69 results on '"Yanzhuo Ma"'
Search Results
2. Circulating mir-483-5p as a novel diagnostic biomarker for acute coronary syndrome and its predictive value for the clinical outcome after PCI
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Yuying Zhao, Xinxing Song, Yanzhuo Ma, Xiang Liu, and Yuhong Peng
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Acute coronary syndrome ,miR-483-5p ,Major adverse cardiovascular events ,Diagnostic ,Predicts ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Abstract Background MicroRNA (miRNA) plays a critical function in the progression of acute coronary syndrome (ACS) and is associated with major adverse cardiovascular events (MACEs) after undergoing percutaneous coronary intervention (PCI). This research was designed to probe the diagnostic accuracy of miR-483-5p in patients with ACS and its predictive value of MACEs. Methods 118 patients with ACS (40 with unstable angina pectoris [UAP] and 78 with acute myocardial infarction [AMI]) and 75 healthy controls were enrolled. Serum miR-483-5p was detected in the subjects by reverse transcription-quantitative real-time PCR (RT-qPCR). ROC curve and logistic regression models were employed to estimate the diagnosis. Patients were monitored for 6 months after PCI to document the occurrence of MACEs. Kaplan-Meier survival was conducted to explore the predictive significance of miR-483-5p for the MACEs. Results Serum miR-483-5p levels were higher in ACS patients and associated with SYNTAX score and Gensini score. miR-483-5p was effective in identifying ACS patients from healthy individuals (AUC = 0.919) and AMI patients from ACS patients (AUC = 0.867), demonstrating a high diagnostic value, proven by logistic regression (OR = 9.664, 95%CI = 4.462–20.928, P
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- 2023
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3. Impact of a medical supply bulk-buy program on treatment of patients with coronary artery disease in China: A single-center study.
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Xinxing Song, Yanzhuo Ma, Zhiwen Li, Xiaoye Wang, Lingfeng Kong, Gang Wang, Yuhong Peng, and Leisheng Ru
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Medicine ,Science - Abstract
BackgroundThe Chinese government recently introduced a program to buy medical supplies in bulk to reduce the patient cost burden. For patients undergoing percutaneous coronary intervention (PCI), little is known about the effect on outcomes of this bulk-buy program.AimsThis study investigated whether the bulk-buy program to decrease the price of stents used in PCI affected clinical decision-making and outcomes.MethodsThis single-center study enrolled patients undergoing PCI from January 2020-December 2021. Prices decreased for stents on January 1, 2021, and balloons on March 1, 2021. Patients were grouped by surgical year as either before (2020) or after (2021) policy implementation. All clinical data were collected. To examine whether clinical decision-making for PCI was affected by the bulk-buy program, procedure appropriateness was analyzed using the 2017 appropriate use criteria (AUC). To assess outcomes, the rates of major adverse cardiac and cerebrovascular events (MACCE) and complications were compared between groups.ResultsStudy participants were 601 patients in 2020 (before bulk buying) and 699 patients in 2021 (after bulk buying). Results of analysis by AUC for procedure appropriateness were 74.5% appropriate, 21.6% may be appropriate, and 3.8% rarely appropriate in 2020, with no differences for patients who underwent PCI in 2021. Between-group comparisons showed MACCE rates of 0.5% in 2020 and 0.6% in 2021, whereas complication rates were 5.5% and 5.7%, respectively. No statistically significant differences were found between groups (p > 0.05).ConclusionThe bulk-buy program did not impact physician clinical decision-making or surgical outcomes for patients undergoing PCI.
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- 2023
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4. A novel use of small ballons to reduce the risk of subintimal hematoma formation during recanalization of chronic total occlusion: two case reports
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Yanzhuo Ma, Xinxing Song, Lingfeng Kong, Gang Wang, Xiaoye Wang, and Leisheng Ru
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Antegrade approach ,Chronic total occlusion ,Percutaneous coronary intervention ,Hematoma formation ,Balloon occlusion ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Abstract Background Subintimal hematoma remains a major challenge associated with unnecessary technical complexity, failure of the antegrade approach or imperfection of revascularization in percutaneous coronary intervention (PCI) for chronic total occlusion (CTO). Some techniques and devices release the hematoma after its formation. Here, we describe a novel use of small ballons to prevent the hematoma formation during antegrade approach in two cases. Case presentation We report two cases of CTO-PCI in which balloon occlusion was successfully applied to prevent haematoma formation. The first case, a 72-year-old female with diabetes, was hospitalized because of unstable angina. Angiography showed right coronary artery (RCA) CTO, which initiated from the proximal part to the trifurcation at the distal part of the RCA. Considering the high likelihood and serious consequences of subintimal haematoma, a small balloon is employed to prevent subintimal hematoma formation. A balloon and microcatheter or double-lumen microcatheter are placed in the proximal coronary CTO lesion; then the balloon was dilated beside the catheter, most of the antegrade blood flow was sealed which reduced the likelihood of haematoma formation. The procedure was successfully completed without subintimal hematoma formation. The second case a 62-year-old male with unstable angina, was hospitalized for PCI. Angiography showed left anterior descending coronary artery CTO. Similar to case 1, we also used a small balloon to prevent hematoma formation. Both patients underwent PCI, which employed a small balloon to prevent hematoma formation and both procedures were successful without complications. Conclusion In patients who underwent CTO-PCI, balloon occlusion offers an alternative for reducing the incidence of subintimal haematomas.
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- 2022
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5. Case report: What course to follow when left bundle branch pacing encounters acute myocardial infarction?
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Xiaojiang Zhang, Yanzhuo Ma, Leisheng Ru, Dongmei Wang, Jie Li, and Shuying Qi
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left bundle branch pacing (LBBP) ,acute myocardial infarction (AMI) ,AV block ,pacemaker dysfunction ,the pacing threshold ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Compared with traditional right ventricular apical pacing, His-bundle pacing (HBP) provides more physiologic pacing by activating the normal conduction system. However, HBP has some limitations including higher pacing thresholds. In addition, disease in the distal His-Purkinje system may prevent the correction of abnormal conduction. Left bundle branch pacing (LBBP) may overcome these disadvantages by providing lower pacing thresholds and relatively narrow QRS duration that improve cardiac function. Here, we describe a rare case of a transient loss of ventricular capture due to acute anterior wall myocardial infarction in an LBB-paced patient. With the improvement of the ischemia, the function of the pacemaker partly recovered. We review the adaptations, advantages, and limitations, and long-term safety of LBBP.
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- 2022
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6. Atherogenic L5 LDL induces cardiomyocyte apoptosis and inhibits KATP channels through CaMKII activation
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Yanzhuo Ma, Nancy Cheng, Junping Sun, Jonathan Xuhai Lu, Shahrzad Abbasi, Geru Wu, An-Sheng Lee, Tatsuya Sawamura, Jie Cheng, Chu-Huang Chen, and Yutao Xi
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Action potential ,ATP-sensitive potassium ,Ca2+/calmodulin-dependent protein kinase II ,Cardiomyocytes ,Electronegative low-density lipoprotein ,Nutritional diseases. Deficiency diseases ,RC620-627 - Abstract
Abstract Background Cardiac Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation plays a critical role in cardiomyocyte (CM) apoptosis and arrhythmia. Functional ATP-sensitive potassium (KATP) channels are essential for cardiac protection during ischemia. In cultured CMs, L5 low-density lipoprotein (LDL) induces apoptosis and QTc prolongation. L5 is a highly electronegative and atherogenic aberrant form of LDL, and its levels are significantly higher in patients with cardiovascular-related diseases. Here, the role of L5 in cardiac injury was studied by evaluating the effects of L5 on CaMKII activity and KATP channel physiology in CMs. Methods Cultured neonatal rat CMs (NRCMs) were treated with a moderate concentration (ie, 7.5 μg/mL) of L5 or L1 (the least electronegative LDL subfraction). NRCMs were examined for apoptosis and viability, CaMKII activity, and the expression of phosphorylated CaMKIIδ and NOX2/gp91phox. The function of KATP and action potentials (APs) was analyzed by using the patch-clamp technique. Results In NRCMs, L5 but not L1 significantly induced cell apoptosis and reduced cell viability. Furthermore, L5 decreased Kir6.2 expression by more than 50%. Patch-clamp analysis showed that L5 reduced the KATP current (IKATP) density induced by pinacidil, a KATP opener. The partial recovery of the inward potassium current during pinacidil washout was susceptible to subsequent inhibition by the IKATP blocker glibenclamide. Suppression of IKATP by L5 significantly prolonged the AP duration. L5 also significantly increased the activity of CaMKII, the phosphorylation of CaMKIIδ, and the expression of NOX2/gp91phox. L5-induced apoptosis was prevented by the addition of the CaMKII inhibitor KN93 and the reactive oxygen species scavenger Mn (III)TBAP. Conclusions L5 but not L1 induces CM damage through the activation of the CaMKII pathway and increases arrhythmogenicity in CMs by modulating the AP duration. These results help to explain the harmful effects of L5 in cardiovascular-related disease.
