Risk of Mycoplasma pneumoniae-related hepatitis in MP pneumonia pediatric patients: a predictive model construction and assessment.

BACKGROUND: A predictive model for risk of Mycoplasma pneumoniae (MP)-related hepatitis in MP pneumonia pediatric patients can improve treatment selection and therapeutic effect. However, currently, no predictive model is available. METHODS: Three hundred seventy-four pneumonia pediatric patients with/without serologically-confirmed MP infection and ninety-three health controls were enrolled. Logistic regressions were performed to identify the determinant variables and develop predictive model. Predictive performance and optimal diagnostic threshold were evaluated using area under the receiver operating characteristic curve (AUROC). Stratification analysis by age and MP-IgM titer was used to optimize model's clinical utility. An external validation set, including 84 MP pneumonia pediatric patients, was used to verify the predictive efficiency. After univariate analysis to screen significant variables, monocyte count (MO), erythrocyte distribution width (RDW) and platelet count (PLT) were identified as independent predictors in multivariate analysis. RESULTS: We constructed MRP model: MO [^109/L] × 4 + RDW [%] - PLT [^109/L] × 0.01. MRP achieved an AUROC of 0.754 and the sensitivity and specificity at cut-off value 10.44 were 71.72 and 61.00 %, respectively in predicting MP-related hepatitis from MP pneumonia. These results were verified by the external validation set, whereas it merely achieved an AUROC of 0.540 in pneumonia without MP infection. The AUROC of MRP was 0.812 and 0.787 in infants and toddlers (0-36 months) and low MP-IgM titer subgroup (1:160-1:320), respectively. It can achieve an AUROC of 0.804 in infants and toddler with low MP-IgM titer subgroup. CONCLUSIONS: MRP is an effective predictive model for risk of MP-related hepatitis in MP pneumonia pediatric patients, especially infants and toddlers with low MP-IgM titer.

lncRNA FBXL19-AS1 is a diagnosis biomarker for paediatric patients with acute myeloid leukemia.

BACKGROUND: Long non-coding RNAs (lncRNA) have emerged as novel clinical biomarkers and therapeutic targets for various tumors because of their disease- and stage-restricted expression. lncRNA FBXL19 antisense RNA 1 (FBXL19-AS1) expression has been confirmed to be up-regulated in several tumors. However, its expression and effects in paediatric acute myeloid leukemia (AML) have not been elucidated. METHODS: Serum FBXL19-AS1 expression was determined in 137 AML patients compared to 43 healthy controls ( < 0.01). RESULTS: Using receiver operating characteristic curve analysis, we observed that serum FBXL19-AS1 provided the highly diagnostic performance for the detection of AML (AUC = 0.841, < 0.001). We also examined the association between serum FBXL19-AS1 expression and clinicopathological factors, finding that its high expression was associated with French-American-British classification ( = 0.011) and cytogenetics ( = 0.021). Survival assays with the Kaplan-Meier method revealed that the overall survival ( = 0.0088) and disease-free-survival ( = 0.0027) of AML patients with high serum FBXL19-AS1 levels were distinctly shorter compared to those with low serum FBXL19-AS1 levels. More importantly, Multivariate analysis identified serum FBXL19-AS1 overexpression as an independent unfavorable prognostic factor for both overall survival and disease-free-survival of AML patients. CONCLUSIONS: Overall, our findings revealed that high expression of serum FBXL19-AS1 might be useful as a novel prognostic and diagnostic biomarker for AML patients.

RBM5 inhibits tumorigenesis of gliomas through inhibition of Wnt/ß-catenin signaling and induction of apoptosis.

BACKGROUND: Gliomas are one of the most common malignant brain tumors and bring a big threat to human life as traditional therapy is unsatisfactory. RBM5 was a RNA-binding motif protein and was reported as a tumor suppressor. But the role of RBM5 in gliomas was unknown. METHODS: The mRNA level of RBM5 was determined in gliomas tissues and cell lines by real-time quantitative PCR (qRT-PCR) assay while the association of RBM5 expression with prognosis was analyzed by Kaplan-Meier method and compared by log-rank test. Lentivirus was used to overexpress RBM5 in gliomas cells. MTT and BrdU incorporation assay were used to determine cell proliferation and DNA synthesis when the ability of cell migration and invasion was analyzed by transwell assay with/without Matrigel. Cell apoptosis rate was determined with fluorescence-activated cell sorting (FACS) method. Then, expression of apoptosis molecules and critical members in Wnt/ß-catenin pathway were detected by western blot analysis. RESULTS: RBM5 was shown to be downregulated in gliomas tissues and gliomas cell lines. And decreased RBM5 expression was clinically correlated with tumor stage, patient age, and poor prognosis of gliomas patients. The proliferation and DNA synthesis was dramatically inhibited when RBM5 was overexpressed in SHG44 or U251 cells. Also, the ability of cell migration and invasion was disrupted. Then, the level of ß-catenin and Cyclin D1 significantly decreased when DKK1 and P-GSK-3ß increased reversely in SHG44 cells, which suggested that RBM5 inhibited canonical Wnt/ß-catenin signaling. Meanwhile, we demonstrated that caspase3-mediated apoptotic pathway was activated by RBM5 as Bax, TNF-α, and cleaved caspase3 were greatly upregulated while antiapoptotic molecule Bcl-2 was downregulated. Additionally, that apoptotic rate increased significantly from less than 1 to 32% in RBM5-overexpressed SHG44 cells further supported the pro-apoptosis role of RBM5 in gliomas cells. CONCLUSIONS: RBM5 plays a suppressor role in human gliomas by inhibiting Wnt/ß-catenin signaling and inducing cell apoptosis. This study improves our knowledge about the carcinogenesis and progression of human gliomas, which would greatly contribute to the therapy for gliomas patients.