0.05). Accessory pathway antegrade and retrograde effective refractory period values were shorter in patients with PAF attacks (P

Forearm ; innervation ; Ganglion Cysts ; surgery ; Humans ; Male ; Middle Aged ; Muscle, Skeletal ; innervation ; surgery ; Tendons ; surgery ; Ulnar Nerve ; surgery

We investigated the genetic diversity and evolution of the M gene of human influenza A viruses in Hangzhou (Zhejiang province, China) from 2009 to 2013, including subtypes of A(H1N1) pdm09 strains and seasonal A(H3N2) strains. Subtypes of analyzed viruses were identified by cell culture and real-time reverse transcription-polymerase chain reaction, followed by cloning, sequencing and phylogenetic analyses of the M gene. Assessment of 5675 throat swabs revealed a positive rate for the influenza virus of 20.46%, and 827 cases were diagnosed as. infections due to influenza A viruses. Seventy-six influenza-A strains were selected randomly from nine stages during six phases of a virus epidemic. Sequences of the M gene showed high homology among six epidemics with identities of amino-acid sequences of 98.98-100%. All strains contained the adamantine-resistant mutation S31N in its M2 protein. Two of the A(H1N1)pdm09 strains had double mutants of V27A/S31N or V271/S31N. One of the seasonal A(H3N2) viruses had another form of double-mutant R45H/S31N. Evolutionary rate of the M gene was much lower than that of the HA gene and NA gene. Compared with A(H3N2) strains, higher positive pressure on the M1 and M2 proteins of A(H1N1) pdm09 viruses was observed. Separate analyses of M1 and M2 proteins revealed very different selection pressures. Knowledge of the genetic diversity and evolution of the M gene of human influenza-A viruses will be valuable for the control and prevention of diseases.
Amino Acid Substitution ; China ; epidemiology ; Evolution, Molecular ; Genetic Variation ; Humans ; Influenza A Virus, H1N1 Subtype ; classification ; genetics ; isolation & purification ; Influenza A Virus, H3N2 Subtype ; classification ; genetics ; isolation & purification ; Influenza, Human ; epidemiology ; virology ; Phylogeny ; Selection, Genetic ; Viral Matrix Proteins ; genetics ; Viral Proteins ; chemistry ; genetics

Objective To investigate the effect of 9-cis retinoid acid(c-RA),a retinoid X receptor(RXR)agonist,on hydrogen peroxide(H2O2)induced apoptosis in cultured rat neonatal cardiomyoeytes,and to explore the mechanism.Method Cultured cardiomyocpes were randomly divided into three groups:normal group treated with vehicle(N group),H2O2 group treated with 100 μmol/L H2O2(H group),and c-RA group pretreated with 100nmol/L c-RA(H+R group).Cell viability was detected by MTT.Morphological changes of apoptotic cardiomyocytes were observed by Hoechst 33258 staining under fluorescence microscope.The apoptotic rate was determined by flow cytometry.Mitochondrial membrane potential(△(ψ)m)was measured by JC-1 dye.Cellular reactive oxygen species(ROS)production was detected by CM-H2DCFDA fluorescent probe.All measurement data wIe expressed as(x±s),and statistically analyzed using one-way ANOVA analysis and Dunnett test.Differences were considered significant when P was＜0.05.Results Treatment with c-RA significantly enhanced cell viability,reduced apoptosis ratio,stabled mitoehondrial membrane potential and reduced level of cellular reactive oxygen species.Conclusions RXR agonist c-RA inhibits H2O2-induced myocyte apoptosis in cultured rat neonatal cardiomyocytes,which may be related to alleviate oxidative stress injury.

To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.
Action Potentials ; Arrhythmia/*etiology ; Heart Ventricles/metabolism ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardial Infarction/*pathology ; Myocytes, Cardiac/*cytology ; Patch-Clamp Techniques ; Potassium Channels/*metabolism

To observe the effects of simvastatin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), high-cholesterol group (HC), high-cholesterol+simvastatin group (HC+S) and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shiftassay (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kappaB-DNA binding activity, MCP-1 protein expression, intima thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kappaB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P<0.05). There was no significant difference in the serum lipids between the LC and HC+S groups (P>0.05), but the NF-kappaB-DNA binding activity, the expression of MCP-1 protein and the intima thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P<0.05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kappaB-DNA binding activity and by reducing the expression of MCP-1 protein.

AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (I to ), delayed rectifier potassium current (I K) and inward rectifier potassium current (I K1 ) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, I to , I K and I K1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of I to , I K,tail and I K1 were reduced significantly in HMI group (P

Objective: To investigate the effects of normal and pathological bone marrow stromal cells(BMSC) on the proliferation and apoptosis of K562 cells in separated culture and contact culture.Methods: On 2,4,7 and 12 d after culture,the growth of K562 cells was observed under optical microscope;the apoptosis of K562 cells was detected by TUNEL. Results: the growth of K562 cells on CML BMSC in contact culture was faster than the else.The growth of K562 cells in contact culture was significantly faster than that in separated culture after 7 d(P

Objective To observe the effects of Fuyanshu Capsule on phenol mucilage-induced endometritis rats and the possible anti-inflammation mechanism of the therapeutic effects.Methods Chronic endometritis in rats was induced by injection of phenol mucilage suspension into the uterus.Sixty female SD rats were randomly divided into 6 groups,namely,sham-operation group (distilled water,10mL/kg),model group,Jinji capsule group (0.65 g/kg),and Fuyanshu Capsule groups (1.8 g/kg,0.9 g/kg and 0.45 g/kg).After the rats were treated 28 days with corresponding medicine by intragastric administration,the pathology of the endometrium and changes of tumor necrosis factor α(TNF-α)and interleukin-2 (IL-2)levels were detected to evaluate the effects of Fuyanshu Capsule. Results Fuyanshu Capsule (1.8 g/kg and 0.9 g/kg)ameliorated the body weight reduction caused by endometritis in rats.Fuyanshu Capsule (1.8 g/kg,0.9 g/kg and 0.45 g/kg)reduced the ratio of the swelling uterus and ovaries to body weight of the rats.It ameliorated obviously the hyperplasia,necrosis and degeneration of endometrial epithelia and infiltration of inflammatory cells.The capsule (1.8 g/kg)decreased the serum IL-2 level in the rats with phenol mucilage-induced endometritis. Conclusion The anti-inflammatory effect of Fuyanshu Capsule on chronic endometritis induced by phenol mucilage in rats may be related to the decrease of IL-2 level.

BACKGROUND:Retinoid X receptor (RXR) plays a central role in the regulation of intracellular receptor signaling pathways. The activation of RXR has protective effect on H2O2-induced apoptosis of H9c2 ventricular cells in rats. But the protective effect and mechanism of activating RXR in cardiomyocytes against hypoxia/reoxygenation (H/R)-induced oxidative iniury are stillunclear. METHODS:The model of H/R injury was established through hypoxia for 2 hours and reoxygenation for 4 hours in H9c2 cardiomyocytes of rats. 9-cis-retinoic acid (9-cis RA) was obtained as an RXR agonist, and HX531 as an RXR antagonist. Cultured cardiomyocytes were randomly divided into four groups:sham group, H/R group, H/R+9-cis RA -pretreated group (100 nmol/L 9-cis RA), and H/R+9-cis RA+HX531-pretreated group (2.5 μmol/L HX531). The cellviability was measured by MTT, apoptosis rate of cardiomyocytes by flow cytometry analysis, and mitochondrial membrane potential (ΔΨm) by JC-1 fluorescent probe, and protein expressions of Bcl-2, Bax and cleaved caspase-9 with Western blotting. Allmeasurement data were expressed as mean±standard deviation, and analyzed using one-way ANOVA and the Dunnett test. Differences were considered significant whenP was <0.05. RESULTS:Pretreatment with RXR agonist enhanced cellviability, reduced apoptosis ratio, and stabled ΔΨm. Dot blotting experiments showed that under H/R stress conditions, Bcl-2 protein level decreased, while Bax and cleaved caspase-9 were increased. 9-cis RA administration before H/R stress prevented these effects, but the protective effects of activating RXR on cardiomyocytes against H/R induced oxidative injury were abolished when pretreated with RXR pan-antagonist HX531. CONCLUSION:The activation of RXR has protective effects against H/R injury in H9c2 cardiomyocytes of rats through attenuating signaling pathway of mitochondria apoptosis.