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

{"title":"Functional capacity and skeletal muscle morphology are linked to N-terminal proBNP but not left ventricular ejection fraction in patients with heart failure.","authors":"Jakob Wang, Thomas Groennebaek, Roni Nielsen, Kasper Pryds, Frank Vincenzo de Paoli, Hans Erik Bøtker, Kristian Vissing","doi":"10.1152/ajpheart.00275.2025","DOIUrl":"10.1152/ajpheart.00275.2025","url":null,"abstract":"<p><p>Chronic heart failure (CHF) involves skeletal muscle abnormalities, including atrophy, inflammation, mitochondrial dysfunction, and fibrosis, which impair contractile function. This study examines whether muscle deterioration correlates with CHF disease severity by assessing the relationship between circulating N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations, left ventricular ejection fraction (LVEF), and muscle characteristics in patients with CHF. In 36 patients with CHF (LVEF ≤ 45%, New York Heart Association class I-III), we measured circulating NT-proBNP concentrations, LVEF, muscle strength and functional measures, and myocellular features, including fiber type-specific cross-sectional area (CSA), muscle stem cell (MuSC) and myonuclei content, and capillary density. Also, muscle mitochondrial function was evaluated. The concentration of NT-proBNP inversely correlated with muscle strength (<i>R</i>² = 0.25, <i>P</i> < 0.01), mean fiber CSA (<i>R</i>² = 0.15, <i>P</i> = 0.04), and MuSC content (<i>R</i>² = 0.37, <i>P</i> < 0.01). Moreover, a nonsignificant inverse correlation was observed for capillary density (<i>R</i>² = 0.12, <i>P</i> = 0.06). The strength of associations between NT-proBNP, fiber CSA, and capillary density was primarily driven by fiber type-specific correlations. Associations with MuSC content were equally strong across fiber types. No correlation was observed for measures of mitochondrial function. For LVEF, a nonsignificant correlation was observed only for overall MuSC content (<i>R</i>² = 0.11, <i>P</i> = 0.07). Skeletal muscle deterioration in patients with CHF correlates with NT-proBNP, but not LVEF, suggesting that NT-proBNP concentration constitutes a stronger indicator of the link between CHF severity and skeletal muscle decline than LVEF as function parameter. Our findings highlight circulating NT-proBNP concentrations as a potential biomarker for the identification of patients at risk of experiencing skeletal muscle deterioration.<b>NEW & NOTEWORTHY</b> In this study, the authors reveal that elevated NT-proBNP levels are inversely associated with muscle function and cellular features in patients with chronic heart failure (CHF), including muscle fiber cross-sectional area, muscle stem cell content, and capillarization. NT-proBNP appears to be a more reliable marker than left ventricular ejection fraction (LVEF) for identifying skeletal muscle abnormalities and predicting muscle loss in CHF, offering potential for early intervention and personalized care.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1344-H1350"},"PeriodicalIF":4.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960049","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":"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":"https://doi.org/10.1152/ajpheart.00345.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetitive Remote Ischemic Preconditioning as a Potential Alternative Intervention to Attenuate Arterial Stiffness in Individuals with Elevated Blood Pressure.","authors":"Money Ghimire, Brittany K Sanchez, Jahyun Kim","doi":"10.1152/ajpheart.00299.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00299.2025","url":null,"abstract":"<p><p>Elevated blood pressure (BP) is associated with increased arterial stiffness and risk of cardiovascular diseases (CVDs). Remote ischemic preconditioning (RIPC) involves 3 or 4 cycles of limb blood flow blockage followed by reperfusion with occlusion pressure between 200-220 mmHg and has been shown to improve vascular function. However, studies in normotensive adults showed no change in arterial stiffness, possibly due to shorter intervention periods (<1 week). Therefore, the purpose of this study was to investigate the effects of 4 weeks of RIPC on arterial stiffness in adults with elevated BP or stage 1 hypertension (EBP), and whether superoxide dismutase (SOD) levels account for this effect. We hypothesized that 4 weeks of RIPC attenuates arterial stiffness measured by carotid-femoral pulse wave velocity (PWV) in individuals with EBP due to SOD upregulation. Young adults with NBP (n=11, 3M/8F, Age 21.0 ± 1.34 yrs, BP 102.9 ± 7.56/ 68.91 ± 4.68 mmHg) and EBP (n=11, 8M/3F, Age 21.64 ± 1.63 yrs, BP 124.5 ± 6.70/ 78.55 ± 6.20 mmHg) underwent 4 weeks of RIPC intervention, and the results showed RIPC reduced PWV in the elevated BP group (5.66 ± 0.99 vs 5.34 ± 0.77 m/s, P=0.0492). Furthermore, serum SOD activity was increased in EBP group after RIPC (13.18 ± 3.60 vs 14.59 ± 4.02 units/mL, P < 0.016) with no significant changes in the normotensive group (P = 0.603). Thus, RIPC may serve as a potential alternative intervention to attenuate arterial stiffness likely via antioxidant upregulation in individuals with EBP.