Relevant bibliographies by topics / Heart – Hypertrophy

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Heart – Hypertrophy'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Heart – Hypertrophy"

1

Kang, Peter M., Patrick Yue, Zhilin Liu, Oleg Tarnavski, Natalya Bodyak, and Seigo Izumo. "Alterations in apoptosis regulatory factors during hypertrophy and heart failure." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (July 2004): H72—H80. http://dx.doi.org/10.1152/ajpheart.00556.2003.

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Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made hypertrophic by a pathological stimulus show increased sensitivity to apoptosis. Examination of the molecular changes associated with these distinct types of hypertrophy revealed changes in Bcl-2 family members and caspases favoring survival during physiological hypertrophy. However, in pathological hypertrophy, there were more diffuse proapoptotic changes, including changes in Fas, the Bcl-2 protein family, and caspases. Therefore, we speculate that this increased sensitivity to apoptotic stimulation along with proapoptotic changes in the apoptosis program may contribute to the development of heart failure seen in pathological cardiac hypertrophy.
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Liu, Yaoqiu, Yahui Shen, Jingai Zhu, Ming Liu, Xing Li, Yumei Chen, Xiangqing Kong, Guixian Song, and Lingmei Qian. "Cardiac-Specific PID1 Overexpression Enhances Pressure Overload-Induced Cardiac Hypertrophy in Mice." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1975–85. http://dx.doi.org/10.1159/000374005.

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Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic stimuli. Methods: Samples of human failing hearts from the left ventricles of dilated cardiomyopathy (DCM) patients undergoing heart transplants were collected. Transgenic mice with cardiomyocyte-specific overexpression of PID1 were generated, and cardiac hypertrophy was induced by transverse aortic constriction (TAC). The extent of cardiac hypertrophy was evaluated by echocardiography as well as pathological and molecular analyses of heart samples. Results: A significant increase in PID1 expression was observed in failing human hearts and TAC-treated wild-type mouse hearts. When compared with TAC-treated wild-type mouse hearts, PID1-TG mouse showed a significant exacerbation of cardiac hypertrophy, fibrosis, and dysfunction. Further analysis of the signaling pathway in vivo suggested that these adverse effects of PID1 were associated with the inhibition of AKT, and activation of MAPK pathway. Conclusion: Under pathological conditions, over-expression of PID1 promotes cardiac hypertrophy by regulating the Akt and MAPK pathway.
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Kee, Hae Jin, and Hyun Kook. "Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/928326.

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Cardiac hypertrophy occurs in association with heart diseases and ultimately results in cardiac dysfunction and heart failure. Histone deacetylases (HDACs) are post-translational modifying enzymes that can deacetylate histones and non-histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro-hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Krüppel like factor 4 (KLF4) or inositol polyphosphate-5-phosphatase f (Inpp5f). Thus, modulators of HDAC2 enzymes, such as selective HDAC inhibitors, are considered to be an important target for heart diseases, especially for preventing cardiac hypertrophy. In contrast, class IIa HDACs have been shown to repress cardiac hypertrophy by inhibiting cardiac-specific transcription factors such as myocyte enhancer factor 2 (MEF2), GATA4, and NFAT in the heart. Studies of class IIa HDACs have shown that the underlying mechanism is regulated by nucleo-cytoplasm shuttling in response to a variety of stress signals. In this review, we focus on the class I and IIa HDACs that play critical roles in mediating cardiac hypertrophy and discuss the non-histone targets of HDACs in heart disease.
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Hu, Chengyun, Feibiao Dai, Jiawu Wang, Lai Jiang, Di Wang, Jie Gao, Jun Huang, et al. "Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice." Oxidative Medicine and Cellular Longevity 2022 (January 29, 2022): 1–12. http://dx.doi.org/10.1155/2022/5067544.

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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.
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Sarkar, Sagartirtha, Douglas W. Leaman, Sudhiranjan Gupta, Parames Sil, David Young, Annitta Morehead, Debabrata Mukherjee, et al. "Cardiac Overexpression of Myotrophin Triggers Myocardial Hypertrophy and Heart Failure in Transgenic Mice." Journal of Biological Chemistry 279, no. 19 (February 16, 2004): 20422–34. http://dx.doi.org/10.1074/jbc.m308488200.

