7 results on '"Azure Duan"'
Search Results
2. Resequencing DCDC5 in the Flanking Region of an LD-SNP Derived from a Kidney-Yang Deficiency Syndrome Family
- Author
-
Wei-Hong Li, Wei Jun Ding, Hong Ya Yang, Wan Zhen Li, Mi Qu Wang, Azure Duan, Ling Ling Tan, Tian E. Zhang, Weiwei Liu, Li Ping Zhou, and Yu Hua Qin
- Subjects
Nonsynonymous substitution ,Genetics ,Linkage disequilibrium ,Article Subject ,Single-nucleotide polymorphism ,lcsh:Other systems of medicine ,Biology ,lcsh:RZ201-999 ,genomic DNA ,Exon ,Complementary and alternative medicine ,Polymorphism (computer science) ,SNP ,Gene ,Research Article - Abstract
Objective. To explore the genetic traits of Kidney-yang deficiency syndrome (KDS).Design. Twelve KDS subjects and three spouses from a typical KDS family were recruited. Their genomic DNA samples were genotyped by Affymetrix 100K single-nucleotide polymorphism (SNP) arrays. The linkage disequilibrium (LD) SNPs were generated using GeneChip DNA analysis software (GDAS, Affymetrix). Genes located within 100 bp of the flanks of LD SNPs were mined via GeneView. 29 exons of the doublecortin domain containing 5 (DCDC5), a representative gene within the flank of an LD SNP, were resequenced.Results. Five LD SNPs display midrange linkage with KDS. Two genes with established functions, DCDC5 and Leucyl-tRNA synthetase, were mined in the flanks of LD SNPs. Resequencing of DCDC5 revealed a nonsynonymous variation, in which 3764T/A was replaced by C/G. Accordingly, the Ser1172was substituted by Pro1172. The S1172P substitution effect was evaluated as “possibly damaging” by PolyPhen.Conclusion. We have identified a genomic variation of DCDC5 based on the LD SNPs derived from a KDS family. DCDC5 and other genes surrounding these SNPs display some relationships with key symptoms of KDS.
- Published
- 2011
3. Observations on Copy Number Variations in a Kidney-yang Deficiency Syndrome Family
- Author
-
Ling Ling Tan, Yong Xiang Gao, Mi Qu Wang, Weiwei Liu, Hong Ya Yang, Shi Lin Yan, Azure Duan, Wei Jun Ding, Wan Zhen Li, Li Ping Zhou, and Min Yan
- Subjects
Genetics ,Kidney ,Disease ,lcsh:Other systems of medicine ,Biology ,lcsh:RZ201-999 ,Homology (biology) ,genomic DNA ,symbols.namesake ,medicine.anatomical_structure ,Complementary and alternative medicine ,mental disorders ,Yang deficiency ,medicine ,Mendelian inheritance ,symbols ,Original Article ,Copy-number variation ,Gene - Abstract
We have performed an analysis of a family with kidney-yang deficiency syndrome (KDS) in order to determine the structural genomic variations through a novel approach designated as “copy number variants” (CNVs). Twelve KDS subjects and three healthy spouses from this family were included in this study. Genomic DNA samples were genotyped utilizing an Affymetrix 100 K single nucleotide polymorphism array, and CNVs were identified by Copy Number Algorithm (CNAT4.0, Affymetrix). Our results demonstrate that 447 deleted and 476 duplicated CNVs are shared among KDS subjects within the family. The homologus ratio of deleted CNVs was as high as 99.78%. One-copy-duplicated CNVs display mid-range homology. For two copies of duplicated CNVs (CNV4), a markedly heterologous ratio was observed. Therefore, with the important exception of CNV4, our data shows that CNVs shared among KDS subjects display typical Mendelian inheritance. A total of 113 genes with established functions were identified from the CNV flanks; significantly enriched genes surrounding CNVs may contribute to certain adaptive benefit. These genes could be classified into categories including: binding and transporter, cell cycle, signal transduction, biogenesis, nerve development, metabolism regulation and immune response. They can also be included into three pathways, that is, signal transduction, metabolic processes and immunological networks. Particularly, the results reported here are consistent with the extensive impairments observed in KDS patients, involving the mass-energy-information-carrying network. In conclusion, this article provides the first set of CNVs from KDS patients that will facilitate our further understanding of the genetic basis of KDS and will allow novel strategies for a rational therapy of this disease.
