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Gotowe bibliografie tematyczne / Endothelial cells

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Gotowa bibliografia na temat „Endothelial cells”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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Artykuły w czasopismach na temat "Endothelial cells"

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Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (1994): 259–65. http://dx.doi.org/10.1046/j.1468-2982.1994.1404259.x.

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Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is s

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Westerweel, Peter E., та Marianne C. Verhaar. "Protective Actions of PPAR-γActivation in Renal Endothelium". PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/635680.

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Renal endothelial damage is pivotal in the initiation and progression of renal disease. Damaged renal endothelium may be regenerated through proliferation of local endothelium and circulation-derived endothelial progenitor cells. Activation of the PPAR-γ-receptors present on endothelial cells affects their cellular behavior. Proliferation, apoptosis, migration, and angiogenesis by endothelial cells are modulated, but may involve both stimulation and inhibition depending on the specific circumstances. PPAR-γ-receptor activation stimulates the production of nitric oxide, C-type natriuretic pepti

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Mebazaa, A., E. Mayoux, K. Maeda, et al. "Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (1993): H1841—H1846. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1841.

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Endocardial endothelium is reported to modulate myocardial contraction by releasing diffusible factors, but the nature of the agent(s) responsible is unknown. In the present study we investigated the potential role of endothelin in these effects. Cultured sheep endocardial endothelial cells were found to express endothelin-1 mRNA and to release endothelin-1 into superfusing solution. This superfusate induced positive inotropic effects in isolated rat cardiac myocytes, associated with an increase in the cytosolic Ca2+ transient. Similar positive inotropic effects were induced by vascular endoth

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Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.

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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immun

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Rosolowsky, L. J., and W. B. Campbell. "Endothelial cells stimulate aldosterone release from bovine adrenal zona glomerulosa cells." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (1994): E107—E117. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e107.

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Intra-adrenal factors promote basal as well as adrenocorticotropic hormone (ACTH)-, angiotensin-, and flow-induced steroid secretion. Because endothelial cells respond to changes in flow and are in a close anatomical relationship to steroidogenic cells, we examined the effect of endothelial cells on the secretion of aldosterone from zona glomerulosa (ZG) cells. Endothelial cells and endothelial cell-conditioned medium (EC-CM) stimulated the release of aldosterone from ZG cells. The stimulatory effect was related to the concentration of endothelial cells or EC-CM. The maximal stimulatory effect

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Dehouck, Marie-Pierre, Paul Vigne, Gérard Torpier, Jean Philippe Breittmayer, Roméo Cecchelli, and Christian Frelin. "Endothelin-1 as a Mediator of Endothelial Cell–Pericyte Interactions in Bovine Brain Capillaries." Journal of Cerebral Blood Flow & Metabolism 17, no. 4 (1997): 464–69. http://dx.doi.org/10.1097/00004647-199704000-00012.

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Endothelial cells and pericytes are closely associated in brain capillaries. Together with astrocytic foot processes, they form the blood–brain barrier. Capillaries were isolated from bovine brain cortex. Pure populations of endothelial cells and pericytes were isolated and cultured in vitro. Polarized monolayers of endothelial cells preferentially secreted immunoreactive endothelin-1 (Et-1) at their abluminal (brain-facing) membrane. They did not express receptors for Et-1. Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments. These

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Zhang, Zhong, Kristie Payne, and Thomas L. Pallone. "Syncytial communication in descending vasa recta includes myoendothelial coupling." American Journal of Physiology-Renal Physiology 307, no. 1 (2014): F41—F52. http://dx.doi.org/10.1152/ajprenal.00178.2014.

