Objective Percutaneous coronary intervention( PCI) is effective in improving the ischemia and prognosis of pa-tients with acute myocardial infarction ( AMI) to reduce the short-term mortality.However, little research has been done on PCI in eld-erly AMI patients.The study aimed to evaluate the efficacy and the safety of percutaneous coronary intervention in elderly AMI patients (≥75 years old) . Methods 213 AMI patients who underwent emergency PCI in Jingling Hospital from January 2012 to December 2013 were divided into 2 groups:elderly group (≥75 years old, n=57) and non-elderly group (<75years old,n=156).Retrospec-tive analysis were made on the clinical data and the coronary intervention features of the patients. Results There were more patients having dyspnea, fatigue and other heart failure symptoms at the onset of first-break AMI in elderly group than in non-elderly group (21.1%vs 3.2%,P<0.0).More women (47.4% vs 16.7%,P<0.01) and more patients with hypertention or diabetes mellitus were found in elderly group.The procedure success rates with TIMI-3 flow grade of post-PCI in both groups were very high (100%). Compared with non-elderly group, the occurrence of the procedure-related complications (3.5%vs 2.6%,P=NS) and major adverse cardiac event rates (8.8%vs 6.4%,P=NS) and in-hospital mortality (5.3%vs 2.6%,P=NS) showed no significant difference.Conclusion There are more atypical clinical symptoms in elderly AMI patients. The emergency PCI in elderly AMI patients can effectively make artery unimpeded with high successful rate, few com-plications and a favorable short-term prognosis.

BACKGROUND:Decreased function and reduced number of CD4+CD25+regulatory T cells have been considered the major manifestation of immunity dysfunction in children with primary nephrotic syndrome. Bone marrow mesenchymal stem cells have immunoregulation effects, which up-regulate CD4+CD25+regulatory T cells, inhibit proliferation of lymphocytes, and have been widely used in many immune diseases.
OBJECTIVE:To investigate the effects of bone marrow mesenchymal stem celltransplantation on the CD4+CD25+regulatory T cells of peripheral blood in rats with primary nephrotic syndrome.
METHODS:Bone marrow mesenchymal stem cells from six Sprague-Dawley rats were isolated, passaged and utilized for cellsuspension preparation. At the third passage, bone marrow mesenchymal stem cells were used for transplantation. The remaining 30 rats were randomly and equal y divided into three groups:normal group, normal saline infusion group, and bone marrow mesenchymal stem cells group. The rat models of primary nephrotic syndrome were established by single injection of adriamycin intravenously through tail vein in the latter two groups. Rats were then treated with bone marrow mesenchymal stem cells (1×10 7 ) (bone marrow mesenchymal stem cells group) or normal saline (normal saline infusion group) through tail vein at the same time after adriamycin administration. The normal group received no treatment.
RESULTS AND CONCLUSION:Compared with the normal group, rats in the normal saline infusion group developed nephropathy characterized by ascites, proteinuria, hypoalbuminemia, hypercholastero-lnemia, and progressive renal injury. However, the proteinurine and clinical severity in bone marrow mesenchymal stem cells group were significantly ameliorated after treatment with bone marrow mesenchymal stem cells. CD4+CD25+Treg/CD4+Treg in the peripheral blood in the bone marrow mesenchymal stem cells group and normal saline infusion group were significantly higher than that in the normal group at 28 days after model establishment (P<0.05), while there was no significant difference between bone marrow mesenchymal stem cells group and normal saline infusion group (P>0.05). The expression of FoxP3 mRNA in the peripheral blood mononuclear cells of the bone marrow mesenchymal stem cells group was significantly higher than that in the normal saline infusion group and normal group (P<0.05). The bone marrow mesenchymal stem cells play a protective effect in rats with primary nephrotic syndrome, which may be related to the increase of local expression of FoxP3 and generation of CD4+CD25+Treg.