- Published
- 2011
4. Insufficient activity of MAPK pathway is a key monitor of Kidney-Yang Deficiency Syndrome
- Author
-
Min Liu, Azure Duan, Ying Zi Zeng, Xiaokun Teng, Wei Jun Ding, Wei-Hong Li, Jennifer Man-Fan Wan, Cong E. Tan, Tian E. Zheng, and Shi Lin Yan
- Subjects
China ,Microarray ,MAP Kinase Signaling System ,Regulator ,Gene Expression ,Urination ,Enzyme-Linked Immunosorbent Assay ,Computational biology ,Oxidative Phosphorylation ,Body Temperature ,Transcriptome ,Adenosine Triphosphate ,Complementary DNA ,Gene expression ,Medicine ,Humans ,Single-Blind Method ,Medicine, Chinese Traditional ,Extracellular Signal-Regulated MAP Kinases ,Gene ,Oligonucleotide Array Sequence Analysis ,Mitogen-Activated Protein Kinase 1 ,Expressed sequence tag ,business.industry ,Reverse Transcriptase Polymerase Chain Reaction ,Gene Expression Profiling ,Gluconeogenesis ,Pedigree ,Gene expression profiling ,Yang Deficiency ,Complementary and alternative medicine ,Kidney Diseases ,business ,Energy Metabolism ,Glycolysis - Abstract
To explore the genetic characteristics and molecular regulator of Kidney-Yang Deficiency Syndrome (KDS).A typical KDS family was collected using a questionnaire of cold feeling and a 40-item scoring table of KDS based on Traditional Chinese Medicine (TCM), by single-blind method repeated annually over three years. Their transcriptomes were assayed by microarray and validated by RT-PCR and ELISA. Simultaneously, 10 healthy volunteers were recruited as controls and the same protocols were performed.This typical KDS family has 35 members, of whom 11 were evaluated as having severe KDS and 6 as having common KDS. Results of the cDNA microarray revealed that there were 420 genes/expressed sequence tags differentially expressed in KDS transcriptomes, indicating a global functional impairment in the mass-energy-information carrying network of KDS patients, involving energy metabolism, signal transduction, development, cell cycle, and immunity. Pathway analysis by gene set enrichment assay (GSEA) and other tools demonstrated that mitogenic activated protein kinase (MAPK) is among the most insufficiently activated pathways, while the oxidative phosphorylation and glycolysis/gluconeogenesis pathways, the two main pathways relevant to ATP synthesis, were among the most excessively activated pathways in KDS patients. Results of RT-PCR and ELISA confirmed the status of insufficient activity of the MAPK pathway.KDS patients undergo overall attenuated functions in the mass-energy-information carrying network. The marked low level of energy output in KDS may be primarily attributed to the insufficient activity of the MAPK pathway, which may be a key monitor for the abnormal energy metabolism and other impaired activities in KDS.
- Published
- 2009
5. Observations on Copy Number Variations in a Kidney-yang Deficiency Syndrome Family.
- Author
-
Wei Wei Liu, Yong Xiang Gao, Li Ping Zhou, Azure Duan, Ling Ling Tan, Wan Zhen Li, Min Yan, Hong Ya Yang, Shi Lin Yan, Mi Qu Wang, and Wei Jun Ding
- Abstract
We have performed an analysis of a family with kidney-yang deficiency syndrome (KDS) in order to determine the structural genomic variations through a novel approach designated as "copy number variants" (CNVs). Twelve KDS subjects and three healthy spouses from this family were included in this study. Genomic DNA samples were genotyped utilizing an Affymetrix 100 K single nucleotide polymorphism array, and CNVs were identified by Copy Number Algorithm (CNAT4.0, Affymetrix). Our results demonstrate that 447 deleted and 476 duplicated CNVs are shared among KDS subjects within the family. The homologus ratio of deleted CNVs was as high as 99.78%. One-copy-duplicated CNVs display mid-range homology. For two copies of duplicated CNVs (CNV
4 ), a markedly heterologous ratio was observed. Therefore, with the important exception of CNV4 , our data shows that CNVs shared among KDS subjects display typical Mendelian inheritance. A total of 113 genes with established functions were identified from the CNV flanks; significantly enriched genes surrounding CNVs may contribute to certain adaptive benefit. These genes could be classified into categories including: binding and transporter, cell cycle, signal transduction, biogenesis, nerve development, metabolism regulation and immune response. They can also be included into three pathways, that is, signal transduction, metabolic processes and immunological networks. Particularly, the results reported here are consistent with the extensive impairments observed in KDS patients, involving the mass-energy-information-carrying network. In conclusion, this article provides the first set of CNVs from KDS patients that will facilitate our further understanding of the genetic basis of KDS and will allow novel strategies for a rational therapy of this disease. [ABSTRACT FROM AUTHOR]- Published
