Elevated IgE responses and eosinophilia observed in patients with atopic dermatitis (AD) may reflect increased responses of type 2 T-helper (Th2) cytokines with a concomitant decrease in interferon-gamma (IFN-gamma) production. However, the cross-regulation of Th1/Th2 derivation and function in AD patients are incompletely characterized. Therefore, we investigated serum levels of several cytokines [interleukin (IL)-18, IL-12, IL-10, IL-2 and IFN-gamma] in patients with AD to assess their possible relationships to the severity of disease. Serum IL-18 levels in AD patients were significantly higher than those in healthy controls [207 pg/mL; 95% confidence interval (CI), 172-242 pg/mL vs. 144 pg/mL; 95% CI, 116-178 pg/mL; P = 0.026]. Those IL-18 levels significantly correlated with eosinophil counts and serum soluble IL-2 receptor (sIL-2R) levels, and showed a tendency to correlate with clinical severity scores and serum IgE levels. IL-2 levels showed a significantly inverse correlation with serum IgE levels, and IL-12 levels clearly correlated with IL-10 levels. These results suggest the value of serum IL-18 levels as a parameter of AD activity and may support a possible role for IL-18 in the pathogenesis of AD. The inverse correlation between IgE levels and IL-2 levels suggests that IgE production may be inhibited by IL-2 in patients with AD. Furthermore, the correlation of IL-12 levels with IL-10 levels may support the previous reports that show the induction of IL-10 production by human natural killer cells and/or T cells stimulated with IL-12 in vitro.

Abstract. Epigenetic reprogramming in early preimplantation embryos, that refers to erasing and remodeling epigenetic marks such as DNA methylation, is essential for differentiation and development. In many species, paternal genome is subjected to genome-wide active demethylation before the DNA replication commences, while maternal genome maintains its methylation status until being demethylated passively during the subsequent cleavage divisions. The purpose of this manuscript was to review the available knowledge about the paternal genome active demethylation process concerning the possible mechanisms, species variation and the factors affecting the active demethylation dynamics such as in vitro protocols for production of pronuclear-stage zygotes. Better understanding the mechanisms by which the epigenetic reprogramming is occurred may contribute to clarify the biological significance of this process. Key words: Active demethylation, Epigenetics, Paternal genome, Pronuclear zygotes (J. Reprod. Dev. 55: [356][357][358][359][360] 2009) ene expression is regulated by both genetic and epigenetic mechanisms. Epigenetics includes modifications of DNA itself (methylation of cytosine in the CpG dinucleotide) and/or the associated protein (phosphorylation, acetylation and methylation of histone) [1]. These modifications can regulate the gene expression without changing the DNA consequences [2]. Each cell type in our body has its own epigenetic signature which reflects different gene expression, and subsequently results in different structure and function among genetically homogenous cells. DNA methylation is one of the most-studied epigenetic mechanisms, and it is recognized as a chief contributor to the stability of gene expression state [3]. DNA Methylation: Nature, Function and ReprogrammingDNA methylation is a process that includes transferring a methyl group from S-adenosylmethionine to C5 positions of the cytosine residues in the CpG dinucleotides by different categories of methyltransferase enzymes (Dnmt1, Dnmt1o, Dnmt2, Dnmt3a, Dnmt3b and Dnmt3L) [4,5]. The CpG dinucleotides are mainly present in a cluster called CpG islands, which are associated with genes, and mostly located in promoters and first exons [6]. These islands are defined as the initiation sites for both transcription and DNA replication, and may represent genomic footprints for replication initiation [7]. Methylation of the CpG dinucleotides in the gene promoter may repress gene expression by interfering with the access of the DNA binding proteins and subsequently blocking the transcription or by binding to the transcriptional repressor MeCP2 [4,8,9]. In spite of great correlation between gene methylation status and gene expression, it is not yet clear whether DNA methylation is the cause of or a subsequence to the transcriptional repression [10]. In an another view for the correlation between gene methylation status and its expression, methylation can increase or decrease the level of gene transcription depending on whether the methylation in...

A rapidly growing, hemorrhagic, exophytic tumor on the upper back of a 44-year-old male patient was investigated. Histological, immunohistochemical, and electron microscopic studies revealed both basal cell carcinoma-like and spindle cell sarcoma-like structures intermingled in the same tumor. Clinical consequences to this patient were mainly dependent on the sarcomatous element.