Objective To explore main influencing factors of quality of life in patients with essential hypertension.Methods 644 patients with essential hypertension were investigated in a cross-sectional study with the questionnaire including demographic information,behaviour,years of hypertension,treatment,Chinese version SF-36 short form of quality of life.Influencing factors was analyzed by variance analysis and stepwise multivariate linear regression.Results Multivariable analysis showed that age,history of mental distress within the last one year,family income,physical exercise,attitude,knowledge,ordinary blood pressure,and community comprehensive management significantly influenced quality of life of patients with hypertension,with their standardized coefficients being-0.204,-0.097,0.102,-0.174,-0.197,0.129,-0.178 and-0.227 respectively.Conclusions To improve hypertension patients' quality of life,it is should be strengthened to control their blood pressure effectively,to enhance their health education and feasible exercise,and to improve their pessimistic attitude with psychological intervention.

Objective Regenerating genes express mainly in gastrointestinal tissues and the injured regenerating pancreatic tissues,which can promote the regeneration of pancreatic β cells and other tissue cells.In recent years,researches on Reg family mainly involved the gene structure of various subtypes of Reg,and its role in diabetes,gastrointestinal cancer,inflammation,anti-microbial and the related mechanisms.Among the various subtypes of Reg,regenerating geneⅢ(Reg3) plays a particularly crucial role in these diseases.Therefore,Reg3 is a promising target for the treatment of these diseases.Based on the relationships of Reg3 with a variety of diseases,our group devote to the role of Reg3 [human REG3A,and mouse Reg3γ(Reg3g)] in type 1 diabetes,inflammation-linked pancreatic carcinogenesis,and the immunological changes participated in these processes.Hence,this review will summarize serial studies on Reg3 and the feasibility of it as drug targets.

Humans ; Mouth Diseases ; drug therapy ; Mouth Mucosa ; pathology ; Thalidomide ; therapeutic use

Objective To research the expression and clinical significance of SALL 4 gene in cervical cancer .Methods The ex-pression of SALL4 in 56 samples of cervical cancer and 35 samples of normal cervical tissues was detected by immunohistochemistry and RT-PCR ,and its relationship with the clinicopathological characteristics of cervical cancer was analyzed .Results The expres-sion of SALL4 mRNA was 2 .56 ± 0 .22 in cervical cancer tissues ,which was significantly higher than 0 .38 ± 0 .03 in the normal cer-vical tissues .the difference between them had statistical significance(t=58 .1 ,P<0 .01);the positive expression rate of SALL4 pro-tein was 80 .4% (45/56) in cervical cancer ,which was significantly higher than 11 .4% (4/35) in the normal cervical tissues (χ2 =41 .177 ,P<0 .01) .The positive expression of SALL4 in the cervical cancer tissues was correlated with the differentiation status of tumor ,which in the middle and high differentiation groups was lower than that in the low differentiation group (χ2 =4 .226 ,P=0 .039) ,but had no correlation with age ,International Federation of Gynecology and Obstetrics (FIGO) stage ,tumor size ,pathologi-cal type and lymph node metastasis(P>0 .05) .Conclusion SALL4 is highly expressed in the cervical cancer tissues and correlated with the tumor differentiation ,which might play an important role in the occurrence and development of cervical cancer .

