Currently there is no effective antiviral therapy for SARS-CoV-2 infection, which frequently leads to fatal inflammatory responses and acute lung injury. Here, we discuss the various mechanisms of SARS-CoV-mediated inflammation. We also assume that SARS-CoV-2 likely shares similar inflammatory responses. Potential therapeutic tools to reduce SARS-CoV-2 -induced inflammatory responses include various methods to block FcR activation. In the absence of a proven clinical FcR blocker, the use of intravenous immunoglobulin to block FcR activation may be a viable option for the urgent treatment of pulmonary inflammation to prevent severe lung injury. Such treatment may also be combined with systemic anti-inflammatory drugs or corticosteroids. However, these strategies, as proposed here, remain to be clinically tested for effectiveness.

Liver fibrosis is a very common condition seen in millions of patients with various liver diseases, and yet no effective treatments are available owing to poorly characterized molecular pathogenesis. Here, we show that leukocyte cell-derived chemotaxin 2 (LECT2) is a functional ligand of Tie1, a poorly characterized endothelial cell (EC)-specific orphan receptor. Upon binding to Tie1, LECT2 interrupts Tie1/Tie2 heterodimerization, facilitates Tie2/Tie2 homodimerization, activates PPAR signaling, and inhibits the migration and tube formations of EC. In vivo studies showed that LECT2 overexpression inhibits portal angiogenesis, promotes sinusoid capillarization, and worsens fibrosis, whereas these changes were reversed in Lect2-KO mice. Adeno-associated viral vector serotype 9 (AAV9)-LECT2 small hairpin RNA (shRNA) treatment significantly attenuates fibrosis. Upregulation of LECT2 is associated with advanced human liver fibrosis staging. We concluded that targeting LECT2/Tie1 signaling may represent a potential therapeutic target for liver fibrosis, and serum LECT2 level may be a potential biomarker for the screening and diagnosis of liver fibrosis. (A) LECT2 inhibited the migration of EA.hy926 cell. Scale bar, 100 mm. (B) LECT2 inhibited tube formation of EA.hy926 cell. Scale bar, 200 mm. (C) Inhibition of LECT2 enhanced migration of EA.hy926 cell. Scale bar, 100 mm. (D) Inhibition of LECT2 enhanced tube formation of EA.hy926 cell. Scale bar, 200 mm. (E) LECT2 inhibited the migration of primary liver sinusoid endothelial cell (LSEC). Scale bar, 100 mm. (F) LECT2 inhibited tube formation of primary LSEC. Scale bar, 200 mm. (G) Liver tissues were immunohistochemically stained for CD31. Arrows indicate portal vessels, and arrowheads indicate capillarization of liver sinusoids. Scale bar, 200 mm. (H) The number of CD31-positive vessels surrounding the portal area was measured. (I) The CD31-positive capillarization of liver sinusoids was measured. (J) Liver tissues were immunohistochemically stained for CD31. Arrows indicate portal vessels, and arrowheads indicate capillarization of liver sinusoids. Scale bar, 200 mm. (K) The number of CD31-positive vessels surrounding the portal area was measured. (L) The CD31-positive capillarization of liver sinusoids was measured.

Evaluation of fish nutritional content information could provide essential guidance for seafood consumption and human health protection. This study investigated the lipid contents, fatty acid compositions, and nutritional qualities of 22 commercially important marine fish species from the Pearl River Estuary (PRE), South China Sea. All the analyzed species had a low to moderate lipid content (0.51-7.35% fat), with no significant differences in fatty acid profiles among fishes from different lipid categories (p > 0.05). Compared with previous studies from other regions, the examined fish species exhibited higher proportions of saturated fatty acids (SFAs, 39.1 ± 4.00%) and lower contents of polyunsaturated fatty acids (PUFAs, 21.6 ± 5.44%), presumably due to the shifted diet influence from increased diatoms and decreased dinoflagellate over the past decades in the PRE. This study further revealed that there was a significantly negative correlation between the trophic levels and levels of PUFAs in the examined species (Pearson's r =-0.42, p = 0.04), likely associated with their differed dietary composition. Considering the health benefit of PUFAs, a few marine fish in PRE with low levels of PUFAs might have no significant contribution to the cardiovascular disease prevention, although fish with different fatty acid profiles most likely contribute differently towards human health. Additional studies are needed in order to comprehensively analyze the nutritional status of fish species in the PRE.

The N-myc downstream-regulated gene 2 (NDRG2) is involved in tumor cell differentiation and apoptosis, but its function in tumor angiogenesis remains to be established. Here, we employed adenovirus overexpressing NDRG2 (Ad-NDRG2) to efficiently up-regulate target gene expression in the NDRG2-low-expressing, breast cancer cell line MCF-7. Moreover, VEGF secretion was decreased in MCF-7 cells infected by Ad-NDRG2, and medium conditioned by these infected cells could significantly inhibit the proliferation, tube formation and invasion of human umbilical vein endothelial cells (HUVECs). Further study indicated that the angiogenesis promoting factors VEGF and HIF-1α were down-regulated, whereas the angiogenesis suppressing factors p53 and VHL were up-regulated in MCF-7 cells infected by Ad-NDRG2. Finally, in a nude mouse model, intratumoral injections of Ad-NDRG2 every 3 days for 20 days significantly inhibited the growth and angiogenesis of xenografted MCF-7 tumors. In summary, these data indicate that NDRG2 may be involved in angiogenesis by impacting the expression of angiogenesis related factors. Thus, specific overexpression of NDRG2 by adenovirus represents a promising approach for the treatment of tumor angiogenesis.