Relevant bibliographies by topics / Myocytes – Physiologie

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

Academic literature on the topic 'Myocytes – Physiologie'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Myocytes – Physiologie"

1

Feuvray, D., and M. Karmazyn. "Echangeur Na+/H+ et régulation du pH des myocytes cardiaques : de la physiologie à la physiopathologie." médecine/sciences 15, no. 3 (1999): 322. http://dx.doi.org/10.4267/10608/1341.

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Dolber, Paul C., Robert P. Bauman, Judith C. Rembert, and Joseph C. Greenfield. "Are interatrial band myocytes maximally hypertrophied in normal canine hearts?" American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (1998): H1225—H1235. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1225.

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In canine right atrial hypertrophy, the cross-sectional area ( A xs) of right atrial myocytes increases, whereas the A xs of the broader interatrial band myocytes does not. In the current study, myocyte reconstructions showed that right atrial myocyte length increased in proportion to A xs in right atrial hypertrophy. On the other hand, mean interatrial band myocyte length in both normal and right atrial hypertrophy dogs was roughly inversely proportional to mean A xs, as expected if interatrial band myocyte volume was constant. Plotting mean A xs vs. myocyte length for individual interatrial
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Krishnan, Anirudh, Emily Chilton, Jaishankar Raman, et al. "Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?" Cells 10, no. 9 (2021): 2501. http://dx.doi.org/10.3390/cells10092501.

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Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts d
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Zhang, Lian-Qin, Xue-Qian Zhang, Timothy I. Musch, Russell L. Moore, and Joseph Y. Cheung. "Sprint training restores normal contractility in postinfarction rat myocytes." Journal of Applied Physiology 89, no. 3 (2000): 1099–105. http://dx.doi.org/10.1152/jappl.2000.89.3.1099.

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The significance of 6–8 wk of high-intensity sprint training (HIST) on contractile abnormalities of myocytes isolated from rat hearts with prior myocardial infarction (MI) was investigated. Compared with the sedentary (Sed) condition, HIST attenuated myocyte hypertrophy observed post-MI primarily by reducing cell lengths but not cell widths. At high extracellular Ca2+ concentration (5 mM) and low pacing frequency (0.1 Hz), conditions that preferentially favored Ca2+ influx over efflux, MI-Sed myocytes shortened less than Sham-Sed myocytes did. HIST significantly improved contraction amplitudes
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Li, F., M. R. McNelis, K. Lustig, and A. M. Gerdes. "Hyperplasia and hypertrophy of chicken cardiac myocytes during posthatching development." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 2 (1997): R518—R526. http://dx.doi.org/10.1152/ajpregu.1997.273.2.r518.

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For characterization of the growth pattern of cardiac myocytes during posthatching development, cardiac myocytes were enzymatically isolated from the ventricles of 1-, 15-, 29-, and 42-day-old chickens for measurement of myocyte nucleation, length, width, volume, and number, and for immunolabeling of cytoskeletal proteins. Ventricular myocyte number increased 156% from day 1 to day 42. Average cell volume increased more than 400%, and myocytes lengthened 125%, but cell width only increased 53% during this period. All myocytes were mononucleated at day 1. At day 15, 18% of myocytes became binuc
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Smolich, J. J., A. M. Walker, G. R. Campbell, and T. M. Adamson. "Left and right ventricular myocardial morphometry in fetal, neonatal, and adult sheep." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 1 (1989): H1—H9. http://dx.doi.org/10.1152/ajpheart.1989.257.1.h1.

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This study has examined left (LV) and right ventricular (RV) myocardial morphometry in perfusion-fixed hearts of late-gestation sheep fetuses, neonatal lambs, and adult sheep. During development, myocyte size, intercapillary distance, and myocyte myofibrillar and mitochondrial volume densities increased, whereas capillary density, the myocyte-to-capillary ratio, and the myocyte matrix volume density decreased. RV myocytes were larger than LV myocytes in cross section in fetuses and 4-day-old lambs. LV and RV myocytes were of similar size in 7-day-old lambs. LV and RV myocytes were of larger in
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Barbera, A., G. D. Giraud, M. D. Reller, J. Maylie, M. J. Morton, and K. L. Thornburg. "Right ventricular systolic pressure load alters myocyte maturation in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 4 (2000): R1157—R1164. http://dx.doi.org/10.1152/ajpregu.2000.279.4.r1157.

