BackgroundAlthough joint involvement is the second most common clinical manifestation after skin involvement in patients with Henoch-Schönlein purpura (HSP), it has not been well characterized. The aim of this study was to profile the clinical characteristics and identify the potential risk factors for kidney damage in HSP patients having joint involvement.MethodsWe retrospectively reviewed 71 cases of HSP patients with joint involvement who attended our hospital between January 2010 and March 2012 and analyzed their epidemiological profile, clinical characteristics, follow-up findings (up to three years) and overall prognosis. Logistic regression analysis was performed to identify risk factors associated with renal symptoms in HSP patients with joint involvement.ResultsAverage age of patients was 8.55 ± 2.13 years with male to female ratio at 1.29:1. The peak age of disease onset was six to 11 years. The most common triggers included upper respiratory infection, vigorous physical activity, and autumn and winter seasons. Forty cases (56.35 %) had gastrointestinal involvement and 37 (52.11 %) had kidney damage; gastrointestinal system, scrotal involvement, and increased D-dimer levels were significantly associated with kidney injury (P < 0.05) by multivariate analysis. Glucocorticoid therapy was effective in alleviating symptoms.ConclusionGastrointestinal symptoms, scrotal involvement, and increased D-dimer are the potential risk factors for kidney damage in HSP patients having joint involvement. Rational use of corticosteroids was probably responsible for the good clinical outcomes.

Context: Our previous study demonstrated that tetrandrine (TET) could reverse the resistance of Candida albicans to fluconazole. Objective: The aim of this study was to investigate the molecular mechanism underlying this action. Materials and methods: Real-time reverse transcription polymerase chain reaction (real-time RT-PCR) was performed to compare the expression levels of the drug resistance genes CDR1, CDR2, MDR1, FLU1 and ERG11 in fluconazole-sensitive CA-3 and resistant CA-16 cells that were either treated with FLC and/or TET or left as untreated controls. In addition, intracellular ATP levels were measured using an ATP assay kit, and the expression level of the energy metabolism gene ADH1 was measured by real-time RT-PCR. Results: Compared with FLC/TET-free conditions, FLC þ TET treatment strains showed statistically different (p50.05) expression of CDR1 and CDR2 (increased in the FLC-sensitive strains, while decreased in the FLC-resistant strains), MDR1 (increased in the FLC-resistant strains), FLU1 and ERG11 (increased in the FLC-sensitive strains), ADH1 (decreased in both the FLC-sensitive and the FLC-resistant strains). And also, the FLC þ TET treatment decreased the intracellular ATP levels in both the FLC-sensitive and the FLC-resistant strains (p50.05). Discussion and conclusion: These results suggest that changes in the expression levels of the drug resistance genes CDR1 and CDR2, the cellular ATP supply and the expression level of the energy metabolism gene ADH1 contribute to the TET-mediated reversal of the fluconazole resistance of C. albicans.

In the present study, we aimed to investigate immune-related signatures and immune infiltration in melanoma. The transcriptome profiling and clinical data of melanoma were downloaded from The Cancer Genome Atlas database, and their matched normal samples were obtained from the Genotype-Tissue Expression database. After merging the genome expression data using Perl, the limma package was used for data normalization. We screened the differentially expressed genes (DEGs) and obtained immune signatures associated with melanoma by an immune-related signature list from the InnateDB database. Univariate Cox regression analysis was used to identify potential prognostic immune genes, and LASSO analysis was used to identify the hub genes. Next, based on the results of multivariate Cox regression analysis, we constructed a risk model for melanoma. We investigated the correlation between risk score and clinical characteristics and overall survival (OS) of patients. Based on the TIMER database, the association between selected immune signatures and immune cell distribution was evaluated. Next, the Wilcoxon rank-sum test was performed using CIBERSORT, which confirmed the differential distribution of immune-infiltrating cells between different risk groups. We obtained a list of 91 differentially expressed immune-related signatures. Functional enrichment analysis indicated that these immune-related DEGs participated in several areas of immune-related crosstalk, including cytokine-cytokine receptor interactions, JAK–STAT signaling pathway, chemokine signaling pathway, and Th17 cell differentiation pathway. A risk model was established based on multivariate Cox analysis results, and Kaplan-Meier analysis was performed. The Kruskal-Wallis test suggested that a high risk score indicated a poorer OS and correlated with higher American Joint Committee on Cancer-TNM (AJCC-TNM) stages and advanced pathological stages ( P < 0.01 ). Furthermore, the association between hub immune signatures and immune cell distribution was evaluated in specific tumor samples. The Wilcoxon rank-sum test was used to estimate immune infiltration density in the two groups, and results showed that the high-risk group exhibited a lower infiltration density, and the dominant immune cells included M0 macrophages ( P = 0.023 ) and activated mast cells ( P = 0.005 ).

Candida albicans, a human fungal pathogen, is able to tolerate certain levels of environmental stresses. Its cell wall plays an important role in cellular homeostasis, responding to environmental stimuli. SRB1 gene encodes a GDP-mannose pyrophosphorylase that catalyzes the formation of the major cell wall component, mannan. The exact relationship between SRB1 and various stresses is not yet fully understood. In current study, C. albicans SC5314 cells were exposed to oxidative, hyperosmotic, and thermal stresses. The expression of SRB1 and related stress response genes, HOG1, CAP1, MKC1, and HSP90, was systematically evaluated in cells exposed to various levels of stress. In addition, the apoptosis and ultrastructural changes of the cells were examined. We found that the expression of SRB1 and related stress response genes significantly increased under oxidative, hyperosmotic, and thermal stresses, and the increased gene expression was correlated with higher percentages of apoptosis and ultrastructural changes in C. albicans cells. We propose that protein glycosylation is associated with stress response that involves SRB1 in C. albicans. Further in-depth studies of SRB1 function should aid our understanding of C. albicans pathogenesis, and provide important clues about the development of novel antifungal compounds for drug resistant C. albicans.