Objective To detect the levels of high mobility group box 1 protein HMGB1),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),C-reactive protein (CRP) in order to explore the clinical significance of HMGB1 in patients with severely traumatic brain injury.Methods A total of 75 patients composed of 40 male and 35 female with severely traumatic brain injury were hospitalized from March 2011 through March 2012.The scores of Glasgow Coma Scale (GCS) were 5-8 within 12 hours after brain injury.Casualties with history of hypertension,diabetes,severe diseases of heart,liver and kidney,and with concurrent trauma of other parts of body were excluded.Another 50 healthy subjects were enrolled as controls.Serum samples were taken from both patients and controls at admission.The levels of HMGB1,TNF-α and IL-6 were measured by using enzyme-linked immunosorbent assay (ELISA).The level of CRP was measured by using automatic biochemistry analyzer.Comparisons of the levels of HMGB1,TNF-α,IL-6and CRP between casuahies and healthy controls were carried out.The correlations of HMGB1 with TNF-α,IL-6,CRP in patients with severe traumatic brain injury were analyzed.Thereafter,75 patients were divided into two groups post hoc:the death group and the survival group.On the 1st day,the 3rd day and the 7th day after trauma,serum HMGB1 was detected.The comparison of HMGB1 was made between death group and survival group by using t-test.Results Serum HMGB1 level in the traumatic patients was higher than that of healthy controls (P ＜ 0.01).Correlative analysis showed that there was a positive correlation between HMGB1 and TNF-α (r =0.365,P＜0.05),IL-6 (r=0.530,P＜0.05),CRP (r=0.661,P＜0.05) in patients with severe traumatic brain injury.Serum HMGB1 level in the death group was higher than the survival group (P ＜ 0.01).Conclusions Increased serum HMGB1 level was found after severe traumatic brain injury.There were positive correlations between HMGB1 and three inflammatory factors,TNF-α,IL-6and CRP.Serum HMGB1 should be used as reliable hiomarker to judge the prognosis of patients with severe traumatic brain injury.

[Objective ] Intrastriatal Parr interneurons are considered to be the junction between striatal input and output neurons. This study purposes to confirm the morphology of Parr neurons and their distribution in striatum. [Method] Adult male SD rats were perfused and the brains were removed. The sections were conducted with a semiconductor-frozen microtome, then single labeling and double labeling were immunocytochemically conducted with PAP technique. Positive neurons were observed, counted, and calculated, and analyzed with SPSS. [Results] The distribution of Parr positive neurons in striatum was inhomogeueous, and was the most dense in the dorsal lateral area (P<0.001) ; the distribution of Parr positive neurons in matrix compartment was apparently more than patch compartment (82.0% vs 18.0%, P<0.001); Parr positive neurons in striaturn were medium-sized cell bodies with polygonal or oval in shape (mean diameter is 11.68 μm), and were larger in the lateral area than that in the medial area (P<0.01) ; the positive dendrites were dense and smooth without dendrite spines; the positive axons 1 were slender and their collaterals extended in striatum. [Conclusion] The characteristic of Parr positive neurons collecting mostly in lateral striatum and matrix eompartment, as well as their traits of intemeurons, indicated that they would affect the striatal projection neuronal function.

To discuss the physiology teaching mode and method for adult higher education and aim to improve high effect and quality of teaching,we should use visual thinking and divergent thinking in class,and employ interactive and elicitation teaching method,pay attention to connect physiology with clinical practice,and make the lectures in class lively to stimulate students'interior incentive,improve students'ablitiy of comprehensive thinking and cultivate students to use physiological knowledge to analyze and solve the problems.

Objective To assess the left ventricular systolic function (LVSF) in patients with implanted dual-chamber(DDD) mode cardiac pacemakers using Two-dimensional Echocardiography (2DE),Real-time Tri-plane Echocardiography (RT-3PE)and Full-volume Three Dimensional Echocardiography (FV-3DE).Methods A total of 30 patients with DDD mode cardiac pacemaker were ex-amined by 2DE, RT-3PE and FV-3DE separately.Left ventricle end diastolic volume (LVEDV), left ventricle end systolic volume (LVESV), and ejection fraction (EF) were measured and compared within the three methods above .Results The measurement of EF with patients of post-operation was higher than the patients of pre-operation.The measurements of EF with 2DE were higher than RT-3PE.The measurements of LVEDV , LVESV and SV with 2DE and RT-3PE were lower than FV-3DE, and EF was higher .There were statistically significant differences in above measurements ( P <0.05 ) .But there were no statistically significant differences in measurements of LVEDV and LVESV between 2DE and RT-3DE ( P >0.05).Conclusions Implanting DDD mode cardiac pace-maker can evaluate LVSF of patients obviously .FV-3DE can evaluate LVSF in patients with DDD mode cardiac pacemaker accurately . The LVEDV, LVESV and SV are underestimated by 2DE and RT-3PE, and EF is overestimated by 2DE and RT-3PE.

