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Journal articles on the topic 'Heart formation'

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Author: Grafiati

Published: 4 June 2021

Last updated: 22 February 2023

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1

Marecki, Bogusław. "The formation of heart-proportion in fetal ontogenesis." Zeitschrift für Morphologie und Anthropologie 79, no. 2 (October 30, 1992): 197–202. http://dx.doi.org/10.1127/zma/79/1992/197.

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2

Pasterkamp, G. "The erythrocyte: a new player in atheromatous core formation." Heart 88, no. 2 (August 1, 2002): 115–16. http://dx.doi.org/10.1136/heart.88.2.115.

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3

Lasater, Phillip M. "The Heart of Self Formation." Dead Sea Discoveries 28, no. 3 (October 6, 2021): 367–95. http://dx.doi.org/10.1163/15685179-bja10025.

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Abstract This article discusses the “heart” as part of the terminology for selfhood in ancient Jewish literature. After discussing a couple of criticisms of studies of the self and showing how these criticisms fail to persuade, the paper examines a range of texts in the Hebrew Bible, the Dead Sea Scrolls, and beyond for conceptions of the moral self. Special attention is given to the legal S tradition in the Scrolls as a fruitful illustration of how the self and law are recurring conceptual companions. In this legal tradition, a universalizing conception of selfhood and agency is rooted in local, practical concerns of a community.

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4

CRACOWSKI, J. L. "Increased formation of F2-isoprostanes in patients with severe heart failure." Heart 84, no. 4 (October 1, 2000): 439–40. http://dx.doi.org/10.1136/heart.84.4.439.

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5

Weidenbach, M. "Infective endocarditis with progressive periaortal abscess formation in a previously healthy girl." Heart 89, no. 7 (July 1, 2003): 730. http://dx.doi.org/10.1136/heart.89.7.730.

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6

Moorman, A. "DEVELOPMENT OF THE HEART: (1) FORMATION OF THE CARDIAC CHAMBERS AND ARTERIAL TRUNKS." Heart 89, no. 7 (July 1, 2003): 806–14. http://dx.doi.org/10.1136/heart.89.7.806.

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7

Camacho, J. A., C. J. Peterson, G. J. White, and H. E. Morgan. "Accelerated ribosome formation and growth in neonatal pig hearts." American Journal of Physiology-Cell Physiology 258, no. 1 (January 1, 1990): C86—C91. http://dx.doi.org/10.1152/ajpcell.1990.258.1.c86.

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Rapid growth (5 mg dry heart/h) of the left ventricular free wall (LVFW) in the newborn pig heart accompanied by lack of growth of the right ventricular free wall (RVFW) represents a unique natural model of cardiac enlargement that is free of pathophysiological influences. By 3 days of life, LVFW was 71% larger than at 4 h of age. Rates of protein synthesis were measured during perfusion of isolated pig hearts with bicarbonate buffer containing glucose, lactate, insulin, and plasma concentrations of amino acids of an aortic pressure of 60 mmHg. In hearts from pigs that were 18 h of age, rates of protein synthesis were the same in RVFW and LVFW, but in 2-day-old pigs the rate was 52% greater in LVFW than RVFW. During the first 3 days of life, RNA content (mg/g) increased 3.4-fold faster in LVFW than RVFW. When RNA content was expressed per total heart portion, the increase was 7.9-fold greater. Because approximately 85% of total RNA is rRNA, these values indicated much more rapid formation of ribosomes in the LVFW than RVFW. When ribosome formation was measured in vitro in hearts from 48-h-old pigs, rates of formation were 39% greater in LVFW than RVFW, and at 18 h of age, ribosome formation was 40% faster in LVFW than RVFW. These findings indicated that formation of new ribosome preceded accelerated synthesis of total heart proteins. These findings indicated that rapid growth of LVFW compared with no growth of RVFW was associated with a 67% faster rate of ribosome formation and a 32% greater rate of protein synthesis.

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8

Heesch, C. M. "Cocaine activates platelets and increases the formation of circulating platelet containing microaggregates in humans." Heart 83, no. 6 (June 1, 2000): 688–95. http://dx.doi.org/10.1136/heart.83.6.688.

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9

Stainier, Didier Y. R. "Zebrafish genetics and vertebrate heart formation." Nature Reviews Genetics 2, no. 1 (January 2001): 39–48. http://dx.doi.org/10.1038/35047564.

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10

Roth, M., O. Reuthebuch, W. P. Klövekorn, and E. P. Bauer. "Thrombus formation of the right heart." European Journal of Cardio-Thoracic Surgery 13, no. 2 (February 1998): 216–17. http://dx.doi.org/10.1016/s1010-7940(97)00307-2.

