In Cantharidin-poisoned rats, nicotinamide-adenine dinucletide dehydrogenase (NADHD) andcytochrome oxidase (CCO) activities of myocardi-um, stomach and intestine were observed in exper-iment histochemically. The result showed thatNADHD and CCO reaction granules were de-creased, stained weakly, and distributed sparselyin myocardium, stomach and intestine of intoxicat-ed rats as compared with the control group. Thus,from the experimental result it was considered thatcantharidin may inhibit the activities of NADHDand CCO in varving degrees.

Based on the histochemical observation ofnicotinamide adenine dinucleotide dehydrogenase(NADHD) and eytochrome oxidase (CCO) activi-ties of myocardium in cantharidine poisoned rats,furthermore, we observed the changes of these en-zymes of the myocardium cytochemically. The re-sult showed that, compared with control group, NADHD and CCO activities were inhibited afteradministration of cantharidin 1 or 2 h, and the in-hibition was found to be more obvious with poison-ing times prolonged, after 24 h, the cristae of mi-tochondria can not be distinguished, and the reac-tion products diffued into stroma to become a ho-mogeneous mass and lost their normal localization.It is indicated that cantharidin might destroy thestructure of mitochondria and interfere the activi-ties of NADHD and CCO of which both are locatedon mitochondria.

Objective To determine the changes of L-type calcium currents(I Ca-L ) of rabbit ischemic myocytes in peri-infarcted zone.Methods Rabbit AMI models were made by ligation of branches of left coronary artery. After 1 week and 2 months, single pericardial myocytes were isolated enzymatically from ischemic zone adjacent to infarcted area and the normal control cells from similar regions in normal rabbit hearts. I Ca-L were recorded by using patch clamp techniques in the whole cell configuration. Results Peak of I Ca-L density of ischemic cells from the peri-infarcted zone was significantly reduced in AMI onc week later ( 3 52 0 93 pA/pF, n=6) compared to control cells ( 5 58 1 53pA/pF,n=10), P0 05 The steady-state inactivation curves were shifted to the hyperpolarizing direction in ischemic cells,the half-maximal voltage dependence of inactivation(V 1/2 ) in ischemic cells was 25 9 7 0 mV in AMI 1W , 21 3 5 6mV in AMI 2M and 13 1 4 2mV in the control cells(compared with control group,P

BACKGROUND:After acute myocardial infarction(AMI),there is still surviving myocardium in and around the infarcted area,which plays an important role in the occurrence of arrhythmia. OBJECTIVE:To study the alterations of the activities of Na+ channel current(INa),L-calcium current(ICa-L),transient outward K+ current(Ito) and inward rectifying K+ current(IK1) in the cardiomyocytes in the infarcted area after AMI. DESIGN: A randomized controlled study. SETTING:Department of Cardiology,Bethune International Peace Hospital. PARTICIPANTS:The experiment was finished in the Central Laboratory of the Department of Cardiology,Bethune International Peace Hospital from January to June 2003.Twenty New Zealand pure big-ear rabbits were randomly divided into AMI group(n=10) and control group(n=10). INTERVENTIONS:Rabbit AMI models were established by ligation of the left anterior descending coronary artery.The ventricular myocytes were separated with the method of enzymatic dissociation technique,and the changes of the ion currents were recorded with the whole cell patch-clamp techniques. MAIN OUTCOME MEASURES:The changes of INa,ICa-L,Ito and IK1 in the cardiomyocytes taken from the infarcted area of epicardium 24 hours after AMI in both the AMI and control groups. RESULTS:Twenty-four hours after AMI,the peak current densities of INa,ICa-L and IK1 in the AMI group [(28.48± 3.53) pA/pF,n=16;(3.91± 0.95) pA/pF,n=12;(26.93 ± 3.48) pA/pF,n=16]were all significantly reduced as compared with those in the control group [(45.50± 5.33) pA/pF,n=12;(5.58± 1.53) pA/pF,n=10;(34.12± 4.21) pA/pF,n=10] (t=3.026,P< 0.01;t=2.985,P< 0.01;t=2.706,P< 0.05).There was no significant difference in the Ito density between the AMI group and control group (P >0.05). CONCLUSION:The reduce of INa,ICa-L and IK1 caused by AMI can result in the decrease of myocardial conduction velocity,the shortening of action potential-time,abnormal repolarization,which is possibly the ionic mechanism for the reentrant ventricular arrhythmia after AMI.

Objective:To produce the mcAb specifically reacting with lung cancer and to purificate its antigen.Methods:The mice were immunized with A549, the mcAb 2B9 was screened by indirect cell ELISA and immunohistochemistry, and its antigen was purificated by immunoaffinity chromatography.Results:A mcAb was obtained, which could react to lung cancer but very little or not to normal lung tissue and other caner tissues, and the antigen of the mcAb was purificated from the cell lysate.Conclusion:A mcAb which can react to lung cancer have been obtained and its antigen was purificated, they may be useful on clinic for diagnosis and prognosis of lung cancer.

