Diversity of the genus Sugiyamaella and description of two new species from rotting wood in China.

Species of the genus Sugiyamaella (Trichomonascaceae, Saccharomycetales), found in rotting wood in China, were investigated using morphology and the molecular phylogeny of a combined ITS and nrLSU dataset. Nine taxa were collected in China: two were new species (viz. Sugiyamaella chuxiong sp. nov. and S. yunanensis sp. nov.) and seven were known species, S. americana, S. ayubii, S. novakii, S. paludigena, S. valenteae, S. valdiviana and S. xiaguanensis. The two new species are illustrated and their morphology and phylogenetic relationships with other Sugiyamaella species are discussed. Our results indicate a potentially great diversity of Sugiyamaella spp. inhabiting rotting wood in China just waiting to be discovered.

Mrakia panshiensis sp. nov. a new member of the Cystofilobasidiales from soil in China, and description of the teleomorphic-stage of M. arctica.

In a study on the fungal diversity in Northeast China, twelve yeast isolates were obtained from soils collected in three provinces, Helongjiang, Jilin and Liaoning. Morphological assessment and phylogenetic analyses of the nuc rDNA internal transcribed spacer (ITS) region and the D1/D2 domains of the nuc 28S rDNA (nuc 28S) gene of the 12 cultures placed them in the genus Mrakia, namely Mrakia aquatica, Mrakia arctica, Mrakia frigida, Mrakia gelida and Mrakia robertii. A total of three isolates represented a hitherto undescribed species, which is described here as M. panshiensis sp. nov. (MB 834813). The species M. panshiensis sp. nov. shares several morphological characters with M. niccombsii, M. aquatica, M. fibulata and M. hoshinonis. These species can be distinguished based on physiological traits and pairwise rDNA sequence similarities. The study also describes for the first time the formation of teliospores by previously described M. arctica.

Interleukin-17A and -17F Gene Polymorphisms in Chinese Population with Chronic Immune Thrombocytopenia.

BACKGROUND: A case-control study was conducted to evaluate the influence of interleukin (IL)-17A and -17F gene polymorphisms on the risk of primary chronic immune thrombocytopenia (ITP). METHODS: The study included 146 Chinese chronic ITP patients and 137 healthy controls. IL-17A G197A and IL-17F A7488G polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: No significant difference in frequencies of IL-17A G197A genotypes and alleles was found between ITP patients and healthy controls, whereas frequencies of IL-17F A7488G allele A were significantly higher in ITP patients than that in healthy controls (31.85% vs. 18.98%; P<0.01). More specifically, patients with ITP had significantly higher frequencies of the IL-17F A7488G AA and AG genotypes compared with healthy controls (AA: 17.12% vs. 9.49%, P=0.02; AG: 29.46% vs. 18.98%, P=0.02). Logistic regression analysis revealed that AA and AG genotypes of IL-17F A7488G were associated with increased risk of ITP (AA: odds ratio (OR)=2.33, 95% CI 1.11-4.89; AG: OR=2.03, 95% CI 1.14-3.61). CONCLUSIONS: Our results suggest that SNPs in IL-17F A7488G but not IL-17A are associated with the development of chronic ITP in China.

Impaired nuclear translocation of glucocorticoid receptors: novel findings from psoriatic epidermal keratinocytes.

Psoriasis is a chronic proliferative skin disease and is usually treated with topical glucocorticoids, which act through the glucocorticoid receptor (GR), a component of the physiological systems essential for immune responses, differentiation, and homeostasis. To investigate the possible role of GR in the pathogenesis of psoriasis, normal and psoriatic lesional skin were recruited. Firstly, the immunolocalization of GR in the skin and cultured epidermal keratinocytes were determined by immunofluorescence. In normal skin and cultured human epidermal keratinocytes, intracellular GR is localized in the nuclei, while in psoriatic skin and cultured keratinocytes, GR is in the cytoplasm. Next, we investigated possible factors associated with the cytoplasmic distribution. We found that VEGF and IFN-γ led to impaired nuclear translocation of GR through p53 and microtubule-inhibitor, vincristine, and inhibited nuclear uptake of GR in normal keratinocytes. In addition to dexamethasone, interleukin (IL)-13 was also able to transfer GR into nuclei of psoriatic keratinocytes. Furthermore, discontinuation of dexamethasone induced cytoplasmic retention of GR in normal keratinocytes. In contrast, energy depletion of normal epidermal keratinocytes did not change the nuclear distribution of GR. To confirm our findings in vivo, an imiquimod-induced psoriasis-like skin mouse model was included. IL-13 ameliorated (but vincristine exacerbated) the skin lesions on the mouse. Taken together, our findings define that impaired nuclear translocation of GR is associated with VEGF, IFN-γ, p53, and microtubule. Therapeutic strategies designed to accumulate GR in the nucleus, such as IL-13, may be beneficial for the therapy of psoriasis.