Gotowe bibliografie tematyczne / Cardiac hypertrophy

Gotowa bibliografia na temat „Cardiac hypertrophy”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 września 2023

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych

Wybierz rodzaj źródła:

Spis treści

Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Cardiac hypertrophy”.

Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.

Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.

Artykuły w czasopismach na temat "Cardiac hypertrophy"

1

Li, Wei-ming, Yi-fan Zhao, Guo-fu Zhu, Wen-hui Peng, Meng-yun Zhu, Xue-jing Yu, Wei Chen, Da-chun Xu i Ya-wei Xu. "Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload". Clinical Science 131, nr 2 (23.12.2016): 141–54. http://dx.doi.org/10.1042/cs20160664.

Pełny tekst źródła
Streszczenie:
Pathological cardiac hypertrophy is an independent risk factor of heart failure. However, we still lack effective methods to reverse cardiac hypertrophy. DUSP12 is a member of the dual specific phosphatase (DUSP) family, which is characterized by its DUSP activity to dephosphorylate both tyrosine and serine/threonine residues on one substrate. Some DUSPs have been identified as being involved in the regulation of cardiac hypertrophy. However, the role of DUSP12 during pathological cardiac hypertrophy is still unclear. In the present study, we observed a significant decrease in DUSP12 expression in hypertrophic hearts and cardiomyocytes. Using a genetic loss-of-function murine model, we demonstrated that DUSP12 deficiency apparently aggravated pressure overload-induced cardiac hypertrophy and fibrosis as well as impaired cardiac function, whereas cardiac-specific overexpression of DUPS12 was capable of reversing this hypertrophic and fibrotic phenotype and improving contractile function. Furthermore, we demonstrated that JNK1/2 activity but neither ERK1/2 nor p38 activity was increased in the DUSP12 deficient group and decreased in the DUSP12 overexpression group both in vitro and in vivo under hypertrophic stress conditions. Pharmacological inhibition of JNK1/2 activity (SP600125) is capable of reversing the hypertrophic phenotype in DUSP12 knockout (KO) mice. DUSP12 protects against pathological cardiac hypertrophy and related pathologies. This regulatory role of DUSP12 is primarily through c-Jun N-terminal kinase (JNK) inhibition. DUSP12 could be a promising therapeutic target of pathological cardiac hypertrophy. DUSP12 is down-regulated in hypertrophic hearts. An absence of DUSP12 aggravated cardiac hypertrophy, whereas cardiomyocyte-specific DUSP12 overexpression can alleviate this hypertrophic phenotype with improved cardiac function. Further study demonstrated that DUSP12 inhibited JNK activity to attenuate pathological cardiac hypertrophy.
Style APA, Harvard, Vancouver, ISO itp.
2

Wehbe, Nadine, Suzanne Nasser, Gianfranco Pintus, Adnan Badran, Ali Eid i Elias Baydoun. "MicroRNAs in Cardiac Hypertrophy". International Journal of Molecular Sciences 20, nr 19 (23.09.2019): 4714. http://dx.doi.org/10.3390/ijms20194714.

Pełny tekst źródła
Streszczenie:
Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.
Style APA, Harvard, Vancouver, ISO itp.
3

Strøm, Claes C., Mogens Kruhøffer, Steen Knudsen, Frank Stensgaard-Hansen, Thomas E. N. Jonassen, Torben F. Ørntoft, Stig Haunsø i Søren P. Sheikh. "Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy". Comparative and Functional Genomics 5, nr 6-7 (2004): 459–70. http://dx.doi.org/10.1002/cfg.428.

Pełny tekst źródła
Streszczenie:
Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in hypertrophic signalling. From gene expression analyses (8740 probe sets,n= 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61 genes whose altered expression had previously been reported. We identified a single common gene program underlying hypertrophic remodelling, regardless of how the hypertrophy was induced. These genes constitute the molecular basis for the existence of one main form of cardiac hypertrophy and may be useful for prediction of a common therapeutic approach. Supplementary material for this article can be found at: http://www.interscience.wiley.com/jpages/1531-6912/suppmat
Style APA, Harvard, Vancouver, ISO itp.
4

Bazgir, Farhad, Julia Nau, Saeideh Nakhaei-Rad, Ehsan Amin, Matthew J. Wolf, Jeffry J. Saucerman, Kristina Lorenz i Mohammad Reza Ahmadian. "The Microenvironment of the Pathogenesis of Cardiac Hypertrophy". Cells 12, nr 13 (4.07.2023): 1780. http://dx.doi.org/10.3390/cells12131780.

Pełny tekst źródła
Streszczenie:
Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades’ advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components.
Style APA, Harvard, Vancouver, ISO itp.
5

Zhang, Yan, Qiang Da, Siyi Cao, Ke Yan, Zhiguang Shi, Qing Miao, Chen Li i in. "HINT1 (Histidine Triad Nucleotide-Binding Protein 1) Attenuates Cardiac Hypertrophy Via Suppressing HOXA5 (Homeobox A5) Expression". Circulation 144, nr 8 (24.08.2021): 638–54. http://dx.doi.org/10.1161/circulationaha.120.051094.

