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Książki na temat „Cardiac hypertrophy”

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

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1

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

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2

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

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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

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9

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

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10

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

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11

T, Kawaguchi Akira, i Linde Leonard M, red. Partial left ventriculectomy: Its theory, results, and perspectives : proceedings of the Cardiac Volume Reduction Forum '97, held in Tokyo on 4 October 1997. Amsterdam: Elsevier, 1998.

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12

1941-, Maron Barry J., red. Diagnosis and management of hypertrophic cardiomyopathy. Malden, Mass: Blackwell Futura, 2004.

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13

Cardiac Volume Reduction Forum (2nd 1998 Tokyo, Japan). Partial left ventriculectomy: Recent evolution for safe and effective application : proceedings of the 2nd International Symposium on Partial Left Ventriculectomy, Tokyo, Japan, 12 December 1998. Redaktorzy Kawaguchi Akira T i Linde Leonard M. Amsterdam: Elsevier, 1999.

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14

Whyte, Gregory P. Cardiac structure, and exercise gas exchange kinetics in elite multi-disciplinary athletes and hypertrophic cardiomyopathy patients. Wolverhampton: University of Wolverhampton, 1998.

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15

1936-, Williams Richard Allen, red. The athlete and heart disease: Diagnosis, evaluation & management. Philadelphia, PA: Lippincott Williams & Wilkins, 1999.

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16

Schipperheyn, J. J., i Henk Keurs. Cardiac Left Ventricular Hypertrophy. Springer London, Limited, 2012.

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17

Swynghedaun, Bernard. Cardiac Hypertrophy and Failure. John Libbey & Co Ltd, 1990.

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18

H.E.D.J. Ter Keurs. Cardiac Left Ventricular Hypertrophy. Springer, 2011.

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19

Dhalla, Naranjan S., Pawan K. Singal, Larry Hryshko i Elissavet Kardami. Signal Transduction and Cardiac Hypertrophy. Springer London, Limited, 2012.

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20

R, Oberman, Yamama Hafeez, Abraham B. Bornstein i Hajira Basit. Heart Failure and Cardiac Hypertrophy. DI Press, 2022.

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21

Dhalla, Naranjan S., Pawan K. Singal, Larry Hryshko i Elissavet Kardami. Signal Transduction and Cardiac Hypertrophy. Springer, 2012.

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22

Jacob, Ruthard. Experimental Cardiac Hypertrophy and Heart Failure. Steinkopff, Dietrich, 2013.

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23

Yamada, Yoshihiro, Marisa Ojala, Bhattacharya Pt i Yamin Liu. Current Progress in Cardiac Hypertrophy Research. DI Press, 2022.

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24

Walsh, Richard A. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Informa Healthcare, 2004.

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25

Walsh, Richard A. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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26

Walsh, Richard A. Molecular Mechanisms of Cardiac Hypertrophy and Failure. CRC Press, 2005. http://dx.doi.org/10.3109/9780203503249.

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27

A, Walsh Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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28

A, Walsh Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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29

A, Walsh Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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30

A, Walsh Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2019.

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31

A, Walsh Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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32

Walsh, Richard. Molecular Mechanisms of Cardiac Hypertrophy and Failure. Taylor & Francis Group, 2005.

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33

Zhang, Hai-Gang, Ya Liu i Xiongwen Chen, red. Cardiac Hypertrophy: From Compensation to Decompensation and Pharmacological Interventions. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-909-7.

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34

(Editor), Naranjan S. Dhalla, Larry Hryshko (Editor), Elissavet Kardami (Editor) i Pawan K. Singal (Editor), red. Signal Transduction and Cardiac Hypertrophy (Progress in Experimental Cardiology). Springer, 2003.

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35

Reckman, Yolan J., i Yigal M. Pinto. The role of non-coding RNA/microRNAs in cardiac disease. Redaktorzy José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso i Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0031.

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In the past two decades, our knowledge about non-coding DNA has increased tremendously. While non-coding DNA was initially discarded as ‘junk DNA’, we are now aware of the important and often crucial roles of RNA transcripts that do not translate into protein. Non-coding RNAs (ncRNAs) play important functions in normal cellular homeostasis and also in many diseases across all organ systems. Among the different ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have been studied the most. In this chapter we discuss the role of miRNAs and lncRNAs in cardiac disease. We present examples of miRNAs with fundamental roles in cardiac development (miR-1), hypertrophy (myomiRs, miR-199, miR-1/133), fibrosis (miR-29, miR-21), myocardial infarction (miR-15, miR17~92), and arrhythmias/conduction (miR-1). We provide examples of lncRNAs related to cardiac hypertrophy (MHRT, CHRF), myocardial infarction (ANRIL, MIAT), and arrhythmias (KCNQ1OT1). We also discuss miRNAs and lncRNAs as potential therapeutic targets or biomarkers in cardiac disease.
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36

Zoccali, Carmine, Davide Bolignano i Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.