Objective To observe the clinical effect of bicyclol combined with polyene phosphatidyl choline in elderly non-alcoholic fatty liver disease (NAFLD).Methods One hundred and twenty elderly patients with NAFLD were divided into 3 groups by block randomization method,40 cases in each group.Therapeutic group was treated by bicyclol combined with polyene phosphatidyl choline; bicyclol group was only treated by bicyclol; and polyene phosphatidyl choline group was only treated by polyene phosphatidyl choline.The blood biochemical indexes,liver ultrasound score and clinical curative effect of 3 groups were compared after treated for 24 weeks.Results The total cholesterol (TC),triglyceride (TG),alanine aminotransferase (ALT),aspartate aminotransferase (AST) and gamma glutamine transferase (GGT) in 3 groups after treatment were lower than those before treatment,and the difference was statistically significant (P ＜ 0.05) ; TC,TG and ALT levels in therapeutic group after treatment were significantly lower than those in bicyclol group and polyene phosphatidyl choline group [(1.36 ± 0.84) mmol/L vs.(2.77 ± 1.27),(2.84 ±1.35) mmol/L; (1.32 ±0.71) mmol/L vs.(1.89 ±0.87),(1.92 ±0.90) mmol/L; (38.26 ± 12.75) U/L vs.(57.83 ± 16.67),(62.07 ± 18.16) U/L],and the difference was statistically significant (P ＜ 0.05).The liver ultrasound score in 3 groups after treatment was significantly decreased compared with that before treatment,and the difference was statistically significant (P ＜ 0.05).Liver ultrasound scores in therapeutic group after treatment were significantly lower than those in bicyclol group and polyene phosphatidyl choline group [(2.08 ± 0.93) scores vs.(3.17 ± 1.14),(3.34 ± 1.07) scores],and the difference was statistically significant (P ＜ 0.05).The total effective rate in therapeutic group was significantly higher than that in bicyclol group and polyene phosphatidyl choline group [85.0％ (34/40) vs.67.5％ (27/40),65.0％ (26/40)],and the difference was statistically significant (P ＜0.05).Conclusions Bicyclol combined with polyene phosphatidyl choline has better clinical effect in elderly patients with NAFLD.It is better than single bicyclol and polyene phosphatidyl choline and worth clinical promotion.

Objective To explore the effect of Toll-like receptor 4 (TLR4) on the peripheral blood mononuclear cells(PBMCs) in the development of rheumatoid arthritis (RA) by inducing the differentiation of Th17 cells.Methods Forty two subjects were recruited to the study,including 22 patients with RA and 20 healthy controls (HC).The percentage of circulating Th17 cells were analyzed using flow cytometry.PBMCs were stimulated with LPS for two days.TLR4 mRNA of the PBMCs and the concentration of IL-6 and TNF-α in the supernatants were analyzed with the real-time qPCR and ELISA respectively.Supematants was then used for CD4+ cord blood mononuclear cells (CBMCs) culture,and IL-17 in the supernatants and the expression of IL-17 mRNA in cells were detected by ELISA and real-time qPCR respectively.The statistical analysis was carried out with t-test.Results The TLR4 mRNA expression in the PBMCs and the percentage of circulating Th17 ceils of RA patients were significantly higher than that of the HC group (P＜0.01).Stimulated by LPS,the expression of TLR4 mRNA increased 3.5 times in the RA group but decreased 0.11 times in the HC group.LPS also increased cytokines production in both groups,while PBMCs from RA patients produced more IL-6 and TNF-α than the cells from healthy subjects (P＜0.01).Compared to the HC group,the IL-17 mRNA expression and IL-17 secretion of CD4+ CBMCs induced by the supematants of RA patients' PBMCs stimulated with LPS was significantly higher(P＜0.01 ); but there was no significant difference between the RA group and the HC group without LPS stimulation (P＞0.05).Conclusion The expression of TLR4 on PBMCs from patients with RA and its response to LPS stimulation are increased,and it has demonstrated high capability in inducing the differentiation of Th 17 cells.

Objective To characterize the clinical presentation of noncardiac chest pain(NCCP), to investigate the quality of life among NCCP patients,and to understand the relation between NCCP and acid reflux and the value of proton pump inhibitor(PPI) in diagnosis of NCCP.Methods Eighty-seven NCCP patients were enrolled to the study.All patients received lansoprzole 30 mg twice daily for 7 days. Patients filled out a questionnaire survey before and after the PPI treatment.The questionnaire included the general personal data,the symptom scale,the medical outcome study 36-item short form healthy survey(SF-36),Zung Self Rating Anxiety Scale(SAS) and Zung Self-rating Depression Scale(SDS).The results were analyzed in comparisons of healthy control group.Results①The most common cause for NCCP was gastroesophageal reflux disease (GERD).The typical reflux syndrome presented among 34.5% of the patients.②Among 87 patients,acid-related NCCP was accounted for 56.3% (49/87), whereas non-acid-related NCCP was accounted for 43.7% (38/87).The sensitivity and specificity of PPI test were 91% and 81%,respectively.③Except the role of role emotional(RE),7 healthy conceptions in the health-related quality of life in NCCP patients were significantly lower than those in healthy volun- teers(P

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) onpromotion 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 induce the 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. Liquid chromatography-mass spectrometry (LC-MS) and co-immunoprecipitation (Co-IP) were conducted to identify proteins interacting with 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 prolifer-ation 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 KRAS/ERK 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.

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.

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.