The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55±8 ms to 86±15 ms during sympathetic stimulation (P<0.01). The TDR (53±9 ms) during parasympathetic stimulation was not significantly different from that of the control (55±8 ms) (P>0.05). The EAD was elicited in the Mid of 2 dogs (16%) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58%) during sympathetic stimulation (P<0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolarization and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.
In order to study the role of annexin II, a recombinant expression vector, pZeoSV2 (+)ANN II, containing the annexin II cDNA, was developed. The 1. 1-kb-length annexin II cDNA was inserted into a expression vector, PZeoSV(+) and transfected into HL-60 cells which had low baseline expression of Ann- II. pZeoSV(+) ANN II was analyzed by restriction mapping and the Ann- II sequence identified. The ability of the transfected cells, non-transfected and mock-transfected cells to stimulate t-PA-depend plasminogen activation was compared. The results showed that HL-60 with pZeoSV(+) ANN II transfection could significantly increase the plasminogen activation (8.9±1.2 U)in vitro with the difference being significant as compared with non-transfected (1.5±0.4 U) and mock-transfected cells (4.2±0.9 U), respectively. Antiannexin II oligonucleotides significantly inhibited the binding ability of t-PA and plasminogen to annexin II, and obviously reduced the plasminogen activationin vitro. The above findings showed human umbilical vein endothelial cells (HUVECs) treated with sense or missense oligonucleotides indicated no significant change in binding of t-PA and PLG. Treatment of HUVECs with antiannexin II oligonucleotides could significantly reduce the plasminogen activation by 2.4–0.3 U as compared with sense oligonucleotide group in binding of t-PA and PLG. These results, therefore, suggest that Ann- II can bind plasminogen and participate in the stimulation of t-PA-dependent activation of plasminogen, and that interference with Ann- II mRNA by antisense oligonucleotide may be a new strategy for the therapy of bleeding in patients with hyperfibrinolysis.
To elucidate role of the three enzymes in hepatocarcinogenesis, hMTH1, hOGG1 and hMYH, mRNA expression were examined by using RT/semi-quantitative real-time PCR and 8-O-HdG levels was studied by HPLC/ECD in HCC and non-tumorous liver tissue of 21 patients with hepatocellular carcinoma (HCC). It was found that the 8-OHdG level in non-tumourous liver tissue was significantly higher than in HCC tissue (P=0.006), and this was correlated with the degree of inflammation. The hMTH1 expression in HCC tissue was significantly higher than in nontumorous liver tissue (P=0.014). Inversely, The hMYHα expression was significantly increased (P=0.039) in non-tumorous liver tissue. No difference was seen in hOGG1 expression in non-tumorous liver and HCC tissue. A significant linear correlation between hMTH1 and hOGG1 expression was found both in HCC tissue (r=0.809,P<0.001) and in non-tumorous liver tissue (r=0. 883,P<0.001). Our findings suggested a reactive rather than pathogenic role of the DNA repair enzymes in the hepatocarcinogenesis.
To elevate the clinical value of3D-FLASH in the diagnosis of anal fistula and compare it with convationd MR sequence, MR sequences, consisting of spin echo T1WI, turbo invertion recovery magnitude (TIRM), fast low-angle shot image (FLASH), mon-enhancement and enhancement substraction and coronary reconstructing, was conducted in15 cases suspected of anal fistula. Comparison was made among the three sequences in display rate of internal fistula, external fistula, the branch of fistule connulas. Our results showed that1 patient had perianal abscess.24 different anal fistulas were identified in14 patients, and10 of them was complicated with perianal abscess and8 of them with complex multi-branch fistula. The display rate of3D-FLASH sequence was much higher than those of T1WI and TIRM in all cases. It is concluded that3D-FLASH squence is an senstive and time-efficient technique for the dignosis of anal fistula.