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1,940 results on '"Yang, Hongbo"'

1. Deformability, inherent mechanical properties and chemical bonding of Al11Nd3 in Al-Nd target material

Author

Wang, Xue-Qian, Song, Run-Xin, Guan, Xu, Li, Shuan, Sun, Shuchen, Yang, Hongbo, Wu, Daogao, Tu, Ganfeng, Li, Song, Yan, Hai-Le, and Zuo, Liang

Subjects
Condensed Matter - Materials Science
Abstract

Microstructure uniformity of the Al-Nd target materials with Al11Nd3 significantly affects the performance of the fabricated film, which is widely used as wiring material in largesize thin-film transistor liquid crystal display (TFT-LCD) panels. Understanding the inherent mechanical properties and chemical bonds of Al11Nd3 is crucial for homogenizing the Al-Nd target. Here, by a combined experimental and ab-initio theoretical study, the microstructure and deformability of the Al-3wt%Nd alloy and the inherent mechanical properties and chemical bonds of Al11Nd3 are investigated comprehensively. The Al-3wt%Nd alloy is composed of the pre-eutectic {\alpha}-Al matrix and the eutectic {\alpha}-Al and a high stable {\alpha}-Al11Nd3 phases. During the plastic deformation, the eutectic microstructure transforms from a cellular to a lamellar shape, while the morphology and dimension of {\alpha}-Al11Nd3 are not changed significantly. By examining ideal tensile strength, elastic moduli, hardness and brittleness-ductility, the hardnessbrittleness of {\alpha}-Al11Nd3 is quantitatively evaluated, accounting for its difficulties of plastic deformation and fragmentation. Combining band structure, population analysis, topological analysis and crystal orbital Hamilton population, it is revealed that {\alpha}-Al11Nd3 possesses two types of chemical bonds: the Nd-Al and Al-Al bonds. The former is a typical ionic bond with electron transfer from Nd to Al, while the latter, dominated by both 3s-3p and 3p-3p interactions, is a weak covalent bond. The mixed chemical bond is responsible for the high hardness-brittleness of {\alpha}-Al11Nd3. This work is expected to lay a foundation for Al-Nd alloy and catalyze the fabrication of high-quality Al-Nd target materials., Comment: 11 figures,5 tables

Published
2024

8. Finite-temperature ductility-brittleness and electronic structures of Al$_{n}$Sc (n=1, 2 and 3)

Author

Wang, Xue-Qian, Zhao, Ying, Liu, Hao-Xuan, Sun, Shuchen, Yang, Hongbo, Zhong, Jiamin, Tu, Ganfeng, Li, Song, Yan, Hai-Le, and Zuo, Liang

Subjects
Condensed Matter - Materials Science, Physics - Computational Physics
Abstract

Finite-temperature ductility-brittleness and electronic structures of Al$_3$Sc, Al$_2$Sc and AlSc are studied comparatively by first-principles calculations and ab-initio molecular dynamics. Results show that Al$_3$Sc and Al$_2$Sc are inherently brittle at both ground state and finite temperatures. By contrast, AlSc possesses a significantly superior ductility evaluated from all Pugh's, Pettifor's and Poisson's ductility-brittleness criteria. At ground state, AlSc meets the criteria of ductile according to Pugh's and Poisson's theories, while it is categorized as the brittle in the frame of Pettifor's picture. With the increasing temperature, the ductility of all the studied compounds exhibits a noticeable improvement. In particular, as the temperature rises, the Cauchy pressure of AlSc undergoes a transition from negative to positive. Thus, at high temperatures (T > 600 K), AlSc is unequivocally classified as the ductile from all criteria considered. In all Al$_3$Sc, Al$_2$Sc and AlSc, the Al-Al bond, originated from s-p and p-p orbital hybridizations, and the Al-Sc bond, dominated by p-d covalent hybridization, are the first and second strongest chemical bonds, respectively. To explain the difference in mechanical properties of the studied compounds, the mean bond strength (MBS) is evaluated. The weaker Al-Al bond in AlSc, leading to a smaller MBS, could be the origin for the softer elastic stiffness and superior intrinsic ductility. The longer length of the Al-Al bond in AlSc is responsible for its weaker bond strength. Furthermore, the enhanced metallicity of the Al-Al bond in AlSc would also contribute to its exceptional ductility., Comment: 14 pages, 10 figures

Published
2023

9. Multiple Liver Metastases in Malignant Insulinoma: A Case Report

Author

LIAO Jinhao, GAO Yuting, WANG Xiang, WANG Zhiwei, XU Qiang, ZHAO Yuxing, CHI Yue, MAO Jiangfeng, and YANG Hongbo

Subjects
hypoglycemia, malignant insulinoma, multidisciplinary treatment, Medicine
Abstract

