BACKGROUNDTumor necrosis factor a receptor 1 (TNFalphaR1) plays an important role in the signal pathway of apoptosis. The objective of this study was to investigate the effects of TNFalphaR1 knockout on the up-regulation of erythropoietin receptor (Epo-R) and the coordinated anti-apoptosis functions during myocardial ischemia-reperfusion injury in mice.

METHODSThe ischemia-reperfusion injury model for cardiomyocytes was performed by ligating the left circumflex branch artery of TNFalphaR1 knockout (P55(-/-)) C17 B6 mice, as well as wild-type (P55(+/+)) C17 B6 mice. Triphenyltetrazolium chloride (TTC) staining was performed to observe the damaged area of the heart. TUNEL staining and DNA fragmentation were used to identify apoptosis. Mitochondrial Bcl-2 and Bax as well as expression of Epo-R and its downstream genes (Jak-2, stat-5, Akt, IkB-alpha, HIF-1alpha) were measured by Western blotting. The gene knockout mice were assigned into those undergoing the apoptosis surgical model group (KO group), and those subjected to sham operation (KOs group). Similarly, wild-type mice were either exposed to the surgical model (WT group) or subject to a sham operation (WTs group).

RESULTSThe myocardial damage ratio of the wild-type group after the operation was significantly higher than that of the knockout group, (50.5 +/- 6.4)% vs (36.9 +/- 6.9)%, P < 0.01. Similarly, TUNEL positive ratio of the wild-type group was significantly higher than that of the knockout group, (63.1 +/- 5.6)% vs (42.1 +/- 4.7)%, P < 0.01. The gray value ratios of Epo-R, Jak-2, stat-5, Akt, IkB-alpha, HIF-1 and mitochondrial Bcl-2 in the KO group were significantly higher than those of the WT group, P < 0.05; however, mitochondrial Bax was significantly lower than that of the WT group significantly (P < 0.05).

CONCLUSIONSUsing the ischemia-reperfusion injury model in mice, cardiomyocytes of TNFalphaR1 knockouts exhibited anti-apoptotic characteristics. This information could be used to coordinate the prevention of myocardial apoptosis by up-regulating and activating the Epo-R pathway.

Animals ; Apoptosis ; Blotting, Western ; Disease Models, Animal ; I-kappa B Proteins ; metabolism ; In Situ Nick-End Labeling ; In Vitro Techniques ; Janus Kinase 2 ; metabolism ; Male ; Mice ; Mice, Knockout ; Myocardial Reperfusion Injury ; genetics ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; NF-KappaB Inhibitor alpha ; Oncogene Protein v-akt ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Receptors, Erythropoietin ; metabolism ; Receptors, Tumor Necrosis Factor ; genetics ; metabolism ; STAT5 Transcription Factor ; metabolism ; Up-Regulation ; bcl-2-Associated X Protein ; metabolism

Aortic Valve/surgery* ; Aortic Valve Stenosis/surgery* ; Cardiac Catheterization ; Heart Rupture ; Heart Valve Prosthesis ; Heart Valve Prosthesis Implantation ; Humans ; Transcatheter Aortic Valve Replacement/adverse effects* ; Treatment Outcome

OBJECTIVETo investigate the feasibility and safety in treatment of coronary bifurcation lesions with 6F-guiding catheter by transradial approach.

METHODSClinical data of 1258 patients who were treated with 6F-guiding catheter by transradial approach from Oct. 2003 to Feb. 2007 were reviewed. The most common approach in the treatment of bifurcations was one-stent technique on the main branch; if the side branch was large enough and the lesion was involved in the ostium and proximal part of side branch, two-stent technique was used.

RESULTOf 295 bifurcation lesions, 204 were originally planed to be treated by one stent; but finally 2 side branches were provisional stented due to dissection in this group. Ninety-one cases were planed to use double-stent technique: 73 with crushing stent (46 step crushing, 24 modified balloon crushing, 3 reverse crushing), 5 with T-stent, 3 with Cullote-stent, 5 with modified V-stent, 5 with step kissing stent. There was no acute myocardial infarction or death occurred but 1 case was complicated with cardiac tamponade secondary from coronary perforation.

CONCLUSIONThe treatment of coronary bifurcation lesions with 6F-guiding catheter by transradial approach is a feasible and safe procedure.

