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144 results on '"Yang, Xi-Qiang"'

2. Targeted Gene Sanger Sequencing Should Remain the First-Tier Genetic Test for Children Suspected to Have the Five Common X-Linked Inborn Errors of Immunity

Author

Chan, Koon-Wing, primary, Wong, Chung-Yin, additional, Leung, Daniel, additional, Yang, Xingtian, additional, Fok, Susanna F. S., additional, Mak, Priscilla H. S., additional, Yao, Lei, additional, Ma, Wen, additional, Mao, Huawei, additional, Zhao, Xiaodong, additional, Liang, Weiling, additional, Singh, Surjit, additional, Barbouche, Mohamed-Ridha, additional, He, Jian-Xin, additional, Jiang, Li-Ping, additional, Liew, Woei-Kang, additional, Le, Minh Huong Thi, additional, Muktiarti, Dina, additional, Santos-Ocampo, Fatima Johanna, additional, Djidjik, Reda, additional, Belaid, Brahim, additional, Ismail, Intan Hakimah, additional, Abdul Latiff, Amir Hamzah, additional, Lee, Way Seah, additional, Chen, Tong-Xin, additional, Liu, Jinrong, additional, Jin, Runming, additional, Wang, Xiaochuan, additional, Chien, Yin Hsiu, additional, Yu, Hsin-Hui, additional, Raj, Dinesh, additional, Raj, Revathi, additional, Vaughan, Jenifer, additional, Urban, Michael, additional, Berg, Sylvia van den, additional, Eley, Brian, additional, Lee, Anselm Chi-Wai, additional, Isa, Mas Suhaila, additional, Ang, Elizabeth Y., additional, Lee, Bee Wah, additional, Yeoh, Allen Eng Juh, additional, Shek, Lynette P., additional, Quynh Le, Nguyen Ngoc, additional, Nguyen, Van Anh Thi, additional, Phan Nguyen Lien, Anh, additional, Capulong, Regina D., additional, Mallillin, Joanne Michelle, additional, Villanueva, Jose Carlo Miguel M., additional, Camonayan, Karol Anne B., additional, Vera, Michelle De, additional, Casis-Hao, Roxanne J., additional, Lobo, Rommel Crisenio M., additional, Foronda, Ruby, additional, Binas, Vicky Wee Eng, additional, Boushaki, Soraya, additional, Kechout, Nadia, additional, Phongsamart, Gun, additional, Wongwaree, Siriporn, additional, Jiratchaya, Chamnanrua, additional, Lao-Araya, Mongkol, additional, Trakultivakorn, Muthita, additional, Suratannon, Narissara, additional, Jirapongsananuruk, Orathai, additional, Chantveerawong, Teerapol, additional, Kamchaisatian, Wasu, additional, Chan, Lee Lee, additional, Koh, Mia Tuang, additional, Wong, Ke Juin, additional, Fong, Siew Moy, additional, Thong, Meow-Keong, additional, Latiff, Zarina Abdul, additional, Noh, Lokman Mohd, additional, Silva, Rajiva de, additional, Jouhadi, Zineb, additional, Al-Saad, Khulood, additional, Vignesh, Pandiarajan, additional, Jindal, Ankur Kumar, additional, Rawat, Amit, additional, Gupta, Anju, additional, Suri, Deepti, additional, Yang, Jing, additional, Au, Elaine Yuen-Ling, additional, Kwok, Janette Siu-Yin, additional, Chan, Siu-Yuen, additional, Hui, Wayland Yuk-Fun, additional, Chua, Gilbert T., additional, Duque, Jaime Rosa, additional, Cheong, Kai-Ning, additional, Chong, Patrick Chun Yin, additional, Ho, Marco Hok Kung, additional, Lee, Tsz-Leung, additional, Wong, Wilfred Hing-Sang, additional, Yang, Wanling, additional, Lee, Pamela P., additional, Tu, Wenwei, additional, Yang, Xi-Qiang, additional, and Lau, Yu Lung, additional

Published
2022
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9. Molecular Diagnosis of Severe Combined Immunodeficiency—Identification of IL2RG, JAK3, IL7R, DCLRE1C, RAG1, and RAG2 Mutations in a Cohort of Chinese and Southeast Asian Children