Malignant insulinoma is a kind of rare and challenging neuroendocrine tumor. It is often accompanied by distant metastasis, among which liver metastasis is most common, and the prognosis is often non-promising. In this paper, we report a case of multiple liver metastases from malignant insulinoma. The patient, a 70-year-old male, was admitted to the hospital due to "episodic consciousness disorder for more than four months." Blood glucose monitoring revealed recurrent hypoglycemia in the early morning, after meals, and at night. Pancreatic perfusion CT and dynamic enhanced MRI of the liver revealed a mass in the uncinate process of the pancreatic head and multiple liver metastases. Percutaneous liver biopsy confirmed the diagnosis of insulinoma. After multidisciplinary discussions, hepatic artery embolization and radiofrequency ablation were performed in stages, in combination with everolimus treatment. Thereafter, the enhanced CT demonstrated that some liver metastases shrank. The patient had regular meals, and the blood sugar gradually increased and remained normal thereafter. This article discusses this case's clinical characteristics and multidisciplinary collaborative diagnosis and treatment, aiming to provide experience for the comprehensive clinical diagnosis and treatment of malignant insulinoma patients.

Published
2024
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32. Clinical Features and Mutation Analysis of Gordon Holmes Syndrome Associated with RNF216 Gene Mutation and a Literature Review

Author

CHEN Meiping, YANG Hongbo, PAN Hui, FENG Feng, ZHU Yicheng, and ZHU Huijuan

Subjects
rnf216 gene, gordon holmes syndrome, hypogonadotropic hypogonadism, cerebellar ataxia, neurodegenerative diseases, Medicine
Abstract

Objective To summarize the clinical characteristics and RNF216 gene mutation of a patient with Gordon Holmes syndrome (GHS), and to improve the understanding of the genetic and clinica characteristics of this disease through literature review. Methods We collected the clinical data of the patient with GHS, extracted the DNA from 2 mL peripheral venous blood of the patient and his parents for whole exome gene detection, and then we analyzed the clinical and genetic characteristics of all previously reported patients with RNF216 gene mutation. Results The young male patient was short in stature at sixyearsold and was diagnosed growth hormone deficiency.He had no secondary sexual characteristics by the age of 15 and was diagnosed hypogonadal hypogonadism.After the age of 22, he gradually developed abnormal gait and had progressive decline in speech, motor, and cognitive functions.Whole exome sequencing revealed a homozygous, nonsense mutation c.1549C>T (p.R517*) in the RNF216 gene.His parents were consanguineous and were heterozygous carriers of the mutations with phenotypic normality.Combined with literature review and this case report results showed that a total of 21 patients of the disease in the world and among them 15 had pathogenic variants of RNF216 gene mutation.7 of the 15 had truncated mutations, 5 had missense mutations, and 1 synonym mutation, 1 splice mutation, and 1 deletion mutation respectively.RNF216 gene mutation can be seen in neurodegenerative diseases with multiple overlapping symptoms of GHS, Huntington-like disease, and 4H syndrome.The main clinical manifestations are hypogonadotropic hypogonadism and early-onset progressive neurological dysfunction in adolescence or early adulthood.The median age of onset of neurological symptoms is 28 years old, featuring cerebellar ataxia, dysarthria, and cognitive impairment, as well as imaging manifestations of extensive white matter lesions and cerebellar atrophy. Conclusions The mutation of RNF216 gene can cause GHS.Genetic testing is helpful to the diagnosis and treatment of rare diseases.

Published
2023
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33. Necrolytic Migratory Erythema—A Case Report of Pancreatic Occupying Lesion

Author

HU Zhonghui, YANG Lu, LIU Yuehua, JIN Hongzhong, XU Qiang, LIU Wenjing, LUO Yaping, YANG Hongbo, and WANG Tao

Subjects
necrolytic migratory erythema, glucagonoma, glucagonoma syndrome, pancreatic occupying lesion, Medicine
Abstract

Glucagonoma is a rare neuroendocrine tumor of α cells of the pancreas. The tumor excessively secretes glucagon and causes glucagonoma syndrome.70%-90% of patients with glucagonoma will develop necrolytic migratory erythema (NME). We reported a patient of glucagonoma syndrome who was presented to the dermatology outpatient clinic with a 2-year-history of recurrent erythema and scaling on the skin migrating throughout the body. A skin biopsy was performed and resulting features matched with NME, whilst imaging examinations suggested a soft tissue density tumor present in the tail of the pancreas with somatostatin receptor expression and laboratory tests found an elevated levels of serum glucagon. After the diagnosis was confirmed, the patient was treated with surgical resection of the glucagonoma and the skin eruptions resolved rapidly in 4 days. Meanwhile, we reviewed relevant literature published in recent years and summarized its clinical characteristics in order to improve its understanding by clinicians, including clinical manifestations, laboratory and imaging examinations, diagnosis and treatments.

