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Objective@#To evaluate the efficacy and safety of nifekalan (NIF) on cardioversion in atrial fibrillation (AF) patients post radiofrequency ablation, and investigate the relevant factors related to the cardioversion efficacy of NIF.@*Methods@#We screened patients with sustained AF rhythm after radiofrequency ablation between November 2016 and July 2018. Participants were treated with intravenous NIF 0.4 mg/kg within 5-10 minutes after ablation. We observed the adverse reaction, and monitored the rhythm, heart rate, QT interval and QTc interval before the medication and at 5, 10, 20, 120 min after the medication. According to the drug outcome of NIF, patients were divided into conversion group and non-conversion group, related factors affecting conversion efficacy were evaluated using logistic regression analysis.@*Results@#(1)A total of 116 patients were enrolled in the study (63 males and 53 females, mean age was (64±18) years). Among them, 72 patients were converted to sinus rhythm, and the overall successful rate was 62.1%. There were 84 patients with persistent AF, of which 50 cases (59.2%) were restored to sinus rhythm. There were 32 patients with paroxysmal AF, 22 cases (68.8%) of them were restored to sinus rhythm. The conversion time was 1.5 to 12 (6.8±3.4)min. (2) In 116 patients, the QT interval and QTc interval were significantly longer after medication than before the drug administration (P<0.01), and peaked at about 10th min, and restored to the level before drug administration at about 120th min. (3) There were 8 cases of bradycardia (6.9%), 3 cases of frequent and short ventricular tachycardia (2.6%). (4) The duration of atrial fibrillation was shorter and left atrial diameter was smaller in the cardioversion group than in the non-cardioversion group (both P<0.05). There were no significant differences in gender, disease history, atrial fibrillation type and structural heart disease between the two groups (P>0.05). (5) Multifactorial logistic regression analysis showed that the duration of atrial fibrillation (OR=0.980, 95%CI 0.966-0.994, P=0.004) and the left atrial diameter (OR=0.888, 95%CI 0.814-0.967, P=0.007) were the factors that influence the cardioversion efficacy of NIF on atrial fibrillation post ablation.@*Conclusions@#The total effective rate of NIF was 62.1% in patients witrh sustained AF post radiofrequency ablation, was 68.8% in patients with paroxysmal AF. Besides, NIF has the advantage of short conversion time and few adverse reactions. Left atrium diameter and AF duration were relevant factors that influence the efficacy of NIF of cardioversion in patients with sustained AF after radiofrequency ablation.
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Objective@#To investigate the effect and related mechanism of homocysteine (Hcy) on calcium overload in neonatal rat atrial cells (NRICs).@*Methods@#NRICs were assigned to 9 groups after culture for 3 days: (1) control group; (2) Hcy group (0, 50, 100, 200, 500 μmol/L for 48 hours); (3) antioxidant group (NAC, 10 μmol/L for 24 hours); (4) Hcy+NAC group (500 μmol/L Hcy for 48 hours, then treated with 10 μmol/L NAC for 24 hours); (5) calcium/calmodulin dependent protein kinase Ⅱδ (CaMKⅡδ) inhibitor group (KN-93, 3 μmol/L KN-93 for 5 hours); (6) specific sodium current inhibitor group (ELE, 1 μmol/L ELE for 5 hours); (7) Hcy+KN-93 group (500 μmol/L Hcy for 48 hours, then treated with 3 μmol/L KN-93 for 5 hours); (8) Hcy+ELE group (500 μmol/L Hcy for 48 hours, then treated with 1 μmol/L ELE for 5 hours; (9) Hcy+KN-93+ELE group (500 μmol/L Hcy for 48 hours, then treated with 3 μmol/L KN-93 and 1 μmol/L ELE for 5 hours). Moreover, NRICs were also treated with CaMKⅡδ-siRNA lentivirus, and Nav1.5-siRNA lentivirus, negative lentivirus carrier containing green fluorescent protein (GFP) for 24 hours. The MOI values of the three groups were 10. Infection efficiency of lentivirus was determined by observing the percentage of GFP fluorescence under inverted fluorescence microscope after transfection for 24 hours, and cultured regularly with simultaneous Puro screening, then cells were grouped as Hcy+CaMKⅡδ-siRNA group, Hcy+Nav1.5-siRNA group and Hcy+negative group. The concentration of Ca2+ in NRICs ([Ca2+]i) of various groups was detected through Fluo-4/AM fluorescence probe, then 2', 7'- two chlorofluorescein diacetate (DCFH-DA) was used as a probe to detect reactive oxygen species (ROS) in NRICs by flow cytometry. The malondialdehyde (MDA) was detected by the activity of superoxide dismutase (SOD) and xanthine oxidase was detected by thiobarbituric acid colorimetry. The protein and mRNA expression level of CaMKⅡδ and Nav1.5 in NRICs were detected by Western blot and quantitative real-time PCR.