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1 hrombosis) by synergistic stimulation of the coagulation system.
2 of enzyme systems, in particular, the blood coagulation system.
3 n between cells of the vessel wall and blood coagulation system.
4 lay among the various processes in the blood coagulation system.
5 ties implicate a role in the fibrinolytic or coagulation system.
6 that local mechanisms exist to regulate the coagulation system.
7 due to concurrent activation of the platelet-coagulation system.
8 ion motif receptors, and cross talk with the coagulation system.
9 ation and dysfunction, and activation of the coagulation system.
10 c disease that provokes dysregulation of the coagulation system.
11 platelets with subsequent alteration of the coagulation system.
12 C) is associated with robust activity of the coagulation system.
13 potentiate several interactions in the blood coagulation system.
14 ical states caused by a malfunctioning blood coagulation system.
15 as associated with activation of the contact coagulation system.
16 mechanism by which ticks inhibit the host's coagulation system.
17 rotein VI on platelets and factor XIa of the coagulation system.
18 oint of care comprehensive assessment of the coagulation system.
19 am in granulocytes through engagement of the coagulation system.
20 ory processes and abnormalities of the blood coagulation system.
21 a (HCC) with a recently engineered microwave coagulation system.
22 c domains of several serine proteases of the coagulation system.
23 (SAA) and of CRP itself, and to activate the coagulation system.
24 saccharide administration also activates the coagulation system.
25 d with APC is unique among inhibitors of the coagulation system.
26 resulting from unfettered activation of the coagulation system.
27 ss, and is associated with activation of the coagulation system.
28 of treatment on vascular reactivity and the coagulation system.
29 th the vascular wall structure and the blood coagulation system.
30 membrane-stabilized proteases of the plasma coagulation system.
31 ctivation or regulation of the complement or coagulation systems.
32 anisms, such as modulation of the immune and coagulation systems.
33 phils, activation of the complement, and the coagulation systems.
34 he vascular endothelium in activation of the coagulation system, a fundamental homeostatic mechanism
35 an approved therapy with a component of the coagulation system (activated protein C) to treat patien
42 vation of the innate immune response and the coagulation system after injury is a phylogenetically an
46 le cell disease have a chronically activated coagulation system and display hemostatic perturbations,
47 tested the hypothesis that activation of the coagulation system and downstream protease-activated rec
48 ttenuated the APAP-induced activation of the coagulation system and hepatocellular injury and diminis
49 may be possible only if these hurdles in the coagulation system and innate immunity can be overcome.
51 t study, a novel interface between the blood coagulation system and platelets is demonstrated by show
52 eads to global dysfunction of the endogenous coagulation system and results in worse outcomes and inc
53 hat thrombin mediates cross-talk between the coagulation system and the adaptive immune system at sit
54 mmarise the complex interactions between the coagulation system and the angiogenic process that occur
55 , fibrinolysis, and interactions between the coagulation system and the vascular endothelium, brain t
57 ose derived from the complement, contact and coagulation systems) and late phase inflammation (Th2 ce
59 ntial, life-threatening alterations in their coagulation system, and currently, there is an approved
60 cting blood to tissues, interacting with the coagulation system, and modulating resistance to blood f
61 Because activation of platelets and of the coagulation system are interdependent mediators of throm
63 actions between neurohormonal, vascular, and coagulation systems are beginning to explain how this ha
65 rch has demonstrated that the complement and coagulation systems are closely integrated with each inf
66 elements of the bradykinin, angiotensin and coagulation systems are co-expressed with ACE2 in alveol
69 ied protein components of the complement and coagulation systems as key pathways implicated in psycho
70 e related to differences in the platelet and coagulation systems between diabetics and nondiabetics,
71 he function of human factor IX in the murine coagulation system, bleeding times were performed in nor
72 ed direct links between mammalian immune and coagulation systems by examining cytokine proproteins fo
73 h all of the membrane-bound reactions of the coagulation system can be localized to the surface of ac
74 (tissue factor/factor VIIa) pathways in the coagulation system, coagulation factor Xa (FXa) has been
76 ces in these processes, in particular in the Coagulation System, could account for the thrombotic phe
79 the renin-angiotensin-aldosterone system and coagulation system, dysregulated immunity, the dysfuncti
80 lement cascade (e.g. C1R, C1S, and VWF), the coagulation system (e.g. THBS1 and VWF), and the regulat
82 f the immune system, the endothelium and the coagulation system: factors required for malarial pathog
83 s, APOepsilon4 was associated with increased coagulation system failure among European American patie
85 r (TF), the protease receptor initiating the coagulation system, functions in vascular development, a
86 s associated with dysregulated complement or coagulation systems impact disease, we performed a retro
88 ghts the involvement of genes related to the coagulation system in determining the severity of COVID-
90 ls" such as horseshoe crabs, the role of the coagulation system in immunity in higher organisms remai
93 e network, the vascular endothelium, and the coagulation system in patients without a history of diab
95 llness, such as from the complement cascade, coagulation system, inflammation and adaptive immune sys
96 sical training has beneficial effects on the coagulation system, inflammatory factors, and sleep qual
97 ings provide an interesting link between the coagulation system, innate immunity, LPS scavenging, and
98 the mechanisms through which the immune and coagulation systems interact and reciprocally regulate o
99 Although it is known that the complement and coagulation systems interact, no studies have investigat
100 d that in most inflamed arthritic joints the coagulation system is activated, leading to the local ge
101 ese studies suggest that a part of the blood coagulation system is adapted to perform a developmental
107 thrombin, the pivotal proenzyme of the blood coagulation system, is demonstrated and activation of th
111 he complex cross talk between platelets, the coagulation system, leukocytes, and the activated endoth
114 dence suggests that the kallikrein-kinin and coagulation system might participate in this process.
116 ere inflammation (negative association), the coagulation system (negative association), and liver X r
118 ith a selectively enhanced activation of the coagulation system (plasma levels of thrombin-antithromb
119 did neither influence the activation of the coagulation system (plasma levels of thrombin/antithromb
120 ssociated with an enhanced activation of the coagulation system post-LAAC (144 [48-192] versus 52 [24
122 ncompatibilities between the pig and primate coagulation systems proved additionally beneficial.
124 The activation of factor X by the extrinsic coagulation system results from the action of an enzyme
125 ave developed a model of the extrinsic blood coagulation system that includes the stoichiometric anti
126 ch implies tissue specific regulation of the coagulation system that is supported by further evidence
127 ized linkage between platelets and the blood coagulation system that may have a significant regulator
128 cleic acid-based approaches to influence the coagulation system, the future of genetic therapies for
129 sclerosis (MS) has been associated with the coagulation system, the temporal and spatial regulation
130 sis, and inflammation; it also activates the coagulation system through direct interaction with tissu
131 ate that PDAC is driven by activation of the coagulation system through tumor cell-derived TF, circul
132 II)) salt was investigated as a flocculation-coagulation system to remove arsenic (As) from water.
136 matory cytokines (i.e. IL-6) and an impaired coagulation system, which can cause serious complication
138 animals developed a severe alteration of the coagulation system, which was concomitant with acute hep
141 tribute to the development of a pathological coagulation system, with resulting chronic inflammation
142 ne network, the vascular endothelium and the coagulation system, with the exception of antithrombin l