First laboratory-confirmed case of scrub typhus in Shijiazhuang City, Hebei Province.

Objective: Defining whether a suspected case was due to scrub typhus through laboratory testing, to understand the prevalence of scrub typhus in Shijiazhuang City, Hebei Province. Methods: An epidemiological investigation was conducted on the suspected case, utilizing Weil-Felix test and indirect immunofluorescence assay (IFA) to detect specific antibodies against O. tsutsugamushi in serum specimens. Additionally, PCR amplification of the 56-kDa and groEL genes was performed, followed by constructing a phylogenetic tree to identify the genotype. Results: The acute phase titer of the Weil-Felix test for the case was 1:160, which increased to 1:320 in the recovery phase. IFA assay revealed IgG titers against O. tsutsugamushi of 1:64 in the acute phase and 1:256 in the recovery phase. Sequence alignment of the PCR amplified fragment showed the highest similarity with the O. tsutsugamushi genotype. Kawasaki sequence, ranging from 99.71 to 100.00%. The strain exhibited the closest genetic relationship with the known O. tsutsugamushi Kawasaki genotype. Conclusion: This study confirms the presence of O. tsutsugamushi in Shijiazhuang City, Hebei Province, with the identified strain belonging to the Kawasaki genotype, marking the first diagnosis of this strain in the region.

Effect of Azelaic Acid on Psoriasis Progression Investigated Based on Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway.

Objective: To probe into the effect of azelaic acid on psoriasis based on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Methods: Psoriasis gene expression data were downloaded from the GEO database for differential expression analysis to identify differentially expressed genes (DEGs). KEGG and GSEA analyses were performed to identify important signaling pathways that may be involved in psoriasis progression for subsequent validation. Thirty-six C57BL/6 mice aged 8 weeks old were randomly assigned into the blank control group (n = 9), negative control group (n = 9), psoriasis model group (n = 9), and azelaic acid treat group (n = 9). Mice models of psoriasis were prepared with imiquimod (IMQ) in the latter two groups, and azelaic acid ointment was applied in azelaic acid treat group. Then, hematoxylin-eosin (HE) staining was carried out to detect the effect of azelaic acid on the pathological damage of mice models of psoriasis in each group. HaCaT cells cultured in vitro were divided into blank control group, negative control group (addition of azelaic acid), IL-17 group (20 ng/mL) and IL-17+azelaic acid group, with 3 replicates for each group. Immunofluorescence assay and Western blotting were used to detect the protein expression of PI3K/AKT signaling pathway related molecules. Results: KEGG analysis showed that DEGs were significantly enriched in PI3K-AKT signaling pathway. GSEA analysis showed that PI3K and MTOR signaling pathways were up-regulated in psoriasis, while AUTOPHAGY signaling pathway was down-regulated. HE staining showed that azelaic acid could significantly inhibit the local skin injury in mice caused by IMQ-induced psoriasis. Moreover, azelaic acid can inhibit the expression of PI3K/AKT signaling pathway related proteins phosphorylated (p)-PI3K, p-AKT, p-mammalian target of rapamycin (mTOR), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), angiogenin-1 and hypoxia-inducible factor-1α (HIF-1α). These results imply that azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis. Conclusion: Azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis.

The protection of NF-κB inhibition on kidney injury of systemic lupus erythematosus mice may be correlated with lncRNA TUG1.