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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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37

Tsoporis, James Nick. Effects of hydralazine on blood pressure and cardiac hypertrophy in the two-kidney, one-clip hypertensive rat. 1985.

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38

Cardim, Nuno, Denis Pellerin i Filipa Xavier Valente. Hypertrophic cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0042.

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Hypertrophic cardiomyopathy is a common inherited heart disease caused by genetic mutations in cardiac sarcomeric proteins. Although most patients are asymptomatic and many remain undiagnosed, the clinical presentation and natural history include sudden cardiac death, heart failure, and atrial fibrillation. Echocardiography plays an essential role in the diagnosis, serial monitoring, prognostic stratification, and family screening. Advances in Doppler myocardial imaging and deformation analysis have improved preclinical diagnosis as well as the differential diagnosis of left ventricular hypertrophy. Finally, echocardiography is closely involved in patient selection and in intraoperative guidance and monitoring of septal reduction procedures. This chapter describes the pathophysiology, clinical presentation, role of echocardiography, morphological features, differential diagnosis, diagnostic criteria in first-degree relatives, echo guidance for the treatment of symptomatic left ventricular outflow tract obstruction, and follow-up and monitoring of patients with hypertrophic cardiomyopathy.
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39

Sah, Rajan. Role of the transient outward potassium current and action potential profile in cardiac excitation-contraction coupling, hypertrophy and failure. 2002.

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40

Maron, Barry J. Diagnosis and Management of Hypertrophic Cardiomyopathy: Sudden Death Prevention. Blackwell Publishing Limited, 2004.

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41

Maron, Barry J. Diagnosis and Management of Hypertrophic Cardiomyopathy. Wiley & Sons, Incorporated, John, 2008.

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42

Maron, Barry J. Diagnosis and Management of Hypertrophic Cardiomyopathy. Wiley & Sons, Incorporated, John, 2008.

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43

Maron, Barry J. Diagnosis and Management of Hypertrophic Cardiomyopathy. Wiley & Sons, Limited, John, 2007.

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44

Kaprielian, Roger. Molecular and cellular mechanisms associated with cardiac hypertrophy following myocardial infarction in rats: Studies on ion channels and intracellular calcium. 2000.

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45

D, Slaughter Graham R. Characterization and identification of the dual-lineage kinase, MUK/DLK in rat myocardium: A possible role in cardiac growth and hypertrophy. 2002.

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46

D’Andrea, Antonello, André La Gerche i Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.

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The term ‘athlete’s heart’ refers to the structural, functional, and electrical adaptations that occur as a result of habitual exercise training. It is characterized by an increase of the internal chamber dimensions and wall thickness of both atria and ventricles. The athlete’s right ventricle also undergoes structural, functional, and electrical remodelling as a result of intense exercise training. Some research suggests that the haemodynamic stress of intense exercise is greater for the right heart and, as a result, right heart remodelling is slightly more profound when compared with the left heart. Echocardiography is the primary tool for the assessment of morphological and functional features of athlete’s heart and facilitates differentiation between physiological and pathological LV hypertrophy. Doppler myocardial and strain imaging can give additional information to the standard indices of global systolic and diastolic function and in selected cases cardiac magnetic resonance imaging may help in the diagnosis of specific myocardial diseases among athletes such as hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy.
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47

Montgomery, Hugh, i Rónan Astin. Normal physiology of the cardiovascular system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0128.

