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1 zine), suggesting that they exhibit superior antipruritic action and limited side effects that likely
2                               The beneficial antipruritic action of RMP may be explained, at least pa
3 Prostaglandin D(2) (PGD(2)) is known to have antipruritic activity by suppressing histamine release.
4  as well as cell transplant-derived GABA are antipruritic against acute itch and in a transgenic mous
5            Systemic muscimol or baclofen are antipruritic against both histamine-dependent and -indep
6 diates its anti-itch effects by boosting the antipruritic agent, PGD(2), by the activation of the p38
7 nd vanilloids may serve as targets for novel antipruritic agents.
8 nd-receptor systems into future therapies as antipruritics and/or analgesics in humans.
9 est potency were evaluated in vivo for their antipruritic as well as sedative action; they proved to
10 may provide a central therapeutic target for antipruritic drug development.
11 ntity of its own, which must be treated with antipruritic drugs, even if the underlying cause is alre
12 ify the critical brain centers mediating the antipruritic effect of butorphanol.
13 onergic antidepressants and demonstrated the antipruritic effect of the TRPC4 inhibitor ML204.
14  muscimol produced a significant synergistic antipruritic effect, with no sedation.
15 examined the connection between seladelpar's antipruritic effects and IL-31 and bile acid levels in p
16 In contrast, KORs mediating the diuretic and antipruritic effects were not regulated by JNK (c-Jun N-
17 , and TRPM8 activation has antiallodynic and antipruritic effects, making it a prime therapeutic targ
18 ggesting a mechanism to explain seladelpar's antipruritic effects.
19 ntihistamine with a H(2)S donor has improved antipruritic efficacy, bifunctional molecules with antih
20 ith atopic dermatitis; however, the specific antipruritic mechanism of action remains unclear.
21                           We also tested the antipruritic properties of intraspinal transplantation o
22 counterstimuli relieve itch, resulting in an antipruritic state that persists for minutes to hours.
23 ritogenic pruritus), which may affect future antipruritic strategies.
24 g a new basis for the development of a novel antipruritic strategy via interrupting IL-20 epidermal p
25 talk between 5-HT1A and GRPR may be a useful antipruritic strategy.
26 r both may serve as a potential approach for antipruritic therapy in atopic dermatitis.
27 ignal transduction as a potential target for antipruritic therapy.
28 ent potential targets for the development of antipruritic therapy.
29 static liver diseases hinders development of antipruritic treatments.