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=== Terminology ===
=== Terminology ===
The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue.
The foundation model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue.


== Function ==
== Function ==
==Clinical significance==
==Clinical significance==
{{Main|Endothelial dysfunction}}
{{Main|Endothelial dysfunction}}
[[Endothelial dysfunction]], or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide synthase|nitric oxide synthesis]] and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in [[reactive oxygen species]], which can impair nitric oxide production and activity via several mechanisms.<ref name="pmid15643116">{{cite journal | author = Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.
[[Endothelial dysfunction]], or the lose of pooper endothelial function, is a halmark for vascular diseeses, iz often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide hiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.


== See also ==
== See also ==

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'{{about|the lining of blood and lymphatic vessels|the endothelium of the cornea|corneal endothelium}} {{refimprove|date=October 2008}} {{Infobox Anatomy | Name = Endothelium | Latin = | GraySubject = | GrayPage = | Image = Endotelijalna ćelija.jpg | Caption = Diagram showing the location of endothelial cells | Image2 = Microvessel.jpg | Caption2 = Endothelial cells, which form the [[tunica intima]], or innermost layer of the vessel, encircle an erythrocyte (E). | Precursor = | System = | Artery = | Vein = | Nerve = | Lymph = | MeshName = | MeshNumber = | Code = {{TerminologiaHistologica|2|00|02.0.02003}} | }} The '''endothelium''' is the thin layer of [[cell (biology)|cells]] that lines the interior surface of [[blood vessel]]s and [[lymphatic vessels]],<ref>{{DorlandsDict|three/000035470|Endothelium}}</ref> forming an interface between circulating [[blood]] or [[lymph]] in the [[lumen (anatomy)|lumen]] and the rest of the vessel wall. The cells that form the endothelium are called '''endothelial cells'''. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells. Vascular endothelial cells line the entire [[circulatory system]], from the [[heart]] to the smallest [[capillaries]]. These cells have unique functions in vascular biology. These functions include [[ultrafiltration|fluid filtration]], such as in the [[glomeruli]] of the kidney, [[muscle tone|blood vessel tone]], [[hemostasis]], [[neutrophil]] recruitment, and [[hormone trafficking]]. Endothelium of the interior surfaces of the heart chambers is called [[endocardium]]. ==Structure== Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer. In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow.<ref>Eskin S.G., C.L. Ives, L.V. McIntire, L.T. Navarro. Microvascular Research. Volume 28, Issue 1, July 1984, Pages 87–94Response of cultured endothelial cells to steady flow. http://dx.doi.org/10.1016/0026-2862(84)90031-1</ref><ref>B L Langille and S L Adamson. Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice. ''Circulation Research''.1981; 48: 481-488.</ref> === Terminology === The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue. == Function == Endothelial cells are involved in many aspects of vascular biology, including: * Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of [[white blood cell]]s into and out of the bloodstream. Excessive or prolonged increases in permeability of the endothelial monolayer, as in cases of chronic inflammation, may lead to tissue [[edema]]/swelling. * [[Coagulation|Blood clotting]] ([[thrombosis]] & [[fibrinolysis]]). The endothelium normally provides a non-thrombogenic surface because it contains, for example, [[heparan sulfate]] which acts as a [[Cofactor (biochemistry)|cofactor]] for activating [[antithrombin]], a protease that inactivates several factors in the coagulation cascade. * [[Inflammation]] * Formation of new blood vessels ([[angiogenesis]]) * [[Vasoconstriction]] and [[vasodilation]], and hence the control of [[blood pressure]] * Repair of damaged or diseased organs via an injection of blood vessel cells<ref>[http://medicalxpress.com/news/2013-10-blood-vessel-cells-regenerate-scientists.html#ajTabs]</ref> * [[Angiopoietin-2]] works with VEGF to facilitate cell proliferation and migration of endothelial cells ==Clinical significance== {{Main|Endothelial dysfunction}} [[Endothelial dysfunction]], or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide synthase|nitric oxide synthesis]] and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in [[reactive oxygen species]], which can impair nitric oxide production and activity via several mechanisms.