目的利用口内扫描仪定量评估正常[牙合]力咬合下后牙长轴角度变化量及牙冠特征点相对位移量,以期为临床提供参考。方法招募北京大学口腔医学院·口腔医院研究生志愿者15名(男性5名,女性10名,年龄22~30岁),用口内扫描仪扫描牙列,扫描获得张口状态上颌和下颌后牙表面数据(U1、L1)作为咬合前数据;嘱志愿者以正常[牙合]力咬合,扫描后牙颊侧获得颊侧咬合数据,作为配准依据。在Geomagic Studio 2013软件中沿上下颌后牙表面数据牙冠龈缘及近远中邻接触区绘制边界线,确定上下颌第二前磨牙及第一、第二磨牙的牙冠长轴、质心及近中功能尖顶点,分割上下颌后牙表面数据为单牙数据。通过单牙数据和颊侧咬合数据对应牙冠颊面共同区域,将单牙数据逐一配准至咬合数据,获得新的上下颌后牙数据(U2、L2),作为咬合后数据。以第一磨牙为基准,测量第一磨牙与邻牙间牙冠长轴夹角及质心距离,计算咬合前后变化量,以咬合后质心距离变小为负值,反之为正值。以第一磨牙牙冠表面为共同区域,分别将L1、U1配准至L2、U2,测量咬合前后第二前磨牙或第二磨牙的牙冠长轴偏转角度、质心及近中功能尖偏移量。采用Wilcoxon符号秩检验比较同颌第二前磨牙与第二磨牙相同测量项目间差异以及上下颌同名牙相同测量项目间差异。结果同颌第二前磨牙与第二磨牙相同测量项目的结果差异均无统计学意义(P>0.05)。下颌第一磨牙与第二前磨牙质心距离的咬合前后变化量[-0.022(0.046)mm]显著大于上颌[-0.006(0.040)mm](P<0.05)。咬合前后下颌第二前磨牙牙冠长轴偏转角度[0.913°(0.647°)]和第二磨牙质心偏移量[0.102(0.106)mm]分别显著大于上颌第二前磨牙和第二磨牙[分别为0.590°(0.550°)和0.074(0.060)mm](P<0.05)。结论咬合前后上下颌第二前磨牙和第二磨牙均可发生牙冠长轴偏转及质心偏移,下颌变化量显著大于上颌。
Th22 cells play a crucial part in pathogenesis of autoimmune diseases.H owever,little is known about a mechanistic process of regulating their *** this study,Jagged-1 signaling suppressed the deviation of naive CD4+T ...
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Th22 cells play a crucial part in pathogenesis of autoimmune diseases.H owever,little is known about a mechanistic process of regulating their *** this study,Jagged-1 signaling suppressed the deviation of naive CD4+T cells into Th22,which could be rescued by DAPT or hes-1 ***-1 contributed to the reduction of Th22 by lessening AHR level,but the knockdown of arnt or ahr could facilitate Th22 *** were the significant interactions among Hes-1,AHR level and ARNT,whereas their up-or down-stream relationships were confirmed by various ***-1 signaling markedly alleviated the joint swelling and clinical scores in the rheumatoid arthritis-bearing mice via the diminished Th22 with the inhibition of TNF-α and *** findings strongly indicate that the activated Jagged-1/Notch pathway suppresses the skewing of naive CD4T cells into Th22 to relieve rheumatoid arthritis through reduction of IL-22 and TNF-α by Hes-1/ARNT/AHR signaling.
Our previous results proved that Jagged-1/Notch signaling inhibits the phenotypic transformation of naive CD4+T cells into Th22 induced by both IL-6 and TNF-α.The current study showed that this process was facilitate...
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Our previous results proved that Jagged-1/Notch signaling inhibits the phenotypic transformation of naive CD4+T cells into Th22 induced by both IL-6 and TNF-α.The current study showed that this process was facilitated by hsp90 knockdown or SNX2112 with the augment of il-22,ahr and arnt,the attenuation of hes-1 as well as the high productions of Th22 cytokines and CCR6,which could be reversed by Hsp90 overexpression or *** Jagged-1 or DAPT caused downregulation or upregulation of Th22 phenotype,no changes were observed at the levels of Hsp90 mRNA and ***,the inhibition or activation of Hsp90 was able to reduce or enhance downstream Hes-1 via interacting with NICD and *** in vivo overexpression of Hsp90 could suppress deviation of Th22,which were rescued by hsp90 *** data demonstrate that Hsp90 can stabilize NICD and AhR to boost Notch signaling transduction,suggesting that it regulates Notch signaling to mediate Th22 differentiation.
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