The CD24 protein and mRNA levels in the cornu ammonis and dentate gyrus regions of the ipsilateral hippocampus were elevated after TBI, and high CD24 expression was widespread in the hippocampal astrocytes after TBI. Specific inhibition of CD24 in the hippocampal astrocytes interfered with the activation of Src homology region 2 containing protein tyrosine phosphatase 2 (SHP2) and extracellular signal regulated kinase (ERK), shortened the neuronal dendritic spines, decreased the GAP43 level and impaired the cognitive functions of the TBI-model mice. These results revealed that elevated hippocampal CD24 in astrocytes participated in neural regeneration in mice after TBI, possibly by activating the SHP2/ERK pathway.Long noncoding RNAs (lncRNAs) play the critical biological role in many malignant tumours. MIR4435-2HG has been proven to be a novel oncogenic lncRNA. However, the exact role and mechanism of MIR4435-2HG in hepatocellular carcinoma (HCC) remain unclear. Here, we found that MIR4435-2HG is overexpressed in HCC tissue compared to normal controls and that high level of MIR4435-2HG indicates a poorer prognosis in HCC patients. MIR4435-2HG enhances the growth and metastasis ability of HCC cells. MIR4435-2HG promotes the expression of YWHAZ by sponging miR-22-3p to liberate YWHAZ mRNA transcripts. MIR4435-2HG facilitates the proliferation and metastasis of HCC by modulating the miR-22-3p/YWHAZ axis. These results demonstrated the role and mechanism of MIR4435-2HG in malignant progression of HCC. MIR4435-2HG may be used as the prognostic marker and treatment target for the patient with HCC.
  Acute lung injury (ALI) is a common disease that usually progresses to acute respiratory distress syndrome (ARDS) with high morbidity and mortality. We aim to analyze the trends in ALI/ARDS, and to compare the differences in aspects of years, countries, institutions, journals, etc.  https://www.selleckchem.com/products/tasquinimod.html  Methods We screened all relevant literature on ALI/ARDS from Web of Science during 2009-2019, and analyzed the research trends in this field by VOSviewer.
 
  We had screened 7,890 publications with a total cited frequency of 164,713. The United States contributed the largest number of publications (2,612, 33.11%), cited frequency (81,376, 48.61%), and the highest H-index (107). 
  published the largest number of literatures on ALI/ARDS, MATTHAY MA published the majority of articles in this field (147), while SLUTSKY AS received the most cited frequency (10015). University of California San Francisco had the largest number of publications (243, 3.08%) among all full-time institutions. In the aspect of clinical research in ALI/ARDS, the keyword "Berlin definition" emerged in recent years, with an average year of 2016.3; in the basic research, the key word "protects" appeared latest, and the average years were 2016.5. The current research trend indicates that basic research is gradually transforming into clinical research.
 
  The United States have made the most significant contribution to the ALI/ARDS field in the last decade. The current research 'hotspot' mainly appeared in clinical research, such as "Berlin definition". In regards to basic research, studies tend to explore the protective mechanisms against ALI/ARDS.
 The United States have made the most significant contribution to the ALI/ARDS field in the last decade. The current research 'hotspot' mainly appeared in clinical research, such as "Berlin definition". In regards to basic research, studies tend to explore the protective mechanisms against ALI/ARDS.Microglia-mediated neuroinflammation is one of the hallmark pathological features following traumatic brain injury (TBI) that contributes to aggravated brain damage and cognitive deficits. These pathologies require novel effective treatments to improve prognosis. Trametinib, a mitogen-activated protein kinase inhibitor approved by the Food and Drug Administration in treating various malignant tumors, has been shown to exert anti-inflammatory effects. The present study demonstrated that TBI mice treated with trametinib exhibited improved cognitive function. Trametinib treatment rescued oligodendrocytes and decreased infiltrating microglial density in the TBI area. Furthermore, this study revealed that ameliorated lipopolysaccharides (LPS) induced inflammatory reaction in microglial cells. Besides, trametinib attenuated inflammation factors expression during the early stages of TBI. In addition, trametinib inhibited LPS-induced microglial chemotactic activity. In conclusion, the results indicate that trametinib efficiently suppresses microglia-induced neuroinflammation and improves cognitive function of TBI mice, providing a potential therapy strategy for TBI patients.Multiple studies have highlighted the importance of long noncoding RNAs in tumorigenesis. However, the molecular mechanisms underlying the role of lncRNAs in breast cancer are not well understood. Recently, the lncRNA HOXC-AS3 has drawn significant attention due to its regulatory effects on the tumorigenesis of human cancers. However, the potential molecular mechanisms whereby it mediates breast cancer progression remain unknown. Based on public breast cancer expression data and using bioinformatics methods, we discovered significantly upregulated expression levels of HOXC-AS3 in diseased tissues. We verified this result in breast cancer samples and found that the expression of HOXC-AS3 was well correlated with the prognosis of breast cancer. In vitro and in vivo experimental evidence suggests that HOXC-AS3 has the potential to regulate tumorigenesis. Further, mechanistic studies demonstrated the potential of HOXC-AS3 in the transcriptional activation of TK1 via its binding to YBX1. Furthermore, the silencing of TK1 reversed HOXC-AS3-mediated increase in breast cancer cell growth and migration. In conclusion, these results indicated the potential value of HOXC-AS as a prognostic biological marker for breast cancer, and possibly, as a therapeutic target.Acute respiratory distress syndrome (ARDS) is a critical clinical disease characterized by diffuse inflammation of lung parenchyma and refractory hypoxemia. Remifentanil has been reported to act as an anti-inflammatory antioxidant in a variety of diseases. However, whether Remifentanil has a protective effect in ARDS and its mechanism remains to be further studied. This study was designed to investigate the effects of Remifentanil on ARDS in neonate rats. In this study, we established the model of acute respiratory distress in neonate rats. To study the effects of Remifentanil on ARDS through a series of in vitro and in vivo experiments. Furthermore, the overexpression vector of recombinant tissue inhibitors of metalloproteinase 1 (TIMP1) was injected into the neonate rat before the operation to explore the effect of TIMP-1 overexpression on acute respiratory distress rats through the above experiments. Remifentanil reduced lung injury in rats with acute respiratory distress, reduced inflammation, oxidative stress and tissue cell apoptosis in rats with acute respiratory distress.