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Using dual cell patch-clamp recording, we examined pericyte, endothelial, and myoendothelial cell-to-cell communication in descending vasa recta. Graded current injections into pericytes or endothelia yielded input resistances of 220 ± 21 and 128 ± 20 MΩ, respectively ( P < 0.05). Injection of positive or negative current into an endothelial cell depolarized and hyperpolarized adjacent endothelial cells, respectively. Similarly, current injection into a pericyte depolarized and hyperpolarized adjacent pericytes. During myoendothelial studies, current injection into a pericyte or an endothel

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CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metaboli

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Faivre-Fiorina, Béatrice, Alexis Caron, Céline Fassot, et al. "Presence of hemoglobin inside aortic endothelial cells after cell-free hemoglobin administration in guinea pigs." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 2 (1999): H766—H770. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h766.

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The endothelium is the production site of several potent vasoactive factors that contribute to the modulation of the vascular tone. Because hemoglobin-based oxygen carriers (HBOC) have been demonstrated to cause vasoconstriction and thereby increase arterial pressure by interacting with endothelium-derived factors such as nitric oxide and endothelin-1, we hypothesized that hemoglobin could penetrate into the endothelial cells. Therefore, we investigated the presence of hemoglobin into guinea pig aortic endothelial cells by immunohistochemical staining after exchange transfusion with a hemoglob

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Jaffredo, T., R. Gautier, A. Eichmann, and F. Dieterlen-Lievre. "Intraaortic hemopoietic cells are derived from endothelial cells during ontogeny." Development 125, no. 22 (1998): 4575–83. http://dx.doi.org/10.1242/dev.125.22.4575.

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We have investigated the developmental relationship of the hemopoietic and endothelial lineages in the floor of the chicken aorta, a site of hemopoietic progenitor emergence in the embryo proper. We show that, prior to the onset of hemopoiesis, the aortic endothelium uniformly expresses the endothelium-specific membrane receptor VEGF-R2. The onset of hemopoiesis can be determined by detecting the common leukocyte antigen CD45. VEGF-R2 and CD45 are expressed in complementary fashion, namely the hemopoietic cluster-bearing floor of the aorta is CD45(+)/VEGF-R2(−), while the rest of the aortic en

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Rozprawy doktorskie na temat "Endothelial cells"

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Holmén, Carolina. "Mechanisms of endothelial cell dysfunction in Wegener's granulomatosis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-443-0/.

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Clayton, Zoe Ellen. "The pro-angiogenic properties of induced pluripotent stem cell derived endothelial cells and induced endothelial cells." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17300.

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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide, (1, 2). Current interventions are ineffective in up to 30% of patients due to the presence of diffuse or extensive atherosclerosis, therefore the development of alternative or supplementary therapies for CVD is a high priority for medical research. Therapeutic angiogenesis, enhancing the growth of new blood vessel networks from the existing vasculature, is a promising strategy for restoring blood flow to ischaemic tissue. Stem cells have shown potential as pro-angiogenic therapies for patients with coronary

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Harrison, Vanessa Jane. "The characterisation of endothelin-converting enzyme in endothelial cells." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307673.

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Ristori, Emma. "Vascular Endothelial Growth Factors and Endothelial Cells Behaviour." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1127960.

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L'endotelio vascolare è un importante tessuto il cui ruolo sia in fisiologia, che in patologia è stato a lungo sottovalutato. Per molti anni, l'inaccessibilità di questo tessuto ha reso difficoltoso valutarne il ruolo fisio-patologico. La disfunzione delle cellule endoteliali è alla base di molti se non tutti gli stati patologici e può manifestarsi a diversi livelli dello sviluppo vascolare: durante la vasculogenesi, durante il processo di angiogenesi oppure durante il rimodellamento vascolare. Il processo di vasculogenesi consiste nella specializzazione di precursori vascolari in arterie e v

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Huang, Lan. "Endothelial Colony Forming Cells (ECFCs): Identification, Specification and Modulation in Cardiovascular Diseases." Thesis, Connect to resource online, 2009. http://hdl.handle.net/1805/2063.

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Thesis (Ph.D.)--Indiana University, 2009.<br>Title from screen (viewed on February 2, 2010). Department of Biochemistry and Molecular Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Mervin C. Yoder, Jr., David A. Ingram, Jr., Lawrence A. Quilliam, Mark D. Pescovitz. Includes vitae. Includes bibliographical references (leaves 171-194).

