Whole-body MRI of juvenile spondyloarthritis: protocols and pictorial review of characteristic patterns.

Spondyloarthritides are a group of inflammatory rheumatological diseases that cause arthritis with a predilection for spinal or sacroiliac involvement in addition to a high association with HLA-B27. Juvenile spondyloarthritis is distinct from adult spondyloarthritis and manifests more frequently as peripheral arthritis and enthesitis. Consequently juvenile spondyloarthritis is often referred to as enthesitis-related arthritis (ERA) subtype under the juvenile idiopathic arthritis (JIA) classification criteria.

Toxicity and outcome of children with treatment related acute myeloid leukemia.

Background: The aim of this study was to evaluate the clinical course and outcome of children with treatment related acute myeloid leukemia (tAML) and compare them to children with primary AML (pAML).

Procedure: We retrospectively reviewed the demographic, treatment, toxicity, and outcome data of children with tAML and treatment related myelodysplastic syndrome (tMDS), treated at our institution between 1975 and 2005. We compared these parameters with matched controlled children with pAML.

Epigenetic basis for the transcriptional hyporesponsiveness of the human inducible nitric oxide synthase gene in vascular endothelial cells.

A marked difference exists in the inducibility of inducible NO synthase (iNOS) between humans and rodents. Although important cis and trans factors in the murine and human iNOS promoters have been characterized using episomal-based approaches, a compelling molecular explanation for why human iNOS is resistant to induction has not been reported. In this study we present evidence that the hyporesponsiveness of the human iNOS promoter is based in part on epigenetic silencing, specifically hypermethylation of CpG dinucleotides and histone H3 lysine 9 methylation.

The expression of endothelial nitric-oxide synthase is controlled by a cell-specific histone code.

Expression of endothelial nitric-oxide synthase (eNOS) mRNA is highly restricted to the endothelial cell layer of medium to large sized arterial blood vessels. Here we assessed the chromatin environment of the eNOS gene in expressing and nonexpressing cell types. Within endothelial cells, but not a variety of nonendothelial cells, the nucleosomes that encompassed the eNOS core promoter and proximal downstream coding regions were highly enriched in acetylated histones H3 and H4 and methylated lysine 4 of histone H3.

Nitric oxide reduces bacterial superantigen-immune cell activation and consequent epithelial abnormalities.

Inhibition of the inducible form of nitric oxide (NO) synthase prolonged the murine enteropathy evoked by the bacterial superantigen, Staphylococcus aureus enterotoxin B (SEB). We examined the ability of NO to alleviate SEB-induced epithelial dysfunction and immune cell activation. Human peripheral blood mononuclear cells (PBMC) were activated by SEB for 24 h +/- the NO donors, S-nitroso-N-acetylpenicillamine and spermine-NONOate.