Journal of Cardiovascular Translational Research最新文献_第2页

Cirbp: A Key Regulator in Hypothermic Cardioprotection of Aged Donor Hearts During Transplantation. Cirbp：移植过程中低温保护衰老供体心脏的关键调控因子

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-15 DOI: 10.1007/s12265-024-10536-4

Danni Meng, Michail Spanos, Junjie Xiao

引用次数: 0

A Kernel Attention-based Transformer Model for Survival Prediction of Heart Disease Patients. 基于核注意力的心脏病患者生存预测变压器模型

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-08-05 DOI: 10.1007/s12265-024-10537-3

Palak Kaushal, Shailendra Singh, Rajesh Vijayvergiya

{"title":"A Kernel Attention-based Transformer Model for Survival Prediction of Heart Disease Patients.","authors":"Palak Kaushal, Shailendra Singh, Rajesh Vijayvergiya","doi":"10.1007/s12265-024-10537-3","DOIUrl":"10.1007/s12265-024-10537-3","url":null,"abstract":"Survival analysis is employed to scrutinize time-to-event data, with emphasis on comprehending the duration until the occurrence of a specific event. In this article, we introduce two novel survival prediction models: CosAttnSurv and CosAttnSurv <math><mo>+</mo></math> DyACT. CosAttnSurv model leverages transformer-based architecture and a softmax-free kernel attention mechanism for survival prediction. Our second model, CosAttnSurv <math><mo>+</mo></math> DyACT, enhances CosAttnSurv with Dynamic Adaptive Computation Time (DyACT) control, optimizing computation efficiency. The proposed models are validated using two public clinical datasets related to heart disease patients. When compared to other state-of-the-art models, our models demonstrated an enhanced discriminative and calibration performance. Furthermore, in comparison to other transformer architecture-based models, our proposed models demonstrate comparable performance while exhibiting significant reduction in both time and memory requirements. Overall, our models offer significant advancements in the field of survival analysis and emphasize the importance of computationally effective time-based predictions, with promising implications for medical decision-making and patient care.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1295-1306"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Influence of LVAD Cannula Outflow Graft Flow Rate and Location on Fluid-Particle Interactions and Thrombi Distribution: A Primary Numerical Study. LVAD 导管外流移植物流速和位置对流体-颗粒相互作用和血栓分布的影响：初步数值研究

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-22 DOI: 10.1007/s12265-024-10547-1

Longyan Li, Li Shi, Xiao Tan, Yixia Zhao

{"title":"Influence of LVAD Cannula Outflow Graft Flow Rate and Location on Fluid-Particle Interactions and Thrombi Distribution: A Primary Numerical Study.","authors":"Longyan Li, Li Shi, Xiao Tan, Yixia Zhao","doi":"10.1007/s12265-024-10547-1","DOIUrl":"10.1007/s12265-024-10547-1","url":null,"abstract":"A left ventricular assist device (LVAD) supports hemodynamics in heart failure patients. To deepen the understanding of hemodynamic changes and the movement of thrombi in the aorta, we examined three distinct LVAD blood flow rates across two implantation sites using the theory of computational fluid dynamics. Our findings revealed the complex dynamics of blood flow during cardiac systole under various scenarios. We also analyzed thrombi residence time and flow probabilities into aortic branches. Simulation results indicate that thrombi distribution in the aorta is significantly influenced by the location of the LVAD outflow graft and the flow rate. When the LVAD outflow graft is implanted into the ascending aorta, higher flow rates may reduce the risk of cerebral thrombosis. However, lower flow rates may reduce the risk of cerebral thrombosis while it is implanted into the descending aorta. The study may offer valuable insights into the LVAD implantation about the risk of cerebrovascular embolism.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1316-1327"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11634971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction. 短期 S100A8/A9 阻断可促进心肌梗死后心脏新生血管的形成

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-15 DOI: 10.1007/s12265-024-10542-6

