Relevant bibliographies by topics / Heart Muscles Diseases

Academic literature on the topic 'Heart Muscles Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Contents

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

Journal articles on the topic "Heart Muscles Diseases":

1

Agafonov, F. D. "The state of the peripheral circulatory system in infectious diseases." Kazan medical journal 25, no. 11 (October 29, 2021): 1210–17. http://dx.doi.org/10.17816/kazmj80472.

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The state of blood circulation and the causes of its disorder, both in chronic and, in particular, in acute infectious diseases, have always been of great interest to both clinicians and pathologists. Since the time of Laennec, who first drew attention to the weakness of the heart muscles in those who died from febrile diseases and emphasized, like Louis, weakness and fragility of the heart muscle, they began to look for the causes of these disorders in the state of the heart muscles. A significant success in the study of diseases of the heart muscle in infectious diseases was the teaching of Virchow about parenchymal inflammation, confirmed by Bttcher for typhoid and Mosler for diphtheria. While these authors spoke only about parenchymal inflammation of the heart muscle, Hayem was able to establish under the same conditions also interstitial myocarditis, and later productive endoarteritis of the coronary vessels, which, causing vascular thrombosis, could be the cause of sudden death during typhoid.
2

Chandragirish S, Harsha B R, and Girish V. Patil. "Morphometric study on papillary muscles of human tricuspid valve-dissection method." Indian Journal of Clinical Anatomy and Physiology 8, no. 3 (October 15, 2021): 190–93. http://dx.doi.org/10.18231/j.ijcap.2021.043.

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Aim of the present study was to observe the measurements of anterior papillary muscles present in tricuspid valve of human heart. Measurements of anterior papillary muscles in tricuspid valve gains utmost importance in cardiac surgeries because they are the causes of myocardial infarction in recent times because of its variations and detection of these causes by advent in modern technologies which will help in treatment of tricuspid valve diseases. This study was carried out on 96 normal formalin fixed human heart specimens. Dissection was performed according to standard techniques. Anterior papillary muscles were observed and length, width and thickness of each muscle were measured and documented. In the present study, numbers of anterior papillary muscles were present with a frequency of 1-3, with most common appearance of 1 muscle in 66 hearts (68.8%) and least common incidence of 3 muscles in 6 hearts (6.3%). Anterior papillary muscles were present in all 96 hearts. In measurements, anterior papillary muscles mean height was 1.49±0.44 cm; mean width was 0.82±0.21 cm and mean thickness was 0.64±0.15 cm respectively. We hope this study will serve to understand the morphometry of anterior papillary muscles better and will help in various surgical procedures and cardiac treatment done on tricuspid valve.
3

Gorkova, N. B., L. M. Starykh, and L. E. Karpova. "A case of early pelvic-brachial progressive muscular dystrophy with severe heart involvement." Kazan medical journal 72, no. 2 (February 15, 1991): 142–44. http://dx.doi.org/10.17816/kazmj106605.

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Progressive muscular dystrophies (PMD) are a group of hereditary diseases characterized by a primary dystrophic process in muscle tissue. The peculiarity and characteristics of cardiac disorders depend both on the nosological form with a characteristic muscle pathology for each of them, and on the stage, severity of the course of the disease and the mass of the affected muscles, and circulatory failure is less pronounced than damage to skeletal muscles.
4

Jörgen Sandell and Mark Davies. "Benefits of sauna on lung capacity, neurocognitive diseases, and heart health." World Journal of Advanced Research and Reviews 17, no. 1 (January 30, 2023): 057–62. http://dx.doi.org/10.30574/wjarr.2023.17.1.1414.

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Sauna refers to passive heat therapy that involves exposure of the body to a high-temperature environment for an appropriately short period, contingent on the therapy’s purpose. Ideally, the therapy aims to raise the internal body temperature by a few degrees, and its effect happens in two phases. The first phase occurs during the first ten minutes, encouraging the body to perspire while maintaining a temperature of around 98.6 degrees. The extra heat is dispersed by increased blood circulation, blood pushing on the skin's surface, and sweating. The body enters the second phase after 10-30 minutes in the sauna. During this period, the body cannot disperse the sauna heat, thereby increasing the body temperature. In return, the heart rate and sweating increase. There are four different types of saunas. These include traditional saunas, usually heated with wood-burning stoves, rocks, or an electric coil. Far-infrared saunas are usually heated by metallic or ceramic elements that produce a small spectrum of light, referred to as far-infrared. Infrared lamp saunas are heated using heat lamps that produce radiant heat. The last type is steam saunas, traditionally heated, but water increases the humidity and air temperatures. During sauna therapy, the heart rate of an individual increase from the standard range up to 120 or 150 beats per minute. Unlike physical activity, sauna therapy does not involve any active function of the skeletal muscles. Even though skeletal muscles are inactive during a sauna session, blood volume is partially redirected to the internal organs' exterior body parts due to decreased venous return. Sauna therapy assists in liberating toxins piled in our tissues, facilitating lymph and blood circulation and strengthening one's immune system. Sauna bathing has mainly been used for purposes of relaxation and pleasure. Today, the activity is increasingly becoming popular as a form of treatment therapy. Several pieces of evidence claim that sauna bathing has numerous health benefits, including hemodynamic regulation processes, reduced risk of vascular diseases, cardiovascular disease, neurocognitive diseases, mortality, pulmonary diseases, stabilized arterial blood pressure, and enhancement of conditions such as flu, headache, and arthritis. However, response to stress from heat can increase muscle blood flow. This report will precisely explore the benefits of sauna bathing on lung capacity and heart health for people with cardiovascular, lung-related or respiratory-related, and neurocognitive diseases.
5

