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structural remodeling in related brain regions in patients with facial synkinesis

Neural Regeneration Research 2021年第12期16卷 2528-2533页

作者： Jia-Jia Wu Ye-Chen Lu Mou-Xiong Zheng Xu-Yun Hua Chun-Lei Shan Wei Ding Jian-Guang Xu Center of Rehabilitation Medicine Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghaiChina Wound Healing Center Ruijin HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina Department of Trauma and Orthopedics Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghaiChina School of Rehabilitation Science Shanghai University of Traditional Chinese MedicineShanghaiChina Department of Plastic and Reconstructive Surgery Shanghai Ninth People’s HospitalShanghai Jiao Tong University School of MedicineShanghaiChina

Facial synkinesis is a troublesome sequelae of facial nerve *** is difficult to recover from synkinesis,despite improved surgical techniques for isolating the peripheral facial nerve ***,it remains unclear whether long-term dysfunction of motor control can lead to irreversible plasticity-induced structural brain *** case-control study thus investigated the structural brain alterations associated with facial *** study was conducted at Shanghai Ninth People’s Hospital,Shanghai Jiao Tong University School of Medicine,*** patients with facial synkinesis(2 male and 18 female,aged 33.35±6.97 years)and 19 healthy volunteers(2 male and 17 female,aged 33.21±6.75 years)underwent magnetic resonance imaging,and voxel-based and surface-based morphometry techniques were used to analyze *** was no significant difference in brain volume between patients with facial synkinesis and healthy *** with facial synkinesis exhibited a significantly reduced cortical thickness in the contralateral superior and inferior temporal gyri and a reduced sulcal depth of the ipsilateral precuneus compared with healthy *** addition,sulcal depth of the ipsilateral precuneus was negatively correlated with the severity of *** findings suggest that there is a structural remodeling of gray matter in patients with facial synkinesis after facial nerve *** study was approved by the Ethics Review Committee of the Ninth People’s Hospital,Shanghai Jiao Tong University School of Medicine,China(approval No.2017-365-T267)on September 13,2017,and was registered with the Chinese Clinical Trial Registry(registration number:ChiCTR1800014630)on January 25,2018.

关键词： brain plasticity cortical thickness depression facial nerve paralysis facial synkinesis peripheral nerve injury sulcal depth structural remodeling surface-based morphometry voxel-based morphometry

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Changes in microRNAs expression are involved in age-related atrial structural remodeling and atrial fibrillation

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Chinese Medical Journal 2013年第8期126卷 1458-1463页

作者： XU Guo-jun GAN Tian-yi TANG Bao-peng CHEN Zu-heng Mahemuti Ailiman ZHOU Xian-hui JIANG Tao SONG Jian-guo GUO Xia LI Yao-dong MIAO Hai-jun ZHANG Yu LI Jin-xin Department of CardiologyFirst Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China Department ofAnimal Experiment First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China Laboratory of Electrophysiology First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China Department of Molecular Biology First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China

Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation （AF） was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. Methods Three groups of dogs were studied： adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AE

关键词： atrial fibrillation aging structural remodeling microRNAs

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Effects of trimetazidine on atrial structural remodeling and platelet activation in dogs with atrial fibrillation

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Chinese Medical Journal 2009年第18期122卷 2180-2183页

作者： HAN Wei LI Wei-min ZHOU Hong-yan HUO Hong WEI Na DONG Guo CAO Yong ZHOU Guo YANG Shu-sen Department of Cardiology First Clinical College of Harbin Medical University Harbin Heilongjiang 150001 China

Atrial fibrillation （AF） is one of the most common .arrhythmias in clinical practice. AF results in electrophysiological alterations which involve increased atrial effective refractory period and atrial effective refractory period dispersion, reduced rate adaptation of atrial effective refractory period, and slowed atrial conduction. These variances promote their own maintenance-AF begets AF.1 Previous study suggested that Ca^2＋ overload and metabolic derangement contributed to electrophysiological remodeling in AF. However, we did not demonstrate a persistent disturbance in energy metabolism during AF in our previous study,

关键词： atrialfibrillation structural remodeling thrombosis trimetazidine

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Calpain I inhibition prevents atrial structural remodeling in a canine model with atrial fibrillation

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Chinese Medical Journal 2008年第1期000卷 32-37页

作者： XUE Hong-jie LI Wei-min LI Yue GONG Yong-tai YANG Bao-feng JIN Cheng-luo SHENG Li CHU Shan ZHANG Li SHAN Hong-bo LIU Jie Department of Cardiology First Clinical Hospital of HarbinMedical University Harbin Heilongjiang 150001 China Department of Pharmacology and Bio-pharmaceutical KeyLaboratory of Heilongjiang Province and State Harbin MedicalUniversity Harbin Heilongjiang 150086 China Department of Uronology Second Clinical Hospital of HarbinMedical University Harbin Heilongjiang 150086 China

Background Atrial fibrillation （AF） is accompanied by atrial structural remodeling. Calpain activity is induced during AE To test a causal relationship between calpain activation and atrial structural changes, N-acetyI-Leu-Leu-Met （ALLM）, a calpain inhibitor, was utilized in a canine AF model. Methods Fifteen dogs were randomly divided into 3 groups： sham-operated group, control group and calpain inhibitor group; each with 5 dogs. Sustained AF was induced by rapid right atrium pacing at 600 beats per minute for 3 weeks. ALLM was administered at a dosage of 1.0 mg-kg-l-d1 in the calpain inhibitor group. Three weeks later, the proteolysis, protein expression of TnT and myosin, calpain I localization and expression and structural changes were examined in left atrial free walls, right atrial free walls and the interatrial septum respectively. Atrial size and contractile function were also measured by echocardiography. Results Long-term rapid atrial pacing induced marked structural changes such as enlarged atrial volume, myolysis, degradation of TnT and myosin, accumulation of glycogen and changes in mitochondrial shape and size, which were paralleled by an increase in calpain activity. The positive correlation between calpain activity and the degree of myolysis （rs=0.90 961, P〈0.0001） was demonstrated. In addition to structural abnormalities, pacing-induced atrial contractile dysfunction was observed in this study. The pacing-induced atrial structural alterations and loss of contractility were partially prevented by the calpain inhibitor ALLM. Conclusions Activation of calpain represents key features in the progression towards overt structural remodeling. Calpain inhibitor, ALLM, suppressed the increased calpain activity and reversed structural remodeling caused by sustained atrial fibrillation in the present model. Calpain inhibition may therefore provide a possibility for therapeutic intervention in AE

关键词： atrial fibrillation structural remodeling calpain inhibitor N-acetyl-leu-leu-met

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