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1 important role in the assembly of the plasma kallikrein-kinin system.
2 at plays a central role in activation of the kallikrein-kinin system.
3 ng cascade, the fibrinolytic system, and the kallikrein-kinin system.
4 ting a disturbed balance between the RAS and kallikrein-kinin systems.
5 ole in the renin-angiotensin-aldosterone and kallikrein-kinin systems.
6 een GPCR that link the renin-angiotensin and kallikrein-kinin systems.
7 nhibitor that rapidly inhibits PKa activity, kallikrein kinin system activation and HK cleavage in pl
8        Effects of KVD900 on PKa activity and kallikrein kinin system activation in whole plasma were
9  monoclonal antibody C11C1 attenuates plasma kallikrein-kinin system activation, local and systemic i
10 se the intriguing possibility that decreased kallikrein-kinin system activity may play an important r
11  rats could be mediated via changes in renal kallikrein-kinin system activity.
12                                          The kallikrein-kinin system, along with the interlocking ren
13 nd anti-inflammatory pathways, including the kallikrein-kinin system and leukocyte activity.
14 ent with the close interrelation between the kallikrein-kinin system and the RAAS.
15                                    The renal kallikrein-kinin system and the renin-angiotensin system
16 ologic assembly and activation of the plasma kallikrein/kinin system and discusses its influence on v
17 interaction between CpaA, FXII, and the KKS (kallikrein-kinin system) and to determine the downstream
18 s also been reported that alterations of the kallikrein-kinin system are associated with formation of
19                  The opposing effects of the kallikrein-kinin system are mediated by bradykinin actin
20               The principal effectors of the kallikrein-kinin system are plasma and tissue kallikrein
21                    The renin-angiotensin and kallikrein-kinin systems are key regulators of vascular
22 The relevance and significance of the plasma kallikrein/kinin system as a risk factor for the develop
23 ein produced in the liver that regulates the kallikrein-kinin system at multiple points.
24                                   One of the kallikrein-kinin system components, kallikrein-binding p
25 vascular remodeling and the up-regulation of Kallikrein-kinin system contribute, at least in part, to
26 ning genetic disease that is associated with kallikrein-kinin system dysregulation.
27                    The renin-angiotensin and kallikrein-kinin systems engage in cross-talk at multipl
28          This is the first report of a local kallikrein-kinin system in adrenergic nerve endings capa
29  Previous findings underline the role of the kallikrein-kinin system in angiogenesis.
30                   To explore the role of the kallikrein-kinin system in relation to ischemia/reperfus
31  opposing roles of the renin-angiotensin and kallikrein-kinin systems in vivo, the distinct propertie
32                   Hemodialysis activates the kallikrein-kinin system, increasing bradykinin.
33                                          The kallikrein-kinin system is developmentally expressed in
34 ion of coagulation cascade components of the kallikrein-kinin system (KKS) and downregulation of kini
35                                          The kallikrein-kinin system (KKS) comprises a cascade of pro
36                                   The plasma kallikrein-kinin system (KKS) consists of serine proteas
37                                          The kallikrein-kinin system (KKS) has been postulated to pla
38                            Modulation of the kallikrein-kinin system (KKS) has been shown to have ben
39          This study examines the role of the kallikrein-kinin system (KKS) in RIHD by investigating t
40 s studies in perfused limbs suggest that the kallikrein-kinin system may participate in the regulatio
41                                          The kallikrein-kinin system participates in blood pressure r
42 r angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of t
43 between MPO and the components of the plasma kallikrein-kinin system resulted in decreased bradykinin
44 or the assembly of the vasoregulatory plasma kallikrein-kinin system; thus we explored whether MPO an
45 on phase of coagulation and functions in the kallikrein-kinin system to generate bradykinin.