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Cardiac hypertrophy and heart failure remain leading causes of death in the United States. Many studies have suggested that, under stress, myocardium releases factors triggering protein synthesis and stimulating myocyte growth. We identified and cloned myotrophin, a 12-kDa protein from hypertrophied human and rat hearts. Myotrophin (whose gene is localized on human chromosome 7q33) stimulates myocyte growth and participates in cellular interaction that initiates cardiac hypertrophyin vitro. In this report, we present data on the pathophysiological significance of myotrophinin vivo, showing the effects of overexpression of cardio-specific myotrophin in transgenic mice in which cardiac hypertrophy occurred by 4 weeks of age and progressed to heart failure by 9-12 months. This hypertrophy was associated with increased expression of proto-oncogenes, hypertrophy marker genes, growth factors, and cytokines, with symptoms that mimicked those of human cardiomyopathy, functionally and morphologically. This model provided a unique opportunity to analyze gene clusters that are differentially up-regulated during initiation of hypertrophyversustransition of hypertrophy to heart failure. Importantly, changes in gene expression observed during initiation of hypertrophy were significantly different from those seen during its transition to heart failure. Our data show that overexpression of myotrophin results in initiation of cardiac hypertrophy that progresses to heart failure, similar to changes in human heart failure. Knowledge of the changes that take place as a result of overexpression of myotrophin at both the cellular and molecular levels will suggest novel strategies for treatment to prevent hypertrophy and its progression to heart failure.
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Qian, Yanxia, Mingming Zhang, Ningtian Zhou, Xiaohan Xu, Jiahui Zhang, Qiang Ding, and Junhong Wang. "A long noncoding RNA CHAIR protects the heart from pathological stress." Clinical Science 134, no. 13 (July 2020): 1843–57. http://dx.doi.org/10.1042/cs20200149.

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Abstract Mammalian genomes have been found to be extensively transcribed. In addition to classic protein coding genes, a large numbers of long noncoding genes (lncRNAs) have been identified, while their functions, especially in heart diseases, remain to be established. We hypothesized that heart failure progression is controlled by tissue-specific lncRNAs. In the present study, we found that the cardiac-enriched lncRNA 4632428C04Rik, named as cardiomyocyte hypertrophic associated inhibitory RNA (CHAIR), is dynamically regulated during heart development, is expressed at low levels in embryonic hearts and accumulated at high levels in adult hearts. More interestingly, the lncRNA was down-regulated during cardiac hypertrophy and failure both in mice and humans. Importantly, loss of lncRNA CHAIR has no effects on normal hearts, whereas it results in accelerated heart function decline, increased hypertrophy, and exacerbated heart failure in response to stress. In contrast, restoring the expression of lncRNA CHAIR rescued the hearts from hypertrophy and failure. DNMT3A was recruited to CHAIR promoter during heart failure to suppress its expression. Reciprocally, CHAIR interacted with DNMT3A to inhibit its DNA-binding activity. Taken together, our data revealed a new cardioprotective lncRNA that represses heart failure through an epigenetic mechanism.
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Zhang, Yan, Qiang Da, Siyi Cao, Ke Yan, Zhiguang Shi, Qing Miao, Chen Li, et al. "HINT1 (Histidine Triad Nucleotide-Binding Protein 1) Attenuates Cardiac Hypertrophy Via Suppressing HOXA5 (Homeobox A5) Expression." Circulation 144, no. 8 (August 24, 2021): 638–54. http://dx.doi.org/10.1161/circulationaha.120.051094.

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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.
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SHANTZ, Lisa M., David J. FEITH, and Anthony E. PEGG. "Targeted overexpression of ornithine decarboxylase enhances β-adrenergic agonist-induced cardiac hypertrophy." Biochemical Journal 358, no. 1 (August 8, 2001): 25–32. http://dx.doi.org/10.1042/bj3580025.