<ref name="pmid15643116">{{cite journal | author = Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. == See also == {{columns-list|3| * [[Epithelium]] * [[Apelin]] * [[Caveolae]] * [[Endocardium]] * [[Endothelial activation]] * [[Endothelial microparticle]]s * [[Endothelial progenitor cell]]s * [[Endothelium-derived relaxing factor]] ([[EDRF]]) * [[Robert F. Furchgott]] (1998 Nobel prize for discovery of EDRF) * [[Platelet activation]] * [[Susac's syndrome]] * [[Tunica intima]] * [[VE-cadherin]] * [[Weibel-Palade body|Weibel-Palade bodies]] * [[Angiocrine growth factors]] }} == References == {{reflist|2}} == External links == * {{eMedicineDictionary|Endothelium}} * {{UCDavisOrganology|Circulatory/vessels/capillaries1/capillaries3}}, "Capillaries, non-fenestrated (EM, Low)" * {{BUHistology|21402ooa}} * [http://www.informaworld.com/smpp/title~content=t713617829 Endothelium Journal of Endothelial Cell Research], [[Informa Healthcare]] * [http://essuir.sumdu.edu.ua/handle/123456789/2689 Endothelium and inflammation] * [http://courses.washington.edu/conj/bloodcells/platelets.htm Platelet Activation], [[University of Washington]] {{Epithelium and epithelial tissue}} {{Cardiovascular system}} [[Category:Angiology]] [[Category:Tissues]]'
New page wikitext, after the edit (new_wikitext)
'{{about|the lining of blood and lymphatic vessels|the endothelium of the cornea|corneal endothelium}} {{refimprove|date=October 2008}} {{Infobox Anatomy | Name = Endothelium | Latin = | GraySubject = | GrayPage = | Image = Endotelijalna ćelija.jpg | Caption = Diagram showing the location of endothelial cells | Image2 = Microvessel.jpg | Caption2 = Endothelial cells, which form the [[tunica intima]], or innermost layer of the vessel, encircle an erythrocyte (E). | Precursor = | System = | Artery = | Vein = | Nerve = | Lymph = | MeshName = | MeshNumber = | Code = {{TerminologiaHistologica|2|00|02.0.02003}} | }} The '''endothelium''' is the thin layer of [[cell (biology)|cells]] that lines the interior surface of [[blood vessel]]s and [[lymphatic vessels]],<ref>{{DorlandsDict|three/000035470|Endothelium}}</ref> forming an interface between circulating [[blood]] or [[lymph]] in the [[lumen (anatomy)|lumen]] and the rest of the vessel wall. The cells that form the endothelium are called '''endothelial cells'''. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells. Vascular endothelial cells line the entire [[circulatory system]], from the [[heart]] to the smallest [[capillaries]]. These cells have unique functions in vascular biology. These functions include [[ultrafiltration|fluid filtration]], such as in the [[glomeruli]] of the kidney, [[muscle tone|blood vessel tone]], [[hemostasis]], [[neutrophil]] recruitment, and [[hormone trafficking]]. Endothelium of the interior surfaces of the heart chambers is called [[endocardium]]. ==Structure== Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer. In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow.<ref>Eskin S.G., C.L. Ives, L.V. McIntire, L.T. Navarro. Microvascular Research. Volume 28, Issue 1, July 1984, Pages 87–94Response of cultured endothelial cells to steady flow. http://dx.doi.org/10.1016/0026-2862(84)90031-1</ref><ref>B L Langille and S L Adamson. Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice. ''Circulation Research''.1981; 48: 481-488.</ref> === Terminology === The foundation model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue. == Function == Endothelial cells are involved in many aspects of vascular biology, including: * Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of [[white blood cell]]s into and out of the bloodstream. Excessive or prolonged increases in permeability of the endothelial monolayer, as in cases of chronic inflammation, may lead to tissue [[edema]]/swelling. * [[Coagulation|Blood clotting]] ([[thrombosis]] & [[fibrinolysis]]). The endothelium normally provides a non-thrombogenic surface because it contains, for example, [[heparan sulfate]] which acts as a [[Cofactor (biochemistry)|cofactor]] for activating [[antithrombin]], a protease that inactivates several factors in the coagulation cascade. * [[Inflammation]] * Formation of new blood vessels ([[angiogenesis]]) * [[Vasoconstriction]] and [[vasodilation]], and hence the control of [[blood pressure]] * Repair of damaged or diseased organs via an injection of blood vessel cells<ref>[http://medicalxpress.com/news/2013-10-blood-vessel-cells-regenerate-scientists.html#ajTabs]</ref> * [[Angiopoietin-2]] works with VEGF to facilitate cell proliferation and migration of endothelial cells ==Clinical significance== {{Main|Endothelial dysfunction}} [[Endothelial dysfunction]], or the lose of pooper endothelial function, is a halmark for vascular diseeses, iz often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide hiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. == See also == {{columns-list|3| * [[Epithelium]] * [[Apelin]] * [[Caveolae]] * [[Endocardium]] * [[Endothelial activation]] * [[Endothelial microparticle]]s * [[Endothelial progenitor cell]]s * [[Endothelium-derived relaxing factor]] ([[EDRF]]) * [[Robert F. Furchgott]] (1998 Nobel prize for discovery of EDRF) * [[Platelet activation]] * [[Susac's syndrome]] * [[Tunica intima]] * [[VE-cadherin]] * [[Weibel-Palade body|Weibel-Palade bodies]] * [[Angiocrine growth factors]] }} == References == {{reflist|2}} == External links == * {{eMedicineDictionary|Endothelium}} * {{UCDavisOrganology|Circulatory/vessels/capillaries1/capillaries3}}, "Capillaries, non-fenestrated (EM, Low)" * {{BUHistology|21402ooa}} * [http://www.informaworld.com/smpp/title~content=t713617829 Endothelium Journal of Endothelial Cell Research], [[Informa Healthcare]] * [http://essuir.sumdu.edu.ua/handle/123456789/2689 Endothelium and inflammation] * [http://courses.washington.edu/conj/bloodcells/platelets.htm Platelet Activation], [[University of Washington]] {{Epithelium and epithelial tissue}} {{Cardiovascular system}} [[Category:Angiology]] [[Category:Tissues]]'
