American journal of physiology. Heart and circulatory physiology最新文献

{"title":"Sex-specific effects of mild kidney dysfunction on vascular function in midlife and older adults.","authors":"Sanna Darvish, McKinley E Coppock, Kevin O Murray, Daniel H Craighead, Michel Chonchol, Kristen L Nowak, Douglas R Seals, Matthew J Rossman","doi":"10.1152/ajpheart.00332.2025","DOIUrl":"10.1152/ajpheart.00332.2025","url":null,"abstract":"<p><p>Mild kidney dysfunction (MKD) increases cardiovascular disease (CVD) risk. Vascular dysfunction, including vascular endothelial dysfunction and aortic stiffening, is a key antecedent to CVD, but the impact of MKD on vascular function in midlife/older (ML/O) adults is not established. Moreover, sex is a biological variable that influences vascular function, but whether sex modulates the effects of MKD on vascular function is unclear. Vascular endothelial function (brachial artery flow-mediated dilation, FMD_BA) and aortic stiffness (carotid-femoral pulse wave velocity, PWV_CF) were compared in 93 ML/O men and postmenopausal women with MKD [estimated glomerular filtration rate (eGFR): 60-89 mL/min/1.73 m²] versus 78 ML/O adults without MKD (healthy controls; eGFR: ≥90 mL/min/1.73 m²) (age: 50+ yr). Circulating markers of inflammation and oxidative stress were also assessed. FMD_BA was lower in men with MKD (4.0 ± 0.3%) versus healthy controls (5.5 ± 0.5%; <i>P</i> = 0.0097) and correlated with eGFR (<i>r</i>_s = 0.30, <i>P</i> = 0.0073). There was no difference in FMD_BA between women with MKD (4.7 ± 0.4%) and healthy controls (4.8 ± 0.5%; <i>P</i> = 0.86) and no relation with eGFR. PWV_CF was higher in men with MKD (9.4 ± 0.2 m/s) versus controls (8.4 ± 0.3 m/s; <i>P</i> = 0.030) and correlated with eGFR (<i>r</i> = -0.34, <i>P</i> = 0.0013). However, PWV_CF was not different between women with MKD (9.3 ± 0.5 m/s) and controls (10.1 ± 0.4 m/s; <i>P</i> = 0.099) and not related to eGFR. The observed effects of MKD on vascular function were independent of traditional CVD risk factors and medication use. There were no differences in markers of inflammation nor oxidative stress between controls and MKD. Our findings suggest that vascular dysfunction may contribute to increased CVD risk associated with MKD in ML/O men but not in postmenopausal women.<b>NEW & NOTEWORTHY</b> Midlife/older (ML/O) adults with mild kidney dysfunction (MKD) are at an increased CVD risk compared with ML/O adults with normal kidney function. We assessed whether ML/O men and postmenopausal women with MKD exhibit vascular dysfunction compared with ML/O adults without MKD. We observed MKD-related vascular dysfunction in men but not in women. Thus, vascular dysfunction may contribute to MKD-associated increases in CVD risk in men but is unlikely to contribute to the increased risk in postmenopausal women.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H401-H408"},"PeriodicalIF":4.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12333382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144582816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiomyocytes Regulate Inflammation in the Failing Heart.","authors":"Harikrishnan Venugopal, Nikolaos G Frangogiannis","doi":"10.1152/ajpheart.00529.2025","DOIUrl":"10.1152/ajpheart.00529.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681878","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}

{"title":"Endothelial TERT drives microvascular phenotype associated with coronary artery disease.","authors":"Erin C Birch, Yoshinori Nishijima, Shelby N Hader, Andreas M Beyer","doi":"10.1152/ajpheart.00342.2025","DOIUrl":"10.1152/ajpheart.00342.2025","url":null,"abstract":"<p><p>Microvascular endothelial dysfunction is a powerful predictor of future atherosclerotic cardiac events. Our previous studies revealed that under pathological states, such as coronary artery disease (CAD), the dilation mechanism switches from nitric oxide (NO)-mediated [determined by NO synthase (NOS) inhibitor] to mitochondria-derived H₂O₂ (determined by H₂O₂ scavenger). Telomerase reverse transcriptase (TERT), the catalytic subunit of telomerase, plays a noncanonical role in preventing the increase of mitochondrial reactive oxygen species in arterioles from subjects with CAD. Activation of TERT can reverse the mechanism of flow-induced, endothelium-dependent dilation from H₂O₂ to NO. Previous studies showed that systemic TERT knockout (KO) mice reduced NO synthase (NOS)-mediated dilation, accompanied by increased release of flow-induced mitochondrial H₂O₂ in microcirculations. In this study, we tested the hypothesis that knocking out the endothelial cell (EC)-specific TERT is sufficient to cause endothelial