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186265","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":"Relative contribution of correcting the diet and voluntary exercise to myocardial recovery in a murine model of heart failure with preserved ejection fraction.","authors":"Emylie-Ann Labbé, Sara-Ève Thibodeau, Èlisabeth Walsh-Wilkinson, Maude Chalifour, Pierre-Olivier Sirois, Juliette Leblanc, Audrey Morin-Grandmont, Marie Arsenault, Jacques Couet","doi":"10.1152/ajpheart.00092.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00092.2025","url":null,"abstract":"<p><p>Using a two-hit murine model of heart failure with preserved ejection fraction (HFpEF), we studied cardiac reverse remodelling (RR) after stopping the causing stress (Angiotensin II (AngII) + High-fat diet (HFD); MHS) and then introducing voluntary exercise (VE) and feeding the animals with a low-fat diet. This led to extensive left ventricle (LV) RR. We then studied the relative contribution to RR of only correcting the diet or allowing VE after stopping AngII. We next evaluated myocardial recovery after an extended period (12 weeks instead of four) by exposing the animals to a second MHS. Our observations revealed a sex-specific response. Stopping AngII but continuing the HFD blocked RR in females, not males. Correcting the diet or implementing VE normalized most gene markers of LV hypertrophy or extracellular matrix remodelling, irrespective of sex. Twelve weeks of recovery was associated with normal LV morphology and function, except for several abnormal diastolic echocardiographic parameters. A second MHS after these 12 weeks led to a loss of ejection fraction in males. The response of females was like that after the first MHS, suggesting a better myocardial recovery. The MHS likely changed myocardial glucose metabolism. Pyruvate dehydrogenase (PDH) activity, which is responsible for pyruvate entry in the mitochondria, was reduced after MHS, and this was accompanied by an increase in PDH phosphorylation and pyruvate dehydrogenase kinase 4 content. RR normalized these. Our results suggest sex-specific RR after stopping the MHS and that myocardial anomalies remaining make males more sensitive to a second HFpEF-inducing stress.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148872","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":"CCR2⁺ MONOCYTE-DERIVED MACROPHAGES DRIVE CARDIAC HYPERTROPHY IN EARLY HFPEF.","authors":"Jana Raman, Steven John Simmonds, Ellen Caluwé, Rick van Leeuwen, Caroline Walschap, Mathias Stroobants, Ümare Cöl, Petra Vandervoort, Stephane Heymans, Elizabeth A V Jones","doi":"10.1152/ajpheart.00022.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00022.2025","url":null,"abstract":"<p><p>Heart Failure with Preserved Ejection Fraction is a chronic syndrome driven by systemic inflammation. Resident and monocyte-derived macrophages play opposing roles in several heart diseases. Though general ablation of macrophages has previously been studied in HFpEF, the individual contribution of these subsets to HFpEF development is unknown. We induced preclinical HFpEF in mice using a model consisting of high-fat diet, chronic low-dose angiotensin II administration, and salt supplemented drinking water. Our model was marked by circulating Ly6C^hi monocytosis and elevated pro-inflammatory CCR2⁺ macrophage infiltration at the expense of the cardioprotective TIMD4⁺ resident macrophage subset. Beyond an inflammatory signature typical of HFpEF, the mouse model also faithfully recreates cardiac fibrosis, hypertrophy, and functional changes in the heart as measured by echocardiography and pressure-volume loops. The experimental mice also show exercise intolerance. Using a loss-of-function genetic model, we found that CCR2 ablation prevented classical macrophage infiltration and improved the resident TIMD4⁺ macrophage representation early in HFpEF development. CCR2^-/- mice showed a higher accumulation of dysfunctional mitochondria in the heart with diffusely organized cristae without worsened mitochondrial fusion (Mitofusin2) or functioning in general (TOM20). Loss of CCR2 did prevent LV hypertrophy in our preclinical model but it did not resolve the cardiac fibrosis or diastolic dysfunction. Mitochondrial damage has been suggested to drive hypertrophy, however, we found that preventing classical macrophage recruitment increased the presence of damaged mitochondria, even though hypertrophy is resolved. In the future, our results can contribute to successful therapeutic immunomodulation to tackle HFpEF, if combined with anti-fibrotic treatment.