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- 2020
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7. A novel real-time intravascular ultrasound double-lumen microcatheter for recanalization of chronic total occlusion: a case report
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Yanzhuo Ma, Yuhong Peng, Gang Wang, and Leisheng Ru
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Percutaneous coronary intervention ,Chronic total occlusion ,Catheter design ,Intravascular ultrasound ,Medicine - Abstract
Abstract Background Chronic total occlusion revascularization remains a challenging problem because of its complexity. We present a case of a patient with chronic total occlusion who was successfully revascularized with the use of a new device called a real-time intravascular ultrasound double-lumen microcatheter. Case presentation A 58-year-old East Asians woman presented to our hospital with a complaint of recurrent chest pain of 5 months’ duration. Angiography revealed chronic total occlusion of the right coronary artery from the right coronary artery ostium to the ostia of the posterolateral and posterior descending branches. A guidewire was passed to the distal right coronary artery but went into the false lumens at the posterior descending and posterolateral ostia after use of the antegrade and retrograde approaches. Hence, we used the new device to pass through the subintimal right coronary artery space with reentry into the true lumen before the posterior descending and posterolateral ostia. A stent was successfully deployed at the posterior descending and posterolateral ostia, and the final result was excellent. Conclusions This device was useful for finding the entry point and for reentry into the true lumen of a chronic total occlusion. It may be a valuable tool for recanalization of complex chronic total occlusion lesions.
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- 2019
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8. Apolipoprotein-J blocks increased cell injury elicited by ox-LDL via inhibiting ROS-CaMKII pathway
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Yanzhuo Ma, Zhi Gong, Kai Nan, Shuying Qi, Yu Chen, Chao Ding, Dongmei Wang, and Leisheng Ru
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Ox-LDL ,Apolipoprotein-J ,Apoptosis ,Neonatal rat ventricular cells ,Nutritional diseases. Deficiency diseases ,RC620-627 - Abstract
Abstract Background Oxidized low-density lipoprotein (ox-LDL) is crucial in cardiac injury. Apolipoprotein-J (ApoJ) contributes to antiapoptotic effects in the heart. We aimed to evaluate the protective effects of ApoJ against ox-LDL cytotoxicity in Neonatal rat ventricular cells (NRVCs). Methods and results NRVCs were damaged by exposure to ox-LDL, as shown by increased caspase-3/7 activity, enhanced caspase-3 expression, and decreased cell viability. ApoJ overexpression, using an adenovirus vector, significantly reduced ox-LDL-induced cell injury. ApoJ also prevented ox-LDL from augmenting reactive oxygen species (ROS) production, as demonstrated by elevated Nox2/gp91phox and P47 expression. Furthermore, ApoJ overexpression reduced CaMKIIδ expression elicited by ox-LDL in cultured NRVCs. Upregulating CaMKIIδ activity, mediated by ox-LDL, was significantly inhibited by ApoJ overexpression. A CaMKIIδ inhibitor, KN93, prevented ApoJ’s protective effect against ox-LDL cytotoxicity. A ROS scavenger, Mn (III)meso-tetrakis (4-benzoic acid) porphyrin (Mn (III)TBAP), also attenuated CaMKIIδ’s increased expression and activity, induced by ox-LDL, and showed similar results to ApoJ by attenuating ox-LDL-induced cell damage, as ApoJ did. Conclusions ApoJ confers cytoprotection to NRVCs against ox-LDL cytotoxicity through the ROS-CaMKII pathways.
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- 2019
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9. Refined Chroma From Luma Prediction in AV1 Based on Color Component Grouping.
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Junyan Huo, Zhenyao Zhang, Jiarun Song, Yanzhuo Ma, and Fuzheng Yang 0001
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- 2024
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10. Unified Cross-Component Linear Model in VVC Based on a Subset of Neighboring Samples.
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Junyan Huo, Hongqing Du, Xinwei Li, Shuai Wan, Hui Yuan 0001, Yanzhuo Ma, and Fuzheng Yang 0001
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- 2022
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11. Data structures based on non-linear relations and data processing methods
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Xingni Zhou, Zhiyuan Ren, Yanzhuo Ma, Kai Fan, Xiang Ji and Xingni Zhou, Zhiyuan Ren, Yanzhuo Ma, Kai Fan, Xiang Ji
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- 2020
12. Data structures based on linear relations
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Xingni Zhou, Zhiyuan Ren, Yanzhuo Ma, Kai Fan, Xiang Ji and Xingni Zhou, Zhiyuan Ren, Yanzhuo Ma, Kai Fan, Xiang Ji
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- 2020
13. Preparation and performance of latanoprost-loaded hydrogels as a lacrimal suppository for the treatment of glaucoma
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Siyu Xiao, Aijie Ma, Yanzhuo Ma, Haiyan Bai, Binghong Zhang, Juan Li, and Hongwei Zhou
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Biomaterials ,Biomedical Engineering - Abstract
Glaucoma is the leading cause of irreversible blindness, and its treatment is attracting widespread attention. Drug-loaded lacrimal suppositories can effectively treat xerophthalmia, but there is little research on the treatment of glaucoma with drug-loaded lacrimal suppositories. This article explored and expanded the non-pharmacological model of lacrimal suppository therapy for glaucoma by using a combination of lacrimal suppository and medication. The drug-loaded lacrimal suppository was rationally designed through the conjugation of gelatin with polyamide (PAM) via the formation of amide linkages, followed by Schiff base reaction grafting with latanoprost. In vitro drug release studies showed that latanoprost released from drug-loaded lacrimal embolus had sustained-release properties with a release time of 33 days and a drug release volume of 82.6%. The biological evaluation of drug-loaded lacrimal thrombus was carried out by IOP test, retinal potential test, and retinal H&E staining. The results showed that the IOP decreased to 27.125 ± 1.1254 mmHg, and the a and b waves of retinal potential increased to 4.39 ± 0.16 μV and 67.9 ± 2.17 μV, respectively. It indicated that latanoprost lacrimal suppository has a good therapeutic effect on glaucoma.
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- 2023
14. Fabrication of anisotropic nanocomposite hydrogels by magnetic field‐induced orientation for mimicking cardiac tissue
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Yanzhuo Ma, Aijie Ma, Tao Luo, Siyu Xiao, and Hongwei Zhou
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Polymers and Plastics ,Materials Chemistry ,General Chemistry ,Surfaces, Coatings and Films - Published
- 2022
15. Scalable Prediction Structure for Multiview Video Coding.
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Junyan Huo, Yilin Chang, Ming Li, and Yanzhuo Ma
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- 2009
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16. Channel-Aware Adaptive Multi-RPS Scheme for Video Error Resilient Transmission over Wireless OFDM Channel.
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Yanzhuo Ma and Yilin Chang
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- 2007
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17. The Impact of the Bulk-Buy Program on the Treatment of Patients with Coronary Artery Disease in China: A Single Center Study
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Xinxing Song, Yanzhuo Ma, Zhiwen Li, Xiaoye Wang, Gang Wang, Yuhong Peng, and Leisheng Ru
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History ,Polymers and Plastics ,Business and International Management ,Industrial and Manufacturing Engineering - Published