Angioplasty, Balloon, Coronary ; methods ; Coronary Angiography ; Coronary Artery Disease ; therapy ; Coronary Vessels ; pathology ; Female ; Humans ; Male ; Radial Artery ; Stents

OBJECTIVETo observe changes in plasma motilin (MOT) level among preterm infants after birth, to investigate the relationship between plasma motilin level and feeding intolerance (FI), and to clarify the possible risk factors.

METHODSA total of 112 preterm infants were divided into feeding tolerance (FT) group (n=59) and FI group (n=53). Their plasma MOT levels were measured by radioimmunoassay on days 1, 4, 7 and 14 of life. The clinical data of FI group were collected and subjected to multivariate logistic regression analysis.

RESULTSCompared with the FT group, the FI group showed significantly lower plasma MOT levels on days 1, 4, 7 and 14 of life (P<0.05), and there was a positive correlation between plasma MOT level and gestational age, age in days, and volume of enteral feeding in the FI group. The lower the gestational age, the longer the FI duration. There was a negative correlation between the plasma MOT level on day 1 of life and the FI duration (r=-0.913, P<0.001). Gestational age and prenatal use of glucocorticoid were protective factors for FI, while fetal distress, placental abnormality and perinatal infection were risk factors for FI.

CONCLUSIONSChange in plasma MOT level may be closely related to the development of FI in preterm infants. Early monitoring of plasma MOT level may be useful for predicting the occurrence of FI.

Enteral Nutrition ; adverse effects ; Female ; Gestational Age ; Humans ; Infant, Newborn ; Infant, Premature ; blood ; Infant, Premature, Diseases ; blood ; Logistic Models ; Male ; Motilin ; blood

OBJECTIVETo investigate the role of B7-H1 expression in IL-10 production, the B7-H1 and IL-10 expression levels in pancreatic carcinoma tissues and to analyze the correlation between B7-H1 expression and IL-10 level.

METHODSThe mRNA and protein levels expressions of B7-H1 and IL-10 in 35 cases of pancreatic cancer and corresponding paracarcinoma tissues and 5 cases of normal pancreas tissues were detected by RT-PCR, Western blot and immunohistochemistry respectively.

RESULTSThe findings for the first time provided the evidences that there was a clear trend for B7-H1 and IL-10 expressions to be most highly expressed in carcinoma tissue, intermediately expressed in paracarcinoma tissue, and expressed at the lowest level in normal pancreatic tissue at mRNA and protein levels. Moreover, there were statistically significant differences in B7-H1 and IL-10 expression between pancreatic carcinoma tissues, corresponding paracarcinoma tissues and normal pancreatic tissues at mRNA and protein levels (P < 0.05). Furthermore, the immunohistochemistry indicated that there were high expression levels of B7-H1 (60.5% +/- 12.7%) and IL-10 (65.3% +/- 16.2%) in pancreatic carcinoma tissues while there were no significant expressions in normal pancreatic tissues. Meanwhile, correlation analysis revealed that B7-H1 expression was significant associated with IL-10 level in tumor tissues at mRNA (P = 0.008, r = 0.841) and protein levels (P = 0.007, r = 0.838).

CONCLUSIONSOver-expression of B7-H1 may be responsible for the increasing IL-10 production in pancreatic cancer, which caused reduced immune response to tumor cells and contributed to pancreatic carcinoma escape from immune attack.

Antigens, CD ; immunology ; B7-H1 Antigen ; Humans ; Immune Evasion ; Interleukin-10 ; immunology ; Pancreatic Neoplasms ; immunology

BACKGROUNDPatients with diabetes mellitus (DM) have a higher risk of thromboembolic events; however, the optimal duration of dual antiplatelet therapy (DAPT) remains unclear. The goal of this study was to assess the efficacy and safety of various DAPT durations in patients with DM undergoing drug-eluting stent implantation.

METHODSWe conducted a literature search for randomized controlled trials (RCTs). We searched databases including EMBASE, PubMed, Cochrane Library, and Scopus up to June 2016. Investigators extracted data independently, including outcomes, characteristics, and study quality. A random-effect model was used to pool odds ratios (OR s) with 95% confidence intervals (CI s) of the clinical outcomes.

