A one time large dose of selenium with label was injected to Se deficient rats. Platelets, liver and PPP were assayed for GSH-Px activity and determined the uptake of Se. The results showed that platelet GSH-Px activity would also be a good index in reflecting the abrupt change of Se status. It can be changed rapidly and significantly. The results also demostrated that platelet GSH-Px trends to reflect GSH-Px in the liver which is the organ with the most labile Se pool. Platelet GSH-Px may be a suitable index of selenium status for determine the bioavilability of selenium from various food sources in short-term human studies. When different form of Se was given, GSH-Px activity in platelet, liver and PPP expressed on a protein basis was similar in the selenite and selenomethionine administered groups. However, Se uptake of platelet, liver and PPP was greater in the selenomethionine versus the selenite group, indicating that selenomethionine was being taken up nonspecifically into platelet protein other than GSH-Px. This fact was also shown by the lower platelet GSH-Px specific activity. There might be another metabolic way for Se. More work is needed to clarify metabolism of selenium in tissue.

AIM: To observe the effects of hypertriglyceridemia and fenofibrate on CD40L expression in platelets in vitro and in vivo. METHODS: In vivo experiments, according to its own strict standards, 20 patients were respectively selected for hypertriglyceridemia group and control group, before and after treatment of fenofibrate for hypertriglyceridemia patients. The CD40 ligand positive rates of platelets by flow cytometry and plasma soluble CD40 ligand by ELISA were examined under the same conditions as control group. The CD40L and sCD40L in each group were compared. In in vitro experiments, all 6 objects plasma was chosen in the same condition except for triglyceridemia, after the co-incubation of these plasma with the same healthy platelets was performed and the interference with wy14643, the CD40 ligand positive rate of platelets by flow cytometry and total platelets CD40 ligand protein content by Western blotting were examined under the same conditions in all objects. The CD40L positive rate and total CD40L content in each group were compared, respectively. RESULTS: The platelet CD40L positive rate and plasma sCD40L concentration in hypertriglyceridemia group were significant higher than those in control group (P<0.01). Followed the TG concentration decreased, the platelet CD40L positive rate and plasma sCD40L concentration decreased after the treatment of fenofibrate, the same as the total platelets CD40L content which was significant higher in hypertriglyceridemia group than that in control group in vitro (P<0.05). No effect of wy14643 on the total CD40L content expression was observed in vitro. CONCLUSION: Hypertriglyceridemia plasma stimulates immune-activation of platelets both in vitro and in vivo. sCD40L may mainly come from CD40L on platelet membrane. PPARα activator of fenofibrate may inhibit the immune-activation of platelets by reducing the concentration of plasma TG, but PPARα activator WY14643 cant inhibit the expression of CD40L and CD40L in vitro.

AIM:To observe the effect of immune-activated platelets and low-density lipoprotein cholesterol (LDL) on the expression and activity of cyclooxygenase-2 (COX-2) and peroxisome proliferator activated receptor ? (PPAR-?) in human umbilical vein endothelial cells (HUVECs) treated with activated platelets and LDL.METHODS:The platelets were activated by ADP.The co-culture system of HUVECs with immune activated platelets and/or LDL were established.The activity of COX-2 and expression of PPAR-? at mRNA and protein levels in HUVECs were detected by RT-PCR and Western blotting.The concentration of PGE2 was measured by ELISA for representing the COX-2 activity.The PPAR-? activity was determined by a nuclear factor assay kit.RESULTS:The COX-2 activity and mRNA expression of PPAR-?,the protein levels of COX-2 and PPAR-? and PGE2 concentration in activated platelets group were significant higher than those in un-activated platelets group (all P

AIM:To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein 22 (HSP22), tumor necrosis factor alpha (TNF-α) and endothelial nitric oxide synthase (eNOS) and the effect of atorvasta-tin intervention.METHODS:Hyperlipidemia model was established in SD rats.Afterwards, the rats were divided into nor-mal control group, high fat group and high fat+atorvastatin intervention group.The expression of HSP22 and TNF-αin the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting.RE-SULTS:No detectable expression of HSP22 and TNF-αin the normal control group was observed.However, the expression of HSP22 and TNF-αwas positive in the high fat group and the atorvastatin intervention group.The mean densities of HSP22 and TNF-αpositive particles were significant lower in the atorvastatin intervention group as compared with high fat group ( both P<0.05) .The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group (P<0.01).However, no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed.CONCLUSION:The expression of HSP22 and TNF-αin the rat aortas is increased in the hyperlipidemia rat model.This effect can be restored by atorvastatin treatment.The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model, but this tendency could not be attenuated by atorvastatin.