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These studies were designed to determine the consequences of constitutive overexpression of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in response to agents that induce cardiac hypertrophy. However, it is not known whether high ODC levels are sufficient for the development of a hypertrophic phenotype. Transgenic mice were generated with cardiac-specific expression of a stable ODC protein using the α-myosin heavy-chain promoter. Founder lines with > 1000-fold overexpression of ODC in the heart were established, resulting in a 50-fold overaccumulation of putrescine, 4-fold elevation in spermidine, a slight increase in spermine and accumulation of large amounts of cadaverine compared with littermate controls. Despite these significant alterations in polyamines, myocardial hypertrophy, as measured by ratio of heart to body weight, did not develop, although atrial natriuretic factor RNA was slightly elevated in transgenic ventricles. However, stimulation of β-adrenergic signalling by isoproterenol resulted in severe hypertrophy and even death in ODC-overexpressing mice without further altering polyamine levels, compared with only a mild hypertrophy in littermates. When β1-adrenergic stimulation was blocked by simultaneous treatment with isoproterenol and the β1 antagonist atenolol, a significant, although reduced, hypertrophy was still present in the hearts of transgenic mice, suggesting that both β1 and β2 adrenergic receptors contribute to the hypertrophic phenotype. Therefore these mice provide a model to study the in vivo co-operativity between high ODC activity and activation of other pathways leading to hypertrophy in the heart.
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Gu, Wei, Yutong Cheng, Su Wang, Tao Sun, and Zhizhong Li. "PHD Finger Protein 19 Promotes Cardiac Hypertrophy via Epigenetically Regulating SIRT2." Cardiovascular Toxicology 21, no. 6 (February 21, 2021): 451–61. http://dx.doi.org/10.1007/s12012-021-09639-0.

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AbstractEpigenetic regulations essentially participate in the development of cardiomyocyte hypertrophy. PHD finger protein 19 (PHF19) is a polycomb protein that controls H3K36me3 and H3K27me3. However, the roles of PHF19 in cardiac hypertrophy remain unknown. Here in this work, we observed that PHF19 promoted cardiac hypertrophy via epigenetically targeting SIRT2. In angiotensin II (Ang II)-induced cardiomyocyte hypertrophy, adenovirus-mediated knockdown of Phf19 reduced the increase in cardiomyocyte size, repressed the expression of hypertrophic marker genes Anp and Bnp, as well as inhibited protein synthesis. By contrast, Phf19 overexpression promoted Ang II-induced cardiomyocyte hypertrophy in vitro. We also knocked down Phf19 expression in mouse hearts in vivo. The results demonstrated that Phf19 knockdown reduced Ang II-induced decline in cardiac fraction shortening and ejection fraction. Phf19 knockdown also inhibited Ang II-mediated increase in heart weight, reduced cardiomyocyte size, and repressed the expression of hypertrophic marker genes in mouse hearts. Further mechanism studies showed that PHF19 suppressed the expression of SIRT2, which contributed to the function of PHF19 during cardiomyocyte hypertrophy. PHF19 bound the promoter of SIRT2 and regulated the balance between H3K27me3 and H3K36me3 to repress the expression of SIRT2 in vitro and in vivo. In human hypertrophic hearts, the overexpression of PHF19 and downregulation of SIRT2 were observed. Of importance, PHF19 expression was positively correlated with hypertrophic marker genes ANP and BNP but negatively correlated with SIRT2 in human hypertrophic hearts. Therefore, our findings demonstrated that PHF19 promoted the development of cardiac hypertrophy via epigenetically regulating SIRT2.
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Funamoto, Masafumi, Yoichi Sunagawa, Yasufumi Katanasaka, Kana Shimizu, Yusuke Miyazaki, Nurmila Sari, Satoshi Shimizu, et al. "Histone Acetylation Domains Are Differentially Induced during Development of Heart Failure in Dahl Salt-Sensitive Rats." International Journal of Molecular Sciences 22, no. 4 (February 10, 2021): 1771. http://dx.doi.org/10.3390/ijms22041771.

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Histone acetylation by epigenetic regulators has been shown to activate the transcription of hypertrophic response genes, which subsequently leads to the development and progression of heart failure. However, nothing is known about the acetylation of the histone tail and globular domains in left ventricular hypertrophy or in heart failure. The acetylation of H3K9 on the promoter of the hypertrophic response gene was significantly increased in the left ventricular hypertrophy stage, whereas the acetylation of H3K122 did not increase in the left ventricular hypertrophy stage but did significantly increase in the heart failure stage. Interestingly, the interaction between the chromatin remodeling factor BRG1 and p300 was significantly increased in the heart failure stage, but not in the left ventricular hypertrophy stage. This study demonstrates that stage-specific acetylation of the histone tail and globular domains occurs during the development and progression of heart failure, providing novel insights into the epigenetic regulatory mechanism governing transcriptional activity in these processes.
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Dissertations / Theses on the topic "Heart – Hypertrophy"

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

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XU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.