Nazir, Muhammad Mudasser, Muhammad Mazhar Ayaz, Atif Nisar Ahmed, Azhar Maqbool, Kamran Ashraf, Muhammad Oneeb, Ghulam Yasin, et al. "Prevalence of Toxoplasma gondii, Neospora caninum, and Sarcocystis Species DNA in the Heart and Breast Muscles of Rock Pigeons (Columbia livia)." Journal of Parasitology Research 2018 (2018): 1–4. http://dx.doi.org/10.1155/2018/6264042.

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Little is known about the prevalence of protozoan parasites in the muscles of rock pigeons (Columbia livia). The muscles from 54 (heart from 45 and breast from 54) rock pigeons were examined for DNA of Toxoplasma gondii, Neospora caninum, and Sarcocystis species using PCR. Twenty-four were female and 30 were males. The birds were part of flocks of pigeons housed at the tombs of saints in Lahore, Pakistan. Birds that died or were euthanized due to poor health were submitted for necropsy at the Department of Parasitology, University of Veterinary and Animal Sciences, Lahore, Pakistan, where DNA isolations and PCR were conducted. Nineteen (35.1%) of the birds were positive for T. gondii DNA. Seven males and 12 females were positive. Breast tissue was always infected in T. gondii positive birds, while the heart was infected in 13 (28.8%) of breast positive birds. Five (9.2%) of the pigeons, 2 males and 3 females, were positive for N. caninum. The distribution of N. caninum DNA was more variable in the muscles of pigeons than T. gondii and was found only in the heart of 1 (female), heart and breast muscle of 2 (male), and only the breast muscle of 2 birds (female). One of the 54 rock pigeons (female) was positive for both T. gondii (heart and breast) and N. caninum (heart only). Two of the positive Neospora caninum amplicons were sequenced and had 97% nucleotide identity with N. caninum isolates. Sarcocystis DNA was not found in any bird. The prevalence of T. gondii in rock pigeons and their predation by cats suggest that they may play an unrecognized role in maintaining environmental contamination with T. gondii oocysts by cats. Our study indicates that rock pigeons are intermediate hosts of N. caninum and this information will aid in understanding the epidemiology of N. caninum.
6

Shaikh, Rumana M. "Cardiovascular Diseases Prediction Using Machine Learning Algorithms." Turkish Journal of Computer and Mathematics Education (TURCOMAT) 12, no. 6 (April 11, 2021): 1083–88. http://dx.doi.org/10.17762/turcomat.v12i6.2426.

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A broad variety of health conditions are involved in heart disease. Several illnesses and disorders come under the heart disease umbrella. Heart disease forms include: In arrhythmia, abnormality of the heart rhythm. Arteriosclerosis, Hardening of the arteries is atherosclerosis. Via cardiomyopathy, this disorder causes muscles in the heart to harden or grow weak. Defects of the congenital heart, heart abnormalities that are present at birth are congenital heart defects. Disease of the coronary arteries (CAD), the accumulation of plaque in the heart's arteries triggers CAD. It's called ischemic heart disease occasionally. Infections of the heart, bacteria, viruses, or parasites may trigger heart infections. Heart diseases namely arrhythmias, coronary heart disease, heart attacks, cardiomyopathy will be detect using the proposed algorithm in this paper. Here I compared three algorithms namely Restricted Boltzmann Machines, Deep Belief Networks and Convolutional Neural Networks for electrocardiogram (ECG) classification for heart disease.
7

Dubuisson, Nicolas, Romain Versele, María A. Davis-López de Carrizosa, Camille M. Selvais, Sonia M. Brichard, and Michel Abou-Samra. "Walking down Skeletal Muscle Lane: From Inflammasome to Disease." Cells 10, no. 11 (November 4, 2021): 3023. http://dx.doi.org/10.3390/cells10113023.

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Over the last decade, innate immune system receptors and sensors called inflammasomes have been identified to play key pathological roles in the development and progression of numerous diseases. Among them, the nucleotide-binding oligomerization domain (NOD-), leucine-rich repeat (LRR-) and pyrin domain-containing protein 3 (NLRP3) inflammasome is probably the best characterized. To date, NLRP3 has been extensively studied in the heart, where its effects and actions have been broadly documented in numerous cardiovascular diseases. However, little is still known about NLRP3 implications in muscle disorders affecting non-cardiac muscles. In this review, we summarize and present the current knowledge regarding the function of NLRP3 in diseased skeletal muscle, and discuss the potential therapeutic options targeting the NLRP3 inflammasome in muscle disorders.
8

Caron, Marc-André, Richard Debigaré, P. N. Richard Dekhuijzen, and François Maltais. "Comparative assessment of the quadriceps and the diaphragm in patients with COPD." Journal of Applied Physiology 107, no. 3 (September 2009): 952–61. http://dx.doi.org/10.1152/japplphysiol.00194.2009.

