Relevant bibliographies by topics / Myocardial

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

Academic literature on the topic 'Myocardial'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Myocardial"

1

A. Meenakshi, Martin, and Erik G. Seth. "Protective role of TAT-HSP70 after myocardial I/R injury." American Journal of BioMedicine 5, no. 3 (September 22, 2017): 279–84. http://dx.doi.org/10.18081/2333-5106/015-04/289-294.

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Myocardial ischemia reperfusion injury I/R adversely affects cardiac function. Heat shock proteins (HSPs) are a highly conserved family of proteins with diverse functions expressed by all cells exposed to environmental stress including myocardila injury. We investigated release of small constitutive heat shock proteins (HSPs) from mouse myocardium and the effects of TAT-HSP70 after myocardial I/R via occluding the left coronary artery (LAD). The results support the hypothesis that elevated HSPs in myocardium after ischemia and reperfusion and contributes to the inflammatory mechanism of myocardial functional injury. Further investigation of the significance of HSPs accumulation to the evolution of myocardial injury.
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2

Micic-Labudovic, Jelena, Tatjana Atanasijevic, Vesna Popovic, Zoran Mihailovic, Slobodan Nikolic, and Dragana Puzovic. "Myocardial bridges: A prospective forensic autopsy study." Srpski arhiv za celokupno lekarstvo 143, no. 3-4 (2015): 153–57. http://dx.doi.org/10.2298/sarh1504153m.

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Introduction. When the coronary artery, located subepicardially, submerges into the myocardium and appears again subepicardially after a short intramural course, it represents an embedded coronary artery, while the part of the myocardium above is a myocardial bridge. Objective. We investigated the frequency of the embedded left coronary artery (LAD) in the autopsy material considering the descending branch of the LAD to be the most important one in the nourishment of the myocardium and myocardial bridges to be the most frequent in its area, as well as clinically important. Methods. A prospective autopsy study of 975 cases was performed, including both, natural (21.33%) and violent (78.67%) deaths. The sample consisted of 74.56% males and 25.44% females. In order to discover myocardyal bridges and their characteristics, the hearts were examined by both transverse cuts and longitudinal openings of the LAD. Results. Myocardial bridge was found in 78 cases (8.00%), more commonly in males (9.35%) than females (4.03%). The average length of the myocardial bridge was 21.85?16.10mm and thickness 3.744?1.48 mm. The common localization of the myocardial bridge was the proximal half of the LAD (89.74%). The upper part of the artery, proximal to the bridge, was a common site of atherosclerotic changes. Myocardial bridge was found in 12.50% of natural deaths, but in 13.38% out of all cases of sudden cardiac deaths. Conclusion. Therefore, the presence of the myocardial bridge by itself is not predominant, but it is certainly a contributing factor to a sudden cardiac death.
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3

Zhong, Ze, Jia-qing Hu, Xin-dong Wu, Yong Sun, and Jun Jiang. "Anti-apoptotic effects of myocardin-related transcription factor-A on rat cardiomyocytes following hypoxia-induced injury." Canadian Journal of Physiology and Pharmacology 94, no. 4 (April 2016): 379–87. http://dx.doi.org/10.1139/cjpp-2014-0461.

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Myocardin-related transcription factor-A (MRTF-A) can transduce both biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction. However, the molecular mechanism that underlies the contribution that MRTF-A provides to the myocardium is not completely understood. The objective of this study was to investigate the effects of MRTF-A on myocardium apoptosis and its mechanisms. Our experiment results showed that MRTF-A expression increased and Bcl-2 expression reduced during myocardial ischemia–reperfusion in rat. Meanwhile, primary cardiomyocytes were pretreated with wild-type MRTF-A or siRNA of MRTF-A before exposure to hypoxia. We found that overexpression of MRTF-A in myocardial cells inhibited apoptosis and the release of cytochrome c. MRTF-A enhanced Bcl-2, which contributes to MRTF-A interaction with Bcl-2 in the nuclei of cardiomyocytes. MRTF-A upregulation expression of Bcl-2 in cardiomyocytes induced by hypoxia was inhibited by PD98059, an ERK1/2 inhibitor. In conclusions, MRTF-A improved myocardial cell survival in a cardiomyocyte model of hypoxia-induced injury; this effect was correlated with the upregulation of anti-apoptotic gene Bcl-2 through the activation of ERK1/2.
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4

Bhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth, and Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development." Journal of Cardiovascular Development and Disease 8, no. 3 (March 2, 2021): 26. http://dx.doi.org/10.3390/jcdd8030026.

