Mutations in SFRP4 cause Pyle’s bone disease with wide metaphyses and increased skeletal fragility.The WNT signaling pathway plays important roles in determining skeletal architecture and SFRP4 is a secreted Frizzled...Mutations in SFRP4 cause Pyle’s bone disease with wide metaphyses and increased skeletal fragility.The WNT signaling pathway plays important roles in determining skeletal architecture and SFRP4 is a secreted Frizzled decoy receptor that inhibits WNT signaling.Seven cohorts of male and female Sfrp4 gene knockout mice,examined through 2 years of age,had a normal lifespan but showed cortical and trabecular bone phenotypes.Mimicking human Erlenmeyer flask deformities,bone cross-sectional areas were elevated 2-fold in the distal femur and proximal tibia but only 30%in femur and tibia shafts.Reduced cortical bone thickness was observed in the vertebral body,midshaft femur and distal tibia.Elevated trabecular bone mass and numbers were observed in the vertebral body,distal femur metaphysis and proximal tibia metaphysis.Midshaft femurs retained extensive trabecular bone through 2 years of age.Vertebral bodies had increased compressive strength,but femur shafts had reduced bending strength.Trabecular,but not cortical,bone parameters in heterozygous Sfrp4mice were modestly affected.Ovariectomy resulted in similar declines in both cortical and trabecular bone mass in wild-type and Sfrp4 KO mice.SFRP4 is critical for metaphyseal bone modeling involved in determining bone width.Sfrp4 KO mice show similar skeletal architecture and bone fragility deficits observed in patients with Pyle’s disease with SFRP4 mutations.展开更多
目的回顾分析院内高血压合并急性心肌梗死中实施加速康复外科(enhanced recovery after surgery,ERAS)理念的新型心脏康复模式的作用。方法纳入时间为2021年1月至2022年12月,将该时间段院内60例高血压合并急性心肌梗死患者进行研究讨论...目的回顾分析院内高血压合并急性心肌梗死中实施加速康复外科(enhanced recovery after surgery,ERAS)理念的新型心脏康复模式的作用。方法纳入时间为2021年1月至2022年12月,将该时间段院内60例高血压合并急性心肌梗死患者进行研究讨论,通过随机分配法安排为对照组(30例实施常规临床干预)、观察组(30例实施ERAS理念的新型心脏康复模式),比较两组血压指标、分泌型卷曲相关蛋白5(Secreted Frizzled Related Protein 5,SFRP5)指标、基质金属蛋白酶8(Matrix metalloproteinase 8,MMP-8)指标。结果观察组血压指标均处于良好状态,且显著比对照组低(P<0.05)。观察组MMP-8指标更低,SFRP5指标更高(P<0.05)。结论ERAS理念的新型心脏康复模式能够降低高血压合并急性心肌梗死患者血压水平,改善SFRP5及MMP-8指标。展开更多
文摘Mutations in SFRP4 cause Pyle’s bone disease with wide metaphyses and increased skeletal fragility.The WNT signaling pathway plays important roles in determining skeletal architecture and SFRP4 is a secreted Frizzled decoy receptor that inhibits WNT signaling.Seven cohorts of male and female Sfrp4 gene knockout mice,examined through 2 years of age,had a normal lifespan but showed cortical and trabecular bone phenotypes.Mimicking human Erlenmeyer flask deformities,bone cross-sectional areas were elevated 2-fold in the distal femur and proximal tibia but only 30%in femur and tibia shafts.Reduced cortical bone thickness was observed in the vertebral body,midshaft femur and distal tibia.Elevated trabecular bone mass and numbers were observed in the vertebral body,distal femur metaphysis and proximal tibia metaphysis.Midshaft femurs retained extensive trabecular bone through 2 years of age.Vertebral bodies had increased compressive strength,but femur shafts had reduced bending strength.Trabecular,but not cortical,bone parameters in heterozygous Sfrp4mice were modestly affected.Ovariectomy resulted in similar declines in both cortical and trabecular bone mass in wild-type and Sfrp4 KO mice.SFRP4 is critical for metaphyseal bone modeling involved in determining bone width.Sfrp4 KO mice show similar skeletal architecture and bone fragility deficits observed in patients with Pyle’s disease with SFRP4 mutations.
文摘目的回顾分析院内高血压合并急性心肌梗死中实施加速康复外科(enhanced recovery after surgery,ERAS)理念的新型心脏康复模式的作用。方法纳入时间为2021年1月至2022年12月,将该时间段院内60例高血压合并急性心肌梗死患者进行研究讨论,通过随机分配法安排为对照组(30例实施常规临床干预)、观察组(30例实施ERAS理念的新型心脏康复模式),比较两组血压指标、分泌型卷曲相关蛋白5(Secreted Frizzled Related Protein 5,SFRP5)指标、基质金属蛋白酶8(Matrix metalloproteinase 8,MMP-8)指标。结果观察组血压指标均处于良好状态,且显著比对照组低(P<0.05)。观察组MMP-8指标更低,SFRP5指标更高(P<0.05)。结论ERAS理念的新型心脏康复模式能够降低高血压合并急性心肌梗死患者血压水平,改善SFRP5及MMP-8指标。
