21 results on '"Wanjin, Chen"'
Search Results
2. COASY variant as a new genetic cause of riboflavin-responsive lipid storage myopathy
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Yilei Zheng, Tongling Liufu, Bing Wen, Chao Zhou, Lingchun Liu, Yusen Qiu, Wenquan Zou, Wei Zhang, Yu Li, Jianfeng Pei, Yiheng Zeng, Wanjin Chen, Chunhua Zhang, Yun Yuan, Guochun Wang, Chuanzhu Yan, Xin Lu, Jianwen Deng, Zhaoxia Wang, and Daojun Hong
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Cytology ,QH573-671 - Published
- 2024
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3. Multidimensional features of sporadic Creutzfeldt-Jakob disease in the elderly: a case report and systematic review
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Jiangfeng Liao, Wenming Hu, Shiheng Chen, Chunyu Huang, Senwei Dong, Wanjin Chen, Xiaochun Chen, and Longfei Chen
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sporadic Creutzfeldt-Jakob disease ,elderly ,clinical features ,diagnosis biomarkers ,neuropathology hallmarks ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
BackgroundAs a rare neurodegenerative disease, sporadic Creutzfeldt-Jakob disease (sCJD) is poorly understood in the elderly populace. This study aims to enunciate the multidimensional features of sCJD in this group.MethodsA case of probable sCJD was reported in a 90-year-old Chinese man with initial dizziness. Then, available English literature of the elderly sCJD cases (aged 80 years and over) was reviewed and analyzed. Patients (15 cases) were subdivided and compared geographically.ResultsIn the elderly sCJD cohort, the onset age was 84.9 ± 4.5 years and the median disease duration was 6.8 months, with respiratory infection/failure as the commonest death cause. Various clinical symptoms were identified, with cognitive disorder (86.7%) as the commonest typical symptom and speech impairment (66.7%) as the most atypical one. Restricted hyperintensities were reported in 60.0% cases on DWI, periodic sharp wave complexes in 73.3% cases on electroencephalogram, and cerebral hypoperfusion/hypometabolism in 26.7% cases on molecular imaging. The sensitive cerebrospinal fluid biomarkers were total tau (83.3%), 14-3-3 protein (75.0%), and PrP RT-QuIC (75.0%). Neuropathological profiles in the cerebral cortex revealed vacuolar spongiosis, neuronal loss, gliosis, and aging-related markers, with synaptic deposit as the commonest PrP pattern (60.0%). The polymorphic PRNP analysis at codon 129 was M/M (90.9%), with MM1 and MM2C as the primary molecular phenotypes. Latency to first clinic visit, hyperintense signals on DWI, and disease duration were significantly different between the patient subgroups.ConclusionThe characteristics of sCJD are multidimensional in the elderly, deepening our understanding of the disease and facilitating an earlier recognition and better care for this group.
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- 2024
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4. ESCRT-I protein UBAP1 controls ventricular expansion and cortical neurogenesis via modulating adherens junctions of radial glial cells
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Danping Lu, Yiqiang Zhi, Huizhen Su, Xiang Lin, Jingjing Lin, Yan Shi, Wenxiang Yi, Chaoyin Hong, Tongtong Zhang, Zhifei Fu, Li-Yu Chen, Zhiqi Zhao, Rong Li, Zhiheng Xu, Wanjin Chen, Ning Wang, and Dan Xu
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CP: Neuroscience ,CP: Developmental biology ,Biology (General) ,QH301-705.5 - Abstract
Summary: Intricate cerebral cortex formation is orchestrated by the precise behavior and division dynamics of radial glial cells (RGCs). Endocytosis functions in the recycling and remodeling of adherens junctions (AJs) in response to changes in RGC activity and function. Here, we show that conditional disruption of ubiquitin-associated protein 1 (UBAP1), a component of endosomal sorting complex required for transport (ESCRT), causes severe brain dysplasia and prenatal ventriculomegaly. UBAP1 depletion disrupts the AJs and polarity of RGCs, leading to failure of apically directed interkinetic nuclear migration. Accordingly, UBAP1 knockout or knockdown results in reduced proliferation and precocious differentiation of neural progenitor cells. Mechanistically, UBAP1 regulates the expression and surface localization of cell adhesion molecules, and β-catenin over-expression significantly rescues the phenotypes of Ubap1 knockdown in vivo. Our study reveals a critical physiological role of the ESCRT machinery in cortical neurogenesis by regulating AJs of RGCs.
