Insulin resistance is the important base of the pathogenesis of type 2 diabetes.Physical exercise can improve insulin sensitivity.This article presents an overview of how physical exercise improves insulin resistance and helps the prevention and treatment of diabetes mellitus by analyzing its influence on the level of insulin receptor and post-receptor and adipose cell cytokine.

Objective To explore the levels of serum interleukin-6 and interleukin-18 in newly diagnosed type 2 diabetes mellitus (T2DM) and investigate their roles. Methods The serum interleukin-6 and interleukin-18 levels were detected in 50 newly, diagnosed T2DM patients (T2DM group) and 40 normal subjects (control group). Fasting blood glucose, fasting insulin, blood lipid, body mass index (BMI) and waist/hip ratio (WHR) were measured. HOMA-IR and HOMA-β were calculated. Results The serum interleukin-6 and interleukin-18 levels in T2DM group were significantly higher than those in control group [(2.56 ± 1.09) ng/L vs (1.81±0.80) ng/L, (5.38±0.91) ng/L vs (4.62±0.59)ng/L] (P <0.01).Interleukin-6 level was positively correlated with HbA_1c,while interleukin-18 level was positively correlated with BMI and WHR. Interleukin-6 and interleukin-18 levels were positively correlated. Interleukin-6 and interhukin-18 could predicted the insulin resistance. Conclusion Interleukin-6 and interleukin-18 take part in the development of T2DM, and can be related to the insulin resistance.

Objective To investigate the effect of EGB on SOD, MDA of ventilator-induced lung injury in rats and its possible mechanisms. Methods Thirty male SD rats were randomly divided into 3 groups: control group (C group), high tidal ventilation group (H group) and EGB group (E group). The setting mechanical ventilation was VT=30 mL/kg, RR=40/min, I/E=1/3, PEEP=0 cmH2 O and FiO2=21%. The broncho-alveolar lavage fluid (BLAF) and serum were obtained for determination of the levels of SOD and MDA at the end of 4 h mechanical ventilation. The Lungs were removed, and the wet-to-dry weight ratio (W/D) and pulmonary pathologic changes were measured. Results As compared with C group, W/D and the levels of MDA were significantly increased in H group, but the levels of SOD were reduced in H group. As compared with H group, W/D and the levels of MDA were significantly decreased in E group, but the levels of SOD were increased in E group. Pulmonary pathologic changes were alleviated in E group comparing with H group. Conclusion EGB injection may have a protective role against hyperoxia and induced pulmonary damage in rats.

Objective To observe the effect of paraoxonase 1 (PON1) application of the new method of arylesterase activity in patients with coronary heart disease,analysis of paraoxonase 1 (PON1) of the clinical value of arylesterase activity in the new testing method.Methods From January 2014 to January 2016 in our hospital 86 patients with coronary heart disease as the research object,and then select the healthy people at the same time to the hospital physical examination of 50 as the control group to take the research object,spectrophotometric method for the determination of coronary heart disease patients and control subjects serum PON1 arylesterase activity,PON1 arylesterase activity at the same time with statistics the different degree of coronary heart disease,PON1 arylesterase activity between patients with coronary heart disease and control group comparison study and different severity of coronary heart disease patients,the patients with coronary heart disease PON1 aromatic ester enzyme activity,age,gender,BMI,TC,total cholesterol,low density lipoprotein cholesterol LDL-C and glycerin three greases TG included in the analysis of factors of coronary heart disease multiple linear regression equation,to determine the changes of patients with coronary artery disease by PON1 arylesterase activity,to provide a reference for clinical treatment.Results The activity of PON1 in patients with coronary heart disease was significantly lower than that of the control group,and the difference was statistically significant (P<0.05).Single branch lesions in patients with PON1 arylesterase activity was significantly higher than that of double vessel lesions and three lesions were double branch lesions in patients with PON1 arylesterase activity was significantly higher than that in three patients,the differences were statistically significant (P<0.05).According to the multiple linear regression analysis showed that coronary heart disease and the patient′s age,gender,BMI,TC,LDL-C,TG and PON1 arylesterase activity (P<0.05),which was related with age,gender,BMI,TC,LDL-C and TG were positively correlated,negatively correlated with PON1 arylesterase activity.Conclusion The PON1 activity of in patients with coronary heart disease is significantly decreased,and the extent of the disease is more severe,the more obvious the decline of PON1,the activity of PON1 shows a negative correlation with coronary heart disease.

Objective To examine the expression of CGRP in congenital pseudarthrosis of tibia(CPT) in order to find the pathogenesis of CPT.Methods Periosteum and bones from CPT patients were collected as experimental group.Immunohistochemistry stain was applied to determine the differences of the expression of CGRP in two groups.Results CGRP was located at vessel wall of periosteum and intracytoplasm of osteoblasts and osteoclasts in bones,its expression was significantly less in periosteum and bones of CPT than that in control group(P

Child, Preschool ; Female ; Humans ; Infant ; Male ; Methionine ; blood ; Tyrosine ; blood ; Tyrosine Transaminase ; deficiency ; Tyrosinemias ; blood ; diagnosis ; enzymology ; pathology ; therapy

OBJECTIVETo study the inhibitory effect of wogonin on the growth and proliferation of breast cancer cells MDA-MB-23, and observe its effect on the adhesion, migration and invasion of MDA-MB-23 cells, in order to further study its molecular mechanism.

