Hochschulschrift
Complement C5a receptor and polymorphonuclear neutrophils- accomplices in atherosclerotic lesion formation
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
Aachen, Techn. Univ., Diss., 2012
- Schlagwort
-
Komplement , Anaphylatoxine , Komplement C5a , Rezeptor , Plaque , Arteriosklerose , Neutrophiler Granulozyt
Kardiovaskuläre Krankheit
- Ereignis
-
Veröffentlichung
- (wo)
-
Aachen
- (wer)
-
Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen
- (wann)
-
2013
- Urheber
- URN
-
urn:nbn:de:hbz:82-opus-43584
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
25.03.2025, 13:55 MEZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Objekttyp
- Hochschulschrift
Beteiligte
- Vijayan, Santosh
- Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen
Entstanden
- 2013
Ähnliche Objekte (12)
Complement C5a receptor and polymorphonuclear neutrophils - accomplices in atherosclerotic lesion formation
Complement Factor C5a Inhibits Apoptosis of Neutrophils—A Mechanism in Polytrauma?
Atherosclerotic lesion: a morphometric study applying a biometric system
Role of CXCL12 and endothelial HIF-1alpha in atherosclerotic lesion stabilization
Numerical simulation of growth of an atherosclerotic lesion with a moving boundary
The role of FLIP long in C5a-modulated spontaneous apoptosis of neutrophils
Impact of a temporary depletion of Regulatory T cells on atherosclerotic lesion development
Role of CXCL12 and endothelial HIF-1 α [alpha] in atherosclerotic lesion stabilization
Complement C5a blockade is sufficient to resolve crystalline thrombotic microangiopathy
Complement C5a-induzierte Funktionsänderung neutrophiler Granulozyten während der systemischen Entzündung
Complement C5a induces pro-inflammatory microvesicle shedding in severely injured patients
Role of complement receptors C5aR and C5L2 in bone metabolism
Complement C5a receptor and polymorphonuclear neutrophils - accomplices in atherosclerotic lesion formation
Complement Factor C5a Inhibits Apoptosis of Neutrophils—A Mechanism in Polytrauma?
Atherosclerotic lesion: a morphometric study applying a biometric system
Role of CXCL12 and endothelial HIF-1alpha in atherosclerotic lesion stabilization
Numerical simulation of growth of an atherosclerotic lesion with a moving boundary
The role of FLIP long in C5a-modulated spontaneous apoptosis of neutrophils
Impact of a temporary depletion of Regulatory T cells on atherosclerotic lesion development
Role of CXCL12 and endothelial HIF-1 α [alpha] in atherosclerotic lesion stabilization
Complement C5a blockade is sufficient to resolve crystalline thrombotic microangiopathy
Complement C5a-induzierte Funktionsänderung neutrophiler Granulozyten während der systemischen Entzündung
Complement C5a induces pro-inflammatory microvesicle shedding in severely injured patients
Role of complement receptors C5aR and C5L2 in bone metabolism
Complement C5a receptor and polymorphonuclear neutrophils - accomplices in atherosclerotic lesion formation
Complement Factor C5a Inhibits Apoptosis of Neutrophils—A Mechanism in Polytrauma?
Atherosclerotic lesion: a morphometric study applying a biometric system
Role of CXCL12 and endothelial HIF-1alpha in atherosclerotic lesion stabilization
Numerical simulation of growth of an atherosclerotic lesion with a moving boundary
The role of FLIP long in C5a-modulated spontaneous apoptosis of neutrophils
Impact of a temporary depletion of Regulatory T cells on atherosclerotic lesion development
Role of CXCL12 and endothelial HIF-1 α [alpha] in atherosclerotic lesion stabilization
Complement C5a blockade is sufficient to resolve crystalline thrombotic microangiopathy
Complement C5a-induzierte Funktionsänderung neutrophiler Granulozyten während der systemischen Entzündung
Complement C5a induces pro-inflammatory microvesicle shedding in severely injured patients