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11

Dor, Yuval, Scott E. Klewer, John A. McDonald, Eli Keshet, and Todd D. Camenisch. "VEGF modulates early heart valve formation." Anatomical Record 271A, no. 1 (January 27, 2003): 202–8. http://dx.doi.org/10.1002/ar.a.10026.

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12

CLARKE, N. R. A. "Mycotic aneurysm formation with dehiscence of a valved aortic conduit resulting in dynamic aortic obstruction." Heart 84, no. 3 (September 1, 2000): 271–75. http://dx.doi.org/10.1136/heart.84.3.271.

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13

Baker, C. S. R. "Repetitive myocardial stunning in pigs is associated with an increased formation of reactive nitrogen species." Heart 87, no. 1 (January 1, 2002): 77–78. http://dx.doi.org/10.1136/heart.87.1.77.

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14

Balcells, Eduardo, Qing C. Meng, Walter H. Johnson, Suzanne Oparil, and Louis J. Dell’Italia. "Angiotensin II formation from ACE and chymase in human and animal hearts: methods and species considerations." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (October 1, 1997): H1769—H1774. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h1769.

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The current study examined the contributions of angiotensin-converting enzyme (ACE) vs. chymase to angiotensin II (ANG II) generation in membrane preparations from left ventricles of humans, dogs, rabbits, and rats and from total heart of mice. ACE and chymase activity were measured in membrane preparations extracted with low or high detergent (LD and HD, respectively) concentrations. We hypothesized that ACE, which is membrane bound in vivo, would be preferentially localized to the HD preparation, whereas chymase, which is localized to the cytoplasm and cardiac interstitium, would be localized to the LD preparation. In human heart, ACE activity was 16-fold higher in the HD than in the LD preparation, whereas chymase activity was 15-fold higher in the LD than in the HD preparation. Total ANG II formation was greater in human heart [15.8 ± 3.4 (SE) μmol ANG II ⋅ g−1 ⋅ min−1] than in dog, rat, rabbit, and mouse hearts (3.90 ± 0.35, 0.41 ± 0.02, 0.61 ± 0.07, and 1.16 ± 0.08 μmol ANG II ⋅ g−1 ⋅ min−1, respectively, P < 0.05, by analysis of variance). ANG II formation from ACE was higher in mouse heart (1.09 ± 0.05 μmol ANG II ⋅ g−1 ⋅ min−1, P < 0.001) than in rabbit, human, dog, and rat hearts (0.55 ± 0.06, 0.34 ± 0.01, 0.32 ± 0.06, and 0.31 ± 0.02 μmol ANG II ⋅ g−1 ⋅ min−1, respectively). In contrast, chymase activity was higher in human heart (15.3 ± 3.4 μmol ANG II ⋅ g−1 ⋅ min−1) than in dog, rat, rabbit, and mouse hearts (3.59 ± 0.29, 0.10 ± 0.01, 0.06 ± 0.01, and 0.07 ± 0.01 μmol ANG II ⋅ g−1 ⋅ min−1, respectively). Our results demonstrate important species differences in the pathways of intracardiac ANG II generation. Chymase predominated over ACE activity in human heart, accounting for extremely high total ANG II formation in human heart compared with dog, rat, rabbit, and mouse hearts.

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15

Meghji, P., K. M. Middleton, and A. C. Newby. "Absolute rates of adenosine formation during ischaemia in rat and pigeon hearts." Biochemical Journal 249, no. 3 (February 1, 1988): 695–703. http://dx.doi.org/10.1042/bj2490695.

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1. The activities of ecto- and cytosolic 5′-nucleotidase (EC 3.1.3.5), adenosine kinase (EC 2.7.1.20), adenosine deaminase (EC 3.5.4.4) and AMP deaminase (EC 3.5.4.6) were compared in ventricular myocardium from man, rats, rabbits, guinea pigs, pigeons and turtles. The most striking variation was in the activity of the ecto-5′-nucleotidase, which was 20 times less active in rabbit heart and 300 times less active in pigeon heart than in rat heart. The cytochemical distribution of ecto-5′-nucleotidase was also highly variable between species. 2. Adenosine formation was quantified in pigeon and rat ventricular myocardium in the presence of inhibitors of adenosine kinase and adenosine deaminase. 3. Both adenosine formation rates and the proportion of ATP catabolized to adenosine were greatest during the first 2 min of total ischaemia at 37 degrees C. Adenosine formation rates were 410 +/- 40 nmol/min per g wet wt. in pigeon hearts and 470 +/- 60 nmol/min per g wet wt. in rat hearts. Formation of adenosine accounted for 46% of ATP plus ADP broken down in pigeon hearts and 88% in rat hearts. 4. The data show that, in both pigeon and rat hearts, adenosine is the major catabolite of ATP in the early stages of normothermic myocardial ischaemia. The activity of ecto-5′-nucleotidase in pigeon ventricle (16 +/- 4 nmol/min per g wet wt.) was insufficient to account for adenosine formation, indicating the existence of an alternative catabolic pathway.

