|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Hemiballism-hemichorea induced by ketotic hyperglycemia: case report with PET study and review of the literature显示文摘Hemiballism-hemichorea(HB-HC)is commonly used to describe the basal ganglion dysfunction in non-ketotic hyperglycemic elderly patients.Here we report two elderly female patients with acute onset of involuntary movements induced by hyperglycemia with positive urine ketones.We described the computed tomography and magnetic resonance imaging findings in these two patients,which is similar to that of non-ketotic hyperglycemic HB-HC patients.FDG-PET was performed and the glucose metabolism in the corresponding lesion in these two patients was contradictory with each other.We tried to clarify the underlying mechanisms of HB-HC and explain the contradictory neuroradiological findings in FDG-PET as being performed at different clinical stages. | Yuyan Tan Xiaoyu Xin Qin Xiao Shengdi Chen Li Cao Huidong Tang | 2014 | Translational Neurodegeneration2014，3，1： | 21 |
| 2 | Freezing of gait in Parkinson’s disease: pathophysiology, risk factors and treatments显示文摘Background Freezing of gait(FOG)is a common,disabling symptom of Parkinson’s disease(PD),but the mechanisms and treatments of FOG remain great challenges for clinicians and researchers.The main focus of this review is to summarize the possible mechanisms underlying FOG,the risk factors for screening and predicting the onset of FOG,and the clinical trials involving various therapeutic strategies.In addition,the limitations and recommendations for future research design are also discussed.Main body In the mechanism section,we briefly introduced the physiological process of gait control and hypotheses about the mechanism of FOG.In the risk factor section,gait disorders,PIGD phenotype,lower striatal DAT uptake were found to be independent risk factors of FOG with consistent evidence.In the treatment section,we summarized the clinical trials of pharmacological and non-pharmacological treatments.Despite the limited effectiveness of current medications for FOG,especially levodopa resistant FOG,there were some drugs that showed promise such as istradefylline and rasagiline.Non-pharmacological treatments encompass invasive brain and spinal cord stimulation,noninvasive repetitive transcranial magnetic stimulation(rTMS)or transcranial direct current stimulation(tDCS)and vagus nerve stimulation(VNS),and physiotherapeutic approaches including cues and other training strategies.Several novel therapeutic strategies seem to be effective,such as rTMS over supplementary motor area(SMA),dual-site DBS,spinal cord stimulation(SCS)and VNS.Of physiotherapy,wearable cueing devices seem to be generally effective and promising.Conclusion FOG model hypotheses are helpful for better understanding and characterizing FOG and they provide clues for further research exploration.Several risk factors of FOG have been identified,but need combinatorial optimization for predicting FOG more precisely.Although firm conclusions cannot be drawn on therapeutic efficacy,the literature suggested that some therapeutic strategies showed promise. | Chao Gao Jun Liu Yuyan Tan Shengdi Chen | 2020 | Translational Neurodegeneration2020，9，2： | 9 |
| 3 | LIN28 coordinately promotes nucleolar/ribosomal functions and represses the 2C-like transcriptional program in pluripotent stem cells显示文摘LIN28 is an RNA binding protein with important roles in early embryo development,stem cell differentiation/re-programming,tumorigenesis and metabolism.Previous studies have focused mainly on its role in the cytosol where it interacts with Let-7 microRNA precursors or mRNAs,and few have addressed LIN28's role within the nucleus.Here,we show that LIN28 displays dynamic temporal and spatial expression during murine embryo development.Maternal LIN28 expression drops upon exit from the 2-cell stage,and zygotic LIN28 protein is induced at the forming nucleolus during 4-cell to blas-tocyst stage development,to become dominantly expressed in the cytosol after implantation.In cultured pluripotent stem cells(PSCs),loss of LIN28 led to nucleolar stress and activation of a 2-cell/4-cell-like transcriptional program characterized by the expression of endogenous retrovirus genes.Mechanistically,LIN28 binds to small nucleolar RNAs and rRNA to maintain nucleolar integrity,and its loss leads to nucleolar phase separation defects,ribosomal stress and activation of P53 which in turn binds to and activates 2C transcription factor Dux.LIN28 also resides in a complex containing the nucleolar factor Nucleolin(NCL)and the transcrip-tional repressor TRIM28,and LIN28 loss leads to reduced occupancy of the NCL/TRIM28 complex on the Dux and rDNA loci,and thus de-repressed Dux and reduced rRNA expression.Lin28 knockout cells with nucleolar stress are more likely to assume a slowly cycling,translationally inert and anabolically inactive state,which is a part of previously unappreciated 2C-like transcriptional program.These findings elucidate novel roles for nucleolar LIN28 in PSCs,and a new mechanism linking 2C program and nucleolar functions in PSCs and early embryo development. | Zhen Sun Hua Yu Jing Zhao Tianyu Tan Hongru Pan Yuqing Zhu Lang Chen Cheng Zhang Li Zhang Anhua Lei Yuyan Xu Xianju Bi Xin Huang Bo Gao Longfei Wang Cristina Correia Ming Chen Qiming Sun Yu Feng Li Shen Hao Wu Jianlong Wang Xiaohua Shen George Q.Daley Hu Li Jin Zhang | 2022 | Protein & Cell2022，13，7： | 4 |
| 4 | Completing China's Interest Rate Liberalization显示文摘 | Yuyan Tan Yang Ji Yiping Huang | 2016 | China & World Economy2016，24，2： | 4 |
