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Gotowa bibliografia na temat „Aging cardiac”

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Data publikacji: 20 lipca 2024

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Artykuły w czasopismach na temat "Aging cardiac"

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Wessells, Robert J., i Rolf Bodmer. "Cardiac aging". Seminars in Cell & Developmental Biology 18, nr 1 (luty 2007): 111–16. http://dx.doi.org/10.1016/j.semcdb.2006.12.011.

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Li, Zhen, i David J. Lefer. "Demystifying Cardiac Aging". Circulation Research 128, nr 4 (19.02.2021): 508–10. http://dx.doi.org/10.1161/circresaha.121.318741.

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LIMACHER, MARIAN C. "Aging and Cardiac Function". Southern Medical Journal 87, nr 5 (maj 1994): S17. http://dx.doi.org/10.1097/00007611-199405000-00003.

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LIMACHER, MARIAN C. "Aging and Cardiac Function". Southern Medical Journal 87, Supplement (maj 1994): S17. http://dx.doi.org/10.1097/00007611-199405001-00003.

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Miyamoto, Shigeki. "Autophagy and cardiac aging". Cell Death & Differentiation 26, nr 4 (28.01.2019): 653–64. http://dx.doi.org/10.1038/s41418-019-0286-9.

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Renlund, Dale G., i Gary Gerstenblith. "Aging and cardiac function". International Journal of Cardiology 10, nr 3 (marzec 1986): 193–96. http://dx.doi.org/10.1016/0167-5273(86)90001-x.

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Czuriga, D., Z. Papp, I. Czuriga i Á. Balogh. "Cardiac aging – a review". European Surgery 43, nr 2 (kwiecień 2011): 69–77. http://dx.doi.org/10.1007/s10353-011-0600-3.

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Obas, Vanessa, i Ramachandran S. Vasan. "The aging heart". Clinical Science 132, nr 13 (9.07.2018): 1367–82. http://dx.doi.org/10.1042/cs20171156.

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As the elderly segment of the world population increases, it is critical to understand the changes in cardiac structure and function during the normal aging process. In this review, we outline the key molecular pathways and cellular processes that underlie the phenotypic changes in the heart and vasculature that accompany aging. Reduced autophagy, increased mitochondrial oxidative stress, telomere attrition, altered signaling in insulin-like growth factor, growth differentiation factor 11, and 5′- AMP-activated protein kinase pathways are among the key molecular mechanisms underlying cardiac aging. Aging promotes structural and functional changes in the atria, ventricles, valves, myocardium, pericardium, the cardiac conduction system, and the vasculature. We highlight the factors known to accelerate and attenuate the intrinsic aging of the heart and vessels in addition to potential preventive and therapeutic avenues. A greater understanding of the processes involved in cardiac aging may facilitate our ability to mitigate the escalating burden of CVD in older individuals and promote healthy cardiac aging.
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Chen, Bijun, Shuaibo Huang i Nikolaos G. Frangogiannis. "Aging, cardiac repair and Smad3". Aging 10, nr 9 (20.09.2018): 2230–32. http://dx.doi.org/10.18632/aging.101567.

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Westin, Oscar, Finn Gustafsson i Emil Fosbøl. "Occult cardiac amyloidosis?" Aging 11, nr 20 (19.10.2019): 8739–40. http://dx.doi.org/10.18632/aging.102383.

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Rozprawy doktorskie na temat "Aging cardiac"

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Inuzuka, Yasutaka. "Suppression of phosphoinositide 3-kinase prevents cardiac aging in mice". Kyoto University, 2009. http://hdl.handle.net/2433/126462.

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Haynes, Premi. "TRANSMURAL HETEROGENEITY OF CELLULAR LEVEL CARDIAC CONTRACTILE PROPERTIES IN AGING AND HEART FAILURE". UKnowledge, 2014. http://uknowledge.uky.edu/physiology_etds/16.

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The left ventricle of the heart relaxes when it fills with blood and contracts to eject blood into circulation to meet the body’s metabolic demands. Dysfunction in either relaxation or contraction of the left ventricle can lead to heart failure. Transmural heterogeneity is thought to contribute to normal ventricular wall motion but it is not well understood how transmural modifications affect the failing left ventricle. The overall hypothesis of this dissertation is that normal left ventricles exhibit transmural heterogeneity in cellular level contractile properties and with aging and heart failure there are region-specific changes in cellular level contractile mechanisms. Age is the biggest risk factor associated with heart failure and therefore we investigated transmural changes in Ca2+ handling and contractile proteins in aging F344 rats before the onset of heart failure. We found that in 22-month old F344 rats there is a region-specific decrease in cardiac troponin I phosphorylation in the sub-epicardium that may contribute to slowed myocyte relaxation in the sub-epicardial cells of the same age. We then investigated the transmural patterns of contractile properties in myocardial tissue samples from patients with heart failure. Force and power output reduced most significantly in the samples from the mid-myocardial region when compared to sub-epicardium and sub-endocardium of the failing hearts. There was a region-specific increase in fibrosis is the mid-myocardium of the failing hearts. Myocardial power output was correlated with key sarcomeric proteins including cardiac troponin I, desmin and myosin light chain-1. The results in this dissertation reveal novel region-specific modifications in contractile properties in aging and heart failure. These transmural effects can potentially contribute to disruption in normal wall motion and lead to ventricular dysfunction.
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Yang, Bo, i 杨波. "Role of lipocalin-2 in cardiac dysfunction associated with aging and dietary obesity". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47869641.

