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Objective @#To screen the core genes of diabetic kidney disease ( DKD) based on bioinformatics , ex- plore the therapeutic targets of DKD , and discuss its possible regulatory mechanism .@*Methods @#The expression da- ta matrix of glomerular transcriptome in patients with DKD in GEO database (GSE30528 , GSE47183) was extrac- ted , and the differentially expressed genes ( DEGs) were screened by bioinformatics methods to identify the core differential genes , and then gene expression and enrichment analysis (GSEA) were conducted to predict effective targets . @*Results @#By screening and identifying the mRNA expression matrix of DKD , five core genes were screened out. Among them , C1orf21 and NPHS1 were significantly down regulated , and CD48 , COL1A2 , and TGFBI were up regulated . NPHS1 and CD48 were significantly related to immune differences , intercellular communication , and cell surface interaction . Through receiver operating characteristic curve ( ROC) analysis and GSEA analysis and drug target prediction , it might be of great significance for the treatment of DKD .@*Conclusion @#The core genes screened in this study have significant correlation with DKD , which may be used as effective markers for the treat- ment of diabetes . And then , this study provides a theoretical basis for the treatment and identification of DKD .
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Objective To evaluate the left ventricular systolic function of uremic patients after peritoneal dialysis measured by two-dimensional speckle tracking imaging. Methods Thirty uremic patients with their left ventricular ejection fraction (LVEF) > 50% who had not been underwent dialysis were enrolled in this study. Thirty healthy volunteers were involved as controls. For both groups, the basic data and routine cardiac ultrasound parameters were measured, and the images were collected to be analyzed by QLab software. The left ventricular 16-segment time-strain curves were obtained, and the peak strain of the systolic phase of each segment was measured. The data of 2 groups were analyzed by two independent samples t-test. After 6 months of peritoneal dialysis, the uremic patients were checked again. By using paired t-test, we analyzed the difference in left ventricular systolic dysfunction of uremic patients before and after peritoneal dialysis. Results (1) Comparison between uremia group (nondialysis patients) and control group: systolic arterial pressure, diastolic arterial pressure and pulse pressure of uremic patients increased (t=-4.445,-4.531 and-2.203, P<0.05); left atrial anterior and posterior diameter (LAAPD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular end diastolic volume (LVEDV), left ventricular end systolic volume (LVESV) and left ventricular mass index (LVMI) of uremic patients were larger. Interventricular septum thickness (IVST), left ventricular posterior wall thickness (LVPWT) and relative wall thickness (RWT) were thicker (t=-6.461,-5.168,-4.660,-3.578,-2.872,-6.819,-6.251,-7.108 and-2.659, P < 0.05); the longitudinal, radial and circumferential directions peak systolic strain of 16 segment myocardial of uremic patients decreased (the longitudinal strain:t=-7.063,-5.391,-3.351,-5.323,-5.586,-7.842,-5.265,-5.587,-5.037,-3.051,-4.584,-3.936,-4.168,-9.783,-9.175 and-3.805; the radial strain: t=3.659, 3.58, 5.368, 2.649, 2.928, 4.344, 2.754, 5.031, 5.025, 2.277, 2.691, 2.731, 3.187, 4.179, 5.292 and 4.429; the circumferential strain: t=-5.158,-3.959,-2.164,-3.592,-2.324,-5.672,-4.946,-7.184,-7.748,-5.014,-2.439,-6.299,-8.072,-8.410,-7.884 and-8.854, P < 0.05).(2)Comparison between uremic patients before and after dialysis:the systolic arterial pressure of uremic patients decreased after dialysis (t=2.833, P < 0.05); LAAPD and LVMI of uremic patients decreased after dialysis (t=4.805, 2.631, P < 0.05); BAS, BA, BIL, BI, BIS, MAS, MAL, MIL, APA and APL longitudinal systolic peak strain and the BAL, MAL, MIS, APS, APL and API radial systolic peak strain of uremic patients increased after dialysis (t=5.199, 4.127, 3.781, 3.380, 4.114, 3.116, 2.840, 3.243, 4.003 and 5.605, P < 0.05; t=-3.343,-3.687,-2.488,-2.921,-3.826 and-3.339, all P < 0.05). There were no statistical differences in circumferential peak systolic strain (P>0.05). Conclusions In uremic patients, the structure of the left ventricle changed, the function of myocardial contraction decreased, and the function of myocardial contraction improved after peritoneal dialysis. 2D-STI was able to quantitatively and objectively evaluate the function of the left ventricular myocardial constriction before and after dialysis.