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- 2024
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5. ACSS2-dependent histone acetylation improves cognition in mouse model of Alzheimer’s disease
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Yingbin Lin, Anlan Lin, Lili Cai, Weibin Huang, Shanzhi Yan, Yuanxiang Wei, Xinglin Ruan, Wenting Fang, Xiaoman Dai, Jinbo Cheng, Jie Zhang, Wanjin Chen, Qinyong Ye, Xiaochun Chen, and Jing Zhang
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Alzheimer’s disease ,ACSS2 ,Synaptic plasticity ,Histone acetylation ,Acetate ,Glutamate receptors ,Neurology. Diseases of the nervous system ,RC346-429 ,Geriatrics ,RC952-954.6 - Abstract
Abstract Background Nuclear acetyl-CoA pools govern histone acetylation that controls synaptic plasticity and contributes to cognitive deterioration in patients with Alzheimer’s disease (AD). Nuclear acetyl-CoA pools are generated partially from local acetate that is metabolized by acetyl-CoA synthetase 2 (ACSS2). However, the underlying mechanism of histone acetylation dysregulation in AD remains poorly understood. Methods We detected ACSS2 expression and histone acetylation levels in the brains of AD patients and 5 × FAD mice. When we altered ACSS2 expression by injecting adeno-associated virus into the dorsal hippocampus of 5 × FAD mice and replenished ACSS2 substrate (acetate), we observed changes in cognitive function by Morris water maze. We next performed RNA-seq, ChIP-qPCR, and electrophysiology to study molecular mechanism underlying ACSS2-mediated spatial learning and memory in 5 × FAD mice. Results We reported that ACSS2 expression and histone acetylation (H3K9, H4K12) were reduced in the hippocampus and prefrontal cortex of 5 × FAD mice. Reduced ACSS2 levels were also observed in the temporal cortex of AD patients. 5 × FAD mice exhibited a low enrichment of acetylated histones on the promoters of NMDARs and AMPARs, together with impaired basal and activity-dependent synaptic plasticity, all of which were rescued by ACSS2 upregulation. Moreover, acetate replenishment enhanced ac-H3K9 and ac-H4K12 in 5 × FAD mice, leading to an increase of NMDARs and AMPARs and a restoration of synaptic plasticity and cognitive function in an ACSS2-dependent manner. Conclusion ACSS2 is a key molecular switch of cognitive impairment and that targeting ACSS2 or acetate administration may serve as a novel therapeutic strategy for the treatment of intermediate or advanced AD. Graphical Abstract Nuclear acetyl-CoA pools are generated partly from local acetate that is metabolized by acetyl-CoA synthetase 2 (ACSS2). Model depicts that ACSS2 expression is downregulated in the brains of 5×FAD model mice and AD patients. Of note, ACSS2 downregulation mediates a reduction in ionotropic glutamate receptor expression through histone acetylation, which exacerbates synaptic plasticity impairment in AD. These deficits can be rescued by ACSS2 upregulation or acetate supplementation (GTA, an FDA-approved food additive), which may serve as a promising therapeutic strategy for AD treatment.