| 5 | Methylation status of DJ-1 in leukocyte DNA of Parkinson’s disease patients显示文摘Background:DJ-1 has been thought as a candidate biomarker for Parkinson’s disease(PD).It was found reduced in PD brains,CSF and saliva,although there were conflicting results.How DJ-1 expression may be regulated is not clear.Recently,blood-based DNA methylation represents a highly promising biomarker for PD by regulating the causative gene expression.Thus,in this study,we try to explore whether blood-based DNA methylation of DJ-1 could be used as a biomarker to differentiate PD patients from normal control(NC),and whether DNA methylation could regulate DJ-1 expression in a SH-SY5Y cell model.Methods:Forty PD patients and 40 NC were recruited in this study.DNA was extracted from peripheral blood leukocytes(PBLs).Methylation status of two CpG islands(CpG1 and CpG2)in promoter region of DJ-1 was explored by bisulfite specific PCR-based sequencing method.Methylation inhibitor 5-Aza-dC was used to treat SH-SY5Y cell line,DJ-1 level was detected in both mRNA and protein level.Results:CpG sites in these two CpG islands(CpG1 and CpG2)of DJ-1 were unmethylated in both PD and NC group.In SH-SY5Y cell model treated by methylation inhibitor,there was no significant change of DJ-1 expression in either mRNA level or protein level.Conclusions:Our results indicated that DNA methylation inhibitor didn’t alter DJ-1 gene expression in SH-SY5Y cell model,and DNA methylation of DJ-1 promoter region in PBLs level might not be an efficient biomarker for PD patients. | Yuyan Tan Li Wu Dunhui Li Xiaoli Liu Jianqing Ding Shengdi Chen | 2016 | Translational Neurodegeneration2016，5，1： | 1 |
| 6 | Ethacrynic acid targets GSTM1 to ameliorate obesity by promoting browning of white adipocytes显示文摘Dear Editor,Obesity is caused by an imbalance between energy intake and expenditure,and has become a global epidemic with over 650 million adults affected.Adipose tissues in mammals are composed of white adipose tissue(WAT)and classical brown adipose tissue(BAT),and their balance is highly related to the occurrence of obesity.The browning of white adipocytes results in“beige”or“brite”adipocytes,which appear functionally similar to classical brown adipocytes,and can be detected in WAT deposits of animals that have been exposed to cold or other inducers(Fu et al.,2015). | Zhaomeng Cui Yang Liu Wei Wan Yuyan Xu Yehui Hu Meng Ding Xin Dou Ruina Wang Hailing Li Yongmei Meng Wei Li Wei Jiang Zengxia Li Yiming Li Minjia Tan Dengke KMa Yu Ding Jun OLiu Cheng Luo Biao Yu Qiqun Tang Yongjun Dang | 2021 | Protein & Cell2021，12，6： | 1 |
| 7 | Organic- montomorillonite modified shape memory epoxy composite显示文摘 | Liu Yuyan Han Chunmiao Tan Huifeng | 2010 | Polym Adv Techn2010，22，12： | 1 |
| 8 | Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets显示文摘Microglia activation is observed in various neurodegenerative diseases.Recent advances in single-cell technologies have revealed that these reactive microglia were with high spatial and temporal heterogeneity.Some identified microglia in specific states correlate with pathological hallmarks and are associated with specific functions. | Chao Gao Jingwen Jiang Yuyan Tan Shengdi Chen | 2023 | Signal Transduction and Targeted Therapy2023，8，10： | 1 |
| 9 | AN IMPROVED JONES-NELSON NONLINEAR MATERIAL MODEL AND RUBBER COMPOSITE LAMINA ANALYSIS显示文摘A Jones-Nelson model has been applied to depict nonlinear stress-strain relations ofcomposite laminae,where mechanical properties were expressed by strain energy density.The nonlin-ear material matrix is only a function of the strain energy density.Then a material model could beconveniently applied under complex stress condition.In this paper,by introducing large displacementstress-strain measurement and varying-Poisson’s ratio idea,an improved Jones-Nelson material modelis presented,where the expanding problem of material properties and convergence problems are over-come.Meanwhile a discuss of the reorientation of fiber and a material nonlinear analysis of rubbercomposite lamina under super large deformation conditions are made.The prediction results of im-proved material model are in fairly good agreement with those of the experiments. | Tan Huifeng Liu Yuyan Du Xingwen | 1998 | Acta Mechanica Solida Sinica1998，11，1： | 0 |
| 10 | Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in APP/PS1 mice via the Nrf2/HO-1 and NF-κB signaling pathways显示文摘Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain.The ketogenic diet,a widely recognized therapeutic intervention for refractory epilepsy,has recently been proposed as a potential treatment for a variety of neurological diseases,including Alzheimer's disease.However,the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains unclear.The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's disease.Male amyloid precursor protein/presenilin 1(APP/PS1)mice were randomly assigned to either a ketogenic diet or control diet group,and received their respective diets for a duration of 3 months.The findings show that ketogenic diet administration enhanced cognitive function,attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice,and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway.Collectively,these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation.This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease. | Jingwen Jiang Hong Pan Fanxia Shen Yuyan Tan Shengdi Chen | 2023 | Neural Regeneration Research2023，18，12： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员