Author

Lee, Pamela P. W., Chan, Koon-Wing, Chen, Tong-Xin, Jiang, Li-Ping, Wang, Xiao-Chuan, Zeng, Hua-Song, Chen, Xiang-Yuan, Liew, Woei-Kang, Chen, Jing, Chu, Kit-Man, Chan, Lee-Lee, Shek, Lynette, Lee, Anselm C. W., Yu, Hsin-Hui, Li, Qiang, Xu, Chen-Guang, Sultan-Ugdoracion, Geraldine, Latiff, Zarina Abdul, Latiff, Amir Hamzah Abdul, Jirapongsananuruk, Orathai, Ho, Marco H. K., Lee, Tsz-Leung, Yang, Xi-Qiang, and Lau, Yu-Lung

Published
2011
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19. Erratum to: Molecular Diagnosis of Severe Combined Immunodeficiency—Identification of IL2RG, JAK3, IL7R, DCLRE1C, RAG1, and RAG2 Mutations in a Cohort of Chinese and Southeast Asian Children

Author

Lee, Pamela P. W., Chan, Koon-Wing, Chen, Tong-Xin, Jiang, Li-Ping, Wang, Xiao-Chuan, Zeng, Hua-Song, Chen, Xiang-Yuan, Liew, Woei-Kang, Chen, Jing, Chu, Kit-Man, Chan, Lee-Lee, Shek, Lynette Pei-Chi, Lee, Anselm C. W., Yu, Hsin-Hui, Li, Qiang, Xu, Chen-Guang, Sultan-Ugdoracion, Geraldine, Latiff, Zarina Abdul, Latiff, Amir Hamzah Abdul, Jirapongsananuruk, Orathai, Ho, Marco H. K., Lee, Tsz-Leung, Yang, Xi-Qiang, and Lau, Yu-Lung

Published
2013
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20. Quantitative photoelectrochemical detection of biological affinity reaction: biotin--avidin interaction

Author

Dong, Dong, Zheng, Dong, Wang, Fu-Quan, Yang, Xi-Qiang, Wang, Na, Li, Yuan-Guang, Guo, Liang-Hong, and Cheng, Jing

Subjects
Chemistry, Analytic -- Research, Chemistry
Abstract

Quantitative detection of a biological affinity reaction, the biotin/avidin recognition, was achieved using our newly developed photoelectrochemical analytical system. The system is based on the operation mechanism of the welldeveloped dye-sensitized photoelectrochemical solar cells and comprises a ruthenium tris(2,2'-bipyridine) (Ru-bipy) derivative as the photoelectrochemical signal-generating molecule, oxalate as the sacrificial electron donor, and tin oxide nanoparticle as the semiconductor electrode material. To perform the affinity reaction, avidin was immobilized on Sn[O.sub.2] electrode by passive adsorption. Biotin-linked bovine serum albumin (BSA) was labeled with an NHS-ester derivative of Ru-bipy. After binding of BSA to the surface-immobilized avidin through biotin, photoelectrochemical measurement was carried out in the presence of oxalate. Anodic photocurrent was turned on and off repeatedly by control of incidental light. The action spectrum of the photocurrent resembled the absorption spectrum of Ru-bipy, proving the photocurrent was generated from the metal complex. A linear relationship between photocurrent and BSA concentration was obtained in the range of 1-100 [micro]g/mL. This is the first case of quantitative photoelectrochemical detection of a biological affinity interaction.

Published
2004

21. The severity of bronchiolitis is not dependent on the co-infection of RSV with other respiratory viruses

Author

Liu En-mei, Bai Hua, Fu Zhou, Chen Jiehua, Deng Yu, Luo Zhengxiu, Yang Xi-qiang, Luo Jian, Wang Li-jia, Zhao Xiao-dong, and Liu Wei

Subjects
biology, business.industry, viruses, Incidence (epidemiology), Human bocavirus, Disease, respiratory system, biology.organism_classification, medicine.disease, Virology, Virus, Infectious Diseases, Human metapneumovirus, Bronchiolitis, Pediatrics, Perinatology and Child Health, Immunology, medicine, Bronchitis, Respiratory system, business
Abstract