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- 2023
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6. Chromatin binding protein HMGN1 promotes HBV cccDNA transcription and replication by regulating the phosphorylation of histone 3
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Ming, Tan, Yuting, Liu, Meiling, Dong, Shengtao, Cheng, Jihua, Ren, Hui, Zhang, Wanjin, Chen, Dian, Li, Tingting, Gao, Juan, Chen, and Zhenzhen, Zhang
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- 2024
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7. Mini-dCas13X–mediated RNA editing restores dystrophin expression in a humanized mouse model of Duchenne muscular dystrophy
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Guoling Li, Ming Jin, Zhifang Li, Qingquan Xiao, Jiajia Lin, Dong Yang, Yuanhua Liu, Xing Wang, Long Xie, Wenqin Ying, Haoqiang Wang, Erwei Zuo, Linyu Shi, Ning Wang, Wanjin Chen, Chunlong Xu, and Hui Yang
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Therapeutics ,Medicine - Abstract
Approximately 10% of monogenic diseases are caused by nonsense point mutations that generate premature termination codons (PTCs), resulting in a truncated protein and nonsense-mediated decay of the mutant mRNAs. Here, we demonstrate a mini-dCas13X–mediated RNA adenine base editing (mxABE) strategy to treat nonsense mutation–related monogenic diseases via A-to-G editing in a genetically humanized mouse model of Duchenne muscular dystrophy (DMD). Initially, we identified a nonsense point mutation (c.4174C>T, p.Gln1392*) in the DMD gene of a patient and validated its pathogenicity in humanized mice. In this model, mxABE packaged in a single adeno-associated virus (AAV) reached A-to-G editing rates up to 84% in vivo, at least 20-fold greater than rates reported in previous studies using other RNA editing modalities. Furthermore, mxABE restored robust expression of dystrophin protein to over 50% of WT levels by enabling PTC read-through in multiple muscle tissues. Importantly, systemic delivery of mxABE by AAV also rescued dystrophin expression to averages of 37%, 6%, and 54% of WT levels in the diaphragm, tibialis anterior, and heart muscle, respectively, as well as rescued muscle function. Our data strongly suggest that mxABE-based strategies may be a viable new treatment modality for DMD and other monogenic diseases.
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- 2023
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8. Prevalence and disease progression of genetically-confirmed facioscapulohumeral muscular dystrophy type 1 (FSHD1) in China between 2001 and 2020: a nationwide population-based study
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Zhiqiang Wang, Liangliang Qiu, Minting Lin, Long Chen, Fuze Zheng, Lin Lin, Feng Lin, Zhixian Ye, Xiaodan Lin, Junjie He, Lili Wang, Xin Lin, Qifang He, Wanjin Chen, Yi Lin, Ying Fu, and Ning Wang
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FSHD1 ,Prevalence ,Independent ambulation loss ,Public aspects of medicine ,RA1-1270 - Abstract
Summary: Background: Facioscapulohumeral muscular dystrophy type 1 (FSHD1) is a rare disease, which is often underdiagnosed due to its heterogeneous presentations and complex molecular genetic basis, leading to a lack of population-based epidemiology data, especially of prevalence and disease progression. Methods: Fujian Neuromedical Centre (FNMC) is a diagnosis centre for clinical-genetic FSHD in China, and the only one employing pulsed-field gel electrophoresis (PFGE)-based Southern blotting for all FSHD1 genetic tests. Three sources distributed across all six spatial zones in China, were used to obtain information regarding FSHD1 events, namely, FNMC, Genetic and Myopathy Group (branches of the Neurology Society of the Chinese Medical Association), and “FSHD-China” (an organization supported by FSHD patients). During 2001-2020, all genetically-confirmed FSHD1 from China were registered in FNMC. Follow-up was conducted in the 20-year period to obtain data on disease progression, which was mainly described in terms of independent ambulation loss. Findings: Of the 1,744 FSHD1 genetic tests (total test number 1,802) included in the analysis, 997 (57.2%) patients from 620 families were diagnosed with FSHD1. The estimated prevalence of genetically-confirmed FSHD1 in China is 0.75 per million (95% confidence interval [CI], 0.70-0.79) during 2001-2020, with 0.78 (95% CI, 0.72-0.85) in males and 0.71 (95% CI, 0.65-0.78) in females. The estimated prevalence increased from 0.22 (95% CI, 0.19-0.26) per