Previous studies suggest that COVID-19 is more likely to infect older adult men, particularly those with chronic comorbidities. [2][3][4] Few infections in children have been reported. We identified all infected infants in China and described demographic, epidemiologic, and clinical features.Methods | For this retrospective study, we identified all hospitalized infants diagnosed with COVID-19 infection between December 8, 2019, and February 6, 2020, in China. The summary number and geographic location of new COVID-19 infections, released daily by the central government, were screened to identify infants (aged 28 days to 1 year). Demographic information, including age, sex, and geographic location, released anonymously by local health departments, were then retrieved and local hospitals and the Centers for Disease Control and Prevention were contacted for demographic data, family clustering (≥1 infected family member residing with the infant), linkage to Wuhan (residing in or visiting Wuhan or contact with visitors from Wuhan ≤2 weeks before the onset of infection), clinical features (symptoms at admission, dates of admission and diagnosis), treatment (intensive care unit or mechanical ventilation), prognosis (any severe complica-

It has been recognized that cancer is not merely a disease of tumor cells, but a disease of imbalance, in which stromal cells and tumor microenvironment play crucial roles. Extracellular matrix (ECM) as the most abundant component in tumor microenvironment can regulate tumor cell behaviors and tissue tension homeostasis. Collagen constitutes the scaffold of tumor microenvironment and affects tumor microenvironment such that it regulates ECM remodeling by collagen degradation and re-deposition, and promotes tumor infiltration, angiogenesis, invasion and migration. While collagen was traditionally regarded as a passive barrier to resist tumor cells, it is now evident that collagen is also actively involved in promoting tumor progression. Collagen changes in tumor microenvironment release biomechanical signals, which are sensed by both tumor cells and stromal cells, trigger a cascade of biological events. In this work, we discuss how collagen can be a double-edged sword in tumor progression, both inhibiting and promoting tumor progression at different stages of cancer development.

Background Emerging evidence supports the pivotal roles of adipocytes in breast cancer progression. Tumour induced beige/brown adipose tissue differentiation contributes to the hypermetabolic state of the breast cancer. However, the mediators and mechanisms remain unclear. Methods Survival probabilities were estimated using the Kaplan–Meier method based on immunohistochemistry results. Biochemical studies were performed to characterize the novel interrelation between breast cancer cells and adipocytes. Results We show that tumour-surrounding adipocytes exhibit an altered phenotype in terms of upregulated beige/brown characteristics and increased catabolism associated with an activated state characterized by the release of metabolites, including free fatty acids, pyruvate, lactate and ketone bodies. Likewise, tumour cells cocultivated with mature adipocytes exhibit metabolic adaptation and an aggressive phenotype in vitro and in vivo. Mechanistically, we show that tumour cells induce beige/brown differentiation and remodel metabolism in resident adipocytes by exosomes from the co-culture system that carry high levels of miRNA-144 and miRNA-126. miRNA-144 promotes beige/brown adipocyte characteristics by downregulating the MAP3K8/ERK1/2/PPARγ axis, and exosomal miRNA-126 remodels metabolism by disrupting IRS/Glut-4 signalling, activating the AMPK/autophagy pathway and stabilizing HIF1α expression in imminent adipocytes. In vivo inhibition of miRNA-144 or miRNA-126 decreases adipocyte–induced tumour growth. Conclusions These results demonstrate that by inducing beige/brown differentiation and enhancing catabolism in recipient adipocytes, exosomal miRNA-144 and miRNA-126 from the tumour-adipocyte interaction reprogram systemic energy metabolism to facilitate tumour progression. Electronic supplementary material The online version of this article (10.1186/s13046-019-1210-3) contains supplementary material, which is available to authorized users.

Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) has been demonstrated as an important regulator in diverse human cancers. However, its function and regulatory mechanism in ischemic stroke remains largely unknown. Here, we report that MEG3 is physically associated with microRNA-21 (miR-21), while miR-21 is downregulated following ischemia in the ischemic core in vitro and in vivo, which is opposite to MEG3. Besides, overexpression of miR-21 protects oxygen–glucose deprivation and reoxygenation (OGD/R)-induced apoptotic cell death. Furthermore, MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with programmed cell death 4 (PDCD4) mRNA for directly binding to miR-21, which mediates ischemic neuronal death. Knockdown of MEG3 protects against ischemic damage and improves overall neurological functions in vivo. Thus, our data uncovers a novel mechanism of lncRNA MEG3 as a ceRNA by targeting miR-21/PDCD4 signaling pathway in regulating ischemic neuronal death, which may help develop new strategies for the therapeutic interventions in cerebral ischemic stroke.

AimsAn ongoing outbreak of 2019 novel coronavirus (SARS-CoV-2) diseases (COVID-19) has been spreading in multiple countries. One of the reasons for the rapid spread is that the virus can be transmitted from infected individuals without symptoms. Revealing the pathological features of early phase COVID-19 pneumonia is important to the understanding of its pathogenesis. The aim of this study was to explore pulmonary pathology of early phase COVID-19 pneumonia in a patient with a benign lung lesion. Methods and resultsWe analyzed the pathological changes of lung tissue from a 55-year-old female patient with early phase SARS-CoV-2 infection. In this case, right lower lobectomy was performed for a benign pulmonary nodule. Detailed clinical, laboratory and radiological data were also described. This case was confirmed to have preoperative SARS-CoV-2 infection by real-time RT-PCR and RNA in situ hybridization on surgically removed lung tissues. Histologically, COVID-19 pneumonia was characterized by exudative inflammation. The closer to the visceral pleura, the more severe the exudation of monocytes and lymphocytes. Perivascular inflammatory infiltration, intraalveolar multinucleated giant cells, pneumocyte hyperplasia and intracytoplasmic viral-like inclusion bodies were seen. However, fibrinous exudate and hyaline membrane formation, which were typical pulmonary features of SARS pneumonia, were not evident in this case. Immunohistochemical staining results showed that an abnormal accumulation of CD4+ helper T lymphocytes and CD163+ M2 macrophages in the lung tissue. Accepted ArticleThis article is protected by copyright. All rights reserved ConclusionThe results highlighted the pulmonary pathological changes of early phase SARS-CoV-2 infection and suggested a role of immune dysfunction in the pathogenesis of COVID-19 pneumonia.