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Among the three transforming growth factor beta (TGFβ) ligands, TGFβ2 is essential for heart development and is produced by multiple cell types, including myocardium. Heterozygous mutations in TGFB2 in patients of connective tissue disorders result in congenital heart defects and adult valve malformations, including mitral valve prolapse (MVP) with or without regurgitation. Tgfb2 germline knockout fetuses exhibit multiple cardiac defects but the role of myocardial-TGFβ2 in heart development is yet to be elucidated. Here, myocardial Tgfb2 conditional knockout (CKO) embryos were generated by crossing Tgfb2flox mice with Tgfb2+/−; cTntCre mice. Tgfb2flox/− embryos were normal, viable. Cell fate mapping was done using dual-fluorescent mT/mG+/− mice. Cre-mediated Tgfb2 deletion was assessed by genomic PCR. RNAscope in situ hybridization was used to detect the loss of myocardial Tgfb2 expression. Histological, morphometric, immunohistochemical, and in situ hybridization analyses of CKOs and littermate controls at different stages of heart development (E12.5–E18.5) were used to determine the role of myocardium-derived TGFβ2 in atrioventricular (AV) cushion remodeling and myocardial development. CKOs exhibit a thin ventricular myocardium, AV cushion remodeling defects and developed incomplete AV septation defects. The loss of myocardial Tgfb2 resulted in impaired cushion maturation and dysregulated cell death. Phosphorylated SMAD2, a surrogate for TGFβ signaling, was “paradoxically” increased in both AV cushion mesenchyme and ventricular myocardium in the CKOs. Our results indicate that TGFβ2 produced by cardiomyocytes acting as cells autonomously on myocardium and via paracrine signaling on AV cushions are required for heart development.
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5

Berry, Mark F., Adam J. Engler, Y. Joseph Woo, Timothy J. Pirolli, Lawrence T. Bish, Vasant Jayasankar, Kevin J. Morine, Timothy J. Gardner, Dennis E. Discher, and H. Lee Sweeney. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSCs) into the acutely ischemic myocardium. Two weeks postinfarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were twofold stiffer than myocardium from noninfarcted animals but softer than myocardium from vehicle-treated infarcted animals. After 8 wk, the following variables were evaluated: MSC engraftment and left ventricular geometry by histological methods, cardiac function with a pressure-volume conductance catheter, myocardial fibrosis by Masson Trichrome staining, vascularity by immunohistochemistry, and apoptosis by TdT-mediated dUTP nick-end labeling assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated postinfarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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6

Khubulava, G. G., A. N. Shishkevich, S. S. Mikhailov, and E. Yu Bessonov. "Myocardial reperfusion syndrome. Pathogenesis, clinic, diagnosis." Bulletin of the Russian Military Medical Academy 22, no. 1 (December 15, 2020): 196–200. http://dx.doi.org/10.17816/brmma25992.

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The basics of pathogenesis, clinic and diagnosis of myocardial reperfusion syndrome are considered. Myocardial reperfusion syndrome is defined. Its relevance as one of the most poorly studied and formidable complications of cardiac reperfusion in myocardial infarction with elevation of the S-T segment has been explained. A brief review of the historical review of this problem and such types of manifestations of myocardial reperfusion syndrome as: diastolic myocardial dysfunction, post-reperfusion disturbances of the heart rhythm, the phenomenon of no-reflow and irreversible damage to the myocardium are briefly reviewed. The modern views on the pathological physiology of diastolic myocardial dysfunction, post-reperfusion damage to the myocardium, and the no-reflow phenomenon are analyzed. A review of current views on the pathological physiology of the development of post-reperfusion disturbances in heart rhythm is carried out. The clinical picture and the effect on the hemodynamics of such a manifestation of myocardial reperfusion syndrome as diastolic myocardial dysfunction are described. A brief description of the clinical picture of irreversible post-reperfusion damage to the myocardium is given. The clinical picture and types of post-reperfusion rhythm disturbances are described. The diagnostics of the no-reflow phenomenon has been analyzed in detail, the coronary angiographic scales for assessing thrombolysis in myocardial infarction and for assessing myocardial perfusion are graphically shown. A description of the basics of diagnosing post-reperfusion disturbances in heart rhythm, diastolic myocardial dysfunction, and post-reperfusion irreversible damage to the myocardium is given. A brief description of the known in the world literature predictors of the development of myocardial reperfusion syndrome is presented.
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Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer, and Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.

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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.
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Brown, TA. "Hibernating myocardium." American Journal of Critical Care 10, no. 2 (March 1, 2001): 84–91. http://dx.doi.org/10.4037/ajcc2001.10.2.84.

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According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.
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9

Xiao, Ying, Tao Wang, Xin Song, Dan Yang, Qing Chu, and Y. James Kang. "Copper promotion of myocardial regeneration." Experimental Biology and Medicine 245, no. 10 (March 8, 2020): 911–21. http://dx.doi.org/10.1177/1535370220911604.