METHODMTT assay was used to detect the effect of wogonin on MDA-MB-23 cell growth. Ki-67 assay was adopted to test the effect of wogonin on cell proliferation. Scratch test, adherence test and invasion chamber assay were taken to detect the effect on the migration and invasion abilities of MDA-MB-231 cells. Proliferation and metastasis-related proteins and relevant signaling pathways were detected by Western blotting.

RESULTWogonin could remarkably inhibit the growth and proliferation of MDA-MB-231 cells, significantly inhibit migration, adhesion and invasion abilities of breast cancer cells at a low concentration, and effectively inhibit the expression of Survivin, Bcl-2, ICAM-1, MMP-2, MMP-9 proteins of MDA-MB-231 cells.

CONCLUSIONWogonin could notably inhibit growth and proliferation of breast cancer cells, and inhibit migration, adhesion and invasion of MDA-MB-231 cells. Its invasive and adhesive effects on MDA-MB-231 cells may be related to the decrease in ICAM-1, MMP-2, MMP-9 expressions.

Breast Neoplasms ; genetics ; metabolism ; pathology ; physiopathology ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Female ; Flavanones ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Neoplasm Invasiveness ; Signal Transduction ; drug effects

Objective To assess the reliability and validity of the Somatic Self-rating Scale(SSS). Methods The sample consisted of 589 outpatients and 64 inpatients, which all the patients completed Zung's Scales at the same time to test criterion validity of the SSS. And 24 inpatients were selected randomly to take a retest after two weeks without antidepressant treatment. Result The test-retest reliability of the SSS was 0.96 and the Cronbach' s αcoefficients was 0.89. The correlation coefficients of the four factors with the total scale score ranged from 0.76 to 0.88, the correlation coefficients of the four factors ranged from 0. 56 to 0.70. The confirmatory factor analysis showed that the fit index for GFI, NFI, NNFI, CFI, IFI were all approaching 0.9, REMEA = 0. 064,x2/df = 3.67. The factor loadings ranged from 0. 427 to 0.732. Correlations with Zung's Scales were in range of 0.74to 0. 80 while the four factors were in range of 0.55 to 0.74. Drawing the ROC curve and the area under the curve was 0.841. Conclusion The SSS has a high reliability and a good validity and can be used in general hospital.

Objective To investigate the effects of dihydrofolate reductase (DHFR) gene expression up-regulating on cisplatin resistance in epithelial ovarian cancer cell lines.Methods The cDNA length of DHFR gene was amplified by PCR and was connected to lentiviral vector pWPI, the recombinant retroviral vector DHFR-pWPI was infected SKOV3 cells by lipofectamine 2000.The groups included DHFR-pWPI-SKOV3 cell, pWPI-SKOV3 cell and SKOV3 cell group.Western blot was used to detect the expression of DHFR.Flow cytometry was applied to measure the cell apoptosis rate of 3 groups cells in different cisplatin concentrations (2.5, 5.0, 10.0, 20.0 μg/ml) and at different time period (24, 48 and 72 hours), and half maximal inhibitory concentration (IC50) treated with cisplatin concentration (6.0, 4.0, 4.9 μg/ml).High performance liquid chromatography (HPLC) was applied to test intracellular cisplatin concentration in different cisplatin concentration (4.0, 6.0, 8.0 μg/ml) at 24 and 48 hours.Transmission electron microscope was used to observe ultrastructural changes cells under IC50 cisplatin concentration.Results The recombinant plasmid DHFR-pWPI was constructed and then infected into SKOV3 cell successfully.(1) The expression of DHFR detected by western blot in transfection group was higher than those in the negative control group and blank control group (10.280±0.009 vs 2.050±0.003 vs 3.480±0.003;P＜0.01).(2) Treated with cisplatin concentration (2.5, 5.0, 10.0, 20.0 μg/ml) at 24, 48 hours, the apoptosis rate detected by flow cytometry results shown that they were lower than those in the negative control group and blank control group (P＜0.05), while treated at the concentration of 5.0 and 10.0 μg/ml for 72 hours, whose apoptosis rate in transfection group was higher than those in the negative control group and blank control group (P＜0.05).When treated cells under IC50 cisplatin concentration (6.0, 4.0, 4.9 μg/ml) at for 24 and 48 hours, the results indicated thatthere were mainly G0/G1 stage cell cycle rate in 3 groups, it was obviously higher in transfection group than those in two control groups (P＜0.05).However, mainly G2/M, S stage cell cycle rate for 72 hours, and S stage cell cycle rate in transfection group obviously higher than those in two control groups, but G2/M stage cell cycle rate were lower (P＜0.01).(3) After treated with cisplatin concentration (4.0 μg/ml) for 24, 48 hours and cisplatin concentration (6.0 μg/ml) for 24 hours, the intracellular cisplatin content tested by HPLC method in the transfection group were significantly lower than those in two control groups (P＜0.01).While, at 6.0 μg/ml of cisplatin concentration for 48 hours and 8.0 μg/ml of cisplatin concentration for 24 and 48 hours, the intracellular cisplatin content of transfection group were obviously higher than those two control groups (P＜0.05).(4) Treated with IC50 (6.0, 4.0, 4.9 μg/ml) cisplatin concentration at different time to obeserve ultrastructural changes by transmission electron microscopy.The results shown that the microwire gathered together at 24 and 48 hours, and the number and structure of mitochondria had obvious change in transfection group, while there was rare microfilament, the number of mitochondria decreased but structure change was not apparent in two control groups.There were appeared expansion of endoplasmic reticulum and had rare normal organelles among three groups.After treated with cisplatin for 72 hours, there were inordinate microfilament, a part of nuclear membrane disappeared, a lot of ribosomes gathered together in two control groups, and there were rare microfilament in transfection group, nuclear membrane completely disappeared, many white cystic matter were seen in cytoplasm, mitochondrial structure disappeared completely, which seems most cells on the verge of death.Conclusion The lentiviral expressing vector harboring human DHFR gene were successfully constructed.When the up-expression of DHFR gene, the drug-resistant in ovarian cancer cell may be increase, which suggest that there were certain contact between resistance increases with microfilament gathered and the change of the mitochondria.

