Translational Research最新文献

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Author Guidelines 作者指导方针
IF 6.4 2区 医学
Translational Research Pub Date : 2025-06-26 DOI: 10.1016/S1931-5244(25)00071-4
{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(25)00071-4","DOIUrl":"10.1016/S1931-5244(25)00071-4","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Information for Readers 读者资讯
IF 6.4 2区 医学
Translational Research Pub Date : 2025-06-26 DOI: 10.1016/S1931-5244(25)00072-6
{"title":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(25)00072-6","DOIUrl":"10.1016/S1931-5244(25)00072-6","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Page IBC"},"PeriodicalIF":6.4,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Editorial Advisory Board 编辑顾问委员会
IF 6.4 2区 医学
Translational Research Pub Date : 2025-06-26 DOI: 10.1016/S1931-5244(25)00070-2
{"title":"Editorial Advisory Board","authors":"","doi":"10.1016/S1931-5244(25)00070-2","DOIUrl":"10.1016/S1931-5244(25)00070-2","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Page ii"},"PeriodicalIF":6.4,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Epigenetically targeting PRMT5 promotes antitumor immunity by inducing endogenous retroviruses expression and triggering viral mimicry response 表观遗传靶向PRMT5通过诱导内源性逆转录病毒表达和触发病毒模仿反应来促进抗肿瘤免疫。
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-29 DOI: 10.1016/j.trsl.2025.05.007
Hua Zhang , Gang Shi , Yamei Li , Chao Wang , Yong Zhang , Yan Luo , Jia Xu , Yusha Qiu , Jinhu Ma , Jin Yang , Dandan Liao , Yihua Chen , Hongxin Deng
{"title":"Epigenetically targeting PRMT5 promotes antitumor immunity by inducing endogenous retroviruses expression and triggering viral mimicry response","authors":"Hua Zhang ,&nbsp;Gang Shi ,&nbsp;Yamei Li ,&nbsp;Chao Wang ,&nbsp;Yong Zhang ,&nbsp;Yan Luo ,&nbsp;Jia Xu ,&nbsp;Yusha Qiu ,&nbsp;Jinhu Ma ,&nbsp;Jin Yang ,&nbsp;Dandan Liao ,&nbsp;Yihua Chen ,&nbsp;Hongxin Deng","doi":"10.1016/j.trsl.2025.05.007","DOIUrl":"10.1016/j.trsl.2025.05.007","url":null,"abstract":"<div><div>Colorectal cancer (CRC) is one of the most common cancers worldwide. Although immune checkpoint blockade (ICB) has transformed CRC treatment, the low response rate and immune resistance remain significant challenges. In recent years, epigenetic therapies have been shown to induce viral mimicry response to overcome immune resistance and increase the effectiveness of ICB. However, as an epigenetic modifier, the intrinsic function of PRMT5 in controlling innate immune signaling, viral mimicry, and the tumor microenvironment in CRC remains to be elucidated. Here, we report that PRMT5 inhibition attenuates CRC growth and epigenetically targeting PRMT5 remolds the tumor immune microenvironment, thereby enhancing the therapeutic efficacy of ICB. Mechanistically, PRMT5 knockdown increases endogenous retroviruses (ERVs) expression and dsRNA formation and causes DNA repair incompetence and genomic instability. These changes, combined with the elevated expression of RIG-I/MDA5/STING, trigger innate immune activation and viral mimicry response, thereby facilitating immune cell infiltration and enhancing ICB effectiveness. Furthermore, PRMT5 knockdown reduces H3R2me2s and H3R8me2s levels, and epigenetically promotes innate immune responses. Our study reveals the tumor intrinsic role of PRMT5 in controlling ERVs and innate sensors expression, providing perspectives for the epigenetically targeting of PRMT5 to induce viral mimicry response and enhance antitumor immunity in CRC.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages 55-68"},"PeriodicalIF":6.4,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
A novel rabbit model of severe ARDS: Synergistic effects of acid aspiration and harmful mechanical ventilation 一种新的严重急性呼吸窘迫综合征兔模型:吸酸和有害机械通气的协同作用。
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-29 DOI: 10.1016/j.trsl.2025.05.009
Petra Košútová , Nikollet Nemcová , Maroš Kolomazník , Andrea Čalkovská , Pavol Mikolka