Unified diff of changes made by edit (edit_diff)
'@@ -28,7 +28,7 @@ Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer. In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow.<ref>Eskin S.G., C.L. Ives, L.V. McIntire, L.T. Navarro. Microvascular Research. Volume 28, Issue 1, July 1984, Pages 87–94Response of cultured endothelial cells to steady flow. http://dx.doi.org/10.1016/0026-2862(84)90031-1</ref><ref>B L Langille and S L Adamson. Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice. ''Circulation Research''.1981; 48: 481-488.</ref> === Terminology === -The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue. +The foundation model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue. == Function == Endothelial cells are involved in many aspects of vascular biology, including: @@ -42,7 +42,7 @@ ==Clinical significance== {{Main|Endothelial dysfunction}} -[[Endothelial dysfunction]], or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide synthase|nitric oxide synthesis]] and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in [[reactive oxygen species]], which can impair nitric oxide production and activity via several mechanisms.<ref name="pmid15643116">{{cite journal | author = Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. +[[Endothelial dysfunction]], or the lose of pooper endothelial function, is a halmark for vascular diseeses, iz often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide hiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi. == See also == {{columns-list|3| '
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[ 0 => 'The foundation model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue.', 1 => '[[Endothelial dysfunction]], or the lose of pooper endothelial function, is a halmark for vascular diseeses, iz often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide hiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.' ]
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[ 0 => 'The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of [[vimentin]] rather than [[keratin]] filaments separate these from epithelial cells.<ref name="urlFMA">{{cite web |url=http://bioportal.bioontology.org/ontologies/FMA/?p=classes&conceptid=http%3A%2F%2Fsig.uw.edu%2Ffma%23Endothelial_cell&jump_to_nav=true |title=FMA |format= |work= |accessdate=2013-09-28}}</ref> Many considered the endothelium a specialized [[epithelial]] tissue.', 1 => '[[Endothelial dysfunction]], or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of [[atherosclerosis]]. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with [[coronary artery disease]], [[diabetes mellitus]], [[hypertension]], [[hypercholesterolemia]], as well as in [[Tobacco smoking|smokers]]. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of [[nitric oxide]], often due to high levels of [[asymmetric dimethylarginine]], which interfere with the normal [[Arginine|L-arginine]]-stimulated [[Nitric oxide synthase|nitric oxide synthesis]] and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in [[reactive oxygen species]], which can impair nitric oxide production and activity via several mechanisms.<ref name="pmid15643116">{{cite journal | author = Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ | title = Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension | journal = J Hypertens | volume = 23 | issue = 1 | pages = 7–17 |date=January 2005 | pmid = 15643116 | doi = 10.1097/00004872-200501000-00004| url = }}</ref> The signalling protein [[ERK5]] is essential for maintaining normal endothelial cell function.<ref name="pmid19909257">{{cite journal | author = Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ.| title = ERK5 and the regulation of endothelial cell function | journal = Biochem Soc Trans. | volume = 37 | issue = 6 | pages = 1254–9 |date=Dec 2009 | pmid = 19909257 | pmc = | doi =10.1042/BST0371254 }}</ref> A further consequence of damage to the endothelium is the release of pathological quantities of [[von Willebrand factor]], which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.' ]
Whether or not the change was made through a Tor exit node (tor_exit_node)
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Unix timestamp of change (timestamp)
1408723385