Pub Date : 2024-04-19DOI: 10.1152/ajpheart.00132.2024
Luciana de Souza Santos, Marília Harumi Higuchi dos Santos Rehder, Marcelo Vailati Negrao, Beatriz R. Goes-Santos, Edgar Toschi-Dias, Camila Jordão Paixão, Ursula Urias, Natali Schiavo Giannetti, Ludhmila A. Hajjar, Roberto Kalil Filho, Carlos E. Negrão
Background: It is unclear whether muscle blood flow (MBF) is altered in long-term Hodgkin Lymphoma (HL) survivors. We test the hypothesis that: 1) MBF response during mental stress (MS) is impaired in long-term HL survivors; 2) Aerobic exercise training combined with local strength exercise (ET) restores MBF responses during MS in these survivors. Methods: Eighteen 5-year HL survivors and 10 aged-paired healthy subjects (HC) were studied. Twenty HL survivors were randomly divided into two groups: Exercise-trained (HLT, n=10) and untrained (HLUT, n=10). Maximal aerobic capacity was evaluated by a cardiopulmonary exercise test and forearm blood flow (FBF) by venous occlusion plethysmography. MS was elicited by Stroop Color Word Test. ET was conducted for four months, three/week for 60 minutes each session. The aerobic exercise intensity corresponded to anaerobic threshold up to 10% below the respiratory compensation point. The strength exercises consisted of 2-3 sets of chest press, pulley and squat exercises, 12-15 repetitions each exercise at 30-50% of the maximal voluntary contraction. Results: Baseline was similar in HL survivors and HC, except peak oxygen consumption (peak VO2, p=0.013) and FBF (p=0.006) that were lower in the HL survivors. FBF responses during MS were lower in HL survivors (p<0.001). ET increased peak VO2 (11.59±3.07%, p=0.002), and FBF at rest (33.74±5.13%, p<0.001) and during MS (24±5.31%, p=0.001). Further analysis showed correlation between the changes in peak VO2 and the changes in FBF during MS (r=0.711, p=0.001). Conclusion: Long-term HL survivors have impaired MBF responses during MS. ET restores MBF responses during MS.
背景：霍奇金淋巴瘤（HL）长期存活者的肌肉血流（MBF）是否会发生变化尚不清楚。我们测试了以下假设1）长期霍奇金淋巴瘤（HL）幸存者在精神压力（MS）期间的肌肉血流反应受损；2）有氧运动训练结合局部力量锻炼（ET）可恢复这些幸存者在精神压力（MS）期间的肌肉血流反应。方法：研究对象为 18 名 5 年的 HL 幸存者和 10 名年龄配对的健康受试者（HC）。20 名 HL 幸存者被随机分为两组：运动训练组（HLT，n=10）和未训练组（HLUT，n=10）。最大有氧能力通过心肺运动测试进行评估，前臂血流量（FBF）通过静脉闭塞胸透进行评估。MS 通过 Stroop 颜色词测试激发。有氧运动持续四个月，每周三次，每次 60 分钟。有氧运动强度与无氧阈值相对应，低于呼吸代偿点 10%。力量练习包括2-3组胸压、滑轮和深蹲练习，每次重复12-15次，最大自主收缩量为30-50%。结果HL 幸存者和 HC 的基线相似，但 HL 幸存者的峰值耗氧量（峰值 VO2，p=0.013）和 FBF（p=0.006）较低。HL 幸存者在 MS 期间的 FBF 反应较低（p<0.001）。ET 增加了峰值 VO2（11.59±3.07%，p=0.002），以及静息时（33.74±5.13%，p<0.001）和 MS 期间（24±5.31%，p=0.001）的 FBF。进一步分析表明，峰值 VO2 的变化与 MS 期间 FBF 的变化之间存在相关性（r=0.711，p=0.001）。结论长期 HL 存活者在 MS 期间的 MBF 反应受损。ET 可恢复 MS 期间的 MBF 反应。
{"title":"Aerobic Exercise Training Combined with Local Strength Exercise Restores Muscle Blood Flow and Maximal Aerobic Capacity in Long-Term Hodgkin Lymphoma Survivors","authors":"Luciana de Souza Santos, Marília Harumi Higuchi dos Santos Rehder, Marcelo Vailati Negrao, Beatriz R. Goes-Santos, Edgar Toschi-Dias, Camila Jordão Paixão, Ursula Urias, Natali Schiavo Giannetti, Ludhmila A. Hajjar, Roberto Kalil Filho, Carlos E. Negrão","doi":"10.1152/ajpheart.00132.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00132.2024","url":null,"abstract":"Background: It is unclear whether muscle blood flow (MBF) is altered in long-term Hodgkin Lymphoma (HL) survivors. We test the hypothesis that: 1) MBF response during mental stress (MS) is impaired in long-term HL survivors; 2) Aerobic exercise training combined with local strength exercise (ET) restores MBF responses during MS in these survivors. Methods: Eighteen 5-year HL survivors and 10 aged-paired healthy subjects (HC) were studied. Twenty HL survivors were randomly divided into two groups: Exercise-trained (HLT, n=10) and untrained (HLUT, n=10). Maximal aerobic capacity was evaluated by a cardiopulmonary exercise test and forearm blood flow (FBF) by venous occlusion plethysmography. MS was elicited by Stroop Color Word Test. ET was conducted for four months, three/week for 60 minutes each session. The aerobic exercise intensity corresponded to anaerobic threshold up to 10% below the respiratory compensation point. The strength exercises consisted of 2-3 sets of chest press, pulley and squat exercises, 12-15 repetitions each exercise at 30-50% of the maximal voluntary contraction. Results: Baseline was similar in HL survivors and HC, except peak oxygen consumption (peak