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The effects of right ventricular (RV) systolic pressure (RVSP) load on fetal myocyte size and maturation were studied. Pulmonary artery (PA) pressure was increased by PA occlusion from mean 47.4 ± 5.0 (±SD) to 71 ± 13.6 mmHg ( P < 0.0001) in eight RVSP-loaded near-term fetal sheep for 10 days. The maximal pressure generated by the RV with acute PA occlusion increased after RVSP load: 78 ± 7 to 101 ± 15 mmHg ( P< 0.005). RVSP-load hearts were heavier (44.7 ± 8.4 g) than five nonloaded hearts (31.8 ± 0.2 g; P < 0.03); heart-to-body weight ratio (10.9 ± 1.1 and 6.5 ± 0.9 g/kg, respective
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Wang, Z., R. Mukherjee, C. F. Lam, and F. G. Spinale. "Spatial characterization of contracting cardiac myocytes by computer-assisted, video-based image processing." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (1996): H769—H779. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h769.

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The goals of the present study were to develop and validate a computer-assisted, video-based image processing (CAVIP) system to measure time-dependent changes in isolated myocyte geometry during contraction and to use the CAVIP system to examine spatial characteristics of the myocyte during contraction in normal myocytes and in myocytes after development of dilated cardiomyopathy (DCM). Myocytes were isolated from the left ventricles of five control pigs and five pigs that developed chronic tachycardia (240 beats/min; 3 wk)-induced DCM. Isolated myocytes were stimulated and recorded using a hi
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Moore, R. L., T. I. Musch, R. V. Yelamarty, et al. "Chronic exercise alters contractility and morphology of isolated rat cardiac myocytes." American Journal of Physiology-Cell Physiology 264, no. 5 (1993): C1180—C1189. http://dx.doi.org/10.1152/ajpcell.1993.264.5.c1180.

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Chronic exercise training elicits positive adaptations in cardiac contractile function and ventricular dimension. The potential contribution of single myocyte morphological and functional adaptations to these global responses to training was determined in this study. Left ventricular cardiac myocytes were isolated from the hearts of sedentary control (Sed) or exercise-trained (TR) rats. Training elicited an approximately 5% increase in resting myocyte length (Sed, 121.0 +/- 2.0 vs. TR, 126.7 +/- 2.0 microns; P < 0.05), whereas resting sarcomere length and midpoint cell width were unaffected
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Chen, Yue-Feng, Suleman Said, Scott E. Campbell, and A. Martin Gerdes. "A method to collect isolated myocytes and whole tissue from the same heart." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H2004—H2006. http://dx.doi.org/10.1152/ajpheart.00479.2007.

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A technique for isolation of cardiac myocytes and collection of whole heart tissue from individual hearts of adult rats is described in this study. After excision of the apical half of the left ventricle (LV) and cauterization of the cut edge, aortas were cannulated and high-quality isolated cardiac myocytes were collected after collagenase perfusion of the basal portion. Myocyte dimensions from the basal portion of cauterized and noncauterized hearts from matching rats were identical. Additionally, myocyte dimensions from the basal and apical halves of the LV were compared with the use of who
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Dissertations / Theses on the topic "Myocytes – Physiologie"

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Tessier, Sophie. "Physiologie et pharmacologie du courant K+ transitoire sortant des myocytes atriaux humains." Paris 11, 1999. http://www.theses.fr/1999PA11T017.

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De nombreuses pathologies cardiaques entraînent des altérations de la structure et du fonctionnement du myocarde auriculaire qui favorisent la survenue du plus fréquent des troubles du rythme, la fibrillation auriculaire. Ces altérations sont liées à des modifications de l'activité électrique et sont principalement marquées par la diminution de la durée du potentiel d'action. Dans les myocytes atriaux humains, le courant K+ transitoire Ito, constitué d'une composante It qui s'inactive rapidement et d'une composante Isus qui s'inactive lentement, contrôle la durée du potentiel d'action et son r
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Passerieux, Emilie. "Corrélation entre l'organisation spatiale du perimysium et des domaines subcellulaires des fibres musculaires squelettiques : implication dans la transmission latérale des forces et conséquences possibles sur les adaptations du muscle à l'exercice physique." Bordeaux 2, 2006. http://www.theses.fr/2006BOR21358.

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Nous avons exploré la possibilité qu’une fraction du tissu conjonctif intramusculaire, le périmysium soit impliqué dans les mécanismes qui sont à l’origine des adaptations musculaires. Pour cela, nous avons montré dans le muscle squelettique Flexor carpi radialis de bœuf que le périmysium transmet latéralement les forces de la contraction musculaire depuis les fibres musculaires jusqu’aux tendons. D’autre part, nous avons montré que sa répartition spatiale correspond à la surface des fibres musculaires à la répartition des intégrines et à la présence des cellules satellites et dans les fibres
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Hatem, Stéphane. "Mecanismes responsables de l'electrogenese et du signal calcique des myocytes cardiaques : physiologie et physiopathologie." Paris 11, 1995. http://www.theses.fr/1995PA112458.