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16

Ashrafian, H. "The mechanism of formation of pulmonary arteriovenous malformations associated with the classic Glenn shunt (superior cavopulmonary anastomosis)." Heart 88, no. 6 (December 1, 2002): 639. http://dx.doi.org/10.1136/heart.88.6.639.

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17

Westwood, M. A. "An incidental case of thrombus formation in a patient with a portacath inserted for regular blood transfusions." Heart 89, no. 3 (March 1, 2003): 244. http://dx.doi.org/10.1136/heart.89.3.244.

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18

Anderson, R. H. "Development of the heart: (3) Formation of the ventricular outflow tracts, arterial valves, and intrapericardial arterial trunks." Heart 89, no. 9 (September 1, 2003): 1110–18. http://dx.doi.org/10.1136/heart.89.9.1110.

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19

Arbustini, E. "Plaque composition in plexogenic and thromboembolic pulmonary hypertension: the critical role of thrombotic material in pultaceous core formation." Heart 88, no. 2 (August 1, 2002): 177–82. http://dx.doi.org/10.1136/heart.88.2.177.

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20

MOORMAN, ANTOON F. M., and VINCENT M. CHRISTOFFELS. "Cardiac Chamber Formation: Development, Genes, and Evolution." Physiological Reviews 83, no. 4 (October 2003): 1223–67. http://dx.doi.org/10.1152/physrev.00006.2003.

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Moorman, Antoon F. M., and Vincent M. Christoffels. Cardiac Chamber Formation: Development, Genes, and Evolution. Physiol Rev 83: 1223-1267, 2003; 10.1152/physrev.00006.2003.—Concepts of cardiac development have greatly influenced the description of the formation of the four-chambered vertebrate heart. Traditionally, the embryonic tubular heart is considered to be a composite of serially arranged segments representing adult cardiac compartments. Conversion of such a serial arrangement into the parallel arrangement of the mammalian heart is difficult to understand. Logical integration of the development of the cardiac conduction system into the serial concept has remained puzzling as well. Therefore, the current description needed reconsideration, and we decided to evaluate the essentialities of cardiac design, its evolutionary and embryonic development, and the molecular pathways recruited to make the four-chambered mammalian heart. The three principal notions taken into consideration are as follows. 1) Both the ancestor chordate heart and the embryonic tubular heart of higher vertebrates consist of poorly developed and poorly coupled “pacemaker-like” cardiac muscle cells with the highest pacemaker activity at the venous pole, causing unidirectional peristaltic contraction waves. 2) From this heart tube, ventricular chambers differentiate ventrally and atrial chambers dorsally. The developing chambers display high proliferative activity and consist of structurally well-developed and well-coupled muscle cells with low pacemaker activity, which permits fast conduction of the impulse and efficacious contraction. The forming chambers remain flanked by slowly proliferating pacemaker-like myocardium that is temporally prevented from differentiating into chamber myocardium. 3) The trabecular myocardium proliferates slowly, consists of structurally poorly developed, but well-coupled, cells and contributes to the ventricular conduction system. The atrial and ventricular chambers of the formed heart are activated and interconnected by derivatives of embryonic myocardium. The topographical arrangement of the distinct cardiac muscle cells in the forming heart explains the embryonic electrocardiogram (ECG), does not require the invention of nodes, and allows a logical transition from a peristaltic tubular heart to a synchronously contracting four-chambered heart. This view on the development of cardiac design unfolds fascinating possibilities for future research.

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21

Bilchuk, Natalia, and Liudmyla Kolotova. "«HEART” AS A BASIS FORMATION OF SPIRITUALITY." Visnyk of the Lviv University, no. 34 (2021): 15–20. http://dx.doi.org/10.30970/pps.2021.34.2.

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22

Kokubo, Hiroki. "Formation of the Heart and Progenitor Cells." Pediatric Cardiology and Cardiac Surgery 38, no. 2 (May 1, 2022): 75–86. http://dx.doi.org/10.9794/jspccs.38.75.