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Chronic obstructive pulmonary disease (COPD) and other chronic diseases such as heart failure are accompanied by skeletal muscle alterations that further enhance morbidity and mortality in affected individuals. Several studies have highlighted important structural and biochemical modifications in limb and respiratory muscles in COPD. Reviewing the similarities and differences between the two most studied muscles in COPD, the quadriceps and the diaphragm, may be helpful in providing important clues about the mechanisms underlying muscle changes associated with this disease. Although oxidative stress is present in both muscles, other muscle alterations are clearly distinct between the quadriceps and the diaphragm. For example, the oxidative metabolism varies in opposite directions, the diaphragm exhibiting increased resistance to fatigue while the quadriceps in COPD is characterized by premature fatigability. Differences in muscle phenotypic expression between the diaphragm and the quadriceps indicate that, in addition to systemic factors, the local microenvironment must participate in the reorganization seen in these two skeletal muscles in COPD.
9

Kovalev, Dmitriy. "Myocarditis complicated by therapy-resistant heart failure." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 2 (February 1, 2020): 55–60. http://dx.doi.org/10.33920/med-10-2002-07.

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Myocarditis is an inflammation of the heart muscles, caused by direct or indirect — through immune mechanisms — exposure to infectious, physical and chemical factors, as well as developing in case of autoimmune diseases and heart transplantation. Inflammatory myocardial diseases are one of the rare nosological forms in cardiology, which, despite its nearly two-century history, still does not have clear guidelines for diagnosis and treatment.
10

Moalla, Wassim, Grégory Dupont, Abdou Temfemo, Yves Maingourd, Matthew Weston, and Said Ahmaidi. "Assessment of exercise capacity and respiratory muscle oxygenation in healthy children and children with congenital heart diseases." Applied Physiology, Nutrition, and Metabolism 33, no. 3 (June 2008): 434–40. http://dx.doi.org/10.1139/h07-196.

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Muscular and cardiorespiratory dysfunction contributes to exercise intolerance. Therefore, the aim of the present study was to characterize the cardiopulmonary response andrespiratory muscle oxygenation of children with congenital heart diseases (CHD) when compared with those of healthy children. Twelve children with CHD in New York Heart Association (NYHA) class II or III, and 14 healthy children participated in the study. All subjects performed conventional spirographic measurements and a cardiopulmonary exercise test on a cycle ergometer. Oxygen uptake (VO2), carbon dioxide production (VCO2), minute ventilation (VE), heart rate (HR), and power output were measured. Oxygenation of respiratory muscles was assessed by near-infrared spectroscopy (NIRS) during exercise and recovery. Pulmonary function was normal and no significant difference was found between groups. At rest, CHD patients had cardiorespiratory variables comparable with those of the healthy group. At submaximal intensity (ventilatory threshold) and at peak exercise, power output, HR, VO2, VCO2, and VE were significantly reduced (p < 0.01) in CHD patients. Respiratory muscles deoxygenated during exercise in both groups. However, deoxygenation was more pronounced in the CHD group than in the healthy children from an intensity of 40% up to exhaustion. Likewise, children with CHD showed a slower recovery of oxygenation than healthy children (113.4 ± 17.5 vs. 74.6 ± 13.0 s; p < 0.001). Compared with healthy children, these results demonstrated that children with CHD have reduced performance and present a defected exercise capacity. Children with CHD showed a more pronounced decrease of respiratory muscle oxygenation and slower recovery of oxygen kinetics.
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You might also be interested in the extended bibliographies on the topic 'Heart Muscles Diseases' for particular source types:
Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Heart Muscles Diseases":

1

Gieseking, Elizabeth Robinson. "Control mechanism for the papillary muscles of the mitral valve : an In Vitro study." Thesis, Georgia Institute of Technology, 1989. http://hdl.handle.net/1853/10912.

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2

Warner, Anke Sigrid. "The expression, regulation and effects of inducible nitric oxide synthase in hibernating myocardium." Title page, contents and summary only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phw279.pdf.

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Amendments inserted at back. "May 2002" Includes bibliographical references (leaves 237-290) Experiments described in this thesis address the potential role of inducible nitric oxide synthase (iNOS) in hibernating myocardium. Specifically it was sought to establish a cellular model of hibernating myocardium and investigate the expression, regulation and effects of iNOS in this model. Experiments were performed using primary cultures of neonatal rat ventricular myocytes.
3

Messaggi-Sartor, Monique 1984. "Respiratory muscle dysfunction in respiratory and non-respiratory diseases : clinical and therapeutic approaches." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/565809.

