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

{"title":"Postnatal development of human atrial cardiomyocytes: linking atrial gene expression profiles and atrial electrophysiology.","authors":"Elise Rougier, Akshata Dhumal, Robert A Rose","doi":"10.1152/ajpheart.00754.2024","DOIUrl":"10.1152/ajpheart.00754.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1519-H1521"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602851","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":"A zebrafish model to study <i>RRAGD</i> variants associated cardiomyopathy.","authors":"Irene Sambri, Francesco Trepiccione","doi":"10.1152/ajpheart.00695.2024","DOIUrl":"10.1152/ajpheart.00695.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1343-H1344"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493022","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":"The multifaceted roles of red blood cells in health and disease.","authors":"Helmut Raphael Lieder","doi":"10.1152/ajpheart.00739.2024","DOIUrl":"10.1152/ajpheart.00739.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1474-H1476"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602857","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":"Creating diversity, equity, inclusion, and accessibility statements for your CV: a resource guide to effectiveness and comprehensiveness.","authors":"Jesse D Moreira-Bouchard, Jason Cunha, Brian S Tao, Hahnbie Kim, Joshua Lepson, Evan J Nessen, Zachary J Milstone, Nathaniel Fisher, Nancy Clinton, Lisa M Roberts, Maria A Serrano, Deepa M Gopal, Emelia J Benjamin, Kaku So-Armah, Jessica L Fetterman","doi":"10.1152/ajpheart.00610.2024","DOIUrl":"10.1152/ajpheart.00610.2024","url":null,"abstract":"<p><p>Diversity in academic medicine and research enhances the quality of the science produced and the efficacy of patient care. Diversity, equity, inclusion, and accessibility (DEIA) statements have recently been suggested or required by academic job postings as a way to measure candidate's commitments to fostering DEIA in their role. In this perspective, we discuss steps to craft effective DEIA statements that convey your actions in, and commitment to, DEIA. We recognize that mandating DEIA statements may actually result in inauthentic or disingenuous statements and offer solutions to encouraging academics to arrive at a meaningful statement that represents their own perspectives on diversity. Last, we provide examples of DEIA statements from three academics at different career points.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1376-H1383"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556957","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":"Differential postnatal cardiovascular course of donor-recipient twins and associated pathophysiology-a cohort study.","authors":"Eugene Ting, Mark Teoh, Arvind Sehgal","doi":"10.1152/ajpheart.00656.2024","DOIUrl":"10.1152/ajpheart.00656.2024","url":null,"abstract":"<p><p>Fetal echocardiography in twin-to-twin transfusion pregnancies treated with photocoagulation noted impaired cardiac function. Systematic information about cardiac structure or function and arterial distensibility after birth is not available. This study evaluated cardiovascular function and arterial dynamic properties in survivors of twin-to-twin transfusion syndrome (TTTS). Eleven pairs of donor-recipient twins were compared with each other and with 20 singletons of comparable gestational age. The twin cohort was born at 31.5 ± 2 wk gestational age; birthweights of donors-recipients were comparable (donors: 1,358 ± 421 g vs. recipients: 1,617 ± 460 g, <i>P</i> = 0.2). Significant intertwin differences were noted for cardiac function parameters. Recipients had greater septal thickness (donors: 2.3 ± 0.15 vs. recipients: 2.7 ± 0.36 mm, <i>P</i> = 0.01) and globularity [lower sphericity index (donors: 1.76 ± 0.1 vs. recipients: 1.62 ± 0.12, <i>P</i> = 0.009)]. They also had lower cardiac function [tricuspid annular plane systolic excursion (donors: 4.6 ± 0.5 vs. recipients: 4.1 ± 0.4 mm, <i>P</i> = 0.02) and right ventricular fractional area change (donors: 30 ± 1 vs. recipients: 27.7 ± 1.3%, <i>P</i> = 0.0001)]. Compared with singletons, differences were statistically more significant for recipients. Arterial distensibility however was more affected in donors [higher arterial wall stiffness index (donors: 2.5 ± 0.2 vs. recipients: 2.2 ± 0.2, <i>P</i> = 0.008) and lower pulsatile diameter (donors: 51 ± 5 vs. recipients: 63 ± 10 µm, <i>P</i> < 0.0001)]. Compared with singletons, the differences were statistically more significant for donors. Evaluation in the neonatal period noted that cardiac function and arterial distensibility are affected in TTTS twins. These cohorts will benefit from close postnatal follow-up for the evolution of cardiac and arterial impairments.