- 2011
- Full Text
- View/download PDF
6. Resequencing DCDC5 in the Flanking Region of an LD-SNP Derived from a Kidney-Yang Deficiency Syndrome Family.
- Author
-
Li Ping Zhou, Wei Wei Liu, Zhang, Tian E., Wei Hong Li, Ling Ling Tan, Wan Zhen Li, Yu Hua Qin, Hong Ya Yang, Azure Duan, Mi Qu Wang, and Wei Jun Ding
- Abstract
Objective. To explore the genetic traits of Kidney-yang deficiency syndrome (KDS). Design. Twelve KDS subjects and three spouses from a typical KDS family were recruited. Their genomic DNA samples were genotyped by Affymetrix 100K single-nucleotide polymorphism (SNP) arrays. The linkage disequilibrium (LD) SNPs were generated using GeneChip DNA analysis software (GDAS, Affymetrix). Genes located within 100 bp of the flanks of LDSNPs were mined via GeneView. 29 exons of the doublecortin domain containing 5 (DCDC5), a representative gene within the flank of an LD SNP, were resequenced. Results. Five LD SNPs display midrange linkage with KDS. Two genes with established functions, DCDC5 and Leucyl-tRNA synthetase, were mined in the flanks of LD SNPs. Resequencing of DCDC5 revealed a nonsynonymous variation, in which 3764T/A was replaced by C/G. Accordingly, the Ser1172 was substituted by Pro1172. The S1172P substitution effect was evaluated as "possibly damaging" by PolyPhen. Conclusion. We have identified a genomic variation of DCDC5 based on the LD SNPs derived from a KDS family. DCDC5 and other genes surrounding these SNPs display some relationships with key symptoms of KDS. [ABSTRACT FROM AUTHOR]
- Published
- 2011
- Full Text
- View/download PDF
7. Insufficient Activity of MAPK Pathway Is a Key Monitor of Kidney-Yang Deficiency Syndrome.
- Author
-
Wei Jun Ding, Shi Lin Yan, Ying Zi Zeng, Wei Hong Li, Azure Duan, Tian E. Zheng, Min Liu, Cong E. Tan, Xiaokun Teng, and Jennifer Wan
- Subjects
MITOGEN-activated protein kinases ,CHINESE medicine ,BLIND experiment ,MITOGENS ,DNA microarrays ,ENERGY metabolism ,CELL cycle ,IMMUNITY - Abstract
Objective: To explore the genetic characteristics and molecular regulator of Kidney-Yang Deficiency Syndrome (KDS). Design: A typical KDS family was collected using a questionnaire of cold feeling and a 40-item scoring table of KDS based on Traditional Chinese Medicine (TCM), by single-blind method repeated annually over three years. Their transcriptomes were assayed by microarray and validated by RT-PCR and ELISA. Simultaneously, 10 healthy volunteers were recruited as controls and the same protocols were performed. Results: This typical KDS family has 35 members, of whom 11 were evaluated as having severe KDS and 6 as having common KDS. Results of the cDNA microarray revealed that there were 420 genes/expressed sequence tags differentially expressed in KDS transcriptomes, indicating a global functional impairment in the mass-energy-information carrying network of KDS patients, involving energy metabolism, signal transduction, development, cell cycle, and immunity. Pathway analysis by gene set enrichment assay (GSEA) and other tools demonstrated that mitogenic activated protein kinase (MAPK) is among the most insufficiently activated pathways, while the oxidative phosphorylation and glycolysis/gluconeogenesis pathways, the two main pathways relevant to ATP synthesis, were among the most excessively activated pathways in KDS patients. Results of RT-PCR and ELISA confirmed the status of insufficient activity of the MAPK pathway. Conclusion: KDS patients undergo overall attenuated functions in the mass-energy-information carrying network. The marked low level of energy output in KDS may be primarily attributed to the insufficient activity of the MAPK pathway, which may be a key monitor for the abnormal energy metabolism and other impaired activities in KDS. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.