Bronchiolitis is one of the most common lower respiratory diseases in infants. A correlation between the severity of bronchiolitis and a co-infection with respiratory syncytial virus (RSV) as well as other viruses has not yet been elucidated. The purpose of this study was to clarify the impact of RSV co-infection with other viruses on the severity of bronchiolitis and airway inflammation. One hundred and twelve hospitalized children with clinical symptoms of bronchiolitis were prospectively enrolled in this study. Nasopharyngeal aspirates were analyzed to identify RSV, human bocavirus, human metapneumovirus and nine other respiratory viral pathogens. Inflammatory cell counting and concentrations of cytokines/chemokines were also evaluated. The severity of the disease was further determined on the basis of symptom score and duration of hospitalization. Viral pathogens were detected in 84 samples (75%). RSV was detected in 62 samples (55.36%), 31 of which also possessed other viruses. No difference was found between children with bronchiolitis that had RSV as the sole infecting viral agent and those that were infected with RSV and other viruses with respect to the prevalence of symptoms prior to admission to the hospital, the duration of hospitalization and the diagnosis of severe bronchiolitis. The median cellularity, concentrations of cytokines and cell counts of nasopharyngeal aspirates were similar between the two groups of children. The severity of bronchiolitis is not dependent on the co-infection of RSV with other respiratory viruses.

Published
2015

22. Erratum to: Clinical and Molecular Features of 38 Children with Chronic Granulomatous Disease in Mainland China

Author

Xu, Huan, primary, Tian, Wen, additional, Li, Shu-Juan, additional, Zhang, Lu-Ying, additional, Liu, Wei, additional, Zhao, Yao, additional, Zhang, Zhi-Yong, additional, Tang, Xue-Mei, additional, Wang, Mo, additional, Wu, Dao-Qi, additional, Shi, Ji-Sheng, additional, Ding, Yuan, additional, Zhao, Xiao-Dong, additional, Yang, Xi-Qiang, additional, and Jiang, Li-Ping, additional

Published
2016
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24. CHILDREN WITH PERSISTENT WHEEZING ASSOCIATED WITH HUMAN BOCAVIRUS INFECTION IN CHINA

Author

Wang Li-jia, Zhao Xiao-dong, Yang Xi-qiang, Luo Zhengxiu, Ding Yuan, Liu En-mei, Deng Yu, and Li Qubei

Subjects
biology, business.industry, Human bocavirus, Airway inflammation, biology.organism_classification, medicine.disease, Virology, Virus, law.invention, law, Pediatrics, Perinatology and Child Health, Immunology, Coinfection, Medicine, Respiratory system, Lower respiratory infection, business, Pathogen, Polymerase chain reaction
Abstract

INTRODUCTION: Human bocavirus (HBoV) is a newly identified human parvovirus that was originally isolated from children with lower respiratory tract disease. The impact of HBoV on childhood persistent wheezing has not been identified. OBJECTIVE: Our aim was to study the impact of HBoV on childhood persistent wheezing. METHODS: In this study, a total of 40 tracheal aspirates were obtained by bronchofibroscope from children with persistent wheezing who had been wheezing for at least >4 weeks. HBoV was detected by polymerase chain reaction. A rapid immunofluorescence method was used for diagnosis of respiratory syncytial virus, adenovirus, influenza A and B, and parainfluenza 1, 2, and 3. RESULTS: In 40 children with persistent wheezing, 13 (32.5%) had DNA sequences that were HBoV-positive. Age of the patients with HBoV-positive infection ranged from 1 month to 2 years. The results of polymerase chain reaction products sequencing proved that these 13 samples were exactly identical to the sequence of HBoV published in GenBank (accession Nos. DQ988934 and DQ457413). Two children with HBoV infection were found to have coinfection with respiratory syncytial virus. CONCLUSIONS: This study confirmed that HBoV is a common pathogen for children with lower respiratory infection and might particularly be attributed to persistent wheezing. However, more studies should be performed to study the mechanism of HBoV on chronic airway inflammation.