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Preload modulates contractile performance, and is determined by end-diastolic volume (EDV) and ventricular compliance. Compliance falls with increasing preload, muscle stiffness or ventricular hypertrophy, making central venous pressure (CVP) a poor surrogate for EDV. Responsiveness to fluid loading can be identified by seeking a change in stroke volume (SV) with changes in cardiac loading. Afterload, the force to be overcome before cardiac muscle can shorten to eject blood, rises with transmural pressure and end-diastolic radius, and inversely with wall thickness. Afterload, being the tension across the ventricular wall, is influenced by pleural pressure. Reductions in afterload increase SV for any cardiac work, as do reductions in vascular resistance. Resistance is modified by changes in arteriolar cross-sectional area. A rise in resistance increases blood pressure and microvascular flow velocity. Increased resistance may reduce CO if cardiac work cannot be augmented sufficiently. Flow autoregulationis the ability of vascular beds to maintain constant flow across varied pressures by adjusting local resistance.
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48

London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Redaktor Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.

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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudden death are the most frequent causes of death in ESRD. Cardiomyopathy of overload with development of left ventricular hypertrophy and fibrosis are the most characteristic alterations and major determinants of prognosis. Left ventricular hypertrophy may result in systolic and/or diastolic dysfunction and is a risk factor for arrhythmias, sudden death, heart failure, and myocardial ischaemia. Arterial disease, whether due to atherosclerosis or arteriosclerosis (or both), represents a major contributory factor to the cardiovascular complications. Arterial disease may result in ischaemic complications (ischaemic heart disease, peripheral artery diseases) or arterial stiffening with direct consequences on left ventricular afterload, decreased coronary perfusion, and microvascular abnormalities (inward remodelling and microvessel rarefaction).
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49

O’Mahony, Constantinos. Hypertrophic cardiomyopathy: prevention of sudden cardiac death. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0354.

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Sudden cardiac death (SCD) secondary to ventricular arrhythmias is the most common mode of death in hypertrophic cardiomyopathy (HCM) and can be effectively prevented with an implantable cardioverter defibrillator (ICD). The risk of SCD in HCM relates to the severity of the phenotype and regular risk stratification is an integral part of routine clinical care. For the primary prevention of SCD, risk stratification involves the assessment of seven readily available clinical parameters (age, maximal left ventricular wall thickness, left atrial diameter, left ventricular outflow tract gradient, non-sustained ventricular tachycardia, unexplained syncope, and family history of SCD) which are used to estimate the risk of SCD within 5 years of clinical evaluation using a statistical risk prediction model (HCM Risk-SCD). The 2014 European Society of Cardiology Guidelines provide a framework to aid clinical decisions and consider patients with a 5-year risk of SCD of less than 4% as low risk and recommend regular assessment while those with a risk of 6% or higher should be considered for an ICD. In patients with an intermediate risk (4% to <6%) ICD implantation may also be considered after taking into account age, co-morbid conditions, socioeconomic factors, and the psychological impact of therapy. Survivors of ventricular fibrillation arrest should receive an ICD for secondary prevention unless their life expectancy is less than 1 year. Following device implantation, patients should be followed up for device- and disease-related complications, particularly heart failure and cerebrovascular disease.
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50

Pierard, Luc A., i Lauro Cortigiani. Stress echocardiography: diagnostic and prognostic values and specific clinical subsets. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0015.

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Stress echocardiography is a widely used method for assessing coronary artery disease, due to its high diagnostic and prognostic value. While inducible ischaemia predicts an unfavourable outcome, its absence is associated with a low risk of future cardiac events. The method provides superior diagnostic and prognostic information than standard exercise electrocardiography and perfusion myocardial imaging in specific clinical subsets, such as women, hypertensive patients, and patients with left bundle branch block. Stress echocardiography allows effective risk assessment also in the diabetic population. The evaluation of coronary flow reserve of the left anterior descending artery by transthoracic Doppler adds diagnostic and prognostic information to that of standard stress test. Stress echocardiography is indicated in the cases when exercise electrocardiography is unfeasible, uninterpretable or gives ambiguous result, and when ischaemia during the test is frequently a false-positive response, as in hypertensive patients, women, and patients with left ventricular hypertrophy. Viability detection represents another application of stress echocardiography. The documentation of a large amount of viable myocardium predicts improved ejection fraction, reverse remodelling, and improved outcome following revascularization in patients with ischaemic cardiomyopathy. Moreover, stress echocardiography can aid significantly in clinical decision-making in patients with valvular heart disease through dynamic assessment of primary or secondary mitral regurgitation, transvalvular gradients, and pulmonary artery systolic pressure, as well as before vascular surgery due to the excellent negative predictive value. Finally, stress echocardiography allows effective risk stratification in patients with hypertrophic cardiomyopathy through evaluation of inducible ischaemia, coronary flow reserve, and intraventricular gradient.
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