Objective To explore the treatment of chronic infective wounds .Methods A retrospective analysis of clinical data in 225 patients were admitted from 2000 to 2010 .Results (1) They were mainly traumatic ulcers ,pressure ulcers ,postoperative ul-cers ,diabetes ulcers ,vascular ulcers in the group ,accounted for 80 .4% (181/225) .(2) Bacterial culture positive rate was 87 .1%(196/225) ,a total of 46 kinds with 342 pathogens were cultured ,gram-positive bacteria 40 .6% (139/342);gram-negative bacteria 57 .6% (197/342);Fungi 1 .8% (6/342) .The main pathogens were S .aureus(52) ,E .coli(43) ,P .aeruginosa(44) ,Klebsiella .SPP (27) ,which were highly resistant to penicillin ,erythromycin ,ampicillin ,gentamicin ,cotrimoxazole and the multidrug resistance rate was 37 .1% (127/342) .Chronic wounds and multidrug resistant bacteria showed rapidly increasing trend from 2007 .(3) 201 pa-tients with topical antibiotic treatment ,208 patients(49 patiens underwent re-operation)underwent operations to close wounds ;213 patiens were recovery ,12 patiens had to leave hospital because economic burden .Conclusion Chronic infective wounds were affect-ed by many factors .emphasizing on debriding ,reasonablechoice ,circulative ,alternate use of antibiotics and wound bed preparation , appling surgery to close wounds in early stage could effectively control wound infection and promote wound healing .

Objective To explore causes and high risk electrocardiogram expression of cardiac syncope caused by malignant rapid ventricular arrhythmia.Methods Forty-eight patients were analysed, they had cardiac syncope once or more that after which were admitted to the hospital. Results The basic causes of cardiac syncope were individed following types in 48 patients: coronary heart disease with acute or dated myocardial infarction,dilated or hypertrophic cardiomyopathy,hypokalaemia were ordinarist inducer.Torsade de pointes(TdP) were most common type of malignant rapid ventricular arrhythmia.They had some high risk electrocardiogram expression: secondary long QT syndrome,Brugada's syndrome,idiopathic abnormal J wave,complex ventricular ectopic beats,acute myocardial infarction with ST-T electrical alternation; or extensive anterior myocardial infarction with tombstone ST segment elevation,dilated cardiomyopathy with advance QRS complex low voltage.They were different electrocardiographic and clinical characteristic. Conclusion The cardiac syncope caused by malignant rapid ventricular arrhythmia is not single and independent clinical entity, which presents different the causes and high risk electrocardiogram expression.

This article was aimed to explore the effect ofSan-Huang (SH) decoction on improving chemosensitivity of MCF-7 cells to epirubicin and inhibition of Aurora kinase A, in order to discuss its underlying mechanism. The inhibition of MCF-7 cells proliferation on breast cancer by SH decoction was determined by CCK-8 assay. RT-PCR and western blot were used to detect the Aurora A, p53 mRNA and protein expression level of MCF-7 cells by SH decoction. The siRNA silenced Aurora A of MCF-7 cells. CCK-8 assay was used to detect the inhibition of MCF-7 cells proliferation. CCK-8 assay and AnnexinV-FITC/PI staining were used to detect the inhibition rate and apoptosis rate of MCF-7 cells treated by the combination of SH decoction and epirubicin. Western blot analysis was used to detect the expression of apoptosis-related proteins. The results showed that SH decoction inhibited the proliferation of MCF-7 cells in a dose-dependent manner (P< 0.05). The effect of 48 h medication was better than 24 h (P < 0.05). There was no statistical difference with medication for 72 h (P > 0.05). SH decoction can regulate the Aurora A, p53 protein and mRNA expression of MCF-7 cells. siRNA silenced Aurora A, which downregulated the inhibition rate of MCF-7 cells by SH decoction for 50.0% (from 49.2% to 24.8%). The combination of SH decoction and epirubicin enhanced the effect of epirubicin on inhibiting the proliferation rate and apoptosis rate of MCF-7 cell, regulated the expression levels of apoptosis-related protein such as c-PARP, c-Caspase 3, Bcl-2, Bax, as well as the protein level of Aurora A. It was concluded that SH decoction can increase the chemosensitivity of MCF-7 cells to epirubicin, which may be related to the inhibition of Aurora Kinase A by SH decoction.