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23

Vagnozzi, Ronald J., Jeffery D. Molkentin, and Steven R. Houser. "New Myocyte Formation in the Adult Heart." Circulation Research 123, no. 2 (July 6, 2018): 159–76. http://dx.doi.org/10.1161/circresaha.118.311208.

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24

Sparks, H. V., and H. Bardenheuer. "Regulation of adenosine formation by the heart." Circulation Research 58, no. 2 (February 1986): 193–201. http://dx.doi.org/10.1161/01.res.58.2.193.

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25

Zhang, Shaobo, and Timothy Saunders. "Cell Matching during Drosophila embryonic heart formation." Mechanisms of Development 145 (July 2017): S156. http://dx.doi.org/10.1016/j.mod.2017.04.443.

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26

Titov, A. M., and P. M. Larionov. "Mechanism of brushite formation in heart valves." Bone 44 (June 2009): S253—S254. http://dx.doi.org/10.1016/j.bone.2009.03.429.

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27

Watanabe, Yusuke, and Margaret Buckingham. "The formation of the embryonic mouse heart." Annals of the New York Academy of Sciences 1188, no. 1 (February 2010): 15–24. http://dx.doi.org/10.1111/j.1749-6632.2009.05078.x.

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28

Osmond, M. K., A. J. Butler, F. C. Voon, and R. Bellairs. "The effects of retinoic acid on heart formation in the early chick embryo." Development 113, no. 4 (December 1, 1991): 1405–17. http://dx.doi.org/10.1242/dev.113.4.1405.

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The vitamin A derivative retinoic acid has previously been shown to have teratogenic effects on heart development in mammalian embryos. The craniomedial migration of the precardiac mesoderm during the early stages of heart formation is thought to depend on a gradient of extracellular fibronectin associated with the underlying endoderm. Here, the effects of retinoic acid on migration of the precardiac mesoderm have been investigated in the early chick embryo. When applied to the whole embryo in culture, the retinoid inhibits the craniomedial migration of the precardiac mesoderm resulting in a heart tube that is stunted cranially, while normal or enlarged caudally. Similarly, a local application of retinoic acid to the heart-forming area disrupts the formation of the cardiogenic crescent and the subsequent development of a single mid-line heart tube. This effect is analogous to removing a segment of endoderm and mesoderm across the heart-forming area and results in various degrees of cardia bifida. At higher concentrations of retinoic acid and earlier developmental stages, two completely separate hearts are produced, while at lower concentrations and later stages there are partial bifurcations. The controls, in which the identical operation is carried out except that dimethyl sulphoxide (DMSO) is used instead of the retinoid, are almost all normal. We propose that one of the teratogenic effects of retinoic acid on the heart is to disrupt the interaction between precardiac cells and the extracellular matrix thus inhibiting their directed migration on the endodermal substratum.

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29

Smith, Rebecca M., Ramjay Visweswaran, Iryna Talkachova, Jillian K. Wothe, and Elena G. Tolkacheva. "Uncoupling the mitochondria facilitates alternans formation in the isolated rabbit heart." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 1 (July 1, 2013): H9—H18. http://dx.doi.org/10.1152/ajpheart.00915.2012.

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Alternans of action potential duration (APD) and intracellular calcium ([Ca2+]i) transients in the whole heart are thought to be markers of increased propensity to ventricular fibrillation during ischemia-reperfusion injuries. During ischemia, ATP production is affected and the mitochondria become uncoupled, which may affect alternans formation in the heart. The aim of our study was to investigate the role of mitochondria on the formation of APD and [Ca2+]i alternans in the isolated rabbit heart. We performed dual voltage and [Ca2+]i optical mapping of isolated rabbit hearts under control conditions, global no-flow ischemia ( n = 6), and after treatment with 50 nM of the mitochondrial uncoupler FCCP ( n = 6). We investigated the formation of alternans of APD, [Ca2+]i amplitude (CaA), and [Ca2+]i duration (CaD) under different rates of pacing. We found that treatment with FCCP leads to the early occurrence of APD, CaD, and CaA alternans; an increase of intraventricular APD but not CaD heterogeneity; and significant reduction in conduction velocity compared with that of control. Furthermore, we demonstrated that FCCP and global ischemia have similar effects on the prolongation of [Ca2+]i transients, whereas ischemia induces a significantly larger reduction of APD compared with that in FCCP treatment. In conclusion, our results demonstrate that uncoupling of mitochondria leads to an earlier occurrence of alternans in the heart. Thus, in conditions of mitochondrial stress, as seen during myocardial ischemia, uncoupled mitochondria may be responsible for the formation of both APD and [Ca2+]i alternans in the heart, which in turn creates a substrate for ventricular arrhythmias.