dysfunction in mice. The third/fourth branch of mesenteric arteries from male EC-specific TERT KO mice (3-5-mo old) were isolated, and endothelial-dependent vasodilator response to flow (FMD) and acetylcholine (ACh) was assessed by videomyography. In control animals, FMD was mediated by NOS, whereas in EC-TERT KO mice, dilation was significantly reduced, and the remaining dilation was mediated by both NOS and H₂O₂, suggesting a switch from NO to H₂O₂-mediated dilation. Similarly, ACh-induced dilation was reduced in EC-TERT KO mice compared with control mice, whereas smooth-muscle-dependent dilation to papaverine was not impaired. In conclusion, knocking down EC-TERT is sufficient to cause endothelial dysfunction and triggers a switch from physiological NO-mediated dilation to pathological H₂O₂-mediated dilation.<b>NEW & NOTEWORTHY</b> Previously established by Ait-Aissa et al. (Ait-Aissa K, Kadlec AO, Hockenberry J, Gutterman DD, Beyer AM. <i>Am J Physiol Heart Circ Physiol</i> 314: H1053-H1060, 2018), systemic TERT KO mice have a loss of NO synthase-mediated dilation to flow, accompanied by compensatory increased release of flow-induced H₂O₂ in coronary and peripheral microcirculations. Our study demonstrates that mice with EC-specific TERT KO exhibit phenotypes similar to systemic TERT deficiency and microvascular pathologies observed in patients with CAD. These findings underscore the critical, noncanonical, and likely mitochondrial-mediated regulation of vascular tone and systemic cardio-metabolic changes.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H267-H270"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The two-pore K⁺ channel TREK-1 regulates pressure overload-induced cardiac remodeling.","authors":"Cemantha M L Johnson, Drew M Nassal, Alexander J Winkle, Benjamin Buck, Xianyao Xu, Xiaoping Wan, Mei Han, Simon Lococo, Nicholas Leahy, Shivangi Mohta, Rebecca Shaheen, Omer Cavus, Aaryan Kohli, Yuanyuan Cao, Mona El Refaey, Sakima Smith, Xun Ai, Isabelle Deschênes, Thomas J Hund","doi":"10.1152/ajpheart.00821.2024","DOIUrl":"10.1152/ajpheart.00821.2024","url":null,"abstract":"<p><p>Heart failure (HF) represents a major burden on the healthcare system, with patients with HF at increased risk for a host of comorbidities, including ventricular arrhythmias. Despite considerable advances in defining cell- and organ-level changes associated with HF, the precise mechanisms driving structural and electrical remodeling remain to be defined. We sought to elucidate the role of the two-pore K⁺ channel TREK-1 in cardiac remodeling in pressure overload-induced HF. Cardiac-specific TREK-1 conditional knockout (TREK1cKO) and floxed control mice were subjected to transaortic contraction (TAC) or sham procedure and evaluated for 6 wk by echocardiography and subsurface electrocardiograms. Ventricular myocytes were isolated for action potential, intracellular Ca²⁺, and contractility measurements. The expression/regulation of key cell signaling pathways was evaluated early in remodeling. TREK1cKO and control mice showed a significant decrease in cardiac systolic function with evidence of hypertrophy as early as 2 wk post-TAC compared with sham. However, TREK1cKO mice displayed a more severe decline in function with enhanced left ventricular chamber dilation (eccentric remodeling) compared with control 6 wk post-TAC. Similarly, TAC TREK1cKO mice demonstrated greater prolongation of the QT and QRS intervals compared with TAC control. TAC TREK1cKO ventricular myocytes exhibited greater action potential prolongation with paradoxical improvements in Ca²⁺ homeostasis and contractility compared with control. Two weeks post-TAC, TREK1cKO hearts exhibited elevation of STAT3 phosphorylation at Y705 compared with control. Our findings reveal a complex interaction between chronic stress, TREK-1, STAT3 regulation, and cardiac remodeling, with TREK-1 exerting both maladaptive and protective effects on overall cardiac function.<b>NEW & NOTEWORTHY</b> A major finding of this study is the involvement of the background K⁺ channel TREK-1 in modulating STAT3 activation, profibrotic gene expression, and fibrosis with implications for the cardiac remodeling response to chronic pressure overload.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H178-H190"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12207601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ET(-1) phone home: a commentary on the complexities of cardiovascular disease risk in postmenopausal women.","authors":"Kyle J Kastrup, Lyndsey E DuBose","doi":"10.1152/ajpheart.00345.2025","DOIUrl":"10.1152/ajpheart.00345.