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Obesity is closely related to many medical complications such as type 2 diabetes, hypertension and heart failure. Obesity and other factors, including elevated blood glucose levels, hypertension, and dyslipidemia, constitute a constellation of symptoms known as the metabolic syndrome, which are the risk factors for coronary artery disease. Lipocalin-2 is a pro-inflammatory adipokine causally involved in the development of obesity-associated metabolic and cardiovascular diseases. Recent clinical and experimental evidences demonstrate an association between augmented circulating lipocalin-2 and cardiac dysfunction. However, little is known about the detailed roles of lipocalin-2 in regulating pathophysiological functions of the heart. The present study was designed to compare the heart functions of mice with normal (WT) or deficient lipocalin-2 (Lcn2-KO) expression and to examine the molecular mechanisms underlying lipocalin-2-mediated deteriorated effects in hearts. Echocardiographic analysis revealed that the myocardial contractile function was significantly improved in hearts of Lcn2-KO mice, under both standard chow and high fat diet conditions. The heart function before and after I/R injury (20-min of global ischemia followed by 60-min of reperfusion) was assessed using the Langendorff perfusion system. Compared with WT littermates, hearts from Lcn2-KO mice showed improved functional recovery and reduced infarct size following I/R. These phenomena can be observed in mice under both standard chow and high fat feeding conditions. Under baseline condition, the mitochondrial function of hearts from Lcn2-KO mice was significantly enhanced, as demonstrated by biochemical analysis of respiratory chain activity, markers of biogenesis and oxidative stress, as well as electron microscopic investigation of the mitochondrial ultrastructure. Acute or chronic administration of lipocalin-2 impaired cardiac functional recovery to I/R and dampened the mitochondrial function in hearts of Lcn2-KO mice. These effects were associated with an extensive modification of the fatty acyl chain compositions of intracellular phospholipids. In particular, lipocalin-2 facilitated the redistribution of linoleic acid (C18:2) among different types of phospholipid, including cardiolipin, which is exclusively located in the mitochondria inner membrane. The direct effects of lipocalin-2 on both H9c2 and NCM cells were also examined. TUNEL assay and flow cytometry analysis demonstrated that lipocalin-2 treatment promoted apoptosis in cardiomyocytes. Lipocalin-2 induced an early phase of phosphatidylserine exposure, followed by Bax-translocation and caspase-3 cleavage. The results collectively suggested that lipocalin-2 initiated the intrinsic mitochondria-mediated apoptotic pathway. In the hearts of Lcn2-KO mice, significantly reduced number of apoptotic cells was observed after I/R injury. In conclusion, lacking of lipocalin-2 improved heart function recovery during I/R injury via mitochondrial function restoration, phospholipids remodeling, and inhibition of cardiomyocytes apoptosis.
published_or_final_version
Pharmacology and Pharmacy
Doctoral
Doctor of Philosophy
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Ueno, Linda Massako. "Effects of aging and regular exercise upon baroreflex sensitivity and cardiac autonomic activities". Kyoto University, 2003. http://hdl.handle.net/2433/148937.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第10300号
人博第187号
14||151(吉田南総合図書館)
新制||人||46(附属図書館)
UT51-2003-H721
京都大学大学院人間・環境学研究科文化・地域環境学専攻
(主査)教授 森谷 敏夫, 教授 中村 榮太郎, 教授 津田 謹輔
学位規則第4条第1項該当
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Amano, Masari. "Effects of exercise training, aging, gender and mental stress upon cardiac autonomic nervous function". Kyoto University, 2003. http://hdl.handle.net/2433/148936.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第10299号
人博第186号
14||150(吉田南総合図書館)
新制||人||45(附属図書館)
UT51-2003-H720
京都大学大学院人間・環境学研究科文化・地域環境学専攻
(主査)教授 森谷 敏夫, 教授 津田 謹輔, 教授 田口 貞善
学位規則第4条第1項該当
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Ramsey, Michael Wiechmann. "Effects of head-up tilt on mean arterial pressure, heart rate, and regional cardiac output distribution in aging rats". Texas A&M University, 2005. http://hdl.handle.net/1969.1/3094.