@*Results@#(1) ROS, MDA and SOD were similar between NAC group and control group, ROS and MDA were significantly increased, while SOD was significantly reduced in Hcy group in a concentration-dependent manner. (2) [Ca2+]i: The level of [Ca2+]i was (155.57+7.25), (187.43+13.07), (248.98+27.22) and (307.36+15.09) nmol/L in 50, 100, 200 and 500 μmol/L Hcy groups, which was significantly higher than that in the control group ((123.18+7.24) nmol/L, P<0.01). In addition, the level of [Ca2+]i in Hcy+NAC group ((222.87+23.71)nmol/L) was significantly lower than that in Hcy 500 μmol/L group ((305.15+39.45) nmol/L, P<0.05), while [Ca2+]i level was similar between NAC group and the control group. (3) The protein expression of CaMKⅡδ and Nav1.5 was significantly upregulated in Hcy groups than in the control group. The protein expression level of CaMKⅡδ-Thr287 was significantly lower in NAC group than in Hcy 500 μmol/L group (P<0.01), however, there was no significant difference on the protein expression levels of CaMKⅡδ-Thr287 and Nav1.5 between NAC group and control group (all P>0.05). (4) The protein expression levels of CaMKⅡδ-Thr287 and the concentration of [Ca2+]i were significantly lower in Hcy+KN-93 group and Hcy+KN-93+ELE group than in Hcy 500 μmol/L group (P<0.05). [Ca2+]i concentration was significantly lower in Hcy+KN-93 group, Hcy+ELE group and KN-93+ELE+Hcy group than in Hcy 500 μmol/L group (P<0.05). (5) The mRNA and protein expression levels of CaMKⅡδ and Nav1.5 in each group infected with lentivirus: the GFP expression was ideal post lentivirus transfection for 24 hours (up to 90%), which was significantly lower in the CaMKⅡδ-siRNA group and Nav1.5-siRNA group than in the negative infection group (all P<0.05), which was similar between negative infection group and control group (P>0.05). Moreover, the mRNA and protein expression levels of CaMKⅡδ and CaMKⅡδ-Thr287 was significantly lower in Hcy+Nav1.5-siRNA group than in Hcy+negative infection group (P<0.05). The protein and mRNA levels of Nav1.5 were similar between Hcy+CaMKⅡδ-siRNA group and Hcy+negative infection group (P>0.05).@*Conclusions@#Hcy can induce calcium overload in NRICs by increasing oxidative stress, upregulating the sodium channel protein, and activating the late sodium current and phosphorylating CaMKⅡδ.
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Objective@#To investigate the current status of application of intra-aortic balloon pump(IABP) and analyze the factors which might impact the application of IABP in patients with acute myocardial infarction complicated with cardiac shock in China.@*Methods@#In China Acute Myocardial Infarction (CAMI) Registry,a nationwide, multicenter(107 hospitals), prospective study, 26 592 patients with acute myocardial infarction were enrolled consecutively between January 1, 2013 and September 30, 2014. After excluding of 30 cases due to missing important data,26 562 cases were analyzed.The application status of IABP was analyzed and multivariate logistic regression analysis was performed to determine the factors related to IABP application.@*Results@#A total of 785(3.0%) patients with acute myocardial infarction received IABP implantation, and 381(49.9%) patients belonged to preventive application of IABP before primary percutaneous coronary intervention,and 6(0.8%) patients were complicated with mechanical complications.There were 118(15.0%) patients with cardiac shock received IABP implantation, which accounted for 12.0%(118/984) of all patients with cardiac shock.Multivariate logistic regression analysis showed that the clinical independent factors of the decision of IABP insertion included dyslipidemia (OR=2.858, 95%CI 1.397-5.846, P=0.004),left ventricular ejection fraction (OR=0.977, 95%CI 0.961-0.994, P=0.009),usage of dopamine (OR=2.817, 95%CI 1.495-5.308, P=0.001), left main disease (OR=2.817, 95%CI 1.495-5.308, P=0.001), GRACE score (OR=1.006, 95%CI 1.000-1.011, P=0.034), receiving primary percutaneous coronary intervention (OR=4.508, 95%CI 1.673-12.146, P=0.003), teritiary hospitals (OR=2.562, 95%CI 1.498-4.384, P=0.001), and higher education of the patients (OR=2.183, 95%CI 1.056-4.509, P=0.016).@*Conclusions@#Among the Chinese acute myocardial infarction patients who received IABP implantation, nearly half application of IABP are preventive implantation before primary percutaneous coronary intervention. Only a few patients complicated with cardiac shock received IABP insertion. The clinical conditions, grade of hospitals, degree of education impact the decision of IABP insertion for the patients with acute myocardial infarction. Clinical Trial Registry National Institutes of Health, NCT018746.