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30

Beinlich, Cathy J., Kenneth M. Baker, Gloria J. White, and Howard E. Morgan. "Control of growth in the neonatal pig heart." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 4 (October 1, 1991): L3—L7. http://dx.doi.org/10.1152/ajplung.1991.261.4.l3.

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The newborn heart is an excellent model in which to study cardiac growth because the neonatal period is a normal situation in which the left ventricle (LV) grows rapidly and the right ventricle grows slowly. Accelerated LV growth is in response to mechanical, neural, and endocrine changes at birth. Faster growth of the LV is accounted for by greater capacity for protein synthesis, as evidenced by greater RNA content. At 18 h of life, ribosomes are formed in preference to total heart protein, but at 48 h of life, faster rates of both ribosome formation and total protein synthesis are observed. In the LV of hearts from 2-day-old pigs, these rates are insensitive to the addition of glucagon, 1-methyl-3-isobutylxanthine, or a combination of norepinephrine and propranolol. These observations could result because of maximal growth stimulation already present in the LV of the newborn heart. To restrain LV growth in the neonatal period, we treated pigs with enalapril maleate, an angiotensin II-converting enzyme inhibitor. Enalapril blocked growth of the LV as well as the increase in RNA content. When hearts from enalapril-treated pigs were perfused in vitro, rates of protein synthesis and ribosome formation in the LV were lower. These studies suggest that angiotensin II is an important factor accounting for rapid growth of the neonatal heart in response to pressure overload at birth. adenosine 3',5'-cyclic monophosphate; angiotensin II; cardiac hypertrophy; glucagon; norepinephrine; protein synthesis; ribosome formation

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31

Beinlich, Cathy J., Kenneth M. Baker, Gloria J. White, and Howard E. Morgan. "Control of growth in the neonatal pig heart." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): 3–7. http://dx.doi.org/10.1152/ajpheart.1991.261.4.3.

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The newborn heart is an excellent model in which to study cardiac growth because the neonatal period is a normal situation in which the left ventricle (LV) grows rapidly and the right ventricle grows slowly. Accelerated LV growth is in response to mechanical, neural, and endocrine changes at birth. Faster growth of the LV is accounted for by greater capacity for protein synthesis, as evidenced by greater RNA content. At 18 h of life, ribosomes are formed in preference to total heart protein, but at 48 h of life, faster rates of both ribosome formation and total protein synthesis are observed. In the LV of hearts from 2-day-old pigs, these rates are insensitive to the addition of glucagon, 1-methyl-3-isobutylxanthine, or a combination of norepinephrine and propranolol. These observations could result because of maximal growth stimulation already present in the LV of the newborn heart. To restrain LV growth in the neonatal period, we treated pigs with enalapril maleate, an angiotensin II-converting enzyme inhibitor. Enalapril blocked growth of the LV as well as the increase in RNA content. When hearts from enalapril-treated pigs were perfused in vitro, rates of protein synthesis and ribosome formation in the LV were lower. These studies suggest that angiotensin II is an important factor accounting for rapid growth of the neonatal heart in response to pressure overload at birth. adenosine 3',5'-cyclic monophosphate; angiotensin II; cardiac hypertrophy; glucagon; norepinephrine; protein synthesis; ribosome formation

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32

Konings, T. C. "Separation of coronary ostium caused by pseudoaneurysm formation after composite valve graft replacement for acute dissection of the ascending aorta." Heart 88, no. 3 (September 1, 2002): 265. http://dx.doi.org/10.1136/heart.88.3.265.

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33

Sater, A. K., and A. G. Jacobson. "The specification of heart mesoderm occurs during gastrulation in Xenopus laevis." Development 105, no. 4 (April 1, 1989): 821–30. http://dx.doi.org/10.1242/dev.105.4.821.

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The establishment of heart mesoderm during Xenopus development has been examined using an assay for heart differentiation in explants and explant combinations in culture. Previous studies using urodele embryos have shown that the heart mesoderm is induced by the prospective pharyngeal endoderm during neurula and postneurula stages. In this study, we find that the specification of heart mesoderm must begin well before the end of gastrulation in Xenopus embryos. Explants of prospective heart mesoderm isolated from mid- or late neurula stages were capable of heart formation in nearly 100% of cases, indicating that the specification of heart mesoderm is complete by midneurula stages. Moreover, inclusion of pharyngeal endoderm had no statistically significant effect upon either the frequency of heart formation or the timing of the initiation of heartbeat in explants of prospective heart mesoderm isolated after the end of gastrulation. When the superficial pharyngeal endoderm was removed at the beginning of gastrulation, experimental embryos formed hearts, as did explants of prospective heart mesoderm from such embryos. These results indicate that the inductive interactions responsible for the establishment of heart mesoderm occur prior to the end of gastrulation and do not require the participation of the superficial pharyngeal endoderm.