Pełny tekst źródła
Streszczenie:
Background: Cardiac hypertrophy is an important prepathology of, and will ultimately lead to, heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. This study aims to elucidate the effects and mechanisms of HINT1 (histidine triad nucleotide–binding protein 1) in cardiac hypertrophy and heart failure. Methods: HINT1 was downregulated in human hypertrophic heart samples compared with nonhypertrophic samples by mass spectrometry analysis. Hint1 knockout mice were challenged with transverse aortic constriction surgery. Cardiac-specific overexpression of HINT1 mice by intravenous injection of adeno-associated virus 9 (AAV9)–encoding Hint1 under the cTnT (cardiac troponin T) promoter were subjected to transverse aortic construction. Unbiased transcriptional analyses were used to identify the downstream targets of HINT1. AAV9 bearing shRNA against Hoxa5 (homeobox A5) was administrated to investigate whether the effects of HINT1 on cardiac hypertrophy were HOXA5-dependent. RNA sequencing analysis was performed to recapitulate possible changes in transcriptome profile.Coimmunoprecipitation assays and cellular fractionation analyses were conducted to examine the mechanism by which HINT1 regulates the expression of HOXA5. Results: The reduction of HINT1 expression was observed in the hearts of hypertrophic patients and pressure overloaded–induced hypertrophic mice, respectively. In Hint1 -deficient mice, cardiac hypertrophy deteriorated after transverse aortic construction. Conversely, cardiac-specific overexpression of HINT1 alleviated cardiac hypertrophy and dysfunction. Unbiased profiler polymerase chain reaction array showed HOXA5 is 1 target for HINT1, and the cardioprotective role of HINT1 was abolished by HOXA5 knockdown in vivo. Hoxa5 was identified to affect hypertrophy through the TGF-β (transforming growth factor β) signal pathway. Mechanically, HINT1 inhibited PKCβ1 (protein kinase C β type 1) membrane translocation and phosphorylation via direct interaction, attenuating the MEK/ERK/YY1 (mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/yin yang 1) signal pathway, downregulating HOXA5 expression, and eventually attenuating cardiac hypertrophy. Conclusions: HINT1 protects against cardiac hypertrophy through suppressing HOXA5 expression. These findings indicate that HINT1 may be a potential target for therapeutic interventions in cardiac hypertrophy and heart failure.
Style APA, Harvard, Vancouver, ISO itp.
6

Lu, Peilei, Danyu Zhang, Fan Ding, Jialu Ma, Yang K. Xiang i Meimi Zhao. "Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis". Cells 12, nr 12 (19.06.2023): 1667. http://dx.doi.org/10.3390/cells12121667.

Pełny tekst źródła
Streszczenie:
Pathological cardiac hypertrophy is one of the notable causes of heart failure. Circular RNAs (circRNAs) have been studied in association with cardiac hypertrophy; however, the mechanisms by which circRNAs regulate cardiac hypertrophy remain unclear. In this study, we identified a new circRNA, named circCacna1c, in cardiac hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated with isoprenaline hydrochloride (ISO) to establish a hypertrophy model. We found that circCacna1c was upregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. Western blot and quantitative real-time polymerase chain reaction showed that silencing circCacna1c inhibited hypertrophic gene expression in ISO-induced H9c2 cells. Mechanistically, circCacna1c competitively bound to miR-29b-2-5p in a dual-luciferase reporter assay, which was downregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. MiR-29b-2-5p inhibited the nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) to control hypertrophic gene expression. After silencing circCacna1c, the expression of miR-29b-2-5p increased, which reduced hypertrophic gene expression by inhibiting NFATc1 expression. Together, these experiments indicate that circCacna1c promotes ISO-induced pathological hypertrophy through the miR-29b-2-5p/NFATc1 axis.
Style APA, Harvard, Vancouver, ISO itp.
7

Li, Yuhao, Yoshihiko Saito, Koichiro Kuwahara, Xianglu Rong, Ichiro Kishimoto, Masaki Harada, Yuichiro Adachi i in. "Guanylyl Cyclase-A Inhibits Angiotensin II Type 2 Receptor-Mediated Pro-Hypertrophic Signaling in the Heart". Endocrinology 150, nr 8 (16.04.2009): 3759–65. http://dx.doi.org/10.1210/en.2008-1353.

Pełny tekst źródła
Streszczenie:
Angiotensin II plays a key role in the development of cardiac hypertrophy. The contribution of the angiotensin II type 1 receptor (AT1) in angiotensin II-induced cardiac hypertrophy is well established, but the role of AT2 signaling remains controversial. Previously, we have shown that natriuretic peptide receptor/guanylyl cyclase-A (GCA) signaling protects the heart from hypertrophy at least in part by inhibiting AT1-mediated pro-hypertrophic signaling. Here, we investigated the role of AT2 in cardiac hypertrophy observed in mice lacking GCA. Real-time RT-PCR and immunoblotting approaches indicated that the cardiac AT2 gene was overexpressed in GCA-deficient mice. Mice lacking AT2 alone did not exhibit an abnormal cardiac phenotype. In contrast, GCA-deficiency-induced increases in heart to body weight ratio, cardiomyocyte cross-sectional area, and collagen accumulation as evidenced by van Gieson staining were attenuated when AT2 was absent. Furthermore, the up-regulated cardiac expression of hypertrophy-related genes in GCA-null animals was also suppressed. Pharmacological blockade of AT2 with PD123319 similarly attenuated cardiac hypertrophy in GCA-deficient mice. In addition, whereas the AT1 antagonist olmesartan attenuated cardiac hypertrophy in GCA-deficient mice, this treatment was without effect on cardiac hypertrophy in GCA/AT2-double null mice, notwithstanding its potent antihypertensive effect in these animals. These results suggest that the interplay of AT2 and AT1 may be important in the development of cardiac hypertrophy. Collectively, our findings support the assertion that GCA inhibits AT2-mediated pro-hypertrophic signaling in heart and offer new insights into endogenous cardioprotective mechanisms during disease pathogenesis.
Style APA, Harvard, Vancouver, ISO itp.
8