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Objective@#To discuss the prevalence and influential factors of stroke among population in Jiangxi Province.@*Methods@#Four cities in urban areas and four counties in rural areas were selected firstly, in which two districts or townships were selected; and then three communities or villages were chosen from each district and township, respectively, using the simple random sampling (SRS) method. Finally 15 269 subjects aging 15 years old or above, living in Jiangxi Province ≥6 months were randomly selected to participate in this survey from November 2013 to August 2014. Information of population characteristics, life behavior way, individual disease history were collected through questionnaire survey, and height, weight, waist circumference, blood pressure, body fat rate, visceral fat index and so on were measured by instruments. Risk factors of stroke prevalence were analyzed by the unconditioned logistic regression analysis.@*Results@#A total of 15 269 participants (6 267 males) from 15 364 eligible participants were included in the statistical analysis. Out of which, 7 793 participants came from urban areas, and their average age was (53.04±17.91) years old. In this study, 226 stroke patients (117 males) were found among15 269 participants, including 122 urban participants and 104 rural participants, whose average age was (67.76±9.74) years old. The prevalence of stroke was 1 480.12/100 000 in 2014, which was separately 1 866.92/100 000 and 1 210.84/100 000 among males and females. The prevalence of people aging (45-49) years old was 413.79/100 000 (6/1 450) , while which among people aging 75 years old and above was 3 311.62/100 000 (61/1 842) . The prevalence of stroke among residents in Jiangxi presented an uprising tendency with age increasing (linear-by-linear association χ2=62.23, P<0.01). The research showed that when other influencing factors including gender, BMI, waist circumference, pulse-pressure difference, VAI, and sleeping time in non-working days were controlled, hypertensive patients had a higher risk of stroke than people without hypertension (OR=6.88, 95%CI: 4.90-9.67), drinkers had a higher risk of stroke than non-drinkers (OR=1.56, 95%CI: 1.17-2.08), compared with people <65 years old, people aged 65-74 years old and ≥75 years old had a higher risk of stroke, the value of OR (95%CI) were 1.88 (1.36-2.59) and 1.97 (1.39-2.80), respectively, compared with people with normal body fat percentage, people whose body fat percentage on high side and people who with high body fat percentage had a higher risk of stroke, the value of OR (95%CI) were 1.71 (1.18-2.48) and 1.74 (1.18-2.56), respectively, people with sleep time >8 h had a higher risk of stroke than those with sleep time of 6-8 h.@*Conclusion@#There was a high stroke prevalence among residents in Jiangxi province. Hypertension, drinking, age, BFP and sleep duration were associated with stroke prevalence. Corresponding measures for high-risk population and risk factors should be strengthened to prevent and control the stroke.
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Objective: To explore the correlation of monocyte to HDL-C ratio (MHR) and post-operative slow lfow or no relfow in patients with ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). Methods: A total of 216 STEMI patients treated in our hospital from 2014-10 to 2016-05 were enrolled. The patients were divided into 2 groups: Slow lfow or no relfow group, the patients with TIMI grade≤2,n=43 and Normal lfow group, n=173. Receiver operating characteristic (ROC) curve was performed to assess the best cut-off value for MHR predicting slow lfow or no relfow with its sensitivity and speciifcity; Logistic regression analysis was conducted to studied weather MHR could be used as an independent risk factor for coronary slow lfow or no relfow in STEMI patients after PCI. Results: Compared with Normal lfow group, Slow lfow or no relfow group had the higher MHR (18.6±9.8) vs (10.9±5.5), P<0.001. Univariate Regression analysis indicated that MHR was a risk factor of slow lfow or no relfow occurrence (OR=2.22, 95% CI 1.58-3.28); multivariate regression analysis presented that MHR was an independent risk factor of slow lfow or no relfow occurrence (OR=1.55, 95% CI 1.01-2.38). ROC curve showed that the best cut-off value for MHR predicting slow lfow or no relfow occurrence was 13.37 with the sensitivity and speciifcity at 67.4% and 70.5% respectively, the area under curve (AUC) was 0.734, 95% CI 0.646-0.822. Conclusion: MHR was an independent risk factor for slow lfow or no relfow occurrence in STEMI patients after PCI.
