Objective To probe the relationship between serum amyloid A and insulin resistance in patient with metabolic syndrome.Methods Parameters of body height,body weight,waistline,SBP,DBP,TG,TC,FPG,and HDL were measured in the group of 40 patients with metabolic syndrome while 30 healthy people were referred as control group.Results The level of serum SAA,HOMA,and IR were significantly higher than those of the control group(P<0.01),and the other parameters were also indicated significantly difference(except the parameters of age,height,TC,and LDL-C).In patients of metabolic syndrome,the SSA had a positive correlation with body weight,waistline systolic pressure LDL-C,FINS,HOMA and IR,while the SSA had a negative correlation with HDL-C.Conclusion SAA is closely associated with insulin resistance,and it may serve as a marker in patients with metabolic syndrome

Objective:Ghrelin is a brain-gut peptide with GH-releasing,apetide-inducing and anti-inflammation activities and with widespread tissue distribution.Ghrelin is the endogenous ligand of GH secretagogue receptor (GHSR),and both ghrelin and the GHSR are expressed in T cells.We therefore examined the effect of Ghrelin on human T cell and its signal transduction.Methods:Ghrelin-activating mTOR pathway in human primary T cell was studied using immunoblotting and inhibitors of the PI3K(LY294002,3-Methyladenine) or mTOR(rapamycin) and antagonist of GHSR1a(Des-Lys-3-GHRP6).Results:The results showed that GHSR1a was expressed on T cells.Ghrelin caused a significant increase in the phosphorylated mTOR,P70S6K,S6K,4E-BP-1,eIF4G,eIF4E by immunoblotting.While the phosphorylated mTOR,P70S6K were abolished by the mTOR inhibitor rapamycin and PI3K inhibitor LY294002,3-methyladenine and also antagonist of GHSR1a,Des-Lys-3-GHRP6.Conclusion:The data document that Ghrelin activates translation of T cells through mTOR pathway.

Objective To investigate clinical significance of plasma D-dimer (D-D),fibrinogen (FIB) and fibrin/fibrinogen degradation product (FDP) in patients with chronic obstructive pulmonary disease (COPD).Methods The level of plasma D-D,FIB and FDP in 150 patients with COPD and 80 healthy persons were detected,and compared.Results The level of plasma D-D,FIB and FDP in COPD patients were significantly higher than those in healthy persons[(2.16 ± 0.61) mg/L vs.(0.55 ± 0.04) mg/L,(5.88 ± 1.52) g/L vs.(3.12 ± 0.35) g/L,(7.18 ± 1.63) mg/L vs.(3.62 ± 1.55) mg/L],there were significant differences (P ＜ 0.01).Conclusion Monitoring the level of plasma D-D,FIB and FDP in COPD patients can provide reliable basis in hypercoagulable state and primary and secondary hyperfibrinolysis.

Objective To explore the role of chemokine CXCL12 and its receptor CXCR4 in the directional migration of human prostate cancer(PCa).Methods The expression of CXCL12/CXCR4 in 18 human PCa samples and human PCa cell lines(PC3,DU145 and LNCap)was determined by immunohistochemistry and immunocytochemistry,respectively.Then the effect of CXCL12 on the migration and invasion of human PCa cell lines Was investigated by Matrigel invasion assay.Results Except 1 PCa sample,positive CXCR4 protein expression was detected in 17 clinical PCa samples.On the contrary,in 18 samples determined,only one sample expressed weak CXCL12 protein.CXCR4 rather than CXCL12 protein was exressed in PCa cell lines PC3,DU145 and LNCap.In addition,CXCL12 promoted the migration and invasion of PCa cell lines in a dose dependent manner in viiro,in which experiments PC3,LNCap cells were pretreated by antibody of CXCL12 or CXCR4 and then it was found the migrations of cells stimulated by CXCL12 were inhibited.Conclusion CXCR4 protein is expressed in human PCa and CXCL12/CXCR4 axis may play a significant role in the metastasis of prostate cancer.

The X-ray computed tomography (CT) appearance of 4 cases with pulmonary cryptococcosis (PC) diagnosed by pathological examination in our hospital was retrospectively analyzed. The appearances of PC on CT were various: solitary lesion in 1 case, multiple lesions in single lobe in 2, and multiple lesions in multiple lobes in 1. There were total 52 lesions in 4 cases; the diameter of nodules or masses was 3 - 75 mm. Cavitations were found in 1 case; lesions appeared obviously enhanced and one lesion showed central necrosis. Two cases underwent pulmonary lobectomy; and 2 cases received core cutting needle biopsies, after antifungal therapy for 3 months to 1 year the lesions showed being absorbed. In summary, the CT appearance of PC is non-specific with various modes and forms. PC should be considered when multiple nodules or masses scattered in subpleural zone, accompanied with ground-glass opacity and obviously enhanced. The examination of pathogen and pathology at the beginning is crucial for improving diagnostic accuracy.

aused by pulmonary cryptococcus infection.Conclusions CT-gnided ACNB was a feasible, safe and accurate method for diagnosing pulmonary lesions, pulmonary malignant lesions less than 20 mm in diameter and complicated with pulmonary maybe affect accuracy.

AIM:To investigate rat Urotensin-II(ra t U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmon ary artery was dissected from the male Sprague -Dawley rats and artery ring width was 3-4 mm. Concentration-response curves wer e gene rated to rat U-II(0 03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0 1 ?mol/ L -10 ?mol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoc onstriction had reached plateau to construct the relaxant concentration-respons e curves and their EC 50 and E max . RESULTS: Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC 50 =7 95?0 4 0, E max =(14 28?6 34)% of the response to 60 mmol/L KCl]; PD 98059 caused c oncentration-dependent relaxations of rat U-II precontracted arteries [EC 50 =5 91?0 45, E max =(81 39?13 65)%]. CONCLUSION: Rat U- II was a potent vasoconstrictor of rat main pulmonary arteries and this response was med iated through MAPK.