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Myocardial regeneration is the key to the functional recovery of ischemic heart. Angiogenesis plays a pivotal role in myocardial regeneration by resetting a rejuvenation microenvironment under ischemic conditions. Hypoxia-inducible factor 1 (HIF-1) is the predominant transcription factor in the regulation of angiogenesis. In prolonged myocardial infarction, HIF-1α, the critical subunit of HIF-1, is accumulated in the infarcted myocardium, but fails to activate angiogenesis, suggesting a missing of a critical factor in the HIF-1 regulation of angiogenesis. Copper is involved in multiple steps of HIF-1 regulation of target gene expression. However, copper is deprived during myocardial ischemic injury, leading to deactivation of HIF-1-regulated angiogenesis. Multiple approaches are applied to increasing copper availability in the ischemic heart, effectively reactivating transcription of HIF-1 target angiogenic genes. Copper-induced angiogenesis thus reconstructs the conduit for the transduction of tissue injury signaling, recruitment of tissue repair materials such as stem cells, and the homing of stem cells, leading to the promotion of myocardial regeneration. Thus, copper promotes myocardial regeneration through reactivation of HIF-1-regulated angiogenesis. This would constitute an alternative therapeutic approach to ischemic heart disease. Impact statement Copper promotes angiogenesis, but the mechanistic insights have not been fully elucidated until recently. In addition, the significance of copper promotion of angiogenesis in myocardial regeneration was increasingly revealed. Copper critically participates in the regulation of hypoxia-inducible factor 1 (HIF-1) of angiogenic gene expression. Interestingly, myocardial ischemia causes copper efflux from the heart, leading to suppression of angiogenesis, although HIF-1α, the critical subunit of HIF-1, remains accumulated in the ischemic myocardium. Strategies targeting copper specific delivery to the ischemic myocardium lead to selective activation of HIF-1-regulated angiogenic gene expression. Vascularization of the ischemic myocardium re-establishes the tissue injury microenvironment, and rebuilds the conduit for communication between the tissue injury signals and the remote regenerative responses including stem cells. This process promotes myocardial regeneration. Thus, a simple and effective copper supplementation to the ischemic myocardium would become a novel therapeutic approach to the treatment of patients with ischemic heart diseases.
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Abdrahmanova, A. I., N. B. Amirov, and N. A. Cibulkin. "Application of Perfusion Single Photon Emission Computed Tomography of the Myocardium in Pain-Free Myocardial Ischemia." Russian Archives of Internal Medicine 10, no. 5 (October 9, 2020): 340–47. http://dx.doi.org/10.20514/2226-6704-2020-10-5-340-347.

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This literature review provides data on the use of single-photon emission computed tomography of myocardium in silent myocardial ischemia. The presence of silent myocardial ischemia increases the risk of cardiovascular complications several times and may be the first manifestation of coronary heart disease. Assessing the state of morphofunctional processes in the myocardium is the main goal of diagnostic imaging using singlephoton emission computed tomography of the myocardium. This allows to get three-dimensional image of left ventricle with information about distribution of perfusion volume across myocardium, makes it possible to more accurately differentiate such condition as silent myocardial ischemia. Conducting single-photon emission computed tomography in ECG synchronization mode allows you to visualize the kinetics of the myocardial walls in different phases of the cardiac cycle and thereby simultaneously assess the functional state of the left ventricular myocardium. Indicators of contractile function of the left ventricular myocardium in areas of transient hypoperfusion can be predictors of cardiac events after myocardial infarction and independent predictors of perioperative cardiac events in patients undergoing cardiac surgery. Performing single-photon emission computed tomography in ECG-synchronization mode allows visualizing kinetics of myocardial walls in different phases of cardiac cycle and thereby simultaneously assessing functional state of left ventricle myocardium. In combination with physical exercise and pharmacological tests, it helps to identify coronary stenosis among patients with silent myocardial ischemia. Perfusion single-photon emission computed tomography of myocardium is a necessary tool for stratification and assessment of prognosis of cardiac diseases in asymptomatic patients.
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Dissertations / Theses on the topic "Myocardial"

1

Egan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction." Thesis, The University of Sydney, 2009. http://hdl.handle.net/2123/5975.