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Dans ce memoire, differents aspects de l'electrogenese et du couplage excitation-contraction des myocytes cardiaques ont ete abordes. (1) a distance de l'arret d'un traitement chronique par les inhibiteurs calciques, il persiste une diminution importante de la densite d'ica-l qui pourrait etre liee a une desensibilisation des recepteurs des dihydropyridines. (2) lors de la dilatation de l'oreillette droite, la diminution d'ica-l est due a une diminution de l'activite des canaux par un mecanisme de dephosphorylation. (3) dans un modele de croissance in vitro des myocytes atriaux humains, l'evol
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Coustes-Chazalette, Delphine. "Muscle et intégrité membranaire." Montpellier 1, 2005. http://www.theses.fr/2005MON13507.

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Dans les organismes pluricellulaires, l'adhérence cellulaire et les systèmes de réparation de la membrane plasmique jouent un rôle fondamental dans le maintien de l'intégrité des tissus. Ces deux fonctions sont d'autant plus importantes lorsqu'un tissu, tel le muscle, est soumis à des contraintes mécaniques importantes. Chez l'homme, trois systèmes majeurs permettent aux fibres musculaires d'assurer leur intégrité et par là même, d'assurer l'intégrité du muscle. Deux systèmes macromoléculaires impliquant d'une part la dystrophine et d'autre part l'intégrine alpha7beta1 permettent aux fibres mu
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Jdaïaa, Hassan. "Étude de la conductance aux ions Ca2+ des membranes impliquées dans le couplage excitation-contraction des fibres musculaires squelettiques de crustacé." Lille 1, 1985. http://www.theses.fr/1985LIL10139.

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Allard, Bruno. "Action des ions sodium dans le couplage excitation-contraction de la fibre musculaire squelettique rapide de grenouille." Lyon 1, 1990. http://www.theses.fr/1990LYO10058.

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Les canaux sodiques constituent l'unite fonctionnelle de l'excitabilite cellulaire. Sur la fibre musculaire squelettique, il a ete montre que les ions sodium peuvent aussi jouer un role dans le couplage excitation-contraction. Notre etue a consisdte en l'evaluation de l'action des ions sodium sur la contraction tetanique de la fibre musculaire rapide isolee de grenouille. Les activites electrique et mecanique de la preparation ont ete enregistrees simultanement grace a la technique de la double separation de mannitol couplee a l'emploi d'un transducteur mecano-electrique. En situation de coura
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Verney, Julien. "Conséquences musculaires d'un entraînement sollicitant endurance et force chez un même sujet âgé : aspects fonctionnels et histomorphologiques." Saint-Etienne, 2008. http://www.theses.fr/2008STET4014.

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Nous avons voulu étudier les effets à la fois spécifiques et non spécifiques de l'entraînement en endurance et en musculation chez un même sujet au niveau fonctionnel mais également au niveau cellulaire. Nous avons entraîné chez dix sujets âgés (73 + - 4 ans) l'hémicorps supérieur en musculation et l'hémicorps inférieur en endurance durant 14 semaines (3 fois par semaine). Des biopsies musculaires ont été effectuées sur le deltoïde (Del) et le vaste externe (VLat) avant et après entraînement pour mesurer des activités enzymatiques musculaires, analyser la typologie et la taille des fibres musc
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Hnia, Karim. "Interaction Utrophine / bêta-dystroglycan dans le muscle et le système nerveux périphérique de la souris déficiente en dystrophine." Montpellier 1, 2006. http://www.theses.fr/2006MON13508.

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L'analyse des différentes interactions entre les membres du complexe associés à la dystrophine (DGC) a été le centre de plusieurs études biochimiques. Le bêta-dystroglycan prend une place primordiale au sein de ce complexe du fait de son rôle de protéine d'ancrage de la dystrophine et/ou de l'utrophine. De part son homologie structurale avec la dystrophine, l'utrophine est exprimée dans le muscle des patients DMD et de la souris modèle de cette pathologie, la souris mdx. De plus en plus d'observations soulignent l'implication du bêta-dystroglycan dans des évènements de signalisation. Comme l'o
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Hédou, Julie. "Analyses fonctionnelle et protéomique du rôle de la O-N-acétylglucosaminylation dans la physiologie du muscle squelettique." Thesis, Lille 1, 2008. http://www.theses.fr/2008LIL10102/document.

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La O-N-acétylglucosaminylation ou O-GlcNAc, est une glycosylation cytosolique et nucléaire correspondant à l'addition d'un motif O-GlcNAc sur des résidus sérine et thréonine des protéines. Cette glycosylation dynamique et réversible est impliquée dans de nombreux processus cellulaires comme la transcription, le cycle cellulaire, la signalisation intracellulaire ... mais également dans des pathologies comme le cancer, les maladies neurodégénératives et le diabète. Peu de travaux se sont intéressés au rôle que la O-GlcNAc pourrait jouer dans le muscle strié. Pourtant, le muscle squelettique est
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Arnaudeau, Serge. "Canaux ioniques et compartiments calciques intracellulaires activés par l'ocytocine et l'acétylcholine dans les myocytes lisses viscéraux (myomètre, intestin)." Bordeaux 2, 1994. http://www.theses.fr/1994BOR28283.

