Three dimensional finite element analysis of optimal distribution model of fillers in vertebroplasty / 中国骨伤

OBJECTIVE@#To establish a three-dimensional finite element model of osteoporosis and to study the stiffness recovery of injured vertebrae and stress analysis of adjacent vertebrae after percutaneous vertebroplasty under different perfusion and distribution conditions by simulating fluid flow into the vertebral body.@*METHODS@#A male healthy volunteer was selected. CT scans were performed from T@*RESULTS@#(1) The VonMises stress of T@*CONCLUSION@#Reliable biomechanical model of lumbar vertebral fracture can be established by using CT scanning data through software simulation. Vertebral fracture and vertebroplasty will cause biomechanical changes of adjacent vertebral bodies. With the increase of bone cement injection, the influence of biomechanical changes will increase significantly. Neighbouring vertebral fractures are more likely. For this experiment, percutaneous vertebroplasty has a suitable amount of cement injection of 4 ml.

effects of doxycycline on Cx43 distribution and cardiac arrhythmia susceptibility of rats after myocardial infarction

This study aims to observe the effects of doxycycline [DOX] on gap junction remodeling after MI and the susceptibility of rats to cardiac arrhythmia. The proximal left anterior descending coronary artery of rats was ligated to establish a myocardial infarction animal model. DOX, methylprednisolone [MP], or vehicle was intraperitoneally injected into the animals for two weeks. Then, the heart size and heart function of all animals were determined through echocardiography. The experimental animals were sacrificed after the electrophysiologic study. Myocardial tissues were sampled to analyze the distribution of Cx43 using immunofluorescence; the Cx43 content was analyzed using western blot analysis; and the MMP-2 and MMP-9 activity in the myocardium was analyzed using gelatin zymography. The distribution of Cx43 in the border of the infarcted myocardia in the MI and MP groups was clearly disrupted and the Cx43 content was significantly reduced. In addition, the distribution of Cx43 in the border of the infarct in the DOX group was relatively regular, whereas two weeks of DOX treatment significantly inhibited MMP activity. Meanwhile, the induction rate of arrhythmia in the rats after DOX treatment was lower than those in the MI and MP groups. The results show that DOX treatment after myocardial infarction improves gap junction remodeling in the myocardial tissue near the infarcted area by inhibiting MMP activity and reducing susceptibility to cardiac arrhythmia

Effect of inhibiting endoxin by antidigoxin antiserum on myocardial ischemia/reperfusion injury in rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of antidigoxin antiserum on oxygen stress induced by myocardial ischemia/reperfusion (MI/R) injury in rats.</p><p><b>METHODS</b>Sprauge Dawley rats were submitted to ligate left anterior descending coronary artery 30 min followed by 45 min reperfusion. Experiment animals were randomly divided into seven groups including sham group, MI/R group, normal salina group, verapamil group and three antidigoxin antiserum groups from low to high dose. The left ventricular myocardial tissue sample of ischemia were processed and measured the level of endoxin and malondialdehyde (MDA), the activities of Na+, K(+) -ATPase and superoxin dismutase (SOD). The myocardia morphology was observed.</p><p><b>RESULTS</b>The levels of endoxin and MDA increased and the activities of Na+, K(+) -ATPase and MDA were inhibited significantly in MI/R and saline groups. Including verapamil group in comparison to MI/R and saline groups, MDA level decreased and SOD activities partly reserved, meanwhile, only in three antidigoxin antiserum groups, the myocardial endoxin level was remarkably decreased, Na+, K(+) -ATPase activities were drastically increased. The myocardial histological morphology was significantly improved.</p><p><b>CONCLUSION</b>Antidigoxin antiserum, an endoxin mutual clone antibody, had the effect of attenuating the damage of oxygen free radicals induced by MI/R via to antagonizing the inhibition effect of endoxin on myocardial membrane Na+, K(+) -ATPase activities.</p>