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The vast majority of children undergoing surgical repair of cardiac lesions do spectacularly well. However a significant proportion, ~ 25%, struggle to progress in the early postoperative period and require additional pharmacological and occasionally mechanical circulatory support. All children typically have some degree of postoperative myocardial dysfunction, with the severe spectrum termed the low cardiac output state (LCOS). LCOS is clinically defined as the requirement for new or escalated inotrope therapy, a widened arteriovenous oxygen difference, cardiac arrest or the need for reinstitution of mechanical circulatory support. LCOS is largely responsible for the morbidity and mortality involved in paediatric cardiac surgery. Despite the predictability of LCOS in the initial postoperative hours, the underlying pathophysiology remains unclear. The period of decline in cardiac function that typifies LCOS is temporally associated with the development of oedema in the tissues of the body, including the heart. This relationship between oedema and dysfunction has increasingly become blurred, with a tendency to elevate the temporal association to a causal link. We sought to explore the causes and contributions to myocardial dysfunction in this setting, including the roles of oedema and ischaemia within the heart. In focusing on oedema and ischaemia we also examined the effects of these insults on relevant myocardial membrane proteins, including those that permit rapid water transport – aquaporins (AQPs), and those involved in membrane mechanics – dystrophin, and membrane repair – dysferlin. Experimental settings which enabled the in vitro dissection of these insults and proteins of interest were combined with a clinically accurate in vivo model. This thesis describes a series of thematically linked experiments that examined LCOS, myocardial oedema and the role of various membrane proteins. We performed isolated cardiomyocyte studies, isolated heart studies as well as a clinically relevant large animal (lamb) cardiopulmonary bypass (CPB) model. Across these models we also explored the role of therapeutically protecting myocardial membranes with Poloxamer 188 (P188) and assessed any influence on myocardial function, oedema and membrane proteins. vi The results from these three models suggest that the clinically accepted dogma of a causative link between myocardial oedema and dysfunction overstates the contribution of myocardial oedema to LCOS. We found that ischaemia/reperfusion was of primary importance in causing myocardial dysfunction. Myocardial oedema without ischaemia had a mild and reversible contribution to myocardial dysfunction, but this was minor in comparison to the gross dysfunction attributable to ischaemia. Isolated cardiomyocytes, with induced oedema, functioned well. Whilst ischaemic cardiomyocytes, with less swelling still had severe contractile dysfunction. Isolated hearts, perfused with an oedema inducing crystalloid perfusate developed myocardial oedema and had minimal reversible systolic and diastolic dysfunction. Isolated hearts which experienced global ischaemia had comparable degrees of myocardial oedema, and significantly greater degrees of myocardial dysfunction that increased in severity with increasing duration of ischaemia. In the lamb CPB model, only those lambs which underwent aortic cross clamping and had a period of ischaemia had poor myocardial function. These lambs also had swollen hearts, raised myocardial AQP1 mRNA and reduced membrane dysferlin protein expression. Membrane dystrophin protein expression was not altered, somewhat unexpectedly with CPB with or without ischaemia. Lambs placed on CPB without ischaemia had good myocardial function, minimal oedema and unchanged membrane protein expression during the survival period. In a blinded lamb CPB trial of P188 there were improved haemodynamics and indicies of myocardial function associated with its use. This was also associated with preservation of dysferlin expression and reduced membrane injury. In parallel isolated heart trials of this therapy, there was a reduction in myocardial oedema associated with its use in non-ischaemic experiments. There was also a suggestion of improved diastolic function in ischaemic experiments, but no change in myocardial water content. In conclusion, we have highlighted the primacy of ischaemia/reperfusion over oedema in contributing to LCOS. We have refuted the accepted dogma that myocardial oedema causes significant dysfunction in itself, with important oedema likely to result from ischaemia. We have shown that AQP1 may be involved in the pathogenesis of the capillary leak syndrome. Finally we have hinted at a role for prophylactic P188 in the vii setting of LCOS, possibly highlighting the role of membrane repair in recovery after surgery. Isolated heart trials of P188 further support a non-rheological mechanism of action and also lend support to the causal separation of myocardial oedema and dysfunction. The integral membrane protein dysferlin, rather than dystrophin, is relevant in the setting of LCOS in the current era.
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2

Egan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction." Faculty of Medicine, 2009. http://hdl.handle.net/2123/5975.