- 2022
18. Model Based Motion Vector Predictor for Zoom Motion.
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Hui Yuan 0001, Yilin Chang, Zhaoyang Lu, and Yanzhuo Ma
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- 2010
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19. Atherogenic L5 LDL induces cardiomyocyte apoptosis and inhibits KATP channels through CaMKII activation
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Nancy Cheng, Shahrzad Abbasi, Geru Wu, Yanzhuo Ma, Chu-Huang Chen, Jie Cheng, Yutao Xi, An-Sheng Lee, Junping Sun, Jonathan Lu, and Tatsuya Sawamura
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Electronegative low-density lipoprotein ,ATP-sensitive potassium ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,030209 endocrinology & metabolism ,030204 cardiovascular system & hematology ,Pharmacology ,Glibenclamide ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Endocrinology ,Ca2+/calmodulin-dependent protein kinase ,medicine ,Viability assay ,lcsh:RC620-627 ,Cardiomyocytes ,chemistry.chemical_classification ,Reactive oxygen species ,Biochemistry (medical) ,Action potential ,lcsh:Nutritional diseases. Deficiency diseases ,chemistry ,Apoptosis ,Pinacidil ,cardiovascular system ,Phosphorylation ,Ca2+/calmodulin-dependent protein kinase II ,Lipoprotein ,medicine.drug - Abstract
Background Cardiac Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation plays a critical role in cardiomyocyte (CM) apoptosis and arrhythmia. Functional ATP-sensitive potassium (KATP) channels are essential for cardiac protection during ischemia. In cultured CMs, L5 low-density lipoprotein (LDL) induces apoptosis and QTc prolongation. L5 is a highly electronegative and atherogenic aberrant form of LDL, and its levels are significantly higher in patients with cardiovascular-related diseases. Here, the role of L5 in cardiac injury was studied by evaluating the effects of L5 on CaMKII activity and KATP channel physiology in CMs. Methods Cultured neonatal rat CMs (NRCMs) were treated with a moderate concentration (ie, 7.5 μg/mL) of L5 or L1 (the least electronegative LDL subfraction). NRCMs were examined for apoptosis and viability, CaMKII activity, and the expression of phosphorylated CaMKIIδ and NOX2/gp91phox. The function of KATP and action potentials (APs) was analyzed by using the patch-clamp technique. Results In NRCMs, L5 but not L1 significantly induced cell apoptosis and reduced cell viability. Furthermore, L5 decreased Kir6.2 expression by more than 50%. Patch-clamp analysis showed that L5 reduced the KATP current (IKATP) density induced by pinacidil, a KATP opener. The partial recovery of the inward potassium current during pinacidil washout was susceptible to subsequent inhibition by the IKATP blocker glibenclamide. Suppression of IKATP by L5 significantly prolonged the AP duration. L5 also significantly increased the activity of CaMKII, the phosphorylation of CaMKIIδ, and the expression of NOX2/gp91phox. L5-induced apoptosis was prevented by the addition of the CaMKII inhibitor KN93 and the reactive oxygen species scavenger Mn (III)TBAP. Conclusions L5 but not L1 induces CM damage through the activation of the CaMKII pathway and increases arrhythmogenicity in CMs by modulating the AP duration. These results help to explain the harmful effects of L5 in cardiovascular-related disease.
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- 2020
20. Volume 2: Data structures based on non-linear relations and data processing methods
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Xiang Ji, Yanzhuo Ma, Zhiyuan Ren, Kai Fan, and Xingni Zhou
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Nonlinear system ,Data processing ,Computer science ,Data structure ,Algorithm ,Volume (compression) - Published
- 2020
21. Apolipoprotein-J blocks increased cell injury elicited by ox-LDL via inhibiting ROS-CaMKII pathway
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Chao Ding, Dong-mei Wang, Yu Chen, Kai Nan, Shuying Qi, Zhi Gong, Yanzhuo Ma, and Leisheng Ru
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Apolipoprotein-J ,Heart Ventricles ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Apoptosis ,030209 endocrinology & metabolism ,030204 cardiovascular system & hematology ,Ox-LDL ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,Endocrinology ,Ca2+/calmodulin-dependent protein kinase ,medicine ,Animals ,Viability assay ,Cytotoxicity ,lcsh:RC620-627 ,Cell damage ,chemistry.chemical_classification ,Reactive oxygen species ,Chemistry ,Research ,Biochemistry (medical) ,Neonatal rat ventricular cells ,medicine.disease ,Cytoprotection ,Cell biology ,Lipoproteins, LDL ,lcsh:Nutritional diseases. Deficiency diseases ,Clusterin ,Animals, Newborn ,lipids (amino acids, peptides, and proteins) ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,Reactive Oxygen Species ,Signal Transduction ,Lipoprotein - Abstract
Background Oxidized low-density lipoprotein (ox-LDL) is crucial in cardiac injury. Apolipoprotein-J (ApoJ) contributes to antiapoptotic effects in the heart. We aimed to evaluate the protective effects of ApoJ against ox-LDL cytotoxicity in Neonatal rat ventricular cells (NRVCs). Methods and results NRVCs were damaged by exposure to ox-LDL, as shown by increased caspase-3/7 activity, enhanced caspase-3 expression, and decreased cell viability. ApoJ overexpression, using an adenovirus vector, significantly reduced ox-LDL-induced cell injury. ApoJ also prevented ox-LDL from augmenting reactive oxygen species (ROS) production, as demonstrated by elevated Nox2/gp91phox and P47 expression. Furthermore, ApoJ overexpression reduced CaMKIIδ expression elicited by ox-LDL in cultured NRVCs. Upregulating CaMKIIδ activity, mediated by ox-LDL, was significantly inhibited by ApoJ overexpression. A CaMKIIδ inhibitor, KN93, prevented ApoJ’s protective effect against ox-LDL cytotoxicity. A ROS scavenger, Mn (III)meso-tetrakis (4-benzoic acid) porphyrin (Mn (III)TBAP), also attenuated CaMKIIδ’s increased expression and activity, induced by ox-LDL, and showed similar results to ApoJ by attenuating ox-LDL-induced cell damage, as ApoJ did. Conclusions ApoJ confers cytoprotection to NRVCs against ox-LDL cytotoxicity through the ROS-CaMKII pathways.
- Published
- 2019
22. Atorvastatin blocks increased l-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress
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Yanzhuo Ma, Lingfeng Kong, Dongmei Wang, and Shuying Qi
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0301 basic medicine ,medicine.medical_specialty ,Atorvastatin ,Biophysics ,030204 cardiovascular system & hematology ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Viability assay ,chemistry.chemical_classification ,Cardioprotection ,Reactive oxygen species ,General Medicine ,Angiotensin II ,030104 developmental biology ,Endocrinology ,chemistry ,Apoptosis ,cardiovascular system ,hormones, hormone substitutes, and hormone antagonists ,Oxidative stress ,Intracellular ,circulatory and respiratory physiology ,medicine.drug - Abstract
Thel-type Ca(2+)current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates theICa,land cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91(phox), p47(phox) ,and Cav1.2 were analyzed. In addition,ICa,lwas recorded using the whole-cell patch-clamp technique, and mechanisms of atorvastatin actions were also investigated. It was found that the number of apoptotic cardiomyocytes was increased and cell viability was significantly decreased after AngII administration. AngII also augmented the expressions of Nox2/gp91(phox)and p47(phox)compared with control cardiomyocytes. Exposure to AngII evokedICa,lin a voltage-dependent manner without affecting theI-Vrelationship. In addition, AngII enhanced membrane Cav1.2 expression. These effects were abolished in the presence of the reactive oxygen species (ROS) scavenger, manganese (III)-tetrakis 4-benzoic acid porphyrin [Mn(III)TBAP], or the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, atorvastatin. These results suggested that atorvastatin mediates cardioprotection against arrhythmias and cell injury by controlling the AngII-ROS cascade.
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- 2016
23. Involvement of MicroRNA-133a in the Protective Effect of Hydrogen Sulfide against Ischemia/Reperfusion-Induced Endoplasmic Reticulum Stress and Cardiomyocyte Apoptosis
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Qian Wang, Lin Ren, Yu Chen, Yanzhuo Ma, and Dongmei Wang
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Cardiotonic Agents ,Eukaryotic Initiation Factor-2 ,Motility ,Apoptosis ,Myocardial Reperfusion Injury ,Transfection ,030226 pharmacology & pharmacy ,Flow cytometry ,Cell Line ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,Annexin ,medicine ,Animals ,Myocytes, Cardiac ,Hydrogen Sulfide ,Heat-Shock Proteins ,Pharmacology ,Cardioprotection ,medicine.diagnostic_test ,Endoplasmic reticulum ,Cell migration ,General Medicine ,Endoplasmic Reticulum Stress ,Rats ,Disease Models, Animal ,MicroRNAs ,Cancer research ,Unfolded protein response ,030217 neurology & neurosurgery ,Transcription Factor CHOP - Abstract
Aim: Myocardial ischemia/reperfusion (I/R) injury is a severe trauma that cells undergo and is associated with cardiomyocyte apoptosis. Recently, miRNAs have been demonstrated to play an important role in cardiovascular biology and disease. However, whether the miR-133a and ER stress play a role in hydrogen sulfide (H2S) protection of cardiomyocytes against I/R-induced apoptosis remains unclear. Methods: The neonatal cardiomyocytes were prepared to be treated with H2S or transfected with miR-133a activator or miR-133a inhibitor, either separately or in combination. Non-treated cardiomyocytes served as control. The ER stress biomarker GRP78, CHOP, and eIF2α expression levels were measured by Western blot. Cell apoptosis was assessed by flow cytometry after staining with the Annexin V- FITC. Proliferation was monitored by BrdU labeling, while cell migration and invasion were determined by Transwell assays. Results: Pre-treatment of H2S and overexpression of miR-133a reversed I/R-induced ER stress and cardiomyocyte apoptosis in vitro and in vivo. The proliferation, migration, and invasion of cardiomyocytes were significantly increased by co-treatment with H2S and overexpression of miR-133a. Conclusion: These findings suggest the protective effect of miR-133a against I/R-induced ER stress and cardiomyocyte apoptosis and its enhancement of cell motility. Thus, cardioprotection by miR-133a overexpression provides a novel therapeutic approach to the treatment of ischemic heart diseases.
