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Hearing Disorders: HELP
Articles by Liangliang Zhang
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, Liang Zhang wrote the following 4 articles about Hearing Disorders.
 
+ Citations + Abstracts
1 Article Suspension array-based deafness genetic screening in 53,033 Chinese newborns identifies high prevalence of 109 G>A in GJB2. 2019

Zou, Yu / Dai, Qi-Qiang / Tao, Wei-Jing / Wen, Xiao-Ling / Feng, De-Feng / Deng, Hua / Zhou, Wei-Ping / Li, Mi / Zhang, Liang. ·Department of Otolaryngology, Guangdong Women and Children Hospital, Guangzhou, 511400, China. · Guangzhou DaAn Clinical Laboratory Center, YunKang Group, Guangzhou, 51000, China. · Translational Medicine Center, Guangdong Women and Children Hospital, Guangzhou, 511400, China. · Translational Medicine Center, Guangdong Women and Children Hospital, Guangzhou, 511400, China. Electronic address: zhangliang1999@tsinghua.org.cn. ·Int J Pediatr Otorhinolaryngol · Pubmed #31442870.

ABSTRACT: OBJECTIVES: More than 50% of congenital hearing loss is attributed to genetic factors. Data of gene mutation associated with hearing loss from large population studies in Chinese population are scarce. In this study, we conducted a comprehensive newborn genetic screening in China to establish the carrier frequency and mutation spectrum of deafness-associated genes. METHODS: A total of 53,033 newborns were screened for hearing defects associated mutations. Twenty hot spot mutations in GJB2, GJB3, SLC26A4 and mitochondria12S rRNA were examined using suspension array analysis. RESULTS: 14,185 newborns (26.75%) were identified with at least one mutated allele. 872 (1.64%) neonates carried homozygous mutations including 112 (0.21%) mitochondrial DNA homoplasmy, 228 (0.43%) were compound heterozygotes, and 11,985 (22.59%) were heterozygotes including 11 (0.02%) mitochondrial DNA heteroplasmy. Top five mutations included 109 G > A, 235 delC, 299-300 delAT in GJB2, IVS7-2 A > G in SLC26A4 and 1555 A > G in mitochondria12S rRNA. Notably, a total of 10,995 neonates (20.73%) carried 109 G > A in GJB2. Moreover, the allele frequencies of 109 G > A were detected 11.61% in Guangdong, 10.44% in Sichuan and 2.88% in Shandong, respectively, a significant difference in prevalence among these geographic regions (p<0.01). In addition, the high frequency of 109 G > A in GJB2 was confirmed by a TaqMan probe-based qPCR assay. Very recently, the ClinGen Hearing Loss Expert Panel reached a consensus and confirmed its pathogenic role in hearing impairment. CONCLUSION: We delineated the mutation profile of common deafness-causing genes in the Chinese population and highlighted the high prevalence of 109 G > A pathogenic mutation. Our study may facilitate early diagnosis/intervention and genetic counseling for hearing impairment in clinical practice.

2 Article [Application of suspension array technology for the genetic diagnosis of non-syndromic hearing loss]. 2018

He, Ling / Feng, Defeng / Zhang, Liang / Liu, Chang / He, Tianwen / Yin, Aihua. ·Guangdong Women and Children's Hospital Affiliated to Guangzhou Medical University, Guangzhou, Guangdong 511442, China. yinaiwa@vip.126.com. ·Zhonghua Yi Xue Yi Chuan Xue Za Zhi · Pubmed #29896730.

ABSTRACT: OBJECTIVE: To assess the value of suspension array technology (SAT) for the genetic diagnosis of non-syndromic hearing loss (NSHL). METHODS: Three hundred and sixteen NSHL patients were simultaneously tested by SAT targeting 20 hotspot mutations within 4 common pathologic genes among the Chinese population as well as 9 deafness gene mutation detection kits. The results of the two approaches were validated by Sanger sequencing. RESULTS: Among the 316 patients, 161 were found to carry a mutation by SAT. Sixty five patients have carried homozygous or compound heterozygous mutations, which yielded a mutation rate of 50.9% and a diagnostic rate of 21.2%. Seventy three patients were found to be carriers by the 9 deafness gene mutation detection kits. These included 34 patients carrying homozygous or compound heterozygous mutations, which yielded a mutation rate of 23.1% and diagnostic rate of 11.4%. Above results were consistent with those of Sanger sequencing. CONCLUSION: SAT is a simple, rapid and accurate method featuring high detection rate for common mutations related to deafness among the Chinese population and has provided an effective means of genetic testing for hereditary deafness.

3 Article A Structure Design Method for Reduction of MRI Acoustic Noise. 2017

Nan, Jiaofen / Zong, Nannan / Chen, Qiqiang / Zhang, Liangliang / Zheng, Qian / Xia, Yongquan. ·School of Computer and Communication Engineering, Zhengzhou University of Light Industry, Zhengzhou 450000, China. ·Comput Math Methods Med · Pubmed #29234459.