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Drawnel, Faye Marie. "Control of myocardial hypertrophic remodelling by integration of calcium signals, kinase cascades and microRNAs." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609969.

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Archer, Caroline Rose. "Interactions between GPCR- and growth factor-activated signalling pathways in the induction of cardiac hypertrophy." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648427.

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Zhong, Tiecheng. "Ang II-Induced Cardiac Remodeling: Role of PI3-Kinase-Dependent Autophagy." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/28800.

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Heart failure (HF) is a pathological state indicating insufficient blood supply to the peripheral tissues from the heart. The pathophysiology of HF is multifactorial like cardiac remodeling including cardiac hypertrophy, perivascular fibrosis and apoptosis to compensate for the heart?s inability to pump enough blood. Cardiac hypertrophy is initially adaptive to hemodynamic overload; however, it chronically contributes to heart failure and sudden cardiac death. The extracellular regulatory factors and intracellular signaling pathways involved in the cardiac remodeling are not yet fully clear. PI3-kinase is an important intracellular kinase in organ size control. Cardiac overexpression of Class I PI3-kinase caused heart enlargement in transgenic mice. Autophagy as a dynamic process involving the degradation of damaged mitochondria prevents ROS overproduction which leads to the cardiac remodeling. Therefore, our aim was to study the relationship between PI3-kinases and Ang II-induced cardiac remodeling via an autophagy-dependent mechanism. Ang II significantly increased autophagy with two distinctive phases: an increasing phase at low doses and a decreasing phase at high doses in cardiomyocytes. The Ang II-induced autophagic depression was attenuated by a Class I PI3-kinase inhibitor and potentiated by Class III PI3-kinase inhibitor. Besides, Ang II-induced cardiac hypertrophy and mitochondria ROS generation were attenuated via blockade of Class I PI3-kinase or mTOR. To further validate our in vitro data, we studied the role of Class I PI3-kinase in Ang II-induced cardiac remodeling in vivo. We successfully transferred Lv-DNp85 (Class I PI3-kinase blockade) and Lv-GFP (control) into adult rat hearts and found that cardiac transfer of Lv-DNp85 did not alter Ang II-induced pressor effect, but attenuated Ang II-induced cardiac hypertrophy, perivascular fibrosis and cardiac dysfunction. Ang II-induced cardiac remodeling was associated with impaired autophagy and mitochondrial ROS overproduction, which were significantly attenuated by Lv-DNp85-induced blockade of Class I PI3-kinase. Taken together, these data suggest that Class I PI3-kinase is involved in Ang II-induced impairment of autophagy via Akt/mTOR pathway, leading to mitochondrial ROS overproduction and cardiac remodeling. These results are not only highly significant from a pathophysiological perspective, but also have important pharmacological implications in the control of cardiac hypertrophy to prevent decompensation and failure in cardiac function.
National Institute of Neurological Disorders and Stroke
National Institutes of Health (NIH, NS55008)
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Müller-Brunotte, Richard. "Diastolic heart function in hypertension-induced left ventricular hypertrophy /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-898-3/.

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Turner, J. E. "Collagen metabolism in normal heart and during cardiac hypertrophy." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47290.

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Loonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.

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p38-mitogen activated protein kinases (p38-MAPKs) are stress activated serine/threonine kinases that are activated during several different cardiac pathologies. Classically, studies have focused solely on p38α signaling in the heart. However, there is also high cardiac expression of the p38γ isoform but little is known about its cardiac function. The aim of this study was to elucidate the signaling pathway of p38γ, with a particular focus on its role in the progression of pathological cardiac hypertrophy. Comparisons of cardiac function and structure of wild type (WT) and p38γ knock out (KO) mice, in response to abdominal aortic banding, found that KO mice developed less ventricular hypertrophy than their corresponding WT controls, and have preserved cardiac function. Basal p38γ myocardial staining was primarily localised at the membranes and throughout the cytoplasm. Following aortic constriction, nuclear staining of p38γ increased, but no accumulation of p38α was observed. This suggests that the two isoforms play distinct roles in the heart. To elucidate its signaling pathway, we generated an analogue sensitive p38γ, which is mutated at a gatekeeper residue, to specifically track and identify its endogenous substrates in the myocardium. The mutation allows only the mutant kinase, but not WT kinases, to utilise analogues of ATP that are expanded at the N6 position and contain a detectable tag on the γ-phosphate. Transfer of this tag to substrates allows subsequent isolation and identification. Furthermore, unlike other p38-MAPKs, p38γ contains a C-terminal PDZ domain interacting motif. We have utilised this motif in co pull-down assays to identify interacting proteins of p38γ in the heart. Using these techniques we have identified, amongst other substrates, LDB3 and calpastatin as novel substrates of p38γ and we have determined the residues that are targeted for phosphorylation. Lastly we have shown that phosphorylation of calpastatin reduces its efficiency as a calpain inhibitor in vitro, hence proposing a mechanism by which p38γ may mediate its pro-hypertrophic role.
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Linehan, Katherine Alison. "Collagen deposition and myocyte hypertrophy in the pressure overloaded heart." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484263.