<b>NEW & NOTEWORTHY</b> Evaluation for fetuses with twin-to-twin transfusion syndrome noted impaired cardiac function in recipients. Systematic data after birth are lacking. We noted greater ventricular dilatation, globularity, and hypertrophied interventricular septum in the recipient. Right ventricular contractility was reduced; differences between recipients-singletons had greater statistical significance compared with donors-singletons. The aorta had greater stiffness and lower distensibility in donors compared with recipients; the differences for arterial indices were statistically more significant with donors-singletons.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1400-H1405"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493029","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":"Load-dependent mechanisms contribute to increased aortic stiffness among women with a history of preeclampsia: relation with cardiovagal baroreflex sensitivity.","authors":"Kristen G Davis, Matthew K Armstrong, Virginia R Nuckols, Meaghan N Smith, Ryan Pewowaruk, Colin J Gimblet, Donna A Santillan, Mark K Santillan, Gary L Pierce","doi":"10.1152/ajpheart.00556.2024","DOIUrl":"10.1152/ajpheart.00556.2024","url":null,"abstract":"<p><p>Preeclampsia, a hypertensive disorder of pregnancy, results in increased lifetime cardiovascular disease (CVD) risk. Total aortic stiffness, a robust risk factor for CVD, is composed of load-dependent (blood pressure load on arterial wall) and structural (intrinsic changes in arterial wall) mechanisms. Total aortic stiffness is also associated with reduced cardiovagal baroreflex sensitivity (BRS). We sought to determine <i>1</i>) whether elevated total aortic stiffness among women with a history of preeclampsia (hxPE) is attributed to load-dependent or structural stiffness, and <i>2</i>) whether either mechanism is associated with lower BRS. Total aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal BRS (sequence technique) were measured among women 1-5 yr postpartum (<i>n</i> = 115; age 34 ± 4 yr; hxPE <i>n</i> = 51; controls <i>n</i> = 64). Structural aortic stiffness was calculated from participant-specific exponential models by standardizing aortic stiffness to a \"reference\" blood pressure. Load-dependent stiffness was calculated as total minus structural stiffness. Total [+0.8 m/s, 95% confidence interval (CI) (-0.99, -0.23), <i>P</i> = 0.002] and load-dependent [+0.4 m/s, 95% CI (-0.56, -0.22), <i>P</i> < 0.001], but not structural [95% CI (-0.52, 0.08), <i>P</i> = 0.16] aortic stiffness were higher among women with a hxPE compared with controls. Women with a hxPE had lower BRS (<i>P</i> = 0.042) that was negatively associated with total [<i>B</i> = -3.24 ms/mmHg, 95% CI (-6.35, -0.13), <i>P</i> = 0.042] and load-dependent [<i>B</i> = -5.91 ms/mmHg, 95% CI (-11.31, -0.51), <i>P</i> = 0.033] aortic stiffness. Load-dependent, not structural, aortic stiffness mechanisms contribute to higher total aortic stiffness among women with a hxPE and are associated with lower cardiovagal BRS. Postpartum monitoring for high BP is critical to reduce increased CVD risk after preeclampsia.<b>NEW & NOTEWORTHY</b> The novel finding is that load-dependent stiffness, not structural stiffness, is the primary mechanism of aortic stiffness, and is associated with reduced baroreflex sensitivity in women with a history of preeclampsia. These findings may help tailor high blood pressure prevention and management strategies in this population to prevent structural aortic stiffening, altered baroreflex control, and increased lifetime cardiovascular disease (CVD) risk.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1406-H1412"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456045","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":"Early pathological mechanisms in a mouse model of heart failure with preserved ejection fraction.","authors":"Paola C Rosas, Liomar A A Neves, Nisha Patel, Duyen Tran, Carlos H Pereira, Karina R Bonilla, Jingjing Zheng, Jun Sun, Francisco J Alvarado, Kathrin Banach","doi":"10.1152/ajpheart.00318.2024","DOIUrl":"10.1152/ajpheart.00318.2024","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) constitutes more than half of all HF cases, yet evidence-based therapies remain lacking due to limited understanding of its underlying pathological mechanisms. Our study aimed to uncover early pathological mechanisms in HFpEF by exposing mice to dietary conditions resembling a Western diet-rich in fats, salt, and low in fiber-alongside excess mineralocorticoids to replicate significant aspects of human HFpEF. Echocardiography was performed at both 3-wk and 6-wk intervals postchallenge, revealing cardiac alterations as early as 3 wk. While ejection fraction remained preserved, mice exhibited signs of diastolic dysfunction, reduced stroke volume, and left atrial enlargement. In addition, changes in pulmonary flow