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OBJECTIVE@#To explore the effect and mechanism of angiotensin II receptor blockers - Irbesartan on occurrence of ventricular arrhythmias in rats with myocardial ischemia.@*METHODS@#Rats with embryonic cardiomyocytes-H9c2 were randomly divided into control group, ischemia group, Irbesartan group and Irbesartan + ischemia group. The cell viability of rats in each group was tested using MTT. Real-time PCR was employed to detect the expression of connexin43 (Cx43) mRNA and western blot to detect the expression of Cx43 and phosphorylated Cx43. SD rats were randomly divided into the sham-operation group (SO), myocardial infarction group (MI), Irbesartan group and MI + Irbesartan group, with 10 rats in each group. HE staining was employed to observe the change in the pathomorphology of left ventricular tissue and TUNEL method to analyze the cell apoptosis in the tissue. The immunofluorescence was adopted to observe the expression and distribution of Cx43 in the left ventricular myocardium and study the change in the expression of Cx43 in the cardiac muscular tissue at mRNA and protein level.@*RESULTS@#The intervention of Irbesartan in the condition of ischemia indicated the significant decrease in the number of necrotic cells. The expression of Cx43 was significantly decreased under the culture of ischemia (P < 0.05), but in the presence of Irbesartan, the expression of Cx43 was increased compared with the ischemia group (P < 0.01). The results of WB assay showed the similar trend of change at mRNA level. There was the significant difference in the score of ventricular arrhythmia between MI group and SO group (P < 0.01). The incidence of ventricular tachycardia or ventricular fibrillation was significantly increased compared with the one in SO group (P < 0.05). There was the significant difference in the overall score between MI + Irbesartan group and MI group (P < 0.05). The expression of Cx43 in the cardiac muscular tissue in MI group was significantly decreased (P < 0.01 vs SO group). But the expression of Cx43 was increased after the treatment with Irbesartan.@*CONCLUSIONS@#Irbesartan can inhibit the injury of H9c2 cardiomyocytes and the decreased expression of Cx43 that are induced by the ischemic myocardial infarction. Irbesartan can also improve the reconstruction of Cx43 in rats with ischemic myocardium to inhibit the myocardial infarction-induced arrhythmias.
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[ ABSTRACT] AIM:To study the effect of livin gene-modified bone marrow mesenchymal stem cells ( BM-MSCs) transplantation on the cardiac function following acute myocardial infarction in a rat model and the expression of livin , caspase-3, caspase-7 and caspase-9 in the livin gene-modified BM-MSCs.METHODS: The MSCs were obtained by the whole bone marrow culture method , and the apoptosis of the MSCs after infection with adenovirus vector carrying enhanced green fluorescent protein ( EGFP) gene and livin recombinant vector ( rAd-livin) were detected by flow cytometry .The ex-pression of livin, caspase-3, caspase-7 and caspase-9 was detected by Western blot .After permanent left anterior descend-ing artery occlusion , the rats were randomized to receive intramyocardial injection of DMEM without cells ( vehicle group ) , or containing MSCs ( MSCs group ) , MSCs ( EGFP ) ( rAd-control/MSCs group ) or MSCs ( livin ) ( rAd-livin/MSCs group).Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum in-creased rate of left ventricular pressure ( -dp/dtmax ) and the maximum decline rate of left ventricular pressure ( +dp/dtmax ) were recorded for evaluating the cardiac functions .RESULTS: The apoptosis of rAd-livin/MSCs was significantly decreased as compared with MSCs and rAd-control/MSCs (P<0.05).Meanwhile, the expression of caspase-3, caspase-7 and caspase-9 was significantly downregulated as compared with the other 2 groups ( P<0.05 ) .The cardiac function in rAd-livin/MSCs group was significantly improved as compared with DMEM group , and those in the other 2 groups got the similar results, but the function in rAd-livin/MSCs group was better improved .Meanwhile, the number of surviving cells in rAd-livin/MSCs group was significantly improved as compared with the other 2 groups .CONCLUSION:The apoptosis of MSCs is decreased after rAd-livin transfection, and the expression of caspase-3, caspase-7 and caspase-9 is also significant-ly downregulated while the expression of livin is significantly upregulated .Transplantation of livin-modified BM-MSCs by lentiviral vector results in better prognosis for treating myocardial infarction by enhancing cell survival .