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Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.

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Altalhi, Wafa. "Biological Effects of Osteopontin on Endothelial Progenitor Cells." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20280.

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Endothelial Progenitor Cells (EPCs) are thought to participate in the healing of injured vascular endothelium by incorporating into the defect sites to mediate endothelial recovery. Recently, osteopontin (OPN) was shown to be fundamental in accelerating estrogen-dependent healing of injured blood vessels. Here, we are investigating the effect OPN has on EPC behavior. Late outgrowth human EPCs (LEPCs) were derived from circulating monocytes isolated by leukophoresis, and grown in culture until passage six. L-EPCs were then assayed for adhesion, spreading, chemotaxis, and haptotaxis, as well as

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Zhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.

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Thesis (M.S.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).

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Prahst, Claudia. "Neuropilin-vascular endothelial growth factor signaling in endothelial cells." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-51230.

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Yang, Weidong. "Oxidative damage of endothelial cells." Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29603.

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This study sought to investigate the consequences of different degrees of oxidative stress on endothelial cells, using a cultured endothelial cell model; principally bovine aortic endothelial cells, subjected to oxidative stress. High concentrations of H2O2 or a superoxide generating system caused rapid endothelial cell death, as evidenced by increased membrane permeability, which could be partially protected by myoglobin. Extracellular H2O2 caused a rapid increase in intracellular peroxidation but was also eliminated by endothelial cells. However, the anti-oxidant capacity of the bovine endot

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Książki na temat "Endothelial cells"

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1941-, Ryan Una S., ed. Endothelial cells. CRC Press, 1988.

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S, Ryan Una, ed. Endothelial cells. CRC Press, 1988.

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Balistreri, Carmela Rita. Endothelial Progenitor Cells. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55107-4.

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Ryan, una s. endothelial cells: Vol. 1. CRC Press, 1995.

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J, Bicknell R., ed. Endothelial cellculture. Cambridge University Press, 1996.

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Fitchett, Caroline Jane. Lysophosphatidate signalling in endothelial cells. University of Wolverhampton, 2002.

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C, Aird William, ed. Endothelial cells in health and disease. Taylor & Francis, 2005.

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Love, Graham P. Endothelin-I as a mediator of injury in vascular endothelial cells. University College Dublin, 1997.

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Ricard, Cervera, Khamashta Munther A. A, and Hughes Graham R. V, eds. Antibodies to endothelial cells and vascular damage. CRC Press, 1994.

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Dauphinee, Shauna M., and Aly Karsan. Endothelial dysfunction and inflammation. Birkhäuser, 2010.

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Części książek na temat "Endothelial cells"

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Stevens, T., G. H. Brough, T. M. Moore, P. Babal, and W. J. Thompson. "Endothelial cells." In Methods in Pulmonary Research. Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8855-4_16.

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Atkins, G. Brandon, Gabriela Orasanu, and Mukesh K. Jain. "Endothelial Cells." In Atherosclerosis. John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch9.

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Sturtzel, Caterina. "Endothelial Cells." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57613-8_4.

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Gooch, Keith J., and Christopher J. Tennant. "Endothelial Cells." In Mechanical Forces: Their Effects on Cells and Tissues. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03420-0_2.

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Carreras, Enric, M. Diaz-Ricart, S. Jodele, O. Penack, and S. Vasu. "Early Complications of Endothelial Origin." In The EBMT Handbook. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_42.

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AbstractDuring HCT, the vascular endothelium is affected by conditioning, IS agents, inflammatory molecules released by injured cells and tissues, endotoxins translocated across injured mucosal barriers, the complex process of engraftment, and in allo-HCT immune alloreactivity. This endothelial damage can affect the entire vascular endothelium or that of specific organs and be the triggering event for several of the early complications grouped under denomination vascular endothelial syndromes of HCT.

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Kuwana, Masataka. "Endothelial Progenitor Cells." In Systemic Sclerosis. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55708-1_3.