Published
2008

27. Molecular Diagnosis of Severe Combined Immunodeficiency—Identification of IL2RG, JAK3, IL7R, DCLRE1C, RAG1, and RAG2 Mutations in a Cohort of Chinese and Southeast Asian Children

Author

Lee, Pamela P. W., primary, Chan, Koon-Wing, additional, Chen, Tong-Xin, additional, Jiang, Li-Ping, additional, Wang, Xiao-Chuan, additional, Zeng, Hua-Song, additional, Chen, Xiang-Yuan, additional, Liew, Woei-Kang, additional, Chen, Jing, additional, Chu, Kit-Man, additional, Chan, Lee-Lee, additional, Shek, Lynette, additional, Lee, Anselm C. W., additional, Yu, Hsin-Hui, additional, Li, Qiang, additional, Xu, Chen-Guang, additional, Sultan-Ugdoracion, Geraldine, additional, Latiff, Zarina Abdul, additional, Latiff, Amir Hamzah Abdul, additional, Jirapongsananuruk, Orathai, additional, Ho, Marco H. K., additional, Lee, Tsz-Leung, additional, Yang, Xi-Qiang, additional, and Lau, Yu-Lung, additional

Published
2010
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29. Clinical Characteristics and Genotype-phenotype Correlation in 62 Patients with X-linked Agammaglobulinemia

Author

Lee, Pamela P. W., primary, Chen, Tong-Xin, additional, Jiang, Li-Ping, additional, Chan, Koon-Wing, additional, Yang, Wanling, additional, Lee, Bee-Wah, additional, Chiang, Wen-Chin, additional, Chen, Xiang-Yuan, additional, Fok, Susanna F. S., additional, Lee, Tsz-Leung, additional, Ho, Marco H. K., additional, Yang, Xi-Qiang, additional, and Lau, Yu-Lung, additional

Published
2009
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40. Clinical, molecular, and T cell subset analyses in a small cohort of Chinese patients with hyper-IgM syndrome type 1.

Author

Tang, Wen-Jing, An, Yun-Fei, Dai, Rong-Xin, Wang, Qing-Hong, Jiang, Li-Ping, Tang, Xue-Mei, Yang, Xi-Qiang, Yu, Jie, Tu, Wen-Wei, and Zhao, Xiao-Dong

Subjects
*IMMUNOLOGIC diseases, *CHINESE people, *T cells, *AUTOIMMUNE diseases, *COHORT analysis, *IMMUNODEFICIENCY, *GENETIC mutation, *PATIENTS, *DISEASES
Abstract

Abstract: Type 1 hyper-IgM syndrome (HIGM1) is a rare primary immunodeficiency disease caused by mutations in the CD40L gene. Patients often present with recurrent infections and autoimmune manifestations. We investigated the clinical and molecular characteristics of HIGM1 in thirteen patients from the Chinese mainland and examined the proportion of CD4+CD25+FoxP3+Treg, Th17, and Th1 cells in the peripheral blood. We identified ten distinct CD40L mutations in eleven patients: one missense mutation, one nonsense mutation, one insertion mutation (in frame), and seven deletions. Six of these mutations were novel. We observed the percentage of Tregs in the peripheral blood of HIGM1 patients decreased markedly compared with that in healthy controls, but no statistically significant differences was found in the percentages of Th17 and Th1. The identified mutations reflect the heterogeneity of the CD40L gene in HIGM1. Precise genetic diagnosis of HIGM1 will enable appropriate therapeutic interventions, reliable detection of carriers, and genetic counseling. Skewed Treg, Th17/Treg, and Th1/Treg profiles may be associated with immune responses to autoimmunity or infection, which requires replication in larger studies. [Copyright &y& Elsevier]

Published
2014
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43. [Analysis of prenatal diagnosis for seven high-risk fetuses with Wiskott-Aldrich syndrome].

Author

Zhao Q, Zhang ZY, Zhao XD, Jiang LP, Zhao Y, and Yang XQ

Subjects
Female, Flow Cytometry, Humans, Male, Pregnancy, Wiskott-Aldrich Syndrome genetics, Wiskott-Aldrich Syndrome Protein blood, Wiskott-Aldrich Syndrome Protein genetics, Amniocentesis, Fetal Diseases diagnosis, Prenatal Diagnosis, Wiskott-Aldrich Syndrome diagnosis
Abstract