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148868","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 dysfunction in chronic kidney disease: a clinical perspective.","authors":"Monique E Cho, Vienna E Brunt, Yan-Ting Shiu, Kanokwan Bunsawat","doi":"10.1152/ajpheart.00908.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00908.2024","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is a progressive multi-systemic disorder that augments the risks of cardiovascular (CV) morbidity and mortality as kidney function declines. The endothelium plays a key role in modulating vascular tone, integrity, and homeostasis by producing and releasing a variety of endothelium-derived relaxing factors, including nitric oxide (NO). Endothelial dysfunction is a salient pathogenic mechanism underlying the development and progression of CKD and is characterized by reduced production of vasodilators and increased production of vasoconstrictors (e.g., endothelin-1). Factors such as uremic milieu, inflammation, and oxidative stress are putative contributors of endothelial dysfunction and reduced NO bioavailability that ultimately impacts functional and structural integrity of the vasculature. Because endothelial dysfunction is an independent predictor of CV morbidity and mortality in patients with CKD, several clinical studies have examined disease-related changes in endothelium-dependent vasodilation across the arterial tree. This review will focus on the clinical evidence regarding CKD-associated endothelial dysfunction involving both micro- and macrovasculature, briefly discuss underlying physiological mechanisms, and summarize available and emerging pharmacotherapies along with a brief summary of exercise training as a lifestyle intervention.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148870","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":"Bend it Like BIN1: How a Membrane-Curving Adaptor Protein Shapes Cardiac Physiology.","authors":"Heather C Spooner, Rose E Dixon","doi":"10.1152/ajpheart.00198.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00198.2025","url":null,"abstract":"<p><p><u>B</u>ridging <u>in</u>tegrator 1, initially named <u>b</u>ox dependent myc-<u>in</u>teracting protein-<u>1</u> (BIN1), and also known as and Amphiphysin 2 is a versatile N-BAR protein that plays essential roles in membrane remodeling, protein trafficking, and cellular organization across multiple tissues. While extensively studied in cancer and Alzheimer's disease, BIN1's critical functions in cardiac physiology and pathology represent an emerging frontier with significant therapeutic implications. This review provides a synopsis of our current understanding of BIN1's structure function relationships, with particular emphasis on cardiac-specific isoforms and their roles in heart function. We examine how BIN1's various domains-including the membrane-curvature forming and sensing BAR domain, phosphoinositide-binding motif, and SH3 protein-protein interaction domains-orchestrate its diverse cellular functions, from t-tubule growth, microfolding, and anchoring to directed protein trafficking and complex assembly. Recent discoveries highlight BIN1's involvement in cardiac aging and disease, where both deficiency and excess of BIN1 can lead to dysfunction. Notably, BIN1 levels are reduced in heart failure while increasing significantly during cardiac aging, suggesting a bidirectional pathophysiology where both insufficient and excessive BIN1 expression can impair cardiac function. We discuss emerging evidence regarding the role of BIN1 in cardiac pathologies, offering potential therapeutic targets. Understanding BIN1's membrane-shaping capabilities and its roles in organizing excitation-contraction coupling machinery could yield novel therapeutic strategies for addressing cardiac dysfunction in various disease contexts.