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Benson, Victoria Louise St Vincent's Clinical School UNSW. "The role of calcineurin in high-renin and low-renin animal models of pressure overload left ventricular hypertrophy." Awarded by:University of New South Wales. St Vincent's Clinical School, 2005. http://handle.unsw.edu.au/1959.4/20843.

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Left ventricular hypertrophy (LVH) in response to pressure overload is associated with increased cardiovascular morbidity and mortality, making its prevention an important therapeutic goal. The role of a calcineurin-dependent molecular pathway in the induction of pressure-overload LVH is controversial. The present study tested the hypothesis that, in the setting of LV pressure overload, activation of the systemic renin-angiotensin system was necessary for activation of this calcineurin pathway. Mild LV pressure overload was induced in male Wistar rats by abdominal aortic constriction (AAC) or transverse aortic arch constriction (TAC), producing well-matched pressure gradients of 37 ?? 8 and 35 ?? 15 mmHg, respectively. Tight transverse aortic arch constriction (TTAC) in additional animals produced a pressure gradient of 75 ?? 15 mmHg. Only AAC increased plasma renin concentration and activated the calcineurin pathway, indicated by increased nuclear NFAT3 content. Plasma renin concentration and nuclear NFAT3 content were unchanged in TAC and TTAC animals. AAC animals developed more LVH 21 days post-banding than TAC and TTAC animals: the slope of the relationship between LV/body weight ratio and systolic blood pressure was much steeper in AAC animals than the combined TAC and TTAC animals (20x10-6 versus 5x10-6, p<0.001). Treatment with the calcineurin inhibitor FK506 did not significantly alter the slope of this relationship in the combined TAC and TTAC animals (8x10-6), but FK506 abolished this relationship in AAC animals (-5x10-6, R =0.0003). These data indicate that activation of the calcineurin pathway occurs only in high-renin hypertension, providing an additional stimulus to LVH induction. Calcineurin plays no role in the induction of LVH in low-renin hypertension, which is much more common clinically.
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Books on the topic "Heart – Hypertrophy"

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S, Dhalla Naranjan, and International Conference on Heart Failure (1994 : Winnipeg, Man.), eds. Heart hypertrophy and failure. Boston: Kluwer, 1995.

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Dhalla, Naranjan S., Grant N. Pierce, Vincenzo Panagia, and Robert E. Beamish, eds. Heart Hypertrophy and Failure. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-1237-6.

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

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Nobuakira, Takeda, Nagano Makoto 1928-, Dhalla Naranjan S, and International Conference on Cardiac Hypertrophy (1998 : Tokyo, Japan), eds. The hypertrophied heart. Boston: Kluwer Academic, 2000.

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Kirshenbaum, Lorrie A., Ian M. C. Dixon, and Pawan K. Singal, eds. Biochemistry of Hypertrophy and Heart Failure. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9238-3.

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Yang, Phillip Chung-Ming. Hypertrophic response in primary single-cell culture of adult rat myocardial cells. [New Haven: s.n.], 1989.

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A, Raineri, Leachman Robert D, and International School of Medical Sciences (1990 : Ettore Majorana Centre for Scientific Culture), eds. The big heart: Proceedings of a course held at the International School of Medical Sciences, Ettore Majorana Centre for Scientific Culture, Italy, 2-8 April 1990. Chur, Switzerland: Harwood Academic Publishers, 1994.

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Swynghedauw, B. Hypertrophie et insuffisance cardiaques. Paris: Editions INSERM, 1990.

