Aortic Valve ; pathology ; Calcinosis ; Heart Defects, Congenital ; pathology ; Heart Valve Diseases ; pathology ; Humans

Aged, 80 and over ; Heart Valve Prosthesis Implantation ; methods ; Humans ; Male ; Prosthesis Failure

Metabolic abnormalities were identified and carotid intima-media-thickness(IMT)was measured in 221 individuals at risk for metabolic syndrome(MS).The results indicated that IMT was significantly thicker in MS individuals than that in non-MS individuals(P＜0.01).And there was a tendency of progressive increase in IMT with increasing components of metabolic syndrome.

objective To explore the role of cytokines and dendritic cells (DCs) in rat high-risk corneal allograft survival pro- longed by superantigen Staphylococcal Enterotoxin B (SEB) and to compare the different effects between SEB and glucocorticoid. Design Experimental study.Participants Fisher 344 and Lewis rats.Methods The Fisher 344 and Lewis inbred rats were used for high-risk penetrating keratoplasty model.All of the Lewis rat recipients were divided into three groups by blinded fashion.GroupⅠand GroupⅡrats were injected intraperitoneally with 0.2ml saline buffer or SEB (75?g/ml) respectively at 4-day intervals on three occasions before transplantation.GroupⅢrats were injected subconjunctivally with 0.1ml dexamethasone (1mg/ml) daily from the first day after surgery for 2 weeks.The allograft survival was examined under slit-lamp.The concentration of interleukin IL-1?,IL-2,IL-4,IL-5,IL-6, IL-10,TNF-?in rat aqueous humor and peripheral blood were measured by liquichip and the cytokine and CD11c,CD80,MHC-Ⅱex- pression in corneal grafts were examined by immunohistochemestry staining.Main Octcome Measures Mean survival time of the allo- grafts,the level of cytokines in aqueous humor,peripheral blood and corneal grafts.Results Compared with group control,the grafts mean survival time was delayed about 3.8d in group SEB (P=0.00) and 7.1d in group dexamethasone(P=0.01).But there was no signifi- cant difference between group SEB and dexamethone (P=0.26).Liquichip test showed that the level of IL-1?in aqueous humor was re- duced and IL-4,IL-6 and IFN-?,ascended.Only IFN-?,and IL-6 could be found in peripheral blood,and the changing shift of them was similar to that in aqueous humor.The immunohistochemistry staining showed that the expression of IL-2 in rat corneal grafts was signif- icantly decreased but IL-4,IL-6 and IL-10 elevated.The expression of DCs in group SEB was similar to that in group control,which was elevated after keratoplasty,but the phenotype of DCs was not the same.There were predominantly mature DCs in group control while immature DCs in group SEB.Conclusions The immunological inhibiting effect of SEB is same to glucocorticoid,but the mecha- nism is different.SEB can modulate immune response,which might induce immune inhibition via the local production of cytokines and effect on DCs maturation involving corneal graft rejection prevention.

Objective To explore the effects and mechanisms of prostaglandin E2 (PGE2) receptor 1 antagonist (SC-19220) on proliferation,prostaglandin synthase and extracellular regulated protein kinases (ERK) signal pathway induced by transforming growth factor β1(TGF-β1) in glomerular mesangial cells.Methods Mouse glomerular mesangial cells (GMCs) were divided into 5 groups:control group,TGF-β1 (10 μg/L) group,TGF-β1 (10 μg/L) plus SC-19220 group (0.1,0.5,1.0 μmol/L).The proliferation of GMCs was measured by CCK-8.The PGE2 in supernatant was measured by ELISA.The expression of connective tissue growth factor (CTGF),laminin (LN),cyclooxygenase 2(COX2),membrane-bound prostaglandin E2 synthase 1 (mPGES1) protein and mRNA was examined by Westem blotting and real-time quantitative PCR,ERK1/2 or phospho-ERK1/2 was measured by Western blotting as well.Results TGF-β1 induced the proliferation of GMCs and increased the secretion of PGE2.Besides,TGF-β1 significantly up-regulated the expression of CTGF,LN,COX2 and mPGES1 mRNA and protein (P ＜ 0.05),and increased the expression of phospho-ERK1/2 protein (P ＜ 0.05).However,SC-19220 significantly attenuated the changes of above-mentioned parameters and their activities (P ＜ 0.05).All the effects of SC-19220 were in dose-dependent manner.Conclusions SC19220 may reduce TGF-β1-induced cell damage by suppressing the activity of ERK1/2,and feedback inhibition of COX2,mPGES1 and PGE2,thus decreases the expression of LN and CTGF.

