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Moreover, YAP may promote repair by down-regulating STAT3 activity, thereby inhibiting VEGF expression. Significance Elucidating the role of YAP in endothelial cell permeability repair process after injury might reveal mechanisms of endothelial barrier repair and provide therapeutic targets for treatment of vascular hyper-permeability disease.Aims We aimed to investigate the effect of sperm miR-34c on early human embryonic development kinetics and clinical outcomes of in vitro fertilization (IVF) patients. Materials and methods After oocyte insemination, residual sperm specimens were collected from 58 patients undergoing IVF. miR-34c expression levels in sperm, oocytes, zygotes, and embryos/blastocysts were detected with qRT-PCR, and embryonic development kinetics were observed using time-lapse technology. To confirm the role of miR-34c in regulation of early embryonic development, miR-34c siRNA was injected into zygotes obtained from in vitro-matured oocytes. A ROC curve was used to determine the cutoff value. Comparisons of embryonic development kinetics and clinical outcomes were performed according to the cutoff value. Key findings The miR-34c expression level was highest in 3PN zygotes, but was not expressed in human oocytes. In the miR-34c siRNA group, embryonic development kinetic parameters t2, t3, t4, and t5 were significantly prolonged, but the cleavage rate and high-quality embryo rate were lower than in the control group. The levels of sperm miR-34c were negatively correlated with t5 and positively correlated with rates of blastocyst formation, high-quality blastocysts, and pregnancy. The miR-34c levels and the blastocyst formation rate were higher in the pregnancy group (p less then 0.05). Logistic regression analysis showed that sperm miR-34c level was significantly correlated with pregnancy (OR 5.056, 95% CI 1.560-16.384; p = 0.007). Significance The sperm miR-34c expression level is associated with embryonic development kinetics and clinical outcomes. Thus, miR-34c expression is beneficial to embryonic development and may be used as an indicator of IVF outcomes.Aims Pathological alterations in the brain can cause microglial activation (MA). Thus, inhibiting MA could provide a new approach for treating neurodegenerative disorders. Main methods To investigate the effect of C16 peptide and angiopoietin-1 (Ang1) on inflammation following MA, we stimulated microglial BV-2 cells with lipopolysaccharide (LPS) and used dexmedetomidine (DEX) as a positive control. Specific inhibitors of Tie2, αvβ3 and α5β1 integrins, and PI3K/Akt were applied to investigate the neuron-protective and anti-inflammatory effects and signaling pathway of C16 + Ang1 treatment in the LPS-induced BV-2 cells. selleck compound Key findings Our results showed that C16 + Ang1 treatment reduced the microglia M1 phenotype but promoted the microglia M2 phenotype. In addition, C16 + Ang1 treatment suppressed leukocyte migration across human pulmonary microvascular endothelial cells, reduced the levels of pro-inflammatory factors [inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, tumor necrosis factor (TNF-α)], and cellular apoptosis factors (caspase-3 and p53), and decreased lactate dehydrogenase (LDH) release, but promoted anti-inflammatory cytokine (IL-10) expression and cell proliferation in the LPS-activated BV-2 cells. The signaling pathways underlying the neuron-protective and anti-inflammatory effects of C16 + Ang1 may be mediated by Tie2-PI3K/Akt, Tie2-integrin and integrin-PI3K/Akt. Significance The neuron-protective and anti-inflammatory effects of C16 + Ang1 treatment included M1 to M2 microglia phenotype switching, blocking leukocyte transmigration, decreasing apoptotic and inflammatory factors, and promoting cellular viability.Glioma is the most common brain malignancy and surgical resection is the primary option for patient with glioma. Anesthetics could be used to inhibit cancer dissemination and metastasis during surgery. This study aims to assess the function of volatile anesthetic sevoflurane in glioma migration and invasion and explore the potential mechanism. Twenty-five patients with glioma were recruited in this study. LN229 and U251 cells were used in vitro experiments. Cell viability was analyzed by MTT analysis. Cell migration and invasion were examined via transwell analysis. microRNA-34a-5p (miR-34a-5p) and matrix metalloproteinase-2 (MMP-2) levels were measured via quantitative real-time polymerase chain reaction. The relationship of miR-34a-5p and MMP-2 was tested via bioinformatics analysis, luciferase reporter analysis, RNA immunoprecipitation and RNA pull-down. Sevoflurane decreased glioma cell migration and invasion. In glioma cells, sevoflurane up-regulated miR-34a-5p abundance and down-regulated MMP-2 level. Overexpression of miR-34a-5p contributed to sevoflurane-caused suppression of migration and invasion, while its knockdown played an opposite effect. MMP-2 was targeted via miR-34a-5p and MMP-2 silence reversed the influence of miR-34a-5p knockdown under sevoflurane. Sevoflurane exposure represses cell migration and invasion, which might be related to inhibition of MMP-2 by up-regulating miR-34a-5p. This study provides a novel mechanism for understanding the pharmacological effects of sevoflurane on glioma.Aim Coronavirus disease 2019 (COVID-19) is a novel highly contagious infection caused by SARS-CoV-2, which has been became a global public health challenge. The pathogenesis of this virus is not yet clearly understood, but there is evidence of a hyper-inflammatory immune response in critically ill patients, which leads to acute respiratory distress syndrome (ARDS) and multi-organ failure. Material and methods A literature review was performed to identify relevant articles on COVID-19 published up to April 30, 2020. The search resulted in 361 total articles. After reviewing the titles and abstracts for inclusion, some irrelevant papers were excluded. Additional relevant articles were identified from a review of citations referenced. Key findings SARS-CoV-2, directly and indirectly, affects the immune system and avoids being eliminated in early stages. On the other hand, the secretion of inflammatory cytokines creates critical conditions that lead to multi-organ failure. Significance The immune system which is affected by the virus tries to respond via a cytokine storm and hyperinflammation, which itself leads to further multi-organ damage and even death.