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1 hemical properties, toxicities, and modes of toxic action.
2 c metabolism, specific and reactive modes of toxic action, activation of adaptive stress response pat
3 philin-based mechanism could account for the toxic actions attributed to certain noncoplanar PCB cong
4 cidal proteins known as colicins exert their toxic action by forming a large, nonselective channel in
5 m dodecylbenzenesulfonate revealed a mode of toxic action consistent with oxidative stress and detrim
8 ty of guanidinocalixarenes in inhibiting LPS toxic action has previously been related to their capaci
13 f nascent proteins in vivo, and this mode of toxic action might underlie its suspected role in the pa
18 ng NO synthesis, both acting by inhibiting a toxic action of NO that is critical to tissue injury.
24 immunity proteins protect bacteria from the toxic action of their own effectors, whilst orphan immun
26 tion with apoE receptors may not mediate the toxic actions of apoE4, because receptor-associated prot
28 yconitine attenuated both the protective and toxic actions of DMXB, but in temporally distinct manner
29 he mechanisms underlying the therapeutic and toxic actions of general anesthetics helps us reframe th
30 arrays would protect the retina against the toxic actions of methanol-derived formic acid in a roden
31 presence of nAChRs sensitizes neurons to the toxic actions of soluble oligomeric Abeta, perhaps contr
33 Here we show that aldosterone exerts direct toxic actions on myocardium by oxidative activation of C
34 he scheme is based on three broad domains of toxic action representing nonspecific toxicity (e.g., na
37 ning aquatic-relevant modes or mechanisms of toxic action to substances, based solely on consideratio
38 etrachlorodibenzo-p-dioxin (TCDD) exerts its toxic action via the aryl hydrocarbon (Ah) receptor, whi
39 he antibody combining site was fast, and its toxic action was unimpeded by this delivery mechanism.