Tanshinone ⅡA has a broad anti-tumor activity and good prospects for clinical application. Its possible mechanism of action involves the regulation of cell cycle, inhibition of cell proliferation, induction of apoptosis, inhibition of tumor invasion, metastasis and inhibition of angiogenesis, and reversal of multidrug resistance. This article reviewed the research progress of anti-tumor effect of tanshinone ⅡA in recent years.

Objective To study the effects of ginsenosides (GS) on spontaneous sleep architecture and Cortical EEG power spectrum. Methods 24 adult SD rats were randomly divided into the control, GS 10 and 100mg/kg groups ( n = 8). Rats were instrumented with sleep-wake recording electrodes. After recovery from surgical operation,rats were orally administered GS 10 and 100mg/kg or distilled water once per day for 6 days. On GS administration day 1 and 6,Polygraphic signs of undisturbed sleep-wake activities were recorded for 12 h after GS administration. Results On GS administration day 1 ,only 100mg/kg GS increased significantly total sleep and the non-rapid eye movement ( NREM ) sleep but decreased wakefulness [(9.40 ± 0.88 ) h, ( 8.00 ± 1. 21 ) h,(2.46 ±0.81)h s (7.55 ±1.59)h,(6.36±1.54)h,(4.38 ±1.62)h,(P＜0.01, P＜0.05, P＜0.01),respectively] ;Low and high dose GS enhanced δ-wave power of NREM sleep and wakefulness (P＜ 0.05 ) but reduced θ-wave power of wakefulness (P＜0.01) and-wave power during NREM, REM sleep and wakefulness (P ＜ 0.01 ),moreover,Low and high dose GS lowered θ-wave power of REM and NREM stage(P＜0.05 ) ,respectively. After 6days of GS administration, Low and high dose GS increased markedly total sleep(P＜0.05 ) and NREM sleep(P＜0.05 ) but decreased wakefulness (P ＜0.05 ) and sleep-wake cycles (P ＜ 0.05, P ＜ 0.01 ); moreover, Low and high dose GS enhanced δ-wave power during NREM sleep and wakefulness (P ＜ 0. 05 ) but reduced θ-wave power of wakefulness(P ＜ 0.05 ) and -wave power during NREM, NEM sleep and wakefulness (P ＜ 0. 05 ), 10mg/kg GS also lowered θ-wave power of NREM sleep (P＜0.01). Conclusion These results demonstrate that GS can regulate spontaneous sleep architecture in time dependent manner,as well as cortical EEG power spectrum in rats.

AIM: To further investigate preventive effects of Shenfu(SF) injection, a Chinese herb drug, on acute renal ischemic reperfusion injury (IRI). METHODS: After SF or normal saline was administered intravenously one time a day for four days, the renal ichemia-reperfusion(I-R) model was established by occlusion of right renal artery and vein for an hour and reperfusion for three hours after left nephroectomy. The activity of superoxide dismutase (SOD), content of malondialdehyde(MDA) in serum and renal tissue, and content of nitric oxide (NO),concentrations of Na + and Ca 2+ , numbers of WBC adhesion in renal tissue were detected and light and electronic microscopy were used for the detection of the renal histological changes. RESULTS: SF lowered significantly MDA content in either renal tissues or serum , concentration of Na +, the number of WBC adhesion, and scores of tubules in renal tissue after renal I-R, and the SOD activity in renal tissues and serum and NO content in renal tissue were obviously increased by SF.In addition,renal histomorphological damage in either light or electronic microscope were lightened by SF. But Ca 2+ concentration in renal tissue appeared to be only mildly affected. CONCLUSION: The mechanisms that SF protects renal structure and function against acute renal IRI may be involved in increasing SOD activity,scavenging directly oxygen free redicals(OFR),raising NO content,inhibiting WBC adhesion and recruiment,preventing Na + influx to form Na + overload.

Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period (ERP),vulnerability window (VW) of atrial fibrillation,and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage (RAA),left atrial appendage (LAA),distal coronary sinus (CSd) and proximal coronary sinus (CSp).Results (1) Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P＜0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P＜0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P＜0.05).(2) Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P＜0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P＜0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.(J Geriatr Cardiol 2008;5:28-32)

ObjectiveTo analyze the characteristic of the T peak-end interval (Tpe) in dilated cardiomyopathy(DCM) patients with heart failure and its significance in evaluation of global dispersion of ventricular repolarization.MethodsFifty-three inpatients were enrolled in this study,which included 28patients with DCM and heart failure (DCM group),and 25 patients with supraventricular tachycardia and without structural heart disease (control group).The Tpe and the dispersion of QT interval (QTd) from the 12-lead surface electrocardiogram(ECG) were acquired and measured,and consequently the corrected numerals of the average of Tpe (Tpe-AVEC),the maximal Tpe (Tpe-MAXC) were acquired.ResultsThe levels of Tpe-AVEC,Tpe-MAXC and QTd in DCM group were significantly higher than those in control group [ ( 106.31 ±26.34) ms vs.(82.72 ± 10.01 ) ms,(234.05 ± 69.75) ms vs.( 119.15 ± 11.55 ) ms,( 119.17 ± 67.62) ms vs.( 39.74 ± 17.04 ) ms ] ( P ＜ 0.05 or ＜ 0.01 ).ConclusionsThe global dispersion of ventricular repolarization is significantly increased in patients with DCM and heart failure.The Tpe-AVEC and Tpe-MAxc are recommended to be used for evaluating the dispersion of ventricular repolarization as the prognostic index in patients with DCM and heart failure.