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Many senescent individuals demonstrate an inability to regulate mean arterial pressure (MAP) in response to standing or head-up tilt; however, whether this aging effect is the result of depressed cardiac function or an inability to reduce peripheral vascular conductance remains unknown. Therefore, the purpose of this research was to investigate the effects of aging on MAP, heart rate (HR), regional blood flow (via radioactive-microspheres), and vascular conductance during head-up tilt in conscious young (4 mo; n=12) and old (24 mo; n=10) male Fischer-344 rats. Heart rate and MAP were measured continuously during normal posture and during 10 minutes of head-up tilt. Blood flow was determined during normal posture and at the end of 10 minutes of head-up tilt. Young rats increased MAP significantly at the onset of head-up tilt and generally maintained the increase in MAP for the duration of head-up tilt, while aged rats showed a significant reduction in MAP after 10 minutes of head-up tilt. In the normal posture, aged rats demonstrated lower blood flow to splanchnic, bone, renal, and skin tissues versus young rats. With tilt there were decreases in blood flow to skin, bone, and hind-limb in both age groups and in fat, splanchnic, reproductive, and renal tissues in the young. Bone blood flow was attenuated with age across both conditions in hind foot, distal femur, femur marrow, and proximal and distal tibia. Head-up tilt caused a decrease in blood flow across both age groups in all bones sampled with the exception of the hind foot. These results provide evidence that the initial maintenance of MAP in aged rats during head-up tilt occurs through decreased regional blood flow and vascular conductance, and that the fall in pressure is not attributable to an increase in tissue blood flow and vascular conductance. Therefore, reductions in arterial pressure during headup tilt are likely a result of an old age-induced reduction in cardiac performance. In addition, this is the first study to demonstrate a decreased bone vascular conductance in both young and old rats during head-up tilt.
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Anstine, Lindsey J. "Valve cell dynamics in developing, mature, and aging heart valves". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1478692972995079.

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LODRINI, ALESSANDRA MARIA. "Cellular senescence and failure in human and animal cardiac myocytes". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/301783.

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Nel corso del mio dottorato sono stata coinvolta principalmente in due progetti con lo scopo di studiare la disfunzione cardiaca indotta da invecchiamento o chemioterapia. Il primo studio aveva lo scopo di riprodurre e caratterizzare i meccanismi dell’invecchiamento utilizzando cardiomiociti (CMs) da cellule staminali pluripotenti indotte umane (hiPSCs) e inoltre testare terapie cardioprotettive, come gli esosomi (Exo) da cellule progenitrici cardiache (CPCs). L’invecchiamento cardiaco coinvolge rimodellamenti a livello dei singoli CMs che predispongono allo scompenso cardiaco e la cui incidenza aumenta con l’avanzare dell’età. Curiosamente, fino ad ora non è stato ancora sviluppato un modello di invecchiamento cardiaco umano. Abbiamo riprogrammato CPCs umane ad iPSC e successivamente le abbiamo differenziate in CMs. Un fenotipo simile alla senescenza (SenCMs) è stato indotto con un breve trattamento (3 ore) con doxorubicina (Dox) a concentrazioni sub-letali (0.2 µM). 24 ore dopo il trattamento, alcuni SenCMs sono stati esposti ad Exo (~2·10^3 particelle/cellula) isolati dal medium di coltura delle CPCs. Il trattamento con Dox induce senescenza, come confermato dall’attivazione di p21 e dalla maggiore positività a SA-β-gal in confronto ai controlli (cCMs). Analisi biochimiche hanno rivelato la presenza di stress ossidativo e un potenziale di membrana mitocondriale depolarizzato nei SenCMs, con una ridotta produzione di ATP dai mitocondri. I SenCMs hanno anche difetti nel calcium handling e un QTc prolungato a causa dell’aumento di INaL. Questi effetti sono mitigati dal trattamento con Exo. Complessivamente, i SenCMs ricapitolano il fenotipo dei CMs invecchiati in termini di markers di senescenza e proprietà elettriche e metaboliche. Inoltre, l’esposizione ad Exo prodotti da CPCs limita molte delle anomalie cardiache indotte dall’invecchiamento. Il secondo studio mirava a valutare la disfunzione cardiaca causata dalla somministrazione in combinazione di Dox e Trastuzumab (Trz) in miociti cardiaci di ratto. Il trattamento combinato con Dox e Trz in pazienti con cancro al seno è limitato a causa della cardiotossicità, che si manifesta con disfunzione contrattile ed aritmie. Il ruolo specifico dei due agenti nella cardiotossicità causata dalla terapia combinata è però non ancora del tutto chiarito. I ratti hanno