million in 2001-2015 to 0.53 (95% CI, 0.49-0.57) per million in 2016-2020 (p < 0.001). The prevalence in Fujian province was 7.10 per million, 4.66 per million, and 2.44 per million, during 2001-2020, 2001-2015, and 2016-2020, respectively. Among the 861 symptomatic plus asymptomatic patients of the total 997 patients, the median onset age at first-ever muscle weakness was 16 years of age (range 1-81); the median number of contracted D4Z4 repeats was 5 units (range 1-9); the median 4qA-allele-specific methylation level was 41% (range 14%-69%). Of the 977 symptomatic patients followed-up during 2001-2020, 117 patients (12.0%) lost independent ambulation. The expected duration from onset of first-ever muscle weakness to onset of independent ambulation loss was 40 years. The group with loss of independent ambulation had a smaller number of contracted D4Z4 repeats (p < 0.001) and had an earlier onset age of first-ever muscle weakness (p < 0.001) compared to the group without loss of independent ambulation. Interpretation: Our research captures the largest genetically-confirmed FSHD1 population worldwide, to calculate its prevalence of 0.75 per million in China from 2001 to 2020. Approximately 12.0% of symptomatic plus asymptomatic patients of FSHD1 will lose independent ambulation in 40 years from onset of first-ever muscle weakness. Funding: This work has been supported by the grants (U2005201, 81870902, N.W.) and (81974193, 81671237, Z.Q.W.) from the National Natural Science Foundation of China; Joint Funds for the Innovation of Science and Technology of Fujian Province (2018Y9082) (N.W.), and the Key Clinical Specialty Discipline Construction Program of Fujian (N.W.).
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- 2022
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9. High level of tumor marker CA19-9 returned to normal after cholecystectomy in calculous cholecystitis patients
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Wanjin Chen, Shouwen Wang, Hongchuan Zhao, Guobin Wang, Rong Qin, Fan Huang, Wei Geng, Zimei Liu, Wei Wang, Ruolin Wu, Liujin Hou, Zhenghui Ye, Xinghua Zhang, Xiaoping Geng, and Xiaojun Yu
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Gastroenterology - Published
- 2023
10. Let-7c-5p down-regulates immune-related CDCA8 to inhibit hepatocellular carcinoma
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Wanjin Chen, Haibo Wang, Yuanlong Shen, Shouwen Wang, Deng Liu, Hongchuan Zhao, Guobin Wang, Fan Huang, Wei Wang, Ruolin Wu, Liujin Hou, Zhenghui Ye, Xinghua Zhang, Xiaoping Geng, and Xiaojun Yu
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Genetics ,General Medicine - Published
- 2023
11. miR-29c Suppresses the Malignant Phenotype of Hepatocellular Carcinoma Cells In Vitro by Mediating TPX2 Associated with Immune Infiltration
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Haibo Wang, Wanjin Chen, Yong Qi, Deng Liu, Zhiqiang Liu, Qikun Zhang, Yujiao Yi, Juanru Wang, and Wenyong Wu
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Physiology ,Gastroenterology - Abstract
miR-29-3p, an important tumor suppressor, with inhibitory effects in multiple cancers that have been studied. Its exact molecular function is in HCC, however, still not been explored clearly. The purpose of our study is to make certain how miR-29c-3p affects HCC through TPX2.Expression profile data of miR-29c-3p and TPX2 were acquired and downloaded from the TCGA database, and the respective differential expression was verified by qPCR and immunohistochemistry. The StarBase and dual luciferase reporter confirmed TPX2 targeting miR-29c-3p. Their effects on the biological functions of Hep3B and HepG2 were investigated by cellular assays.miR-29-3p was found to be significantly down-regulated in HCC, and the miR-29-3p low expression group had a poor prognosis. Overexpression of miR-29-3p was detrimental to invasion and migration ability of HCC cells and promoted their apoptosis. We identified miR-29c-3p targeting TPX2 by predictive analysis. TPX2 was significantly upregulated in HCC, and patients with high TPX2 expression had a poor prognosis. TPX2 knockdown partially counteracted the promoting effect of miR-29-3p inhibition on hepatocellular carcinoma cells, and its effect on hepatocellular carcinoma cell biology was similar to miR-29c-3p overexpression.miR-29c, a key gene regulating HCC, is lowly expressed in HCC, its overexpression can remarkably inhibit the biological function of tumor cells. miR-29c can perform this function by regulating the expression of TPX2.