- Published
- 2018
24. Exhaustive exercise decreases L-type calcium current by activating endoplasmic reticulum stress
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Lingfeng Kong, Dongmei Wang, Shuying Qi, and Yanzhuo Ma
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Male ,medicine.medical_specialty ,Calcium Channels, L-Type ,chemistry.chemical_element ,Apoptosis ,Physical Therapy, Sports Therapy and Rehabilitation ,Calcium ,CHOP ,Rats, Sprague-Dawley ,Salubrinal ,Dephosphorylation ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Physical Conditioning, Animal ,Internal medicine ,medicine ,Animals ,Orthopedics and Sports Medicine ,Patch clamp ,Endoplasmic reticulum ,Electric Conductivity ,030229 sport sciences ,Endoplasmic Reticulum Stress ,Rats ,Disease Models, Animal ,Endocrinology ,chemistry ,030220 oncology & carcinogenesis ,Unfolded protein response - Abstract
BACKGROUND This study investigated effects of exhaustive exercise on L-type calcium current (ICa,L) and the putative intracellular cascade responsible for the effects. METHODS Rats were randomly divided into three treatment groups: sedentary (without exercise), exercised to exhaustion and salubrinal injection before each exhaustive exercise period. Exercise group rats were forced to swim until exhaustion each time for 9 days with 5% body weight attached to the head. Salubrinal (1 mg/kg) or an equivalent volume of placebo solution (dimethyl sulfoxide) was injected via the intraperitoneal route daily for the first 3 days, followed by subcutaneous injections of salubrinal (0.5 mg/kg) or placebo solution daily for 9 days (starting 30 min before exercise). After a 1-day recovery period, whole-cell patch clamping was used to investigate the L-type Ca2+ current (ICa,L), with sedentary control rats. Additionally, endoplasmic reticulum (ER) chaperone protein levels were analyzed. RESULTS Exhaustive exercise triggered ER stress, demonstrated by elevated expression of ER stress markers: phospho-eIF2α, CCAT/enhancer-binding homologous protein (CHOP) and caspase-12. Compared to controls, ICa,L was inhibited by exhaustive exercise, which was blocked by salubrinal, a selective eIF2α dephosphorylation inhibitor used to inhibit ER stress. These results suggest that ER stress participates in regulation of ICa,L. However, exhaustive exercise did not change the voltage dependence of steady-state activation and inactivation of ICaL, and salubrinal infusion caused no difference in voltage dependence of steady-state activation and inactivation of ICa,L. CONCLUSIONS Exhaustive exercise activates ER stress, thus inhibiting ICaL, which may change the action potential duration and contribute to proarrhythmia.
- Published
- 2017
25. Advanced Glycation End Products Accelerate Ischemia/Reperfusion Injury Through Receptor of Advanced End Product/Nitrative Thioredoxin Inactivation in Cardiac Microvascular Endothelial Cells
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Wayne Bond Lau, Chenhai Xia, Lu Yang, Ronghua Luan, Lu Sun, Rutao Wang, Ling Tao, Haichang Wang, Kun Lian, Yanzhuo Ma, Rong-qing Zhang, and Yi Liu
- Subjects
Glycation End Products, Advanced ,Male ,Physiology ,Primary Cell Culture ,Receptor for Advanced Glycation End Products ,Clinical Biochemistry ,Population ,Myocardial Ischemia ,Ischemia ,Myocardial Reperfusion Injury ,Pharmacology ,Nitric Oxide ,medicine.disease_cause ,Biochemistry ,Nitric oxide ,chemistry.chemical_compound ,Thioredoxins ,Superoxides ,Glycation ,Animals ,Medicine ,Rats, Wistar ,Receptors, Immunologic ,education ,Molecular Biology ,Cells, Cultured ,General Environmental Science ,education.field_of_study ,Nitrates ,L-Lactate Dehydrogenase ,biology ,business.industry ,Endothelial Cells ,Serum Albumin, Bovine ,Cell Biology ,medicine.disease ,Cell Hypoxia ,Rats ,Nitric oxide synthase ,Oxidative Stress ,chemistry ,Microvessels ,biology.protein ,General Earth and Planetary Sciences ,business ,Reperfusion injury ,Peroxynitrite ,Oxidative stress - Abstract
The advanced glycation end products (AGEs) are associated with increased cardiac endothelial injury. However, no causative link has been established between increased AGEs and enhanced endothelial injury after ischemia/reperfusion. More importantly, the molecular mechanisms by which AGEs may increase endothelial injury remain unknown. Adult rat cardiac microvascular endothelial cells (CMECs) were isolated and incubated with AGE-modified bovine serum albumin (BSA) or BSA. After AGE-BSA or BSA preculture, CMECs were subjected to simulated ischemia (SI)/reperfusion (R). AGE-BSA increased SI/R injury as evidenced by enhanced lactate dehydrogenase release and caspase-3 activity. Moreover, AGE-BSA significantly increased SI/R-induced oxidative/nitrative stress in CMECs (as measured by increased inducible nitric oxide synthase expression, total nitric oxide production, superoxide generation, and peroxynitrite formation) and increased SI/R-induced nitrative inactivation of thioredoxin-1 (Trx-1), an essential cytoprotective molecule. Supplementation of EUK134 (peroxynitrite decomposition catalyst), human Trx-1, or soluble receptor of advanced end product (sRAGE) (a RAGE decoy) in AGE-BSA precultured cells attenuated SI/R-induced oxidative/nitrative stress, reduced SI/R-induced Trx-1 nitration, preserved Trx-1 activity, and reduced SI/R injury. Our results demonstrated that AGEs may increase SI/R-induced endothelial injury by increasing oxidative/nitrative injury and subsequent nitrative inactivation of Trx-1. Interventions blocking RAGE signaling or restoring Trx activity may be novel therapies to mitigate endothelial ischemia/reperfusion injury in the diabetic population.
- Published
- 2011
26. Model Based Motion Vector Predictor for Zoom Motion
- Author
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Zhaoyang Lu, Hui Yuan, Yilin Chang, and Yanzhuo Ma
- Subjects
Motion analysis ,Computer science ,business.industry ,Applied Mathematics ,ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISION ,Iterative reconstruction ,Motion vector ,Motion (physics) ,Quarter-pixel motion ,Motion field ,Motion estimation ,Signal Processing ,Linear motion ,Computer vision ,Artificial intelligence ,Electrical and Electronic Engineering ,Zoom ,business ,ComputingMethodologies_COMPUTERGRAPHICS - Abstract
As zoom motion is common in video applications, a linear motion model is derived to describe zoom motion based on the analyses of camera imaging principles. Based on the motion model, a motion vector predictor for videos involving zoom motion is proposed. A rate distortion (RD) criterion is used to choose the optimal motion vector predictor between the one utilized in H.264/AVC and the one derived from the linear motion model. Experimental results demonstrate that by implementing the proposed method into Key Technology Area test platform version 2.2r1(KTA2.2r1), the maximum and average bit rate savings can be achieved as high as 7.66% and 4.90% respectively, while maintaining the same quality of reconstructed videos.
- Published
- 2010
27. Atorvastatin blocks increased l-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress
- Author
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Yanzhuo, Ma, Lingfeng, Kong, Shuying, Qi, and Dongmei, Wang
- Subjects
Calcium Channels, L-Type ,Angiotensin II ,Original Articles ,Cell Line ,Rats ,Rats, Sprague-Dawley ,Oxidative Stress ,Animals, Newborn ,cardiovascular system ,Atorvastatin ,Animals ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,Reactive Oxygen Species ,hormones, hormone substitutes, and hormone antagonists - Abstract
The l-type Ca2+ current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates the ICa,l and cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91phox, p47phox, and Cav1.2 were analyzed. In addition, ICa,l was recorded using the whole-cell patch-clamp technique, and mechanisms of atorvastatin actions were also investigated. It was found that the number of apoptotic cardiomyocytes was increased and cell viability was significantly decreased after AngII administration. AngII also augmented the expressions of Nox2/gp91phox and p47phox compared with control cardiomyocytes. Exposure to AngII evoked ICa,l in a voltage-dependent manner without affecting the I–V relationship. In addition, AngII enhanced membrane Cav1.2 expression. These effects were abolished in the presence of the reactive oxygen species (ROS) scavenger, manganese (III)-tetrakis 4-benzoic acid porphyrin [Mn(III)TBAP], or the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, atorvastatin. These results suggested that atorvastatin mediates cardioprotection against arrhythmias and cell injury by controlling the AngII–ROS cascade.