ricevuto 6 dosi di Dox, Trz o entrambi in maniera sequenziale. La disfunzione del ventricolo sinistro (LV) mediata da Dox era aggravata dalla somministrazione di Trz. Il trattamento con Dox, ma non con Trz, induceva danno ai tubuli T, prolungamento della durata del potenziale d’azione (APD), aumento dell’incidenza di post-depolarizzazioni tardive (DADs), decadimenti dei transienti di Ca2+ più lenti e la fuoriuscita di Ca2+ dal reticolo in Ca2+ sparks o Ca2+ embers. Il trattamento in combinazione esacerbava queste anomalie. Trz, ma non Dox, riduceva l’ampiezza dei transienti di Ca2+ e il contenuto di Ca2+ nel reticolo sarcoplasmatico (SR). Entrambi gli agenti aumentavano le onde di Ca2+ spontanee e diminuivano l’espressione di SERCA. Questi risultati suggeriscono che Dox, ma non Trz, potrebbe causare danno ai tubuli T in vivo e, inoltre, indurre cambiamenti nei parametri elettrici e nel Ca2+-handling. Mentre Dox induceva cambiamenti reversibili nei parametri elettrofisiologici, la successiva somministrazione di Trz impediva il rescue. Questi risultati illustrano il ruolo specifico di Dox e Trz e il loro ruolo nella cardiotossicità.
During my PhD I was involved mainly in two research projects aimed to study myocardial dysfunction induced by aging or chemotherapy. The first study aimed to reproduce and characterize mechanisms involved in aging using cardiomyocytes (CMs) from human induced pluripotent stem cells (hiPSCs), and to test cardioprotective therapies, like cardiac progenitor cell (CPC)-derived exosomes (Exo). Aging of the heart involves adverse remodeling in CMs which results in heart failure with incidence that increases with age. Interestingly, till now we lacked a human model of cardiac aging. We reprogrammed CPCs into hiPSCs and subsequently differentiated in hiPSC-derived CMs. A senescence-like phenotype (SenCMs) was induced by short exposure (3 hours) to doxorubicin (Dox) at sub-lethal concentration (0.2 µM). 24h following DOX treatment, SenCMs were exposed to Exo (~2·103 particles/cell) collected from culture media of CPCs by ultracentrifugation. Dox treatment induced senescence, as confirmed by activation of p21 and increased SA-β-gal positivity compared to control CMs (cCMs). Biochemical analysis revealed presence of oxidative stress and a depolarized mitochondrial membrane potential due to the treatment, which resulted in decreased ATP production by mitochondria. SenCMs also showed impaired calcium handling and prolonged QTc vs. cCMs due to upregulation of INaL. These effects were mitigated by exposure to Exo. Overall, SenCMs recapitulate the phenotype of aged CMs in terms of senescence markers and electrical and metabolic properties. Additionally, exposure to CPC-derived Exo limited age-related cardiac anomalies. The second study aimed to study the cardiac dysfunction dependent on the combined administration of Dox and trastuzumab (Trz) through evaluation of cardiac performance, T-tubule organization, and electrophysiological changes in cardiac myocytes from an in-vivo rat model. Combined treatment with Dox and Trz in patients with HER2-positive cancer is limited by cardiotoxicity, as manifested by contractile dysfunction and arrhythmia. The respective roles of the two agents in the cardiotoxicity of the combined therapy are incompletely understood. Adult rats received 6 doses of either Dox or Trz, or the two agents sequentially. Dox-mediated left ventricular (LV) dysfunction was aggravated by Trz administration. Dox treatment, but not Trz, induced T-tubule disarray. Moreover, Dox, but not Trz monotherapy, induced prolonged action potential duration (APD), increased incidence of delayed afterdepolarizations (DADs) and beat-to-beat variability of repolarization (BVR), and slower Ca2+ transient decay. Although APD, DADs, BVR and Ca2+ transient decay recovered over time after the cessation of Dox treatment, subsequent Trz administration exacerbated these abnormalities. Trz, but not Dox, reduced Ca2+ transient amplitude and SR Ca2+ content. Both agents increased Ca2+ waves and downregulated SERCA. Finally, Dox increased resting Ca2+ waves, Ca2+ spark frequency, spark-mediated sarcoplasmic reticulum (SR) leak, and long-lasting Ca2+ release events (so-called Ca2+ “embers”). These results suggest that Dox, but not Trz, may cause T-tubule disarray in cardiac myocytes in vivo while also inducing overall larger changes in electrical parameters and intracellular Ca2+ handling. While Dox-induced changes in electrical parameters are reversible, subsequent Trz administration prevents their recovery. These findings illustrate the specific roles of Dox and Trz, and their interactions in cardiotoxicity and arrhythmogenicity.
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ZENI, FILIPPO. "Circulating levels of soluble Receptor for Advanced Glycation End-products (sRAGE) decrease with aging and may predict age-related cardiac remodeling". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/170797.