RESULTSSix RCTs totaling 6040 patients with DM were included in the study. Shorter-duration DAPT resulted in an increased rate of stent thrombosis (ST) (OR, 1.83, 95% CI: 1.03-3.26, P = 0.04), but did not increase the risk of myocardial infarction (OR, 1.33, 95% CI: 0.71-2.47, P = 0.37), stroke (OR, 0.96, 95% CI: 0.52-1.77, P = 0.90), target vessel revascularization (OR, 1.19, 95% CI: 0.46-3.07, P = 0.71), all-cause death (OR: 0.72, 95% CI: 0.48-1.09, P = 0.12), or cardiac death (OR, 0.82, 95% CI: 0.49-1.36, P = 0.44) significantly. Shorter-duration DAPT was associated with a decreased risk of major bleeding (OR, 0.60, 95% CI: 0.38-0.94, P = 0.02).

CONCLUSIONIn patients with DM, longer-duration DAPT had a lower risk of ST, but was associated with an increased bleeding risk.

Diabetes Mellitus ; therapy ; Drug-Eluting Stents ; adverse effects ; Humans ; Platelet Aggregation Inhibitors ; therapeutic use ; Randomized Controlled Trials as Topic ; Thrombosis ; prevention & control

OBJECTIVETo measure the serum level of secretory type II phospholipase A2 (sPLA2) in patients with coronary heart disease and investigate the possible relationship with IL-8 and LPA.

METHODSA total of 110 patients with acute coronary syndrome (ACS), 63 patients with stable coronary heart disease (SCHD) group and 89 non-CHD control patients were studied. Serum levels of sPLA2, IL-8, LPA and hs-CRP were measured and the correlation among these parameters was observed.

RESULTSThe levels of serum sPLA2 [(68 +/- 17) U/ml], IL-8 [(182 +/- 80) pg/ml] and LPA [(2.85 +/- 0.36) micromol/L] were significantly higher in CHD patients than those in controls [sPLA2: (55 +/- 12) U/ml; IL-8: (119 +/- 33) pg/ml; LPA: (2.34 +/- 0.36) micromol/L, all P < 0.01], and sPLA2 and IL-8 were also significantly higher in ACS patients [sPLA2: (71 +/- 18) U/ml; IL-8: (195 +/- 78) pg/ml] than those in SCHD patients [sPLA2: (63 +/- 12) U/ml; IL-8: (159 +/- 79) pg/ml, both P < 0.01]. Serum sPLA2 level was positively correlated with hs-CRP, IL-8 and LPA (r = 0.203, P = 0.007; r = 0.658, P < 0.01; r = 0.231, P = 0.005, respectively). The relative risk of having CHD is 6.248 (P < 0.01) with the sPLA2 level above 63.75 U/ml.

CONCLUSIONElevated serum sPLA2 level is a risk factor for CHD.

Adult ; Aged ; Aged, 80 and over ; C-Reactive Protein ; metabolism ; Coronary Angiography ; Coronary Disease ; blood ; diagnostic imaging ; Female ; Group II Phospholipases A2 ; Humans ; Interleukin-8 ; blood ; Lysophospholipids ; blood ; Male ; Middle Aged ; Phospholipases A ; blood ; Phospholipases A2

The purpose of this study is to investigate the effect of chelerythrine on the hypertrophy of cardiomyocytes of neonatal rats induced by different glucose levels and its mechanism. Using cultured neonatal ventricular myocytes as a model, groups were divided as: control (5 mmol x L(-1)); high glucose level (10, 15, 20, and 25.5 mmol x L(-1)); high glucose level (25.5 mmol x L(-1)) add different concentrations of chelerythrine (1 and 8 micromol x L(-1)); and control glucose level (5 mmol x L(-1)) add different concentrations of chelerythrine (1 and 8 micromol x L(-1)). Different groups of cardiomyocytes after adding corresponding treat factors were cultured for 48 hours. Cardiomyocytes' diameters and protein level were measured and the expression of PKC-alpha, PKC-beta2, p-PKC-alpha, and p-PKC-beta2 were measured by Western blotting. Compared with control group, neonatal myocytes cultured in high glucose levels showed increased cellular volumes, protein level and expression of PKC-alpha, PKC-beta2, p-PKC-alpha, p-PKC-beta2. When chelerythrine was added, cellular volumes, protein level and expression of PKC-alpha, PKC-beta2, p-PKC-alpha, p-PKC-beta2 were significantly reduced. But in 1 micromol x L(-1) chelerythrine group, the expression of PKC-beta2 was not significantly reduced. The result suggested that chelerythrine can reverse the hypertrophy induced by different glucose levels on the cardiac myocytes, it may have protective effect against diabetic cardiomyopathy via PKC passageway.
Animals ; Animals, Newborn ; Benzophenanthridines ; pharmacology ; Cells, Cultured ; Diabetes Mellitus, Experimental ; drug therapy ; metabolism ; Dose-Response Relationship, Drug ; Glucose ; administration & dosage ; Hypertrophy ; chemically induced ; pathology ; Hypoglycemic Agents ; pharmacology ; Myocytes, Cardiac ; drug effects ; pathology ; Phosphorylation ; Protein Kinase C ; antagonists & inhibitors ; metabolism ; Protein Kinase C beta ; Protein Kinase C-alpha ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo determine the effect of proton pump inhibitor (PPI) on in-stent restenosis (ISR) in patients receiving clopidogrel therapy.