- Published
- 2015
28. Apolipoprotein-J prevents angiotensin II-induced apoptosis in neonatal rat ventricular cells
- Author
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Chao Ding, Leisheng Ru, Yanzhuo Ma, Lingfeng Kong, Kai Nan, Dong-mei Wang, and Shuying Qi
- Subjects
MAPK/ERK pathway ,medicine.medical_specialty ,AngII ,Endocrinology, Diabetes and Metabolism ,p38 mitogen-activated protein kinases ,Clinical Biochemistry ,Apoptosis ,Rats, Sprague-Dawley ,Phosphatidylinositol 3-Kinases ,chemistry.chemical_compound ,Endocrinology ,Downregulation and upregulation ,Internal medicine ,Animals ,Medicine ,Myocytes, Cardiac ,LY294002 ,Protein kinase A ,Protein kinase B ,Cells, Cultured ,PI3K/AKT/mTOR pathway ,Biochemistry, medical ,ApoJ ,business.industry ,Angiotensin II ,Research ,Biochemistry (medical) ,NF-kappa B ,Protective Factors ,Neonatal rat ventricular cells ,Clusterin ,Animals, Newborn ,chemistry ,cardiovascular system ,Mitogen-Activated Protein Kinases ,business ,hormones, hormone substitutes, and hormone antagonists ,Signal Transduction - Abstract
Background Up-regulation of angiotensin II (AngII) occurs in cardiac diseases, such as congestive heart failure, cardiac hypertrophy, myocardial ischemia and atrial fibrillation, which represent major health problems. Evidence from in vivo studies suggests that the level of Apolipoprotein-J (ApoJ) is also elevated but plays a protective role in cardiovascular disease. This study aimed to evaluate the protective effects of ApoJ against cytotoxicity of AngII in neonatal rat ventricular cells (NRVCs). Methods and results In culture, NRVCs were damaged by exposure to AngII, and ApoJ overexpression using an adenovirus vector significantly reduced the AngII-induced cell injury. ApoJ also prevented AngII from augmenting Nox2/gp91phox expression. The reactive oxygen species (ROS) scavenger, Mn(III)TBAP, showed similar results of attenuating AngII-induced cell damage. Furthermore, ApoJ overexpression increased phosphorylation of Akt, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 diminished the antioxidant effects of ApoJ, and prevented the protective effect of ApoJ against the cytotoxicity of AngII. Moreover, upregulation of nuclear factor κB (NF-κB) p65 expression and phosphorylation of p38 mitogen-activated protein kinase (MAPK) mediated by AngII in cultured NRVCs were significantly inhibited by overexpression of ApoJ. The p38 MAPK inhibitor SB203580 and the NF-κB inhibitor PDTC protected NRVCs from injury caused by AngII. Conclusions ApoJ serves as a cytoprotective protein in NRVCs against cytotoxicity of AngII through the PI3K-Akt-ROS and MAPK/ NF-κB pathways.
- Published
- 2015
29. Adaptive Granularity selection in Reference Picture Memory Compression
- Author
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Lijuan Kang and Yanzhuo Ma
- Subjects
Motion compensation ,Computer science ,business.industry ,Motion estimation ,Bandwidth (signal processing) ,Wireless ,Memory bandwidth ,Video processing ,Parallel computing ,Granularity ,business ,Block size ,Algorithm - Abstract
design because of the large scale of data, and the high power consumption especially for wireless terminals. An adaptive and random access-obeyed reference pictures memory compression (RPMC) scheme based on as small granularity as 2x2 blocks for 2-bit truncation is proposed in this paper to solve the problems. The impact of granularity in RPMC to memory access bandwidth during motion estimation and/or motion compensation is analyzed firstly. Then an adaptive RPMC scheme based on 2x2 block size is proposed, based on min-max scalar quantization (MMSQ). Finally, the results based on HM are provided which show that compared with the common used 4x4 block-based methods, little performance loss is introduced. At the same time, based on the adaptively merge scheme, the average memory access bandwidth is saved than the 4x4 block based method by up to 17%.
- Published
- 2015
30. The alternative crosstalk between RAGE and nitrative thioredoxin inactivation during diabetic myocardial ischemia-reperfusion injury
- Author
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Aibing Xu, Lu Sun, Lu Yang, Chenhai Xia, Kun Lian, Walter J. Koch, Rutao Wang, Yanzhuo Ma, Haichang Wang, Wayne Bond Lau, Ling Tao, Chao Gao, Yi Liu, Jingyi Liu, Erhe Gao, Yan Qu, and Xiaoyan Lu
- Subjects
Male ,medicine.medical_specialty ,animal structures ,Physiology ,Endocrinology, Diabetes and Metabolism ,Receptor for Advanced Glycation End Products ,Nitric Oxide Synthase Type II ,Myocardial Reperfusion Injury ,Diabetes Mellitus, Experimental ,chemistry.chemical_compound ,Mice ,Thioredoxins ,Superoxides ,Physiology (medical) ,Internal medicine ,medicine ,Organometallic Compounds ,Animals ,cardiovascular diseases ,Enzyme Inhibitors ,RNA, Small Interfering ,Receptors, Immunologic ,Cardioprotection ,NADPH oxidase ,Membrane Glycoproteins ,biology ,business.industry ,Nitrotyrosine ,Lysine ,Acetophenones ,NADPH Oxidases ,Free Radical Scavengers ,medicine.disease ,Salicylates ,Nitric oxide synthase ,Mice, Inbred C57BL ,Endocrinology ,chemistry ,Apocynin ,NADPH Oxidase 2 ,cardiovascular system ,biology.protein ,Advanced glycation end-product ,Tyrosine ,Imines ,business ,Reperfusion injury ,Peroxynitrite - Abstract
The receptor for advanced glycation end products (RAGE) and thioredoxin (Trx) play opposing roles in diabetic myocardial ischemia-reperfusion (MI/R) injury. We recently demonstrated nitrative modification of Trx leads to its inactivation and loss of cardioprotection. The present study is to determine the relationship between augmented RAGE expression and diminished Trx activity pertaining to exacerbated MI/R injury in the diabetic heart. The diabetic state was induced in mice by multiple intraperitoneal low-dose streptozotocin injections. RAGE small-interfering RNA (siRNA) or soluble RAGE (sRAGE, a RAGE decoy) was via intramyocardial and intraperitoneal injection before MI/R, respectively. Mice were subjected to 30 min of myocardial infarction followed by 3 or 24 h of reperfusion. At 10 min before reperfusion, diabetic mice were randomized to receive EUK134 (peroxynitrite scavenger), recombinant hTrx-1, nitrated Trx-1, apocynin (a NADPH oxidase inhibitor), or 1400W [an inducible nitric oxide synthase (iNOS) inhibitor] administration. The diabetic heart manifested increased RAGE expression and Nε-(carboxymethyl)lysine (CML, major advanced glycation end product subtype) content, reduced Trx-1 activity, and increased Trx nitration after MI/R. RAGE siRNA or administration of sRAGE in diabetic mice decreased MI/R-induced iNOS and gp91phox expression, reduced Trx nitration, preserved Trx activity, and decreased infarct size. Apocynin or 1400W significantly decreased nitrotyrosine production and restored Trx activity. Conversely, administration of either EUK134 or reduced hTrx, but not nitrated hTrx, attenuated MI/R-induced superoxide production, RAGE expression, and CML content and decreased cardiomyocyte apoptosis in diabetic mice. Collectively, we demonstrate that RAGE modulates the MI/R injury in a Trx nitrative inactivation fashion. Conversely, nitrative modification of Trx blocked its inhibitory effect upon RAGE expression in the diabetic heart. This is the first direct evidence demonstrating the alternative cross talk between RAGE overexpression and nitrative Trx inactivation, suggesting that interventions interfering with their interaction may be novel means of mitigating diabetic MI/R injury.