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H89-H90"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12186302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-fat feeding has sex-dependent effects on the structure and biomechanical properties of cerebral parenchymal arterioles and cognitive function.","authors":"Jessica T Yen, Theresa A Landsell, Erinn Laimon-Thomson, Martina Yen, William F Jackson, Anne M Dorrance","doi":"10.1152/ajpheart.00295.2024","DOIUrl":"10.1152/ajpheart.00295.2024","url":null,"abstract":"<p><p>One-third of dementia cases could be prevented by correcting modifiable risk factors, including obesity caused by consuming a high-fat (HF) diet consumption. Dementia is associated with white matter injury, which is associated with impaired cerebral parenchymal arteriole (PA) function. Yet, the impact of HF feeding on PAs remains understudied. We tested the hypothesis that HF feeding would result in structural and biomechanical remodeling of the PAs from male and female rats. We also proposed that HF feeding would impair endothelium-dependent dilation and that these changes would be associated with cognitive decline and neuroinflammation. Three-week-old male and female Sprague-Dawley rats were fed a control or HF diet for 20-24 wk. HF feeding increased body weight and blood pressure in both sexes but caused hyperglycemia only in females. Pial artery blood flow was unchanged by HF feeding in both sexes. The PAs from HF-fed females exhibited inward remodeling; PAs from males were not remodeled but were less distensible. Endothelial function and myogenic tone generation in the PAs were not impacted by HF feeding in either sex. The changes observed in the males were associated with impaired spatial memory and reduced cerebral myelin basic protein expression. HF feeding increased the number of microglia in both sexes, but soma size was only increased in the males. These data suggest that HF feeding impairs cognitive function in males, which is associated with increased stiffness in PAs and increased microglial hypertrophy, whereas HF-fed females remain cognitively normal despite exhibiting significant PA remodeling.<b>NEW & NOTEWORTHY</b> Female rats fed a high-fat diet exhibited inward remodeling of the cerebral parenchymal arterioles; this structural change did not impact cerebral blood flow or cognition. In males, parenchymal arterioles from high-fat fed rats were less distensible; this biomechanical change was associated with cognitive decline and neuroinflammation but not cerebral hypoperfusion. Endothelial function was not impacted by high-fat feeding in either sex. These studies suggest that the pathophysiology of obesity-associated dementia differs between the sexes.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1-H15"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12199659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum for Wang et al., volume 327, 2024, p. H642-H659.","authors":"","doi":"10.1152/ajpheart.00110.2024_COR","DOIUrl":"https://doi.org/10.1152/ajpheart.00110.2024_COR","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"329 1","pages":"H214"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537783","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}

{"title":"A novel assessment of anthracycline-induced cardiotoxicity: topological flow data analysis in childhood cancer survivors.","authors":"Tatsuki Nishiyama, Ken Takahashi, Yusuke Akatsuka, Hirohisa Kago, Azusa Akiya, Yu Hosono, Sachie Shigemitsu, Akinori Yaguchi, Osamu Tomita, Junya Fujimura, Masahiro Saito, Keiichi Itatani, Takashi Sakajo, Hiromichi Shoji","doi":"10.1152/ajpheart.00136.2025","DOIUrl":"10.1152/ajpheart.00136.2025","url":null,"abstract":"<p><p>Anthracycline chemotherapy improves survival rates in childhood cancer patients but poses a significant risk of late-onset cardiotoxicity, potentially leading to cardiac dysfunction and heart failure. Recently, flow dynamics parameters derived from two-dimensional fluid dynamics may be sensitive indicators of cardiac dysfunction. Topological flow data analysis (TFDA) mathematically defines vortical flow structures and offers a novel approach to cardiac function assessment. This study aimed to use TFDA to analyze the left ventricular flow patterns in 90 childhood cancer survivors (CCSs) treated with anthracyclines (median age 15.1 yr) and 90 age-matched control subjects. The TFDA parameters, including vortex number, size, circulation, width of mitral inflow, and saddle points, were calculated and compared across the three age subgroups: <i>C1</i> (4-12 yr), <i>C2</i> (13-19 yr), and <i>C3</i> (20-36 yr). The CCSs in <i>group C3</i> exhibited a reduced left ventricular ejection fraction within the normal