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1 5), suggesting impaired vasoconstriction and 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 t biomarker of tolerance than donor-specific hyporeactivity.
7 , preschool) was associated with more global hyporeactivity across the cortico-striatal circuit.
8                            As a result, both hyporeactivity and hypotension are reversed, generation
9 n, CMV infection, OB, donor antigen-specific hyporeactivity, and pulmonary function.
10                               Similar immune hyporeactivity, associated with an elevated risk of succ
11                 DSBM may, thus, induce graft hyporeactivity by impairing intragraft immune activation
12 diagnoses and patterns of patient hyper- and hyporeactivity demonstrated abnormal activation in the a
13 rent depression severity was associated with hyporeactivity exclusively in the nucleus accumbens in r
14 plant correlated with donor antigen-specific hyporeactivity (i.e., decreased proliferative response t
15 aride-induced hypotension and cardiovascular hyporeactivity in animal models of septic shock and in m
16 tal-hypertensive rats show in vitro vascular hyporeactivity in large part mediated by the endothelium
17 reotide treatment prevents in vitro vascular hyporeactivity in prehepatic portal-hypertensive rats, a
18      MEG also reduced the degree of vascular hyporeactivity in rat thoracic aortic rings exposed to p
19 arly phase of hypotension and cardiovascular hyporeactivity in sepsis, and the cellular sources of in
20 g adolescence was associated with more focal hyporeactivity in the nucleus accumbens, while depressio
21 ith functional endothelium but, in contrast, hyporeactivity in vessels without functional endothelium
22 toxicity but does contribute to the vascular hyporeactivity induced by endotoxin in vitro and in vivo
23 tration actually confers donor-specific (DS) hyporeactivity is unknown.
24 lated with questionnaire measures of sensory hyporeactivity, large intra-individual variability may p
25                                     Vascular hyporeactivity of ex vivo aortas was ameliorated.
26                                      The SMA hyporeactivity of PVL-20G and RAL rats was corrected by
27 de also reduced PARS activation and vascular hyporeactivity of rat thoracic aortas exposed to ONOO- (
28  of remitted depression suggest network-wide hyporeactivity of striatal (caudate, putamen, nucleus ac
29 sease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis
30   Thus, it remains unclear which patterns of hyporeactivity represent a trait-like indicator of depre
31 arly phase of hypotension and cardiovascular hyporeactivity seen in septic shock.
32 hese animals did not express iNOS or display hyporeactivity to ACh or SPER-NO.
33  and associated with an in vivo and in vitro hyporeactivity to alloantigens.
34 40401 protects against hypotension, vascular hyporeactivity to catecholamines, and mortality associat
35 deactivation would appear to account for the hyporeactivity to exogenous catecholamines observed in s
36  of knockout mice demonstrated a generalized hyporeactivity to methacholine-induced airflow changes (
37 asculature of PVL-20G and RAL animals showed hyporeactivity to methoxamine (P < 0.01).
38 otension, which was associated with a marked hyporeactivity to norepinephrine in ex vivo thoracic aor
39 ther treatment with M40401 could reverse the hyporeactivity to norepinephrine typifying early septic
40  implicated in the vasodilation and vascular hyporeactivity underlying septic shock.
41  intragraft CD8+ cells, and (3) DSBM induces hyporeactivity up until the day of the allograft placeme
42 e two recipient populations to determine why hyporeactivity was lower in the CCTT group than at our c
43       A lower rate of donor antigen-specific hyporeactivity was seen in the CCTT recipients (6 of 79=
44 isease protection was attributable to T cell hyporeactivity, which was secondary to changes in thymic