Endothelial dysfunction was closely related with AS , NO bioavailability ( production and utilization of endothelial NO ) was decreased by oxidative stress , lipid infiltration , inflammatory factor expression , vascular tone alteration and so on , which play an important role in endothelial dysfunction .Enhanced arginine , activityand asym-metric dimethylarginine together with increased hyperhomocysteinemia all promote AS by intervening NO bioavail -ability.Diabetes mellitus, obesity, chronic kidney disease , smoking and so on also involved in AS via influencing NO bioavailability and NO level .

0.05]. Conclusion:Besides the enlargement of LA,the volume of LAA and the area of LAA ostium were significantly increased in AF patients.Preprocedural assessment of LAA ostium should be helpful for the selection of occlusion devices.Because LAA is be very close to LCX,the selection of AF ablation strategies should be carefully taken to avoid possible damage of LCX.

Background Atrial electrical remodeling(AER)plays an important role in the pathogenesis and maintenance of atrialfibrillation.However,little is known about modulation of vagal activilty to AER.This study aimed to investigate the relationshipbetween vagal moduation and AER. Methods Twenty four adult mongrel dogs under general anesthesia were randomized into 3groups.Sympathetic activity was blocked by administration of metoprolol in 3 groups.The changes in vagal modulation to atria afterAER were observed in 10 dogs without vagal interruption in group A.The effects of vagal intervention on AER were investigated in 8dogs with administration of atropine in group B.The impact of aggressively vagal activity on AER was studied in 6 dogs with bilateralcervical vag sympathetic trunLks stimulation during AER in group C.Bilateral cervicall vagosympathetic trunks were decentralized.Multipolar catheters wereplaced into high right atria(RA),coronary sinus(CS)and rightventricle(RV).AER was induced by 600 bpmpacing through RA catheter for 30 minutes.Attial effective refractory period(ERP)and vulnerability window (VW)of atrial fibrillationwere measured with and without vagal stimulation before and after AER.Results In group A,ERP decreased significantly at baselineand during vagal stimulation after AER compared with that beforeAER(all P＜0.05).In group B,ERP remaind unchanged at baselineand vagal stimulation after AER compared with tbat before AER (all P＞0.05).In group C,ERP shortened significantly at baseline andvagal stimulation after AER compared with that before AER(all P＜0.05).ERP shortening after AER in Groups A and C increasedsignificantly than that in group B (all P＜0.05).Atrial fibrillation could not be induced at baseline(VW close to 0) before and after AERin three groups.VW became widen significantly during vagal stimulation after AER compared with that before AER in Groups A and C(all P＜0.05),while VW remained unchanged in group B (VW close to 0).Conclusions Short-term AER results in the decrease inERP.AER is accompanied by the increases in atrial vagal modulation.The increased vagal activity and vagal stimulation promote AER,thereby increase the susceptibility to atrial fibrillation.The interrupted vagal activity attenuates AER.thereby suppresses the atriaIfibrillation mediated by vagal stimutlation.

Adult rats were implanted with sleep-wake recording electrodes in our experiments. Polygraphic signs of undisturbed sleep-wake activities were recorded for 24 h before cocaine administration, cocaine withdrawal day 1 (acute), day 8 (subacute), and day 14 (subchronic). Western blot method was performed to examine the expression levels of adenosine receptor subtypes in hypothalamus and cerebellum. Non rapid eye movement (NREM) sleep was significantly increased during nighttime (P < 0.01) and daytime (P < 0.05) on withdrawal day 8. The increase of NREM sleep was significant during nighttime (P < 0.01) and slight during daytime on withdrawal day 14, whereas both daytime and nighttime rapid eye movement (REM) sleeps were reduced markedly (P < 0.01) on withdrawal day 8 and 14. In addition, A2A receptor level was significantly enhanced on cocaine withdrawal day 8 and day 14 (P < 0.05), whereas A1 receptor level reduced markedly on withdrawal day 14 (P < 0.05). However, compared with that in the control group, no significant changes existed among adenosine A1, A2A and A2B receptors in rat cerebellum on cocaine withdrawal day 1, day 8 and day 14. Our findings suggest that sleep disorder caused by subacute and subchronic cocaine abstinence may be associated with over-expression of adenosine A2A receptor in rat hypothalamus to some extent.
Animals ; Cocaine ; adverse effects ; Dyssomnias ; chemically induced ; Electroencephalography ; Hypothalamus ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Receptor, Adenosine A2A ; metabolism ; Substance Withdrawal Syndrome

Portal hypertensive gastropathy (PHG) is a disease caused by cirrhotic (or non-cirrhotic) portal hypertension, with a typical feature of snake-skin appearance of the gastric mucosa under endoscope. Many studies have shown that portal hypertension is a necessary condition for the development and progression of PHG. PHG is often complicated by acute or chronic upper gastrointestinal bleeding, which may be the direct reason for patients to visit the hospital. Therefore, the study of the diagnosis and treatment of PHG is very important in clinical practice. This article reviews the research advances in the pathogenesis, classification, diagnosis, and treatment of PHG.