We aimed to know the effect of nuclear factor-kappa B (NF-κB) inhibition on the kidney injury of systemic lupus erythematosus (SLE) mice. Pristane-induced SLE mice were treated with pyrrolidine dithiocarbamate (PDTC, 50 or 100 mg/kg), a NF-κB inhibitor. Histopathological changes were observed by hematoxylin & eosin, Masson and periodic schiff-methenamine stainings. Long noncoding RNA Taurine upregulated gene 1 (LncRNA TUG1) was measured by real-time reverse transcription PCR, NF-κB p65 expression by western blotting, levels of inflammatory cytokines, antinuclear antibodies (ANA), and antidouble stranded DNA (anti-dsDNA) by enzyme-linked immunosorbent assay, and the deposition of IgG and C3 by immunofluorescence. The kidney of SLE mice exhibited interstitial inflammatory cell infiltration, interstitial fibrous proliferation, glomerular mesangial proliferation, and crescent formation, which was mitigated after PDTC administration. The levels of BUN, Cr, ANA, and anti-dsDNA and the pro-inflammatory factors in SLE mice were increased with obvious deposition of IgG and C3, but they were also reversed by PDTC. Furthermore, the NF-κB p65 expression in the nucleus in the SLE mice was decreased with the up-regulation of TUG1 expression and NF-κB p65 expression in the cytoplasm after PDTC treatment. Correlation analysis revealed the negative correlation between the TUG1 expression and NF-κB p65 in the nucleus in the kidney tissues. NF-κB inhibition with PDTC protected against the kidney injury of pristine-induced SLE mice possibly via up-regulating lncRNA TUG1, and further clinical studies are needed to clarify whether NF-κB inhibition may be a therapeutic modality for the kidney injury of SLE.

Clinical significance of reduced expression of lncRNA TUG1 in the peripheral blood of systemic lupus erythematosus patients.

OBJECTIVE: To investigate the expression and clinical significance of long non-coding RNA taurine up-regulated gene 1 (lncRNA TUG1) in the peripheral blood of systemic lupus erythematosus (SLE) patients. METHODS: With the peripheral blood mononuclear cells (PBMCs: T-cells, B-cells and monocytes) collected from SLE patients and healthy controls, TUG1 expression was determined to identify the correlation with the clinicopathological features of SLE patients. Thereby, the diagnostic value of TUG1 expression in diagnosis of SLE was evaluated by receiver operating characteristic (ROC) curve analysis. RESULTS: As compared to healthy controls, SLE patients manifested a lower expression of TUG1 in PBMCs, which was further decreased in SLE patients with lupus nephritis (P < .05). The lowest level of TUG1 was found in monocytes, rather than T-cells or B-cells (P < .05). Negative correlations were identified between TUG1 levels and SLE Disease Activity Index score (r = -.904, P < .001), erythrocyte sedimentation rate (r = -.779, P < .001), disease duration (r = -.503, P < .001) and 24-hour urinary protein (r = -.807, P < .001). Complement C3 levels were positively associated with TUG1 expression (r = .817, P < .001). In addition, the area under the ROC curve of diagnostic efficiency for SLE based on TUG1 was 0.982, and 0.930 for SLE with lupus nephritis. CONCLUSIONS: The levels of lncRNA TUG1 was markedly lower in the SLE patients, which was more obvious in SLE patients with lupus nephritis, and thus, it could be a promising clinical diagnostic tool for SLE patients or SLE patients with lupus nephritis.

Uncovering potential lncRNAs and nearby mRNAs in systemic lupus erythematosus from the Gene Expression Omnibus dataset.

Aim: The aim of this study was to find potential differentially expressed long noncoding RNAs (lncRNAs) and mRNAs in systemic lupus erythematosus. Materials & methods: Differentially expressed lncRNAs and mRNAs were obtained in the Gene Expression Omnibus dataset. Functional annotation of differentially expressed mRNAs was performed, followed by protein-protein interaction network analysis. Then, the interaction network of lncRNA-nearby targeted mRNA was built. Results: Several interaction pairs of lncRNA-nearby targeted mRNA including NRIR-RSAD2, RP11-153M7.5-TLR2, RP4-758J18.2-CCNL2, RP11-69E11.4-PABPC4 and RP11-496I9.1-IRF7/HRAS/PHRF1 were identified. Measles and MAPK were significantly enriched signaling pathways of differentially expressed mRNAs. Conclusion: Our study identified several differentially expressed lncRNAs and mRNAs. And their interactions may play a crucial role in the process of systemic lupus erythematosus.