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Articles by J Song
Total Records ( 6 ) for J Song
  P Du , G Feng , J Flatow , J Song , M Holko , W. A Kibbe and S. M. Lin

Subjective methods have been reported to adapt a general-purpose ontology for a specific application. For example, Gene Ontology (GO) Slim was created from GO to generate a highly aggregated report of the human-genome annotation. We propose statistical methods to adapt the general purpose, OBO Foundry Disease Ontology (DO) for the identification of gene-disease associations. Thus, we need a simplified definition of disease categories derived from implicated genes. On the basis of the assumption that the DO terms having similar associated genes are closely related, we group the DO terms based on the similarity of gene-to-DO mapping profiles. Two types of binary distance metrics are defined to measure the overall and subset similarity between DO terms. A compactness-scalable fuzzy clustering method is then applied to group similar DO terms. To reduce false clustering, the semantic similarities between DO terms are also used to constrain clustering results. As such, the DO terms are aggregated and the redundant DO terms are largely removed. Using these methods, we constructed a simplified vocabulary list from the DO called Disease Ontology Lite (DOLite). We demonstrated that DOLite results in more interpretable results than DO for gene-disease association tests. The resultant DOLite has been used in the Functional Disease Ontology (FunDO) Web application at

  I Kleiter , J Song , D Lukas , M Hasan , B Neumann , A. L Croxford , X Pedre , N Hovelmeyer , N Yogev , A Mildner , M Prinz , E Wiese , K Reifenberg , S Bittner , H Wiendl , L Steinman , C Becker , U Bogdahn , M. F Neurath , A Steinbrecher and A. Waisman

Autoreactive CD4+ T lymphocytes play a vital role in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Since the discovery of T helper 17 cells, there is an ongoing debate whether T helper 1, T helper 17 or both subtypes of T lymphocytes are important for the initiation of autoimmune neuroinflammation. We examined peripheral blood CD4+ cells from patients with active and stable relapsing–remitting multiple sclerosis, and used mice with conditional deletion or over-expression of the transforming growth factor-β inhibitor Smad7, to delineate the role of Smad7 in T cell differentiation and autoimmune neuroinflammation. We found that Smad7 is up-regulated in peripheral CD4+ cells from patients with multiple sclerosis during relapse but not remission, and that expression of Smad7 strongly correlates with T-bet, a transcription factor defining T helper 1 responses. Concordantly, mice with transgenic over-expression of Smad7 in T cells developed an enhanced disease course during experimental autoimmune encephalomyelitis, accompanied by elevated infiltration of inflammatory cells and T helper 1 responses in the central nervous system. On the contrary, mice with a T cell-specific deletion of Smad7 had reduced disease and central nervous system inflammation. Lack of Smad7 in T cells blunted T cell proliferation and T helper 1 responses in the periphery but left T helper 17 responses unaltered. Furthermore, frequencies of regulatory T cells were increased in the central nervous system of mice with a T cell-specific deletion and reduced in mice with a T cell-specific over-expression of Smad7. Downstream effects of transforming growth factor-β on in vitro differentiation of naïve T cells to T helper 1, T helper 17 and regulatory T cell phenotypes were enhanced in T cells lacking Smad7. Finally, Smad7 was induced during T helper 1 differentiation and inhibited during T helper 17 differentiation. Taken together, the level of Smad7 in T cells determines T helper 1 polarization and regulates inflammatory cellular responses. Since a Smad7 deletion in T cells leads to immunosuppression, Smad7 may be a potential new therapeutic target in multiple sclerosis.

  D Zhang , X Jiang , P Fang , Y Yan , J Song , S Gupta , A. I Schafer , W Durante , W. D Kruger , X Yang and H. Wang

Background— Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease. Monocytes display inflammatory and resident subsets and commit to specific functions in atherogenesis. In this study, we examined the hypothesis that HHcy modulates monocyte heterogeneity and leads to atherosclerosis.