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Verdecchia, Paolo. Management of left ventricular hypertrophy. London: Science Press, 2001.

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H, Messerli Franz, and Cruickshank J. M, eds. Left ventricular hypertrophy and its regression. London: Science Press, 1992.

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Book chapters on the topic "Heart – Hypertrophy"

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Heart Hypertrophy." In Encyclopedia of Molecular Mechanisms of Disease, 782–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_878.

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Tio, R. A., R. de Boer, D. J. van Veldhuisen, and W. H. van Gilst. "The Role of Vascular Failure in Heart Failure." In Left Ventricular Hypertrophy, 15–20. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_2.

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Bontaş, Ecaterina, Florentina Radu-Ioniţă, and Liviu Stan. "Hypertrophy and Dilatation, Markers of Dysfunction." In Right Heart Pathology, 179–201. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5_8.

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Pluim, B. M., A. van der Laarse, and E. E. van der Wall. "The Athlete’s Heart: A Physiological or a Pathological Phenomenon?" In Left Ventricular Hypertrophy, 85–106. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_7.

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Reichek, Nathaniel, and Martin G. St. John Sutton. "Left Ventricular Hypertrophy." In Two-Dimensional Real-Time Ultrasonic Imaging of the Heart, 125–34. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2559-8_12.

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Chien, Kenneth R. "Molecular Physiology of Ventricular Hypertrophy." In Diastolic Relaxation of the Heart, 33–40. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2594-3_5.

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Marín-García, José. "Signaling in Hypertrophy and Heart Failure." In Signaling in the Heart, 287–321. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-9461-5_15.

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Lamb, H. J., A. de Roos, and E. E. van der Wall. "Left Ventricular Hypertrophic Heart Disease Studied by MR Imaging and 31P-MR Spectroscopy." In Left Ventricular Hypertrophy, 107–19. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_8.

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Zimmer, H. G. "Thyroid Hormones and Cardiac Hypertrophy." In Heart Function in Health and Disease, 239–50. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3090-9_18.

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Duncker, D. J. G. M. "Perfusion Abnormalities in the Hypertrophied Left Ventricle: Link Between Compensated Hypertrophy and Heart Failure?" In Left Ventricular Hypertrophy, 21–41. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_3.

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Conference papers on the topic "Heart – Hypertrophy"

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Tretyn, Aleksandra, Soni Pullamsetti, Klaus-Dieter Schlueter, Wiebke Janssen, Hossein A. Ghofrani, Norbert Weissmann, Friedrich Grimminger, Werner Seeger, and Ralph T. Schermuly. "Wnt-Signaling Pathway In Experimental Right Heart Hypertrophy." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4982.

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García-Pelagio, Karla P., Ling Chen, and Robert J. Bloch. "Absence of synemin causes hypertrophy in murine heart." In MEDICAL PHYSICS: Fourteenth Mexican Symposium on Medical Physics. Author(s), 2016. http://dx.doi.org/10.1063/1.4954099.

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Farrar, G. E., and A. I. Veress. "A Coupled Model of LV Growth and Mechanics Applied to Pressure Overload Hypertrophy." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14557.

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Hypertension currently affects approximately one third the population in the United States, and represents a major economic burden on the health care system with an estimated annual direct and indirect cost of $50.6 billion [1]. In the case of systemic hypertension, the left ventricle (LV) must work against increased pressure load to pump blood to the body. Over time, this excessive work causes hypertrophy of the myocardium (thickening of the myofibers). While initially a compensatory mechanism, hypertrophy can eventually lead to heart failure (HF) [2]. Predictive modeling of the hypertrophic growth will lead to a better understanding of the disease mechanisms, which in turn has the potential to lead to better treatment strategies.
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Xu Zhenyao and Fu Yinjie. "Application Of The Heart Model To Simulating Ventricle Hypertrophy." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.595856.

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Zhenyao, Xu, and Fu Yinjie. "Application of the heart model to simulating ventricle hypertrophy." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761242.

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Weixler, V., R. Lapusca, A. Guariento, M. Saeed, D. McCully, P. del Nido, and I. Friehs. "Preventing Right Heart Failure in Pressure-Overload Hypertrophy through Transplantation of Autologous Mitochondria." In 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.