VO<sub>2</sub>, <i>p</i>=0.013) and FBF (<i>p</i>=0.006) that were lower in the HL survivors. FBF responses during MS were lower in HL survivors (<i>p</i><0.001). ET increased peak VO<sub>2</sub> (11.59±3.07%, <i>p</i>=0.002), and FBF at rest (33.74±5.13%, <i>p</i><0.001) and during MS (24±5.31%, <i>p</i>=0.001). Further analysis showed correlation between the changes in peak VO<sub>2</sub> and the changes in FBF during MS (r=0.711, <i>p</i>=0.001). Conclusion: Long-term HL survivors have impaired MBF responses during MS. ET restores MBF responses during MS.","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"47 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140630418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-12DOI: 10.1152/ajpheart.00119.2024
Flobater I. Gawargi, Hamid R. Shahshahan, Paras K. Mishra
Cardiovascular research relies heavily on the veracity of in vitro cardiomyocyte models, with HL-1 and H9c2 cell lines at the forefront due to their cardiomyocyte-like properties. However, the variability stemming from non-standardized culturing and transfection methods poses a significant challenge to data uniformity and reliability. In this study, we introduce meticulously crafted protocols to enhance the culture and transfection of HL-1 and H9c2 cells, emphasizing the reduction of cytotoxic effects while improving transfection efficiency. Through the examination of polymer-based and lipid-based transfection methods, we offer a comparative analysis that underscores the heightened efficiency and reduced toxicity of these approaches. Our research provides an extensive array of step-by-step procedures designed to foster robust cell cultures and outlines troubleshooting practices to rectify issues of low transfection rates. We discuss the merits and drawbacks of both transfection techniques, equipping researchers with the knowledge to choose the most fitting method for their experimental goals. By offering a definitive guide to these cell lines' culturing and transfection, our work seeks to set a new standard in procedural consistency, ensuring that the cardiovascular research community can achieve more dependable and reproducible results, thereby pushing the boundaries of current methodologies toward impactful clinical applications.
{"title":"Tailoring Transfection for Cardiomyocyte Cell Lines: Balancing Efficiency and Toxicity in Lipid versus Polymer-Based Transfection Methods in H9c2 and HL-1 Cells","authors":"Flobater I. Gawargi, Hamid R. Shahshahan, Paras K. Mishra","doi":"10.1152/ajpheart.00119.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00119.2024","url":null,"abstract":"Cardiovascular research relies heavily on the veracity of in vitro cardiomyocyte models, with HL-1 and H9c2 cell lines at the forefront due to their cardiomyocyte-like properties. However, the variability stemming from non-standardized culturing and transfection methods poses a significant challenge to data uniformity and reliability. In this study, we introduce meticulously crafted protocols to enhance the culture and transfection of HL-1 and H9c2 cells, emphasizing the reduction of cytotoxic effects while improving transfection efficiency. Through the examination of polymer-based and lipid-based transfection methods, we offer a comparative analysis that underscores the heightened efficiency and reduced toxicity of these approaches. Our research provides an extensive array of step-by-step procedures designed to foster robust cell cultures and outlines troubleshooting practices to rectify issues of low transfection rates. We discuss the merits and drawbacks of both transfection techniques, equipping researchers with the knowledge to choose the most fitting method for their experimental goals. By offering a definitive guide to these cell lines' culturing and transfection, our work seeks to set a new standard in procedural consistency, ensuring that the cardiovascular research community can achieve more dependable and reproducible results, thereby pushing the boundaries of current methodologies toward impactful clinical applications.","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-12DOI: 10.1152/ajpheart.00550.2023
Dorit Koren, Kristen L. Knutson, Brian K. Burke, Kimberly L. Drews, Fida Bacha, Lorraine Katz, Marsha D. Marcus, Siripoom McKay, Kristen Nadeau, Babak Mokhlesi
American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print.