Li, Yu, Bo He, Chao Zhang, Yanji He, Tianyang Xia i Chunyu Zeng. "Naringenin Attenuates Isoprenaline-Induced Cardiac Hypertrophy by Suppressing Oxidative Stress through the AMPK/NOX2/MAPK Signaling Pathway". Nutrients 15, nr 6 (9.03.2023): 1340. http://dx.doi.org/10.3390/nu15061340.

Pełny tekst źródła
Streszczenie:
Cardiac hypertrophy is accompanied by increased myocardial oxidative stress, and whether naringenin, a natural antioxidant, is effective in the therapy of cardiac hypertrophy remains unknown. In the present study, different dosage regimens (25, 50, and 100 mg/kg/d for three weeks) of naringenin (NAR) were orally gavaged in an isoprenaline (ISO) (7.5mg/kg)-induced cardiac hypertrophic C57BL/6J mouse model. The administration of ISO led to significant cardiac hypertrophy, which was alleviated by pretreatment with naringenin in both in vivo and in vitro experiments. Naringenin inhibited ISO-induced oxidative stress, as demonstrated by the increased SOD activity, decreased MDA level and NOX2 expression, and inhibited MAPK signaling. Meanwhile, after the pretreatment with compound C (a selective AMPK inhibitor), the anti-hypertrophic and anti-oxidative stress effects of naringenin were blocked, suggesting the protective effect of naringenin on cardiac hypertrophy. Our present study indicated that naringenin attenuated ISO-induced cardiac hypertrophy by regulating the AMPK/NOX2/MAPK signaling pathway.
Style APA, Harvard, Vancouver, ISO itp.
9

Johansson, Markus, Benyapa Tangruksa, Sepideh Heydarkhan-Hagvall, Anders Jeppsson, Peter Sartipy i Jane Synnergren. "Data Mining Identifies CCN2 and THBS1 as Biomarker Candidates for Cardiac Hypertrophy". Life 12, nr 5 (12.05.2022): 726. http://dx.doi.org/10.3390/life12050726.

Pełny tekst źródła
Streszczenie:
Cardiac hypertrophy is a condition that may contribute to the development of heart failure. In this study, we compare the gene-expression patterns of our in vitro stem-cell-based cardiac hypertrophy model with the gene expression of biopsies collected from hypertrophic human hearts. Twenty-five differentially expressed genes (DEGs) from both groups were identified and the expression of selected corresponding secreted proteins were validated using ELISA and Western blot. Several biomarkers, including CCN2, THBS1, NPPA, and NPPB, were identified, which showed significant overexpressions in the hypertrophic samples in both the cardiac biopsies and in the endothelin-1-treated cells, both at gene and protein levels. The protein-interaction network analysis revealed CCN2 as a central node among the 25 overlapping DEGs, suggesting that this gene might play an important role in the development of cardiac hypertrophy. GO-enrichment analysis of the 25 DEGs revealed many biological processes associated with cardiac function and the development of cardiac hypertrophy. In conclusion, we identified important similarities between ET-1-stimulated human-stem-cell-derived cardiomyocytes and human hypertrophic cardiac tissue. Novel putative cardiac hypertrophy biomarkers were identified and validated on the protein level, lending support for further investigations to assess their potential for future clinical applications.
Style APA, Harvard, Vancouver, ISO itp.
10

Hu, Chengyun, Feibiao Dai, Jiawu Wang, Lai Jiang, Di Wang, Jie Gao, Jun Huang i in. "Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice". Oxidative Medicine and Cellular Longevity 2022 (29.01.2022): 1–12. http://dx.doi.org/10.1155/2022/5067544.

Pełny tekst źródła
Streszczenie:
A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis. Importantly, heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) pathway activation. These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure.
Style APA, Harvard, Vancouver, ISO itp.
Więcej źródeł

Rozprawy doktorskie na temat "Cardiac hypertrophy"

1

Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
2

Clarke, Samantha Jayne. "Biochemical adaptations in cardiac hypertrophy". Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395503.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
3

Schans, Veerle Anna Maria van de. "Wnt signaling and cardiac hypertrophy". [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=14684.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
4

Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy". Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.