METHODSTotal 439 patients underwent percutaneous coronary intervention (PCI) were enrolled in the study,including 250 post-PCI patients discharged on clopidogrel alone and 189 patients discharged on clopidogrel with PPI. The in-stent restenosis (ISR) ratio of the patients in these two groups were observed.

RESULTSDuring a mean follow-up period of (13 ± 5.9) months, the post-PCI patients discharged on concomitant clopidogrel-PPI therapy had higher risk of ISR than those discharged on clopidogrel alone (19.6% Compared with 8%, P<0.001).

CONCLUSIONConcomitant use of clopidogrel and PPI after hospital discharge would increase the risk of ISR for post-PCI patients.

Angioplasty, Balloon, Coronary ; Coronary Restenosis ; etiology ; Drug Antagonism ; Drug Therapy, Combination ; Follow-Up Studies ; Humans ; Platelet Aggregation Inhibitors ; therapeutic use ; Proton Pump Inhibitors ; therapeutic use ; Retrospective Studies ; Risk ; Stents ; Ticlopidine ; analogs & derivatives ; therapeutic use

OBJECTIVESTo measure the plasma levels of urokinase plasminogen activator (uPA), urokinase plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1), and study the relationship between the plasma levels of uPA, PAI-1 and the serum albumin (Alb), collagen type IV (CIV), the serum hyaluronic acid (HA), prothrombin time (PT) and prothrombin activity (PTA) in patients with different stages of liver cirrhosis following chronic hepatitis B.

METHODS72 cases with liver cirrhosis of different stages were classified according to child-pugh's categories A, B, C, in which there were 23 cases in child A, 29 cases in child B, and 20 cases in child C. The plasma levels of uPA, uPAR, PAI-1 and the serum levels of HA, CIV were detected by ELISA. The serum PCIII concentration was determined by radioimmunoassay.

RESULTSWith the progression of hepatic fibrosis, the plasma levels of uPA, uPAR and PAI-1 were (1.36+/-0.43) microg/L, (3.03+/-1.48) microg/L and (24.09+/-7.14) microg/L respectively in group A, (1.79+/-0.62) microg/L, (4.80+/-2.22) microg/L and (41.40+/-17.52) microg/L respectively in group B. The highest levels were in child C, whose levels were (1.88+/-0.64) microg/L, (4.82+/-2.02) microg/L and (52.60+/-16.87) microg/L respectively, compared with group A and group B, t value were from 2.81 to 7.38, all of P value were less than 0.01. There was negative correlation between the plasma levels of uPA and the serum PCIII (r=-0.4785, P<0.05) in child A, but, positive correlation between the plasma PAI-1 and the serum HA (r=0.5447, P<0.01) in child C. The value of PAI-1/uPA was significantly decreased in child A, but increased in child B and child C.

CONCLUSIONIn the late of liver cirrhosis, increased PAI-1 together with uPA, uPAR are associated with overall inhibition of matrix degradation. The plasma levels of uPA and PAI-1 were correlation to the progression of liver cirrhosis.

Female ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; blood ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 ; blood ; Receptors, Cell Surface ; blood ; Receptors, Urokinase Plasminogen Activator ; Urokinase-Type Plasminogen Activator ; blood