Objective To study the effect of myocardial infarction induced by distal left ascending artery occlusion on left ventrieular(LV) synchronism. Methods Routine echocardiography and vector velocity imaging were performed within 2 hours before and 7-14 days after myocardial infarction by occluding distal left ascending coronary arteries in experimental pigs. Routine eehocardiographie parameters of LV, including end diastolic and systolic diameters, volumes, and spherical indexes were measured or calculated. Six segmental peak systolic velocity, strain and strain rate were compared between pre- and post-myocardial infarction. Results After myocardial infarction, LV end diastolic, end systolic long diameter and end systolic volume increased with decreased ejection fraction. With the 6 segmental systolic velocity, strain and strain rate significantly reduced,the mean 6-segmental time to peak strain rate delayed significantly. Conclusions Abnormal synchronism after myocardial infarction may aggravate LV systolic dysfunction.

Objective:To observe the effect of xylitol on the cyclooxygenase(COX)-2 expression of renal tubule in diabetic rats.Methods:The Wistar rats were randomly divided into normal control group(group NC),diabetes control group(group DC),5% xylitol-treated group(group 5%),10% xylitol-treated group(group 10%)and 20% xylitol-treated group(group 20%).At the end of 8 weeks,the expression of COX-2 in kidney tissue,the level of serum uric acid,allantoin and creatinine were tested in rat groups.Results:The levels of serum uric acid and allantoin were higher in group 5% and group 10% compared with that of group DC.The differences in levels of serum uric acid and allantoin were statistical significance between group 10% and group DC(P ＜ 0.05),whereas,the lower levels of serum uric acid and allantoin were found in group 20% compared with those of group DC(P ＞ 0.05).The levels of urine uric acid and allantoin were lower in group 5% and group 10% than those of group DC(urine uric acid,P＞ 0.05 and allantoin,P＜ 0.05),whereas,group 20% had higher levels of urine uric acid and allantoin than those of group DC(P＜ 0.05).The fractional excretion of uric acid(FEUA)was lower in group 5% and group 10% compared with that of group DC(P ＜ 0.05).The FEUA was higher in group 20% than that of group DC(P ＜ 0.05).The expression of COX-2 was significantly increased in group 5% and group 10% compared with that of group DC(P ＜ 0.05),but the expression of COX-2 decreased in group 20%(P ＜ 0.05).Conclusion:The lower and mediate doses of dietary xylitol could aggravate the tubular injury through increasing the level of serum uric acid and the expression of COX-2 in renal tubule.The higher doses of xylitol could increase the excretion of uric acid and down-regulate the expression of COX-2 in renal tubule.

Objective:To investigate the effect and mechanism of PPAR-γ agonist Pioglitazone (PGZ) on the proliferation of malignant mesothelioma (MM) cells.Methods:In December 2019, MM cell lines MSTO-211H and NCI-H2452 were incubated with different final concentrations of PGZ (0, 10, 50, 100, 150, and 200 μmol/L) for different periods of time (24 h, 48 h, and 72 h) , and then the cell proliferation level was detected by CCK8 assay. After given various final concentration of PGZ (0, 10, 50, 100, 150, 200 μmol/L) the for 72 hours, the changes of number and morphology of MM cells were observed under an inverted microscope. The expressions of PPAR-γ and HMGB1 mRNA were determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) after treatment of MM cells with PGZ of 0, 10, 50, 100 μmol/L for 72 h. The MM cells were treated with PGZ at concentration of 0, 100 μmol/L for 72 h, and the protein expressions of HMGB1 were examined using Western blotting and immunofluorescence; the protein expressions of Ki67 were assessed by immunohistochemistry.Results:The cell viability rate of MM cells was decreased after treated with PGZ ( P<0.05) . Cell number in PGZ-treated group was significantly less than that in control group and morphology changes were observed under light microscope. QRT-PCR results revealed significantly increased PPAR-γ mRNA expression in the PGZ-treated group compared to the control group ( P<0.05) . There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 μmol/L) as compared to the control group in MSTO-211H ( P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences ( P>0.05) . Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H ( P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences ( P>0.05) . Immunohistochemistry results showed increased expression of proliferation marker Ki-67. Conclusion:Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-γ.

Objective:To investigate the effect and mechanism of PPAR-γ agonist Pioglitazone (PGZ) on the proliferation of malignant mesothelioma (MM) cells.Methods:In December 2019, MM cell lines MSTO-211H and NCI-H2452 were incubated with different final concentrations of PGZ (0, 10, 50, 100, 150, and 200 μmol/L) for different periods of time (24 h, 48 h, and 72 h) , and then the cell proliferation level was detected by CCK8 assay. After given various final concentration of PGZ (0, 10, 50, 100, 150, 200 μmol/L) the for 72 hours, the changes of number and morphology of MM cells were observed under an inverted microscope. The expressions of PPAR-γ and HMGB1 mRNA were determined by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) after treatment of MM cells with PGZ of 0, 10, 50, 100 μmol/L for 72 h. The MM cells were treated with PGZ at concentration of 0, 100 μmol/L for 72 h, and the protein expressions of HMGB1 were examined using Western blotting and immunofluorescence; the protein expressions of Ki67 were assessed by immunohistochemistry.Results:The cell viability rate of MM cells was decreased after treated with PGZ ( P<0.05) . Cell number in PGZ-treated group was significantly less than that in control group and morphology changes were observed under light microscope. QRT-PCR results revealed significantly increased PPAR-γ mRNA expression in the PGZ-treated group compared to the control group ( P<0.05) . There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 μmol/L) as compared to the control group in MSTO-211H ( P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences ( P>0.05) . Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H ( P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences ( P>0.05) . Immunohistochemistry results showed increased expression of proliferation marker Ki-67. Conclusion:Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-γ.

Four hundred and four male patients with primary gout were enrolled. According to the degree of nonalcoholic fatty liver diseases (NAFLD), the patients were divided into simple gout ( n=121), gout combined with mild NAFLD ( n=149) and gout combined with moderate-severe NAFLD ( n=134). The height, weight, waist, hip, blood pressure and blood biochemistry parameters of patients were measured. The degree of NAFLD was negatively correlated with the age of patients in three groups. The BMI, ratio of waist/hip, count of red cells, hemoglobin, hematocrit, red blood cell distribution width ( SD and CV), triglyceride, alanine aminotransferase and HOMA-IR were increased with the increasing of NAFLD severity (all P<0.05). Red blood cell count, hemoglobin, alanine aminotransferase, serum uric acid increased with the increasing of NAFLD severity (all P<0.05). Platelet, serum urea nitrogen and serum creatinine were decreased with the increase of NAFLD severity. Logistic regression showed that BMI, hemoglobin and HOMA-IR were independent risk factors for NAFLD. The prevalence and the severity of NAFLD was increased with increasing quadrates of hemoglobin. Taking group Q1 as a control, OR of NAFLD in group Q2 was 1.166(95 %CI:0.638-2.133), OR in group Q3 was 2.011(95 %CI:1.122-3.605)and OR in group Q4 was 3.120(95 %CI:1.613-6.034). The result indicates that hemoglobin levels are associated with the development and the severity of NAFLD in male patients with primary gout.