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Objective The goal of this study is to understand the function of FKBP51 in resistant to high fat diet-induced obesity using FKBP51 knockout ( KO) mice and in vitro adipocyte differentiation.Methods Four-week old male FKBP51 KO and wild type ( WT) mice were fed separately with regular or high fat diet for 6 weeks.The body weight and food consumption were recorded weekly, the energy expenditure differences ( O2 consumption, CO2 production, respiratory exchange ratio, and heat production) of each group were monitored using the MM-100 metabolism cages system for 24 hours, then the liver from the above animals were stained with the Oil red-O to detect the lipid accumulation and the expression of metabolic genes.In addition, induction of adipocyte differentiation of immortalized MEF cells from WT and FKBP51 KO mice were used to observe the effect of FKBP51 gene on lipogenesis.Results Compared to WT mice, FKBP51 KO mice has less weight increment, and less lipid accumulation in the liver, but with no difference on food consumption during high-fat diet fed.Moreover, FKBP51 KO mice exhibited more O2 consumption, CO2 production and heated production under both RD and HF diet conditions.The PEPCK, G6Pase and UCP-1 genes up-regulation.In addition, lipid content was reduced in FKBP51 gene deficient MEF cells after adipocyte differentiation.Conclusions The FKBP51 gene plays an important role in high fat diet-induced obesity through the energy metabolism enhancement and lipogenesis inhibition.
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Objective To explore the value of real-time tissue elastography (RTE) with tissue dispersion quantitative analysis technique for assessment of liver fibrosis stage.Methods 51 rats were injected 6％ thioacetamide to induce liver fibrosis model,and 9 rats were injected saline as control group.In modeling 4 weeks,8 weeks,12 weeks respectively,14 rats in group of liver fibrosis model and 3 rats in control group were randomly selected to RTE.All the rats underwent tissue dispersion quantitative analysis,to obtain 12 quantitative parameters of elasticity,which included average relative strain value (MEAN),standard deviation of relative strain value (SD),area ratio of low-strain region (％ AREA),complexity (COMP),kurtosis (KURT),skewness (SKEW),contrast (CONT),entropy (ENT),inverse difference moment (IDM),angular second moment (ASM),correlation (CORR) and liver elasticity index (LF index).Subsequently,rats were sacrificed and their livers were taken for pathology analysis.Liver fibrosis model group was divided into S0,S1,S2,S3,S4 group.The 12 quantitative parameters of elasticity were compared with each group.Results 49 rats were successfully modeled,and 42 rats were analyzed.Except COMP,KURT,CORR,the other quantitative parameters had statistically differences (P ＜ 0.05).The other 9 parameters were correlated with liver fibrosis stage.Among these parameters,MEAN,％ AREA and LF index had higher related coefficient(r =-0.831,0.882,0.866).The ROC curve was made by MEAN,LF index and ％AREA to estimate the fibrosis stage,when S≥S1,S≥S2,S≥S3,S =S4,the areas under the ROCcurve were 0.884,0.925,0.934,0.962 (MEAN);0.917,0.958,0.984,0.962 (％AREA);0.917,0.948,0.966,0.967 (LF index),respectively.Conclusions As a non-invasive examination,RTE dispersion quantitative analysis technology can be used to quantitatively assess liver fibrosis.