The essential medium of B115 composed of 1% tryptone, 0.25% yeast extract and 0.5% sodium chloride was determined by using an orthogonal design. The orthogonal design was also employed in testing the optimum additions. It was composed of 0.1%(NH_(4))_(2)SO_(4),1.4%K_(2)HPO_(4), 0.6% KH_(2)PO_(4) and 0.1% (Na_(3)C_(6)H_(5)O_(7)). The yield of B115 cultured in optimum medium was compared with the one in essential medium. Statistic analysis showed that the growth of B115 was most significantly improved by adding K~(+)、NH~+_(4) and (Na_(3)C_(6)H_(5)O_(7)) to essential medium. The antibacterial effect of Bacillus subtilis strain B115 on pathogenic Aeromonas was studied. The results showed different antibacterial effects of B115 on different aeromonads. There were obvious antibacterial effects on BSK-10 and CL990920, while no effect on the growth of TL970424.

0.05).Conclusions SNP of 2350G→A in ACE gene is associated with MI,AA genotype is probably a genetic marker of MI in Han nationality.

AIMTo explore effects of Ginsenosides (Rb1, Rg1) on the expression of Bcl-2, Bax in the serum of kidney ischemia/reperfusion inducing apoptosis of HK-2 cells.

METHODSThe serum of rabbits with renal ischemia/reperfusion (SIR) and the control serum of rabbits (SC) were acquired and cultured with HK-2 cells. Detected apoptosis with TUNEL assay. The experiment was designed as: control group,ischemia/ reperfusion group, Rb1 blocking group and Rg1 blocking group. To detect the expression of Bcl-2, Bax with immunocytochemistry after 24 hours' cultured.

RESULTSThe expression of Bax in Rb1 blocking group and Rg1 blocking group were significantly decreased (P < 0.01), the ratios of Bcl-2/Bax were increased as compared with ischemia/reperfusion group.

CONCLUSIONRb1 and Rg1 have protective effects on apoptosis of HK-2 cells induced by serum of kidney ischemia/reperfusion.

Animals ; Apoptosis ; drug effects ; Cell Line ; Female ; Ginsenosides ; pharmacology ; Ischemia ; blood ; Kidney ; blood supply ; Kidney Tubules, Proximal ; cytology ; Male ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rabbits ; Reperfusion Injury ; blood ; Serum ; physiology ; bcl-2-Associated X Protein ; genetics ; metabolism

OBJECTIVETo study the characteristics of gene expression of adrenal cortical steroid synthetase and its regulatory factor in mice with H22 liver cancer of different patterns.

METHODSSyndromes revealed in mice with H22 tumor were differentiated by quantified four diagnostic methods and syndrome differentiation, and mice with commonly encountered patterns (A: evil-toxin accumulation pattern, B: qi-deficiency pattern, C: yang-qi deficiency pattern and D: qi-yin-yang deficiency pattern) were screened out for subjecting to the study. Two batches of GeneChip Mouse Exon 1.0 ST Array detection were performed in the selected mice for detecting the gene expressions of adrenal cortical steroid synthetase and its regulatory factor, with the analysis performed put stress on the differential expressions in mice of various syndrome patterns.

