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author:("Hu, buau")
1.  Chitinase 3–like 1 Suppresses Injury and Promotes Fibroproliferative Responses in Mammalian Lung Fibrosis 
Science translational medicine  2014;6(240):240ra76.
Epithelial injury, alternative macrophage accumulation, and fibroproliferation coexist in the lungs of patients with idiopathic pulmonary fibrosis (IPF). Chitinase 3–like 1 (CHI3L1) is a prototypic chitinase-like protein that has been retained over species and evolutionary time. However, the regulation of CHI3L1 in IPF and its ability to regulate injury and/or fibroproliferative repair have not been fully defined. We demonstrated that CHI3L1 levels were elevated in patients with IPF. High levels of CHI3L1 are associated with progression—as defined by lung transplantation or death—and with scavenger receptor–expressing circulating monocytes in an ambulatory IPF population. In preterminal acute exacerbations of IPF, CHI3L1 levels were reduced and associated with increased levels of apoptosis. We also demonstrated that in bleomycin-treated mice, CHI3L1 expression was acutely and transiently decreased during the injury phase and returned toward and eventually exceeded baseline levels during the fibrotic phase. In this model, CHI3L1 played a protective role in injury by ameliorating inflammation and cell death, and a profibrotic role in the repair phase by augmenting alternative macrophage activation, fibroblast proliferation, and matrix deposition. Using three-dimensional culture system of a human fibroblast cell line, we found that CHI3L1 is sufficient to induce low grade myofibroblast transformation. In combination, these studies demonstrate that CHI3L1 is stimulated in IPF, where it represents an attempt to diminish injury and induce repair. They also demonstrate that high levels of CHI3L1 are associated with disease progression in ambulatory patients and that a failure of the CHI3L1 antiapoptotic response might contribute to preterminal disease exacerbations.
doi:10.1126/scitranslmed.3007096
PMCID: PMC4340473  PMID: 24920662
2.  LOT: a tool for linkage analysis of ordinal traits for pedigree data 
Bioinformatics  2008;24(15):1737-1739.
Summary: Existing linkage-analysis methods address binary or quantitative traits. However, many complex diseases and human conditions, particularly behavioral disorders, are rated on ordinal scales. Herein, we introduce, LOT, a tool that performs linkage analysis of ordinal traits for pedigree data. It implements a latent-variable proportional-odds logistic model that relates inheritance patterns to the distribution of the ordinal trait. The likelihood-ratio test is used for testing evidence of linkage.
Availability: The LOT program is available for download at http://c2s2.yale.edu/software/LOT/
Contact: heping.zhang@yale.edu
doi:10.1093/bioinformatics/btn258
PMCID: PMC2566542  PMID: 18535081
3.  LOT 
Bioinformatics (Oxford, England)  2008;24(15):1737-1739.
Summary
Existing linkage-analysis methods address binary or quantitative traits. However, many complex diseases and human conditions, particularly behavioral disorders, are rated on ordinal scales. Herein, we introduce, LOT, a tool that performs linkage analysis of ordinal traits for pedigree data. It implements a latent-variable proportional-odds logistic model that relates inheritance patterns to the distribution of the ordinal trait. The likelihood-ratio test is used for testing evidence of linkage.
doi:10.1093/bioinformatics/btn258
PMCID: PMC2566542  PMID: 18535081

Results 1-3 (3)