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Respiratory muscle dysfunction is a clinical condition that may be present in both respiratory and non-respiratory diseases. This impairment of muscle function can have a negative effect on clinical outcomes, contributing to a further worsening of the patient’s clinical condition. This doctoral thesis has been directed by the ‘Rehabilitation Research Group’ (RERG) in collaboration with the Muscle Wasting and Cachexia in Chronic Respiratory Diseases and Lung Cancer Group (Lung Cancer and Muscle Research Group) of the Institut Hospital del Mar d’Investigacions Mèdiques (IMIM) in Barcelona. Muscle dysfunction has been a priority area of research in these groups from different perspectives: exercise and muscle training in the RERG, Physiopathology and Molecular Biology in the Lung Cancer and Muscle Research Group. The large number of published studies in journals with high impact factor endorses the quality and leadership of these research groups. Up to then, research on RMT had focused on patients with chronic obstructive pulmonary disease, but had been scarcely addressed in other conditions. In the last 5 years, the RERG has aimed to study the effects of RMT in other respiratory diseases (bronchiectasis, lung cancer) and in non-respiratory diseases. The study of respiratory muscle dysfunction in stroke patients has made it possible to start an increasing collaboration with neurorehabilitation researchers, in which RMT plays a role in the management of patients with dysphagia.
La disfunción muscular respiratoria es una condición clínica que puede estar presente tanto en las enfermedades respiratorias como no respiratorias. Este deterioro de la función muscular puede tener un efecto negativo en los resultados clínicos, lo que contribuye a un mayor empeoramiento de la condición clínica del paciente. Esta tesis doctoral ha sido dirigida por el "Grupo de Investigación en Rehabilitación" (RERG) en colaboración con el Grupo de Investigación de Enfermedades Respiratorias Crónicas y Cáncer de Pulmón (Grupo de Investigación de Cáncer de Pulmón y Músculo) del Instituto Hospital del Mar de Investigaciones Mèdiques (IMIM) en Barcelona. La disfunción muscular ha sido un área prioritaria de investigación en estos grupos desde diferentes perspectivas: ejercicio y entrenamiento muscular en el RERG, Fisiopatología y Biología Molecular en el Cáncer de Pulmón y el Grupo de Investigación Muscular. El gran número de estudios publicados en revistas con alto factor de impacto refuerza la calidad y liderazgo de estos grupos de investigación. Hasta entonces, la investigación sobre RMT se había centrado en los pacientes con enfermedad pulmonar obstructiva crónica, pero apenas se había abordado en otras condiciones. En los últimos 5 años, el RERG se ha propuesto estudiar los efectos de la RMT en otras enfermedades respiratorias (bronquiectasias, cáncer de pulmón) y en enfermedades no respiratorias. El estudio de la disfunción de los músculos respiratorios en los pacientes con ictus ha permitido iniciar una creciente colaboración con los investigadores de neurorehabilitación, en los que RMT desempeña un papel en el tratamiento de los pacientes con disfagia.
4

Spinner, Erin M. "Tricuspid valve mechanics: understanding the effect of annular dilatation and papillary muscle displacement." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/45754.

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Tricuspid regurgitation (TR), back flow of blood from the right ventricle to the right atrium, has been reported in approximately 85% of the population, with 16% having mild or severe TR. Patients with untreated moderate to severe TR are likely to experience decreased exercise capacity and have increased morbidity and mortality, thus affecting the patient's quality of life. Current methods of repair offer limited rates of success, and many patients require further operations to correct returning levels of TR. Incomplete repair may be due to incomplete understanding of the functional anatomy and mechanics of the TV and the underlying causes of TR. It was hypothesized that alterations in the geometry of tricuspid valve annular and subvalvular apparatus induced by ventricular dilatation determine the severity of TR. In vivo measurements of papillary muscle (PM) position in patients with single or biventricular dilatation revealed PM displacement away from the center of the annulus as compared to control patients. Additionally, pulmonary arterial pressure, annulus area, ventricular size and apical displacement of the anterior PM were highly correlated with the severity of TR. An in vitro right-heart simulator was developed to investigate isolated mechanics of TR. Through these in vitro studies it was demonstrated that the tricuspid valve begins to leak at only 40% dilation, much lower than the mitral valve. Additionally, it was shown that isolated PM displacement resulted in significant TR. The highest levels of TR were achieved with a combination of annular dilatation and PM displacement. Alterations in leaflet coaptation, as quantified by measuring the amount of leaflet available for coaptation and leaflet mobility were observed with annular dilatation and PM displacement, both isolated and combined. The changes in leaflet coaptation resulted in redistribution of the forces on the chords originating from the anterior PM and inserting into the anterior and posterior leaflets. The findings herein provide the clinical and scientific community with a mechanistic understanding of the tricuspid valve to further improve intervention and repair of TV disease.
5

Yentrapalli, Venkata Ramesh. "Novel radiation targets in the endothelium and heart muscle." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-90429.