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34

Prasch, Jürgen, Eva Bernhart, Helga Reicher, Manfred Kollroser, Gerald N. Rechberger, Chintan N. Koyani, Christopher Trummer, et al. "Myeloperoxidase-Derived 2-Chlorohexadecanal Is Generated in Mouse Heart during Endotoxemia and Induces Modification of Distinct Cardiomyocyte Protein Subsets In Vitro." International Journal of Molecular Sciences 21, no. 23 (December 3, 2020): 9235. http://dx.doi.org/10.3390/ijms21239235.

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Sepsis is a major cause of mortality in critically ill patients and associated with cardiac dysfunction, a complication linked to immunological and metabolic aberrations. Cardiac neutrophil infiltration and subsequent release of myeloperoxidase (MPO) leads to the formation of the oxidant hypochlorous acid (HOCl) that is able to chemically modify plasmalogens (ether-phospholipids) abundantly present in the heart. This reaction gives rise to the formation of reactive lipid species including aldehydes and chlorinated fatty acids. During the present study, we tested whether endotoxemia increases MPO-dependent lipid oxidation/modification in the mouse heart. In hearts of lipopolysaccharide-injected mice, we observed significantly higher infiltration of MPO-positive cells, increased fatty acid content, and formation of 2-chlorohexadecanal (2-ClHDA), an MPO-derived plasmalogen modification product. Using murine HL-1 cardiomyocytes as in vitro model, we show that exogenously added HOCl attacks the cellular plasmalogen pool and gives rise to the formation of 2-ClHDA. Addition of 2-ClHDA to HL-1 cardiomyocytes resulted in conversion to 2-chlorohexadecanoic acid and 2-chlorohexadecanol, indicating fatty aldehyde dehydrogenase-mediated redox metabolism. However, a recovery of only 40% indicated the formation of non-extractable (protein) adducts. To identify protein targets, we used a clickable alkynyl analog, 2-chlorohexadec-15-yn-1-al (2-ClHDyA). After Huisgen 1,3-dipolar cycloaddition of 5-tetramethylrhodamine azide (N3-TAMRA) and two dimensional-gel electrophoresis (2D-GE), we were able to identify 51 proteins that form adducts with 2-ClHDyA. Gene ontology enrichment analyses revealed an overrepresentation of heat shock and chaperone, energy metabolism, and cytoskeletal proteins as major targets. Our observations in a murine endotoxemia model demonstrate formation of HOCl-modified lipids in the heart, while pathway analysis in vitro revealed that the chlorinated aldehyde targets specific protein subsets, which are central to cardiac function.

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35

Ascione, L. "Relation between early mitral regurgitation and left ventricular thrombus formation after acute myocardial infarction: results of the GISSI-3 echo substudy." Heart 88, no. 2 (August 1, 2002): 131–36. http://dx.doi.org/10.1136/heart.88.2.131.

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36

Ozdemir, E. Sila, Anna M. Koester, and Xiaolin Nan. "Ras Multimers on the Membrane: Many Ways for a Heart-to-Heart Conversation." Genes 13, no. 2 (January 25, 2022): 219. http://dx.doi.org/10.3390/genes13020219.

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Formation of Ras multimers, including dimers and nanoclusters, has emerged as an exciting, new front of research in the ‘old’ field of Ras biomedicine. With significant advances made in the past few years, we are beginning to understand the structure of Ras multimers and, albeit preliminary, mechanisms that regulate their formation in vitro and in cells. Here we aim to synthesize the knowledge accrued thus far on Ras multimers, particularly the presence of multiple globular (G-) domain interfaces, and discuss how membrane nanodomain composition and structure would influence Ras multimer formation. We end with some general thoughts on the potential implications of Ras multimers in basic and translational biology.

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37

Risebro, Catherine A., and Paul R. Riley. "Formation of the Ventricles." Scientific World JOURNAL 6 (2006): 1862–80. http://dx.doi.org/10.1100/tsw.2006.316.

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The formation of the ventricles of the heart involves numerous carefully regulated temporal events, including the initial specification and deployment of ventricular progenitors, subsequent growth and maturation of the ventricles through “ballooning” of chamber myocardium, the emergence of trabeculations, the generation of the compact myocardium, and the formation of the interventricular septum. Several genes have been identified through studies on mouse knockout and transgenic models, which have contributed to our understanding of the molecular events governing these developmental processes. Interpretation of these studies highlights the fact that even the smallest perturbation at any stage of ventricular development may lead to cardiac malformations that result in either early embryonic mortality or a manifestation of congenital heart disease.

