Accumulating studies have proved that systemic inflammation is one of the important pathophysiologic mechanisms of heart failure. This article focuses on the sources of inflammation mediators and the causes of inflammation activation in heart failure including hemodynamic changes and oxidative stress, Toll-like receptors, microbial antigens and microorganisms, endotoxin hypothesis and neurohormonal activation. Furthermore, the effects of inflammation mediators such as cytokines and chemokines on heart failure are introduced. All lead to the conclusion that heart failure is a process with complex inflammation.

Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells (VSMCs), which were regulated by sterol regulatory element binding proteins(SREBPs).Methods ① Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed, and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.② Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group (n=6), low concentration simvastatin group (n=6) and high concentration simvastatin group (n=6). Besides, normal control group (sham operation group, n=8) was established. Intragastric group and high concentration simvastation group, respectively, while those in normal control group and atherosclerotic injured group were given same amount of normal saline. Rats were sacrificed 4 weeks later. Plasma lipid levels were examined by enzymic method, ratios of intima/(intima + tunics media) of thoracic aorta and left common carotid artery were determined, and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR. Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs. Low concentration simvastatin didn't promote the proliferation and migration of VSMCs, while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs, which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs. Moreover, high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA. Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.

Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells(VSMCs),which were regulated by sterol regulatory element binding proteins(SREBPs).Methods①Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed,and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.②Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group(n =6),low concentration simvastatin group(n=6) and high concentration simvastatin group(n=6).Besides,normal control group(sham operation group,n=8) was established.Intragastric administration of simvastation of 0.5 mg?kg~(-1)?d~(-1) and 2.5 mg?kg~(-1)?d~(-1) was conducted in low concentration simvastatin group and high concentration simvastation group,respectively,while those in normal control group and atherosclerotic injured group were given same amount of normal saline.Rats were sacrificed 4 weeks later.Plasma lipid levels were examined by enzymic method,ratios of intima/(intima+tunica media) of thoracic aorta and left common carotid artery were determined,and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR.Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs.Low concentration simvastatin didn't promote the proliferation and migration of VSMCs,while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs,which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs.Moreover,high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA.Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.

Background Granulocyte colony-stimulating factor(G-CSF)has been reported to have beneficial effect on cardiac dysfunction in post infarction and doxorubicin-induced cardiomyopathy.Objective To investigate the effects of G-CSF on cardiac remodeling in cardiac hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ).Methods Thirty-six male wild type mice(WT)were allocated randomly to receive subcutaneously G-CSF(10 ?g/kg per day, n=9),or Ang Ⅱ(2.88 mg/kg per day,n=9),or Ang Ⅱ plus G-CSF(Ang Ⅱ 2.88 mg/kg+G-CSF 10 ?g/kg,n =9)for 4 weeks with untreated WT(n=9)as controls.Blood pressure and cardiac function were measured. Heart weight/body weight ratio,myocyte cross-sectional area and fibrosis area were determined.The mRNA ex- pression of osteopontin(OPN)in myocardium was detected by RT-PCR.The expressions of angiotensin converting enzyme(ACE),ACE2 and phosph-p70S6 kinase protein in myocardium were assessed by Western-Blot.Results Ang Ⅱ significantly elevated blood pressure(SBP,Ang Ⅱ:139.7?1.6 vs WT:108.7?2.3 mmHg,P0.05),but significantly attenuated the myocyte cross-sectional area(Ang Ⅱ+G-CSF:181.06?0.11 vs Ang Ⅱ:202.02?0.16 ?m~2,P