Razvan Gheorghita Mares, Viorel Iulian Suica, Elena Uyy, Raluca Maria Boteanu, Luminita Ivan, Iuliu Gabriel Cocuz, Adrian Horatiu Sabau, Vikas Yadav, Istvan Adorjan Szabo, Ovidiu Simion Cotoi, Mihaela Elena Tomut, Gabriel Jakobsson, Maya Simionescu, Felicia Antohe, Alexandru Schiopu

{"title":"Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.","authors":"Razvan Gheorghita Mares, Viorel Iulian Suica, Elena Uyy, Raluca Maria Boteanu, Luminita Ivan, Iuliu Gabriel Cocuz, Adrian Horatiu Sabau, Vikas Yadav, Istvan Adorjan Szabo, Ovidiu Simion Cotoi, Mihaela Elena Tomut, Gabriel Jakobsson, Maya Simionescu, Felicia Antohe, Alexandru Schiopu","doi":"10.1007/s12265-024-10542-6","DOIUrl":"10.1007/s12265-024-10542-6","url":null,"abstract":"Acute-phase inhibition of the pro-inflammatory alarmin S100A8/A9 improves cardiac function post-myocardial infarction (MI), but the mechanisms underlying the long-term benefits of this short-term treatment remain to be elucidated. Here, we assessed the effects of S100A8/A9 blockade with the small-molecule inhibitor ABR-238901 on myocardial neovascularization in mice with induced MI. The treatment significantly reduced S100A9 and increased neovascularization in the myocardium, assessed by CD31 staining. Proteomic analysis by mass-spectrometry showed strong myocardial upregulation of the pro-angiogenic proteins filamin A (~ 10-fold) and reticulon 4 (~ 5-fold), and downregulation of the anti-angiogenic proteins Ras homolog gene family member A (RhoA, ~ 4.7-fold), neutrophilic granule protein (Ngp, ~ 4.0-fold), and cathelicidin antimicrobial peptide (Camp, ~ 4.4-fold) versus controls. In-vitro, ABR-238901 protected against apoptosis induced by recombinant human S100A8/A9 in human umbilical vein endothelial cells (HUVECs). In conclusion, S100A8/A9 blockade promotes post-MI myocardial neovascularization by favorably modulating pro-angiogenic proteins in the myocardium and by inhibiting endothelial cell apoptosis.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1389-1399"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11634919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Silencing DOCK2 Attenuates Cardiac Fibrosis Following Myocardial Infarction in Mice Via Targeting PI3K/Akt and Wnt/β-Catenin Pathways. 通过靶向 PI3K/Akt 和 Wnt/β-Catenin 通路，沉默 DOCK2 可减轻小鼠心肌梗死后的心肌纤维化。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-11 DOI: 10.1007/s12265-024-10533-7

Guangquan Hu, Jin Chen, Min Chen, Kai Yang, Yuchen Wang, Ziyang Ma, Huangxin Bao, Xiaojie Ding

{"title":"Silencing DOCK2 Attenuates Cardiac Fibrosis Following Myocardial Infarction in Mice Via Targeting PI3K/Akt and Wnt/β-Catenin Pathways.","authors":"Guangquan Hu, Jin Chen, Min Chen, Kai Yang, Yuchen Wang, Ziyang Ma, Huangxin Bao, Xiaojie Ding","doi":"10.1007/s12265-024-10533-7","DOIUrl":"10.1007/s12265-024-10533-7","url":null,"abstract":"Cardiac fibrosis following myocardial infarction (MI) seriously affects the prognosis and survival rate of patients. This study aimed to determine the effect and regulation mechanism of the dedicator of cytokinesis 2 (DOCK2) during this process. Experiments were carried out in mice in vivo, and in Ang II treated cardiac fibroblasts (CFs) in vitro. DOCK2 was increased in mouse myocardial tissues after MI and Ang II-treated CFs. In MI mice, DOCK2 silencing improved cardiac function, and ameliorated cardiac fibrosis. DOCK2 knockdown suppressed the activation of CFs and decreased the expression of α-SMA, collagen I, and collagen III. Suppression of DOCK2 mitigated Ang II induced migration of CFs. DOCK2 inhibition reduced the activity of the PI3K/Akt and Wnt/β-catenin pathways, while this change could be reversed by the pathway activators, SC79 and SKL2001. In summary, DOCK2 suppression improves cardiac dysfunction and attenuates cardiac fibrosis after MI via attenuating PI3K/Akt and Wnt/β-catenin pathways.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1442-1454"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of Methylation in Ferroptosis. 甲基化在铁变态反应中的作用

