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1 ately 25-50 are reduced, with 6-8 considered hyperreactive.
2 ased from endothelium is ultralarge (UL) and hyperreactive.
3 not conclude whether or not asthmatic ASM is hyperreactive.
4 hat natural ovarian steroids directly reduce hyperreactive 5-HT and thromboxane A2-stimulated Ca2+ an
5 y exposed workers and control subjects to be hyperreactive (95% confidence interval, 1.8-25.2; p = 0.
6 against syngeneic MHC-II(+) skin grafts, (2) hyperreactive against third-party MHC-II(+) skin grafts,
9 class had diminished lung function and more hyperreactive airways compared with all other classes.
11 rs the TCR threshold and renders lymphocytes hyperreactive and capable of unwanted immune responses.
12 Platelets from patients with diabetes are hyperreactive and demonstrate increased adhesiveness, ag
14 ollapse, 23% of highly exposed subjects were hyperreactive as compared with only 11% of moderately ex
16 ically silencing these neurons abolished the hyperreactive broncho-constrictions, even in the presenc
17 rlapping with those identified previously as hyperreactive by administration of exogenous reagents (t
18 e c oxidase-negative/succinate dehydrogenase-hyperreactive (COX-/SDH++) fibers from normal aging huma
19 work is the first to directly identify seven hyperreactive cysteines: 1040, 1303, 2436, 2565, 2606, 2
21 ibody-drug conjugates, and identification of hyperreactive methionine residues in whole proteomes.
22 ll transfer from long-term exposed mice into hyperreactive mice also restored normal airway responsiv
23 how that normal responsiveness in previously hyperreactive mice, achieved after long-term allergen ch
24 represents an important mechanism behind the hyperreactive nature of basophils that has long been obs
25 the rs956115 marker of the IRS-1 gene have a hyperreactive platelet phenotype and increased risk of M
28 anges in platelet gene expression creating a hyperreactive platelet, despite antiplatelet therapy.
29 tion in humans, but can cumulatively lead to hyperreactive platelets and increase risk for negative o
33 et therapies, and it has been suggested that hyperreactive reticulated platelets underlie this altere
34 ted for reducing the rate of CPM labeling of hyperreactive SR thiols (IC50 = 0.3 and 1.8 microM, resp
37 nd dose-dependently interact with a class of hyperreactive sulfhydryl groups localized on ryanodine-s
38 lcoumarin (CPM) to measure the reactivity of hyperreactive sulfhydryl moieties on sarcoplasmic reticu
39 itions previously shown to selectively label hyperreactive sulfhydryls and eliminate redox sensing.
40 ely and reversibly alters the redox state of hyperreactive sulfhydryls localized in the RyR/Ca2+ chan
45 lated to their ability to selectively modify hyperreactive thiols regulating normal functioning of mi
47 ound that pre-GT WASp-deficient B cells were hyperreactive to B cell receptor stimulation (BCR stimul
48 onsequence, TIPE2 knockout myeloid cells are hyperreactive to Poly (I:C) stimulation, and TIPE2 knock
51 ence of E3Q EcFpg, the Sp nucleotide (nt) is hyperreactive toward cleavage by MPE-Fe(II)-generated hy
53 age (IL-6), resulting in the accumulation of hyperreactive ULVWF in plasma and on the surface of endo
54 ease with thrombospondin motif) converts the hyperreactive unusually large (UL) forms of von Willebra
57 These findings suggest an important role for hyperreactive VWF in SCD pathology and connect SCD to ot
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