{"title":"A novel rabbit model of severe ARDS: Synergistic effects of acid aspiration and harmful mechanical ventilation","authors":"Petra Košútová ,&nbsp;Nikollet Nemcová ,&nbsp;Maroš Kolomazník ,&nbsp;Andrea Čalkovská ,&nbsp;Pavol Mikolka","doi":"10.1016/j.trsl.2025.05.009","DOIUrl":"10.1016/j.trsl.2025.05.009","url":null,"abstract":"<div><h3>Background</h3><div>Acute respiratory distress syndrome (ARDS) is characterised by severe inflammation and pulmonary edema, often leading to respiratory failure. This study aims to develop a stable and relevant rabbit model of severe ARDS using hydrochloric acid (HCl) aspiration and ventilator-induced lung injury (VILI).</div></div><div><h3>Methods</h3><div>Adult New Zealand rabbits were divided into four groups: Saline (<em>n</em> = 9), 1-hit 3.0 (HCl 3 ml/kg, <em>n</em> = 7), 1-hit 6.0 (HCl 6 ml/kg, <em>n</em> = 7), and 2-hit (HCl 3 ml/kg and ventilation with V<sub>T</sub> 20 ml/kg, zero PEEP, RR 20-30 bpm, and FiO<sub>2</sub> 1.0 to mimic VILI, <em>n</em> = 14). PaO<sub>2</sub>/FiO<sub>2</sub> ratio, oxygenation index, oxygen saturation, PaCO<sub>2</sub>, ventilation efficiency index and alveolar-arterial gradient were evaluated every hour for 4 h after induction of lung injury. The <em>post-mortem</em> analysis included total and differential cell counts in bronchoalveolar lavage fluid (BALF), evaluation of lung edema formation, biochemical and histological examination of lung tissue<em>.</em></div></div><div><h3>Results</h3><div>In the 2-hit group, we observed a significant deterioration of all lung function parameters (P/F ratio, oxygenation index, ventilation efficiency index, and alveolar-arterial gradient) compared to the saline group. Similarly, a deterioration was observed in the 1-hit 6.0 group. When analysing the inflammatory profile, we observed significantly increased levels of chemokines and cytokines (TNFα, IL-1β, IL-6, IL-8, ET-1, MCP, H1F, MIP) and oxidative stress parameters (3NT, MDA, AOPP, catalase and GSH/GSSG) in BALF in the 2-hit group compared to the saline group. Intratracheal administration of HCl alone did not have a significant impact on inflammation as the combination of two insults. An increased wet-to-dry lung weight ratio (W/D), indicative of pulmonary edema, was observed in both the 2-hit and 1-hit 6.0 groups compared to the saline group. An increased level of protein content in BALF and total lung injury score were observed in the 2-hit group compared to the saline group, 1-hit 3.0 and 1-hit 6.0.</div></div><div><h3>Conclusion</h3><div>The combination of hydrochloric acid aspiration and ventilator-induced lung injury reliably reproduces key features of severe ARDS, offering a robust and clinically relevant model for investigating its complex pathophysiology and evaluating novel therapeutic interventions.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages 43-54"},"PeriodicalIF":6.4,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Information for Readers 读者资讯
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-28 DOI: 10.1016/S1931-5244(25)00060-X
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引用次数: 0
Author Guidelines 作者指导方针
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-28 DOI: 10.1016/S1931-5244(25)00059-3
{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(25)00059-3","DOIUrl":"10.1016/S1931-5244(25)00059-3","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Editorial Advisory Board 编辑顾问委员会
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-28 DOI: 10.1016/S1931-5244(25)00058-1
{"title":"Editorial Advisory Board","authors":"","doi":"10.1016/S1931-5244(25)00058-1","DOIUrl":"10.1016/S1931-5244(25)00058-1","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Page ii"},"PeriodicalIF":6.4,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Predictive modeling of ARDS mortality integrating biomarker/cytokine, clinical and metabolomic data 整合生物标志物/细胞因子、临床和代谢组学数据的ARDS死亡率预测模型。
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-24 DOI: 10.1016/j.trsl.2025.05.005
Ruslan Rafikov , Debrah M. Thompson , Olga Rafikova , Sara M. Camp , Roberto A. Ribas , Ramon C. Sun , Matthew S. Gentry , Nancy G. Casanova , Joe G N Garcia
{"title":"Predictive modeling of ARDS mortality integrating biomarker/cytokine, clinical and metabolomic data","authors":"Ruslan Rafikov ,&nbsp;Debrah M. Thompson ,&nbsp;Olga Rafikova ,&nbsp;Sara M. Camp ,&nbsp;Roberto A. Ribas ,&nbsp;Ramon C. Sun ,&nbsp;Matthew S. Gentry ,&nbsp;Nancy G. Casanova ,&nbsp;Joe G N Garcia","doi":"10.1016/j.trsl.2025.05.005","DOIUrl":"10.1016/j.trsl.2025.05.005","url":null,"abstract":"<div><div>Acute Respiratory Distress Syndrome (ARDS), characterized by the rapid onset of respiratory failure and mortality rates of ∼40%, remains a significant challenge in critical care medicine. Despite advances in supportive care, accurate prediction of ARDS mortality remains challenging, resulting in