Today, nonalcoholic fatty liver disease remains the most dominant chronic liver disease. Cyclic guanosine monophosphate-adenosine monosphosphate synthase (cGAS) is a cytosolic DNA sensor that catalyzes the synthesis of cyclic guanosine monophosphate, activates stimulator of interferon genes (STING), and releases type-I interferon cytokines to trigger immune responses. Exogenous or endogenous DNA acts as a cGAS ligand to activate the cGAS-STING signaling pathway, which plays a role in hepatitis, nonalcoholic fatty liver disease, liver cancer and other diseases, and affects liver disease progression and metabolism through mechanisms such as autophagy. This article reviews the activation of cGAS-STING pathway and its molecular immunological role in nonalcoholic fatty liver disease progression.

OBJECTIVE: To explore the genetic basis of cerebral palsy (CP). METHODS: A pair of twins with cerebral palsy and different phenotypes were subjected to whole genome sequencing, and other 8 children with CP were subjected to whole exome sequencing. Genetic variations were screened by a self-designed filtration process in order to explore the CP-related biological pathways and genes. RESULTS: Three biological pathways related to CP were identified, which included axon guiding, transmission across chemical synapses and protein-protein interactions at synapses, and 25 susceptibility genes for CP were identified. CONCLUSION The molecular mechanism of CP has been explored, which may provide clues for development of new treatment for CP.
Cerebral Palsy ; genetics ; Child ; Genetic Testing ; Humans ; Phenotype ; Whole Exome Sequencing ; Whole Genome Sequencing

Objective:To analyze the expression of CD44 in non-alcoholic fatty liver disease (NAFLD) accompanied with hepatitis B virus (HBV) infection and its clinical significance.Methods:Blood sample of hospitalized patients with NAFLD, chronic hepatitis B, cirrhosis, and healthy population (control) was collected. The study was approved by the hospital ethics committee. Serum CD44 level and clinopathological characteristics were analyzed quantitatively by enzyme-linked immunosorbent-assay. Flow cytometry was used to analyze the proportion of CD44 +T lymphocytes in patients with NAFLD and chronic hepatitis B. NAFLD model was prepared with high-fat diet to verify the abnormal expression of CD44. Results:Compared with the healthy control group, the expression of serum CD44 in the cirrhosis group, chronic hepatitis B group and NAFLD group was increased, and the difference between the groups were statistically significant ( P < 0.01). NAFLD patients graded as mild or severe group were equally accompanied by hepatocyte injury, abnormal blood glucose, lipid or CD44. In NAFLD patients accompanied with HBV infection, serum CD44 concentrations were significantly higher in HBsAg, HBeAg and HBV DNA positive group than HBsAg, HBeAg and HBV DNA negative group ( P < 0.01). The proportion of CD44 +T lymphocytes in peripheral blood of NAFLD and chronic hepatitis B group were 78.2% ± 16.3% and 68.5% ± 20.9%, respectively, and both groups (NAFLD and chronic hepatitis B) were significantly higher than the healthy control group (46.5% ± 20.5%) ( P < 0.05). The high-fat diet model confirmed that in rat liver tissues the CD44 was overexpressed with fat deposition accompanied with liver cell damage, especially remarkable in liver tissues containing carcinogens. Conclusion:The abnormal expression of CD44 in patients with NAFLD may be related to the malignant transformation of HBV-related liver disease.