range, and the longitudinal strain decreased in <i>groups C2</i> and <i>C3</i>. Regarding TFDA parameters, the number of abnormal vortices in the early diastolic frames increased across all CCSs, with significant reductions in the width of the effective mitral inflow in <i>groups C2</i> and <i>C3</i>. Systolic circulation was reduced across all CCSs, and diastolic circulation was decreased in <i>groups C2</i> and <i>C3</i>, which correlated with age, time since chemotherapy, and cumulative anthracycline dose. TFDA parameters identified cardiac dysfunction before conventional echocardiographic markers, highlighting its potential as a novel and sensitive tool for the early detection and long-term monitoring of cardiotoxicity in CCSs and supporting its integration into clinical practice.<b>NEW & NOTEWORTHY</b> This study suggests that topological flow data analysis (TFDA) is a novel and sensitive method for assessing cardiotoxicity in childhood cancer survivors. By analyzing vortical flow parameters, including circulation and abnormal vortices, TFDA detected anthracycline-induced cardiotoxicity earlier than conventional echocardiographic indicators. The findings reveal age- and dose-dependent cardiac dysfunction, emphasizing TFDA's potential as a highly sensitive tool for long-term cardiovascular monitoring and early intervention in high-risk populations.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H41-H50"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959647","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}

{"title":"Splenic modulation of the early inflammatory response to regional and global ischemia/reperfusion injury in swine.","authors":"Tyler J Rolland, Emily R Hudson, Luke A Graser, Sumbule Zahra, Daniel Cucinotta, Brian R Weil","doi":"10.1152/ajpheart.00714.2024","DOIUrl":"10.1152/ajpheart.00714.2024","url":null,"abstract":"<p><p>The spleen has been identified as a source of proinflammatory leukocytes mobilized after local ischemic injury in rodents. However, the role of the spleen in the inflammatory response to regional or global ischemia/reperfusion injury (IRI) in larger mammals is unknown. We investigated the spleen's contribution to early IRI-associated inflammation in porcine models of acute reperfused myocardial infarction (AMI) and sudden cardiac arrest (SCA). Swine were randomized to splenectomy (SPLX; <i>n</i> = 15) or sham surgery (SHAM; <i>n</i> = 15) 1 wk before a 75 min coronary occlusion (AMI; <i>n</i> = 6/group) or 8 min of ventricular fibrillation and cardiopulmonary resuscitation (CPR) (SCA; <i>n</i> = 9/group). Hemodynamic assessment and echocardiography were performed before and after IRI, with serial blood sampling to assess leukocyte mobilization and cytokine release. Heart and brain samples were collected for postmortem evaluation of injury and leukocyte infiltration. Early post-IRI leukocyte mobilization, cytokine levels, and leukocyte infiltration were similar between groups in each protocol. After SCA, SHAM animals showed a significant 41 ± 15% increase in hematocrit and 30 ± 12% rise in arterial O₂ content during CPR that was absent after SPLX. These differences persisted for up to 90 min and were associated with prolonged time to return of spontaneous circulation (ROSC) and increased vasopressor support in the SPLX group. Contrary to findings in rodents, the spleen is not required for the early inflammatory response to regional or global IRI in swine. However, splenic erythrocyte mobilization during SCA leads to an increase in arterial O₂ content that is associated with earlier ROSC and reduced reliance on vasopressors during CPR and the postresuscitation period.<b>NEW & NOTEWORTHY</b> Acute reperfused myocardial infarction (AMI) and sudden cardiac arrest (SCA) are characterized by ischemia-reperfusion injury (IRI) and inflammation. Although prior studies implicated the spleen as a primary source of inflammatory leukocytes after regional IRI in rodents, our findings indicate that, in swine, the spleen is not required for leukocyte mobilization after AMI or SCA. However, splenic erythrocyte mobilization during whole body IRI increases arterial oxygen content during CPR and may influence outcomes after SCA.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H16-H31"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum for Methawasin et al., volume 328, 2025, p. H719-H733.","authors":"","doi":"10.1152/ajpheart.00575.2024_COR","DOIUrl":"https://doi.org/10.1152/ajpheart.00575.2024_COR","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"329 1","pages":"H213"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526058","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}