INTRODUCTION: Although mandibular repositioning devices were found to be very effective for treating obstructive sleep apnea (OSAS), they can cause side effects such as temporomandibular joint disorder and occlusal deviation. A semi-rigid device with a low frequency of side effects, the Silensor,(Erkodent Gmbh, Tuttlingen, Germany) was reported previously. The purpose of this study is to determine whether the Silensor is effective for treating OSAS. MATERIALS AND METHODS: Thirty-five OSAS patients (27 males and 8 females) who were treated with the Silensor were enrolled in this study. The mean age and body mass index of the patients were 52.2 years (23-72 years) and 24.5 kg/m(2)(19.3-31.6 kg/m(2)), respectively. The patients were classified into two groups based on the length of the apparatus connector: 0-2 or 3-4 mm. A polysomnography test was performed twice, at the first visit and after the improvement of subjective symptoms. These data were statistically analyzed using the Wilcoxon signed-rank test. RESULTS: The apnea-hypopnea index significantly improved in all OSAS patients, the mild to moderate OSAS patients, severe OSAS patients, 0- to 2-mm group, and the 3- to 4-mm group (91.4 %; p < 0.01, 88.9 %; p < 0.01, 100 %; p < 0.05, 86.4 %; p < 0.01, 100 %; p < 0.01, respectively). The only side effects of the Silensor were broken apparatus and damage to the buccal mucosa. DISCUSSION: The Silensor is useful for the treatment of OSAS. In particular, the Silensor is suitable for the first phase of OSAS treatment with oral appliances because the efficacy of the Silensor was equal to that of other oral appliances and had few side effects.

The evolution of multicellular metazoans from a unicellular ancestor is one of the most important advances in the history of life. Protein tyrosine kinases play important roles in cell-to-cell communication, cell adhesion, and differentiation in metazoans; thus, elucidating their origins and early evolution is crucial for understanding the origin of metazoans. Although tyrosine kinases exist in choanoflagellates, few data are available about their existence in other premetazoan lineages. To unravel the origin of tyrosine kinases, we performed a genomic and polymerase chain reaction (PCR)-based survey of the genes that encode tyrosine kinases in the two described filasterean species, Capsaspora owczarzaki and Ministeria vibrans, the closest relatives to the Metazoa and Choanoflagellata clades. We present 103 tyrosine kinase-encoding genes identified in the whole genome sequence of C. owczarzaki and 15 tyrosine kinase-encoding genes cloned by PCR from M. vibrans. Through detailed phylogenetic analysis, comparison of the organizations of the protein domains, and resequencing and revision of tyrosine kinase sequences previously found in some whole genome sequences, we demonstrate that the basic repertoire of metazoan cytoplasmic tyrosine kinases was established before the divergence of filastereans from the Metazoa and Choanoflagellata clades. In contrast, the receptor tyrosine kinases diversified extensively in each of the filasterean, choanoflagellate, and metazoan clades. This difference in the divergence patterns between cytoplasmic tyrosine kinases and receptor tyrosine kinases suggests that receptor tyrosine kinases that had been used for receiving environmental cues were subsequently recruited as a communication tool between cells at the onset of metazoan multicellularity.

Angiogenin is a member of the ribonuclease superfamily that is associated with the angiogenic process. Angiogenesis is regarded as an important step to support primary and metastatic tumor growth. In cutaneous T cell lymphoma (CTCL), angiogenesis in lesional skin is increased, suggesting that interaction between tumor cells and their microvasculature are likely to occur during progression of CTCL. Patients with hematological malignancies show increased serum angiogenin levels, which are related with poor overall survival. To investigate possible roles of angiogenin in development of CTCL, we measured serum angiogenin levels in 36 patients with CTCL and 21 healthy controls by enzyme-linked immunosorbent assay. We also investigated angiogenin mRNA and protein expression in lesional skin of CTCL by quantitative RT-PCR and immunohistochemistry. Serum angiogenin levels in patients with CTCL were significantly higher than those in healthy controls. When classified with types of skin lesions, serum angiogenin levels were elevated only in erythrodermic CTCL patients. Angiogenin mRNA expression levels in lesional skin were significantly elevated in erythrodermic CTCL compared to normal skin. Immunohistochemical study revealed that angiogenin was expressed by keratinocytes, endothelial cells, and infiltrating lymphocytes in CTCL. Our results suggest that enhanced angiogenin expression may be related with a poor prognosis of erythrodermic CTCL. As angiogenin acts as an inhibitor of polymorphonuclear leukocyte degranulation, angiogenin may also be linked to impaired host defense in erythrodermic CTCL.