Objective To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats. Methods The models of acute myocardial infarction were established in 16 rata by ligation of left anterior descending branch of left coronary artery through chest incision, and the animal were divided into control group(n=8) and experiment group (n=8). The hearts of another 2 rats were obtained for normal myocardial tissue sections as controls. Monoclonal antibody of ICAM-1 was infused from the caudal vein in experimental group, and no invervention was conducted for control group. Blood samples were obtained from caudal vein on the first, third, seventh and fourteenth day after operation in these two groups. Serum concentration of ICAM-1 was measured by ELISA, positive rate of CD34 cells in peripheral blood was detected by flow cytometry, and the parameters of concentration of ICAM-1 and positive rate of CD34 cells at each time point were compared between groups. Results The concentration of ICAM-1 in peripheral blood of experiment group reached the lowest of (59.01±2.22) pg/mL on the seventh day. The concentrations of ICAM-1 in peripheral blood of experiment group were lower than those in control group, and there were significant differences between these two groups on the seventh and fourteenth day(P < 0.01). The positive rate of CD34 cells in peripheral blood of experiment group reached the highest of (12±2.11)% on the seventh day. The positive rates of CD34 cells in peripheral blood of experiment group were higher than those in control group, and there were significant differences between these two groups on the third, seventh and fourteenth day(P<0.05 or P<0.01). Conclusion ICAM-1 can inhibit the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats.

Objective To investigate the accuracy of three-dimensional reconstruction coronary angiography with CardiOp-B system in the evaluation of coronary artery stenosis, and make comparison with conventional quantitative coronary angiography(QCA). Methods The imaging data of 33 patients (39 vessel segments) who underwent coronary angiography and received interventional therapy were collected. The vessel diameter, vessel area, diameter of reference vessel rate of stenosed area and lesion length detected by three-dimensional reconstruction coronary angiography and QCA were compared. Results There was no significant difference in the detected minimal vessel diameter, minimal vessel area, diameter of reference vessel, rate of stenosed area and lesion length between three-dimensional reconstruction coronary angiography and QCA in these 39 vessel segments (P > 0.05), while the lesion length detected by three-dimensional reconstruction coronary angiography was significantly longer than that detected by QCA(P < 0.05). Conclusion Three-dimentional reconstruction of coronary angiography with CardiOp-B system demonstrates higher accuracy in the quantitative analysis of coronary artery stenosis compared with conventional QCA.

ObjectiveTo explore the procedures and methods for genetic diagnosis in one nonsyndromic variants of congenital neutropenia (NSVCN) patient and its pathogenic mutation.Methods Genomic DNA was prepared from one NSVCN patient who had progressed to chronic myelomonocytic leukemia and ELA2,HAX1,WASp and GFI1 genes were amplified and sequenced.Results A novel compound heterogeneous mutation consisting of two frame-shift mutations (c.430-1insG and c.655- 9del5bp) was found in HAX1 gene.ConclusionA practically genetic diagnosis procedure for NSVCN has been established,and the novel HAX1 gene mutation may contribute to the etiology of NSVCN.

Objective To detect the expression level of aquaporin 8 (AQP8) in patients with functional constipation(FC) or constipated irritable bowel syndrome (IBS-C),and the correlation between the expression of AQP8 and clinical features.Methods From March to December 2014,a total of 16 patients with IBS-C and 19 patients with FC met Rome Ⅲ criteria were collected,and nine healthy individuals were assigned to control group at the same period.The ascending and decending colonic tissues mucosa of FC,IBS-C and control group were taken under endoscope.The expression of AQP8 at mRNA and protein level was detected by real-time polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC).The differences in AQP8 mRNA expression and AQP8 relative area were analyzed by Kruskal-Wallis test among groups,and Pearson correlation coefficient was performed for correlation analysis between the expression and clinical features.Results The relative expressions of AQP8 mRNA of ascending colon and descending colon of FC patients (1.38,0.61 to 4.09;2.65,0.82 to 7.52) and IBS-C patients (2.23,0.82 to 4.67;1.35,0.51 to 2.03) were higher than those of control group (0.56,0.19 to 0.97;0.38,0.21 to 1.19),and the differences were statistically significant (ZFc =-2.435,-3.149,ZIBS-C =-2.690,-2.152;all P＜0.05).AQP8 mRNA expression of descending colon in patients with FC was higher than that of patients with IBS-C,and the difference was statistically significant (Z =-2.003,P =0.045).The expression of AQP8 in patients with FC and IBS-C was positively correlated with disease course (ascending colon r=0.57 and 0.53;descending colon r=0.49 and 0.54,all P＜0.05),and was negatively correlated with frequency of defecation (ascending colon r=-0.82 and-0.61;descending colon r=-0.49 and-0.53,all P＜0.05).There was no correlation between the expression of AQP8 and age,gender,onset age,presence of abdominal symptoms of the patients (all P＞ 0.05).Most of AQP8 of FC group was expressed in cytoplasm of colonic mucosa epithelial cells,while that of IBS-C group and control group was mostly expressed at apical membrane and basal membrane of epithelial cells.The results of semi-quantification demonstrated that AQP8 relative area of descending colon of FC and IBS-C group increased compared with that of control group (3.42％ (1.24％ to 5.61％),2.45％(1.72％ to 4.27％) vs 1.18％ (0.35％ to 2.81％);Z=-2.534,-2.151,both P＜0.05).Meanwhile,AQP8 relative area of ascending colon of FC group increased compared with that of control group (2.46％(1.48％ to 4.18％) vs 1.14％(1.29％ to 2.15％) Z=-2.041,P＜0.05).Conclusion There are differences in AQP8 expression quantity and location in cells of descending colon between patients with FC and patients with IBS-C,which is a way for differentiation these two diseases.