RESULTSData obtained from the two batches detection showed well repeatability, in which similar genes of high or low expression emerged. The adrenal cortical steroid synthetase genes, such as Cyp11a1, Star, Cyp11b2, Cyp21a1, Hsd3b and Hsd17b were highly expressed, with few difference among the four patterns. However, Cyp11a1 was down-regulated and Cyp1b2 up-regulated in all patterns; Hsd3b1 and Cyp21a1 down-regulated in pattern A and B, but up-regulated in pattern C and D. As for the expressions of the relative regulatory factors, Cyb5b and Wnt4 were down-regulated but Fdx1, Fdxr, Hsd11b1, Por, Agt and Nr 0b1 were up-regulated in all patterns; Nr5al down-regulated in pattern A but up-regulated in other three patterns; Nr4al and Nr4a2 up-regulated in pattern A and down-regulated in the others.

CONCLUSIONSThe adrenal cortical steroid synthetase genes are rather conservative and stable in mice bearing H22 liver cancer, part of the expression might be correlated to the condition of disease and essence of syndromes, embodying the differences among different patterns in the same disease.

Adrenal Cortex ; metabolism ; Animals ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Liver Neoplasms ; diagnosis ; genetics ; metabolism ; Male ; Medicine, Chinese Traditional ; Mice ; Mice, Inbred Strains ; Oligonucleotide Array Sequence Analysis ; Oxidoreductases ; genetics ; metabolism ; Steroids ; biosynthesis ; Yang Deficiency ; Yin Deficiency

OBJECTIVETo investigate the effects of non-neuronal muscarinic receptors (NNMR) stimulation on atherosclerosis and endothelial cells activation.

METHODSAtherosclerosis model was established in ApoE-/- mice by a high fat diet for 7 weeks. During the experimental periods, animals were received a low (7 mg/kg/d) or a high (21 mg/kg/d) dose of arecoline by gavage. At the termination of the treatments, serum total cholesterol and NO levels were measured, and the aorta morphology was analyzed by hematoxylin and eosin staining. The gene expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in the thoracic aortas was determined by RT-PCR, and the MCP-1 protein expression and NF-κB activity were detected by Western blot analysis. NO production, MCP-1 secretion in cultured rat aortic endothelial cells (RAECs), and monocyte-endothelium adhesion assay were also performed after arecoline treatments.

RESULTSArecoline efficiently decreased atherosclerotic plaque areas, increased serum nitric oxide (NO) content, suppressed the mRNA and protein expression of MCP-1, and modulated the IκB-α degradation and P65 phosphorylation in the aortae of ApoE-/- mice. Furthermore, arecoline promoted NO production and suppressed MCP-1 secretion in cultured RAECs after ox-LDL exposure, and either atropine or NG-nitro-L-arginine methylester could abrogate these effects. Arecoline also significantly inhibited the adherence of U937 monocytes to the ox-LDL injured human umbilical vein endothelial cells, which could be abolished by atropine.

CONCLUSIONOur results indicate that arecoline attenuates the progression of atherosclerosis and inhibits endothelial cells activation and adherence by stimulating endothelial NNMR. These effects, at least in part, are due to its modulation on NF-κB activity.

Animals ; Aorta ; cytology ; Apolipoproteins E ; Arecoline ; pharmacology ; Atherosclerosis ; physiopathology ; prevention & control ; Cell Adhesion Molecules ; metabolism ; Chemokine CCL2 ; metabolism ; Cholesterol ; blood ; Disease Progression ; Endothelial Cells ; cytology ; drug effects ; Endothelium, Vascular ; Human Umbilical Vein Endothelial Cells ; cytology ; Humans ; I-kappa B Proteins ; metabolism ; Lipoproteins, LDL ; Mice ; Mice, Knockout ; Monocytes ; cytology ; NF-KappaB Inhibitor alpha ; Nitric Oxide ; blood ; Nitroarginine ; pharmacology ; Rats ; Receptors, Muscarinic ; physiology ; Transcription Factor RelA ; metabolism