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Objective To explore the effect and mechanism of angiotensin II receptor blockers – Irbesartan on occurrence of ventricular arrhythmias in rats with myocardial ischemia. Methods Rats with embryonic cardiomyocytes-H9c2 were randomly divided into control group, ischemia group, Irbesartan group and Irbesartan + ischemia group. The cell viability of rats in each group was tested using MTT. Real-time PCR was employed to detect the expression of connexin43 (Cx43) mRNA and western blot to detect the expression of Cx43 and phosphorylated Cx43. SD rats were randomly divided into the sham-operation group (SO), myocardial infarction group (MI), Irbesartan group and MI + Irbesartan group, with 10 rats in each group. HE staining was employed to observe the change in the pathomorphology of left ventricular tissue and TUNEL method to analyze the cell apoptosis in the tissue. The immunofluorescence was adopted to observe the expression and distribution of Cx43 in the left ventricular myocardium and study the change in the expression of Cx43 in the cardiac muscular tissue at mRNA and protein level. Results The intervention of Irbesartan in the condition of ischemia indicated the significant decrease in the number of necrotic cells. The expression of Cx43 was significantly decreased under the culture of ischemia (P < 0.05), but in the presence of Irbesartan, the expression of Cx43 was increased compared with the ischemia group (P < 0.01). The results of WB assay showed the similar trend of change at mRNA level. There was the significant difference in the score of ventricular arrhythmia between MI group and SO group (P < 0.01). The incidence of ventricular tachycardia or ventricular fibrillation was significantly increased compared with the one in SO group (P < 0.05). There was the significant difference in the overall score between MI + Irbesartan group and MI group (P < 0.05). The expression of Cx43 in the cardiac muscular tissue in MI group was significantly decreased (P < 0.01 vs SO group). But the expression of Cx43 was increased after the treatment with Irbesartan. Conclusions Irbesartan can inhibit the injury of H9c2 cardiomyocytes and the decreased expression of Cx43 that are induced by the ischemic myocardial infarction. Irbesartan can also improve the reconstruction of Cx43 in rats with ischemic myocardium to inhibit the myocardial infarction-induced arrhythmias.
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In this study, we analyzed two cases of pure cerebral fat embolism and reviewed related literatures to explore the pathogenesis, clinical manifestations, diagnosis and treatment of cerebral fat embolism, improve the treatment efficiency and reduce the misdiagnosis rate. In our cases, patients fully returned to consciousness at the different times with good prognosis, normal vital signs and without obvious sequelae. For patients with the limb fractures, who developed coma without chest distress, dyspnea or other pulmonary symptoms 12 or 24 h post injury, cerebral fat embolism should be highly suspected, except for those with intracranial lesions, such as delayed traumatic intracerebral hemorrhage, etc. The early diagnosis and comprehensive treatment can improve prognosis.
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Adult , Humans , Male , Embolism, Fat , Diagnosis , Therapeutics , Intracranial Embolism , Diagnosis , TherapeuticsABSTRACT
Inflammasomes are multiprotein complexes that can recognize pathogenic microorganisms and stress -asso-ciated endogenous molecules and play an important role in innate immune system .Inflammasomes cause inflamma-tion response by inducing maturation of inflammatory cytokines interleukin ( IL)-1βand IL-18 through activation of caspase-1 ,and involve in the pathogenesis of various diseases such as cryopyrin-associated periodic syndrome , is-chemia-reperfusion injury and atherosclerosis .