AIM: To detect the effects of resveratrol (RSV) on the expression of microRNA-21 (miR-21) in primarily cultured neonatal rat atrial myocytes with electric remodeling induced by rapid electrical stimulation (RES).Furthermore, to find out the possible mechanism of miR-21 regulating electrical remodeling.METHODS: The neonatal rat atrial myocytes were isolated by double-enzyme (trypsin and collagenase I) digestion and differential adhesion method.The atrial fibrillation (AF) model was induced by RES.Atrial myocytes were randomly divided into 4 groups: control group, RSV group, RES group, and RSV+RES group.To further detect whether RSV regulated electric remodeling by miR-21, except the 4 groups, we add miR-21 over-expression group and miR-21 inhibitor group: RES+negative control (NC) group, RES+miR-21 mimics group, RES+miR-21 mimics+RSV group, RES+miR-21 inhibitor group, and RES+miR-21 inhibitor+RSV group.The optimal concentration and pretreatment time of resveratrol were determined by CCK-8 assay.The expression of miR-21 and the mRNA expression of L-type calcium channels CACNA1C and CACNB2 in atrial myocytes were detected by qPCR.The protein expression of L-type calcium channels Cav1.2 and Cavβ2 in the atrial myocytes was analyzed by Western blot.RESULTS: The expression of miR-21 in RES group was significantly increased compared with control group, while preconditioning with RSV decreased the expression of miR-21.Compared with RES+miR-21 mimics group, the expression of miR-21 in RES+miR-21 mimics+RSV group was significantly decreased.Meanwhile, the mRNA expression of CACNA1C and CACNB2, and the protein levels of Cav1.2 and Cavβ2 were increased (P<0.05).Compared with RES group, the expression of miR-21 in RES+miR-21 inhibitor group and RES+miR-21 inhibitor+RSV group was decreased, while the mRNA expression of CACNA1C and CACNB2, and the protein levels of Cav1.2 and Cavβ2 were increased.However, no difference of the expression of miR-21, the mRNA expression of CACNA1C and CACNB2, and the protein levels of Cav1.2 and Cavβ2 among RSV+RES, RES+miR-21 inhibitor and RES+miR-21 inhibitor+RSV groups was observed (P<0.05).CONCLUSION: In AF model induced by RES, RSV may reduce electric remodeling by inhibiting the expression of miR-21 and regulating the downstream target genes.

Objective To investigate the expression of stem cell associated protein CD90 in primary hepatocellular carcinoma (HCC) and its relationship with clinical pathological characters ;to analyze the relation between CD90 and epithelial mesenchymal transition (EMT) markers E‐cadherin (E‐cad) and N‐cadherin (N‐cad) .Methods The expressions of CD90 ,E‐cad and N‐cad in 53 tissues of HCC were detected by immunohistochemistry streptavidin‐perosidase (SP ) method , and 10 surrounding of liver benign lesions were studied as control .The expression of E‐cad and N‐cad in CD90 positive cells of two HCC cell lines (M HCC97‐L and HCCLM‐3 ) was measured by flow cytometry .Chi square test and Spearman rank correlation analysis were performed for count data .Independent sample t test was used for measurement data comparison .Results There was no CD90 expression in control liver tissue . The positive rate of CD90 expression in HCC tissue was (34% ,18/53) ,and the difference between two groups was statistically significant (χ2 = 4 .755 , P< 0 .05) .The expression of CD90 in HCC was positively correlated with portal vein cancer embolus (r= 0 .378 , P< 0 .05) and was negatively correlated with histological differentiation degree and capsular infiltration (r= -0 .398 and -0 .519 ,both P<0 .05) .The expression of CD90 was negatively correlated with the expression of E‐cad (r= -0 .341 , P<0 .05) ,however was positively correlated with the expression of N‐cad (r=0 .441 ,P<0 .05) .The positive expression rate of E‐cad in CD90 positive HCCLM‐3 cells was lower than that of MHCC97‐L cells ((2 .56 ± 0 .29)% and (4 .31 ± 0 .18)% ,t= 8 .757 ,P< 0 .05) ,while the positive expression rate of N‐cad was higher than that of MHCC97‐L cells ((8 .10 ± 1 .45)% and (5 .51 ± 0 .44)% ,t= -9 .667 ,P<0 .05) .Conclusions The expression of stem cell associated protein CD90 is correlated with the EMT of HCC .Their interaction promote tumor infiltration metastasis w hich may be a new target of HCC treatment .