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Background: L'invecchiamento è un inevitabile fattore di rischio in età avanzata che può influenzare l'insorgenza e la progressione di diverse malattie. Infatti, l'elevata incidenza di malattie cardiovascolari negli anziani è principalmente imputabile al fisiologico rimodellamento cardiaco associato ad un invecchiamento intrinseco. RAGE è un recettore capace di legare diverse molecole e coinvolto in molte malattie legate all'età. La sua isoforma solubile (sRAGE) agisce come un recettore decoy bloccando l'attivazione del recettore legato alla membrana, e suoi livelli circolanti sono stati trovati alterati in diverse patologie croniche ed acute. Il ruolo delle isoforme di RAGE durante l’invecchiamento e, in particolare, nell’invecchiamento cardiaco, non è mai stato studiato. Inoltre, la scoperta di biomarcatori affidabili in grado di valutare lo stato di salute individuale dei soggetti ha importanti applicazioni nel campo della prevenzione, della diagnosi e della gestione della malattia. In tale contesto, lo scopo di questo studio è stato quello di verificare se sRAGE sia un biomarcatore di invecchiamento e di rimodellamento cardiaco legato all’invecchiamento, e valutare il contributo delle isoforme RAGE nell’invecchiamento cardiaco. Risultati: È stato collezionato il siero di soggetti sani, di entrambi i sessi, di età compresa tra i 20 e i 92 anni ed i livelli di sRAGE sono stati valutati mediante ELISA. Abbiamo trovato una significativa diminuzione di sRAGE circolante nei maschi, mentre solo una tendenza nelle femmine. Di conseguenza, abbiamo osservato una forte correlazione di sRAGE con l'età cronologica nei soggetti maschi, ma non nei soggetti di sesso femminile. Topi maschi e femmine a diverse età (2.5-12-22 mesi, Giovani, adulti (MA) e Vecchi, rispettivamente) sono stati sottoposti a ecocardiografia 2D per determinare le dimensioni e la funzione del ventricolo sinistro (LV) durante l'invecchiamento. sRAGE serico diminuisce in maniera simile in entrambi i sessi tra il gruppo Giovani e il gruppo MA, e correla inversamente con le dimensioni e la funzione del LV, in particolare nei machi. Nessuna quantità rilevabile di RAGE è stata trovata nei lisati proteici del LV a tutte le età. Topi Rage-/- hanno mostrato un significativo aumento dei volumi e dei diametri del LV in diastole e in sistole, ed una concomitante diminuzione della frazione di eiezione (EF) e di accorciamento (FS), rispetto agli animali Rage+/+ di pari età durante l'invecchiamento con le più forti differenze presenti tra i gruppi MA. Inoltre, topi MA Rage-/- hanno mostrato la maggiore deposizione di collagene e l’aumento dell'espressione di geni marcatori di scompenso cardiaco (BNP e Ankrd1) rispetto alla controparte Rage+/+. Al contrario, nessuna differenza in termini di dimensioni dei cardiomiociti è stata osservata a qualsiasi età tra i due genotipi. Infine, l’analisi funzionale di annotazione del microarray, basata sull'interazione fra età-genotipo, ha rivelato che la mancanza cronica di RAGE influenza l'espressione di geni associati alla funzione contrattile, al processo di presentazione dell'antigene e dell'immunità adattativa, del pathway dell’insulina, della morte cellulare e dell’apoptosi. Abbiamo anche trovato una correlazione tra i volumi e i diametri del LV in diastole e in sistole e i geni differenzialmente espressi, i quali sono coinvolti in diversi processi come la contrazione muscolare, la fibrosi e la regolazione dell'apoptosi. Conclusioni: I nostri risultati indicano che sRAGE è un biomarcatore serico di invecchiamento sano e di rimodellamento cardiaco legato all'età, preferenzialmente nei maschi. L'assenza di RAGE aggrava l’avverso rimodellamento cardiaco legato all'età. Proponiamo che, tra le isoforme RAGE, sRAGE possa giocare un ruolo fondamentale nell’invecchiamento cardiaco.
Background: Aging is an unavoidable risk factor in later life that can influence the onset and progression of many diseases. In fact, the high incidence of cardiovascular diseases in the elderly is mainly attributable to cardiac remodelling associated to physiological intrinsic aging. RAGE is a multi-ligand receptor involved in many age-related disorders. Its soluble isoform (sRAGE) acts as a decoy receptor being able to block the activation of the membrane-bound receptor, and its circulation levels have been found altered in several chronic and acute pathologies. The role of RAGE isoforms in aging and, in particular, cardiac senescence has never been investigated. Moreover, the finding of reliable biomarkers able to assess individual health status of subjects has important applications in prevention, diagnosis, and disease management. In this context, the aim of this study was to ascertain whether sRAGE is a biomarker of aging and age-related cardiac remodelling, and evaluate the contribution of RAGE isoforms to cardiac aging. Results: Serum of male and female from 20 to 92 years old healthy subjects was collected and sRAGE levels were evaluated by ELISA. We found a significant decrease of circulating sRAGE in males while only a trend in females. Accordingly, we observed a strong correlation of sRAGE with chronological age in male but not in female subjects. Male and female mice at different age (2.5-12-22-months, Young, Middle Age (MA) and Old, respectively) undergone 2D-echocardiography to determine the left ventricle (LV) dimensions and function during aging. Serum sRAGE similarly declines from the Young to the MA group in both sexes, and inversely correlate with LV dimensions and function, preferentially in males. No detectable amount of RAGE protein was found in LV at all ages. Rage-/- mice displayed a significant increase of LV volumes and diameters in diastole and systole, and a concomitant decrease in ejection fraction (EF) and fractional shortening (FS), compared to age-matched wt animals during aging with the strongest differences present between the MA groups. Moreover, MA Rage-/- mice exhibited higher deposition of collagen and expression of heart failure marker genes (BNP and Ankrd1) in respect to the wt counterpart. Conversely, no differences in cardiomyocytes size were observed at any age between the two genotypes. Finally, microarray functional annotation analysis based on the interaction between age-genotype revealed that the chronic lack of RAGE affected the expression of genes associated to contractile fibre function, antigen presenting process and adaptive immunity, insulin pathway, cell death and apoptosis. We also found a correlation between LV volumes and diameters in diastole and systole and differentially expressed genes involved in several processes like muscle contraction, fibrosis, wound healing and regulation of apoptosis. Conclusions: Our results indicate that sRAGE is a serum biomarker of healthy aging and age-related cardiac remodeling, preferentially in males. The absence of RAGE in mice exacerbates adverse cardiac remodeling with age. We propose that, among RAGE isoforms, sRAGE may play a pivotal role in cardiac senescence.
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Sheikh, Hajer Nisar. "Tropomyosin Phosphorylation in Cardiac Health and Disease". University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1242913472.