美国生理学杂志-心脏与循环生理学》，提前出版。
{"title":"The Association of Self-Reported Sleep and Circadian Measures with Glycemic Control and Diabetes Complications among Young Adults with Type 2 Diabetes","authors":"Dorit Koren, Kristen L. Knutson, Brian K. Burke, Kimberly L. Drews, Fida Bacha, Lorraine Katz, Marsha D. Marcus, Siripoom McKay, Kristen Nadeau, Babak Mokhlesi","doi":"10.1152/ajpheart.00550.2023","DOIUrl":"https://doi.org/10.1152/ajpheart.00550.2023","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-12DOI: 10.1152/ajpheart.00116.2024
Vidhya Krishnan, Nikki Atanasova, Preetinder K. Aujla, Devon Hupka, Caroline A. Owen, Zamaneh Kassiri
Cardiac hypertrophy is a common feature in several cardiomyopathies. We previously reported that loss of ADAM15 (disintegrin and metalloproteinase 15) worsened cardiac hypertrophy and dilated cardiomyopathy following cardiac pressure overload. Here, we investigated the impact of ADAM15 loss in female mice following cardiac pressure overload induced by transverse aortic constriction (TAC). Female Adam15-/-mice developed the same degree of cardiac hypertrophy, dilation and dysfunction as the parallel female wildtype (WT) mice at 6 weeks post-TAC. To determine if this is due to the protective effects of estrogen which could mask the negative impact of Adam15 loss, WT and Adam15-/- mice underwent ovariectomy (OVx) 2 weeks prior to TAC. Cardiac structure and function analyses were performed at 6 weeks post-TAC. OVx similarly impacted females of both genotypes post-TAC. Calcineurin (Cn) activity was increased post-OVx-TAC, and more in Adam15-/- mice, however this increase was not reflected in the total-to-phospho NFAT levels. Integrin α7 expression, which was upstream of Cn activation in male Adam15-/--TAC mice, remained unchanged in female mice. However, activation of the Mitogen Activated Protein Kinases (ERK, JNK, P38) were greater in Adam15-/--OVx-TAC compared to WT-OVx-TAC mice. In addition, ADAM15 protein levels were significantly increased post-TAC in male but not in female WT mice. Myocardial fibrosis was comparable in non-OVx WT-TAC and Adam15-/--TAC mice. OVx increased the perivascular fibrosis more in Adam15-/- compared to WT mice post-TAC. Our data demonstrate that loss of ovarian hormones did not fully replicate the male phenotype in the female Adam15-/- mice post-TAC. Since ADAM15 levels were increased in males but not in females post-TAC, it is plausible that ADAM15 does not play a prominent role in post-TAC events in female mice. Our findings highlight the significance of factors other than sex hormones in mediating cardiomyopathies in females, which require a more thorough understanding.