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Objective: To study the effects of acute cold stress on connexin43 (Cx43) protein expression with drug intervention, and cell to cell conduction with its mechanism in neonatal rats’ myocardial cells. Methods: The primary neonatal rats’ myocardial cell culture was conducted in 4 groups. Group① , the cells were normally cultured, Group②, the cells were cultured at 4℃, Group③, the cells were cultured at 0℃and Group④, the anti-arrhythmia peptide (AAP 10) was added in Group②and Group③. The apoptosis rate of myocardial cells was evaluated by lfow cytometry assay, mRNA and protein expressions of CX43 were examined by RT-PCR and Western blot analysis, and CX43 phosphorylation product (P-CX43) was detected. Results: Compared with normally cultured cells, the myocardial cell apoptosis rate was obviously increased by acute cold stress at 4℃and 0℃with time extension. The mRNA expression of Cx43 was decreased at varying degrees at 4℃and 0℃stimulation, the protein expression of Cx43 was decreased at varying degrees at 4℃and 0℃stimulation with time extension, and P-Cx43 level was decreased. While the APP 10 intervention may obviously elevate the protein levels of Cx43 and P-Cx43. Conclusion: Acute cold stress could reduce the protein expression of CX43 and P-CX43, while APP 10 intervention may elevate such expression and improve the cell to cell conduction in neonatal rats’ myocardial cells.
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AIM:To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein 22 (HSP22), tumor necrosis factor alpha (TNF-α) and endothelial nitric oxide synthase (eNOS) and the effect of atorvasta-tin intervention.METHODS:Hyperlipidemia model was established in SD rats.Afterwards, the rats were divided into nor-mal control group, high fat group and high fat+atorvastatin intervention group.The expression of HSP22 and TNF-αin the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting.RE-SULTS:No detectable expression of HSP22 and TNF-αin the normal control group was observed.However, the expression of HSP22 and TNF-αwas positive in the high fat group and the atorvastatin intervention group.The mean densities of HSP22 and TNF-αpositive particles were significant lower in the atorvastatin intervention group as compared with high fat group ( both P<0.05) .The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group (P<0.01).However, no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed.CONCLUSION:The expression of HSP22 and TNF-αin the rat aortas is increased in the hyperlipidemia rat model.This effect can be restored by atorvastatin treatment.The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model, but this tendency could not be attenuated by atorvastatin.
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Objective To investigate the interventional treatment strategy for occluding the intercristal ventricular septal defect (VSD) in order to improve the surgical safety and success rate. Methods During the period from January 2012 to December 2013, a total of 31 patients with intercristal VSD were admitted to authors’ hospital to receive interventional catheter occlusion therapy. Preoperative color Doppler ultrasound echocardiography showed that on the short axis view of the aorta the VSD interrupted port was situated at 12:00 - 1:00 o’clock region. Left ventricular and above aortic valve angiography indicated that the VSD location, shape and size, the split vent size on the left ventricle side and its distance from the aortic valve could be correctly measured when the VSD shunt was visualized , which were very helpful in guiding the operator to select the suitable occluder as well as to adjust the release pattern of the occluder. Postoperative imaging findings of the left ventricular and above aortic valve angiography were compared with the preoperative ones. Results Successful occlusion of VSD was obtained in 22 patients , in 13 among them the left ventricular angiography showed that the direction of blood flow beam at the defect hole was from the left ventricle to the right ventricle in an obliquely upward direction. The basal width of the defect on the left ventricle side was (5.12 ± 1.38) mm, and(6 - 10) mm occluder was employed. In the remaining 9 patients the left ventricular angiography showed that the direction of blood flow beam at the defect hole was from the left ventricle to the right ventricle in a direction almost parallel to the aortic valve , and the basal width of the defect on the left ventricle side was (7.18 ± 1.26) mm, and (9 - 12) mm zero-bias occluder was adopted. Interventional occlusion of VSD was unsuccessful in 9 cases as the intercristal hole was rather larger, and two of them had coexisting aortic sinus aneurysm complicated by mid-to-severe degree aortic valve regurgitation. Conclusion Based on the precise analysis of angiographic images by experienced radiologists optimal treatment scheme can be worked out. If conditions permit, symmetrical occluder should be employed so far as possible in order to reduce the degree of operation difficulty and improve the surgical safety and the success rate as well.