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Książki na temat "Aging cardiac"

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United States. Congress. Senate. Special Committee on Aging. Pacemakers revisited: A saga of benign neglect : hearing before the Special Committee on Aging, United States Senate, Ninety-ninth Congres, first session, Washington, DC, May 10, 1985. Washington: U.S. G.P.O., 1986.

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Office, General Accounting. Medicare's policies and prospective payment rates for cardiac pacemaker surgeries need review and revision: Report to the Chairman, Special Committee on Aging, United States Senate. Washington, D.C: U.S. General Accounting Office, 1985.

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Fried, Robert, i Richard Carlton. Omega-Factor: Promoting Health, Preventing Premature Aging and Reducing the Risk of Sudden Cardiac Death. Taylor & Francis Group, 2023.

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Fried, Robert, i Richard Carlton. Omega-Factor: Promoting Health, Preventing Premature Aging and Reducing the Risk of Sudden Cardiac Death. Taylor & Francis Group, 2023.

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Fried, Robert, i Richard Carlton. Omega-Factor: Promoting Health, Preventing Premature Aging and Reducing the Risk of Sudden Cardiac Death. Taylor & Francis Group, 2023.

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Fried, Robert, i Richard Carlton. Omega-Factor: Promoting Health, Preventing Premature Aging and Reducing the Risk of Sudden Cardiac Death. Taylor & Francis Group, 2023.

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Fried, Robert, i Richard Carlton. Omega-Factor: Promoting Health, Preventing Premature Aging and Reducing the Risk of Sudden Cardiac Death. Taylor & Francis Group, 2023.

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Cardiothoracic surgery in the elderly. New York: Springer, 2011.

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Cardiothoracic surgery in the elderly. New York: Springer, 2011.

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Katlic, Mark R. Cardiothoracic Surgery in the Elderly. Springer New York, 2014.

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Części książek na temat "Aging cardiac"

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Dai, Dao-Fu, Robert J. Wessells, Rolf Bodmer i Peter S. Rabinovitch. "Cardiac Aging". W The Comparative Biology of Aging, 259–86. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3465-6_12.

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Chantler, Paul D., i Edward G. Lakatta. "Heart and Arterial Aging". W Cardiac Adaptations, 111–44. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5203-4_7.

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Fenton, Richard A., Mojca Lorbar i James G. Dobson. "Adenosine and Cardiac Aging". W Developments in Cardiovascular Medicine, 143–58. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5603-9_9.

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Cesselli, Daniela, Federica D’Aurizio, Patrizia Marcon, Natascha Bergamin, Carlo Alberto Beltrami i Antonio Paolo Beltrami. "Cardiac Stem Cell Senescence". W Stem Cells and Aging, 81–97. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-317-6_7.

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Jugdutt, Bodh I., i Anwar Jelani. "Aging and Markers of Adverse Remodeling After Myocardial Infarction". W Cardiac Remodeling, 487–512. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_27.

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Knowlton, Anne A. "Estrogen, Cardiac Protection and Aging". W Integrative Biology of Women’s Health, 157–74. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8630-5_9.

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Bolli, Roberto, i Piero Anversa. "Stem Cells and Cardiac Aging". W Cardiovascular Regeneration and Stem Cell Therapy, 171–81. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988909.ch18.

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Seara, Fernando A. C., Leonardo Maciel, Tais Hanae Kasai-Brunswick, Jose H. M. Nascimento i Antonio C. Campos-de-Carvalho. "Extracellular Vesicles and Cardiac Aging". W Advances in Experimental Medicine and Biology, 33–56. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-1443-2_3.

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Adams, Kent J. "Cardiac Rehabilitation and Exercise". W Handbook of Clinical Nutrition and Aging, 419–36. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-391-0_17.

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Zhao, Cuimei, Guoping Li i Jin Li. "Non-coding RNAs and Cardiac Aging". W Advances in Experimental Medicine and Biology, 247–58. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1671-9_14.

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Streszczenia konferencji na temat "Aging cardiac"

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Lai, Yi-Homg, Yi Yuan, Yu-Xian Liang i Jia-Han Yu. "Comparison of aging effect between cardiac complexity and baroreceptor sensitivity". W 2021 International Conference on Information Technology and Biomedical Engineering (ICITBE). IEEE, 2021. http://dx.doi.org/10.1109/icitbe54178.2021.00068.

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Dimitrakopoulos, Georgios N., Konstantina Dimitrakopoulou, Ioannis A. Maraziotis, Kyriakos Sgarbas i Anastasios Bezerianos. "Supervised method for construction of microRNA-mRNA networks: Application in cardiac tissue aging dataset". W 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6943593.

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Starc, V., i T. T. Schlegel. "The effect of aging and cardiac disease on that portion of QT interval variability that is independent of Heart Rate Variability". W 2008 35th Annual Computers in Cardiology Conference. IEEE, 2008. http://dx.doi.org/10.1109/cic.2008.4749041.

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Heyne, E., R. Musleh, L. G. Koch, S. L. Britton, T. Doenst i M. Schwarzer. "Aging Is Not Related to Increased Cardiac Mitochondrial ROS Production in a Rat Model of Genetically Determined High or Low Exercise Capacity". W 51st Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742786.

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Zhingre Sanchez, Jorge D., Emma A. Schinstock, Michael G. Bateman i Paul A. Iaizzo. "The Development and Testing of a Fixation Apparatus for Inducing the Coaptation of the Cardiac Atrioventricular Valves". W 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3298.

