Obiective To investigate the influence of rapid atrial pacing(RAP)on the expression of ?1c subunit of L-type calcium channel,and the protective effect of verapamil.Methods 30 rabbits were randomly assigned into RAP group and verapamil pre-conditioned group.Each group was further divided into 5 subgroups(n=3 for each subgroup).Electrode was embedded in the right atrium through right external jugular vein.Pacing was performed for 6h,12h,24h and 48h in different subgroups.No pacing in the sham operation group.For verapamil pre-conditioned group,the drug was intravenously administered(0.2mg/kg)30 minutes before the initiation of rapid atrial pacing.Right atrium tissue was harvested for determination of mRNA and protein expression of L-type calcium channel subunits by reverse transcription polymerase chain reaction(RT-PCR)and Western blot.Results The mRNA level of ?1c subunit started to be reduced 6h after rapid atrial pacing(RAP)and continued to decline as pacing continued,and the expression of protein was parallel with mRNA.Otherwise,the mRNA level of ?1c subunit started to decrease 24h after RAP and continued to decline while pacing continued,and the expression of protein paralleled with that of mRNA in verapamil pre-conditioned group.Verapamil can attenuate the down-regulation of L-type calcium channel of the atrium induced by RAP only at 24h after RAP,but the effect was less intent.Conclusion mRNA and protein expression level of L-type calcium channel subunits decreased after RAP,The calcium channel blocker verapamil can attenuate the down-regulation of L-type calcium channel of atrium induced by RAP resulting in a decrease or postponement of calcium overload in atrial myocytes,thus exerting protective effects on atrial electrical remodeling,but such effects vanished after prolonged pacing.

By analyzing the status of Cardiovascular Surgery advanced students,we discussed the characteristics and problems of clinical teaching for advanced students of Cardiovascular Surgery.Strategies of clinical teaching for advanced students of cardiovascular surgery are explored to improve the quality of clinical teaching.

To determine whether the pathological changes caused by injury to the spinal cord can be correlated with values obtained by the Magnetic Motor Evoked Potential (MEPs) technique, we studied spinal cords from 41 adult cats who were divided into 4 groups. The groups ranged from normal cats whose spinal cords were not compressed, to slightly, moderately and severely injured. MEPs were recorded before compression and in 30 minutes, 6 hours, 1 week, 2 week and 4 week after the compression unit was installed. Pathological changes with increased pressure were seen in blood vessels, nerve cells and fibers, Nissl substance and the central canal. A reversal of pathological changes was observed in slight or moderate injury during the 4 weeks of the experiment. Extensive injury, however, caused irreversible changes in the nerve cells with loss of motor function. The latency of MEPs at 30 minutes and 6 hours in the slightly injured group was 0.37 and 0.38 times greater than the baseline and returned to normal levels in 4 weeks. In the moderately injured group, the latency was increased 0.77 and 0.81 times and in the severely injured 1.32 and 1.36 times over the baseline. Recovery in the second group was partial and not at all in the severely injured. Thus, there appears to be good correlation between observed pathological changes, motor functions and MEPs.

In this study, the leukemia K562 cell line was used as a model to elucidate the anticancer effects and preliminary mechanisms of PAMs. MTT assay showed that PAMs could cause cytotoxicities in K562 cells in dose- and time-dependent manners. AO-EB, Annexin-FITC/PI staining showed that the killing effects of PAMs in K562 cells were related to apoptosis, which was further confirmed by the following molecular and enzymatic assay. The mRNA levels of pro-apoptotic genes caspase-3, caspase-9 and bax were remarkably increased while the anti-apoptotic gene bcl-2 was significantly decreased determined by fluorescent quantitative PCR. Western blotting disclosed that PAMs could up-regulate caspase-3 and down-regulate anti-apoptotic survivin protein expression. The latter was also consistent with the results that PAMs could increase the enzymatic activities of both caspase-3 and caspase-9. All these results suggested that PAMs could effectively inhibit the proliferation of K562 cells and the mechanisms may be closely related to apoptosis induction. The work provides evidence basis for PAMs to be potentially developed as anti-cancer leukemia Chinese medicine.

Objective To investigate the ameliorative effect of Lentinan (LNT) on sodium arsenite (SA)-induced hepatic lipid deposition in mice. Methods C57BL/6 mice were used as the experimental subjects, which were divided into control group, SA-exposed group, LNT + SA-exposed group and LNT control group. Blood and liver tissue samples were collected at the end of the experiment, and serum glutathione transaminase (ALT) and glutathione aminotransferase (AST) levels were detected by enzyme-linked immunosorbent assay (ELISA). A part of liver tissues was stained with hematoxylin-eosin (HE) or oil red O to observe the characteristics of liver pathological damage and lipid deposition, and another part of liver tissues was used to detect triglyceride (TG) and Adiponectin (APN) levels by ELISA. Results Compared with control group or LNT control group, SA-exposed group showed the increased levels of AST and ALT, showing the characteristics of liver histopathological damage and lipid deposition, and the APN level decreased while the TG level increased (P<0.05). Compared with SA-exposed group, the levels of AST and ALT decreased in LNT + SA-exposed group, showing the reduced degree of liver tissue damage and lipid deposition, and APN level upregulated while TG level downregulated (P<0.05). Conclusion Chronic SA exposure induces liver function damage, APN downregulation and lipid deposition in C57BL/6 mice, while LNT intervention leads to the significantly improvement of hepatic damage and lipid deposition, which may be related to the elevated APN level in liver.