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Worldwide, people are being exposed to natural and man-made sources of radiation. Epidemiological studies have shown an increased risk of vascular diseases in populations that have been exposed to ionizing radiation. Vascular endothelium is implicated as one of the targets for radiation leading to the development of cardiovascular diseases. However, the molecular mechanisms behind the development of radiation-induced cardiovascular disease in acute or chronic exposed people are not fully elucidated. The hypothesis that chronic low dose rate ionizing radiation accelerates the onset of senescence of primary human umbilical vein endothelial cells has been tested in papers I and II presented in this thesis. In vitro studies show that, when exposed to continuous low dose rate gamma radiation these cells enter premature senescence much earlier than non-irradiated control cells. Quantitative proteomic analysis using isotope coded protein labeling coupled to LC-ESI-mass spectrometry and followed by protein network analysis identified changes in senescence-related biological pathways including cytoskeletal organisation, cell-cell communication and adhesion, and inflammation influenced by radiation. Moreover, the role of PI3K/Akt/mTOR pathway was implicated during the senescence process. Thus, chronic low dose rated endothelial senescence may contribute to increased risk of radiation-induced cardiovascular disease. Paper III analyse the long-term effects of local high doses of radiation to the heart using a mouse model. The results from proteomic and bioinformatics analysis indicated that an impaired activity of the peroxisome proliferator-activated receptor-alpha (PPARA) is involved in mediating the radiation response. Ionizing radiation markedly changed the phosphorylation and ubiquitination status of PPARA. This was reflected by the decreased expression of PPARA target genes involved in energy metabolism and mitochondrial respiratory chain. This in vivo study suggests that alteration of cardiac metabolism contributes to the impairment of heart structure and function after radiation. Taken together, these in vitro and in vivo studies provide novel information on the pathways in heart and endothelial cells that are affected over longer periods of time by ionizing radiation.
6

Pandofino, Alexandra. "A molecular analysis of the basis of cardiovirulence of Coxsackievirus B3." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267166.

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7

Colegrave, Melanie. "Expression of #beta#-cardiac myosin in a myogenic cell line." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342254.

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8

Vesier, Carol Cockerham. "The role of papillary muscle-mitral valve geometry in systolic anterior motion of the mitral valve." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/10279.

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9

Chung, Jae-Hoon. "Regulation of Human Cardiac Muscle Contraction and Relaxation in Health and Disease." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1522851185767187.

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10

Johnson, Andrew William. "Metabolic control of energetics in human heart and skeletal muscle." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:82c0dce6-a162-4c08-b061-3ea7f2e35134.

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Myocardial and skeletal muscle high energy phosphate metabolism is abnormal in heart failure, but the pathophysiology is not understood. Plasma non-esterified fatty acids (NEFA) increase in heart failure due to increased sympathetic drive, and regulate the transcription of mitochondrial uncoupling protein-3 (UCP3), through peroxisome proliferator-activated receptor-α. The aim of the work in this thesis was to determine whether cardiac PCr/ATP ratios and skeletal muscle PCr kinetics during exercise were related to cardiac and skeletal muscle UCP3 levels respectively, thus providing a mechanism for the apparent mitochondrial dysfunction observed in heart failure. Patients having cardiac surgery underwent pre-operative testing, including cardiac and gastrocnemius 31P magnetic resonance spectroscopy. Intra-operatively, ventricular, atrial and skeletal muscle biopsies were taken for measurement of mitochondrial protein levels by immunoblotting, along with mitochondrial function by tissue respiration rates. Fasting plasma NEFA concentrations increased in patients with ventricular dysfunction and with New York Heart Association (NYHA) class. Ventricular UCP3 levels increased and cardiac PCr/ATP decreased with NYHA class, however, demonstrated no relationship to each other. In skeletal muscle, maximal rates of oxidative ATP synthesis (Qmax) related to functional capacity. Skeletal muscle UCP3 levels increased with NYHA class but were unrelated to skeletal muscle Qmax. Tissue respiration experiments revealed no relationship between ventricular function and indices of mitochondrial coupling, furthermore, indices of mitochondrial coupling were unrelated to tissue UCP3 levels. No evidence was found to support mitochondrial uncoupling, mediated through UCP3, as a cause of the abnormalities in cardiac and skeletal muscle high energy phosphate metabolism.
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Books on the topic "Heart Muscles Diseases":

1

Williams, Andrew D. Skeletal muscle in heart failure and type 2 diabetes. New York: Nova Biomedical Books, 2010.

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2

Goodwin, J. F., ed. Heart Muscle Disease. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7.

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3

International Symposium on the Clinical Value of the Anaerobic Threshold in Heart and Lung Diseases (1985 Verzuno, Italy). The anaerobic threshold: Physiological and clinical significance. Edited by Tavazzi L and Di Prampero P. E. Basel: Karger, 1986.

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4

Sörnmo, Leif. Bioelectrical signal processing in cardiac and neurological applications. Amsterdam: Elsevier Academic Press, 2005.

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5

Nuno, Azóia, and Dobreiro Pedra, eds. Treadmill exercise and its effects on cardiovascular fitness, depression, and muscle aerobic function. Hauppauge, N.Y: Nova Science Publisher, 2009.

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6

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

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7

OHOLO Conference (34th 1989 Elat, Israel). Calcium channel modulators in heart and smooth muscle: Basic mechanisms and pharmacological aspects : proceedings of the 33rd [i.e. 34th] Oholo Conference, Eilat, Israel, 1989. Rehovot, Israel: Balaban Publishers, 1990.

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L, Archer Stephen, and Rusch Nancy Jean, eds. Potassium channels in cardiovascular biology. New York: Kluwer Academic/Plenum, 2001.