- Published
- 2012
31. Cardiac-derived adiponectin induced by long-term insulin treatment ameliorates myocardial ischemia/reperfusion injury in type 1 diabetic mice via AMPK signaling
- Author
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Wenjun Yan, Yanzhuo Ma, Qiujun Yu, Yi Liu, Haifeng Zhang, Jingyi Liu, Yan Qu, Wayne Bond Lau, Haifeng Pei, Kun Lian, Ling Tao, Xiaoyan Lu, Chengxiang Li, Peilin Liu, and Weijie Li
- Subjects
Blood Glucose ,Male ,medicine.medical_specialty ,animal structures ,Physiology ,medicine.medical_treatment ,Intraperitoneal injection ,Myocardial Reperfusion Injury ,AMP-Activated Protein Kinases ,Streptozocin ,Mice ,Physiology (medical) ,Diabetes mellitus ,Internal medicine ,medicine ,Animals ,Insulin ,Cardioprotection ,Type 1 diabetes ,Adiponectin ,business.industry ,AMPK ,medicine.disease ,Mice, Inbred C57BL ,Endocrinology ,Diabetes Mellitus, Type 1 ,Female ,Cardiology and Cardiovascular Medicine ,business ,Reperfusion injury ,hormones, hormone substitutes, and hormone antagonists ,Signal Transduction - Abstract
Type 1 diabetes (T1DM) portends poor prognosis concerning ischemic heart disease. Adiponectin (APN), an adipocytokine possessing insulin sensitizing and metabolic regulatory effects, has been recognized as a potent cardioprotective molecule. However, the relationship between APN and T1DM remains controversial and the role of cardiac-derived APN in T1DM is unclear. This study is aimed to investigate the dynamic change of both plasma and cardiac-derived APN expressions in T1DM, and the particular role of cardiac-derived APN in T1DM against myocardial ischemia/reperfusion (MI/R) injury. T1DM was established via intraperitoneal injection of streptozocin and followed by twice-daily subcutaneous injection of insulin or vehicle for 14 days. Non-diabetic mice of wild type and APN knockout were subjected to insulin or vehicle injection. MI/R was induced in Langendorff-perfused hearts. Compared to non-diabetic mice, plasma APN levels of diabetic mice significantly increased at 7 days, and slightly decreased at 14 days, while cardiac-derived APN levels gradually decreased over time. The MI/R injury measured as infarct size and cardiomyocyte apoptosis nearly doubled in diabetic mice. 14 days of insulin treatment increased both plasma and cardiac-derived APN levels in diabetic mice and attenuated myocardial injury via increasing AMPK phosphorylation in T1DM, which was partly reversed by Compound C (an AMPK inhibitor). Moreover, APN deficiency aggravated MI/R injury and partly abolished the protective effect of insulin treatment against MI/R injury, which was associated with decreased AMPK phosphorylation. The results suggest that cardiac-derived APN stimulated by long-term insulin treatment in T1DM exerts cardioprotection against MI/R injury via myocardial AMPK activation.
- Published
- 2012
32. Efficient Prediction Structure for Key Pictures in Multiview Video Coding
- Author
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Yilin Chang, Junyan Huo, and Yanzhuo Ma
- Subjects
H.262/MPEG-2 Part 2 ,Motion compensation ,business.industry ,Computer science ,Iso standards ,computer.file_format ,Coding tree unit ,Computer vision ,Artificial intelligence ,Iec standards ,Multiview Video Coding ,business ,computer ,Context-adaptive binary arithmetic coding ,Coding (social sciences) - Abstract
Compared to simulcast, the utilization of inter-view prediction at key pictures can dramatically improve the compression efficiency of multiview video coding (MVC). The reconstructed key picture in previous adjacent view is used as the inter-view reference picture of the key picture in the current coding view. The efficiency of inter-view prediction may deteriorate due to the existence of mismatch between views. An efficient prediction structure for key pictures is proposed by introducing multiple reference pictures prediction scheme. Experimental results show that average gains of 0.219dB can be achieved for key pictures compared to the reference prediction structure of MVC.
- Published
- 2011
33. Downregulation of adiponectin induced by tumor necrosis factor α is involved in the aggravation of posttraumatic myocardial ischemia/reperfusion injury
- Author
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Ling Tao, Haichang Wang, Erhe Gao, Kun Lian, Chenhai Xia, Yan Qu, Rutao Wang, Xufeng Wei, Wayne Bond Lau, Tao Yin, Shaowei Liu, Haifeng Pei, Yi Liu, Yanzhuo Ma, Walter J. Koch, Wei Yi, and Lu Sun
- Subjects
Male ,medicine.medical_specialty ,Exacerbation ,Myocardial Infarction ,Down-Regulation ,Apoptosis ,Enzyme-Linked Immunosorbent Assay ,Myocardial Reperfusion Injury ,Critical Care and Intensive Care Medicine ,Nitric Oxide ,Receptors, Tumor Necrosis Factor ,Etanercept ,Mice ,Random Allocation ,Downregulation and upregulation ,Superoxides ,Internal medicine ,medicine ,Animals ,Myocytes, Cardiac ,Myocardial infarction ,Mice, Knockout ,Analysis of Variance ,Adiponectin ,business.industry ,Tumor Necrosis Factor-alpha ,medicine.disease ,Cardiovascular physiology ,Disease Models, Animal ,Oxidative Stress ,Anesthesia ,Immunoglobulin G ,Cardiology ,Wounds and Injuries ,Tumor necrosis factor alpha ,business ,Reperfusion injury ,medicine.drug - Abstract
Recent clinical observations have indicated that nonlethal mechanical trauma significantly increases myocardial infarction risk even in the presence of completely normal coronary arteries. We investigated the molecular mechanisms responsible for exacerbation of ischemic myocardial injury after nonlethal mechanical trauma with a special focus on the role of tumor necrosis factor α and its potential downstream effector adiponectin, a novel adipokine with anti-inflammatory and cardioprotective properties.Laboratory study.University research unit.Male adult adiponectin knockout mice and wild-type mice.The animals were subjected to nonlethal mechanical trauma using the Noble-Collip drum (40 rpm ± 5 mins) followed by myocardial ischemia/reperfusion injury 7 days posttrauma. We also investigated the effects of neutralizing tumor necrosis factor α with etanercept and exogenous adiponectin supplementation on ischemic myocardial injury after trauma.Trauma significantly sensitized myocardium to ischemia/reperfusion injury as evidenced by increased apoptosis, enlarged infarct size, and decreased cardiac function. Plasma adiponectin concentrations were reduced after traumatic injury (the nadir occurring 3 days posttrauma), an effect abrogated by etanercept-mediated tumor necrosis factor α blockade. The downregulation of adiponectin was accompanied by increased myocardial superoxide and nitric oxide generation and peroxynitrite formation. Both etanercept and exogenous adiponectin supplementation (on day 3 posttrauma or 10 mins before reperfusion on day 7 posttrauma) markedly inhibited oxidative/nitrative stress and ischemia/reperfusion injury in posttraumatic ischemic/reperfused hearts of wild-type mice, whereas only adiponectin supplementation (but not tumor necrosis factor α inhibition) substantially attenuated posttraumatic ischemia/reperfusion injury in adiponectin knockout mice.Tumor necrosis factor α-induced downregulation of adiponectin and the resultant enhanced oxidative/nitrative stress are involved in exacerbated posttraumatic ischemic myocardial injury. Therapeutic approaches blocking tumor necrosis factor α production or restoring adiponectin might have prophylactic value against secondary myocardial ischemic injury after a primary nonlethal mechanical trauma.
- Published
- 2011
34. Notice of Retraction: A novel 3-D Interleaving method for video transmission over OFDM in mobile wireless channels
- Author
-
Junyan Huo, Yanzhuo Ma, and Yilin Chang
- Subjects
Interleaving ,Computer science ,business.industry ,Orthogonal frequency-division multiplexing ,Data_CODINGANDINFORMATIONTHEORY ,Domain (software engineering) ,Frequency domain ,Bit error rate ,Electronic engineering ,Fading ,Mobile telephony ,Spatial frequency ,business ,Computer hardware - Abstract
Reliable video transmission over mobile wireless channels faces many challenges due to the time-varying multi-path fading. In this paper, a novel 3-D interleaving method, called Spatial Frequency Temporal Interleaving (SFTI), is proposed for video transmission over OFDM systems in this kind of channels. SFTI means the video data will be interleaved both at bit level in spatial domain, which can disperse the error bits to make the channel coding more effective, and slice level in Frequency and temporal domain, which can alleviate the impact of burst bit errors by limiting the bit errors in some area of the picture, thus the error concealment is facilitated. Simulation results show that the proposed method can improve the quality of the reconstructed video.
- Published
- 2010
35. A Flexible Reference Picture Selection Method for Spatial DIRECT Mode in Multiview Video Coding
- Author
-
Yilin Chang, Yanzhuo Ma, Sixin Lin, and Junyan Huo
- Subjects
Motion compensation ,Computer science ,business.industry ,Algorithmic efficiency ,Encoding (memory) ,Macroblock ,Direct mode ,Computer vision ,Visual communication ,Artificial intelligence ,Multiview Video Coding ,Quantization (image processing) ,business - Abstract
The motion information of the macroblock signaled as the spatial DIRECT mode can be derived from the neighboring blocks. The closest reference picture in the reference picture list used by the neighboring blocks is selected as the reference picture of the macroblock. Both temporal and interview reference pictures are put into the reference picture list in order to improve the coding efficiency in MVC. A flexible reference picture selection method taking the diversity of reference picture list into account is proposed in this paper. The experimental results show that the proposed method can improve coding efficiency especially when the interview reference pictures are put ahead of the temporal reference pictures.
