ABSTRACT
Somatostatin, also called somatotropin release-inhibiting factor (SRIF), is a kind of neurotransmitter, neuromodulator and neurotrophic factor, which participates in a variety of physiological functions in the central nervous system by activating the five G-protein-coupled receptors (sst 1-sst 5). SRIF and its receptors are extensively expressed and distributed in retina.Activation of SRIF receptors modulates voltage-gated K + and Ca 2+ channels, and regulates multiple intracellular signaling pathways in retinal cells, then influences neurotransmitter release and synaptic transmission, which plays an important role in the regulation of retinal visual information processing.In addition, SRIF and its receptors may provide protective effects against retinal injuries, such as retinal ischemia, excitotoxic injury and diabetic retinopathy.In this article, connected with related previous researches of our team, the distribution of SRIF and its receptor in retina, as well as the role of SRIF and its receptor in the physiological regulation and neuroprotection of retina were reviewed.
ABSTRACT
Ras-related C3 botulinum toxin substrate 1 (Rac1), a member of the Rho GTPase family which plays important roles in dendritic spine morphology and plasticity, is a key regulator of cytoskeletal reorganization in dendrites and spines. Here, we investigated whether and how Rac1 modulates synaptic transmission in mouse retinal ganglion cells (RGCs) using selective conditional knockout of Rac1 (Rac1-cKO). Rac1-cKO significantly reduced the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents, while glycine/GABA receptor-mediated miniature inhibitory postsynaptic currents were not affected. Although the total GluA1 protein level was increased in Rac1-cKO mice, its expression in the membrane component was unchanged. Rac1-cKO did not affect spine-like branch density in single dendrites, but significantly reduced the dendritic complexity, which resulted in a decrease in the total number of dendritic spine-like branches. These results suggest that Rac1 selectively affects excitatory synaptic transmission in RGCs by modulating dendritic complexity.
ABSTRACT
Mother-to-child vertical transmission is the main mode of transmission of chronic hepatitis B in China. The probability of failure in blocking vertical transmission is about 10% in pregnant mothers with a high viral load, and therefore, correct management of hepatitis B virus (HBV) is of great importance during pregnancy. In addition, viral treatment during pregnancy should take into account the risk of vertical transmission, the health of pregnant women, and the safety of fetus, and each treatment method or prevention option needs to be carefully evaluated. Reasonable antiviral methods, drug selection, and drug withdrawal time can reduce the probability of mother-to-child transmission. This article summarizes the modes of mother-to-child vertical transmission of chronic hepatitis B and related blocking strategies, so as to provide a reference for improving the blocking rate of vertical transmission of HBV.
ABSTRACT
Objective To investigate the prognostic factors for patients with hepatitis B virus-related acute-on-chronic liver failure,and to provide a basis for clinical diagnosis and treatment.Methods A total of 172 patients with hepatitis B virus (HBV)-related acute-on-chronic liver failure who were admitted to The First Hospital of Jilin University from January 1,2006 to January 1,2016 and had complete medical records and follow-up data were enrolled,and a retrospective analysis was performed for their clinical data and laboratory markers to determine prognostic factors.The independent-samples t test was used for comparison of continuous data between groups,the chi-square test was used for comparison of categorical data between groups,and a multivariate logistic regression analysis was performed for the indices determined to be statistically significant by the univariate analysis to screen out independent risk factors for the prognosis of patients with HBV-related acute-on-chronic liver failure.Results The multivariate logistic regression analysis was performed for the indices determined to be statistically significant by the univariate analysis,and the results showed that the prognostic factors were total bilirubin (TBil),prothrombin time activity (PTA),Na +,total cholesterol (TC),Child-Turcotte-Pugh (CTP) score,age ≥50 years,the presence of liver cirrhosis,bilirubin-enzyme separation,and complications.The multivariate regression analysis was performed for the complications determined to affect prognosis by the univariate analysis,and the results showed that the complications as risk factors were hepatic encephalopathy,hepatorenal syndrome,and infection.Conclusion TBil,PTA,Na +,TC,CTP score,age ≥50 years,the presence of liver cirrhosis,bilirubin-enzyme separation,and complications are independent risk factors for the prognosis of patients with HBV-related acute -on-chronic liver failure.Liver failure patients with hepatic encephalopathy,hepatorenal syndrome,and infection tend to have poorer prognosis.Therefore,early judgment of the prognosis of patients with liver failure is of great importance in the prevention and treatment of related complications.
ABSTRACT
Mouse double minute 2 (Mdm2) gene was isolated from a cDNA library derived from transformed mouse 3T3 cells, and was classified as an oncogene as it confers 3T3 and Rat2 cells tumorigenicity when overexpressed. It encodes a nucleocytoplasmic shuttling ubiquitin E3 ligase, with its main target being tumor suppressor p53, which is mutated in more than 50% of human primary tumors. Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related). Activated p53 inhibits cell proliferation, induces apoptosis or senescence, and maintains genome integrity. Mdm2 is also a target gene of p53 transcription factor. Thus, Mdm2 and p53 form a feedback regulatory loop. External and internal cues, through multiple signaling pathways, can act on Mdm2 to regulate p53 levels and cell proliferation, death, and senescence. This review will focus on how Mdm2 is regulated under genotoxic stress, and by the Akt1-mTOR-S6K1 pathway that is activated by insulin, growth factors, amino acids, or energy status.