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- 2022
12. Dosage effect of multiple genes accounts for multisystem disorder of myotonic dystrophy type 1
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Lan Bao, Chen Ding, Yifu Ding, Ping Hu, Qian Yu, Yongjian Ma, Wenjun Yang, Hongye Wang, Na Li, Xinyi Liu, Zhenfei Xie, Yanbo Cheng, Lifang Jin, Yan Li, Liuqing Xu, Qiong Wang, Wanjin Chen, Wei Tang, Kai Wang, Qing Li, Jinsong Li, Qi Yin, Fan Zhang, Cuiqing Zhong, and Bin Zhou
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Mutation ,Mutant ,Cell Biology ,Biology ,medicine.disease ,medicine.disease_cause ,Myotonic dystrophy ,Phenotype ,Cell biology ,chemistry.chemical_compound ,chemistry ,medicine ,MBNL1 ,Stem cell ,Trinucleotide repeat expansion ,Molecular Biology ,Gene - Abstract
Multisystem manifestations in myotonic dystrophy type 1 (DM1) may be due to dosage reduction in multiple genes induced by aberrant expansion of CTG repeats in DMPK, including DMPK, its neighboring genes (SIX5 or DMWD) and downstream MBNL1. However, direct evidence is lacking. Here, we develop a new strategy to generate mice carrying multigene heterozygous mutations to mimic dosage reduction in one step by injection of haploid embryonic stem cells with mutant Dmpk, Six5 and Mbnl1 into oocytes. The triple heterozygous mutant mice exhibit adult-onset DM1 phenotypes. With the additional mutation in Dmwd, the quadruple heterozygous mutant mice recapitulate many major manifestations in congenital DM1. Moreover, muscle stem cells in both models display reduced stemness, providing a unique model for screening small molecules for treatment of DM1. Our results suggest that the complex symptoms of DM1 result from the reduced dosage of multiple genes.
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- 2019
13. Advances in detecting and reducing off-target effects generated by CRISPR-mediated genome editing
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Jin-Jing Li, Erwei Zuo, Shunyan Hong, Hui Yang, and Wanjin Chen
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Gene Editing ,0303 health sciences ,Chromatin Immunoprecipitation ,Whole Genome Sequencing ,High-Throughput Nucleotide Sequencing ,Computational biology ,Biology ,Genome ,03 medical and health sciences ,0302 clinical medicine ,Genome editing ,CRISPR-Associated Protein 9 ,Genetics ,CRISPR ,Humans ,Clustered Regularly Interspaced Short Palindromic Repeats ,Molecular Biology ,030217 neurology & neurosurgery ,030304 developmental biology ,RNA, Guide, Kinetoplastida - Abstract
CRISPR-mediated genome editing is a revolutionary technology for genome manipulation that uses the CRISPR-Cas systems and base editors. Currently, poor efficiency and off-target problems have impeded the application of CRISPR systems. The on-target efficiency has been improved in several advanced versions of CRISPR systems, whereas the off-target detection still remains a key challenge. Here, we outline the different versions of CRISPR systems and off-target detection strategies, discuss the merits and limitations of off-target detection methods, and provide potential implications for further gene editing research.
