1.Effect of zygoma combined with mandibular angel plastic surgery on temporomandibular joint condyle
Qiang ZHANG ; Yuecheng GUO ; Jun GUO ; Zheng LI ; Baofeng YUAN ; Yi ZHAO
Chinese Journal of Medical Aesthetics and Cosmetology 2016;22(1):29-31
Objective To observe the temporomandibular joint spaces changes after the plastic surgery of combined zygoma with mandibular angel.Methods We randomly selected 59 patients with prominent zygoma and mandibular angle,screening periodontal disease,TMJ pain and partial jaw.Bilateral zygomatic arch coarctation,jaw edge of the mandibular angle ostectomy and the mandibular body outer panel split were used.All patients accepted CT scan and three-dimensional reconstruction before operation,10 days after operation and 6 months after operation,and then image analysis softwares were used to measure the line distance of corresponding angle (0°,60°,120°,and 180°)at the TMJ sagittal plane.The 0° (EE 'pitch) and 60° (AA'pitch) represented for pre-space,the 60° and 120° (PP'pitch) was upper-space,the 120° and 180° (SS'pitch) was posterior-space.Results 0° and 60° had the same change trend,which slightly increased at 10 days after operation.The difference before operation and 10 days,6 months after operation were not statistically significant (P > 0.05);120° and 180° had the same change trend,which increased at 10 days after operation.The difference between before operation and 10 days after operation was statistically significant (P < 0.05),but the difference between before operation and 6 months after operation was not statistically significant (P> 0.05).Conclusions In the short term after plastic surgery of zygoma combined with mandibular angel,the TMJ upper and posterior spaces are changed,and the interspace reduced.This may indicate that the TMJ has compensatory ability,and short-term changes can return to normal.
2.The expression levels of miR-21 and TGF-β1 in cardiac remodelin affer myocardial infarction
Fengping HE ; Xin XU ; Shebing ZHANG ; Baofeng CHEN ; Zhanzhong MA ; Shuguo YUAN ; Xiuyan HUANG ; Fenglian LIU ; Shiping FAN ; Dongnan WU
International Journal of Laboratory Medicine 2016;37(18):2513-2516
Objective To detect the change of exoression level of plasma microRNA‐21(miR‐21) and TGF‐β1 in cardiac remode‐lin affer acute myocardial infarction(AMI) of the pateins .Methods 200 pateints with AMI and 100 normal controls(age ,sex matched) were enrolled .Blood samples were obtained from the normal controls and patients with AMI on the 3 days ,7 days and 14 days .Real‐time PCR was developed to detect the expression of miR‐21 and TGF‐β1 in plasma .Results The expression of miR‐21 was significantly up‐regulation in the 3 days ,7 days and 14 days in MI group than that cntrol group ,0 .74 ± 0 .21 vs .2 .62 ± 0 .23 , vs .3 .67 ± 0 .25 ,vs .4 .13 ± 0 .27 up‐regulation in the 3 days ,7 days and 14 days in MI group than that cntrol group ,0 .98 ± 0 .18 vs .2 .35 ± 0 .24 ,vs .3 .67 ± 0 .25 ,vs .4 .13 ± 0 .27 ,P<0 .05 ,respectively .The expression of miR‐21 and TGF‐β1 were up‐regulation with the change of cardiac function .Positive relationship between miRNA‐21 expression and LVDd (r=0 .757 ,P<0 .05);Positive relationship between TGF‐β1 mRNA expression and LVDd(r=0 .701 ,P<0 .05) .Conclusion The expression of miR‐21 and TGF‐β1 were up‐regulation in cardiac remodelin affer AMI of the pateins ,which involved in regulation in cardiac remodelin affer AMI .
3.Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts upregulating metastasis associated protein 3.
Dan XIAO ; Yue ZHANG ; Rui WANG ; Yujie FU ; Tong ZHOU ; Hongtao DIAO ; Zhixia WANG ; Yuan LIN ; Zhange LI ; Lin WEN ; Xujuan KANG ; Philipp KOPYLOV ; Dmitri SHCHEKOCHIKHIN ; Yong ZHANG ; Baofeng YANG
Acta Pharmaceutica Sinica B 2019;9(4):724-733
Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.