Background and purpose:Dihydrofolate reductase (DHFR) is expressed highly in platinum-resis-tant ovarian cancer. This study aimed to explore the relationship between the silence ofDHFR gene and platinum drug resistance in ovarian cancer, and lay the foundation for the treatment of platinum-resistant ovarian cancer.Methods:To design targeting hairpin siRNA ofDHFR gene, the optimal siRNA silent sequence was selected, and lentiviral vector carryingDHFR gene was constructed successfully, named DHFR-pGCSIL-SKOV3 cell. Flow cytometry was used to detect the cell apoptosis of DHFR-pGCSIL-SKOV3 cells, pGCSIL-SKOV3 cells and SKOV3 cells incubated in various concentrations of cisplatin (2.5, 5.0, 10.0 and 20.0 μg/mL) at different time points (24, 48 and 72 h), and cell cycle changes of these cells at IC50 cisplatin concentration (4.4 μg/mL). High performance liquid chromatography was used to test intracellular concentration of cisplatin at different induction concentration of cisplatin (2.5, 5.0 and 7.5 μg/mL) and various time points (24 and 48 h). Ultrastructural changes of these cells at concentration of cisplatin IC50 (4.4 μg/mL) were observed by transmission electron microscope.Results:After annealing double-strand nucleotide was connected to pGCSIL/GFP vector, sequencing result was correct. SKOV3 cell were transfected with virus particles followed by Western blot detection of interference effect. Flow cytometry was used to detect apoptosis in three groups of cells, and increased apoptosis rate was found at the raised cisplatin concentration (2.5, 5.0, 10.0 and 20.0 μg/mL) at 24, 48 and 72 h in DHFR-pGCSIL-SKOV3, pGCSIL-SKOV3 and SKOV3 cells. The apoptosis rate in DHFR-pGCSIL-SKOV3 was signiifcantly higher than that in pGCSIL-SKOV3 and SKOV3 cells at 24 and 48 h (P<0.05). Flow cytometry was adopted to test cells cycle of 3 groups at different time period under IC50 cisplatin concentration (4.4 μg/mL), the results indicated that G0/G1 phase cell rate of DHFR-pGCSIL-SKOV3 was much more than the others, of which G2/M and S phase cell rates were on the contrary. While at 72 h, 3 groups were mainly G2/M and S phase cell rates, DHFR-pGC-SIL-SKOV3 was lower than the others. High performance liquid chromatography method was used to detect intracellu-lar cisplatin concentration at 24 and 48 h after the cells were incubated at various concentrations of cisplatin (2.5 and 5.0μg/mL). The results showed the intracellular cisplatin content of DHFR-pGCSIL-SKOV3 cell was signiifcantly higher than that of pGCSIL-SKOV3 and SKOV3 cells. However, after incubation at cisplatin concentration of 7.5 μg/mL, the intracellular cisplatin content of DHFR-pGCSIL-SKOV3 cell was signiifcantly lower than that of pGCSIL-SKOV3 and SKOV3 cells at 24 h, while higher than pGCSIL-SKOV3 and SKOV3 cells at 48 h (P=0.034,P=0.014). We observed ultrastructural changes of three different cell lines induced by IC50 cisplatin concentration(4.4 μg/mL) at different time points by the electron microscope. We found that the microiflaments were increased and gathered together and mitochondrial structure was also changed obviously without the drug. However, there was rare microiflament in three groups of cells at 24 and 48 h, while at 72 h, obviously increased inordinate microiflaments were observed.Conclusion:We successfully constructed pGCSIL lentivirus interference carrier carryingDHFR gene. The research indicates that down-regulation ofDHFR gene is related to cisplatin drug resistance in ovarian cancer. The results laid the foundation for us to investigate the molecular mechanisms of multidrug-resistance in tumor.