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Doctor of Philosophy(PhD)
The vast majority of children undergoing surgical repair of cardiac lesions do spectacularly well. However a significant proportion, ~ 25%, struggle to progress in the early postoperative period and require additional pharmacological and occasionally mechanical circulatory support. All children typically have some degree of postoperative myocardial dysfunction, with the severe spectrum termed the low cardiac output state (LCOS). LCOS is clinically defined as the requirement for new or escalated inotrope therapy, a widened arteriovenous oxygen difference, cardiac arrest or the need for reinstitution of mechanical circulatory support. LCOS is largely responsible for the morbidity and mortality involved in paediatric cardiac surgery. Despite the predictability of LCOS in the initial postoperative hours, the underlying pathophysiology remains unclear. The period of decline in cardiac function that typifies LCOS is temporally associated with the development of oedema in the tissues of the body, including the heart. This relationship between oedema and dysfunction has increasingly become blurred, with a tendency to elevate the temporal association to a causal link. We sought to explore the causes and contributions to myocardial dysfunction in this setting, including the roles of oedema and ischaemia within the heart. In focusing on oedema and ischaemia we also examined the effects of these insults on relevant myocardial membrane proteins, including those that permit rapid water transport – aquaporins (AQPs), and those involved in membrane mechanics – dystrophin, and membrane repair – dysferlin. Experimental settings which enabled the in vitro dissection of these insults and proteins of interest were combined with a clinically accurate in vivo model. This thesis describes a series of thematically linked experiments that examined LCOS, myocardial oedema and the role of various membrane proteins. We performed isolated cardiomyocyte studies, isolated heart studies as well as a clinically relevant large animal (lamb) cardiopulmonary bypass (CPB) model. Across these models we also explored the role of therapeutically protecting myocardial membranes with Poloxamer 188 (P188) and assessed any influence on myocardial function, oedema and membrane proteins. vi The results from these three models suggest that the clinically accepted dogma of a causative link between myocardial oedema and dysfunction overstates the contribution of myocardial oedema to LCOS. We found that ischaemia/reperfusion was of primary importance in causing myocardial dysfunction. Myocardial oedema without ischaemia had a mild and reversible contribution to myocardial dysfunction, but this was minor in comparison to the gross dysfunction attributable to ischaemia. Isolated cardiomyocytes, with induced oedema, functioned well. Whilst ischaemic cardiomyocytes, with less swelling still had severe contractile dysfunction. Isolated hearts, perfused with an oedema inducing crystalloid perfusate developed myocardial oedema and had minimal reversible systolic and diastolic dysfunction. Isolated hearts which experienced global ischaemia had comparable degrees of myocardial oedema, and significantly greater degrees of myocardial dysfunction that increased in severity with increasing duration of ischaemia. In the lamb CPB model, only those lambs which underwent aortic cross clamping and had a period of ischaemia had poor myocardial function. These lambs also had swollen hearts, raised myocardial AQP1 mRNA and reduced membrane dysferlin protein expression. Membrane dystrophin protein expression was not altered, somewhat unexpectedly with CPB with or without ischaemia. Lambs placed on CPB without ischaemia had good myocardial function, minimal oedema and unchanged membrane protein expression during the survival period. In a blinded lamb CPB trial of P188 there were improved haemodynamics and indicies of myocardial function associated with its use. This was also associated with preservation of dysferlin expression and reduced membrane injury. In parallel isolated heart trials of this therapy, there was a reduction in myocardial oedema associated with its use in non-ischaemic experiments. There was also a suggestion of improved diastolic function in ischaemic experiments, but no change in myocardial water content. In conclusion, we have highlighted the primacy of ischaemia/reperfusion over oedema in contributing to LCOS. We have refuted the accepted dogma that myocardial oedema causes significant dysfunction in itself, with important oedema likely to result from ischaemia. We have shown that AQP1 may be involved in the pathogenesis of the capillary leak syndrome. Finally we have hinted at a role for prophylactic P188 in the vii setting of LCOS, possibly highlighting the role of membrane repair in recovery after surgery. Isolated heart trials of P188 further support a non-rheological mechanism of action and also lend support to the causal separation of myocardial oedema and dysfunction. The integral membrane protein dysferlin, rather than dystrophin, is relevant in the setting of LCOS in the current era.
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3

Zhou, Xiaopeng. "Myocardial T1 Mapping Techniques for Quantification of Myocardial Fibrosis." Cleveland State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=csu1355418392.

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4

Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.

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5

Park, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Pyrimidine nucleoside reverse transcriptase inhibitors (NRTIs), one of the primary classes of HIV/AIDS antiretroviral drugs, are known to cause mitochondrial toxicity by inhibiting polymerase gamma during extending mitochondrial DNA replication. Extensive, prolonged use of NRTIs, such as zidovudine (3'-azido-2',3'-deoxythymidine; AZT), is associated with cardiovascular complications, such as dilated cardiomyopathy, the most common form of heart failure in which cardiac fibrosis is seen. Moreover, cardiac fibrosis is part of the pathological response of the heart during the progression of heart failure. Thus, we hypothesized that AZT treatment will contribute to the progression of cardiac fibrosis indirectly. Our study specifically focused on the effects of AZT and the development of cardiac fibrosis in the myocardium of wildtype (WT) and Y955CB transgenic mice (TG). Y955CB TG expresses a dominant negative cardiac specific mutant mitochondrial DNA polymerase gamma and were used to enhance the mtDNA toxic effect of AZT. To estimate fibrosis, myocardial collagen levels in each treatment group were assessed using both the hydroxyproline assay and histological image analysis. WT mice treated with AZT 0.22 mg/day for 35 days revealed no change in the level of hydroxyproline. However, a significant increase in hydroxyproline abundance correlated with histologically detectable fibrosis in vehicle-treated Y955CB TG mice. Interestingly, there was no additional increase in the abundance of collagen in AZT-treated Y955CB mice. Taken together, these data demonstrate that Y955CB TG displays an increase in the collagen level of the heart, concomitant with its documented cardiomyopathy. However AZT treatment was insufficient to increase the abundance of collagen in the heart.
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6

Dwivedi, Girish. "A Comparison between Myocardial Contrast Echocardiography and Radionuclide Myocardial perfusion Imaging in Patients with Acute Myocardial Infarction." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521583.

