[Analysis on transmission chain of a cluster epidemic of COVID-19, Nanchang].

Objective: Based on an investigation of an outbreak of COVID-19 in Nanchang, to understand the transmission process, analyze the infectivity of the cases in incubation period and asymptomatic carrier, and evaluate the transmission risks in different exposures. Methods: Case investigation was based on the traditional epidemiological survey, combined with analysis based on big data about population movement trajectories. Transmission chain was identified to indicate transmission relationship. Results: A total of 27 cases were found in this cluster epidemic, including 25 confirmed cases, 1 suspected case (index case) and 1 asymptomatic carrier. A total of 347 close contacts were found. The secondary attack rate was 7.2% (25/347). The infection rates in close contacts of the first, second, third and fourth generation cases were 52.6% (10/19), 6.1% (13/213), 2.3% (2/88) and 0.0% (0/27), respectively. Asymptomatic carrier caused household transmission. The infection rates in close contacts after having meals, sharing rooms/beds, having work contacts, having neighbor contacts, having same time medical services or sharing wards and sharing vehicles with the patients were 10.6%(17/160), 10.0%(20/201), 5.3%(5/94), 0.0%(0/30), 0.0%(0/18) and 0.0%(0/17), respectively. Conclusions: The infection source of this cluster epidemic was a suspected case from Wuhan. Analysis based on big data about population movement trajectories can help to search the cases and close contacts accurately. The proposed epidemic prevention and control measures based on this investigation were effective.

Arresting of miR-186 and releasing of H19 by DDX43 facilitate tumorigenesis and CML progression.

Cancer-testis (CT) antigens, rarely in normal tissues except testis, are expressed in many tumor types. In recent years, DDX43 has been shown to be expressed in several malignancies. However, the role of DDX43 during tumorigenesis is not well established. In the present study, we explored the function of DDX43 in chronic myeloid leukemia (CML). We found that DDX43 overexpression in CML cell lines enhanced survival and colony formation, inhibited cell apoptosis, promoted tumorigenesis, and CML progression. In contrast, silencing of DDX43 inhibited cell survival and tumorigenesis. Upregulated H19 and downregulated miR-186 were identified in DDX43-transfected cells. Furthermore, we demonstrated that miR-186 targeted DDX43, and overexpressed miR-186 increased apoptosis and decreased cell survival. We also showed that DDX43 regulated the expression of H19 through demethylation and silencing H19 inhibited cell survival. Taken together, these results indicate that DDX43 provides critical support to the progression of CML by enhancing cell survival, colony formation, and inhibiting cell apoptosis, thereby implicating DDX43 as a potential therapeutic target in CML.

Low miR-34c expression is associated with poor outcome in de novo acute myeloid leukemia.

INTRODUCTION: MicroRNA-34c (miR-34c) has been found to play important roles in tumorigenesis. However, little is known about miR-34c expression and the impact on prognosis in acute myeloid leukemia (AML). METHODS: Real-time quantitative PCR (qRT-PCR) was performed to analyze the status of miR-34c expression in 122 patients with de novo AML and 62 normal controls. RESULTS: MiR-34c expression in AML was significantly downregulated compared to controls (P < 0.001). Receiver operating characteristic curves (ROC) indicated the distinguishing value of miR-34c for discriminating whole-cohort AML, non-M3 AML, and cytogenetically normal AML (CN-AML) patients from healthy controls. No significant differences were found between low miR-34c-expressing and high miR-34c-expressing patients in age, sex, hemoglobin, platelet count, percentage of blasts in bone marrow (BM), WHO classifications, karyotypes, and eight gene mutations, but low miR-34c cases had higher white blood cells (WBC) than high miR-34c cases (P = 0.035). MiR-34c low-expressed patients had similar rates of complete remission (CR) as miR-34c high-expressed patients in whole-cohort AML, non-M3 AML, and CN-AML patients (P = 0.347, 0.314 and 0.167, respectively). Kaplan-Meier analysis indicated that patients with low miR-34c level had markedly shorter overall survival (OS) time in whole-cohort AML, non-M3 AML, and CN-AML patients (P = 0.033, 0.024 and 0.001, respectively). Furthermore, multivariate analysis confirmed that low miR-34c expression was an independent risk factor not only in whole-cohort AML (P = 0.040) but also in non-M3 AML (P = 0.015) and CN-AML patients (P = 0.021). CONCLUSIONS: Our findings indicate that low miR-34c level is a novel promising biomarker in predicting prognosis in patients with de novo AML.