Objective: To observe the intervening effect of resveratrol on coxsackie virus B3m-induced mycocarditis in Balb/c mice and explore its mechanism. Methods: An animal model of viral mycocarditis induced by coxsackie virus B3m (CVB3m) was used, taking ribavirin as control drug, to examine the changes of general condition, mortality, the weights of heart, liver and spleen, serum MDA and NO levels, and cardiac histology in Balb/c mice. Results: By comparison with ribavirin, it was found that in the mice model of viral mycocarditis induced by coxsackie virus B3m resveratrol significantly improved the changes of general condition, mortality, the weights of heart, liver and spleen, serum MDA and NO levels, and cardiac histology. Conclusion: It suggested that resveratrol might have some chemopreventive and chemotherapeutic effects in the treatment of viral mycocarditis.

Objective To examine the expression of potassium channel mRNA in myocardial tissue of mice with low selenium.Methods Forty C57BL/6 mice were randomly divided into four groups according to body weight(18-22 g),10 mice in each group,half male and half female.The low-selenium treatment groups were fed with low-selenium diet(selenium content was 0.004 mg/kg) for 4,12 and 24 weeks,respectively,and the control group was fed with normal diet(selenium content was 0.256 mg/kg).The mice were killed by cutting neck method,hearts were taken out and RNA was extracted by Trizol method.The expressions of potassium ion channel genes (KCNA4,KCND2,KCND3,KCNE1,KCNE2,KCNJ2,KCNJ12 and KCNQ1) at the mRNA level in heart were determined using real-time polymerase chain reaction.Results In low-selenium 4 weeks group,the mRNA expressions of KCNA4 gene(25.3 ± 0.09) and KCND2 gene(4.85 ± 0.05) were higher than that of the control group (1.00 ± 0.00,1.00 ± 0.00,all P ＜ 0.05); in low-selenium 24 weeks group,the mRNA expression of KCNJ12 gene (22.7 ± 0.10) was higher than that of the control group(1.00 ± 0.00,P ＜ 0.05); the mRNA expressions of KCND3,KCNE1,KCNE2,KCNJ2,KCNQ1 genes were compared with the corresponding control groups,the differences were not statistically significant(all P ＞ 0.05).Conclusions Low selenium can affect the mRNA expression of mouse cardiac potassium ion channel genes.

Objective To observe the influence of selenocysteine synthase(SEPSECS) on injury of human umbilical vein endothelial cell line EVC-304 induced by hydrogen peroxide (H2O2). Methods Transfection was conducted to transfect EVC-304 which was maintained in vitro. The cells were divided into four groups: control group, SEPSECS over-expression group, empty vector group and SEPSECS silenced expression group, then Real-time PCR and Western blotting were performed to detected SEPSECS mRNA and protein expression , respectively. Flow cytometry(FCM) was performed to detect cell cycle. Different concentrations of H2O2, which including 0, 200, 400, 600, 800, 1 000 μmol/L, were used to treat EVC-304 . Then malonaldehyde (MDA), superoxide dismutase(SOD) secreted by the cells which were treated with H2O2 for 6 h, were checked by MDA or SOD kit. Results The SEPSECS mRNA expressions of control, SEPSECS silenced expression, empty vector and SEPSECS over-expression groups were 1.03 ± 0.24, 0.43 ± 0.11, 0.98 ± 0.27 and 1.61 ± 0.13, respectively. The protein expressions of control, SEPSECS silenced expression, empty vector and SEPSECS over-expression groups were 1.00 ± 0.26, 0.51 ± 0.10, 1.12 ± 0.38 and 1.51 ± 0.20, respectively. There was a significant difference between control and SEPSECS silenced expression groups (all P<0.05), at the same time , this phenomenon was also observed between empty vector and SEPSECS over-expression groups (all P<0.05). The level of MDA was increased along with the H2O2 concentration. Besides, cell cycle was also tested, however, significant difference was not observed(all P > 0.05). Meanwhile, MDA of SEPSECS silenced expression groups[(15.8 ± 0.5),(19.6 ± 1.5)μmol/L] were significantly higher than control groups[(12.4 ± 0.1),(17.1 ± 0.5)μmol/L, all P < 0.05], on the other hand, MDA of SEPSECS over-expression groups[(10.8 ± 0.4),(14.2 ± 1.1)μmol/L] were lower than empty vector groups [(12.7 ± 0.7),(16.2 ± 1.1)μmol/L, all P < 0.05], when the H2O2 concentration was 800 or 1 000μmol/L. The level of SOD was decreased along with the H2O2 concentration. SOD of SEPSECS silenced expression groups[(7.7 ± 0.4),(2.4 ± 0.3)μmol/L] were lower than control groups[(10.0 ± 1.0),(6.0 ± 0.6)μmol/L, all P < 0.05], on the contrary, SOD of SEPSECS over-expression groups[(11.3 ± 0.6),(12.7 ± 1.6)μmol/L] were higher than empty vector groups[(9.2 ± 0.6),(6.7 ± 0.2)μmol/L, all P < 0.05], when the H2O2 concentration was 800 or 1 000μmol/L. Conclusion Expression of SEPSECS has a significant protective role on damaged EVC-304 which was induced by H2O2.