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Wang, Tammy, Jocelyn Wong, and Anita Honkanen. Glycogen Storage Diseases. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0048.

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Glycogen storage diseases result from deficiencies of various enzymes or proteins in the pathways of glycogen metabolism. The reduction in effective glucose storage and/or mobilization results in hypoglycemia and accumulation of glycogen in tissues. Diagnosis can occur at any age, from infancy to adulthood, depending on the pathway affected and the degree of enzyme deficiency. The clinical presentation varies, but the most commonly affected organ systems include the heart, liver, and skeletal muscles. In addition to the morbidity that can occur from dysfunction of these organs, important anesthetic implications include administration of glucose-containing fluids to avoid hypoglycemia, monitoring for acidosis, and caution with use of depolarizing muscle relaxants because of the potential risk of hyperkalemia and rhabdomyolysis. Inheritance is commonly autosomal recessive.
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Ramrakha, Punit, and Jonathan Hill, eds. Heart muscle diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0008.

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Classification 418Dilated cardiomyopathy 420Dilated cardiomyopathy: treatment 422Hypertrophic cardiomyopathy 424Hypertrophic cardiomyopathy: investigations 428Hypertrophic cardiomyopathy: treatment 430Restrictive cardiomyopathy 432Cardiac amyloidosis 434Cardiac amyloidosis: treatment 436Fabry disease 438Arrhythmogenic right ventricular cardiomyopathy (ARVC) 440ARVC: management 442Left ventricular non-compaction ...
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Book chapters on the topic "Heart Muscles Diseases":

1

Bogaert, J., and A. M. Taylor. "Heart Muscle Diseases." In Clinical Cardiac MRI, 275–353. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/174_2011_358.

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2

Wenger, N. K. "Specific heart muscle diseases." In Heart Muscle Disease, 95–139. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_5.

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3

Oakley, C. M. "Amyloid heart disease." In Heart Muscle Disease, 141–53. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_6.

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Goodwin, J. F. "Cardiomyopathies and specific heart muscle diseases: definition, terminology and classification." In Heart Muscle Disease, 1–5. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_1.

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Perloff, J. K., J. F. Goodwin, D. D. Sugrue, and W. J. McKenna. "Hypertrophic Cardiomyopathy." In Heart Muscle Disease, 7–56. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_2.

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Olsen, E. G. J., and R. O. Brandenburg. "Dilated (Congestive) Cardiomyopathy." In Heart Muscle Disease, 57–86. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_3.

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Davies, J. "Restrictive cardiomyopathy." In Heart Muscle Disease, 87–94. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_4.

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Criley, J. M., R. J. Siegel, J. P. Murgo, J. W. Miller, H. Kuhn, E. D. Wigle, M. Henderson, Z. Sasson, C. Pollick, and H. Rakowski. "Hypertrophic Cardiomyopathy—The Obstructive Dilemma." In Heart Muscle Disease, 157–262. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_7.

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Lowry, P. J., W. A. Littler, and H. D. Bolte. "Dilated (Congestive) Cardiomyopathy—The evidence for and Against a Disorder of Cellular Immunity and Infection." In Heart Muscle Disease, 263–84. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7_8.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Heart Muscle Diseases, Toxic." In Encyclopedia of Molecular Mechanisms of Disease, 783–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1760.

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Conference papers on the topic "Heart Muscles Diseases":

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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly more dystrophin-positive fibers were found within the myocardium than in the GN. We hypothesized that the differences in mechanical loading of the two environments influenced the transplantation and explored whether using MDSCs exposed to mechanical stimulation prior to transplantation could improve transplantation. Our study shows increased engraftment into the heart and GN muscle for cells pretreated with mechanical stretch for 24 hours. This increase was significant for transplantation into the heart. These studies have implications in a variety of applications including mechanotransduction, stem cell biology, and Duchenne muscular dystrophy.
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Moussa, Heba Adel Mohamed Lotfy, Gawaher Saleh Abbas Mahgoub, Mashael Ali H. I. Al-Badr, and Huseyin Cagatay Yalcin. "Investigating the Cardiac Effects of Sildenafil loaded Nanoparticles on Heart Failure using the Zebrafish Embryo Model." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0217.

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Background: Cardiovascular diseases (CVDs) are the first cause of death worldwide. Vasolidator agents are used to relax cardiac muscle, but their extremely short half-lifes limit their effectiveness. Sildenafil is such an agent used to relax the blood vessels muscles and increase the blood flow. The conventional drug can lead to serious problems in patients duo to the systematic drug delivery. Use of Nanomedicine potentially can enhance delivery of this agent while reducing the systematic effect of the drug. Aim: The purpose of the research is to examine the effectiveness sildenafil loaded nanoparticles in rescuing heart failure using zebrafish embryo model. Methods: There will be five experimental groups. The zebrafish will be treated with Aristolochic Acid (AA) at 24 hour per fertilization (hpf) to create the heart injury group. The treatment groups will be heart injury followed by a dose of either Sildenafil or Sildenafil loaded nanoparticles at 36 hpf. Two control groups will be the negative control (exposed to egg water) and vehicle control (exposed to the Dimethylsulfoxide (DMSO)).To evaluate the drug effects on embryo, toxicity assessment (Survival rate, tail flicking and hatching rate), cardiotoxicity assessment and gene expression of heart injury marker via RT-PCR will be conducted. Results: Preliminary findings demonstrate, loading Sildenafil to nanoparticles enhances its effectiveness dramatically. The experiments are ongoing to confirm the results. Conclusion: Nanomedicine is a powerful approach to enhance cardiovascular therapy. Vasodilator drugs in particular will benefit from this improvement as demonstrated with our findings
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Mesihović-Dinarević, Senka. "WHAT IS NEW IN CARDIOVASCULAR MEDICINE?" In Symposium with International Participation HEART AND … Akademija nauka i umjetnosti Bosne i Hercegovine, 2019. http://dx.doi.org/10.5644/pi2019.181.03.