{"title":"Loss of ADAM15 in female mice does not worsen pressure overload cardiomyopathy, independent of ovarian hormones","authors":"Vidhya Krishnan, Nikki Atanasova, Preetinder K. Aujla, Devon Hupka, Caroline A. Owen, Zamaneh Kassiri","doi":"10.1152/ajpheart.00116.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00116.2024","url":null,"abstract":"Cardiac hypertrophy is a common feature in several cardiomyopathies. We previously reported that loss of ADAM15 (disintegrin and metalloproteinase 15) worsened cardiac hypertrophy and dilated cardiomyopathy following cardiac pressure overload. Here, we investigated the impact of ADAM15 loss in female mice following cardiac pressure overload induced by transverse aortic constriction (TAC). Female <i>Adam15<sup>-/-</sup></i><sup></sup>mice developed the same degree of cardiac hypertrophy, dilation and dysfunction as the parallel female wildtype (WT) mice at 6 weeks post-TAC. To determine if this is due to the protective effects of estrogen which could mask the negative impact of <i>Adam15</i> loss, WT and <i>Adam15</i><sup>-/-</sup> mice underwent ovariectomy (OVx) 2 weeks prior to TAC. Cardiac structure and function analyses were performed at 6 weeks post-TAC. OVx similarly impacted females of both genotypes post-TAC. Calcineurin (Cn) activity was increased post-OVx-TAC, and more in <i>Adam15</i><sup>-/-</sup> mice, however this increase was not reflected in the total-to-phospho NFAT levels. Integrin α7 expression, which was upstream of Cn activation in male <i>Adam15</i><sup>-/-</sup>-TAC mice, remained unchanged in female mice. However, activation of the Mitogen Activated Protein Kinases (ERK, JNK, P38) were greater in <i>Adam15</i><sup>-/-</sup>-OVx-TAC compared to WT-OVx-TAC mice. In addition, ADAM15 protein levels were significantly increased post-TAC in male but not in female WT mice. Myocardial fibrosis was comparable in non-OVx WT-TAC and <i>Adam15</i><sup>-/-</sup>-TAC mice. OVx increased the perivascular fibrosis more in<i> Adam15</i><sup>-/-</sup> compared to WT mice post-TAC. Our data demonstrate that loss of ovarian hormones did not fully replicate the male phenotype in the female <i>Adam15</i><sup>-/-</sup> mice post-TAC. Since ADAM15 levels were increased in males but not in females post-TAC, it is plausible that ADAM15 does not play a prominent role in post-TAC events in female mice. Our findings highlight the significance of factors other than sex hormones in mediating cardiomyopathies in females, which require a more thorough understanding.","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"125 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1152/ajpheart.00054.2024
Hualong Bai, M. Alyssa Varsanik, Carly Thaxton, Yuichi Ohashi, Luis Gonzalez, Weichang Zhang, Yukihiko Aoyagi, Masaki Kano, Bogdan Yatsula, Zhuo Li, Luka Pocivavsek, Alan Dardik
Background: Clinical failure of arteriovenous fistulae (AVF) is frequently due to juxta-anastomotic neointimal hyperplasia (JANIH). Although the mouse AVF model recapitulates human AVF maturation, previous studies focused on the outflow vein distal to the anastomosis. We hypothesized that the juxta-anastomotic area (JAA) has increased NIH compared to the outflow vein. Method: AVF were created in C57BL/6 mice without or with chronic kidney disease (CKD). Temporal and spatial changes of the JAA were examined using histology and immunofluorescence. Computational techniques were used to model the AVF. RNA-seq and bioinformatic analyses were performed to compare the JAA with the outflow vein. The jugular vein to carotid artery AVF model was created in Wistar rats. Result: The neointima in the JAA shows increased volume compared to the outflow vein. Computational modeling shows increased volume of disturbed flow at the JAA compared to the outflow vein. Endothelial cells are immediately lost from the wall contralateral to the fistula exit, followed by thrombus formation and JANIH. Gene Ontology (GO) enrichment analysis of the 1862 differentially expressed genes (DEG) between the JANIH and the outflow vein identified 525 overexpressed genes. The rat jugular vein to carotid artery AVF showed changes similar to the mouse AVF. Conclusion: Disturbed flow through the JAA correlates with rapid endothelial cell loss, thrombus formation, and JANIH; late endothelialization of the JAA channel correlates with late AVF patency. Early thrombus formation in the JAA may influence later development of JANIH.
{"title":"Disturbed flow in the juxta-anastomotic area of an arteriovenous fistula correlates with endothelial loss, acute thrombus formation and neointimal hyperplasia","authors":"Hualong Bai, M. Alyssa Varsanik, Carly Thaxton, Yuichi Ohashi, Luis Gonzalez, Weichang Zhang, Yukihiko Aoyagi, Masaki Kano, Bogdan Yatsula, Zhuo Li, Luka Pocivavsek, Alan Dardik","doi":"10.1152/ajpheart.00054.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00054.2024","url":null,"abstract":"Background: Clinical failure of arteriovenous fistulae (AVF) is frequently due to juxta-anastomotic neointimal hyperplasia (JANIH). Although the mouse AVF model recapitulates human AVF maturation, previous studies focused on the outflow vein distal to the anastomosis. We hypothesized that the juxta-anastomotic area (JAA) has increased NIH compared to the outflow vein. Method: AVF were created in C57BL/6 mice without or with chronic kidney disease (CKD). Temporal and spatial changes of the JAA were examined using histology and immunofluorescence. Computational techniques were used to model the AVF. RNA-seq and bioinformatic analyses were performed to compare the JAA with the outflow vein. The jugular vein to carotid artery AVF model was created in Wistar rats. Result: The neointima in the JAA shows increased volume compared to the outflow vein. Computational modeling shows increased volume of disturbed flow at the JAA compared to the outflow vein. Endothelial cells are immediately lost from the wall contralateral to the fistula exit, followed by thrombus formation and JANIH. Gene Ontology (GO) enrichment analysis of the 1862 differentially expressed genes (DEG) between the JANIH and the outflow vein identified 525 overexpressed genes. The rat jugular vein to carotid artery AVF showed changes similar to the mouse AVF. Conclusion: Disturbed flow through the JAA correlates with rapid endothelial cell loss, thrombus formation, and JANIH; late endothelialization of the JAA channel correlates with late AVF patency. Early thrombus formation in the JAA may influence later development of JANIH.","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"79 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1152/ajpheart.00171.2024
Koya Lumbao-Conradson, Ronald J. Vagnozzi
American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print.
