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1 effects of PCMV activation in the recipient (consumptive coagulopathy).
2 yonic blood vessel endothelium causes lethal consumptive coagulopathy.
3 bosis after 3 weeks, terminating in a lethal consumptive coagulopathy.
4 hemodynamic instability, capillary leak, and consumptive coagulopathy.
5 eir illness, both patients had evidence of a consumptive coagulopathy.
6 ot displaying platelet reductions typical of consumptive coagulopathies.
7                                              Consumptive coagulopathy and anemia occurred on days 7 t
8           This suggests that, while managing consumptive coagulopathy and hyperfibrinolysis both seem
9 see text]g/ml), representative biomarkers of consumptive coagulopathy and hyperfibrinolysis respectiv
10 ter estimates about the underlying nature of consumptive coagulopathy and hyperfibrinolysis with surv
11 two prominently described phenotypes of TIC, consumptive coagulopathy and hyperfibrinolysis, affect s
12        Treatment with RA101295 also improved consumptive coagulopathy and preserved endothelial antic
13                        BACKGROUNDFeatures of consumptive coagulopathy and thromboinflammation are pro
14 oach to prevent sepsis-induced inflammation, consumptive coagulopathy, and subsequent organ failure a
15 time and decreased fibrinogen, indicative of consumptive coagulopathy; and SYK expression in tissues.
16     Although D-dimer, sepsis physiology, and consumptive coagulopathy are indicators of mortality, cu
17  extremities and multiple organ systems, and consumptive coagulopathy as the disease end-point provid
18 r than hepatocytes likely contributes to the consumptive coagulopathy associated with severe YF in pr
19 he time of rejection or the development of a consumptive coagulopathy, biopsy specimens were obtained
20 proach to the treatment of sepsis-associated consumptive coagulopathy, but its application is limited
21        A rapidly progressive disorder termed consumptive coagulopathy (CC) has been observed frequent
22 njury and possibly an increased incidence of consumptive coagulopathy (CC).
23 utively dysregulated hemostasis, including a consumptive coagulopathy, characterized by compensatory
24 mbined with the expression of tissue factor, consumptive coagulopathy developed irrespective of histo
25            Embryos lacking TM develop lethal consumptive coagulopathy during this period, and no live
26 V) has been implicated in the development of consumptive coagulopathies in severely envenomed patient
27 ed in prolonged graft survival and prevented consumptive coagulopathy in all recipients.
28 tic microangiopathy in the graft or systemic consumptive coagulopathy in the recipient.
29        Delayed bleeding is often ascribed to consumptive coagulopathy initiated by exposed brain tiss
30 e degree of hemostatic stress of a non-overt consumptive coagulopathy (nonovert DIC).
31           Clinical or laboratory features of consumptive coagulopathy occurred in 7 of 12 baboons.
32 ion and tissue factor expression; in vivo, a consumptive coagulopathy occurred when there was xenorea
33 ion tests are most useful in detecting overt consumptive coagulopathy (overt DIC) near the time of ch
34  Blood, Hijazi et al challenge the view that consumptive coagulopathy that accompanies traumatic brai
35 lated factor VIIa/TF action and a consequent consumptive coagulopathy underlies the bleeding diathesi
36           However, only macaques developed a consumptive coagulopathy whereas YFV-infected hFRG mice