ABSTRACT: The acoustic problem of the split gradient coil is one challenge in a Magnetic Resonance Imaging and Linear Accelerator (MRI-LINAC) system. In this paper, we aimed to develop a scheme to reduce the acoustic noise of the split gradient coil. First, a split gradient assembly with an asymmetric configuration was designed to avoid vibration in same resonant modes for the two assembly cylinders. Next, the outer ends of the split main magnet were constructed using horn structures, which can distribute the acoustic field away from patient region. Finally, a finite element method (FEM) was used to quantitatively evaluate the effectiveness of the above acoustic noise reduction scheme. Simulation results found that the noise could be maximally reduced by 6.9 dB and 5.6 dB inside and outside the central gap of the split MRI system, respectively, by increasing the length of one gradient assembly cylinder by 20 cm. The optimized horn length was observed to be 55 cm, which could reduce noise by up to 7.4 dB and 5.4 dB inside and outside the central gap, respectively. The proposed design could effectively reduce the acoustic noise without any influence on the application of other noise reduction methods.

4 Article A de novo silencer causes elimination of MITF-M expression and profound hearing loss in pigs. 2016

Chen, Lei / Guo, Weiwei / Ren, Lili / Yang, Mingyao / Zhao, Yaofeng / Guo, Zongyi / Yi, Haijin / Li, Mingzhou / Hu, Yiqing / Long, Xi / Sun, Boyuan / Li, Jinxiu / Zhai, Suoqiang / Zhang, Tinghuan / Tian, Shilin / Meng, Qingyong / Yu, Ning / Zhu, Dan / Tang, Guoqing / Tang, Qianzi / Ren, Liming / Liu, Ke / Zhang, Shihua / Che, Tiandong / Yu, Zhengquan / Wu, Nan / Jing, Lan / Zhang, Ran / Cong, Tao / Chen, Siqing / Zhao, Yiqiang / Zhang, Yue / Bai, Xiaoqing / Guo, Ying / Zhao, Lidong / Zhang, Fengming / Zhao, Hui / Zhang, Liang / Hou, Zhaohui / Zhao, Jiugang / Li, Jianan / Zhang, Lijuan / Sun, Wei / Zou, Xiangang / Wang, Tao / Ge, Liangpeng / Liu, Zuohua / Hu, Xiaoxiang / Wang, Jingyong / Yang, Shiming / Li, Ning. ·State Key Laboratory for Agrobiotechnology, College of Biological Sciences, National Engineering Laboratory for Animal Breeding, China Agricultural University, Beijing, 100193, China. · Key Laboratory of Pig Industry Sciences (Ministry of Agriculture), Chongqing Academy of Animal Science, Chongqing, 402460, China. · Department of Otolaryngology, Head & Neck Surgery, Institute of Otolaryngology, Chinese PLA General Hospital, Beijing, 100853, China. · Institute of Animal Genetics and Breeding, College of Animal Science and Technology, Sichuan Agricultural University, Ya'an, Sichuan, 625014, China. · Department of Communicative Disorders and Sciences, Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, New York, USA. · Key Laboratory of Pig Industry Sciences (Ministry of Agriculture), Chongqing Academy of Animal Science, Chongqing, 402460, China. kingyou@vip.sina.com. · Department of Otolaryngology, Head & Neck Surgery, Institute of Otolaryngology, Chinese PLA General Hospital, Beijing, 100853, China. yangsm301@263.net. · State Key Laboratory for Agrobiotechnology, College of Biological Sciences, National Engineering Laboratory for Animal Breeding, China Agricultural University, Beijing, 100193, China. ninglcau@cau.edu.cn. ·BMC Biol · Pubmed #27349893.

ABSTRACT: BACKGROUND: Genesis of novel gene regulatory modules is largely responsible for morphological and functional evolution. De novo generation of novel cis-regulatory elements (CREs) is much rarer than genomic events that alter existing CREs such as transposition, promoter switching or co-option. Only one case of de novo generation has been reported to date, in fish and without involvement of phenotype alteration. Yet, this event likely occurs in other animals and helps drive genetic/phenotypic variation. RESULTS: Using a porcine model of spontaneous hearing loss not previously characterized we performed gene mapping and mutation screening to determine the genetic foundation of the phenotype. We identified a mutation in the non-regulatory region of the melanocyte-specific promoter of microphthalmia-associated transcription factor (MITF) gene that generated a novel silencer. The consequent elimination of expression of the MITF-M isoform led to early degeneration of the intermediate cells of the cochlear stria vascularis and profound hearing loss, as well as depigmentation, all of which resemble the typical phenotype of Waardenburg syndrome in humans. The mutation exclusively affected MITF-M and no other isoforms. The essential function of Mitf-m in hearing development was further validated using a knock-out mouse model. CONCLUSIONS: Elimination of the MITF-M isoform alone is sufficient to cause deafness and depigmentation. To our knowledge, this study provides the first evidence of a de novo CRE in mammals that produces a systemic functional effect.