This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.

Pim kinases contribute to tumor formation and development of lymphoma, which shows enhanced DNA replication, DNA recombination and repair. Endothelial cells^(ECs) express all the three members of Pim kinase gene family. We hypothesized that DNA repair gene would regulate Pim expression in ECs. Human umbilical vein endothelial cells (HUVECs) were isolated and maintained in M199 culture medium. The cellular distribution of Pim-3 in ECs was determined by immunofluorescent staining. The siRNA fragments were synthesized and transfected by using Lipofectamine LTX. The total cellular RNA was extracted from the cells by using Trizol reagent. cDNAs were quantified by semi-quantity PCR. The effects of LY294002 and wortmannin on RNA stability in ECs were also examined. Our data showed that LY294002 and wortmannin, phosphatidylinositol 3-kinase (PI3K) and PI3K-like kinase inhibitors, increased Pim mRNA expression in ECs without altering the mRNA stability. RNA interference (RNAi) targeting DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated (ATM) increased mRNA expression of Pim-3 and Pim-1, respectively. Silencing of Akt decreased Pim-1 instead of Pm-2 and Pim-3 gene expression in ECs. But etoposide, a nucleoside analogue, which could activate DNA-PKcs and ATM, increased Pim expression in ECs. Our study indicates that the expression of Pim kinases is physiologically related to DNA-PKcs and ATM in ECs.

Objective To investigate the changes of compliance in large arteries and carotid artery intima-media thickness(IMT)in patients with metabolic syndrome.Methods There were 64 patients with metabolic syndrome and 56 age-matched control subjects.Their carotid-femoral pulse wave velocities(C-FPWV)were measured by the Complior SP and their carotid artery IMT were detected by B-mode ultrasound.At the same time their height,weight,waist circumstance,hip girth,blood pressure,blood glucose,blood lipid,BMI and waist to hip ratio(WHR)were measured.Results Compared with the control,the patients with metabolic syndrome had higher C-FPWV(P

Objective To investigate the related factors of nosocomial infection after severe thoracic trauma so as to provide basis and interventions for lowering nosocomial infection rate.Methods A retrospective case series study was conducted in 148 cases of severe thoracic trauma surgically treated from January 2014 to January 2016.There were 98 males and 50 females with an average age of 34.7 years.The abbreviated injury scale (AIS) was ≥ 3 points.The incidence of nosocomial infection was statistically analyzed.The possible factors related to nosocomial infection were analyzed,including age,gender,previous basic diseases,coma,blood transplantation,surgical procedure,operation time,tracheal intubation time,postoperative tracheotomy,and postoperative ICU hospitalization.Results Nosocomial infection occurred in 18 cases,with infection rate of 12.2％.There were 11 cases of pulmonary infection,four urinary tract infection,two incision infection,and one thoracic cavity infection.There were four cases (22％) of Gram-positive bacteria as pathogen,both of which were Staphylococcus aureus.A total of 12 cases (67％) were Gram-negative bacteria,among which four were infected with Klebsiella pneumonia,three with Acinetobacter baumannii,three with Pseudomonas aeruginosa,and two with Escherichia coli.Two cases were infected by fungi.The incidence of infection was correlated with the patients' age (≥ 60 years),previous basic disease,coma,operation methods,operation time (≥3 hours),endotracheal intubation time (≥24 hours),tracheotomy after surgery,and postoperative hospitalization duration in the ICU (P ＜ 0.05),rather than gender and blood transplantation.Conclusions The most common pathogen of nosocomial infection in severe thoracic trauma patients is Gram-negative bacteria.The older age,previous basic diseases,coma,thoracotomy,long operation time,long tracheal intubation time,tracheotomy and long ICU hospital stay are the risk factors for nosocomial infection.More attention should be paid to these risk factors in order to minimize the occurrence of postoperative hospital infection,and to reduce the harm to patients.

This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.
Animals ; Animals, Newborn ; Male ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocardial Reperfusion Injury ; metabolism ; Myocardium ; metabolism ; Oxidative Stress ; physiology ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Up-Regulation