Objective:To establish a protein biochip flat to identify the subtype of interfon by adopting the 6 mAb which we have prepared.Methods: Recombinant human interferon was onto the NHS modified gold biochips.then the protein biochips were incubated with the 6 mAb.Cy3 conjugated sheep anti-mouse IgG was used to detect the antigen-antibody.Arrays are imaged using a fluorescence scanner (GenePix4100A) at 532 nm for Cy3.This method was compared with the traditional ones:ELISA,Western blot.Results:The results showed that this flat had speciality to identify the subtype of interfon. Conclusion: The protein biochip plat can provide a practical method to identify the subtype of interfon.It also has some advantages:high quantities;simple operation;low sample dosage and high repetition.

Objective To evaluate the regional cerebral metabolic changes in different episodes by magnetic resonance spectroscopy (MRS) after explosive brain injury in rabbits. Methods Fortyfive New Zealand white rabbits were randomly divided into eight groups, ie, normal control group( 10 rabbits) and trauma group (35 rabbits). The explosive injury in trauma group was induced by explosion of 600 mg TNT equivalent of paper detonators at 6.5 cm above the rabbit brain. The rabbits in trauma group was divided into 1,6, 12, 24 hours, 3, 7, 14 days subgroups (6 rabbits per group). The survival rate was observed at different time points after explosive injury. The MRS was used to detect the regional cerebral metabolic changes including N-acetylaspartate (NAA)/creatine (Cr) ratio and choline(Cho)/Cr ratio as well as evolution of blast injuries over time. Results The rabbits survived for overseven days in the trauma groups, with typical brain contusion manifested by pathological and conventional MRI. Compared with the normal control group, the NAA/Cr ratio was markedly decreased at one hour after injury, slightly rose again at 24 hours and fell again after seven days. The Cho/Cr ratio was markedly increased at one hour after injury, slightly fell again at 12 hours and rose again at three days after injury.Conclusions MRS can manifest the regional cerebral metabolic changes of rabbits with explosive injury at different time points and hence provide a theoretical basis for understanding the local tissue changes and determining the type of tissue damage after blast injury.

Objective To investigate the distribution of uranium in rats after inhalation with depleted uranium aerosols. Methods The depleted uranium aerosols were inhaled by Wistar rats. At 30, 90, 180, 270, 360, and 540 d after inhalation, the rata were sacrificed and tissue samples were collected. The contents of uranium in lung, kidney, liver, heart, brain, thighbone, spleen and thymus were measured by laser time-dependent spectroscopy analysis. Resulits The uranium contents of lung increased in the high-dosc and low-dose groups [(499833.3 ± 14214.8) ng/g and (25 424.0 ± 6193.4)ng/g, respectively] after inhalation, and significantly differed from the control (28.8 ± 13.9)ng/g, (P < 0.05).At 30 d after inhalation, the contents of uranium in lung, kidney and thighbone were higher than those of control, and then decreased time-dependently. At 60 d, the contents of uranium in liver, heart, brain, spleen and thymus were higher than those of control. Curve of the eontenta were biphasie, whieh went up first, reached at peak value and then went down. The contents of uranium were high in lung, thighbone, brain and thymus. Conclusions After inhalation of depleted uranium aerosols, lung and thighbone are the primary reservoirs for uranium redistributed, and accumulations in brain and thymus suggest other two organs for unanticipated injury by depleted uranium.

AIM: To study the current density of transient outward potassium current (I_(to)) in cells from the epicardial zone of the 1-week and 2-month infarcted rabbit heart. METHODS: Rabbits were infarcted by ligation of the left anterior descending coronary artery, 1 week as well as 2 months later, the single ventricular myocytes were isolated enzymatically from the infracted area of 1-week infracted rabbit heart (PMI-1 week) and 2-month infracted heart (PMI-2 months), region remote from the infracted zone of 2-month infracted heart (REM-2 months) and free wall of left ventricule from noninfarcted heart (CON). I_(to) was recorded using whole cell patch-clamp techniques. (RESULTS:) Membrane capacitance of myocytes in REM-2 months group was signifitantly larger than that in CON. I_(to)current density (at +60 mV) was significantly reduced in PMI-1 week [(7.5?2.4) pA/pF, n=12] and PMI-2 months [(10.6?4.1) pA/pF, n=18] compared with CON [(17.4?5.2) pA/pF, n=16], P

AIM: To study the effect of experimental acute necrotizing pancreatitis (ANP) on sodium and L-type calcium current in rat cardiomyocytes. METHODS: I Na and I Ca-L were recorded using whole cell patch-clamp techniques from left ventricular myocytes in ANP model established by retrograde injection of 3 5% sodium taurocholate 2 5 mL/kg into pancreatic duct. RESULTS: Peak I Na current density (at -30 mV) was significantly reduced in ANP [(12 45?2 26) pA/pF, n =16] compared with sham [(25 32?3 31) pA/pF, n= 14], P