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38

Martin, Kendall E., and Joshua S. Waxman. "Atrial and Sinoatrial Node Development in the Zebrafish Heart." Journal of Cardiovascular Development and Disease 8, no. 2 (February 9, 2021): 15. http://dx.doi.org/10.3390/jcdd8020015.

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Proper development and function of the vertebrate heart is vital for embryonic and postnatal life. Many congenital heart defects in humans are associated with disruption of genes that direct the formation or maintenance of atrial and pacemaker cardiomyocytes at the venous pole of the heart. Zebrafish are an outstanding model for studying vertebrate cardiogenesis, due to the conservation of molecular mechanisms underlying early heart development, external development, and ease of genetic manipulation. Here, we discuss early developmental mechanisms that instruct appropriate formation of the venous pole in zebrafish embryos. We primarily focus on signals that determine atrial chamber size and the specialized pacemaker cells of the sinoatrial node through directing proper specification and differentiation, as well as contemporary insights into the plasticity and maintenance of cardiomyocyte identity in embryonic zebrafish hearts. Finally, we integrate how these insights into zebrafish cardiogenesis can serve as models for human atrial defects and arrhythmias.

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39

Panagopoulou, Panagiota, Constantinos H. Davos, Derek J. Milner, Emily Varela, JoAnn Cameron, Douglas L. Mann, and Yassemi Capetanaki. "Desmin mediates TNF-α–induced aggregate formation and intercalated disk reorganization in heart failure." Journal of Cell Biology 181, no. 5 (June 2, 2008): 761–75. http://dx.doi.org/10.1083/jcb.200710049.

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We explored the involvement of the muscle-specific intermediate filament protein desmin in the model of tumor necrosis factor α (TNF-α)–induced cardiomyopathy. We demonstrate that in mice overexpressing TNF-α in the heart (α–myosin heavy chain promoter-driven secretable TNF-α [MHCsTNF]), desmin is modified, loses its intercalated disk (ID) localization, and forms aggregates that colocalize with heat shock protein 25 and ubiquitin. Additionally, other ID proteins such as desmoplakin and β-catenin show similar localization changes in a desmin-dependent fashion. To address underlying mechanisms, we examined whether desmin is a substrate for caspase-6 in vivo as well as the implications of desmin cleavage in MHCsTNF mice. We generated transgenic mice with cardiac-restricted expression of a desmin mutant (D263E) and proved that it is resistant to caspase cleavage in the MHCsTNF myocardium. The aggregates are diminished in these mice, and D263E desmin, desmoplakin, and β-catenin largely retain their proper ID localization. Importantly, D263E desmin expression attenuated cardiomyocyte apoptosis, prevented left ventricular wall thinning, and improved the function of MHCsTNF hearts.

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Eaton, Philip, Jian-Mei Li, David J. Hearse, and Michael J. Shattock. "Formation of 4-hydroxy-2-nonenal-modified proteins in ischemic rat heart." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 3 (March 1, 1999): H935—H943. http://dx.doi.org/10.1152/ajpheart.1999.276.3.h935.

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4-Hydroxy-2-nonenal (HNE) is a major lipid peroxidation product formed during oxidative stress. Because of its reactivity with nucleophilic compounds, particularly metabolites and proteins containing thiol groups, HNE is cytotoxic. The aim of this study was to assess the extent and time course for the formation of HNE-modified proteins during ischemia and ischemia plus reperfusion in isolated rat hearts. With an antibody to HNE-Cys/His/Lys and densitometry of Western blots, we quantified the amount of HNE-protein adduct in the heart. By taking biopsies from single hearts ( n = 5) at various times (0, 5, 10, 15, 20, 35, and 40 min) after onset of zero-flow global ischemia, we showed a progressive, time-dependent increase (which peaked after 30 min) in HNE-mediated modification of a discrete number of proteins. In studies with individual hearts ( n = 4/group), control aerobic perfusion (70 min) resulted in a very low level (296 arbitrary units) of HNE-protein adduct formation; by contrast, after 30-min ischemia HNE-adduct content increased by >50-fold (15,356 units, P < 0.05). In other studies ( n = 4/group), administration of N-(2-mercaptopropionyl)glycine (MPG, 1 mM) to the heart for 5 min immediately before 30-min ischemia reduced HNE-protein adduct formation during ischemia by ∼75%. In studies ( n = 4/group) that included reperfusion of hearts after 5, 10, 15, or 30 min of ischemia, there was no further increase in the extent of HNE-protein adduct formation over that seen with ischemia alone. Similarly, in experiments with MPG, reperfusion did not significantly influence the tissue content of HNE-protein adduct. Western immunoblot results were confirmed in studies using in situ immunofluorescent localization of HNE-protein in cryosections. In conclusion, ischemia causes a major increase in HNE-protein adduct that would be expected to reflect a toxic sequence of events that might act to compromise tissue survival during ischemia and recovery on reperfusion.