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- 2019
14. Dosage effect of multiple genes accounts for multisystem disorder of myotonic dystrophy type 1
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Yifu Ding, Yanbo Cheng, Lan Bao, Kai Wang, Fan Zhang, Hongye Wang, Wenjun Yang, Liuqing Xu, Qiong Wang, Cuiqing Zhong, Yan Li, Wanjin Chen, Lifang Jin, Xinyi Liu, Na Li, Bin Zhou, Qi Yin, Jinsong Li, Boran Chang, Chen Ding, Qian Yu, Ping Hu, Zhenfei Xie, and Wei Tang
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Genetics ,musculoskeletal diseases ,Mutation ,congenital, hereditary, and neonatal diseases and abnormalities ,Mutant ,Biology ,medicine.disease ,medicine.disease_cause ,Gene dosage ,Phenotype ,Myotonic dystrophy ,chemistry.chemical_compound ,chemistry ,medicine ,MBNL1 ,Stem cell ,Gene - Abstract
Multisystem manifestations in myotonic dystrophy type 1 (DM1) may be due to dosage reduction in multiple genes induced by aberrant expansion of CTG repeats in DMPK, including Dmpk and its neighboring genes (Six5 or Dmwd) and downstream Mbnl1. However, the direct evidences are lack. Here, we develop a new strategy to generate mice carrying multigene mutations in one step by injection of haploid embryonic stem cells with mutant Dmpk, Six5 and Mbnl1 into oocytes. The triple heterozygous mutant mice exhibit adult-onset DM1 phenotypes. With the additional mutation in Dmwd, quadruple heterozygous mutant mice recapitulate many major manifestations in congenital DM1. Moreover, muscle stem cells in both models display reduced stemness. Our results suggest that the complex symptoms of DM1 result from the reduced gene dosage of multiple genes.
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- 2019
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15. Dosage effect of multiple genes accounts for multisystem disorder of myotonic dystrophy type 1
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Qi, Yin, Hongye, Wang, Na, Li, Yifu, Ding, Zhenfei, Xie, Lifang, Jin, Yan, Li, Qiong, Wang, Xinyi, Liu, Liuqing, Xu, Qing, Li, Yongjian, Ma, Yanbo, Cheng, Kai, Wang, Cuiqing, Zhong, Qian, Yu, Wei, Tang, Wanjin, Chen, Wenjun, Yang, Fan, Zhang, Chen, Ding, Lan, Bao, Bin, Zhou, Ping, Hu, and Jinsong, Li
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Homeodomain Proteins ,Mice, Knockout ,Heterozygote ,Base Sequence ,Cloning, Organism ,Stem Cells ,Gene Dosage ,Nuclear Proteins ,RNA-Binding Proteins ,Cell Differentiation ,Research Highlight ,Myotonin-Protein Kinase ,DNA-Binding Proteins ,Phenotype ,Mutation ,Animals ,Humans ,Myotonic Dystrophy ,Muscle, Skeletal - Abstract
Multisystem manifestations in myotonic dystrophy type 1 (DM1) may be due to dosage reduction in multiple genes induced by aberrant expansion of CTG repeats in DMPK, including DMPK, its neighboring genes (SIX5 or DMWD) and downstream MBNL1. However, direct evidence is lacking. Here, we develop a new strategy to generate mice carrying multigene heterozygous mutations to mimic dosage reduction in one step by injection of haploid embryonic stem cells with mutant Dmpk, Six5 and Mbnl1 into oocytes. The triple heterozygous mutant mice exhibit adult-onset DM1 phenotypes. With the additional mutation in Dmwd, the quadruple heterozygous mutant mice recapitulate many major manifestations in congenital DM1. Moreover, muscle stem cells in both models display reduced stemness, providing a unique model for screening small molecules for treatment of DM1. Our results suggest that the complex symptoms of DM1 result from the reduced dosage of multiple genes.
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- 2018
16. A study on the Fermi resonance of phenol under the effects of pressure and temperature by Raman spectroscopy
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Zhong Hua, Cheng-Zhi Liu, Cunbo Fan, Chenglin Sun, Zuowei Li, DongFei Li, and WanJin Chen
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Analytical chemistry ,Crystal structure ,Atomic and Molecular Physics, and Optics ,Analytical Chemistry ,symbols.namesake ,chemistry.chemical_compound ,chemistry ,Ribbon ,symbols ,Phenol ,Fermi resonance ,Raman spectroscopy ,Instrumentation ,Spectroscopy ,Coupling coefficient of resonators ,Fermi Gamma-ray Space Telescope ,Ambient pressure - Abstract
The ν1-ν18a Fermi resonance (FR) of phenol were investigated by pressure-dependent Raman spectroscopy from atmospheric up to P=15.2GPa and temperature-dependent Raman spectroscopy from 40 down to T=-180°C, respectively. In the case of pressure, we found the Fermi coupling coefficient W, which were calculated based on the FR theory, exposed a value turnover between 1.912 and 2.244GPa in the process of increasing the pressure. This turnover phenomenon of the Fermi coupling coefficient W has been ascribed to the crystal structure of phenol evolving towards a more symmetric structure with pressure, from a structure like a pseudo-threefold helical chain at ambient pressure to like a ribbon arrangement at 1.912GPa, then to adopt a herringbone arrangement at much higher pressure. On the other hand, we also found the Fermi coupling coefficient W exhibited monotonic reduction without turnover points appearing by decreasing the temperature. The tendencies of the Fermi coupling coefficient W with temperature were in good agreement with the pressure dependence of the Fermi coupling coefficient W in the region of ambient to 1.912GPa, indicating that the effect of pressure and temperature on the FR of phenol in this region might be the same. A conformation evolving induced by pressure and temperature on the ν1 and ν18a FR of phenol have been analyzed.