Background  B-cell-activating factor belonging to the tumor necrosis factor family (BAFF) is known for its role in the survival and maturation of B cells. It is recently suggested that BAFF also plays important roles in T cell activation in T-cell mediated diseases such as psoriasis. Objectives  To investigate the role of BAFF in cutaneous T cell lymphoma (CTCL). Methods  BAFF messenger RNA (mRNA) expression in skin samples (24 CTCL cases and 7 healthy controls), and in skin-derived fibroblasts (5 CTCL cases and 5 healthy controls) was examined by quantitative reverse transcription-PCR. We also performed immunohistochemical staining for BAFF and its receptors. Serum BAFF levels were measured in patients with CTCL (n = 46), atopic dermatitis (n = 36), or psoriasis (n = 27) and 27 healthy controls by enzyme-linked immunosorbent assay. Results  Lesional skin of CTCL contained higher levels of BAFF mRNA than normal skin and the expression levels correlated with disease activity. BAFF mRNA expression levels were elevated in fibroblasts from CTCL skin. Tumor cells in the lesional skin of CTCL expressed BAFF and its receptors, while fibroblasts expressed only BAFF. Serum BAFF levels of CTCL patients were significantly higher than those of healthy controls and correlated with types of skin lesions and clinical stages. They also significantly correlated with serum sIL-2R and LDH levels. Conclusions  BAFF expression in CTCL skin and serum BAFF levels are significantly increased and correlate with the severity in CTCL. These results suggest that BAFF may have important roles in the development of CTCL.

We report on the phenotypic, molecular phylogenetic and pathogenic characterization of a novel azuki bean (Vigna angularis) root-rot (BRR) pathogen from Hokkaido, Japan, which is formally described herein as Fusarium azukicola. This species can be distinguished phenotypically from the other Phaseolus/Vigna BRR and soybean sudden-death syndrome (SDS) pathogens by the production of wider and longer 4-septate conidia cultured on SNA. Molecular phylogenetic analyzes of four anonymous intergenic loci, a portion of the translation elongation factor (EF-1α) gene and the nuclear ribosomal intergenic spacer region (IGS rDNA) strongly support the genealogical exclusivity of F. azukicola with respect to the other soybean SDS and BRR pathogens within Clade 2 of the F. solani species complex (FSSC). Evolutionary relationships of F. azukicola to other members of the SDS-BRR clade, however, are unresolved by phylogenetic analyses of the individual and combined datasets, with the exception of the IGS rDNA partition, which strongly supports it as a sister to the soybean SDS pathogen F. brasiliense. A previously published multilocus genotyping assay is updated to include primer probes that successfully distinguish F. azukicola from the other soybean SDS and BRR pathogens. Results of a pathogenicity experiment reveal that the F. azukicola isolates are able to induce root-rot symptoms on azuki bean, mung bean (Vigna radiata), kidney bean (Phaseolus vulgaris) and soybean (Glycine max), as well as typical SDS foliar symptoms on soybean. Our hypothesis is that F. azukicola evolved in South America and was introduced to Hokkaido, Japan, on azuki bean, but its possible route of introduction remains unknown.

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The mode of thioether macrocyclization of peptides containing an N-terminal 2-chloroacetyl group and two or three competing cysteine residues at downstream positions has been extensively studied, leading to a strategy for designated formation of overlapping-bicyclic peptides or dumbbell-type bicyclic peptides.

Background  CC chemokine ligand (CCL) 18 is expressed by monocytes and dendritic cells (DCs), and has potent chemotactic activity for T cells, B cells and DCs. CCL18 expression is up-regulated in lesional skin of atopic dermatitis and bullous pemphigoid, suggesting its important roles in the development of these skin diseases. Objective  To investigate roles of CCL18 in cutaneous T-cell lymphoma (CTCL). Methods  The CCL18 messenger RNA (mRNA) expression in CTCL skin (n = 21) and in normal skin (n = 7) was examined by quantitative RT-PCR. CCL18 expression was also examined by immunohistochemistry. Serum CCL18 levels were measured in 38 patients with CTCL and 20 healthy controls by enzyme-linked immunosorbent assay. We also analysed correlation between serum CCL18 levels and other clinical and laboratory data. Results  The CTCL lesional skin contained higher levels of CCL18 mRNA than normal skin. CCL18 was expressed by dermal macrophages and DCs in CTCL skin. Serum CCL18 levels in patients with CTCL were significantly higher than those of healthy controls and correlated with types of skin lesions. They also significantly correlated with modified severity-weighted assessment scores, serum sIL-2R, LDH, IL-4, IL-10, IL-31, CCL17 and CCL26 levels. Patients with high serum levels of CCL18 showed significantly poor prognosis compared with those with low CCL18 levels. Conclusion  CCL18 mRNA is up-regulated in CTCL lesional skin, and serum CCL18 levels are significantly increased and correlated with the severity of CTCL. These results suggest that CCL18 may be associated with the development of CTCL.