Objective To investigate the changes of expression of peroxisome proliferator-activated receptor γ (PPARγ) and its coregulators and monocyte chemotactic factor (MCP-1) treated with intedeukin-1β (IL-1β), and to analyze the mechanism of interaction of these factors. Methods Renal tubular cells (HK-2 cells) were cultured in vitro. Total cellular RNA was isolated for real-lime quantitative polymerase chain reaction (real-time PCR), nuclear extracts were prepared for Western blot analysis and EMSA. The supernatant was collected for ELISA after the treatment of IL-1β at different concentrations and time points. Results Under stimulus of different concentrations of IL-1β (0～20 μg/L) for 24 hours, the mRNA expression of PPARγ, SRC-1, SRC-2 and PGC-1 decreased significantly (P<0.05), meanwhile NCoR increased obviously (P<0.05). In further time-dependent experiment, the mRNA levels of SRC-2 and PGC-1 decreased by 57% and 48%, respectively, at 1 hour after treatment with 10 μg/L IL-1β (P<0.05). The expression of SRC-1 decreased by 43%only after 2 hours (P<0.05). The expression of NCoR was not obviously changed until stimulated by IL-1β for 8 hours (2.17 folds, P<0.05), then it decreased slowly. In the same time-dependent experiment, Western blot analysis showed that IL-1β (10 μg/L) significantly decreased the protein level of PPARγ at 4 hours (P<0.05). ELISA analysis revealed that the secretion of MCP-1 kept on rising and reached the peak (160.56±2.80) ng/L at 8 hours (P<0.01), then decreased to (50.82±1.25) ng/L at 24 hours (P<0.01). IL-1β could down-regulate the DNA binding activity of PPARγ, and the activity of NF-κB was up-regulated. Conclusions PPARγ and its eoregulators are closely related to MCP-1 and NF-κB during inflammation response in kidney. The activation of NF-κB by IL-1β leads to the decrease of PPARγ, and its coactivators expression levels, however the expression of MCP-1 and NCoR in renal tubular epithelial cells is up-regulated. PPARγ together with its coregulators participate in the inflammation response in kidney.

ObjectiveTo investigate the role of MG-132, a specific dipeptide proteasome inhibitor, on the proliferation, apoptosis and the related proteins in renal interstitial fibroblasts. MethodsRenal interstitial fibroblasts (NRK-49F) were induced by transforming growth factor β1 (TGF-β1, 5 μg/L) and pro-treated with MG-132 (0～5 μmol/L). The cell proliferation was measured with MTT method. Cell cycle and apoptosis were analyzed by flow cytometry. The apoptosis was also analyzed by Annexin V/PI staining and DNA ladder. Expression of p53, p27, p21, caspase-3, Bcl-2 and Bax protein was examined by Western blot. ResultsTGF-β1 (5 μg/L) could stimulate the proliferation of NRK-49F. MG-132 (0.25～5 μmol/L) could inhibit TGF-β1-induced proliferation in a dose-dependent manner through G1-arrest. TGF-β1 alone could not induce apoptosis (3.880%±0.365% vs 4.723%±1.582%). But pretreatment of MG-132 (0.1～2.5 μmol/L) could significantly induce apoptosis of TGF-β1-stimulated NRK-49F in a dose-dependent manner. Typical DNA ladder was also confirmed in these two groups in the DNA fragments analysis after being incubated with 2.5 μmol/L MG-132 with or without 5 μg/L TGF-β1. Western blot showed that MG-132 could activate the cell-cycle and apoptosis-related proteins such as p53, p21, caspase-3, Bax and inhibit Bcl-2 in a dose-dependent manner, while expression of p27 remained unchanged. ConclusionsProteasome inhibitor MG-132 can inhibit proliferation and induce the cell apoptosis in renal interstitial fibroblasts stimulated by TGF-β1. The mechanism may be associated to the mediation of p53, p21, caspase-3, Bcl-2 and bax pathways. Protoasome inhibitor may be a new strategy to treat renal interstitial fibrosis.