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Makowiec, Danuta, Joanna Wdowczyk, and Marcin Gruchala. "Variability of heart rate variability indexes for estimates of left ventricular hypertrophy in subjects shortly after a heart transplant*." In 2022 12th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2022. http://dx.doi.org/10.1109/esgco55423.2022.9931353.

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Luitel, Himal, Akylbek Sydykov, Baktybek Kojonazarov, Bhola K. Dahal, Djuro Kosanovic, Werner Seeger, Hossein A. Ghofrani, and Ralph T. Schermuly. "Contribution Of Progenitor Cells In Experimental Right Heart Hypertrophy Induced By Pulmonary Artery Ligation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4980.

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Lammers, Steven R., Phil H. Kao, Lian Tian, Kendall Hunter, H. Jerry Qi, Joseph Albietz, Stephen Hofmeister, Kurt Stenmark, and Robin Shandas. "Quantification of Elastin Residual Stretch in Fresh Artery Tissue: Impact on Artery Material Properties and Pulmonary Hypertension Pathophysiology." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206793.

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Pulmonary arterial hypertension (PAH) is characterized as a chronic elevation in mean pulmonary artery pressure (MPAP) resulting from increased hydrodynamic resistance and decreased hydraulic capacitance of the pulmonary circulatory system. These hemodynamic changes cause the heart to operate outside optimum pump efficiency. The heart compensates for the efficiency loss through ventricular hypertrophy which, if left untreated, will continue until cardiac failure results.
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Wang, Lulu, and Ahmed Al-Jumaily. "A New GUI Device for Monitoring Cardiovascular Status." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-65361.

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Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Pulse wave velocity (PWV) is widely recognized as a significant marker of cardiovascular status monitoring, and it is correlated with many cardiovascular risk factors, including age, blood pressure, pulse pressure, hypertrophy and heart diseases. Aortic PWV is a direct measurement of aortic stiffness and is considered to be the gold standard of arterial stiffness measurements. This paper describes the development of a wireless healthcare device includes graphic user interface (GUI) to monitor the severity of CVD by measuring and analysing the PWV values under MATLAB environment. The GUI build presents the data into a simple and friendly program. It consists of patient information part and data analysis which is able to detect the severity of hypertrophy and heart diseases. The proposed device may serve as new clinical computer-aided diagnostic tool to help the healthcare professionals to monitor the severity of CVD due to its properties of non-invasive, effort-independent, and continuous monitoring.
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Reports on the topic "Heart – Hypertrophy"

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Cahaner, Avigdor, Sacit F. Bilgili, Orna Halevy, Roger J. Lien, and Kellye S. Joiner. effects of enhanced hypertrophy, reduced oxygen supply and heat load on breast meat yield and quality in broilers. United States Department of Agriculture, November 2014. http://dx.doi.org/10.32747/2014.7699855.bard.

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Original objectivesThe objectives of this project were to evaluate the growth performance, meat yield and quality attributes of broiler strains widely differing in their genetic potential under normal temperature vs. warm temperature (short and long-term) conditions. Strain differences in breast muscle accretion rate, metabolic responses under heat load and, gross and histopathological changes in breast muscle under thermal load was also to be characterized. BackgroundTremendous genetic progress has been made in broiler chicken growth rate and meat yield since the 1950s. Higher growth rate is driven by higher rates of feed intake and metabolism, resulting in elevated internal heat production. Hot rearing conditions negatively affect broiler growth by hindering dissipation of heat and may lead to a lethal elevation in body temperature. To avoid heat-induced mortality, broilers reduce feed intake, leading to depressed growth rate, lower weight gain, reduce breast meat yield and quality. Thus, the genetic potential of contemporary commercial broilers (CCB) is not fully expressed under hot conditions. Major conclusions, solutions, and achievementsResearch conducted in Israel focused on three broiler strains – CCB, Featherless, Feathered sibs (i.e., sharing similar genetic background). Complimentary research trials conducted at Auburn utilized CCB (Cobb 500, Cobb 700, Ross 308, Ross 708), contrasting their performance to slow growing strains. Warm rearing conditions consistently reduced feed intake, growth rate, feed efficiency, body weight uniformity and breast muscle yield, especially pronounced with CCB and magnified with age. Breast meat quality was also negatively affected, as measured by higher drip loss and paler meat color. Exposure to continuous or short-term heat stress induced respiratory alkalosis. Breast muscle histomorphometrics confirmed enhanced myofiber hypertrophy in CCB. Featherless broilers exhibited a significant increase in blood-vessel density under warm conditions. Rapid growth and muscle accretion rate was correlated to various myopathies (white striping, woody and necrotic) as well as to increases in plasma creatinekinase levels. Whether the trigger(s) of muscle damage is loss of cellular membrane integrity due to oxidative damage or tissue lactate accumulation, or to loss of inter-compartmental cation homeostasis is yet to be determined. Based on genome-wide single-nucleotide polymorphism array genotyping, identification of the gene with the recessive mutation Scaleless (sc) facilitated the development a dCAPS assay to discriminate between sc carrier (sc/+) and non-carrier (+/+) individuals. ImplicationsThis project confirmed that featherless broiler strains grow efficiently with high yield and quality of breast meat, even under warm rearing conditions that significantly depress the overall performance of CCB. Therefore, broiler meat production in hot regions and climates can be substantially improved by introducing the featherless gene into contemporary commercial broiler stocks. This approach has become more feasible with the development of dCAPS assay. A novel modification of the PCR protocol (using whole blood samples instead of extracted DNA) may contribute to the efficient development of commercial featherless broiler strains. Such strains will allow expansion of the broiler meat production in developing countries in warm climates, where energy intensive environmental control of rearing facilities are not economical and easily achievable.
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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.