Objective To investigate the effects of low density lipoprotein receptor (LDLr) pathway on podocyte injury in diabetic nephropathy (DN) under inflammatory stress.Methods Male db/db mice and db/m mice were randomly divided into four groups (8 mice in each group):db/m group (control),casein injected db/m group (db/m + casein),db/db group (db/db),and casein injected db/db group (db/db + casein).An inflamed model of DN was established according to our previous study.24-hour urinary protein was measured every week.The plasma lipid profile was detected by clinical biochemistry assay.Podocyte changes were evaluated by electron microscope and immunofluorescent staining.Lipid accumulation in the kidney was evaluated by oil red O staining and intracellular cholesterol quantitative assay.The protein expression of Wilm's tumor-1 (WT-1),nephrin,α-smooth muscle actin (t-SMA),and molecules correlated with LDLr pathway were examined by immunohistochemical staining or Western blotting.The colocalized protein expression of LDLr with WT-1 was examined by immunofluorescent staining and laser confocal microscopy.Results There were no differences in plasma levels of LDL and HDL among four groups.Compared with db/db group,the db/db+ casein group showed markedly increased 24-hour urinary protein,more significant podocyte foot process effacement and podocyte damage,increased lipid droplet accumulation in kidneys,increased protein expressions of LDLr,SCAP and SREBP-2 in kidneys (all P ＜ 0.05).Interestingly,increased LDLr protein expression in kidneys of db/db mice was negatively correlated with decreased nephrin protein expression (r =-0.855,P ＜ 0.01) and positively correlated with increased α-SMA protein expression (r=0.768,P ＜ 0.01).Conclusions The disruption of LDLr pathway induced by inflammation contributes to podocyte injuries in diabetic nephropathy.

Ob jective To construct and screen out the RPL 23-siRNA interference fragments ,providing the basis for the following experiments about the correlation with RPL 23 and gastric cancer .Methods The RPL23-siRNA,synthesized chemically through lipofection ,were selected from three target sequences by RNA in-terference and detected by real -time PCR and Western blot .Results Compared with normal cell group and RPL23 control group ,the mRNA and protein expression of RPL 23 in the other 3 interference groups were signifi-cantly decreased(P<0.01).Multiple comparisons showed that the interference efficiency of RPL 23 -siRNA1 group was significantly higher than that of RPL 23-siRNA2 group and RPL23-siRNA3 group(P<0.01).Con-clusion The RPL23-siRNA interference fragment can be successfully constructed and screened out ,which pro-vides the basis for the following experiments .

Objective To investigate the potential role of CXC chemokine ligand 16 (CXCL16)/CXC chemokine receptor 6 (CXCR6) pathway in the progression of diabetic nephropathy (DN). Methods 8?week old male db/db mice were randomly divided into DN group and DN inflamed group. 10% casein was subcutaneously injected to induce the DN mouse model with inflammation. In vitro, HK?2 cells were treated with high glucose (HG), and IL?1β+HG to investigate the effect of inflammatory stress on HK?2 cells. Further knockdown CXCL16 was mediated by RNA interference to determine the effects of CXCl16, then cells were divided into HG+IL?1βgroup, HG+IL?1β + siCXCL16 group and HG + IL?1β + vehicle group. Changes of renal function in mice were assessed by 24 h proteinuria and N?acetyl?β?D?glucosaminidase (NAG) during 8 weeks. The ultra?microstructure was checked by electron microscopy at 8th week. Lipid accumulation in kidneys and HK?2 were observed by Filipin staining and quantitative assay of intracellular free cholesterol. The protein expressions of CXCl16, CXCR6, a disintegrin and metalloproteinase?10 (ADAM10), fibronectin and α smooth muscle actin (α?SMA) in renal tissue were detected by immunohistochemistry and Western blotting. The mRNA and protein expressions of CXCl16, CXCR6, ADAM10, fibronectin andα?SMA in HK?2 cells were detected by real?time PCR and Western blotting, and protein expressions of CXCl16, CXCR6 and ADAM10 in HK?2 cells were also tested by cell immunofluorescence. Results Mice in DN inflamed group had higher 24 h proteinuria and NAG than those in DN group, and the differences between two groups shown statistical significance at 8th week (all P<0.05). Compared with DN mice, DN inflamed mice had more vacuoles within renal tubular cells, with mitochondrial swelling, deformation and decrease. Lipid accumulation and protein expressions of fibronectin and α?SMA were increased in DN inflamed group when compared with DN group (all P<0.05). Further, the expressions of CXCL16, CXCR6, ADAM10 were significantly increased in DN inflamed group (all P<0.05). In vitro, the mRNA and protein expressions of CXCL16, CXCR6, ADAM10, fibronectin and α?SMA, and lipid accumulation were increased in high glucose plus IL?1βgroup when compared with high glucose group (all P<0.05). However, after siRNA of CXCL16 transfection, the mRNA and protein expressions of CXCL16, CXCR6, ADAM10, fibronectin andα?SMA were down?regulated in HG+IL?1β+siCXCL16 group as compared with high glucose+IL?1βgroup (all P<0.05). Furthermore, lipid accumulation was decreased (P<0.05). Conclusion Inflammation accelerates tubulointerstitial injury in DN partly through the activation of CXCL16 pathway, which may facilitate the lipid accumulation in tubular epithelial cells.