Pełny tekst źródła
Streszczenie:
Abstract :Cardiac hypertrophy has been identified as the most important independent risk factor for cardiovascular-related morbidity and mortality and is therefore regarded as a pathological condition. Despite this, beneficial physiological forms also appear to exist, such as in response to exercise, leading to maintained or improved cardiac function. The aim of this thesis was to examine two distinct rodent models, an endurance run-trained rat, and the DOCA-salt hypertensive rat, representing physiological and pathological hypertrophy, respectively, in order to develop a better understanding of the molecular changes associated with each condition. The thesis also examined the effect of dietary supplementation of L-arginine to the pathological model, a treatment that has been shown to ameliorate/prevent many of the cardiovascular impairments. Studies examined selected candidate genes (qRT-PCR), including conventional biomarkers of hypertrophy and exploratory analysis of adenosine-related genes (given adenosine’s established regulatory and protective role in the heart, yet minimally studied in cardiac hypertrophy), and explored global transcriptomic shifts via microarrays. The hypothesis of this work was that cardiac hypertrophy lies on a continuum, with similarities existing at the cardiac transcriptional level between early (adaptive) stages of pathological hypertrophy (DOCA-salt rat) and later stages of physiological hypertrophy (endurance run-trained rat). Examination of ten biomarkers of hypertrophy (ANF, BNP, -MHC, -MHC, cardiac -actin, skeletal -actin, SERCA2, PPAR, Coll I and III) revealed that the pathological model displayed alterations in the expression of many of these molecules in line with the literature. These changes were not observed in the physiological model. This therefore reinforces the value of conventional biomarkers in delineating pathological vs. physiological hypertrophies, and reveals fundamental differences in genesis of these two forms of hypertrophy. The adenosine system (receptors and purine handling molecules) was altered in the pathological hypertrophy model as evidenced by the modulation of genes corresponding to A3AR, Ada, and Adk, with a potential shift from purine salvage towards degradation of adenosine to inosine. Furthermore, this study represents the first report of altered regulation of the nucleoside transporter ENT3 in a pathological condition. None of these changes were seen in the physiological model with only modulation of the A2aAR evident. Examination of the transcriptional response to physiological hypertrophy revealed that short (6 week) and long (12 week) training programmes resulted in different profiles, likely reflecting progression of the hypertrophy process. The short programme stimulated genes associated with the mitochondria, oxidoreductase, receptor binding and coenzymemetabolismand repressed the expression of transcripts associated with phosphorylation, catalytic activity, defence/immunity and energy pathways. Thus, initial changes observed are primarily of a metabolic and signalling nature. In contrast, the longer programme resulted in shifts in protein handling and synthesis, and genes involved in structural molecule activity, nucleotide binding and cellular homeostasis. These patterns support a progression with time from initial metabolic adaptations to longer term shifts in protein phenotype and structural adaptations, consistent with longer term changes in heart structure. Similarly, the pathologicalmodel displayed different time-dependent gene expression profiles. Overall, the pattern of changewith early (2week) treatment is suggestive of changes in intracellular signalling and increasing transcriptional capacity with the later changes (at 4 weeks) indicative of structural adaptations (intra- and extracellularly) togetherwith an inflammation response. Genes coding for calciumhandling, ion channels, and gap junctions were altered throughout themodel andmay contribute to electrical conduction defects and cardiac dysfunction. The adrenergic signalling pathway was modulated as associated signalling molecules were down-regulated. The study revealed many expected and novel changes, of which further study should focus on: calcium regulation, metabolic regulation, gap junctions, and (as might be exii pected) signalling via the adrenergic pathway, insulin-like growth factor, PI3K, and Jak/STAT. L-Arginine modulated biomarker expression in pathological hypertrophy, with stimulation of PPAR and SERCA2 with little or no effect on the adenosine-related genes. L-Arginine affected the overall transcriptional response to DOCA-salt treatment, stimulating genes involved in cell growth andmaintenance, nerve transmission, heparin and glycosaminoglycan binding, peptide binding and protein targeting, as well as the repression of genes related to apoptosis (favouring a pro-apoptotic state), intracellular organisation and biogenesis, and enzyme inhibitor activity. The beneficial effects of L-arginine in the setting of pathological hypertrophy may be due to modulation of metabolism, improving calcium handling and overall enhancing cellular functioning. This work demonstrates that cardiac hypertrophy is clearly different at the transcriptional level depending upon the aetiology. This repudiated the hypothesis of the thesis that cardiac hypertrophy lies on a continuum with similarities existing at the cardiac transcriptional level between early (adaptive) stages of pathological hypertrophy and later stages of physiological hypertrophy. Whilst some of the data was in accordance with current knowledge of these states, novel changes were also discovered, contributing to our understanding of the molecular aspects of cardiac hypertrophy.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
Full Text
Style APA, Harvard, Vancouver, ISO itp.
5

Akki, Ashwin. "Lipid overload studies in cardiac hypertrophy". Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441778.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
6

Stirparo, G. G. "DEFINITION OF TRANSCRIPTIONAL LANDSCAPE IN CARDIAC MATURATION AND CARDIAC HYPERTROPHY". Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/247064.