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7

Treibel, Thomas Alexander. "Aortic stenosis : a myocardial disease : insights from myocardial tissue characterisation." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1574742/.

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Aortic stenosis (AS) is a disease of not just the valve, but also of the myocardium. Patient symptoms and outcome are determined by the myocardial response; a crucial but poorly understood process. Diffuse and focal myocardial fibrosis play a key role. Until recently, both could only be assessed using invasive histology, but now cardiovascular magnetic resonance (CMR) offers late gadolinium enhancement (LGE) and extracellular volume fraction (ECV) techniques. In this thesis, I developed new methods to quantify ECV by synthetic ECV and cardiac CT. I then explored myocardial remodelling and fibrosis in patients with severe AS undergoing aortic valve replacement (AVR) using myocardial biopsy, CMR, biomarkers and a wide range of clinical parameters. Prior to AVR, CMR in patients with severe AS revealed important differences in myocardial remodelling between sexes, otherwise missed on echocardiography alone. Given apparently equal valve severity, the myocardial response to AS appeared unexpectedly maladaptive in men compared to women. Intra-operative myocardial biopsy revealed three pattern of fibrosis: endocardial fibrosis, microscars (mainly in the subendomyocardium), and diffuse interstitial fibrosis. Biopsy best captured the transmural gradient of fibrosis and microscars, while on CMR, LGE captured mainly microscars and ECV captured mid-myocardial related functional changes beyond LGE. Combining LGE and ECV allowed better stratification of AS patients. Incidentally, I found that 6% of AS patients older then 65 years had wild-type transthyretin amyloid deposits on cardiac biopsy, which was associated with poor outcome. This is now the basis of a BHF research fellowship. Following AVR, I demonstrated for the first time non-invasively that diffuse fibrosis regresses (focal fibrosis did not), which is accompanied by structural and functional improvements suggesting that human diffuse fibrosis is plastic, measurable by CMR and a potential therapeutic target.
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8

White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.

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Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The causes of stunning are not fully elucidated, however two major hypotheses currently exist; firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free radical (OFR) that may occur in a dramatic ‘surge’ at the onset of reperfusion. Treatment of ischemic myocardium with calcium channel blockers and / or OFR scavengers has been successfully shown to prevent stunning in various animal models. Whilst much is known about the physiological and biochemical changes that occur in stunned myocardium, very little is known about events at the molecular level. Since stunning occurs after only brief (15 minutes low-flow in the rabbit model) ischemia and subsequent reperfusion, we hypothesized that these molecular events are not predominated by large changes in protein expression and abundance, yet rather by subtle and / or transient changes to protein post-translational modifications (PTM). Such changes at the protein level are best analysed using the technologies encompassed under the term ‘proteomics’.
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Singh, Hardial. "Quantitative assessment of myocardial ischaemia with thallium-201 myocardial perfusion imaging." Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/19297.

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Frostfeldt, Gunnar. "Coagulation Inhibition and Development of Myocardial Damage in ST-Elevation Myocardial Infarction." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5322-8/.

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Books on the topic "Myocardial"

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Salerno, Tomas A., and Marco Ricci, eds. Myocardial Protection. Elmsford, New York, USA: Blackwell Publishing, 2003. http://dx.doi.org/10.1002/9780470987452.

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Iskandrian, Ami E., and Ernst E. Van Der Wall, eds. Myocardial Viability. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5.

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Kaski, Juan Carlos, and David W. Holt, eds. Myocardial Damage. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2380-0.

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Cokkinos, Dennis V., ed. Myocardial Preservation. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4.

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Iskandrian, Abdulmassih S., and Ernst E. Van Der Wall, eds. Myocardial viability. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1170-6.

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Dhalla, Naranjan S., Ian R. Innes, and Robert E. Beamish, eds. Myocardial Ischemia. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5.

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Wainwright, Cherry L., and James R. Parratt. Myocardial Preconditioning. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22206-5.

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Cokkinos, Dennis V., Constantinos Pantos, Gerd Heusch, and Heinrich Taegtmeyer, eds. Myocardial Ischemia. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6.

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A, Salerno Tomas, and Ricci Marco, eds. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.

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H, Marwick Thomas, Yu Cheuk-Man, and Sun Jingping, eds. Myocardial imaging. Malden, Mass: Blackwell Pub., 2007.

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Book chapters on the topic "Myocardial"

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Cokkinos, Dennis V. "Myocardial Hibernation." In Myocardial Preservation, 185–202. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_10.

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Cokkinos, Dennis V. "Myocardial Stunning." In Myocardial Preservation, 171–84. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_9.

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Pantos, Constantinos, Iordanis Mourouzis, and Dennis V. Cokkinos. "Myocardial Ischemia." In Myocardial Ischemia, 11–76. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6_2.

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Schwaiger, Markus, and Ulrich Schricke. "Hibernating and stunned myocardium: Pathophysiological considerations." In Myocardial Viability, 1–20. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_1.