BACKGROUND: Our previous study showed that the activation of local renin-angiotensin system in heart and vessels contributed to hypertension and cardiovascular remodeling. However, whether oxygen free radical plays an important role in this process is still unclear. OBJECTIVE: To investigate the interventional effects of Ebselen, a kind of anti-oxidative drug, on rats administered by Nw-Nitro-L-arginine methyl easter (L-NAME) (L-NAME), inhibitor of nitric oxide synthase (NOS) for a long term, and probe into the role of oxygen free radicals (OFR) in hyper- tension and cardiovascular remodeling of NO-deficient rats. DESIGN: A randomized grouping and controlled animal trial. SETTING: Department of Cardiology, the Second Affiliated Hospital of Nanchang University, Institute of Cardiology, Nanchang University. MATERIALS: The experiment was completed from January 2002 to March 2003 at the Animal Experimental Lab, Institute of Cardiology, Nanchang University and the Key Molecular Medical Lab of Jiangxi Province. Twenty-four Wistar rats were divided to three groups according to the random number table method: normal control group (n=8), L-NAME group (n=8), L-NAME + Ebselen group (n=8). METHODS: ①Normal control group: The rats could eat and drink routinely, and they were administrated by skim milk ball (net weigh = 4 g) before feed every night. ② L-NAME group: The rats received L-NAME in the dose of 50 mg/kg mixed in one skim milk ball everyday before feed every night. ③ L-NAME + Ebselen group: The rats were admin istered by one skim milk ball (net weigh = 2 g) mixed with L-NAME (50 mg/kg) and one skim milk ball (net weigh = 2 g) mixed with ebselen (30 mg/kg). The systolic blood pressure (SBP) was detected before LNAME was given and at the ends of the 1st, 2nd, 4th,6th and 8th weeks respectively. The rats were killed under anesthesia at the end of the 8th week, the plasma and homogenate of myocardium of apex were taken to detect the biochemical indexes, the other heart tissues were used for the histological detections. MAIN OUTCOME MEASURE: ① Dynamic changes of blood pressure were observed. The levels of NO and malondialdehyde (MDA), activities of angiotensin-converting enzyme (ACE) and superoxide dismutase (SOD) in plasma and myocardium of apex were measured. The production of superoxide anion and the levels of angiotensin Ⅱ type 1 receptor (AT1R) protein expression in myocardium of apex were determined. ③ The pathomor- phological indexes were determined. RESULTS: All the 24 rats were involved in the analysis of results without deletion. ① SBP: At the ends of the 1st, 2nd, 4th 6th and 8th weeks, SBP elevated gradually in the L-NAME group, which were significantly higher than those in the control group at the same time (P ＜ 0.05-0.01). At the end of the 8th week, the SBP was significantly lower in the L- NAME + Ebselen group than in the L-NAME group (P ＜ 0.05). ② Bio chemical indexes in plasma and homogenate of myocardium of apex: The NO level and SOD activity in myocardial tissue were significantly lower in the L-NAME group than in the normal control group (P ＜ 0.05-0.01), but significantly higher in the L-NAME + Ebselen group than in the L- NAME group (P ＜ 0.05-0.01). The production of superoxide anion, ACE activity and level of AT1R expression were all significantly higher in the L-NAME group than in the normal control group (P ＜ 0.05), but signifi- cantly lower in the L-NAME + Ebselen group than in the L-NAME group. ③ Pathomorphological indexes: The ratio of cardiac mass to body mass, thickness of left ventricle and ratio of thickness to lumen diameter of small artery were all significantly higher in the L-NAME group and L- NAME + Ebselen group than in the normal control group (P ＜ 0.05-0.01), and the thickness of left ventricle and ratio of thickness to lumen diameter of small artery were significantly lower in the L-NAME + Ebselen group than in the L-NAME group (P ＜ 0.05) CONCLUSION: Ebselen, an anti-oxidative drug, enable to attenuate the development of hypertension and cardiovascular remodeling in NO-deficient rats. By activating renin-angiotensin system (RAS), OFR may accelerate the formation of hypertension and cardiovascular remodeling, and the increased production of OFR may contribute to the development of cardiovascular remodeling. It is indicated that RAS may play an important role in the development of hypertension and cardiovascular remodeling induced by NO-deficiency

OBJECTIVETo evaluate the clinical effect of semi-attached quad-helix appliance in expanding the narrow maxillary arches in patients with cleft lip and palate.

METHODS15 cases with cleft lip and palate were selected and treated by semi-attached quad-helix appliance. Before, during, and after treatment, the dental arch width between cuspid, the first premolar and first molar were measured.

RESULTSThe upper dental arches of all patients were expanded effectively in about five months. After orthodontic treatment, the upper dental arches were expanded, and the teeth were alined regularly, which provided good conditions for alveolar bone grafting.

CONCLUSIONThe semi-attached quad-helix appliance with the fixed orthodontic treatment can expand the narrow maxillary arches in patients with cleft lip and palate effectively and conveniently.

Keshan disease was an endemic cardiomyopathy in China. The very low selenium intake of local people was considered to be an important causal factor. The main pathological characteristics of this disease was multifo-cal necrosis and fibrous replacement of myocardium that was scattered throughout the wall of all chambers.Two patterns of myocardial necrosis, myofibrillar pattern and mitochondrial pattern were distinguished in electron microscopy. The myofibrillar pattern was characterized by myofibril segmentation. It agreed well with the contraction band necrosis described in light microscopy. It was mainly seen in acute Keshan heart and might be related to circulatory disorders. Mitochondrial pattern was identical with myocytolysis of conventional pathology. It represented the typical lesion of Keshan disease.Mitochondria showed early and conspicuous changes in involved myo-cytes. Myofibrillar damage seemed to be secondary to the mitochondrial injury in the development of myocytolysis.Histochemical studies revealed that the acid phosphatase activity was obviously increased in muscle fibers surrounding the necrotic foci, and the succinic dehydrogenase activity was greatly reduced in damaged myocardio-cytes.