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Objective: To explore the regulative role of extracellular regulated protein kinase-5 (ERK5)/Bcl-2 interacting mediator of cell death (Bim) pathway in hypothermal stimulation induced neonatal rat’s cardiomyocytes (CMs) damage and apoptosis. Methods: CMs were cultured for hypothermal stimulation and the speciifc siRNA was used to down-regulate the ERK5 or Bim in CMs. The cell apoptosis was detected by lfow cytometry, protein expression was examined by Western blot analysis, the intracellular Ca2+, reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) were evaluated by lfuorescent labeling and lfow cytometry. Results: In hypothermal stimulated CMs, ERK5 siRNA could promote Bim protein expression, but Bim siRNA could not inlfuence ERK5, while attenuated p-ERK5 expression. ERK5 siRNA induced higher apoptosis rate, while Bim siRNA could decrease such effect. ERK5 siRNA increased the intracellular Ca2+overloading, ROS activation andΔΨm damage, while Bim siRNA played the role to against those effects in hypothermal stimulated CMs. Conclusion: Our study revealed that ERK5/Bim pathway played the important regulative roll in hypothermal stimulation induced neonatal rat’s CMs damage and apoptosis.
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Clinicians,as the finders of clinical problems,the refiners of scientific questions and the cooperators of basic and clinic research,play key roles in translational medicine.Clinicians' playing an important part in the process will give the promotion of both the development of translational medicine and improvement of the health condition of the people.
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OBJECTIVE: Interventional occlusion of intracristal ventricular septal defects (IVSD) is a node point. Reports concerning angiography features and successful occlusion of IVSD using domestic occluder are rare. The aim of this paper is to investigate the angiography features of IVSD and the experience of interventional occlusion with domestic occluder. METHODS: Totally 46 cases of IVSD were diagnosed by color Doppler echocardiography that they had interventional indications.According to the short axis view of aortic, they were divided into 4 groups: A (11:30-12:00), B (12:00-12:30), C (12:30-13:00) and D (13:00-13:30). Different groups were performed with adequate angle angiography to show ventricular septal defect, as well as to decide strategy, which to choose occluder and occluded methods.RESULTS: All 46 patients were occluded successful. Technical success rate was 100%, without related complications. A group included 10 cases, B group 13 cases, C group 16 cases and D group 7 cases. The left anterior oblique angle of IVSD left ventricular angiography was greater than other type of VSD, and increased gradually with the changes in the defect location (Group A to D). According to the defect size and different groups, the defects were successfully occluded with symmetric,decentered, zere-decentered type occluder. Modified pigtail catheter was good value in practice occlusion of IVSD.CONCLUSIONS: Left anterior oblique angle in IVSD left ventricular angiography should be bigger. Domestic occluder is safe,effective, with less complication and cost, which can be the first choose for patients with LVSD.
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Objective To study the effect of Cardiotrophin-1 (CT-1) on cardiocyte hypoxia-reoxygenation injury,and to investigate the signaling pathways involved in the protective effect. Method This study was carried out in Key Lab of Molecular Medicine in Jiangxi Province. Cardiomyocytes from the hearts of 2-day-old Sprague-Dawley neonatal rats were prepared by a modified method. Five groups were included in the study. Group (ⅰ): control, Group (ⅱ): hypoxia/reoxygeuation, Group (ⅲ): hypoxia / reoxygenation + CT-1, Group (iv) : CT- 1 + hypoxia/ reoxygenation + LY294002 (PIK3/Akt inhibitor), Group (ⅴ): CT-1 + hypoxia / reoxygenation +DMSO. The concentration of CT-1 was 10 ng/mL. Myocytes survival rote was evaluated by MTS method, apopto-sis, mitochondrial permeability transition pore (△ψm) and reactive oxygen species(ROS) were detected by flow cy-tometer, phosphorylased GSK-3β and PI3K protein by western blotting. Analysis of variance and q test as statistical methods was used to analyze the data. Results Cardiomyocyte apoptosis and ROS increased markedly after hy-poxia/reoxygenation,but cardiomyocyte survival rate and the level of △ψm [(40.55±4.25) vs. (86.28±7.15), P < 0.01]decreased significantly. With CT-1 intervention, cardiomyocyte survival rate increased markedly (87%),apoptosis and ROS reduced significantly. The level of △ψm increased, the level of phosphorylased GSK-3β and phosphorylased PI3K protein obviously increased. The effect of CT-1 was inhibited by LY294002, but no significant effect was observed on ceils survival in DMSO group, which confirmed that LY294002 specifically in-volved blocking the protective effect of CT-1. Conclusions CT-1 can protect cardiac cells against hypoxia- reoxy-genation injury, these effects are dependent upon its ability to activate the PI3K/GSK-3β pathway.