Published
2023
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39. Author Correction: An atlas of dynamic chromatin landscapes in mouse fetal development

Author

Gorkin, David U, Barozzi, Iros, Zhao, Yuan, Zhang, Yanxiao, Huang, Hui, Lee, Ah Young, Li, Bin, Chiou, Joshua, Wildberg, Andre, Ding, Bo, Zhang, Bo, Wang, Mengchi, Strattan, J Seth, Davidson, Jean M, Qiu, Yunjiang, Afzal, Veena, Akiyama, Jennifer A, Plajzer-Frick, Ingrid, Novak, Catherine S, Kato, Momoe, Garvin, Tyler H, Pham, Quan T, Harrington, Anne N, Mannion, Brandon J, Lee, Elizabeth A, Fukuda-Yuzawa, Yoko, He, Yupeng, Preissl, Sebastian, Chee, Sora, Han, Jee Yun, Williams, Brian A, Trout, Diane, Amrhein, Henry, Yang, Hongbo, Cherry, J Michael, Wang, Wei, Gaulton, Kyle, Ecker, Joseph R, Shen, Yin, Dickel, Diane E, Visel, Axel, Pennacchio, Len A, and Ren, Bing

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Pediatric, General Science & Technology
Abstract

A Correction to this paper has been published: https://doi.org/10.1038/s41586-020-03089-4.

Published
2021

43. Author Correction: An atlas of dynamic chromatin landscapes in mouse fetal development

Author

Gorkin, David U, Barozzi, Iros, Zhao, Yuan, Zhang, Yanxiao, Huang, Hui, Lee, Ah Young, Li, Bin, Chiou, Joshua, Wildberg, Andre, Ding, Bo, Zhang, Bo, Wang, Mengchi, Strattan, J Seth, Davidson, Jean M, Qiu, Yunjiang, Afzal, Veena, Akiyama, Jennifer A, Plajzer-Frick, Ingrid, Novak, Catherine S, Kato, Momoe, Garvin, Tyler H, Pham, Quan T, Harrington, Anne N, Mannion, Brandon J, Lee, Elizabeth A, Fukuda-Yuzawa, Yoko, He, Yupeng, Preissl, Sebastian, Chee, Sora, Han, Jee Yun, Williams, Brian A, Trout, Diane, Amrhein, Henry, Yang, Hongbo, Cherry, J Michael, Wang, Wei, Gaulton, Kyle, Ecker, Joseph R, Shen, Yin, Dickel, Diane E, Visel, Axel, Pennacchio, Len A, and Ren, Bing

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, General Science & Technology
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

45. Subtype-specific 3D genome alteration in acute myeloid leukaemia

Author

Xu, Jie, Song, Fan, Lyu, Huijue, Kobayashi, Mikoto, Zhang, Baozhen, Zhao, Ziyu, Hou, Ye, Wang, Xiaotao, Luan, Yu, Jia, Bei, Stasiak, Lena, Wong, Josiah Hiu-yuen, Wang, Qixuan, Jin, Qi, Jin, Qiushi, Fu, Yihao, Yang, Hongbo, Hardison, Ross C., Dovat, Sinisa, Platanias, Leonidas C., Diao, Yarui, Yang, Yue, Yamada, Tomoko, Viny, Aaron D., Levine, Ross L., Claxton, David, Broach, James. R., Zheng, Hong, and Yue, Feng

Published
2022
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49. An atlas of dynamic chromatin landscapes in mouse fetal development

Author

Gorkin, David U, Barozzi, Iros, Zhao, Yuan, Zhang, Yanxiao, Huang, Hui, Lee, Ah Young, Li, Bin, Chiou, Joshua, Wildberg, Andre, Ding, Bo, Zhang, Bo, Wang, Mengchi, Strattan, J Seth, Davidson, Jean M, Qiu, Yunjiang, Afzal, Veena, Akiyama, Jennifer A, Plajzer-Frick, Ingrid, Novak, Catherine S, Kato, Momoe, Garvin, Tyler H, Pham, Quan T, Harrington, Anne N, Mannion, Brandon J, Lee, Elizabeth A, Fukuda-Yuzawa, Yoko, He, Yupeng, Preissl, Sebastian, Chee, Sora, Han, Jee Yun, Williams, Brian A, Trout, Diane, Amrhein, Henry, Yang, Hongbo, Cherry, J Michael, Wang, Wei, Gaulton, Kyle, Ecker, Joseph R, Shen, Yin, Dickel, Diane E, Visel, Axel, Pennacchio, Len A, and Ren, Bing

