Compared to adults, pediatric patients with COVID-19 showed distinctive characteristics in clinical presentation and CT imaging. Pediatric patients tend to have milder clinical symptoms, fewer CT findings, and lesser extent of disease in the lungs. Moreover, peribronchial distribution and bronchial wall thickening, less frequent findings in the adult population with COVID-19, were more commonly seen in pediatric patients. Key Points: 1. Fever was less prevalent in pediatric patients than in adults (6/14, 42.9% vs 39/47, 83%; p = 0.008). 2. Compared with adults, pediatric patients had a lower rate of positive CT findings and milder clinical grade (p = 0.004, p = 0.001 respectively). 3. CT features did not differ in two groups, except for bronchial wall thickening, which was more common in pediatric patients (p =0.048).

BackgroundMicroRNAs (miRNAs) can act as oncogenes or tumor suppressors by controlling cell proliferation, differentiation, metastasis and apoptosis, and miRNA dysregulation is involved in the development of pancreatic cancer (PC). Our previous study demonstrated that Gabra3 plays critical roles in cancer progression. However, whether Gabra3 is regulated by miRNAs in PC remains unknown.MethodsThe expression levels of miR-92b-3p and Gabra3 were measured by quantitative PCR (qPCR), immunoblotting, in situ hybridization (ISH) and immunohistochemistry (IHC). The proliferation rate of PC cells was detected by MTS assay. Wound-healing and transwell assays were used to examine the invasive abilities of PC cells. Dual-luciferase reporter assays were used to determine how miR-92b-3p regulates Gabra3. Xenograft mouse models were used to assess the role of miR-92b-3p in PC tumor formation in vivo.ResultsHere, we provide evidence that miR-92b-3p acted as a tumor suppressor in PC by regulating Gabra3 expression. MiR-92b-3p expression levels were lower in PC tissues than corresponding noncancerous pancreatic (CNP) tissues and were associated with a poor prognosis in PC patients. MiR-92b-3p overexpression suppressed the proliferation and invasion of PC cells in both in vivo and in vitro models. Conversely, miR-92b-3p knockdown induced an aggressive phenotype in PC cells. Mechanistically, miR-92b-3p overexpression suppressed Gabra3 expression, which then led to the inactivation of important oncogenic pathways, including the AKT/mTOR and JNK pathways.ConclusionOur results suggest that miR-92b-3p acted as a tumor suppressor by targeting Gabra3-associated oncogenic pathways; these results provide novel insight into future treatments for PC patients.Electronic supplementary materialThe online version of this article (10.1186/s12943-017-0723-7) contains supplementary material, which is available to authorized users.

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