Pełny tekst źródła
Streszczenie:
Heart failure (HF) is a syndrome resulting from a complex genetic predisposition and multiple environmental factors: it is a leading cause of morbidity and mortality. Specific gene expression patterns are activated in the hypertrophic and failing heart and are thought to contribute to the development of HF. Many regulatory molecules are involved in the control of gene expression: among these, long non-coding RNA (lncRNA) is gaining importance for several cellular process and diseases. However, little is still known about its involvement in HF. Many functions have been attributed to lncRNAs, such as cell proliferation, apoptosis and cell invasion, indicating that they may represent a major regulatory component of the eukaryotic genome. Not surprisingly, lncRNAs have been found implicated in several aspects of cancer, and in many neuronal diseases. Despite this, and the known role of other ncRNAs, such as miRNA, in HF, the function of lncRNAs in this pathologic state has been not studied. Thus, the general hypothesis behind this project is that lncRNAs have an important role in defining gene expression re-programming in HF. Consequently, the overall scientific objective of this proposal is to study the role of lncRNAs in gene transcription regulation accompanying heart failure. To this end, we propose to use high-throughput RNA sequencing (RNA-seq) to identify lncRNAs that are modulated in cardiomyocytes during HF. In order do to this, we performed RNA-seq on cardiomyocytes isolated from mice after 1, 2, 4 and 7 days of transverse aortic constriction (TAC) and from sham-operated mice. The importance of this study lies not only in the furthering of our understanding of the pathological mechanisms leading HF, but aims to generate – in the light of recent progress in RNA-based therapeutic strategies – data that may be instrumental to the development of improved therapeutic strategies for this increasingly frequent pathology.
Style APA, Harvard, Vancouver, ISO itp.
7

Aro, J. (Jani). "Novel load-inducible factors in cardiac hypertrophy". Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212173.

Pełny tekst źródła
Streszczenie:
Abstract Cardiac hypertrophy is an adaptive response to increased cardiac workload. It is initially beneficial, since it helps to maintain cardiac output, but ultimately it is considered as an independent predictor for heart failure and sudden cardiac death. The cardiac hypertrophic response is triggered by mechanical and neurohumoral stimuli and is associated with the activation of complex changes in gene programming and intracellular signaling pathways. The purpose of this study was to investigate the expression of some novel load-induced factors i.e. melusin, thrombospondin (TSP)-1 and -4 and LIM and cysteine-rich domains protein 1 (LMCD1)/dyxin during the hypertrophic response. Melusin was expressed in cardiac tissue both in the atria and ventricles, furthermore its expression was very rapidly activated in response to multiple hypertrophic stimuli predominantly in the left atria. Melusin gene expression was activated when cultured cardiac myocytes were subjected to mechanical stretch or hypertrophic agonists such as endothelin-1 or angiotensin (Ang II). TSP-1 and TSP-4 gene expressions were rapidly activated at an early stage of pressure overload. Myocardial infarction (MI) induced the expression of both TSP-4 and TSP-1 mRNA in the heart. TSP-4 may also be an endothelial cell-specific marker of pressure overload since its expression was limited to endothelial cells in the adult heart. The expression of LMCD1/dyxin was found to be induced during the cardiac hypertrophic response and after MI. By itself, mechanical load was a critical regulator of LMCD1/dyxin gene expression. LMCD1/dyxin is a putative novel p38 mitogen-activated protein kinase (MAPK) target since adenovirus-mediated overexpression of p38 MAPK upregulated LMCD1/dyxin expression. In addition, during the Ang II-induced pressure overload p38 MAPK phosphorylation levels correlated with the early induction of LMCD1/dyxin expression. In conclusion, this study provides new information on the expression of melusin, TSP-1 and -4 and LMCD1/dyxin in the cardiac hypertrophic response. Early induction of their gene expression may represent an initial step in the adaptive and protective remodeling processes following increased workload in the heart
Tiivistelmä Sydänlihas mukautuu lisääntyneeseen kuormitukseen lihassolujen koon kasvun eli hypertrofian avulla. Pitkittyessään hypertrofinen kasvu on kuitenkin tärkeä sydämen vajaatoimintaa ja äkkikuolemaa ennakoiva riskitekijä. Hypertrofisessa vasteessa mekaaninen venytys sekä neurohumoraaliset tekijät saavat aikaan solunsisäisten signaalinvälitysreittien aktivoitumisen, mikä johtaa lisääntyneeseen geenien luentaan ja proteiinituotantoon. Väitöskirjassa tutkittiin uusien kuormitusaktivoituvien tekijöiden, melusiinin, trombospondiini (TSP) -1:n ja -4:n sekä dyksiinin ilmentymistä hypertrofisen vasteen aikana. Melusiinia ilmentyy sydämessä sekä kammioissa että eteisissä, mutta painekuormituksen myötä se aktivoituu nopeasti pääasiassa vasemmassa eteisessä. Sydänlihassolujen soluviljelymallissa melusiinin luenta lisääntyy suoraan mekaanisen venytyksen ja hypertrofisten agonistien vaikutuksesta. Painekuormitus aktivoi nopeasti myös TSP-1:n ja -4:n luentaa sydämessä. TSP-1:n ja -4:n geeniluenta lisääntyy myös kokeellisessa sydäninfarktimallissa. Lisäksi sydämessä TSP-4:ää havaittiin olevan ensisijaisesti endoteelisoluissa. Dyksiinin ilmentyminen lisääntyi sekä painekuormituksen että sydäninfarktin aiheuttaman sydänlihaksen uudelleenmuovautumisen aikana. Mekaaninen kuormitus riitti jo yksinään aktivoimaan dyksiinin geeniluentaa sydämessä. Lisäksi mitogeeni-aktivoituvan p38-proteiinikinaasin havaittiin säätelevän dyksiinin ilmentämistä. Väitöskirjatyössä saatiin uutta tietoa sydänlihaksen kuormituksen aikaisista muutoksista geenien luennassa sydänlihaksessa. Työssä osoitettiin, että painekuormitus aktivoi sydämessä aiemmin vähän tutkittujen geenien, melusiinin, TSP-1:n ja -4:n sekä dyksiinin, ilmentymistä. Näiden tekijöiden aktivoituminen hypertrofisen vasteen alkuvaiheessa antaa viitettä siitä, että tekijät osallistuvat kuormittuneen sydänlihaskudoksen uudelleenmuovautumiseen. Melusiini voi toimia erityisesti eteiskudosta kuormitukselta suojaavissa mekanismeissa, kun taas TSP-4 osoittautui aktivoituvan painekuormituksessa nimenomaan endoteelisoluissa
Style APA, Harvard, Vancouver, ISO itp.
8