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Van Der Wall, Ernst E., Jeroen J. Bax, Hubert W. Vliegen, Albert V. G. Bruschke, and Albert De Roos. "Role of magnetic resonance techniques in viability assessment." In Myocardial Viability, 177–97. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_10.

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Iskandrian, Ami E. "Viability assessment: clinical applications." In Myocardial Viability, 199–227. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_11.

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Iskandrian, Ami S., and Ernst E. Van Der Wall. "Summary." In Myocardial Viability, 229–31. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_12.

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Baliga, Ragavendra R., Jutta Schaper, and Jagat Narula. "Role of apoptosis in myocardial hibernation and myocardial stunning." In Myocardial Viability, 21–45. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_2.

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Schelbert, Heinrich R. "Assessment of myocardial viability with positron emission tomography." In Myocardial Viability, 47–72. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_3.

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Bax, Jeroen J., Jean-Louis J. Vanoverschelde, and Ernst E. Van Der Wall. "Assessment of myocardial viability by thallium-201." In Myocardial Viability, 73–89. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_4.

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Conference papers on the topic "Myocardial"

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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Tracy Ling, Yik Tung, Vincent Sayseng, and Elisa Konofagou. "Myocardial Elastography for Evaluating the Evolution of Strains and Strain Rates in Canine Myocardium After Myocardial Infarction." In 2022 IEEE International Ultrasonics Symposium (IUS). IEEE, 2022. http://dx.doi.org/10.1109/ius54386.2022.9957783.

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Veress, A. I., A. Giannakidis, and G. T. Gullberg. "Mechanical Effects of Myofibril Disarray on Cardiac Function." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14696.

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Myocardial disarray is a fiber distribution that deviates away from the tightly organized, parallel alignment of myocardial fibers that characterizes the normal myocardium. This coherently-organized distribution of the myofibers results in the twisting contraction of the normal left ventricle (LV). With myofiber disarray, the fibers have random directionality, either locally or globally, within the LV.
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Zhang, Song, John A. Crow, Robert C. Cooper, Ronald M. McLaughlin, Shane Burgess, Ali Borazjani, and Jun Liao. "Detection of Myocardial Fiber Disruption in Artificial Lesions With 3D DT-MRI Tract Models." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193121.

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In the United States, it is estimated that in 2008 approximately 1.2 million people will suffer a new or recurrent myocardial infarction. In 2005, the latest full year for which statistics are available, 16 million Americans (7.3% of the population) had some form of coronary heart disease. Loss of myocardium as a result of myocardial infarction increases wall stress locally and globally and triggers adaptive responses at the molecular, cellular, and tissue levels. These adaptive responses can lead to left ventricular dilation and congestive heart failure. Accurate non-invasive evaluation of myocardial structural degeneration (damage) and left ventricular remodeling following an infarct would have both prognostic and therapeutic value clinically.
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Hu, Zhenhua, Dimitris Metaxas, and Leon Axel. "Heart Composite Material Model for Stress-Strain Analysis." In ASME 2003 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/detc2003/vib-48334.

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Mechanical properties of the myocardium have been investigated intensively in the past four decades. Due to the non-linearity and history dependence of myocardial deformation, many complex strain energy functions have been used to describe the stress-strain relationship in the myocardium. These functions are good at fitting in-vitro experimental data from myocardial stretch testing into strain energy functions. However, it is difficult to model in-vivo myocardium by using strain energy functions. In a previous paper [1], we have implemented a transversely anisotropic material model to estimate in-vivo strain and stress in the myocardium. In this work, the fiber orientation is updated at each time step from the end of diastole to the end of systole; the stiffness matrix is recalculated using the current fiber orientation. We also extend our model to include residual ventricular stresses and time-dependent blood pressure in the ventricular cavities.
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Mehri, Sounira, Wided Khamlaoui, and Mohamed Hammami. "Acute myocardial infarction." In the Fourth International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3234698.3234741.

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Singelyn, J. M., J. A. DeQuach, and K. L. Christman. "Injectable myocardial matrix as a scaffold for myocardial tissue engineering." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334839.

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Bradley, Joshua, J. Bradley, EB Schelbert, LJ Bonnett, GA Lewis, J. Lagan, C. Orsborne, et al. "31 Remote myocardial fibrosis predicts adverse outcome following myocardial infarction." In British Society of Cardiovascular Magnetic Resonance (BSCMR) Annual Congress 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2022-bscmr.30.

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Baron, N., N. Kachenoura, F. Beygui, P. Cluze, P. Grenier, A. Herment, and F. Frouin. "Quantification of myocardial edema and necrosis during acute myocardial infarction." In 2008 35th Annual Computers in Cardiology Conference. IEEE, 2008. http://dx.doi.org/10.1109/cic.2008.4749158.