- Published
- 2008
36. A moving objects extraction method based on true motion information
- Author
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Yilin Chang, Hui Yuan, and Yanzhuo Ma
- Subjects
Computer science ,business.industry ,ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISION ,Pattern recognition ,Motion (physics) ,Match moving ,Feature (computer vision) ,Search algorithm ,Motion estimation ,Median filter ,Segmentation ,Computer vision ,Artificial intelligence ,Cluster analysis ,business - Abstract
In this paper, a moving objects extraction method based on true motion information is proposed. First of all, three dimensional recursive search algorithm (3DRS) combined with median filter is used instead of full search in searching for motion vectors (MVs) which reflect the true motion of objects in video sequences. After that a new parameter segmentation factor (SF) is constructed to describe motion feature of each block in a picture. Thus, moving objects extraction with the fuzzy C-means clustering algorithm (FCM) over SFs is implemented, during which gathering degree is used to distinguish the foreground which refers to the moving objects from the background. Experimental results show that this method is effective for still scenes or scenes with consistent global motion.
- Published
- 2008
37. Channel-Aware Adaptive Multi-RPS Scheme for Video Error Resilient Transmission over Wireless OFDM Channel
- Author
-
Yilin Chang and Yanzhuo Ma
- Subjects
Propagation of uncertainty ,Interleaving ,Orthogonal frequency-division multiplexing ,Computer science ,business.industry ,Real-time computing ,Data_CODINGANDINFORMATIONTHEORY ,Broadband wireless communications ,Electronic engineering ,Wireless ,business ,Encoder ,Coding (social sciences) ,Communication channel - Abstract
Orthogonal Frequency Division Multiplexing (OFDM) is a promising technique in broadband wireless communication systems. This paper presents a novel multi-reference scheme based on 3D interleaving for video coding and transmission over OFDM channel. Initially, a combining interleaving method in spatial, frequency and temporal domains, called SFTI, is proposed. With SFTI, different slices within one frame are transmitted in different sub-channels of OFDM, whose SNR can be estimated, and the transmission status of slices through these sub-channels are real-time feedback to the encoder. Based on the feedback information, a multi-reference scheme for video coding is proposed where the well-transmitted slices are selected as the reference picture of its consequent pictures in inter-frame coding to eliminate the impairment caused by error propagation in video transmission over wireless OFDM channels. Extensive experimental results have demonstrated the effectiveness of the proposed methods in error resilience.
- Published
- 2007
38. A Cross-Layer H.264/AVC Video Transmission Method Over Wireless OFDM
- Author
-
Yilin Chang and Yanzhuo Ma
- Subjects
Interleaving ,business.industry ,Computer science ,Orthogonal frequency-division multiplexing ,ComputerSystemsOrganization_COMPUTER-COMMUNICATIONNETWORKS ,Real-time computing ,Data_CODINGANDINFORMATIONTHEORY ,Video quality ,Scalable Video Coding ,Wireless ,business ,Encoder ,Computer hardware ,Data transmission ,Communication channel - Abstract
This paper focuses on the issue of cross-layer control for H.264/AVC video transmission over OFDM. Jointly considering the error resilient (ER) tools provided by H.264/AVC and the characteristics of OFDM channels, a cross-layer scheme is proposed, in which a cross-layer allocator is used to allocate channel resources for different priority video data transmission, and feedback transmission status information to H.264/AVC encoder for error resilient encoding. By allocation, a 3-D interleaving is implemented to improve the reliance of the communication, and a cross-layer feedback is operated to inform the encoder for a more resilient coding processing to obtain optimal transmission quality. The experimental results indicate that the proposed scheme can dramatically improve the received video quality over wireless OFDM.
- Published
- 2007
39. Atorvastatin blocks increased L-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress.
- Author
-
Yanzhuo Ma, Lingfeng Kong, Shuying Qi, and Dongmei Wang
- Published
- 2016
- Full Text
- View/download PDF
40. MOST NEGATIVELY CHARGED SUBFRACTION (L5) INDUCES CARDIOMYOCYTES DAMAGE AND REDUCTION OF CARDIAC ATP-SENSITIVE K+ CHANNELS
- Author
-
Yanzhuo Ma, Chu-Huang Chen, Jie Cheng, Geru Wu, Jonathan Lu, Nancy Cheng, Yutao Xi, and Shahrzad Abbasi
- Subjects
Reduction (complexity) ,business.industry ,Biophysics ,Medicine ,Cardiology and Cardiovascular Medicine ,business - Published
- 2012
41. Adiponectin multimers and their bioactivities were down-regulated in newly diagnosed Chinese type 2 diabetes patients
- Author
-
Aibing Xu, Kun Lian, Qian Huang, Wen Jin, Rutao Wang, Chenhai Xia, Yi Liu, Lu Sun, and Yanzhuo Ma
- Subjects
Gene isoform ,medicine.medical_specialty ,biology ,Adiponectin ,medicine.diagnostic_test ,business.industry ,nutritional and metabolic diseases ,AMPK ,Type 2 diabetes ,medicine.disease ,biology.organism_classification ,Endocrinology ,Western blot ,Enos ,Diabetes mellitus ,Internal medicine ,Medicine ,Phosphorylation ,Cardiology and Cardiovascular Medicine ,business ,hormones, hormone substitutes, and hormone antagonists - Abstract
Objective Adiponectin, circulates as trimer, hexamer and high molecular weight form (HMW) in blood. Both adiponectin complexes concentration and their bioactivities are decreased in pathological state. Moreover, DsbA-L, a key regulator for adiponectin biosynthesis, is down-regulated in obese humans. However, the alterations of adiponectin multimers distribution, bioactivities and DsbA-L level in newly diagnosed Chinese type 2 diabetes (T2DM) patients are unknown. The objective of present study was to compare plasma adiponectin isoform status along with their bioactivities and DsbA-L concentration in T2DM with control subjects. Methods Plasma total adiponectin was measured by ELISA. Adiponectin multimers were analysed by western blot followed SDS-PAGE under nonheating nonreducing conditions. Plasma adiponectin multimers were isolated by chromotography techniques from plasma in ten T2DM and ten healthy control subjects respectively. Adiponectin bioactivity was detected by incubating HUVEC with isolated adiponectin isoforms and determining the phosphorylation level of AMPK and eNOS. DsbA-L protein expression level was determined by western blot. Results 189 T2DM (48.7±9.4 y) and 123 healthy people (42.8±8.0 y) were enrolled. In comparison with healthy control group, total adiponectin (p Conclusion This study directly demonstrated for the first time that human HMW adiponectin bioactivity was decreased in type 2 diabetes. We also provide a target for regulating HMW adiponectin concentration in diabetic patients.
- Published
- 2011
42. Apolipoprotein-J prevents angiotensin II-induced apoptosis in neonatal rat ventricular cells.
- Author
-
Yanzhuo Ma, Lingfeng Kong, Kai Nan, Shuying Qi, Leisheng Ru, Chao Ding, and Dongmei Wang
- Subjects
- *
APOLIPOPROTEIN J , *APOLIPOPROTEIN genetics , *ANGIOTENSIN II , *ANGIOTENSIN receptor genetics , *ATRIAL fibrillation prevention - Abstract
Background: Up-regulation of angiotensin II (AngII) occurs in cardiac diseases, such as congestive heart failure, cardiac hypertrophy, myocardial ischemia and atrial fibrillation, which represent major health problems. Evidence from in vivo studies suggests that the level of Apolipoprotein-J (ApoJ) is also elevated but plays a protective role in cardiovascular disease. This study aimed to evaluate the protective effects of ApoJ against cytotoxicity of AngII in neonatal rat ventricular cells (NRVCs). Methods and results: In culture, NRVCs were damaged by exposure to AngII, and ApoJ overexpression using an adenovirus vector significantly reduced the AngII-induced cell injury. ApoJ also prevented AngII from augmenting Nox2/gp91phox expression. The reactive oxygen species (ROS) scavenger, Mn(III)TBAP, showed similar results of attenuating AngII-induced cell damage. Furthermore, ApoJ overexpression increased phosphorylation of Akt, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 diminished the antioxidant effects of ApoJ, and prevented the protective effect of ApoJ against the cytotoxicity of AngII. Moreover, upregulation of nuclear factor κB (NF-κB) p65 expression and phosphorylation of p38 mitogen-activated protein kinase (MAPK) mediated by AngII in cultured NRVCs were significantly inhibited by overexpression of ApoJ. The p38 MAPK inhibitor SB203580 and the NF-κB inhibitor PDTC protected NRVCs from injury caused by AngII. Conclusions: ApoJ serves as a cytoprotective protein in NRVCs against cytotoxicity of AngII through the PI3K-Akt- ROS and MAPK/ NF-κB pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
43. Efficient Prediction Structure for Key Pictures in Multiview Video Coding.
- Author
-
Junyan Huo, Yilin Chang, and Yanzhuo Ma
- Published
- 2011
- Full Text
- View/download PDF
44. A novel 3-D Interleaving method for video transmission over OFDM in mobile wireless channels.
- Author
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Yanzhuo Ma, Yilin Chang, and Junyan Huo
- Published
- 2010
- Full Text
- View/download PDF
45. A Flexible Reference Picture Selection Method for Spatial DIRECT Mode in Multiview Video Coding.
- Author
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Junyan Huo, Yilin Chang, Yanzhuo Ma, and Sixin Lin
- Published
- 2008
- Full Text
- View/download PDF
46. A Cross-Layer H.264/AVC Video Transmission Method Over Wireless OFDM.
- Author
-
Yanzhuo Ma and Yilin Chang
- Published
- 2007
- Full Text
- View/download PDF
47. The alternative crosstalk between RAGE and nitrative thioredoxin inactivation during diabetic myocardial ischemia-reperfusion injury.
