掌侧入路微创加压螺钉固定术治疗腕舟骨骨折的临床观察

目的观察掌侧入路微创加压螺钉固定术治疗腕舟骨骨折的临床疗效。方法以90例腕舟骨骨折患者为研究对象,分为研究组(n=45)和对照组(n=45),对照组患者行背侧入路微创加压螺钉固定术,研究组患者行掌侧入路微创加压螺钉固定术。记录手术相关指标;观察术后并发症发生情况;比较术后不同复诊时间腕关节康复情况。结果两组患者术中出血量和手术时间差异均无统计学意义(P>0.05),研究组患者骨折愈合时间显著短于对照组水平(P<0.05)。术后3个月和6个月,研究组Mayo评分及腕关节功能优良率显著高于对照组水平(P<0.05),而术后12个月,两组患者上述指标差异无统计学意义(P>0.05)。研究组术后并发症总体发生率(11.11%)显著低于对照组水平(28.89%)(P<0.05)。结论掌侧入路微创加压螺钉固定术可有效缩短腕舟骨骨折患者骨折愈合周期,促进腕关节功能快速恢复,降低术后并发症发生率。

柴北缘宽沟口—红旗沟韧性剪切带及其金成矿动力机制探讨

在介绍宽沟口—红旗沟韧性剪切带基本特征和含矿性的同时,用"断裂阀-构造泵吸-周期性破裂愈合"的构造-流体耦合成矿动力机制,论述了该剪切带的形成、发育的全过程,并论述了该剪切带构造动力对成矿系统的启动、运行机制和对成矿物质的运动学、几何学特征的控制以及由此产生的成矿过程、聚矿能力和成矿产物之差异。

江西临川茅排金矿韧性剪切带特征及其金成矿动力机制探讨

在介绍茅排韧性剪切带基本特征和含矿性的同时,用"断裂阀—构造泵吸—周期性破裂愈合"的构造—流体耦合成矿动力机制,论述了该剪切带的形成、发育的全过程,并论述了该剪切带构造动力对成矿系统的启动、运行机制和对成矿物质的运动学、几何学特征的控制以及由此产生的成矿过程、聚矿能力和成矿产物之差异。

外固定架更换为髓内钉治疗GustiloⅢ型开放性胫骨骨折的临床探索

目的探索外固定架更换为髓内钉内固定治疗GustiloⅢ型开放性胫骨骨折的临床效果。方法选择该院于2016年1月—2018年1月期间收治的GustiloⅢ型开放性胫骨骨折患者54例,以数字表作参考将患者随机划分为观察组与对照组,每组各27例。对照组患者接受外固定架治疗,观察组患者接受外固定架治疗+胫骨髓内钉固定治疗,比较两组患者治疗后的骨折愈合有效率、骨折愈合周期以及并发症发生率。结果观察组患者的骨折愈合率为88.89%,高于对照组患者的66.67%,数据比对,组间差异有统计学意义(χ^2=3.8571,P<0.05);观察组患者的骨折愈合周期为(9.56±2.14)个月,短于对照组患者的(11.73±3.06)个月,数据组间差异有统计学意义(t=3.0196,P<0.05);观察组患者的并发症发生率为3.70%,对照组患者的并发症发生率为25.93%,数据比对差异有统计学意义(χ^2=5.2826,P<0.05)。结论GustiloⅢ型开放性胫骨骨折患者临床治疗期间,对患者行外固定架治疗+胫骨髓内钉固定治疗,不仅可以临床效果确切,还能减少患者出现并发症的风险,缩短患者康复周期,应用价值非常显著,临床应做大力推广。

Expression of positive and negative regulators of cell cycle during wound healing

OBJECTIVE: To detect the expression of cell cycle positive regulators cyclin D(1), cyclin E, CDK(2), CDK(4) and negative regulators p21(cip1), p27(kip1), p16(ink4a) and p15(ink4b) during wound healing in rats. METHODS: Open wounds of full-thickness skin, diameter 1.8 cm, on rat backs were used as the wound model. Wound tissues were harvested on postwounding days 3, 5, 7, 9, 11, 14, 21 and 30. Ki67 expression in granulation tissue was detected by immunohistochemical assay. The patterns of the expression of cyclin D(1), cyclin E, CDK(2), CDK(4) and p21(cip1), p27(kip1), p16(ink4a), p15(ink4b) were detected by Western blot. RESULTS: Cell proliferation in granulation tissue took place predominantly within the first week after injury, with the proliferation peak occurring at postwounding day 5. There were no dramatic variations in the expression of cyclin D(1), CDK(2) and CDK(4) during wound healing. Up-regulated cyclin E was maintained from day 3 to 11 after injury, and then was down-regulated. No expression of p16(ink4a) and p15(ink4b) was found. p21(cip1) was expressed only from day 7 to 14, with peak expression observed on day 9. Constitutive p27(kip1) was expressed throughout wound healing with low levels in the proliferating period of day 3 to 5 and with increased levels in the post-mitotic and remodeling stage. The expression of p21(cip1) and p27(kip1) showed an inverse gradient to that of Ki67. CONCLUSION: p21(cip1) and p27(kip1) play a supervising role in preventing the hyperproliferative tendency in tissue repair.