delayed delivery of targeted interventions and effective disease management. Traditional critical illness severity scores lack specificity for ARDS, underscoring the need for more precise prognostic tools for ARDS mortality. To address this crucial gap, we employed a multimodal approach to predict ARDS patients utilizing a comprehensive dataset comprised of integrated clinical, metabolomic, and biochemical/cytokine data from ARDS patients (collected within hours of ICU admission) to develop and validate predictive models of ARDS mortality risk. The most robust multimodal data model generated demonstrated superior predictive capability with an area under the curve (AUC) of 0.868 on the test set and 0.959 on the validation set. Notably, this model achieved perfect specificity in identifying non-survivors in the validation cohort, highlighting potential utility in guiding early and targeted interventions in ICU settings. Metabolomic analysis revealed significant alterations in crucial pathways associated with ARDS mortality with tryptophan metabolism, particularly the kynurenine pathway, emerging as the most significantly enriched metabolic route, as well as the NAD+ metabolism/nicotinamide phosphoribosyltransferase (NAMPT) and glycosaminoglycan biosynthesis pathways. These metabolic derangements were strongly confirmed by lipidomic/metabolomic analysis of lung tissues from a porcine sepsis/ARDS model. Together, these findings demonstrate the promise of integrating multimodal data to improve ARDS prognostication and to provide important insights into the complex metabolic derangements underlying severe ARDS. Identification of metabolic signatures, such as kynurenine and NAD+ metabolism/NAMPT pathways, may serve as a foundation for developing personalized and effective targeted interventions and management strategies for ARDS patients.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages 31-42"},"PeriodicalIF":6.4,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
sFRP5 ameliorates atherosclerosis by suppressing the JNK/TLR9 pathway in macrophages sFRP5通过抑制巨噬细胞的JNK/TLR9通路改善动脉粥样硬化。
IF 6.4 2区 医学
Translational Research Pub Date : 2025-05-22 DOI: 10.1016/j.trsl.2025.05.004
Yue Yu , Han Chen , Rui Wang , Fei Xu, Jiasheng Yin, Tongtong Zang, Changyi Zhou, Chengpeng Liu, Chaofu Li, Li Shen, Junbo Ge
{"title":"sFRP5 ameliorates atherosclerosis by suppressing the JNK/TLR9 pathway in macrophages","authors":"Yue Yu ,&nbsp;Han Chen ,&nbsp;Rui Wang ,&nbsp;Fei Xu,&nbsp;Jiasheng Yin,&nbsp;Tongtong Zang,&nbsp;Changyi Zhou,&nbsp;Chengpeng Liu,&nbsp;Chaofu Li,&nbsp;Li Shen,&nbsp;Junbo Ge","doi":"10.1016/j.trsl.2025.05.004","DOIUrl":"10.1016/j.trsl.2025.05.004","url":null,"abstract":"<div><div>Secreted frizzled related protein 5 (sFRP5), an anti-inflammatory adipokine, plays a crucial role in various diseases, and its serum levels are low in patients with coronary artery disease (CAD). However, its role in atherosclerosis remains unclear. Therefore, we investigated the correlation between sFRP5 and plaque stability, along with the molecular mechanisms underlying atherosclerosis. In patients with CAD, serum sFRP5 levels were positively correlated with plaque stability, a predictor of thin-cap fibroatheromas (TCFAs). Recombinant sFRP5 (r-sFRP5) supplementation significantly increased plaque stability and ameliorated atherosclerosis progression in <em>ApoE<sup>-/-</sup></em> mice. Aortic RNA-sequencing (RNA-seq) revealed sFRP5-mediated regulation in inflammatory cells. Our experiments confirmed that sFRP5 inhibits inflammation and macrophage migration. Mechanistically, Toll-like receptor 9 (TLR9) was identified as a downstream target of sFRP5, and sFRP5 suppressed TLR9 expression by decreasing c-Jun N-terminal kinase (JNK) phosphorylation. These findings suggest that serum sFRP5 levels are associated with plaque stability and play a protective role in atherosclerosis by attenuating inflammation and macrophage infiltration via inhibition of the JNK/TLR9 pathway, thereby ameliorating the progression of atherosclerosis. This study highlights the potential of sFRP5 as both a biomarker and therapeutic target for plaque stability in atherosclerosis.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages 1-13"},"PeriodicalIF":6.4,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144133401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
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