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Kmieć, Zbigniew. "Sinusoidal Endothelial Cells." In Cooperation of Liver Cells in Health and Disease. Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56553-3_3.

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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, et al. "Endothelial Progenitor Cells." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2334.

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Stolz, Donna Beer. "Sinusoidal Endothelial Cells." In Molecular Pathology Library. Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_7.

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Fischer, Johannes C. "Endothelial Progenitor Cells." In Cellular Diagnostics. KARGER, 2008. http://dx.doi.org/10.1159/000209168.

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Streszczenia konferencji na temat "Endothelial cells"

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Carter, A. J., W. G. Eisert, and T. H. Mμller. "DIFFERENTIAL STIMULATION OF INOSITOL TRISPHOSPHATE ACCUMULATION IN CULTURED HUMAN ENDOTHELIAL CELLS BY THROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644736.

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Vascular endothelial cells possess specific receptors for thrombin, and thrombin can interact with these receptors to activate the endothelial cells. However, the signal transduction mechanisms which mediate the cellular responses are not yet characterised. The aim of this study therefore, was to determine whether thrombin influenced the inositol phosphate transduction pathway in cultured human endothelial cells. Endothelial cells were isolated from both large and small vessels; these were human umbilical vein and the microvasculature of human omentum respectively. The endothelial cells staine

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de Agostini, A., J. Marcum, and R. Rosenberg. "THE BINDING OF ANTITHROMBIN TO CAPILLARY ENDOTHELIAL CELLS GROWN IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643343.

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Cloned endothelial cells from rat epididymal fat pads synthesize anticoagulantly active heparan sulfate proteoglycans containing the disaccharide, GlcA→ AMN-3,6-O-SO3, which is a marker for the antithrombin-binding domain of heparin. To demonstrate that antithrombin (AT) binds to cell surface heparan sulfate, a binding assay employing 125I-AT and cell monolayers has been developed. Post-confluent endothelial cells (7 days) were incubated with radiolabeled AT for 1 h at 4° and washed with PBS. Bound radioactivity was quantitated after solubilizing whole cells. Under these conditions, ∼1% (2174±

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Krishnan, Ramaswamy, Elizabeth Peruski Canovic, Andreea L. Iordan, et al. "Cytoskeletal Fluidization and Resolidification are Required for Reorientation of Endothelial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80431.

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Vascular endothelial cells are subjected to routine mechanical stretch. In response, cellular microstructures rearrange locally as the cell body realigns globally [1–5]. These responses, which underlie the vital functions of the endothelium, are often explained in terms of upstream mechanosensing and downstream cell signaling [2–5].

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Weidert, Eric, Payal Khanna, Francisco Vital-Lopez, and Cheng Dong. "Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80364.

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Metastasis is a complex process mediated by both adhesion molecules and chemokine secretion [1]. One important event during cancer metastasis is tumor cell extravasation through the endothelium [1]. In melanoma cancer, tumor cell extravasation is mediated by very late antigen (VLA)-4 molecule adhesion to vascular cell adhesion molecules (VCAM)-1 on endothelial cells [2]. High expression levels of VLA-4 integrin are associated with a marked increase in melanoma extravasation through endothelial layers [2]. The binding of VLA-4 to VCAM -1 induces the activation of downstream mitogen activated pr

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Shatos, M., J. Doherty, D. Allen, and J. Hoak. "ALTERATIONS IN VASCULAR ENDOTHELIAL CELL FUNCTION BY OXYGEN-FREE RADICALS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643365.

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The vascular endothelium is a target for oxidant-induced damage in many disease states including hyperoxia, inflammation, ischemia and reperfusion injury. However, little is known concerning oxidant injury to endothelial cells and its relationship to hemostasis. Our studies have focused on the ability of oxygen free radicals to injure and/or alter selected vascular endothelial cell functions pertinent to the regulation of hemostasis. Xanthine and xanthine oxidase, a well-characterized generating system for the production of the superoxide anion radical (O− 2) was used to sublethally injure hum

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Reutelingsperger, C. P. M., W. Buurman, G. Horn-stra, and H. C. Horn-stra. "IMMUNOLOGICAL AND CHEMICAL DETECTION OF VAC IN CULTURED ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643913.

