Background A link between HBV and PLK1 was clearly evidenced in HBV-driven carcinogenesis, and we have also recently shown that PLK1 is a proviral factor in the early phases of HBV infection. Moreover, we have shown that BI-2536, a small molecule PLK1 inhibitor, was very efficient at inhibiting HBV DNA neosynthesis, notably by affecting nucleocapsid assembly as a result of the modulation of HBc phosphorylation. Yet, as small molecule kinase inhibitors often feature poor selectivity, a more specific and safer strategy to target PLK1 would be needed for a potential development against chronic HBV infections. Methods Here, we analysed using both freshly isolated primary human hepatocytes and differentiated HepaRG, the anti-HBV properties of an LNP-encapsulated PLK1-targeting siRNA. Standard assays were used to monitor the effect of LNP siPLK1, or controls (LNP siHBV and LNP siNon-Targeting), on HBV replication and cell viability. Results A dose as low as 100ng/mL of LNP-siPLK1 resulted in a >75% decrease in secreted HBV DNA (viral particles), which was comparable to that obtained with LNP siHBV or 10 µM of Tenofovir (TFV), without affecting cell viability. Interestingly, and in contrast to that obtained with TFV, a strong inhibition of viral RNA and HBe/HBsAg secretions was also observed under LNP siPLK1 treatment. This correlated with a significant intracellular decrease of vRNA accumulation, which was independent of any change in cccDNA levels, thus suggesting a transcriptional or post-transcriptional modulation. Such an effect was not obtained with a biochemical approach of PLK1 inhibition, suggesting an enzymatic-independent role of PLK1. Conclusions This study emphasizes that a specific PLK1 inhibition could help achieving an improved HBsAg loss in CHB patients, likely in combination with other HBsAg-targeting strategies.Since the outbreak of coronavirus disease (COVID-19) that was discovered in 2019 in Wuhan, China, no standard therapy guideline has been set despite the severity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its high infectivity. The globally pandemic outbreak suggests that COVID-19 was highly infectious and difficult to control. A dual-combination of ribavirin and interferon-α has been the widely used regimen for the treatment of this disease in China. However, due to the varying results of treatment with these drugs, a novel antiviral combination therapy is urgently needed. This case reports the usage of lopinavir/ritonavir-based combination antiviral regimen for a patient with SARS-CoV-2 infection.Stroke is a leading cause of death and disability worldwide. The purpose of this study was to investigate the possible role of the microRNA (miRNA or miR) miR-137 in ischemic stroke. miRNAs are very stable in the blood and may serve as potential diagnostic and therapeutic markers. Wild-type, Src-/- and miR-137-/- mice were treated with p38 siRNA or Erk2 siRNA to identify their roles in the inflammatory response, oxidative stress, neuronal injury and cognitive impairment in brain tissues of mice following middle cerebral artery occlusion (MCAO) operation. We evaluated several factors including; inflammatory responses, oxidative stress, viability and apoptosis of astrocytes in order to identify the functions of miR-137 and Src in ischemic stroke. miR-137 alleviated the inflammatory response, oxidative stress, neuronal injury and cognitive impairment, and restricted apoptosis via targeting Src and inactivating the MAPK signaling pathway. Furthermore, up-regulation of miR-137 or inhibition of Src inhibited the secretion of inflammatory factors, suppressed oxidative stress, and reduced apoptosis of astrocytes. In conclusion, our work suggests that, in mice, miR-137 confers neuroprotective effects against ischemic stroke via attenuation of oxidative, apoptotic, and inflammatory pathways through inhibiting Src-dependent MAPK signaling pathway.Liver fibrosis is the reversible deposition of extracellular matrix (ECM) and scar formation after liver damage by various stimuli. The interaction between NOX4/ROS and RhoA/ROCK1 in liver fibrosis is not yet clear. Ursolic acid (UA) is a traditional Chinese medicine with anti-fibrotic effects, but the molecular mechanism underlying these effects is still unclear. We investigated the interaction between NOX4/ROS and RhoA/ROCK1 during liver fibrosis and whether these molecules are targets for the anti-fibrotic effects of UA. First, we confirmed that UA reversed CCl4-induced liver fibrosis. In the NOX4 intervention and RhoA intervention groups, related experimental analyses confirmed the decrease in CCl4-induced liver fibrosis. Next, we determined that the expression of NOX4 and RhoA/ROCK1 was decreased in UA-treated liver fibrotic mice. Furthermore, RhoA/ROCK1 expression was decreased in the NOX4 intervention group, but there was no significant change in the expression of NOX4 in the RhoA intervention group. Finally, we found that liver fibrotic mice showed a decline in their microbiota diversity and abundance, a change in their microbiota composition, and a reduction in the number of potential beneficial bacteria. However, in UA-treated liver fibrotic mice, the microbiota dysbiosis was ameliorated. In conclusion, the NOX4/ROS and RhoA/ROCK1 signalling pathways are closely linked to the development of liver fibrosis. UA can reverse liver fibrosis by inhibiting the NOX4/ROS and RhoA/ROCK1 signalling pathways, which may interact with each other.Background The coronavirus disease (COVID-19) was discovered in China in December 2019. It has developed into a threatening international public health emergency.  https://www.selleckchem.com/products/terephthalic-acid.html  With the exception of China, the number of cases continues to increase worldwide. A number of studies about disease diagnosis and treatment have been carried out, and many clinically proven effective results have been achieved. Although information technology can improve the transferring of such knowledge to clinical practice rapidly, data interoperability is still a challenge due to the heterogeneous nature of hospital information systems. This issue becomes even more serious if the knowledge for diagnosis and treatment is updated rapidly as is the case for COVID-19. An open, semantic-sharing, and collaborative-information modeling framework is needed to rapidly develop a shared data model for exchanging data among systems. openEHR is such a framework and is supported by many open software packages that help to promote information sharing and interoperability.