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As the prevalence of mitral and tricuspid valvular disease continues to grow with the aging population [1,2], there is a growing critical need to treat high mortality risk patients using minimally invasive and/or non-surgical percutaneous procedures. However, these transcatheter procedures, especially those aimed at repairing or replacing the mitral and tricuspid valves, are mostly still in development and/or early clinical testing. Catheter delivery, prosthesis fixation, and/or demonstrating device efficacy are major challenges currently being addressed [3,4]. Although in situ animal models can assess catheter systems with clinical imaging, direct visualization of tissue-device interactions in real human heart anatomies are desired. In vitro delivery and implantations of valvular prototypes in human heart specimens can be instrumental for accurate device testing and gaining important design insights. Such investigations can be performed on a pulsatile flow apparatus, utilizing perfusion fixed human hearts with mitral and/or tricuspid valves eliciting coaptation and relative function. The employment of endoscopic cameras provides direct visualization and can be coupled with echocardiography, providing novel insights relative to these transcatheter devices in a dynamic environment. However, these investigative approaches require appropriately fixed human heart specimens that will allow for dynamic valve movement. This study discusses the design, construction, and implementation of a novel fixation apparatus to promote the coaptation of the mitral and tricuspid valves in swine and fresh human heart specimen.
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Men, Jing, Airong Li, Zhiwen Yang, Jixu Yu, Rudolph Tanzi i Chao Zhou. "Heartbeat recovery after cardiac arrest and association of maximum pace-able heart rate with aging via optogenetic pacing and OCM imaging of Drosophila (Conference Presentation)". W Optical Coherence Tomography and Coherence Domain Optical Methods in Biomedicine XXIV, redaktorzy Joseph A. Izatt i James G. Fujimoto. SPIE, 2020. http://dx.doi.org/10.1117/12.2549151.

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Coelho, Patricia, Ana Rodrigues, Maria Vieira, Joana Liberal i Francisco Rodrigues. "The influence of Monfortinho thermal waters on human health". W III SEVEN INTERNATIONAL MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/seveniiimulti2023-241.

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The thermal waters have numerous medicinal advantages, highlighting their anti-inflammatory and immuno-modulatory properties, useful in the treatment of various pathologies of the respiratory, gastrointestinal, muscoloskeletal, skin, among others (Prandelli et al, 2013; Zajac, 2021; Franz et al, 2021). Several studies demonstrate the importance that this type of water presents in cardiovascular pathologies, namely in its use as protectors of the most important risk factors for the triggering of these pathologies (Laukkanen et al, 2015; Laukkanen et al, 2018). Some authors report that balneotherapy is associated with normalization of lipid profile parameters (Heinonen &; Laukkanen, 2018; Esperland et al, 2022) as well as reducing susceptibility to viral infections (Kunutsor et al., 2017; Kunutsor et al., 2021). There is also the component associated with skin and the delay of aging, as demonstrated in studies in the area (Vaz et al, 2022). Of course, there are studies that demonstrate the possibility of the existence of some intercurrences, with special incidence in the cardiac area and in the psychiatric area - note, however, that the studies referred to point to the pre-existence of pathology (Zaccardi et al, 2017; Laukkanen et al 2018).
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Duvall, Julia, Rachael Granberry, Lucy E. Dunne, Brad Holschuh, Christopher Johnson, Kevin Kelly, Bruce Johnson i Michael Joyner. "The Design and Development of Active Compression Garments for Orthostatic Intolerance". W 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3480.

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Current compression garments are often made from a spandex-type elastic material with static levels of compression and can become uncomfortable and difficult to don/doff [1]. This limits their usability, especially for unhealthy or aging populations. The only current alternative to elastic compression stockings are inflatable compression sleeves that are controllable, but highly immobile and must be tethered to an inflation source [2]. Neither design offers a solution that is simultaneously low profile, mobile, and controllable. Here we present the design and development of compression garments with embedded shape-changing materials that can produce controllable compression without the need for a bulky inflation system. This active materials approach enables dynamic control over the degree, timing and location of compression, and allows for graded, synchronized, pulsed, and peristaltic compression patterns, which provide the medical benefit of moving fluid in the body [2]. Such a design combines the best features of both elastic and inflatable compression garments: a slim, low-profile form factor that is easy to don/doff and provides dynamic control. Shape memory alloy (SMA) coil actuators, as described by Holschuh et al., [3] have the ability to apply compressive forces to the body when paired with passive textiles and wrapped circumferentially around the body. These actuators are engineered to contract when heated, creating controllable forces and displacements that are modulated through an applied current. SMA compression garments (SMA-CG) have important applications, from consumer uses to clinical interventions, including: augmenting venous return for conditions of orthostatic intolerance (e.g., postural orthostatic tachycardia syndrome (POTS)); cardiac rehabilitation in heart failure patients; lymphedema venous insufficiency; reducing deep vein thrombosis (DVT) risk; sports performance; and countermeasures for flight or space flight. While the potential uses for this technology are broad, the basic design is similar across many conditions. Key research areas include: 1) identifying and addressing design considerations relevant to prototype development of SMA-CG; 2) determining the compression thresholds needed to dynamically oppose orthostatic changes; and 3) evaluating the effectiveness of the prototypes for augmented venous return by synchronizing compression during cardiac diastole. Here, we focus on the first question: design of SMA-CG prototypes.
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Fira, Monica, Liviu Goras, Victor-Andrei Maiorescu i Mihaela Catalina Luca. "Compressed Sensing and Classification of Cardiac Beats using Patient Specific Dictionaries". W 2nd International Conference on Information and Communication Technologies for Ageing Well and e-Health. SCITEPRESS - Science and and Technology Publications, 2016. http://dx.doi.org/10.5220/0005793401730179.