velocities were noted by the 3-wk mark, suggesting elevated pulmonary pressure. Extracardiac comorbidities included organ congestion, increased adiposity, impaired glucose tolerance, and hypercholesterolemia. Molecular analyses unveiled evidence of low-grade inflammation, oxidative stress, and impaired NO-cGMP-PKG signaling, contributing to the observed decrease in titin phosphorylation, thereby impacting myocardial stiffness. In addition, impaired nitric oxide (NO) signaling might have influenced the alterations observed in coronary flow reserve. Moreover, dysregulation of calcium signaling in cardiomyocytes and reduced sarcoplasmic reticulum (SR) load were observed. Interestingly, elevated phosphorylation of cMyBP-C was linked to preserved ejection fraction despite reduced SR load. We also observed intestinal atrophy, possibly due to a high-fat diet, low dietary fiber intake, and diminished gut perfusion, potentially contributing to systemic low-grade inflammation. These findings reveal how excess mineralocorticoid salt-induced hypertension and dietary factors, like high-fat and low-fiber intake, contribute to cardiac dysfunction and metabolic disturbances, offering insights into early HFpEF pathology in this model.<b>NEW & NOTEWORTHY</b> Our study demonstrates that feeding mice a Western diet rich in fat and salt and low in fiber alongside excess mineralocorticoids replicates aspects of human HFpEF. Cardiac alterations including diastolic dysfunction and decreased stroke volume with preserved ejection fraction were observed. Extracardiac effects included organ congestion, adiposity, glucose intolerance, and intestinal atrophy. Molecular analysis revealed inflammation, oxidative stress, impaired NO-cGMP-PKG signaling pathways, and altered calcium signaling in cardiomyocytes, shedding light on early pathological changes in HFpEF.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1524-H1543"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556958","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":"Red blood cells from patients with ST-elevation myocardial infarction and elevated C-reactive protein levels induce endothelial dysfunction.","authors":"John Tengbom, Rawan Humoud, Eftychia Kontidou, Tong Jiao, Jiangning Yang, Ulf Hedin, Zhichao Zhou, Juliane Jurga, Aida Collado, Ali Mahdi, John Pernow","doi":"10.1152/ajpheart.00443.2024","DOIUrl":"10.1152/ajpheart.00443.2024","url":null,"abstract":"<p><p>Endothelial dysfunction is an early consequence of vascular inflammation and a driver of coronary atherosclerotic disease leading to myocardial infarction. The red blood cells (RBCs) mediate endothelial dysfunction in patients at cardiovascular risk, but their role in patients with acute myocardial infarction is unknown. This study aimed to investigate if RBCs from patients with ST-elevation myocardial infarction (STEMI) induced endothelial dysfunction and the role of systemic inflammation in this effect. RBCs from patients with STEMI and aged-matched healthy controls were coincubated with rat aortic segments for 18 h followed by evaluation of endothelium-dependent (EDR) and endothelium-independent relaxation (EIDR). RBCs and aortic segments were also analyzed for arginase and oxidative stress. The patients were divided into groups depending on C-reactive protein (CRP) levels at admission. RBCs from patients with STEMI and CRP levels ≥2 mg/L induced impairment of EDR, but not EIDR, compared with RBCs from STEMI and CRP <2 mg/L and healthy controls. Aortic expression of arginase 1 was increased following incubation with RBCs from patients with STEMI and CRP ≥2, and arginase inhibition prevented the RBC-induced endothelial dysfunction. RBCs from patients with STEMI and CRP ≥2 had increased reactive oxygen species compared with RBCs from patients with CRP <2 and healthy controls. Vascular inhibition of NADPH oxidases and increased dismutation of superoxide improved EDR. RBCs from patients with STEMI and low-grade inflammation induce endothelial dysfunction through a mechanism involving arginase 1 as well as increased RBC and vascular superoxide by NADPH oxidases.<b>NEW & NOTEWORTHY</b> Red blood cells from patients with STEMI and systemic inflammation induce endothelial dysfunction ex vivo. The RBC-induced endothelial dysfunction is mediated through increased arginase 1 and a shift in the redox balance toward oxidative stress. Inhibition of arginase or free radicals attenuates the impairment of endothelial function. The study suggests that red blood cells deserve attention as a key player in systemic inflammation and STEMI.