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Objective@#To learn the health literacy status, trend and associated factors of Ningbo residents from 2015 to 2019, so as to provide basis for developing health policies and interventions. @*Methods@#The monitoring data of health literacy of Ningbo residents from 2015 to 2019 was collected. The health literacy level was calculated and standardized by the population data of the sixth national census of Ningbo in 2010; five-year absolute growth and growth rate were used to reflect the changing trend. Multivariate logistic regression model was employed to analyze the influencing factors for the health literacy level. @*Results@#The health literacy levels from 2015 to 2019 were 15.44%, 21.73%, 22.41%, 27.60% and 30.03%, with an annual increase trend ( P<0.05 ). The five-year absolute growth and growth rate were 14.59% and 94.49%. The Results of multivariate logistic regression analysis indicated that the year ( OR=1.158, 95%CI: 1.132-1.184 ), age ( 25-<35岁 years, OR=1.235, 95%CI: 1.039-1.468; 35-<45岁 years, OR=1.416, 95%CI: 1.193-1.681; 45-<55岁 years, OR=1.221, 95%CI: 1.024-1.455 ) , education level ( primary school, OR=1.790, 95%CI: 1.461-2.195; junior high school, OR=2.574, 95%CI: 2.102-3.154; high school/vocational high school/technical secondary school, OR=4.863, 95%CI: 3.943-5.998; college or above, OR=8.829, 95%CI: 7.109-10.965 ) , urban areas ( OR=0.934, 95%CI: 0.874-0.998 ) and occupation ( farmers, OR=0.692, 95%CI: 0.608-0.787; workers, OR=0.746, 95%CI: 0.664-0.837; enterprise staff, OR=0.822, 95%CI: 0.745-0.906; others, OR=1.106, 95%CI: 1.009-1.211 ) were the influencing factors for health literacy level. @*Conclusion@# The health literacy level of Ningbo residents shows an upward trend from 2015 to 2019, which are associated with age, education level, area and occupation.
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OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) on promotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to inducethe liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells. qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1.Immunoprecipitation was used to determine the receptor of PID1. Chromatin immunoprecipitation (ChIP) was operated to measure the modification of H3K4me3 of PID1 promoter. RESULTS PID1 restriction improved insulin resistance, hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover, PID1 liver- specific protooncogenes via hydrodynamics- based transfection established a primary hepatocellular carcinoma mouse model, induced an immunosuppressive environment, with the reduction of CD3 +, CD4 +, CD8 +T cells, retarded maturation of dendritic cells (DCs), pronounced differentiation of regulatory T cells (Tregs), and recruitment of MDSC. In addition, PID1 overexpression activated proliferation related genes, promoted anti- inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor (EGFR) and activation of downstream MAPK pathway. As such, PID1 exist trimethylation of histone H3 at lysine 4 (H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function. IR accelerates liver cancer development and progression partially dependent on the activation of PID1.
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OBJECTIVE To investigate enhanced immune function of methionine encephalin (MENK) and its anti-tumor mechanism in CT26 colon cancer mouse model. METHODS 3×106 CT26 cells were implanted subcutaneously in BALB/c mice. Four days after, MENK was peritoneally administrated at the concentration of 20 mg·kg-1 for 14 d. The percentage of MDSCs in bone marrow, spleen, blood, tumor and liver were detected by flow cytometry. Non- esterified fatty acid (NEFA), triglycerides (TG) and total cholesterol (T-CHO) in liver homogenate were tested by a NEFA test kit, a TG test kit and a T- CHO test kit respectively. qRT- PCR and Western blot were used to measure mRNA and protein levels of inflammation-, glycometabolsim- and lipometabolsim-associated indexes in liver. RESULTS MENK decreased percentages of MDSCs in bone marrow, spleen, blood and tumor in colon cancer mice. MENK-treated mice displayed elevated ratio of CD4+T and CD8+T cells in spleen as well as increased T and B lymphocytes proliferation. Meanwhile, MENK also ameliorated liver damage reflected by lower levels of GPT and GOT in serum and reduced risks of cancer- associated index including inflammation, high lipid and high glucose. Furthermore, MENK lowered down the levels of NEFA, TG and T- CHO in liver homogenate. MENK treatment decreased expression of p- STAT3, increased expression of p-AKT, IRS1 and Glut4 at protein level as well as reduced lipogenesis-associated genes and elevated glycolysis-associated genes in liver of tumor bearing mice. Also, abated expression of genes associated with MDSCs generation (M-CSF, GM-CSF, IL-6, IL-1β) and migration (S100A9, KC) was observed within shrunken subcutaneous tumor by MENK intervention. CONCLUSION MENK has the ability to strength immune function against colon cancer by reducing MDSCs and improving liver metabolism.