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L'ocytocine, médiateur de la parturition, provoque une mobilisation du calcium dans les cellules myométriales via l'activation d'une protéine G de type Gq/G11 insensible à la toxine pertussique. Celle-ci permet la stimulation d'une phospholipase C spécifique des phosphatidylinositides et la production d'IP3 responsable de la libération du calcium stocké. L'augmentation de calcium intracellulaire n'implique pas de récepteurs à la ryanodine et ne se produit qi'à partir d'un seul stock calcique sensible à l'IP3, disposé à la périphérie et au centre de la cellule. Elle permet l'activation de condu
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Books on the topic "Myocytes – Physiologie"

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S, Sideman, Beyar Rafael, Landesberg Amir, and New York Academy of Sciences, eds. Interactive and integrative cardiology. Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Larry and Horti Fairberg Cardiac Workshop (6th 2009 Haifa, Israel). Analysis of cardiac development: From embryo to old age. Edited by Beyar Rafael, Landesberg Amir, and New York Academy of Sciences. Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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(Editor), Samuel Sideman, Rafael Beyar (Editor), and Amir Landesberg (Editor), eds. The Communicative Cardiac Cell (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2005.

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

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Larry and Horti Fairberg Cardiac Workshop. Cardiac Engineering: From Genes and Cells to Structure and Function (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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Cardiac Engineering: From Genes And Cells To Structure And Function (Annals of the New York Academy of Sciences, V. 1015). New York Academy of Sciences, 2004.

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Book chapters on the topic "Myocytes – Physiologie"

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Barnett, Vincent A. "Cellular Myocytes." In Handbook of Cardiac Anatomy, Physiology, and Devices. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-372-5_10.

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Barnett, Vincent A. "Cellular Myocytes." In Handbook of Cardiac Anatomy, Physiology, and Devices. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19464-6_12.

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Nayler, Winifred G., and M. J. Daly. "Calcium and the Injured Cardiac Myocyte." In Physiology and Pathophysiology of the Heart. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_25.

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Evans, Rhys, Kenneth T. MacLeod, Steven B. Marston, Nicholas J. Severs, and Peter H. Sugden. "Cardiac physiology." In Oxford Textbook of Medicine. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.160103_update_002.

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The function of the heart is to provide the tissues of the body with sufficient oxygenated blood and metabolites to meet the moment-to-moment needs as dictated by physical activity and postural and emotional changes. Cardiac myocytes are the contractile cells of the heart and constitute the bulk of heart mass. There are differences between the myocytes of the ventricles, the atria, and the conduction system: ventricular myocytes are elongated cells, packed with myofibrils (the contractile apparatus) and mitochondria (for ATP production). Myofibrils are repeating units (sarcomeres) made up of thin actin filaments anchored at the Z-discs at either end of the sarcomere, and thick myosin filaments which interdigitate and interact with the thin filaments. Contraction results from sarcomere shortening produced by the ATP-dependent movement of the thin and thick filaments relative to one another. Transverse (T-) tubules facilitate extracellular Ca...
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Hamrell, Burt B. "Ventricular myocyte electrophysiology." In Cardiovascular Physiology. CRC Press, 2018. http://dx.doi.org/10.1201/9781315105208-2.

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Hamrell, Burt B. "Electrical properties and cardiac myocyte structure." In Cardiovascular Physiology. CRC Press, 2018. http://dx.doi.org/10.1201/9781315105208-6.

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AOKI, HIROKI, and SEIGO IZUMO. "Signal Transduction of Cardiac Myocyte Hypertrophy." In Heart Physiology and Pathophysiology. Elsevier, 2001. http://dx.doi.org/10.1016/b978-012656975-9/50060-2.

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Severs, Nicholas J. "Functional Morphology of the Cardiac Myocyte." In Muscle and Exercise Physiology. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-814593-7.00021-9.

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"Cardiac myocyte excitation and contraction." In Cardiovascular Physiology: Questions for Self Assessment. CRC Press, 2009. http://dx.doi.org/10.1201/b13483-6.

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Conference papers on the topic "Myocytes – Physiologie"

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Yan, Xiao Hong, Yuan Wang, Ya Lan Ding, Min Hu, Gui Mei Wang, and Xiao Min Guo. "ATF6 activated endoplasmic reticulum stress involved in cardioprotection of hydrogen sulfide postconditioning against cardiac myocytes apoptosis by ischemia reperfusion in vivo." In Annual International Conference on Advanced Research: Physiology. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-607x_arp14.16.

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