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- 2015
17. Crystal and electronic structures of superhard B2CN : An ab initio study
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Dan Zhou, Hui Wang, Weitao Zheng, Wanjin Chen, Baojia Wu, Quan Li, and Zhijian Wu
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Superconductivity ,Materials science ,Condensed matter physics ,business.industry ,Ab initio ,Diamond ,General Chemistry ,engineering.material ,Condensed Matter Physics ,Crystal ,Metal ,Semiconductor ,visual_art ,Materials Chemistry ,Coulomb ,visual_art.visual_art_medium ,engineering ,Orthorhombic crystal system ,business - Abstract
With the increasing demand for specific applications in high pressure and electronic devices, the search for superhard superconducting materials remains a topic of great interest. Using particle swarm optimization algorithm, we report five competitive structures with clear tetrahedrally sp(3) hybridization, among which two metallic orthorhombic structures (Pmm2 and Pmma) with the maximal stable bonds (C-C + B-N) are energetically more favorable than earlier proposed structures. Further first principles calculations suggest that the predicted five structures possess simultaneously superhard and superconducting properties. The five structures are with the similar calculated hardness (56-58 GPa), but show distinct difference in superconducting critical temperature, ranging from 2 to 53 K (with the Coulomb parameter mu* of 0.13). (C) 2011 Elsevier Ltd. All rights reserved.
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- 2012
18. Superhard phases of B2O: An isoelectronic compound of diamond
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Yanhui Liu, Yanming Ma, Wanjin Chen, Yang Xia, Quan Li, Hui Wang, and Hongbo Wang
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Chemistry ,Mechanical Engineering ,Ab initio ,General Chemistry ,Crystal structure ,Electronic, Optical and Magnetic Materials ,Crystal structure prediction ,Pseudopotential ,Crystallography ,Tetragonal crystal system ,Ab initio quantum chemistry methods ,Materials Chemistry ,Density functional theory ,Electrical and Electronic Engineering ,Local-density approximation - Abstract
Using ab initio crystal structure prediction, we have predicted several polytypic structures for B 2 O under high pressure. The structural parameters, total energies, electronic properties and hardness of the obtained structures have been studied using pseudopotential density functional theory within the local density approximation. We find that a monoclinic C 2 /m phase is the most energetically favorable structure; however, its X-ray diffraction pattern could not fit into the experimental data [J. Mater. Sci. Lett. 6 (1987) 683]. Instead, X-ray diffraction patterns of the energetically less stable tetragonal P 4 2 mc and designed P -4 m 2 structures are in overall agreement with the experimental data. The simulated hardness of P 4 2 mc and P -4 m 2 are 40.5 and 44.8 GPa, respectively, in accordance with the experimental values of 33.5 ~ 40.5 GPa.