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1431-H1441"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399137","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":"Multidirectional blood flow in the femoral artery via vector flow imaging: Doppler ultrasound imaging insights.","authors":"Jeremy N Cohen, Jessica N Jasiak, Hassan Nahas, Alfred C H Yu, Jason S Au","doi":"10.1152/ajpheart.00690.2024","DOIUrl":"10.1152/ajpheart.00690.2024","url":null,"abstract":"<p><p>The accuracy of femoral artery blood flow measurements via Doppler ultrasound hinges on assumptions of laminar flow upstream of the femoral bifurcation. Existing scanning guidelines recommend a minimum proximity to the flow divider of 2-3 cm for avoiding multidirectional blood flow yet lack experimental evidence to support this recommendation. This study aimed to determine the minimum distance required to avoid multidirectional flow contamination near the femoral bifurcation and to assess the reliability of vector flow imaging (VFI) in these measurements. Twenty healthy adults (10 females, 25 ± 4 yr) participated in this study. Ultrasound VFI was used to visualize blood flow patterns and quantify flow uniformity via vector concentration coefficient (VCC), and multidirectional flow length was quantified at rest in triplicate (<i>n</i> = 20), postisometric contraction (<i>n</i> = 20), and during thigh cuffing (<i>n</i> = 10). At rest, the mean multidirectional flow length was 3.12 ± 0.59 cm, which decreased to 2.80 ± 0.66 cm postcontraction (<i>P</i> = 0.02). Thigh cuffing (80 mmHg) resulted in a multidirectional flow length of 2.75 ± 0.64 cm, not significantly different from rest (<i>P</i> = 0.69). Males exhibited a shorter multidirectional flow length compared with females (mean difference: 0.31 ± 0.71 cm, <i>P</i> = 0.05). The VCC increased from 0.39 ± 0.08 at rest to 0.57 ± 0.15 postcontraction (<i>P</i> < 0.01), indicating increased flow uniformity. Reliability metrics demonstrated good-to-excellent reproducibility at rest, with intraclass correlation coefficient [ICC(3,1)] = 0.85 and 0.84 and coefficient of variation (CV)% = 7.1 ± 6.2% and 7.5 ± 4.5% for multidirectional flow length and VCC, respectively. Our data suggest a minimum scanning proximity of 3.5 cm to the femoral bifurcation to ensure that blood flow assessments are free of multidirectional flow and invite further study in different body positions and arteries of interest to increase rigor in this area.<b>NEW & NOTEWORTHY</b> Current ultrasound scanning guidelines to avoid multidirectional flow contamination in the femoral artery of 2-3 cm lack supporting evidence. We used vector flow imaging to report the multidirectional flow length during rest and manipulation of downstream vessel resistance in males and females. We suggest measurements at least 3.5 cm upstream from the femoral bifurcation to minimize multidirectional flows. This study also supports reliability of vector flow imaging for femoral artery assessments, with good-to-excellent reproducibility of results.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1467-H1473"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556961","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":"Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.","authors":"Gaurav Sharma, Shyam S Chaurasia, Mark A Carlson, Paras K Mishra","doi":"10.1152/ajpheart.00539.2024","DOIUrl":"10.1152/ajpheart.00539.2024","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is characterized by chronic hyperglycemia, and despite intensive glycemic control, the risk of heart failure in patients with diabetes remains high. Diabetes-induced heart failure (DHF) presents a unique metabolic challenge, driven by significant alterations in cardiac substrate metabolism, including increased reliance on fatty acid oxidation, reduced glucose utilization, and impaired mitochondrial function. These metabolic alterations lead to oxidative stress, lipotoxicity, and energy deficits, contributing to the progression of heart failure. Emerging research has identified novel mechanisms involved in the metabolic remodeling of diabetic hearts, such as autophagy dysregulation, epigenetic modifications, polyamine regulation, and branched-chain amino acid (BCAA) metabolism. These processes exacerbate mitochondrial dysfunction and metabolic inflexibility, further impairing cardiac function. Therapeutic interventions targeting these pathways-such as enhancing glucose oxidation, modulating fatty acid metabolism, and optimizing ketone body utilization-show promise in restoring metabolic homeostasis and improving cardiac outcomes. This review explores the key molecular mechanisms driving metabolic remodeling in diabetic hearts, highlights advanced methodologies, and presents the latest therapeutic strategies for mitigating the progression of DHF. Understanding these emerging pathways offers new opportunities to develop targeted therapies that address the root metabolic causes of heart failure in diabetes.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1327-H1342"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493034","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}