Objective: To investigate the value of gene analysis of amniotic fluid exfoliated cells and WASP detection from cord blood in prenatal diagnosis of high-risk fetus with Wiskott-Aldrich syndrome., Method: Seven patients with Wiskott-Aldrich syndrome were diagnosed by gene analysis and WASP detected by flow cytometry from 2008 to 2010. After detailed inquiry for medical history and gene analysis of related family members, seven pedigree trees were drawn, including 15 carriers of abnormal genes. From 2008 to 2011, seven samples of amniotic cell gotten by amniocentesis were collected from seven high-risk pregnant women with abnormal gene during 18 to 20 gestational weeks. WASP gene was amplified by polymerase chain reaction (PCR) from DNA of amniotic cell gotten and sequencing was performed directly on the PCR products forward and reversely. Embryo blood sample was collected from one high-risk fetus by needle puncture of umbilical blood vessel and WASP expression was detected by flow cytometry. Karyotyping was performed in amniotic cell gotten cultivated by orthotopic slice and G band staining. Gene analysis of WASP, WASP expression detected by flow cytometry and evaluation of immune function were reexamined in high-risk fetus after delivery., Result: Amniocentesis and culture of amniotic cell succeeded in all the seven fetuses. Gene analysis and karyotyping showed that one male fetus and four female fetuses were normal and two female fetuses were carriers. WASP expression detected from embryo blood sample of the patient was normal. After delivery, the result of gene analysis, WASP detection and evaluation of immune function was the same as that of prenatal diagnosis., Conclusion: Karyotyping, gene analysis and WASP detection of cord blood can provide reliable service of prenatal diagnosis for high-risk pregnant women with Wiskott-Aldrich syndrome.

Published
2012

49. [Comparation of inflammation between wild mice and severe combined immunodeficiency mice with endotoxemia induced by lipopolysaccharide].

Author

Luo C, Yang XQ, Li X, Liu W, and Wang LJ

Subjects
Alanine Transaminase metabolism, Animals, Aspartate Aminotransferases metabolism, Blood Urea Nitrogen, Chemokine CCL2 blood, Endotoxemia chemically induced, Endotoxemia metabolism, Inflammation chemically induced, Inflammation immunology, Inflammation metabolism, Interferon-gamma blood, Interleukin-6 blood, Lipopolysaccharides, Liver pathology, Lung pathology, Male, Mice, Mice, Inbred BALB C, Mice, SCID, Tumor Necrosis Factor-alpha blood, Endotoxemia pathology, Inflammation pathology
Abstract

Aim: To compare the inflammation between wild BALB/c mice and mice with severe combined immunodeficiency (SCID) with endotoxemia induced by lipopolysaccharide (LPS)., Methods: Endotoxemia models of wild and SCID mice were established by injecting LPS intraperitoneally. Serum was taken before and 3 h, 6 h, 12 h after injecting LPS, liver and lung were taken 12 h after injecting LPS. Alanine transarninase (ALT), aspartate aminotransferase (AST) and blood urea nitrogen (BUN) levels were measured by automatic biochemical analyzer. Liver and lung inflammation injury were observed by H.E staining. TNF-α, IFN-γ, IL-6 and MCP-1 levels in serum were detected by Cytometric Bead Array (CBA)., Results: (1) All of SCID mice (8/8) were dead at 12-24 h after injecting LPS, and only one BALB/c mouse (1/8) was dead. (2) ALT and AST levels of SCID mice 12 h after injecting LPS were higer than those of BALB/c mice(P<0.05), but there was no difference of BUN levels between them. (3) The blind liver and lung pathology scores of SCID mice were higher than those of BALB/c mice (P<0.05). (4) TNF-α, IFN-γ, IL-6 and MCP-1 levels in serum at 3 h, 6 h, 12 h after injecting LPS increased significantly, and the cytokine levels of SCID mice were higher than those of BALB/c mice(P<0.05)., Conclusion: SCID mice don't only excessively secrete inflammatory cytokines after injecting LPS, but also lead to more severe endotoxemia and inflammation injury of organs, which are the important cause of mouse death. The above results also show that the adjustment deficiency of adaptive immunoresponse, abnormal augmentation of innate immunoresponse may be an important cause of severe SIRS of endangering life.

Published
2011

50. [Discussions on the use of promethazine].

Author

Wang XC, Hong JG, and Yang XQ

Subjects
Contraindications, Humans, Infant, Infant, Newborn, Promethazine therapeutic use, Promethazine adverse effects
Published
2010

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