|1.||Colman, Robert W: 14 articles (12/2010 - 07/2002)|
|2.||Pixley, Robin A: 8 articles (12/2010 - 07/2002)|
|3.||Isordia-Salas, Irma: 8 articles (11/2005 - 07/2002)|
|4.||Sainz, Irma M: 5 articles (09/2007 - 09/2004)|
|5.||Agelan, Alexis: 3 articles (12/2010 - 09/2004)|
|6.||Liu, Yuchuan: 3 articles (12/2010 - 09/2007)|
|7.||Martínez-Murillo, Carlos: 3 articles (11/2005 - 09/2004)|
|8.||Sartor, R Balfour: 3 articles (08/2005 - 07/2002)|
|9.||Adam, Albert: 3 articles (08/2005 - 07/2002)|
|10.||Renné, Thomas: 2 articles (09/2015 - 09/2008)|
11/01/2005 - "[High molecular weight kininogen in inflammation and angiogenesis: a review of its properties and therapeutic applications]."
01/01/2005 - "The role of plasma high molecular weight kininogen in experimental intestinal and systemic inflammation."
09/01/2004 - "The role of plasma high molecular weight kininogen in experimental intestinal and systemic inflammation."
10/15/2003 - "The mutation Ser511Asn leads to N-glycosylation and increases the cleavage of high molecular weight kininogen in rats genetically susceptible to inflammation."
01/01/2005 - "The fact that deficiency of plasma high molecular weight kininogen in the genetically susceptible Lewis rat results in decreased chronic enterocolitis and systemic inflammation also supports our hypothesis. "
06/01/2003 - "A 6-year-old male with vertebral-basilar artery thrombosis was recognized to have high-molecular-weight kininogen (HK) deficiency. "
09/01/1999 - "Brown-Norway Katholiek strain rats with an absence of low- and high-molecular-weight kininogen due to a single point mutation, A163T, were compared in the thrombosis model to the wild-type animals, which were otherwise genetically identical. "
07/01/2004 - "gC1q-R/p33 (gC1q-R) is a multifunctional and multicompartmental cellular protein, which is postulated to play a role in inflammation and thrombosis by interacting with C1q and high molecular weight kininogen (HK). "
03/27/2014 - "To determine the extent to which catheter thrombosis is triggered by the contact or extrinsic pathway of coagulation, we used antisense oligonucleotides (ASOs) to selectively knock down factor (f)XII, fXI, or high-molecular-weight kininogen (HK), key components of the contact pathway, or fVII, which is essential for the extrinsic pathway. "
01/01/2010 - "The presence of paradoxical "lupus anticoagulants" in certain thrombosis-prone SLE patient plasmas, marked by delayed clotting in clinical plasma test, was explained by the consumption of contact system proteins, especially high molecular weight kininogen. "
11/01/1984 - "Replacement therapy with C 1-inhibitor preparation for an edema attack revealed that clinical improvement paralleled the increase in blood levels of high molecular weight kininogen. "
03/07/2000 - "LlTI inhibits kinin release from high molecular weight kininogen by human plasma kallikrein in vitro and, administered intravenously, causes a decrease in paw edema induced by carrageenin or heat in male Wistar rats. "
10/01/1989 - "Therefore, we conclude that bradykinin generated by plasma kallikrein-induced cleavage of HMWK is not involved in the pathogenesis of edema due to acute exposure to high altitude."
05/01/2008 - "Several of the key processes that underlie the development of diabetic retinopathy, such as increased vascular permeability, edema, neovascularization, and inflammatory changes, have been associated with the KKS, and recent work has shown that components of the KKS, including plasma kallikrein, factor XIIa, and high-molecular-weight kininogen, are present in the vitreous of people with diabetic retinopathy. "
09/01/2008 - "This review focuses on articles, which report phenotypization of animals deficient in the contact system proteins factor XII, factor XI and high-molecular-weight kininogen, as well as novel links between factor XII and edema formation, discovery of new in-vivo activators of factor XII, and functions of the factor XII downstream protease factor XI. Recent studies improved understanding of the factor XII-driven contact system in hemostasis, thrombosis, and inflammation. "
01/01/1979 - "The significant reduction of high molecular weight-kininogen in synovial fluid of patients with active rheumatoid arthritis."
01/01/2006 - "High molecular weight kininogen (HK) is a plasma protein that is cleaved by plasma kallikrein in the clinical settings of sepsis and chronic inflammatory diseases such as rheumatoid arthritis and Crohn's disease. "
10/13/1983 - "Consumption of high-molecular-weight kininogen in hereditary angioedema."
08/01/1986 - "The anti-light chain Mab demonstrated in vivo activation and cleavage of HMWK during an angioedema attack in a patient with hereditary angioedema and C1-inhibitor deficiency."
01/01/1990 - "Immunoblot assays for detection of changes in the structure of HMWK and prekallikrein may be objective laboratory studies for documenting clinical attacks of hereditary angioedema, their onset, and their resolution."
01/01/2011 - "Bradykinin (BK), generated from high-molecular-weight kininogen (HK) is the major mediator of swelling attacks in hereditary angioedema (HAE), a disease associated with C1-inhibitor deficiency. "
05/05/1983 - "Prekallikrein activation and high-molecular-weight kininogen consumption in hereditary angioedema."
|1.||Factor XII (Hageman Factor)
|2.||Factor XI (Plasma Thromboplastin Antecedent)
|3.||Proteins (Proteins, Gene)
|4.||High-Molecular-Weight Kininogen (Kininogen, High Molecular Weight)
|8.||Low-Molecular-Weight Kininogen (Kininogen, Low Molecular Weight)
|10.||Peptidyl-Dipeptidase A (Angiotensin Converting Enzyme)
|1.||Renal Dialysis (Hemodialysis)