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109400","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":"Reduced peak pressure gradient in patients with aortic stenosis and type 2 diabetes.","authors":"Kosuke Minai, Kazuo Ogawa, Toshikazu Tanaka, Makoto Kawai, Jun Yoshida, Keisuke Shirasaki, Ryosuke Itakura, Seigo Yamashita, Tomohisa Nagoshi, Takayuki Ogawa, Michifumi Tokuda, Michihiro Yoshimura","doi":"10.1152/ajpheart.00255.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00255.2025","url":null,"abstract":"<p><p>Diabetes impairs energy metabolism throughout the body, including the heart. However, the clinical effect of diabetes on left ventricular (LV) contractility remains unclear. To address this knowledge gap, we investigated the effect of diabetes on patients with aortic stenosis (AS), a model of increased LV afterload. We analyzed data from 276 consecutive patients with AS who underwent transthoracic surgery, echocardiography, cardiac catheterization, and fasting blood sampling. The peak aortic velocity was determined using continuous-wave Doppler echocardiography, and the peak pressure gradient (peak-PG) was calculated using the simplified Bernoulli equation. The aortic valve area (AVA) was determined using planimetry Risk factors, including age, glycated hemoglobin (HbA1c), homeostatic model assessment for insulin resistance (HOMA-IR) level, sex, hemoglobin level, hypertension, and dyslipidemia, that influenced the peak PG were examined using regression analysis. Structural equation modeling (SEM) was performed to identify the direct and indirect effects of these variables on the peak PG. SEM revealed a significant association between the AVA and peak-PG (<i>p</i><0.001). The peak- PG significantly decreased with higher HbA1c (<i>p</i><0.001) and increased with age (<i>p</i>=0.004). Other factors, including HOMA-IR, sex, hypertension, and dyslipidemia, had no significant effects. AVA decreased significantly with age (<i>p</i>=0.007) and increased with sex (male) (<i>p</i>=0.034). Diabetes reduces LV contractility, as evidenced in patients with AS. Insufficient glucose metabolism may contribute to LV dysfunction. Clinically, the severity of AS in patients with diabetes should not be underestimated based on the PG alone.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109401","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 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 Deschenes, Thomas J Hund","doi":"10.1152/ajpheart.00821.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00821.2024","url":null,"abstract":"<p><p>Heart failure (HF) represents a major burden on the healthcare system with HF patients 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 weeks by echocardiography and sub-surface electrocardiograms. Ventricular myocytes were isolated for action potential, intracellular Ca²⁺, and contractility measurements. The expression/regulation of key cell signaling pathways were evaluated early in remodeling. TREK1cKO and control mice showed a significant decrease in cardiac systolic function with evidence of hypertrophy as early as 2 weeks post-TAC compared to sham. However, TREK1cKO mice displayed a more severe decline in function with enhanced left ventricular chamber dilation (eccentric remodeling) compared to control 6 weeks post-TAC. Similarly, TAC TREK1cKO mice demonstrated greater prolongation of the QT and QRS intervals compared to TAC control. TAC TREK1cKO ventricular myocytes exhibited greater action potential prolongation with paradoxical improvements in Ca²⁺ homeostasis and contractility compared to control. 2 weeks post-TAC, TREK1cKO hearts exhibited elevation of STAT3 phosphorylation at Y705 compared to 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.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Women's Cardiovascular Health at Risk: An Urgent Call to Protect the U.S. Biomedical Research System and Prevent Setbacks in Women's Health Research.","authors":"Styliani Goulopoulou, Donna A Santillan, Julia Unternaehrer","doi":"10.1152/ajpheart.00182.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00182.2025","url":null,"abstract":"<p><p>This paper calls on the scientific community and academic institutions to take urgent actions to protect research and infrastructure, ensuring that hard-won gains in understanding sex-specific cardiovascular disease mechanisms are not lost in an already underfunded field. We provide a roadmap with recommended actions and implementation strategies to address challenges and threats to women's cardiovascular health research.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101170","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}