Atrial Fibrillation ; surgery ; Catheter Ablation ; Humans

Atrial Fibrillation ; surgery ; Catheter Ablation ; Humans

Animals ; Arrhythmias, Cardiac ; etiology ; therapy ; Captopril ; therapeutic use ; Disease Models, Animal ; Electric Stimulation Therapy ; methods ; Myocardial Ischemia ; physiopathology ; therapy ; Rabbits ; Ventricular Fibrillation

Objective To study the frequency of diffuse large B-cell lymphoma (DLBCL) with multi-genetic alteration, and its correlation with c-myc, bcl-2 and bcl-6 protein expression. Methods 50 cases diagnosed with DLBCL from January 2012 to December 2016 were collected. The expression of c-myc, bcl-2 and bcl-6 was analyzed by immunohistochemistry. Interphase fluorescence in situ hybridization (I-FISH) analysis was performed to identify the genetic alteration of c-myc, bcl-2 and bcl-6. Results In all cases, there were 27 males and 23 females with a median age of 50 years (range: 3-85 years). 23 (46.00 %) cases were defined as primary nodal DLBCL and 27 (54.00 %) cases were primary extra-nodal DLBCL, with gastrointestinal tract (48.15 %, 13/27) being the most common site of involvement. c-myc protein expression was detected in 94.00 % (47/50) cases, in which 82.00 % (41/47) cases exhibited high levels of c-myc expression with positive nuclear staining observed in over 40.00 % of tumor cells. The positive rate of bcl-2 protein was 84.00 % (42/50), 76 % (38/50) cases presented with high-level bcl-2 expression. Concurrent high expression of c-myc and bcl-2 were presented in 18 cases (36.00%). FISH analysis demonstrated c-myc gene rearrangement in 7 cases (14.00 %) and amplification in 2 cases (4.00 %). bcl-2 gene rearrangement was detected in 6 cases (12.00 %) and 4 cases (8.00 %) exhibited gene amplification. bcl-6 gene rearrangement was identified in 8 cases (16.00%), amplification in 3 cases (6.00%), and 1 case concomitantly harbored the rearrangement and amplification of bcl-6. Multi-genetic alterations were defined in 4 cases with 3 cases fulfilling the criteria for double-hit lymphoma (DHL) and 1 case for triple-hit lymphoma (THL). For the cases with concomitant high-level expression of c-myc and bcl-2 proteins, 3 cases (16.67 %) was detected with multi-genetic alterations, including 2 cases for DHL and 1 case for THL. Conclusions The proportion of DLBCL with multi-genetic alterations is 8.00 % in this study. The genetic alterations are not consistently correlated with the protein expression. The molecular genetic testing is reliable for the identification of DHL.

Aim To investigate estradiol inhibition of neointimal proliferation after rat carotid artery balloon injury. Methods Eight to ten-week-old SD rats (male,n=21,female,n=21) were divided into intact control(n=7),gonadectomy control(n=7) and estradiol (n=7, gonadectomy)groups in each sex. Left carotid artery was not injured with 2.0 F PTCA balloon until estradiol was injected for three days. Rats were killed 2 wk after injury. Neointimal areas and media area, ratios of intimal areas/media areas were measured with computer. Results Male neointimal areas and ratios of intimal areas /media areas in estradiol group were less than those in intact control group significantly(all P0.05). Conclusions Estrdiol inhibits neointimal proliferation after the gonadectomy in rats undergoing carotid artery balloon injury.

Objective To modify the method of gavage administration in guinea pigs. Methods Fourty awake guinea pigs were kept rearing on the hind legs and leaning on a vertical fixture to avoid their escaping forward. A 1 mL injector was inserted into the mouth to the depth when the molar teeth were passed. Another fourty guinea pigs under general anesthesia were reversed at trendelenburg position and a children suction tube with an outer diameter of 2 mm was inserted into the stomach. Results All of the 80 guinea pigs were administered by modified gavage smoothly for seven consecutive days by one operator each time. None endured much pain or digestive tract injury, or died from air way perfusion by mistake. Conclusions We successfully modified the gavage method in guinea pigs, which would definitely take guinea pigs involved in intragastical pharmacal experiments besides the routine of rats and mice.

OBJECTIVETo determine effects of activating protein kinase C (PKC) on ventricular action potential duration restitution (APDR) and Burst stimulus induced arrhythmia in Langendorff-perfused rabbit hearts.

METHODSMale rabbits were equally divided into three groups randomly: control group (Tyrode's solution perfusion), PKC agonist phorbol-12-myristate-13-acetate (PMA, 100 nmol/L) group and PKC inhibitor bisindolylmaleimide (BIM, 500 nmol/L) group. Thirty minutes after perfusion, the monophasic action potential (MAP) and effective refractory period (ERP) were determined in right basal ventricle (RB), right apex (RA), left basal ventricle (LB) and left apex (LA) of all the animals, and APDR curve was drawn. Burst stimulus method was used to induce ventricular arrhythmia in perfused rabbit hearts; Real-time PCR was used to detect the mRNA expression of PKC in four different areas of ventricle.

