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1 t biomarker of tolerance than donor-specific hyporeactivity.
2 in the development of donor antigen-specific hyporeactivity.
3 and donor-specific mixed lymphocyte reaction hyporeactivity.
4 eaction demonstrated in vitro donor-specific hyporeactivity.
5 /W, 8-hourly) corrects the in vitro vascular hyporeactivity.
6 5), suggesting impaired vasoconstriction and hyporeactivity.
11 plant correlated with donor antigen-specific hyporeactivity (i.e., decreased proliferative response t
12 aride-induced hypotension and cardiovascular hyporeactivity in animal models of septic shock and in m
13 tal-hypertensive rats show in vitro vascular hyporeactivity in large part mediated by the endothelium
14 reotide treatment prevents in vitro vascular hyporeactivity in prehepatic portal-hypertensive rats, a
16 arly phase of hypotension and cardiovascular hyporeactivity in sepsis, and the cellular sources of in
17 ith functional endothelium but, in contrast, hyporeactivity in vessels without functional endothelium
18 toxicity but does contribute to the vascular hyporeactivity induced by endotoxin in vitro and in vivo
22 de also reduced PARS activation and vascular hyporeactivity of rat thoracic aortas exposed to ONOO- (
23 sease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis
27 40401 protects against hypotension, vascular hyporeactivity to catecholamines, and mortality associat
28 deactivation would appear to account for the hyporeactivity to exogenous catecholamines observed in s
29 of knockout mice demonstrated a generalized hyporeactivity to methacholine-induced airflow changes (
31 otension, which was associated with a marked hyporeactivity to norepinephrine in ex vivo thoracic aor
32 ther treatment with M40401 could reverse the hyporeactivity to norepinephrine typifying early septic
34 intragraft CD8+ cells, and (3) DSBM induces hyporeactivity up until the day of the allograft placeme
35 e two recipient populations to determine why hyporeactivity was lower in the CCTT group than at our c
37 isease protection was attributable to T cell hyporeactivity, which was secondary to changes in thymic
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