Sin, Yuan Yan. "The roles of HSP20 in cardiac hypertrophy". Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3581/.

Pełny tekst źródła
Streszczenie:
Cardiac hypertrophy often develops to compensate for hemodynamic overload and is associated with heart failure. Recent studies have revealed that overexpression and PKA-mediated phosphorylation of heat shock protein 20 (HSP20) at Ser16 can attenuate hypertrophic growth of cardiomyocytes and trigger cardioprotective functions following sustained β-adrenergic stimulation (Fan et al., 2004, 2005, 2006). However, the molecular mechanism of HSP20 induced cardioprotection remains to be fully elucidated. In order to gain insight into the protective mode of action of HSP20, I attempted to (1) investigate the spatiotemporal control of PKA-mediated phosphorylation of HSP20, as well as (2) identifying novel protein binding partners for HSP20 utilising cutting edge ProtoArray technology. Initially, I set up an in vitro hypertrophy model using sustained isoprenaline (ISO)-stimulated neonatal rat cardiomyocytes. Cell size, protein synthesis and fetal gene expression were assessed as parameters of hypertrophic growth. In the first section of my studies, members of the cAMP-specific PDE4 family were shown to form signalling complexes with HSP20, and that the PKA-mediated phosphorylation of HSP20 could be modulated by PDE4. Based on peptide array data, a cell-permeable peptide ‘bs906’ was developed to inhibit the interaction of PDE4 with HSP20. Interestingly, the disruption of the PDE4-HSP20 complex was shown to induce PKA-mediated phosphorylation of HSP20 and trigger cardioprotection against the hypertrophic response measured in neonatal cardiomyocytes upon chronic β-adrenergic stimulation. In the second part of my studies, protein kinase D1 (PKD1) was identified as one interacting partner that robustly associated with HSP20. This interaction was confirmed by biochemical and immunocytochemical means. Using similar approaches to those used for the PDE4-HSP20 interaction, a cell-permeable peptide ‘HJL09’ was generated to promote disruption of the PKD1-HSP20 complex. Experimentation using the peptide concluded that the disruption of the PKD1-HSP20 complex reduced HSP20 phosphorylation and attenuated the hypertrophic response in cultured cardiomyocytes as shown by reduced increases in cell size, protein content and actin reorganisation. In undertaking this work, I also defined a novel PKD phosphorylation site (Ser16) on HSP20 that conforms to the PKD phosphorylation motif of RxxS (also a PKA site). My biochemical data suggested that PKD1 may regulate the cardioprotective function of HSP20 via phosphorylation at Ser16. In situ proximity ligation assay (PLA) further revealed a role of HSP20 as ‘molecular escort’ in targeting the nuclear translocation of PKD1. This function, in part, may be responsible for the induction of fetal gene reexpression as selective disruption of PKD1-HSP20 complex using ‘HJL09’ hindered the nuclear influx of the complex, thereby attenuating hypertrophic signalling. In summary, these studies describe some exciting findings which provide further insight into novel signalling mechanism of cardiac hypertrophy in neonatal rat cardiomyocytes. I have shown that PKA and PKD1 exhibiting opposite functions despite sharing the phosphorylation site on HSP20. In this regard, HSP20 functions as a molecular nexus for the opposing actions of the PKA and PKD1 signalling pathways in hypertrophy, suggesting that crosstalk may occur between anti-hypertrophic and pro-hypertrophic pathways. The identification and characterisation of these complexes should help to build a better understanding of the hypertrophic signalling pathway, and may provide novel therapeutic strategies for the treatment of cardiac hypertrophy.
Style APA, Harvard, Vancouver, ISO itp.
9

Butler, Thomas J. "Impact of dietary manipulation on cardiac hypertrophy". Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:15371.