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Seong, Jaehoon, Ajay K. Wakhloo i Baruch B. Lieber. "Morphological Age-Depended Development of the Human Carotid Bifurcation". W ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2545.

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Abstract The development, significance and function of the human carotid sinus are not clearly understood. The arterial wall of carotid sinus is densely enervated and it contains baroreceptive neural terminals. It has been hypothesized that the dilation, which may involve all vessels of the carotid bifurcation, serves to support pressure sensing. Another hypothesis based on phenomenological observations presumes that the function of the sinus is to slow the blood flow and reduce the pulsatility in order to protect the brain (1). Yet another postulate states that the sinus is an ontogenetic or phylogenic residual. More recently, in vitro and computational models have been used to investigate carotid hemodynamics. Complex flow patterns have been found in the carotid sinus. These patterns have been implicated in the carotid bulb heterogeneity and subsequent development of atherosclerosis at this site. However, long term development of this unique sinus morphology has not been investigated. It is of both fundamental and clinical interest to form an understanding of the hemodynamics and developmental forces that play a role in remodeling of the carotid bifurcation and maturation of the sinus. This understanding can lead to better prognostication and therapy of carotid disease. Therefore, a study of the morphological development of the human carotid bulb was initiated. Carotid bulbs from various human developmental stages were evaluated to test the hypothesis that morphology of the sinus reflects an acclimated change in response to alterations in cerebral blood supply with aging. This acclimation attempts to diminish hydraulic losses in the carotid bifurcation through reduced flow disturbances. Under basal conditions, a high level of blood supply to the brain is maintained that consumes about 15% of cardiac output. Furthermore, it may protect the brain from highly pulsatile blood flow conditions and/or the sinus wall from high shear stress. Initially, we analyzed the sinus morphology and the angle of the carotid bifurcation in four human developmental stages, namely newborn, pediatric, adolescent and adult patients (Groups I, II, III, and IV, respectively). The analysis was performed using biplane digital subtraction angiograms to characterize changes that occur as the brain matures.
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Raporty organizacyjne na temat "Aging cardiac"

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Slaughter-Acey, Jaime, Kathryn Behrens, Amy M. Claussen, Timothy Usset, Carrie Neerland, Sameerah Bilal-Roby, Huda Bashir i in. Social and Structural Determinants of Maternal Morbidity and Mortality: An Evidence Map. Agency for Healthcare Research and Quality (AHRQ), grudzień 2023. http://dx.doi.org/10.23970/ahrqepccer264.

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Objective. The purpose was to review available evidence of risk factors associated with maternal morbidity and mortality in the United States during the prenatal and postpartum periods to inform a National Institutes of Health Pathways to Prevention Workshop: Identifying Risks and Interventions to Optimize Postpartum Health, held November 29–December 1, 2022. Data sources. We searched MEDLINE®, CINAHL®, and the Social Sciences Citation Index through November 2022. Review methods. We searched for observational studies examining exposures related to social and structural determinants of health and at least one health or healthcare-related outcome for pregnant and birthing people. We extracted basic study information and grouped studies by social and structural determinants of health domains and maternal outcomes. We prioritized studies according to study design and rigor of analytic approaches to address selection bias based on the ROBINS-E. We summarize all included studies and provide additional descriptions of direction of association between potential risk exposures and outcomes. Results. We identified 8,378 unique references, with 118 included studies reporting social and structural determinants of health associated with maternal health outcomes. Studies covered risk factors broadly, including identity and discrimination, socioeconomic, violence, trauma, psychological stress, structural/institutional, rural/urban, environment, comorbidities, hospital, and healthcare use factors. However, the risk factors we identified represent only a subset of potential social and structural determinants of interest. We found an unexpectedly large volume of research on violence and trauma relative to other potential exposures of interest for pregnant people. Outcome domains included maternal mortality, severe maternal morbidity, hypertensive disorders, gestational diabetes, cardio/metabolic disorders, weathering (the physiological effect of premature aging caused by chronic stressful experiences), depression, other mental health or substance use disorders, and cost/healthcare use outcomes. Depression/other mental health outcomes represented a large proportion of medical outcomes captured. Risk of bias was high, and rarely did studies report the excess risk attributable to a specific exposure. Conclusions. Identifying risk factors pregnant and birthing people face is vitally important. Limited depth and quality of available research within each social and structural determinant of health impeded our ability to outline specific pathways, including risk factor interdependence. While more recently published literature showed a trend toward increased rigor, future research can emphasize techniques that estimate the causal impacts of risk factors. Improved reporting in studies, along with organized and curated catalogues of maternal health exposures and their presumed mechanisms, would make it easier to examine exposures in the future. In the longer term, the field could be advanced by datasets designed to more fully capture the data required to robustly examine racism and other social and structural determinants of health, in combination with their intersections and feedback loops with other biologic/medical risk factors.
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