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AIM: To observe the change of subunit of NADPH oxidation enzyme complex nox - 1 protein in cardiocyte hypoxia - reoxygenation injury and the role of cardiotrophin -1.METHODS: Cardiomyocytes from the hearts of 1 -3 d old neonatal rats were prepared by a modified method. Five groups were included in the study: control; hypoxia/ reoxygenation; hypoxia/reoxygenation + CT - 1; CT - 1 + hypoxia/reoxygenation + LY294002 (PIK3/Akt inhibitor) ; CT -1 + hypoxia/reoxygenation + PD98059 (ERK inhibitor) ; CT - 1 + hypoxia/reoxygenation + DMSO. The concentration of CT -1 was 10 μg/L. The survival rate of myocytes was evaluated by MTS method. Apoptosis, mitochondrial permeability transition pore ( △ψm) and reactive oxygen species ( ROS) were detected by flow cytometry. Nox - 1 protein was determined by Western blotting. RESULTS: Apoptosis of cardiomyocytes and the level of ROS (19.7% ±1.4% vs 2.1% ± 0.5% , 14.07% ± 1.25% vs 3.54% ± 0.86% , P < 0.05 ) increased markedly after hypoxia/reoxygenation, but cardio-myocyte survival rate and the level of△ψm (40.55% ±4.25% vs 86.28% ±7.15% , P <0.01) decreased significantly. The expression of nox - 1 protein was upregulated markedly. With CT - 1 intervention, cardiomyocyte survival rate increased markedly, apoptosis, both ROS and expression of nox - 1 protein reduced significantly. The level of△ψm increased obviously. The effect of CT - 1 was inhibited by LY294002.No significant effect was observed on cells survival in DMSO group, which confirmed that LY294002 was specifically involved in blocking the protective effect of CT - 1.CONCLUSION : The expression of subunit of NADPH oxidation enzyme complex nox - 1 protein is upregulated markedly in cardiocyte hypoxia - reoxygenation injury.CT - 1 protects cardiac cells against hypoxia - reoxygenation injury by downregulating the expression of nox -1 protein to decrease the level of ROS.
ABSTRACT
Integrin-linked kinase (ILK) is a widely expressed protein kinase that relate to cellular growth and differentiation. It is most abundant in the heart. Recently, many researches revealed that ILK is highly relevant to cardiac response to biomechanical stresses. Also, ILK plays important roles in regulation of the occurrence and development of cardiac hypertrophy, dilated cardiomyopathy, viral myocarditis and myocardial senescence via correlation to several classical signal transduction pathway. Meanwhile, ILK functions in protection after myocardial infarction. This article will try to summarize the effects and relevant mechanism of ILK in above-mentioned aspects, overall reveals the roles of ILK in heart and its potential clinical significance.
ABSTRACT
OBJECTIVE: To purify hVEGF_(121)/EGFP fusion protein using transfected BMSCs as culture media, in addition, to detect the function of hVEGF_(121)/EGFP fusion protein in vitro.METHODS: The pEGFP-N_2-hVEGF_(121) recombinant plasmid, which was constructed in the preliminary work of our study group,was used to extract the plasmid DNA. BMSCs were transfected with pEGFP-N2-hVEGF_(121) by positive ionic liposome transfection method. Under a fluorescent microscopy, the expression of hVEGF_(121)/EGFP fusion protein was detected. The hVEGF_(121)/EGFP fusion protein was purified with Am icon ultrafiltration centrifuge tube and the expression of fusion protein was detected by Western-Blotting method.RESULTS: The BMSCs, which transfected with pEGFP-N2-hVEGF_(121), was observed under the fluorescent microscope. Western blotting confirmed that pEGFP-N_2-hVEGF_(121) fusion protein expressed in the culture media of transfected BMCS. MTT results showed the number of human umbilical vein endothelial cells in the fusion protein team was significantly greater than that in the control group (P < 0.05), and Miles test confirmed that pEGFP-N_2-hVEGF_(121) fusion protein increased the permeability of the blood vessel wall.CONCLUSION: ①This study successfully confirmed the pEGFP-N_2-hVEGF_(121) recombinant plasmid, which carrying VEGF_(121)/EGFP fusion protein, can be expressed in BMSCs.②The VEGF_(121)/EGFP fusion protein have the function of wild-type VEGF in vitro.