OBJECTIVETo study the blood pressure (BP) changes in the liver transplant recipients.

METHODSA total of 206 patients without preoperation hypertension received liver transplantation in our hospital from February 2001 to July 2005. The BP level and serum immunosuppressant concentration at preoperation and various time points post operation were determined.

RESULTSCompared with the preoperation, the average systolic and diastolic pressure was significantly increased at the 2 week, 1, 2, 4 and 6 months post operation. The mobility of hypertension increased significantly after liver transplantation, with the highest mobility (46.49%) at the 1st month post operation. There was no linear correlation between the immunosuppressant (FK506) concentration and the BP level at any time point.

CONCLUSIONThere was a high hypertension incidence after liver transplantation. Although the use of immunosuppressive drugs accompanied with the BP increase, there was no linear correlation between the immunosuppressant concentration and the BP level post operation.

Blood Pressure ; Female ; Follow-Up Studies ; Humans ; Hypertension ; etiology ; Immunosuppressive Agents ; adverse effects ; Liver Transplantation ; adverse effects ; Male ; Middle Aged ; Postoperative Complications ; physiopathology ; Retrospective Studies

Objective To investigate the incidence of acute kidney injury (AKI) post-orthotopic liver transplant (OLT) and its association with prognosis. Methods Data of 28 patients received single OLT in our hospital from 2004 to 2006 were retrospectively analyzed. The incidence of AKI was investigated by new acute kidney injury network (AKIN) criteria. The follow-up was over one year. The prognosis of AKI patients at day 28 and 1 year was evaluated by Kaplan-Meier survival analysis. The association between AKI and prognosis was examined. Results A total of 193 patients were enrolled. The average age was (48.07±10.02) years old. The ratio of male to female was 4:1. One hundred and sixteen (60.1%) patients of post-OLT AKI were found, whose AKI stage 1, 2 and 3 were 50.0%, 21.6% and 28.4% respectively. Ten (8.6%) patients required renal replacement therapy (RRT) after OLT. In AKI post-OLT patients, day 28 and 1 year mortality were significantly higher than those in non-AKI patients (15.5% vs 0, 25.9% vs 3.9%, respectively, both P<0.05). Kaplan-Meier survival analysis showed the 1-year survival rates of AKI stage 1, 2, 3 post-OLT and non-AKl were 84.0%, 81.0%, 42.4% and 90.9%, respectively. The 1-year survival rate of non-AKI was significantly higher than that of AKI stage 1, 2, 3. The 1-year survival rate of AKI stage 3 was significantly lower than that of stage 1 and 2. There was no significant difference between AKI stage 1 and 2. Sct at 1 year post-OLT was significantly higher than that of baseline [(88.35±37.15) vs (73.70±33.88) μmol/L, P<0.05). The change of Scr value at 1 year compared to baseline in AKI patients was similar to non-AKI patients. However such change in AKI stage 2 and 3 was higher than that in stage 1. Conclusions The incidence of AKI post-OLT is quite high and associated to the poor prognosis in short and long periods. Renal function may decrease gradually which is associated to the AKI stage pest-OLTI.