寰枢椎后路柔性固定的生物力学研究

目的分析细棒、PEEK棒固定对寰枢关节稳定性的影响。方法采用6具新鲜成人枕骨(occipital bone,Oc)~颈椎C4节段进行测试,模拟以下手术及固定状态:①完整状态;②损伤状态:枢椎齿状突II型骨折;③坚强固定:寰枢椎均采用普通椎弓根螺钉固定,直径3.5 mm钛棒连接;④PEEK棒:直径3.5 mm的PEEK棒连接;⑤细棒:直径2.0 mm钛棒连接。采用重复测量实验设计,在完整、损伤和不同的固定状态下,通过脊柱试验机对标本分别施加1.5 N·m的前屈/后伸、左/右侧弯和左/右轴向旋转的纯力偶矩。采用Optotrak三维运动测量系统连续采集标本运动,分析寰枢椎之间角度运动范围和中性区。结果采用直径3.5 mm的钛棒,2.0 mm的细棒以及3.5 mm的PEEK棒固定后,在前屈、后伸、侧弯和旋转方向上均显著减小了固定节段的运动范围(P<0.05)。直径3.5 mm和2.0 mm的棒固定后的运动范围,在各个方向上无显著性差异。PEEK棒固定的运动范围仅在侧弯方向上大于坚强固定(P=0.005),其他方向无显著性差异。3种固定方式在屈伸、侧弯和旋转方向上均显著减小了固定节段的中性区(P<0.05)。各种固定方式之间相比较,无显著性差异(P>0.05)。结论在寰枢关节采用直径2.0 mm的细棒固定,与坚强固定的稳定性相当。采用直径3.5 mm的PEEK棒固定,在前屈、后伸、旋转方向上与坚强固定的稳定性相当,在侧弯方向上弱于坚强固定。     

研究辛伐他汀联合二甲双胍治疗糖尿病胰岛素抵抗的疗效

目的探究辛伐他汀联合二甲双胍治疗糖尿病胰岛素抵抗的疗效。方法选取2019年3月至2020年3月本院收治的92例糖尿病胰岛素抵抗患者作为研究对象,随机分为对照组与实验组,各46例,对照组单独应用二甲双胍治疗,实验组联合应用辛伐他汀、二甲双胍进行治疗,比较两组疗效。结果实验组治疗总有效率高于对照组(P<0.05);治疗后,实验组TC、LDL-C、FPG、2 h PG均低于对照组,HDL-C高于对照组(P<0.05);治疗后2、8、12周,实验组TC、LDL-C、FPG、2 h PG逐渐降低、HDL-C逐渐升高(P<0.05);对照组TC、LDL-C、FPG、2 h PG无明显变化,差异无统计学意义;两组不良反应发生率比较差异无统计学意义。结论辛伐他汀联合二甲双胍治疗糖尿病胰岛素抵抗疗效高于单一治疗方案,且药物联用未增加不良反应风险,疗效显著,安全性高,值得临床推广应用。     

Genomic variants within chromosome 14q32.32 regulate bone mass through MARK3 signaling in osteoblasts

Bone mineral density (BMD) is a highly heritable predictor of osteoporotic fracture. GWAS have identified hundreds of loci influencing BMD, but few have been functionally analyzed. In this study, we show that SNPs within a BMD locus on chromosome 14q32.32 alter splicing and expression of PAR-1a/microtubule affinity regulating kinase 3 (MARK3), a conserved serine/threonine kinase known to regulate bioenergetics, cell division, and polarity. Mice lacking Mark3 either globally or selectively in osteoblasts have increased bone mass at maturity. RNA profiling from Mark3-deficient osteoblasts suggested changes in the expression of components of the Notch signaling pathway. Mark3-deficient osteoblasts exhibited greater matrix mineralization compared with controls that was accompanied by reduced Jag1/Hes1 expression and diminished downstream JNK signaling. Overexpression of Jag1 in Mark3-deficient osteoblasts both in vitro and in vivo normalized mineralization capacity and bone mass, respectively. Together, these findings reveal a mechanism whereby genetically regulated alterations in Mark3 expression perturb cell signaling in osteoblasts to influence bone mass.