Kadom N.,Boston University |
Rosman N.P.,Boston University |
Jubouri S.,Childrens National Medical Center |
Trofimova A.,Childrens National Medical Center |
And 2 more authors.
Pediatric Radiology | Year: 2015
Background: Horner syndrome in children is rare. The frequency and spectrum of malignancy as the cause of Horner syndrome in children remains unclear. Also unclear is whether the imaging work-up should include the entire oculo-sympathetic pathway or should be more targeted. In addition, the value of cross-sectional angiographic imaging in Horner syndrome is uncertain. Objective: To review imaging pathology in a cohort of children with Horner syndrome at a major academic pediatric medical center. Materials and methods: We reviewed a 22-year period of CT and MR imaging studies in children with a clinical diagnosis of Horner syndrome referred for imaging. Results: We found 38 patients who fulfilled study criteria of Horner syndrome and 6/38 had relevant imaging findings: 2/6 etiologies were neoplastic (congenital neuroblastoma and central astrocytoma), 1/6 had a vascular abnormality (hypoplastic carotid artery), 1/6 had maldevelopment (Chiari I malformation), and 2/6 had inflammatory/traumatic etiology (viral cervical lymphadenopathy, post jugular vein cannulation). There was a similar number of congenital and acquired pathologies. The malignancies were found at any level of the oculosympathetic pathway. Conclusion: There are treatable causes, including malignancies, in children presenting with Horner syndrome, which justify imaging work-up of the entire oculosympathetic pathway, unless the lesion level can be determined clinically. © 2015, Springer-Verlag Berlin Heidelberg. Source
Wolf L.,Yeshiva University |
Gao C.S.,National Eye Institute NEI |
Gueta K.,Tel Aviv University |
Xie Q.,Yeshiva University |
And 11 more authors.
G3: Genes, Genomes, Genetics | Year: 2013
MicroRNAs (miRNAs) and fibroblast growth factor (FGF) signaling regulate a wide range of cellular functions, including cell specification, proliferation,migration, differentiation, and survival. In lens, both these systems control lens fiber cell differentiation; however, a possible link between these processes remains to be examined. Herein, the functional requirement for miRNAs in differentiating lens fiber cells was demonstrated via conditional inactivation of Dicer1 in mouse (Mus musculus) lens. To dissect the miRNAdependent pathways during lens differentiation, we used a rat (Rattus norvegicus) lens epithelial explant system, induced by FGF2 to differentiate, followed by mRNA and miRNA expression profiling. Transcriptome and miRNome analysis identified extensive FGF2-regulated cellular responses that were both independent and dependent on miRNAs. We identified 131 FGF2-regulated miRNAs. Seventy-six of these miRNAs had at least two in silico predicted and inversely regulated target mRNAs. Genes modulated by the greatest number of FGF-regulated miRNAs include DNA-binding transcription factors Nfib, Nfat5/OREBP, c-Maf, Ets1, and NMyc. Activated FGF signaling influenced bone morphogenetic factor/transforming growth factor-b, Notch, and Wnt signaling cascades implicated earlier in lens differentiation. Specific miRNA:mRNA interaction networks were predicted for c-Maf, N-Myc, and Nfib (DNA-binding transcription factors); Cnot6, Cpsf6, Dicer1, and Tnrc6b (RNA to miRNA processing); and Ash1l, Med1/PBP, and Kdm5b/Jarid1b/Plu1 (chromatin remodeling). Three miRNAs, including miR-143, miR-155, and miR-301a, down-regulated expression of c-Maf in the 39-UTR luciferase reporter assays. These present studies demonstrate for the first time global impact of activated FGF signaling in lens cell culture system and predicted novel gene regulatory networks connected by multiple miRNAs that regulate lens differentiation. © 2013 Wolf et al. Source
Wang R.-X.,National Eye Institute NEI |
Wang R.-X.,Chinese Institute of Basic Medical Sciences |
Yu C.-R.,National Eye Institute NEI |
Dambuza I.M.,National Eye Institute NEI |
And 6 more authors.
Nature Medicine | Year: 2014
Interleukin-10 (IL-10)-producing regulatory B (B reg) cells suppress autoimmune disease, and increased numbers of B reg cells prevent host defense to infection and promote tumor growth and metastasis by converting resting CD4 + T cells to regulatory T (T reg) cells. The mechanisms mediating the induction and development of B reg cells remain unclear. Here we show that IL-35 induces B reg cells and promotes their conversion to a B reg subset that produces IL-35 as well as IL-10. Treatment of mice with IL-35 conferred protection from experimental autoimmune uveitis (EAU), and mice lacking IL-35 (p35 knockout (KO) mice) or defective in IL-35 signaling (IL-12Rβ 22 KO mice) produced less B reg cells endogenously or after treatment with IL-35 and developed severe uveitis. Adoptive transfer of B reg cells induced by recombinant IL-35 suppressed EAU when transferred to mice with established disease, inhibiting pathogenic T helper type 17 (T H 17) and T H 1 cells while promoting T reg cell expansion. In B cells, IL-35 activates STAT1 and STAT3 through the IL-35 receptor comprising the IL-12Rβ 22 and IL-27Rβ± subunits. As IL-35 also induced the conversion of human B cells into B reg cells, these findings suggest that IL-35 may be used to induce autologous B reg and IL-35 + B reg cells and treat autoimmune and inflammatory disease. © 2014 Nature America, Inc. All rights reserved. Source