Methods and Results— We established a novel atherosclerosis-susceptible mouse model with both severe HHcy and hypercholesterolemia in which the mouse cystathionine β-synthase (CBS) and apolipoprotein E (apoE) genes are deficient and an inducible human CBS transgene is introduced to circumvent the neonatal lethality of the CBS deficiency (Tg-hCBS apoE–/– Cbs–/– mice). Severe HHcy accelerated atherosclerosis and inflammatory monocyte/macrophage accumulation in lesions and increased plasma tumor necrosis factor- and monocyte chemoattractant protein-1 levels in Tg-hCBS apoE–/– Cbs–/– mice fed a high-fat diet. Furthermore, we characterized monocyte heterogeneity in Tg-hCBS apoE–/– Cbs–/– mice and another severe HHcy mouse model (Tg-S466L Cbs–/–) with a disease-relevant mutation (Tg-S466L) that lacks hyperlipidemia. HHcy increased monocyte population and selective expansion of inflammatory Ly-6Chi and Ly-6Cmid monocyte subsets in blood, spleen, and bone marrow of Tg-S466L Cbs–/– and Tg-hCBS apoE–/– Cbs–/– mice. These changes were exacerbated in Tg-S466L Cbs–/– mice with aging. Addition of l-homocysteine (100 to 500 µmol/L), but not l-cysteine, maintained the Ly-6Chi subset and induced the Ly-6Cmid subset in cultured mouse primary splenocytes. Homocysteine-induced differentiation of the Ly-6Cmid subset was prevented by catalase plus superoxide dismutase and the NAD(P)H oxidase inhibitor apocynin.

Conclusion— HHcy promotes differentiation of inflammatory monocyte subsets and their accumulation in atherosclerotic lesions via NAD(P)H oxidase–mediated oxidant stress.

  G. E Liu , Y Hou , B Zhu , M. F Cardone , L Jiang , A Cellamare , A Mitra , L. J Alexander , L. L Coutinho , M. E Dell'Aquila , L. C Gasbarre , G Lacalandra , R. W Li , L. K Matukumalli , D Nonneman , L. C. d. A Regitano , T. P. L Smith , J Song , T. S Sonstegard , C. P Van Tassell , M Ventura , E. E Eichler , T. G McDaneld and J. W. Keele

Genomic structural variation is an important and abundant source of genetic and phenotypic variation. Here, we describe the first systematic and genome-wide analysis of copy number variations (CNVs) in modern domesticated cattle using array comparative genomic hybridization (array CGH), quantitative PCR (qPCR), and fluorescent in situ hybridization (FISH). The array CGH panel included 90 animals from 11 Bos taurus, three Bos indicus, and three composite breeds for beef, dairy, or dual purpose. We identified over 200 candidate CNV regions (CNVRs) in total and 177 within known chromosomes, which harbor or are adjacent to gains or losses. These 177 high-confidence CNVRs cover 28.1 megabases or ~1.07% of the genome. Over 50% of the CNVRs (89/177) were found in multiple animals or breeds and analysis revealed breed-specific frequency differences and reflected aspects of the known ancestry of these cattle breeds. Selected CNVs were further validated by independent methods using qPCR and FISH. Approximately 67% of the CNVRs (119/177) completely or partially span cattle genes and 61% of the CNVRs (108/177) directly overlap with segmental duplications. The CNVRs span about 400 annotated cattle genes that are significantly enriched for specific biological functions, such as immunity, lactation, reproduction, and rumination. Multiple gene families, including ULBP, have gone through ruminant lineage-specific gene amplification. We detected and confirmed marked differences in their CNV frequencies across diverse breeds, indicating that some cattle CNVs are likely to arise independently in breeds and contribute to breed differences. Our results provide a valuable resource beyond microsatellites and single nucleotide polymorphisms to explore the full dimension of genetic variability for future cattle genomic research.

  B Wang , L Li , F Ni , J Song , J Wang , Y Mu , X Ma and Y. Cao

Pluripotency associated transcription factor, SAL-Like 4 (SALL4), might play an important role in conferring totipotency on oocytes. In the present study, we screened SALL4 coding regions for mutations in 100 Han Chinese women with non-syndromic ovarian failure and discovered two novel non-synonymous variants in the SALL4 gene: c.541G>A (p.Val181Met) and c.2449A>G. (p.Thr817Ala). The former variant was located in an evolutionary conserved region of SALL4 protein and might affect its function. This is the first report to suggest that SALL4 might be a potential candidate gene of premature ovarian failure.

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