Hsueh P-R, Asymptomatic carrier state, acute respiratory disease, and pneumonia due to severe acute respiratory syndrome coronavirus 2 (SARSCoV-2): Facts and myths, Journal of Microbiology, Immunology and Infection, https://doi.

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BackgroundLysyl oxidase-like 4 (LOXL4) has been found to be dysregulated in several human malignancies, including hepatocellular carcinoma (HCC). However, the role of LOXL4 in HCC progression remains largely unclear. In this study, we investigated the clinical significance and biological involvement of LOXL4 in the progression of HCC.MethodsLOXL4 expression was measured in HCC tissues and cell lines. Overexpression, shRNA-mediated knockdown, recombinant human LOXL4 (rhLOXL4), and deletion mutants were applied to study the function of LOXL4 in HCC. Exosomes derived from HCC cell lines were assessed for the ability to promote cancer progression in standard assays. The effects of LOXL4 on the FAK/Src pathway were examined by western blotting.ResultsLOXL4 was commonly upregulated in HCC tissues and predicted a poor prognosis. Elevated LOXL4 was associated with tumor differentiation, vascular invasion, and tumor-node-metastasis (TNM) stage. Overexpression of LOXL4 promoted, whereas knockdown of LOXL4 inhibited cell migration and invasion of HCC in vitro, and overexpressed LOXL4 promoted intrahepatic and pulmonary metastases of HCC in vivo. Most interestingly, we found that HCC-derived exosomes transferred LOXL4 between HCC cells, and intracellular but not extracellular LOXL4 promoted cell migration by activating the FAK/Src pathway dependent on its amine oxidase activity through a hydrogen peroxide-mediated mechanism. In addition, HCC-derived exosomes transferred LOXL4 to human umbilical vein endothelial cells (HUVECs) though a paracrine mechanism to promote angiogenesis.ConclusionsTaken together, our data demonstrate a novel function of LOXL4 in tumor metastasis mediated by exosomes through regulation of the FAK/Src pathway and angiogenesis in HCC.Electronic supplementary materialThe online version of this article (10.1186/s12943-019-0948-8) contains supplementary material, which is available to authorized users.

Proliferating cells often have increased glucose consumption and lactate excretion relative to the same cells in the quiescent state, a phenomenon known as the Warburg effect. Despite an increase in glycolysis, however, here we show that non-transformed mouse fibroblasts also increase oxidative phosphorylation (OXPHOS) by nearly two-fold and mitochondrial coupling efficiency by ~30% during proliferation. Both increases are supported by mitochondrial fusion. Impairing mitochondrial fusion by knocking down mitofusion-2 (Mfn2) was sufficient to attenuate proliferation, while overexpressing Mfn2 increased proliferation. Interestingly, impairing mitochondrial fusion decreased OXPHOS but did not deplete ATP levels. Instead, inhibition caused cells to transition from excreting aspartate to consuming it. Transforming fibroblasts with the Ras oncogene induced mitochondrial biogenesis, which further elevated OXPHOS. Notably, transformed fibroblasts continued to have elongated mitochondria and their proliferation remained sensitive to inhibition of Mfn2. Our results suggest that cell proliferation requires increased OXPHOS as supported by mitochondrial fusion.

One-dimensional microstructure has been regarded as one of the most desirable configurations for magnetic carbon-based microwave absorbing materials (MAMs). Herein, pea-like Fe/Fe 3 C nanoparticles embedded in nitrogen-doped carbon nanotubes (Fe/Fe 3 C@NCNTs) are successfully prepared through a direct pyrolysis of the mixture of FeCl 3 •6H 2 O and melamine under inert atmosphere. The chemical composition and microstructural feature of these Fe/ Fe 3 C@NCNTs composites are highly dependent on the pyrolysis temperature. As a result, their electromagnetic properties can be also manipulated, where dielectric loss gradually decreases with the increasing pyrolysis temperature and magnetic loss presents a reverse variation trend. When the pyrolysis temperature reaches 600 °C, the as-obtained composite, Fe/Fe 3 C@NCNTs-600 can perform a maximum reflection loss of −46.0 dB at 3.6 GHz with a thickness of 4.97 mm and a qualified bandwidth of 14.8 GHz with the integrated thickness from 1.00 to 5.00 mm. It is very interesting that the microwave absorption performance of this new kind of composites is not so susceptible to the pyrolysis temperature as those common magnetic carbon-based MAMs because there is an effective balance between dielectric loss and magnetic loss, which accounts for a very stable attenuation ability when the pyrolysis temperature range changes from 600 to 700 °C. These favorable characteristics, including low-cost raw materials, easy preparation, and stable performance, may render Fe/Fe 3 C@NCNTs composites as a novel kind of MAMs in the future.

Overall, our findings provide evidence that SPON2 is a critical factor in mediating the immune response against tumor cell growth and migration in HCC. PrecisMatricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signalling events to perform dual functions in HCC microenvironment.

Helicobacter pylori has developed several mechanisms to evade the intracellular killing after phagocytosis. In this study, we reported that some Taiwanese clinical isolated H. pylori can multiply in human monocytic cells, such as THP-1 or U937 cells, but not in murine macrophage Raw264.7 cells. After internalization, there was a 5- to 10-fold increment of re-cultivable H. pylori from the infected THP-1 cells at 12 hrs post infection. The dividing H. pylori was found in a double-layer vesicle, which is characteristic of autophagosome. The formation of autophagosomes is associated with the multiplication of H. pylori in THP-1 cells. Its modulation with rapamycin or 3-MA affects the level of H. pylori replication. Furthermore, the VacA or CagA mutants of H. pylori have lower levels of multiplication in macrophages. We conclude that H. pylori infection induces autophagosome formation, and these autophagic vesicles were adapted for the multiplication of H. pylori in the host.