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Recently we reported the presence in human umbilical cord vessels of an anticoagulatory protein (VAC, Mr = 32,000) which inhibits phospholipid dependent procoagulant reactions through a high affinity binding, in the presence of calcium, to the phospholipid surface. The mechanism of anticoagulation differs fundamentally from those of the well-known physiological anticoagulants.Polyclonal antibodies, raised in rabbits against purified VAC, bind in cultured endothelial cell lysates to an antigen with Mr = 32,000, as was revealed with immunoblotting techniques. It is demonstrated with chemical tec

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Szatmary, Alex C., Rohan J. Banton, and Charles D. Eggleton. "Deformation of White Blood Cells Firmly Adhered to Endothelium." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80894.

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Circulating white blood cells adhere to endothelium near an infection site; this occurs because infection causes ligands to be expressed on activated endothelium. Initially, a white blood cell rolls on the substrate, but eventually forms a firm adhesion, allowing it to crawl through the endothelial layer toward the infected tissue. A computational model of bond kinetics, cell deformability, and fluid dynamics was used to model the forces experienced by a cell during this process. The cell was modeled as a fluid-filled membrane; on its surface were hundreds of deformable microvilli—little finge

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Lim, Yi Chung, and David S. Long. "Aortic Hemodynamics and Endothelial Gene Expression: An Animal Specific Approach." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53312.

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Atherosclerosis is a major cause of morbidity and mortality in the developed world. This disease is identified by endothelial dysfunction, inflammation and the accumulation of lipids and cellular elements within the intima of medium and large-sized arteries. Within these arteries, the distribution of atherosclerotic lesions is non-uniform; the inner wall of curved sections and the outer walls of bifurcations are susceptible sites. Evidence suggests that the focal nature of the disease is mediated in part by local fluid mechanical stresses at the interface between flowing blood and the vessel w

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Lewis, R. M., P. B. Jahrling, B. P. Griffin, and T. M. Cosgriff. "THE EFFECTS OF HEMORRHAGIC FEVER VIRUS INFECTION OF ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643352.

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Pichindé viral infection of strain 13 guinea pigs is a model for Lassa fever virus in humans. Infected animals show impaired platelet function and altered coagulation parameters. Human endothelial cells and the human endothe1ia1-1 ike cell line, EA926, were infected with Pichinde virus. Following infection, cultures were monitored by phase contract microscopy for cytopathic effect (CPE). Assays of supernatant were used to document viral growth and to measure those endothelial-produced components that might affect hemostasis. In addition, the cells were stimulated with phorbol ester (PMA), whic

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Safwan-Zaiter, Hasan, Kay-Dietrich Wagner, and Nicole Wagner. "The Senescence Marker p16Ink4a—A Player of Liver Endothelial Cells Physiology." In Cells 2023. MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021013.

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Raporty organizacyjne na temat "Endothelial cells"

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Paul, Satashree. Flavivirus and its Threat. Science Repository, 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada415526.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells With a VEGF-Triggered Cell Death Receptor. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada423810.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada476353.

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Pumiglia, Kevin. Molecular Regulation of Endothelial Cells by NF-1. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada567663.

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Pumiglia, Kevin. Molecular Regulation of Endothelial Cells by NF-1. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada579995.

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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infar

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Merkle, Carrie J. Studies on Breast Cancer Cell Interactions with Aged Endothelial Cells in Culture and Rat Models. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada455981.

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Avraham, Hava. Studies of Vascular Endothelial Growth Factor (VEGF) Signaling in Breast Cancer Cells. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada395916.

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Avraham, Hava. Studies of Vascular Endothelial Growth Factor (VEGF) Signaling in Breast Cancer Cells. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada412712.

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