RESULTSCompared with the control group, the ERP, 90% of monophasic action potential duration (MAPD(90)) and ERP/MAPD(90) were significantly shortened (all P < 0.01), the max slopes (S(max)) of APDR curve were significantly steeper (RB: 1.22 ± 0.23 vs. 0.65 ± 0.19; RA: 2.99 ± 0.29 vs. 1.02 ± 0.18; LB: 1.84 ± 0.21 vs. 0.85 ± 0.12; LA: 4.02 ± 0.32 vs.1.12 ± 0.23, all P < 0.01) and the incidences of ventricular arrhythmia were significantly increased in the PMA group. All parameters were similar between the BIM group and the control group (all P > 0.05).

CONCLUSIONActivating PKC could enhance the max slopes of APDR curve at various ventricular areas and subsequently increase arrhythmia susceptibility in Langendorff-perfused rabbit hearts.

Action Potentials ; Animals ; Arrhythmias, Cardiac ; physiopathology ; Heart ; drug effects ; physiopathology ; Male ; Protein Kinase C ; pharmacology ; Rabbits

OBJECTIVETo investigate the effects of losartan on mRNA expression of myocardial sarcoplasmic reticulum calcium handling proteins (SERCA2, RyR2 and PLB) and the role of which in prevention of chronic heart failure in rabbit.

METHODSAfter chronic heart failure was induced by ligation of the left anterior descending artery in rabbits, the animals were treated with losartan. At 8 weeks after ligation, left ventricular function, hemodynamic parameters, and SERCA2, RyR2, PLB mRNA expressions were observed.

RESULTSCompared with the control group (group C), LVEDP in the infarcted group (group I) increased (P < 0.01), while +dp/dt(max) and -dp/dt(max) decreased significantly (P < 0.01). LVEDP was lower but +dp/dt(max) and -dp/dt(max) significantly higher in the losartan treated group (group L) than those in group I (P < 0.05). SERCA2, RyR2, and PLB mRNA expressions in group I were remarkably lower than those in group L (P < 0.01) and group C (P < 0.01), respectively.

CONCLUSIONLosartan can improve cardiac function, probably owing to its upregulating mRNA expressions of myocardial sarcoplasmic reticulum Ca(2+) handling proteins (RyR2, SERCA2 and PLB) in the prevention of heart failure.

Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Animals ; Calcium ; metabolism ; Calcium Channels ; drug effects ; Calmodulin ; biosynthesis ; genetics ; Female ; Heart Failure ; drug therapy ; metabolism ; Losartan ; pharmacology ; Male ; Rabbits ; Ryanodine Receptor Calcium Release Channel ; biosynthesis ; Sarcoplasmic Reticulum ; drug effects ; metabolism

BACKGROUNDNifekalant may prevent atrial fibrillation (AF) and possibly be useful in treatment of atrial tachyarrhythmia in patients with severe heart failure. This study investigated the electophysiologic effect of nifekalant on the acute atrial remodeling in rapid atrial pacing (RAP) model of canine.

METHODSTwelve mongrel dogs subjected to rapid stimulation (400 beats/min) at left atrial appendage (LAA) for 24 hours, were randomized into the control group (rapid pacing only, n = 6) and the nifekalant group (intravenous nifekalant therapy immediately after RAP, n = 6). Atrial electrophysiological parameters were measured in right atrium, coronary sinus, LAA, posterior wall of left atrium (PWLA) and left superior pulmonary vein (LSPV), before and after the RAP.

RESULTSIn the control group, the effective refractory periods (ERP) were shortened greatly at all sites, paced dogs had substantially shorter ERPs in the high right atrium, LAA, and LSPV, but fewer changes in the PWLA, the coefficient variation of ERP (COV ERP) was increased significantly. After rapid atrial stimulation, the inducibility of AF increased significantly [induction number: pre-RAP vs post-RAP, 1.00 +/- 0.89 vs 8.17 +/- 2.79, P < 0.01; duration of AF: pre-RAP vs post-RAP, (450.34 +/- 362.59) ms vs (9975.77 +/- 4376.99) ms, P < 0.01]. In the nifekalant group, although the ERPs were prolonged at all sites compared with those in pre-RAP state, only the value at LSPV differed significantly from that in pre-RAP state [pre-RAP vs post-RAP, (102.50 +/- 5.24) ms vs (132.51 +/- 5.20) ms, P < 0.01]; the COV ERP did not change statistically in this group. The inducibility of AF slightly increased but insignificantly after pacing [induction number: pre-RAP vs post-RAP, 0.83 +/- 0.75 vs 1.67 +/- 0.82, P = 0.19; duration of AF: pre-RAP vs post-RAP, (378.67 +/- 317.88) ms vs (1124.08 +/- 1109.77) ms, P = 0.06]. Conduction time values did not alter significantly in either of the two groups after RAP.

CONCLUSIONSIn canine RAP model, nifekalant inhibited ERP shortening and ERP heterogeneity increasing, decreased AF induction. Nifekalant can reverse acute electrical remodeling effect in this model.

Animals ; Anti-Arrhythmia Agents ; pharmacology ; Cardiac Pacing, Artificial ; Dogs ; Female ; Male ; Pyrimidinones ; pharmacology ; Refractory Period, Electrophysiological ; drug effects