Pełny tekst źródła
Streszczenie:
Left ventricular hypertrophy (LVH) is a significant risk factor for the development of heart failure (HF), the incidence of which is increased by obesity. Diets high in fat and sugar have been linked with the development of the metabolic syndrome and obesity, and may expose the heart to a unique environment via the differential actions of dietary macronutrients. The main objectives of this study were to determine the effect of differing dietary regimens upon (i) the progression of LVH and whole organism morphology (ii) function and metabolism in the hypertrophied heart, and (iii) cardiac ceramide content. Cardiac hypertrophy was surgically induced in male Sprague-Dawley rats via abdominal aortic constriction (AC). Animals were assigned to either a diet containing 5% sucrose/7% fat (standard diet, SD), 9 % sucrose/45 % fat (high-fat diet, HFD), or 14% sucrose/44% fat (western diet, WD) for 9 weeks. LVH was observed in all AC groups but was greatest in those fed a SD or WD. Both HFD and WD resulted in a significant increase in abdominal fat mass, which was positively associated with serum concentrations of leptin. In vitro cardiac function was unaltered by any dietary regimen alone, but was significantly enhanced in hypertrophied hearts from HFD and WD-fed animals, consistent with a compensated phase of hypertrophic remodelling. This was accompanied by a small reduction in palmitate oxidation and increased reliance upon lactate, an effect which was exacerbated in hearts from WD-fed animals. In WD-fed animals, there was a substantial increase in cardiac triglyceride (TG), which was not affected by AC. PPARα protein was reduced following AC in the hearts of animals fed a SD or WD, whereas the HFD prevented this decline. CD36 protein expression was not different between control and AC animals, but was highest in those fed a WD. In addition to elevated TG, WD hearts also exhibited a significant accumulation of long-chain ceramide species (C16-C24) compared with other dietary groups; consistent with metabolic remodelling. This effect was observed independent of AC. In order to simulate a model of HF, WD animals were treated with adriamycin (ADR), and cardiac ceramide content was further increased with the specific accumulation of C16 and C18 ceramide. These findings suggest that dietary macronutrient composition can have a profound effect upon the progression of LVH. Furthermore, the enhanced ceramide content in WD hearts indicates that the macronutrient composition of this dietary profile is most deleterious to the hypertrophied heart. Prolonged exposure of the hypertrophied heart to the WD may lead to increased apoptosis and accelerate the transition to HF.
Style APA, Harvard, Vancouver, ISO itp.
10

Crampton, Matthew S., i n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy". Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.

Pełny tekst źródła
Streszczenie:
Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
Style APA, Harvard, Vancouver, ISO itp.
Więcej źródeł

Książki na temat "Cardiac hypertrophy"

1

Adami, J. George. Notes upon cardiac hypertrophy. [S.l: s.n., 1985.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
2

B, Swynghedauw, red. Cardiac hypertrophy and failure. London: Libbey, 1990.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
3

World Heart Congress (17th 2001 Winnipeg, Man.). Signal transduction and cardiac hypertrophy. Redaktor Dhalla Naranjan S. Boston: Kluwer Academic Pub., 2003.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
4

Dhalla, Naranjan S., Larry V. Hryshko, Elissavet Kardami i Pawan K. Singal, red. Signal Transduction and Cardiac Hypertrophy. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
5

C, Claycomb William, Di Nardo Paolo i New York Academy of Sciences., red. Cardiac growth and regeneration. New York, N.Y: New York Academy of Sciences, 1995.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
6

M, Carlson Bruce, red. Growth and hyperplasia of cardiac muscle cells. London, U.K: Harwood Academic Publishers, 1991.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
7

Jenkins, Kim. The role of phosphoinositide hydrolysis and protein kinase C activation in cardiac myocyte hypertrophy. Birmingham: University of Birmingham, 1994.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
8

Heinrich, Taegtmeyer, red. A symposium, from increased energy metabolism to cardiac hypertrophy and failure: Mediators and molecular mechanisms. New York: Excerpta Medica, 1998.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
9

Green, Nicola Kim. Regulation of rat myocardial gene expression by thyroid status and in experimental models of cardiac hypertrophy. Birmingham: University of Birmingham, 1991.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
10

Kassiri, Zamaneh. Frequency-and hypertrophy-mediated alterations in twith force and intracellular calcium transients in rat cardiac trabecula. Ottawa: National Library of Canada, 1998.

Znajdź pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
Więcej źródeł

Części książek na temat "Cardiac hypertrophy"

1

Canale, Enrico D., Gordon R. Campbell, Joseph J. Smolich i Julie H. Campbell. "Cardiac Hypertrophy". W Cardiac Muscle, 189–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-50115-9_8.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
2

Cokkinos, Dennis V. "Cardiac Hypertrophy". W Myocardial Preservation, 63–86. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_5.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
3

Marian, Ali J., i James T. Willerson. "Cardiac Hypertrophy". W Cardiovascular Medicine, 1177–88. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_54.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
4

Tomanek, Robert J. "Cardiac Hypertrophy". W Coronary Vasculature, 221–46. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4887-7_11.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
5

Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann i in. "Cardiac Hypertrophy". W Encyclopedia of Molecular Mechanisms of Disease, 273. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8879.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
6

Müller, Alison L., i Naranjan S. Dhalla. "Differences in Concentric Cardiac Hypertrophy and Eccentric Hypertrophy". W Cardiac Adaptations, 147–66. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5203-4_8.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
7