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The rapid pace of change continues to be a hallmark in cardiovascular medicine and many see that pace accelerating in adult cardiovascular medicine as well as in paediatric cardiology medicine. Cardiovascular medicine is an area of clinical practice with a continually rapid expansion of knowledge, guidelines, best practices and new technology. Cardiovascular diseases are the leading cause of mortality in the world and cause major costs for the health sector and economy. Primary care clinicians are challenged to optimally manage a multitude of diseases including congestive heart failure, coronary artery disease, valvular diseases, arrhythmias, lipid disorders, and hypertension. Multimodality imaging techniques are being used more frequently as their utility is better appreciated. Echocardiography has been the mainstay approach, cardiac computerized tomography and magnetic resonance imaging provide a good imaging alternative for patients with multiple complex surgeries. 3D printing has seen a rapid growth in use for planning treatments for patients with congenital heart disease. Simulation using 3D models is emerging as a fundamental resource for teaching procedural techniques and a new standard of care. Artificial intelligence holds the greatest potential for revolutionizing medicine. Innovative technologies in the world of cardiovascular health are expanding every day: wearable computing technologies, bioresorbable stents, leadless pacemaker, valve-in-valve procedure, protein patch for heart muscle growth and others. As a part of lifelong learning process for all professionals in cardiovascular medicine, the imperative is to have continuity of reviewing novelties, with results data from numerous researches in order to treat patient according to best practices and evidence-based medicine.
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Schroer, Alison K., and W. David Merryman. "Integrin-Focal Adhesion Coupling and Substrate Stiffness Affect Smooth Muscle Alpha Actin Expression in Fibroblasts." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80887.

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Fibroblast cells play a key role in producing and maintaining connective tissue throughout the body. The ability of these cells to differentiate into a more active myofibroblastic phenotype is important during development and wound healing, but prolonged myofibroblast activation can lead to overproduction of extracellular matrix proteins and stiffening of the surrounding tissue. This stiffening can cause heightened differentiation of neighboring fibroblast through force transduction pathways and can lead to detrimental fibrotic pathologies in many organ systems. Atherosclerosis, interstitial lung disease, cirrhosis and heart valve disease are fibrotic diseases that cause significant cost and mortality in our society. Understanding the processes by which cells sense and respond to substrate stiffness is crucial to the treatment of connective tissue diseases. One primary indicator of the myofibroblastic phenotype is the production of α smooth muscle actin (αSMA) bundles called stress fibers which help transmit stress inside the cell and increases the contractility of the cells and their surrounding tissue [1].
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van der Horst, Arjen, Frits L. Boogaard, Marcel C. M. Rutten, and Frans N. van de Vosse. "A 1D Wave Propagation Model of Coronary Flow in a Beating Heart." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53367.

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Due to recent developments in miniaturized sensors on guide-wires, assessment of coronary artery disease with intracoronary pressure and flow measurements has become available. However, direct quantification is still limited to the large epicardial vessels, which means that microvascular disease can only be determined from upstream measurements using an appropriate model of the vessels and their interaction with the cardiac muscle [1].
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Raskina, Tatiana, Inessa Grigoreva, Olga Barbarash, Alexander Kokov, and Vladislava Masenko. "AB0848 BMD AND MUSCLE MASS IN PATIENTS WITH ISCHEMIC HEART DISEASE." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3662.

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Etebari, Ali, Olga Pierrakos, and Pavlos P. Vlachos. "Automatic MRI Image Segmentation and Left Ventricle Surface Reconstruction for Characterizing Myocardial Muscle Function." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32251.

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Normal left ventricular function is characterized by synchronous firing of myocardial muscle fibers. Healthy myocardial function is essential in maintaining cardiac output, and any disturbance to the contracting muscle cells can be detrimental to the health of the heart. A method for non-invasively monitoring left ventricle (LV) operation is necessary for documenting the progression of heart disease and malfunction, such that the point at which disease becomes irreversible can be determined.
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Dolensky, Joseph R., Lauren D. C. Casa, and Ajit P. Yoganathan. "The Effect of Pulmonary Hypertension on Tricuspid Valve Coaptation in Normal and Pathologic Valve Geometries: An In Vitro Study." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80184.