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-29 DOI: 10.1007/s12265-024-10539-1

Yushu Xie, Jie Xie, Liang Li

引用次数: 0

Circulating circ_0069094 is Correlated with the Present and Endothelial Injury of Acute Coronary Syndrome. 循环中的 circ_0069094 与急性冠状动脉综合征的发生和内皮损伤有关。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-09 DOI: 10.1007/s12265-024-10532-8

Zhen Gao, Peng Wu, Hezhong Zhu, Jieqiong Chen, Wei Liu, Jiangtao Huo, Chaoyong He, Yang Duan, Jiajuan Chen

引用次数: 0

Inhibition of Hsp90 K284 Acetylation Aalleviates Cardiac Injury After Ischemia-Reperfusion Injury. 抑制 Hsp90 K284 乙酰化可缓解缺血再灌注损伤后的心脏损伤

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-07-24 DOI: 10.1007/s12265-024-10548-0

Dongyu Zhan, Na Zhang, Li Zhao, Zhirui Sun, Chunyang Cang

引用次数: 0

CRISPR/Cas9 Mediated Deletion of the Uox Gene Generates a Mouse Model of Hyperuricemia with Multiple Complications. CRISPR/Cas9 介导的 Uox 基因缺失产生了一种具有多种并发症的高尿酸血症小鼠模型。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-06-10 DOI: 10.1007/s12265-024-10526-6

Linzi Zeng, Shalaimaiti Shali, Yabiao Gao, Xingchen Du, Xiaoxia Zhu, Lin Li, Yuxiang Dai, Ping Zhou

{"title":"CRISPR/Cas9 Mediated Deletion of the Uox Gene Generates a Mouse Model of Hyperuricemia with Multiple Complications.","authors":"Linzi Zeng, Shalaimaiti Shali, Yabiao Gao, Xingchen Du, Xiaoxia Zhu, Lin Li, Yuxiang Dai, Ping Zhou","doi":"10.1007/s12265-024-10526-6","DOIUrl":"10.1007/s12265-024-10526-6","url":null,"abstract":"Hyperuricemia is a common metabolic disorder with severe complications. We aimed to develop a mouse model for spontaneous hyperuricemia. Uox-/- mouse model was generated on C57BL/6J background by deleting exon 2-4 of Uox using the CRISPR/Cas9 system. The prototypic Uox -/-mice had 5.5-fold increased serum uric acid (1351.04±276.58μmol/L) as compared to the wild type mice (P<0.0001), but died by 4 weeks. After allopurinol (3ug/g) intervention, they all survived > 8 weeks. The serum uric acid was 612.55±146.98μmol/L in the 8-week-old allopurinol-rescued Uox -/-mice, which manifested multiple complications including severe renal insufficiency, hypertension, left ventricular remodeling and systolic dysfunction, aortic endothelial dysfunction, hepatic steatosis and elevated liver enzymes, as well as hyperglycemia and hypercholesteremia. The present Uox-/- mice developed spontaneous hyperuricemia complicated with urate nephropathy, cardiovascular disease and cardiometabolic disorders, and may provide a novel tool to study hyperuricemia associated early-onset cardiovascular disorders in human.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"1455-1465"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141296131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Force Analysis Using Self-Expandable Valve Fluoroscopic Imaging: a way Through Artificial Intelligence. 利用自膨胀瓣膜透视成像进行受力分析：一种通过人工智能的方法。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-12-01 Epub Date: 2024-08-01 DOI: 10.1007/s12265-024-10550-6

Yiming Qi, Xiaochun Zhang, Zhiyun Shen, Yixiu Liang, Shasha Chen, Wenzhi Pan, Daxin Zhou, Junbo Ge

引用次数: 0