Romanò, Massimo. "Cardiac Chamber Hypertrophy". W Text Atlas of Practical Electrocardiography, 201–8. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5741-8_12.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
8

Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis i in. "Pathological Cardiac Hypertrophy". W Encyclopedia of Exercise Medicine in Health and Disease, 690. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2841.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
9

Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis i in. "Physiological Cardiac Hypertrophy". W Encyclopedia of Exercise Medicine in Health and Disease, 711. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2877.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
10

Kalmar, Jayne M., Brigid M. Lynch, Christine M. Friedenreich, Lee W. Jones, A. N. Bosch, Alessandro Blandino, Elisabetta Toso i in. "Cardiac Hypertrophy, Pathological". W Encyclopedia of Exercise Medicine in Health and Disease, 168–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_38.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.

Streszczenia konferencji na temat "Cardiac hypertrophy"

1

Sutar, Rajendra G., i A. G. Kothari. "Detection of cardiac hypertrophy by ECG analysis". W 2012 International Conference on Communication, Information & Computing Technology (ICCICT). IEEE, 2012. http://dx.doi.org/10.1109/iccict.2012.6398192.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
2

Damani, Devanshi N., Anoushka Kapoor, Priyadharshini Sivasubramaniam, Nasibeh Farahani, Moein Enayati, Jeffrey B. Geske, Michael J. Ackerman i in. "Biventricular Involvement In Hypertrophic Cardiomyopathy: Preliminary Analysis Of Cardiac MRIs With Visual Right Ventricular Hypertrophy". W 2022 IEEE 10th International Conference on Healthcare Informatics (ICHI). IEEE, 2022. http://dx.doi.org/10.1109/ichi54592.2022.00031.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
3

Panico, Karine, Giovanni Weber, Marcela S. Carneiro-Ramos i Jo�o Salinet. "Electrophysiological Effects on Renal Ischaemia/Reperfusion-Induced Cardiac Hypertrophy". W 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.301-394.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
4

Wang, Zhonghai, Cai Yuan, Yonghong Shao, Amy D. Bradshaw, Thomas K. Borg i Bruce Z. Gao. "Polarization-resolved SHG microscopy in cardiac hypertrophy study (Conference Presentation)". W Diagnostic and Therapeutic Applications of Light in Cardiology, redaktorzy Guillermo J. Tearney, Kenton W. Gregory i Laura Marcu. SPIE, 2017. http://dx.doi.org/10.1117/12.2253161.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
5

Carneiro-Ramos, Marcela, Carolina Junho, Gabrielle Nepomuceno i Herculano Martinho. "Probing renal ischemia reperfusion-induced cardiac hypertrophy by a Raman spectroscopy". W Diagnostic and Therapeutic Applications of Light in Cardiology 2021, redaktorzy Laura Marcu i Gijs van Soest. SPIE, 2021. http://dx.doi.org/10.1117/12.2583128.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
6

Damerjian, V., O. Tankyevych, A. Guellich, T. Damy i E. Petit. "Ultrasound image texture characterization with Gabor wavelets for cardiac hypertrophy differentiation". W 2016 IEEE 13th International Symposium on Biomedical Imaging (ISBI 2016). IEEE, 2016. http://dx.doi.org/10.1109/isbi.2016.7493208.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
7

Clerk, Angela, Kerry Rostron, Daniel Meijles, Stephen Fuller i Peter Sugden. "85 Enhanced nuclear RSK1 signalling promotes cardiac hypertrophy in mice in vivo, but compromises compensated hypertrophy induced by phenylephrine". W British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.85.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
8

Weixler, V., R. Lapusca, A. Guariento, M. Saeed, D. McCully, P. del Nido i I. Friehs. "Preventing Right Heart Failure in Pressure-Overload Hypertrophy through Transplantation of Autologous Mitochondria". W 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678837.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
9

Bhatia, Raghav, Shafik Khoury, Joseph Westaby, Elijah Behr, Michael Papadakis, Sanjay Sharma, Gherardo Finocchiaro i Mary Sheppard. "1 Mitral valve abnormalities in decedents of sudden cardiac death due to hypertrophic cardiomyopathy and idiopathic left ventricular hypertrophy". W British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.1.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
10

Bhatia, Raghav, Shafik Khoury, Joseph Westaby, Elijah Behr, Michael Papadakis, Sanjay Sharma, Gherardo Finocchiaro i Mary Sheppard. "1 Mitral valve abnormalities in decedents of sudden cardiac death due to hypertrophic cardiomyopathy and idiopathic left ventricular hypertrophy". W British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.1.

Pełny tekst źródła
Style APA, Harvard, Vancouver, ISO itp.
Możesz być także zainteresowany rozszerzonymi bibliografiami na temat „Cardiac hypertrophy” dla poszczególnych typów źródeł:
Artykuły w czasopismach Rozprawy doktorskie Książki
Oferujemy zniżki na wszystkie plany premium dla autorów, których prace zostały uwzględnione w tematycznych zestawieniach literatury. Skontaktuj się z nami, aby uzyskać unikalny kod promocyjny!

Do bibliografii