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Pulmonary hypertension (PHTN) is a pathological condition defined as a mean pulmonary artery pressure (mPAP) greater than 25 mmHg. PHTN can result from a number of lung and heart pathologies, including abnormalities of the pulmonary vasculature, left heart disease, chronic lung disease, and chronic thrombotic disease [1]. Regardless of the cause, the increased afterload on the right heart results in right ventricle (RV) hypertrophy and dilatation and tricuspid regurgitation (TR) [2]. RV dilatation is thought to result in the displacement of the tricuspid valve (TV) papillary muscles (PM) and dilatation of the TV annulus, negatively impacting TV function.
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Sewell-Loftin, M. K., and W. David Merryman. "The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53604.

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Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following the production of αSMA, there is an increase in the synthesis of extracellular matrix (ECM) proteins, most notably type I collagen; this increase in ECM proteins causes the stiffening of the tissue characteristic of fibrotic disease. In non-disease states (such as wound healing or tissue development), the myofibroblasts will either deactivate, becoming fibroblasts again, or apoptose before tissue fibrosis occurs. However, when myofibroblasts persist, increased ECM protein deposition causes increased tissue stiffness and activates neighboring cells, causing the fibrosis to propagate. Currently there are no therapies to prevent or reverse fibrosis. Therefore a more thorough understanding of the dynamic mechanical environment and signaling pathways involved in the activation of fibroblasts is required to develop potential treatments.
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Ivanov, Zhanna A., Robert C. Scott, Jenna Rosano, Barbara Krynska, and Mohammad F. Kiani. "Engineering Cardiac Tissue Using Stem Cell Therapy to Mend the Broken Heart." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203624.

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Myocardial infarction (MI) is one of the most severe forms of coronary artery disease and is the leading cause of death in the United States [1]. Current treatments for an MI are either highly invasive, such as coronary artery bypass grafting and stent angioplasty, or might have undesirable long-term effects as is the case with pharmacological interventions. However, newly emerging methodologies, such as a less invasive stem cell therapy, aim to cure the disease rather than just alleviate its symptoms. This new tissue engineering technology has shown promise in restoring the homeostasis of the heart muscle after MI in preclinical and clinical studies [2]. However, controversies regarding inconsistent methodologies and a lack of mechanistic understanding of its actions have hampered progress in this field [3].

Reports on the topic "Heart Muscles Diseases":

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Kanner, Joseph, Edwin Frankel, Stella Harel, and Bruce German. Grapes, Wines and By-products as Potential Sources of Antioxidants. United States Department of Agriculture, January 1995. http://dx.doi.org/10.32747/1995.7568767.bard.

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Several grape varieties and red wines were found to contain large concentration of phenolic compounds which work as antioxidant in-vitro and in-vivo. Wastes from wine production contain antioxidants in large amounts, between 2-6% on dry material basis. Red wines but also white wines were found to prevent lipid peroxidation of turkey muscle tissues stored at 5oC. The antioxidant reaction of flavonoids found in red wines against lipid peroxidation were found to depend on the structure of the molecule. Red wine flavonoids containing an orthodihydroxy structure around the B ring were found highly active against LDL and membrane lipid peroxidation. The antioxidant activity of red wine polyphenols were also found to be dependent on the catalyzer used. In the presence of H2O2-activated myoglobin, the inhibition efficiency was malvidin 3-glucoside>catechin>malvidin>resveratol. However, in the presence of an iron redox cycle catalyzer, the order of effectiveness was resveratol>malvidin 3-glucoside = malvidin>catechin. Differences in protein binding were found to affect antioxidant activity in inhibiting LDL oxidation. A model protein such as BSA, was investigated on the antioxidant activity of phenolic compounds, grape extracts, and red wines in a lecithin-liposome model system. Ferulic acid followed by malvidin and rutin were the most efficient in inhibiting both lipid and protein oxidation. Catechin, a flavonal found in red-wines in relatively high concentration was found to inhibit myoglobin catalyzed linoleate membrane lipid peroxidation at a relatively very low concentration. This effect was studied by the determination of the by-products generated from linoleate during oxidation. The study showed that hydroperoxides are catalytically broken down, not to an alcohol but most probably to a non-radical adduct. The ability of wine-phenolics to reduce iron and from complexes with metals were also demonstrated. Low concentration of wine phenolics were found to inhibit lipoxygenase type II activity. An attempt to understand the bioavailability in humans of antocyanins from red wine showed that two antocyanins from red wine were found unchanged in human urine. Other antocyanins seems to undergo molecular modification. In hypercholesterolemic hamsters, aortic lipid deposition was significantly less in animals fed diets supplemented with either catechin or vitamin E. The rate of LDL accumulation in the carotid arteries was also significantly lower in the catechin and vitamin E animal groups. These results suggested a novel mechanism by which wine phenolics are associated with decreased risk of coronary heart diseases. This study proves in part our hypothesis that the "French Paradox" could be explained by the action of the antioxidant effects of phenolic compounds found at high concentration in red wines. The results of this study argue that it is in the interest of public health to increase the consumption of dietary plant falvonoids. Our results and these from others, show that the consumption of red wine or plant derived polyphenolics can change the antioxidant tone of animal and human plasma and its isolated components towards oxidative reactions. However, we need more research to better understand bioavailability and the mechanism of how polyphenolics affect health and disease.

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