;Ⅱ型为水平撕裂;Ⅲ型为垂直撕裂,并根据移位情况和形态分为Ⅲa、Ⅲb、Ⅲc三种亚型;Ⅳ型为松散型,发生在前角;Ⅴ型为缺失型,半月板前角-前体部消磨殆尽。对于常规手术入路无法处理的Ⅰb型和Ⅱ型损伤,附加外下入路进行操作并视情况进行Outside-in缝合。87例患者均获得随访,平均随访25.1±5.7月(19~31月)。末次随访时IKDC评分和Lysholm评分均显著高于术前(分别为64.5±7.4 vs 84.3±6.9和73.3±5.1 vs 90.1±5.0,均P<0.05)。结论:基于不同分型采取相应手术策略是治疗外侧半月板前角-前体部损伤的有效方法。
文摘Androgen receptor （AR） is able to promote stress-induced cell death independently of its transcription activity in androgen-independent prostate cancer cells. Yet, the underlying mechanism is incompletely understood. Here, we report that stress-induced proteasomal degradation of AR contributes to its pro-death activity. Upon exposure to ul- traviolet fight and staurosporine, AR underwent proteasomal degradation. Blockade of AR degradation significantly suppressed stress-induced apoptosis in androgen-independent prostate cancer cells. Ectopic expression of the AR N-terminal （AR-N） domain, which lacks DNA- and ligand-binding abilities, led to cell death without any additional death stimuli. Truncation analysis revealed that AR-N domain contains several sub-domains that regulate the pro- death activity of AR, specifically the first 105 amino acids, which function as a minimal pro-death domain acting upstream of caspases. The pro-apoptotic activity of AR N-terminal fragments was suppressed by ectopic expression of Bcl-2 or selected caspase inhibitors. Thus, our results reveal a novel mechanism by which AR promotes stressinduced cell death in androgen-independent prostate cancer cells.