- Published
- 2011
19. Association between G2385R and R1628P polymorphism of LRRK2 gene and sporadic Parkinson's disease in a Han-Chinese population in south-eastern China
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Qi-Fang Lin, Ning Wang, Yi Lin, Wanjin Chen, Wei-Hong Zheng, Bin Cai, and Jiang-Ping Cai
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Adult ,Male ,medicine.medical_specialty ,China ,Population ,Dermatology ,Biology ,Protein Serine-Threonine Kinases ,Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ,Gastroenterology ,Young Adult ,Asian People ,Polymorphism (computer science) ,Risk Factors ,Internal medicine ,medicine ,Humans ,Allele ,Risk factor ,education ,Genotyping ,Genetic Association Studies ,Aged ,Genetics ,Aged, 80 and over ,education.field_of_study ,Polymorphism, Genetic ,Parkinson Disease ,General Medicine ,Odds ratio ,Middle Aged ,LRRK2 ,Confidence interval ,Psychiatry and Mental health ,Female ,Neurology (clinical) - Abstract
The G2385R and R1628P polymorphisms of the leucine-rich repeat kinase 2 (LRRK2) gene have been reported to be associated with Parkinson’s disease (PD), but no data are available on Han-Chinese population of south-eastern China. This study aimed to investigate whether G2385R and R1628P variants are associated with sporadic PD in this population. Total 1,060 subjects were enrolled; including 550 unrelated healthy controls and 510 patients with sporadic PD. Genotyping of polymorphisms was performed by PCR–restriction fragment length polymorphism analysis. All variant samples were sequenced for further confirmation. The results showed that the A allele of the G2385R variant was significantly enriched in sporadic PD patient group (4.8 %) when compared with control group [1.1 %; odds ratio (OR) 4.58, 95 % confidence interval (CI) 2.42–8.65, P
- Published
- 2012
20. Superconductivity at 28 K in CaB3C3 predicted from first-principles
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Wanjin Chen
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Pseudopotential ,Superconductivity ,Condensed Matter::Materials Science ,Electron pair ,Materials science ,Condensed matter physics ,Phonon ,Ab initio quantum chemistry methods ,Condensed Matter::Superconductivity ,General Physics and Astronomy ,Density functional theory ,Electron ,Electronic structure - Abstract
The structural parameters, electronic properties, and superconducting state in the graphite-like BxC1−x intercalation compound, CaB3C3, have been studied using pseudopotential density functional theory within the generalized gradient approximation. Electronic and electron–phonon coupling calculations reveal that CaB3C3 is hole conducting and superconducting with critical temperature 28.2 K, which is much higher than that of CaC6 (11.5 K). The excellent superconducting state in CaB3C3 stems from the simultaneous presence of highly mobile and extremely confined conduction electrons, which enhances electron pairing and superconductivity. The current calculations might stimulate further theoretical and experimental investigation in search of new superconducting states in graphite-like BxC1−x intercalated compounds.
- Published
- 2013
21. [The construction of urine-derived cell lines from patients with spinal muscular atrophy].
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Wanjin C, Qijie Z, Jin H, Xiang L, and Ning W
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- Cell Line, Humans, Mutation, Survival of Motor Neuron 1 Protein analysis, Muscular Atrophy, Spinal urine, Survival of Motor Neuron 1 Protein genetics, Urine cytology
- Abstract
Spinal muscular atrophy (SMA) is a common neurodegenerative disease in childhood and infancy, clinically characterized by progressive and symmetric muscular weakness and atrophy. Few effective therapies are available now, and SMA is one of the most common genetic causes of infantile mortality. SMA patient-derived cells are beneficial in basic research on this disease, but the most common model cell, fibroblasts can only be obtained through invasive procedures such as muscle or skin biopsy, which are unwelcome to patients and their families. In this study, fresh urine from SMA patients and healthy controls was collected and centrifuged, and the urine sediment was cultured in vitro. The growth characteristics of urine-derived cells were observed, and the survival of motor neuron (SMN) gene, and the amount and localization of SMN protein in different urine cell lines were investigated. In total, 25 urine cell lines from 11 SMA patients and 14 healthy controls were established. These urine-derived cells expand robustly in vitro with stable cell morphological characteristics. The urine cell lines derived from patients carry the SMN1 gene defect and express a low level of SMN protein, while the intracellular localization of SMN protein is normal. Urine-derived cell culture technology is simple, non-invasive and highly reproducible, a way of obtaining and storing rare cell samples from SMA patients with which to study the pathogenesis of SMA.
- Published
- 2014
- Full Text
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