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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Yahav, Shlomo, John Brake, and Orna Halevy. Pre-natal Epigenetic Adaptation to Improve Thermotolerance Acquisition and Performance of Fast-growing Meat-type Chickens. United States Department of Agriculture, September 2009. http://dx.doi.org/10.32747/2009.7592120.bard.

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: The necessity to improve broiler thermotolerance and performance led to the following hypothesis: (a) thethermoregulatory-response threshold for heat production can be altered by thermal manipulation (TM) during incubation so as to improve the acquisition of thermotolerance in the post-hatch broiler;and (b) TM during embryogenesis will improve myoblast proliferation during the embryonic and post-hatch periods with subsequent enhanced muscle growth and meat production. The original objectives of this study were as follow: 1. to assess the timing, temperature, duration, and turning frequency required for optimal TM during embryogenesis; 2. to evaluate the effect of TM during embryogenesis on thermoregulation (heat production and heat dissipation) during four phases: (1) embryogenesis, (2) at hatch, (3) during growth, and (4) during heat challenge near marketing age; 3. to investigate the stimulatory effect of thermotolerance on hormones that regulate thermogenesis and stress (T₄, T₃, corticosterone, glucagon); 4. to determine the effect of TM on performance (BW gain, feed intake, feed efficiency, carcass yield, breast muscle yield) of broiler chickens; and 5. to study the effect of TM during embryogenesis on skeletal muscle growth, including myoblast proliferation and fiber development, in the embryo and post-hatch chicks.This study has achieved all the original objectives. Only the plasma glucagon concentration (objective 3) was not measured as a result of technical obstacles. Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” In order to sustain or even improve broiler performance, TM during the period of embryogenesis when satellite cell population normally expand should increase absolute pectoralis muscle weight in broilers post-hatch. Major conclusions: Intermittent TM (39.5°C for 12 h/day) during embryogenesis when the thyroid and adrenal axis was developing and maturing (E7 to E16 inclusive) had a long lasting thermoregulatory effect that improved thermotolerance of broiler chickens exposed to acute thermal stress at market age by lowering their functional Tb set point, thus lowering metabolic rate at hatch, improving sensible heat loss, and significantly decreasing the level of stress. Increased machine ventilation rate was required during TM so as to supply the oxygen required for the periods of increased embryonic development. Enhancing embryonic development was found to be accomplished by a combination of pre-incubation heating of embryos for 12 h at 30°C, followed by increasing incubation temperature to 38°C during the first 3 days of incubation. It was further facilitated by increasing turning frequency of the eggs to 48 or 96 times daily. TM during critical phases of muscle development in the late-term chick embryo (E16 to E18) for 3 or 6 hours (39.5°C) had an immediate stimulatory effect on myoblast proliferation that lasted for up to two weeks post-hatch; this was followed by increased hypertrophy at later ages. The various incubation temperatures and TM durations focused on the fine-tuning of muscle development and growth processes during late-term embryogenesis as well as in post-hatch chickens.
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