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Liu, Chi-Feng, Chia-Hsien Lin, Chin-Fa Chen, Tian-Chyuan Huang, and Song-Chow Lin. "Antioxidative Effects of Tetramethylpyrazine on Acute Ethanol-Induced Lipid Peroxidation." American Journal of Chinese Medicine 33, no. 06 (January 2005): 981–88. http://dx.doi.org/10.1142/s0192415x05003570.

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Acute p.o. administration of 99.5% ethanol (0.1 ml) to fasted mice produced heart toxicity. Pretreatment with p.o. administration of tetramethylpyrazine (TMP) could prevent such toxicity effectively and dose-dependently. The maximal antioxidative effect against 99.5% ethanol-induced heart toxicity could be observed at 1 hour after TMP administration. In order to further investigate the heart protective mechanism of TMP, both lipid peroxidation level in vivo and superoxide scavenging activity were conducted. TMP exhibited a dose-dependently anti-lipid peroxidation effect in mice heart homogenate, and results indicated that 99.5% ethanol-induced intoxicated mice hearts have higher malonic dialdehyde (MDA) levels compared with those in TMP administrated mice hearts. These results suggest that the potentially heart protective mechanism of TMP could be contributed, at least in part, to its prominent anti-lipid peroxidation and anti-free radical formation effects, hence it could protect the heart from lipid peroxidation-induced heart toxicity.

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Zhumaeva, Z. J., and I. S. Manasova. "Risk factors of formation of congenital heart diseases." ACADEMICIA: An International Multidisciplinary Research Journal 10, no. 2 (2020): 266. http://dx.doi.org/10.5958/2249-7137.2020.00042.7.

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NEWBY, ANDREW C., and PARVIZ MEGHJI. "The mechanism of adenosine formation in the heart." Biochemical Society Transactions 14, no. 6 (December 1, 1986): 1110–11. http://dx.doi.org/10.1042/bst0141110.

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Thampy, K. G. "Formation of malonyl coenzyme A in rat heart." Journal of Biological Chemistry 264, no. 30 (October 1989): 17631–34. http://dx.doi.org/10.1016/s0021-9258(19)84614-8.

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Ryckebusch, L., Z. Wang, N. Bertrand, S. C. Lin, X. Chi, R. Schwartz, S. Zaffran, and K. Niederreither. "Retinoic acid deficiency alters second heart field formation." Proceedings of the National Academy of Sciences 105, no. 8 (February 19, 2008): 2913–18. http://dx.doi.org/10.1073/pnas.0712344105.

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Cunningham, Thomas J., Michael S. Yu, Wesley L. McKeithan, Sean Spiering, Florent Carrette, Chun-Teng Huang, Paul J. Bushway, et al. "Id genes are essential for early heart formation." Genes & Development 31, no. 13 (July 1, 2017): 1325–38. http://dx.doi.org/10.1101/gad.300400.117.

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Diep, Quy N., Odd BrØrs, and Thomas Bøhmer. "Formation of pivaloylcarnitine in isolated rat heart cells." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1259, no. 2 (November 1995): 161–65. http://dx.doi.org/10.1016/0005-2760(95)00151-2.

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Spyridopoulos, Ioakim, and Helen M. Arthur. "Microvessels of the heart: Formation, regeneration, and dysfunction." Microcirculation 24, no. 1 (January 2017): e12338. http://dx.doi.org/10.1111/micc.12338.

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Joziasse, Irene C., Jasper J. Smagt, Kelly Smith, Jeroen Bakkers, Gert-Jan Sieswerda, Barbara J. M. Mulder, and Peter A. Doevendans. "Genes in congenital heart disease: atrioventricular valve formation." Basic Research in Cardiology 103, no. 3 (April 7, 2008): 216–27. http://dx.doi.org/10.1007/s00395-008-0713-4.

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Sasaki, Y. "Role of endothelial cell denudation and smooth muscle cell dedifferentiation in neointimal formation of human vein grafts after coronary artery bypass grafting: therapeutic implications." Heart 83, no. 1 (January 1, 2000): 69–75. http://dx.doi.org/10.1136/heart.83.1.69.

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