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Biomedical and Clinical Sciences, Genetics, Human Genome, Biotechnology, Pediatric, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Animals, Chromatin, Chromatin Immunoprecipitation Sequencing, Datasets as Topic, Disease, Enhancer Elements, Genetic, Female, Fetal Development, Gene Expression Regulation, Developmental, Genetic Variation, Histones, Humans, Male, Mice, Mice, Inbred C57BL, Molecular Sequence Annotation, Organ Specificity, Regulatory Sequences, Nucleic Acid, Reproducibility of Results, Transposases, General Science & Technology
Abstract

The Encyclopedia of DNA Elements (ENCODE) project has established a genomic resource for mammalian development, profiling a diverse panel of mouse tissues at 8 developmental stages from 10.5 days after conception until birth, including transcriptomes, methylomes and chromatin states. Here we systematically examined the state and accessibility of chromatin in the developing mouse fetus. In total we performed 1,128 chromatin immunoprecipitation with sequencing (ChIP-seq) assays for histone modifications and 132 assay for transposase-accessible chromatin using sequencing (ATAC-seq) assays for chromatin accessibility across 72 distinct tissue-stages. We used integrative analysis to develop a unified set of chromatin state annotations, infer the identities of dynamic enhancers and key transcriptional regulators, and characterize the relationship between chromatin state and accessibility during developmental gene regulation. We also leveraged these data to link enhancers to putative target genes and demonstrate tissue-specific enrichments of sequence variants associated with disease in humans. The mouse ENCODE data sets provide a compendium of resources for biomedical researchers and achieve, to our knowledge, the most comprehensive view of chromatin dynamics during mammalian fetal development to date.

Published
2020

50. An integrative ENCODE resource for cancer genomics.

Author

Zhang, Jing, Lee, Donghoon, Dhiman, Vineet, Jiang, Peng, Xu, Jie, McGillivray, Patrick, Yang, Hongbo, Liu, Jason, Meyerson, William, Clarke, Declan, Gu, Mengting, Li, Shantao, Lou, Shaoke, Xu, Jinrui, Lochovsky, Lucas, Ung, Matthew, Ma, Lijia, Yu, Shan, Cao, Qin, Harmanci, Arif, Yan, Koon-Kiu, Sethi, Anurag, Gürsoy, Gamze, Schoenberg, Michael, Rozowsky, Joel, Warrell, Jonathan, Emani, Prashant, Yang, Yucheng, Galeev, Timur, Kong, Xiangmeng, Liu, Shuang, Li, Xiaotong, Krishnan, Jayanth, Feng, Yanlin, Rivera-Mulia, Juan, Adrian, Jessica, Broach, James, Bolt, Michael, Moran, Jennifer, Fitzgerald, Dominic, Dileep, Vishnu, Liu, Tingting, Mei, Shenglin, Sasaki, Takayo, Trevilla-Garcia, Claudia, Wang, Su, Wang, Yanli, Zang, Chongzhi, Wang, Daifeng, Klein, Robert, Snyder, Michael, Gilbert, David, Yip, Kevin, Cheng, Chao, Yue, Feng, Liu, X, White, Kevin, and Gerstein, Mark

Subjects
Cell Line, Tumor, Cell Transformation, Neoplastic, Databases, Genetic, Gene Regulatory Networks, Genomics, Humans, Mutation, Neoplasms, Reproducibility of Results, Transcription Factors
Abstract

ENCODE comprises thousands of functional genomics datasets, and the encyclopedia covers hundreds of cell types, providing a universal annotation for genome interpretation. However, for particular applications, it may be advantageous to use a customized annotation. Here, we develop such a custom annotation by leveraging advanced assays, such as eCLIP, Hi-C, and whole-genome STARR-seq on a number of data-rich ENCODE cell types. A key aspect of this annotation is comprehensive and experimentally derived networks of both transcription factors and RNA-binding proteins (TFs and RBPs). Cancer, a disease of system-wide dysregulation, is an ideal application for such a network-based annotation. Specifically, for cancer-associated cell types, we put regulators into hierarchies and measure their network change (rewiring) during oncogenesis. We also extensively survey TF-RBP crosstalk, highlighting how SUB1, a previously uncharacterized RBP, drives aberrant tumor expression and amplifies the effect of MYC, a well-known oncogenic TF. Furthermore, we show how our annotation allows us to place oncogenic transformations in the context of a broad cell space; here, many normal-to-tumor transitions move towards a stem-like state, while oncogene knockdowns show an opposing trend. Finally, we organize the resource into a coherent workflow to prioritize key elements and variants, in addition to regulators. We showcase the application of this prioritization to somatic burdening, cancer differential expression and GWAS. Targeted validations of the prioritized regulators, elements and variants using siRNA knockdowns, CRISPR-based editing, and luciferase assays demonstrate the value of the ENCODE resource.

Published
2020

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