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Vasilchenko, S. Yu, A. A. Stratonnikov, A. I. Volkova, V. B. Loschenov, E. A. Sheptak, and S. S. Kharnas. "Investigation of myocardial photodynamic revascularization method on ischemic rat myocardium model." In SPIE Proceedings, edited by Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.697420.

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Reports on the topic "Myocardial"

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Moridi, Mina, Parinaz Onikzeh, Aida Kazemi, and Hadi Zamanian. CABG versus myotomy in symptomatic myocardial bridge patients : A systematic Review and Meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0088.

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Review question / Objective: The aim of this study is to find which surgical intervention in myocardial bridge ( myotomy or CABG) is more effective in reducing adverse outcomes in symptomatic patients resistant to optimal medical therapy ? Condition being studied: Myocardial bridge : A myocardial bridge (MB) is a congenital heart defect in which a bridge of muscle fibers (myocardium) overlying a section of a coronary artery and the artery is squeezed and normal blood flow is disrupted. Most bridges don't seem to cause symptoms. However, some people can experience angina, or chest pain. In patients with symptoms, first line treatment is medication and if they have symptoms despite optimal medical treatment , invasive measures like CABG or myotomy should be taken.
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Voynalovich-Khanova, Y. A. SYNDROME OF MYOCARDIAL REMODELING (CLINICAL OBSERVATION). "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-46-49.

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Li, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li, and Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.

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Review question / Objective: Whether acupuncture is effective for infarction size on myocardial ischemia rat models. Condition being studied: Myocardial ischemia is a typical pathological condition of coronary heart disease (CHD), which has been a global issue with high incidence and mortality. Myocardial infarction caused by myocardial ischemia leads to cardiac dysfunction, and the size of myocardial infarction also determines the recovery and prognosis of cardiac function. Acupuncture, a long history of traditional Chinese medicine, is widely used to treat symptoms like thoracalgia and palpitation. Many researches based on rat experiments have shown that acupuncture affects infarction size, cardiac function, myocardial enzyme or arrhythmias severity on myocardial ischemia models; nevertheless, few literatures have systematically reviewed these studies, assessing the risk of bias, quality of evidence, validity of results, and summarizing potential mechanisms. A systematic review of animal studies can benefit future experimental designs, promote the conduct and report of basic researches and provide some guidance to translate the achievements of basic researches to clinical application in acupuncture for myocardial ischemia. Therefore, we will conduct this systematic review and meta analysis to evaluate effects of acupuncture on infarction size on myocardial ischemia rat models.
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McDonough, Kathleen H., and Harvey I. Miller. Myocardial Dysfunction Contributes to Irreversible Hemorrhagic Shock. Fort Belvoir, VA: Defense Technical Information Center, February 2001. http://dx.doi.org/10.21236/ada389358.

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Pickard, Jeb S., and Joe E. Burton. Flying Waivers for History of Angioplasty and Myocardial Infraction. Fort Belvoir, VA: Defense Technical Information Center, November 1994. http://dx.doi.org/10.21236/ada292505.

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Hassanzadeh, Sara, Sina Neshat, Afshin Heidari, and Masoud Moslehi. Myocardial Perfusion Imaging in the Era of COVID-19. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0063.

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Review question / Objective: This review studies all aspects of myocardial perfusion imaging with single-photon emission computed tomography (MPI SPECT) after the COVID-19 pandemic. Condition being studied: Many imaging modalities have been reduced after the COVID-19 pandemic. Our focus in this review is to see if the number of MPIs is lowered or not and, if so, why. Furthermore, it is possible that a combination of CT attenuation correction and MPI could yield findings. In this study, we'll also look for these probable findings. Third, we know from previous studies that COVID might cause cardiac injuries in some people. Since MPI is a cardiovascular imaging technique, it might shows those injuries. So we'll review articles to find out in patients with active COVID infection, long COVID, or previous COVID cases what findings in MPI those cardiac injuries can cause.
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Dejong, Marla J., Kyungeh An, Candace C. Cherrington, and Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada427523.

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Crowley, James P., C. R. Valeri, and Joseph Chazan. Myocardial Infarction and Transfusion Requirements in Transfusion Dependent Anemic Patients. Fort Belvoir, VA: Defense Technical Information Center, May 1990. http://dx.doi.org/10.21236/ada360239.

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QIN, Xiaoyu, Chunai WANG, Jie ZHANG, Shuwei WANG, and Weiqi ZHANG. Effectiveness and safety of electroacupuncture for myocardial protection in cardiopulmonary bypass patients with myocardial ischemia-reperfusion injury：a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0045.

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Naydenov, Stefan, Nikolay Runev, Emil Manov, Nadya Naydenova, Mikhail Matveev, and Plamen Krastev. Diagnostic Potential of Signal-Averaged Orthogonal Electrocardiography in Acute Myocardial Infarction. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2021. http://dx.doi.org/10.7546/crabs.2021.02.16.

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