- Author
-
Yi Liu, Yan Qu, Rutao Wang, Yanzhuo Ma, Chenhai Xia, Chao Gao, Jingyi Liu, Kun Lian, Aibing Xu, Xiaoyan Lu, Lu Sun, Lu Yang, Lau, Wayne B., Erhe Gao, Koch, Walter, Haichang Wang, and Ling Tao
- Abstract
The receptor for advanced glycation end products (RAGE) and thioredoxin (Trx) play opposing roles in diabetic myocardial ischemia-reperfusion (MI/R) injury. We recently demonstrated nitrative modification of Trx leads to its inactivation and loss of cardioprotection. The present study is to determine the relationship between augmented RAGE expression and diminished Trx activity pertaining to exacerbated MI/R injury in the diabetic heart. The diabetic state was induced in mice by multiple intraperitoneal low-dose streptozotocin injections. RAGE small-interfering RNA (siRNA) or soluble RAGE (sRAGE, a RAGE decoy) was via intramyocardial and intraperitoneal injection before MI/R, respectively. Mice were subjected to 30 min of myocardial infarction followed by 3 or 24 h of reperfusion. At 10 min before reperfusion, diabetic mice were randomized to receive EUK134 (peroxynitrite scavenger), recombinant hTrx-1, nitrated Trx-1, apocynin (a NADPH oxidase inhibitor), or 1400W [an inducible nitric oxide synthase (iNOS) inhibitor] administration. The diabetic heart manifested increased RAGE expression and Nε-(carboxymethyl) lysine (CML, major advanced glycation end product subtype) content, reduced Trx-1 activity, and increased Trx nitration after MI/R. RAGE siRNA or administration of sRAGE in diabetic mice decreased MI/R-induced iNOS and gp91
phox expression, reduced Trx nitration, preserved Trx activity, and decreased infarct size. Apocynin or 1400W significantly decreased nitrotyrosine production and restored Trx activity. Conversely, administration of either EUK134 or reduced hTrx, but not nitrated hTrx, attenuated MI/R-induced superoxide production, RAGE expression, and CML content and decreased cardiomyocyte apoptosis in diabetic mice. Collectively, we demonstrate that RAGE modulates the MI/R injury in a Trx nitrative inactivation fashion. Conversely, nitrative modification of Trx blocked its inhibitory effect upon RAGE expression in the diabetic heart. This is the first direct evidence demonstrating the alternative cross talk between RAGE overexpression and nitrative Trx inactivation, suggesting that interventions interfering with their interaction may be novel means of mitigating diabetic MI/R injury. [ABSTRACT FROM AUTHOR]- Published
- 2012
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48. Advanced Glycation End Products Accelerate Ischemia/Reperfusion Injury Through Receptor of Advanced End Product/Nitrative Thioredoxin Inactivation in Cardiac Microvascular Endothelial Cells.
- Author
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Yi Liu, Yanzhuo Ma, Rutao Wang, Chenhai Xia, Rongqing Zhang, Kun Lian, Ronghua Luan, Lu Sun, Lu Yang, Wayne B. Lau, Haichang Wang, and Ling Tao
- Subjects
- *
GLYCOSYLATION , *ISCHEMIA , *REPERFUSION injury , *THIOREDOXIN , *ENDOTHELIUM , *LACTATE dehydrogenase , *ENZYME kinetics - Abstract
AbstractThe advanced glycation end products (AGEs) are associated with increased cardiac endothelial injury. However, no causative link has been established between increased AGEs and enhanced endothelial injury after ischemia/reperfusion. More importantly, the molecular mechanisms by which AGEs may increase endothelial injury remain unknown. Adult rat cardiac microvascular endothelial cells (CMECs) were isolated and incubated with AGE-modified bovine serum albumin (BSA) or BSA. After AGE-BSA or BSA preculture, CMECs were subjected to simulated ischemia (SI)/reperfusion (R). AGE-BSA increased SI/R injury as evidenced by enhanced lactate dehydrogenase release and caspase-3 activity. Moreover, AGE-BSA significantly increased SI/R-induced oxidative/nitrative stress in CMECs (as measured by increased inducible nitric oxide synthase expression, total nitric oxide production, superoxide generation, and peroxynitrite formation) and increased SI/R-induced nitrative inactivation of thioredoxin-1 (Trx-1), an essential cytoprotective molecule. Supplementation of EUK134 (peroxynitrite decomposition catalyst), human Trx-1, or soluble receptor of advanced end product (sRAGE) (a RAGE decoy) in AGE-BSA precultured cells attenuated SI/R-induced oxidative/nitrative stress, reduced SI/R-induced Trx-1 nitration, preserved Trx-1 activity, and reduced SI/R injury. Our results demonstrated that AGEs may increase SI/R-induced endothelial injury by increasing oxidative/nitrative injury and subsequent nitrative inactivation of Trx-1. Interventions blocking RAGE signaling or restoring Trx activity may be novel therapies to mitigate endothelial ischemia/reperfusion injury in the diabetic population. Antioxid. Redox Signal.15, 1769â1778. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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49. Dynamic alteration of adiponectin/adiponectin receptor expression and its impact on myocardial ischemia/reperfusion in type 1 diabetic mice.
- Author
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Yanzhuo Ma, Yi Liu, Shaowei Liu, Yan Qu, Rutao Wang, Chenhai Xia, Haifeng Pei, Kun Lian, Tao Yin, Xiaoyan Lu, Lu Sun, Lu Yang, Yanjie Cao, Lau, Wayne Bond, Erhe Gao, Haichang Wang, and Ling Tao
- Subjects
- *
ADIPONECTIN , *CORONARY heart disease risk factors , *MYOCARDIAL reperfusion , *PEOPLE with diabetes , *LABORATORY mice , *ADENOSINE monophosphate , *PROTEIN kinases , *APOPTOSIS - Abstract
The present study determined the dynamic change of adiponectin (APN, a cardioprotective adipokine), its receptor expression, and their impact upon myocardial ischemia/reperfusion (MI/R) injury during type 1 diabetes mellitus (T1DM) progression, and involved underlying mechanisms. Diabetic state was induced in mice via multiple intraperitoneal injections of low-dose streptozotocin. The dynamic change of plasma APN concentration and cardiac APN receptor-1 and -2 (AdipoR1/2) expression were assessed immediately after diabetes onset (0 wk) and 1, 3, 5, and 7 wk thereafter. Indicators of MI/R injury (infarct size, apoptosis, and LDH release) were determined at 0, 1, and 7 wk of DM duration. The effect of APN on MI/R injury was determined in mice subjected to different diabetic durations. Plasma APN levels (total and HMW form) increased, whereas cardiac AdipoR1 expression decreased early after T1DM onset. With T1DM progression, APN levels were reduced and cardiac AdipoR1 expression increased. MI/R injury was exacerbated with T1DM progression in a time-dependent manner. Administration of globular APN (gAD) failed to attenuate MI/R injury in 1-wk T1DM mice, while an AMP-activated protein kinase (AMPK) activator (AICAR) reduced MI/R injury. However, administration of gAD (and AICAR) reduced infarct size and cardiomyocyte apoptosis in 7-wk T1DM mice. In conclusion, our results demonstrate a dynamic dysfunction of APN/AdipoR1 during T1DM progression. Reduced cardiac AdipoR1 expression and APN concentration may be responsible for increased I/R injury susceptibility at early and late T1DM stages, respectively. Interventions bolstering AdipoR1 expression during early T1DM stages and APN supplementation during advanced T1DM stages may potentially reduce the myocardial ischemic injury in diabetic patients. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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50. Downregulation of adiponectin induced by tumor necrosis factor α is involved in the aggravation of posttraumatic myocardial ischemia/reperfusion injury.
- Author
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Shaowei Liu, Tao Yin, Xufeng Wei, Wei Yi, Yan Qu, Yi Liu, Rutao Wang, Kun Lian, Chenhai Xia, Haifeng Pei, Lu Sun, Yanzhuo Ma, Lau, Wayne Bond, Erhe Gao, Koch, Walter J., Haichang Wang, and Ling Tao
- Published
- 2011
- Full Text
- View/download PDF
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