美国生理学杂志-心脏与循环生理学》，提前出版。
{"title":"Unstrain my Heart: Can Cardiac Macrophages Reverse Remodel Fibrosis?","authors":"Koya Lumbao-Conradson, Ronald J. Vagnozzi","doi":"10.1152/ajpheart.00171.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00171.2024","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1152/ajpheart.00706.2023
Ala Yousef, Deanna K. Sosnowski, Liye Fang, Renald James Legaspi, Jacob Korodimas, Andy Lee, Katharine E. Magor, John M. Seubert
American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print.
美国生理学杂志-心脏与循环生理学》，提前出版。
{"title":"Cardioprotective Response and Senescence in Aged sEH Null Female Mice Exposed to LPS","authors":"Ala Yousef, Deanna K. Sosnowski, Liye Fang, Renald James Legaspi, Jacob Korodimas, Andy Lee, Katharine E. Magor, John M. Seubert","doi":"10.1152/ajpheart.00706.2023","DOIUrl":"https://doi.org/10.1152/ajpheart.00706.2023","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1152/ajpheart.00151.2024
Chantal L. Rytz, Keila Turino Miranda, Paul E. Ronksley, Nathalie Saad, Satish R. Raj, Ranjani Somayaji, Sandra M. Dumanski, Heather Ganshorn, Dina N. Greene, David Collister, Amelia M. Newbert, Lindsay Peace, Sofia B. Ahmed
American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print.
美国生理学杂志-心脏与循环生理学》，提前出版。
{"title":"Association between Serum Estradiol and Cardiovascular Health among Transgender Adults Using Gender-Affirming Estrogen Therapy","authors":"Chantal L. Rytz, Keila Turino Miranda, Paul E. Ronksley, Nathalie Saad, Satish R. Raj, Ranjani Somayaji, Sandra M. Dumanski, Heather Ganshorn, Dina N. Greene, David Collister, Amelia M. Newbert, Lindsay Peace, Sofia B. Ahmed","doi":"10.1152/ajpheart.00151.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00151.2024","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"202 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1152/ajpheart.00025.2024
Tara-Yesomi Wenegieme, Dalia Elased, Kelia E. McMichael, Jananie Rockwood, Khanzada Hasrat, Adaku C. Ume, Andrea G. Marshall, Kit Neikirk, Annet Kirabo, Khalid M. Elased, Antentor Hinton, Clintoria R. Williams
American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print.
美国生理学杂志-心脏与循环生理学》，提前出版。
{"title":"Strategies for Inducing and Validating Zinc Deficiency and Zinc Repletion","authors":"Tara-Yesomi Wenegieme, Dalia Elased, Kelia E. McMichael, Jananie Rockwood, Khanzada Hasrat, Adaku C. Ume, Andrea G. Marshall, Kit Neikirk, Annet Kirabo, Khalid M. Elased, Antentor Hinton, Clintoria R. Williams","doi":"10.1152/ajpheart.00025.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00025.2024","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Ahead of Print. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Corrigendum for Ferreira et al., volume 325, 2023, p. H774–H789","authors":"","doi":"10.1152/ajpheart.00200.2023_cor","DOIUrl":"https://doi.org/10.1152/ajpheart.00200.2023_cor","url":null,"abstract":"American Journal of Physiology-Heart and Circulatory Physiology, Volume 326, Issue 4, Page H1060-H1060, April 2024. <br/>","PeriodicalId":7640,"journal":{"name":"American Journal of Physiology - Heart and Circulatory Physiology","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140569571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：