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1  mediated by HO using the chemical inhibitor tin protoporphyrin.
2 ity by EFS was inhibited by the HO inhibitor Tin protoporphyrin (1 x 10(-4) mol/L).
3                 Inhibition of HO activity by tin protoporphyrin 9 reverses the component of endotheli
4             Enzyme studies demonstrated that tin protoporphyrin-9 is a selective inhibitor of HO with
5                                              Tin protoporphyrin, a selective inhibitor of HO, reverse
6                  In contrast, treatment with tin protoporphyrin abolished the benefit of BC1 gene tra
7                          Inhibition of HO by tin protoporphyrin abrogated the impairment of resistanc
8 amycin and, more importantly, the effects of tin protoporphyrin, an inhibitor of HO activity, on the
9 toporphyrin, an inducer of HO-1 activity, or tin protoporphyrin, an inhibitor of HO-1.
10                                 In contrast, tin protoporphyrin and tin mesoporphyrin did not display
11                          The HO-1 inhibitor, tin protoporphyrin, blocked MP4CO protection, consistent
12  Inhibition of HO activity by treatment with tin protoporphyrin blunted survival advantage in Tg mice
13 closporin A), inhibition of HO-1 activity by tin protoporphyrin, caused graft rejection in 3--7 days.
14 treatment of Ad-HO-1 with the HO-1 inhibitor tin protoporphyrin completely restored each morphometric
15                 Heme oxygenase inhibition by tin protoporphyrin exacerbates stasis in sickle mice.
16         Under inhibition of HO-1 activity by tin protoporphyrin, exogenous CO suppressed graft reject
17 nhibition of heme oxygenase via injection of tin protoporphyrin IX (20 micromol/kg intraperitoneally)
18 Th3/(+) We observed that HO inhibition using tin protoporphyrin IX (SnPP) decreased heme-iron recycli
19 ence and absence of neurohumoral inhibitors (tin protoporphyrin IX [SnPP IX] for CO synthesis, N(omeg
20 cts of PMA are prevented by the HO inhibitor tin protoporphyrin IX and in cultures from mice with del
21                                              Tin protoporphyrin IX did not affect heme oxygenase-1 ex
22 n vivo heme oxygenase enzyme inhibition with tin protoporphyrin IX in common bile duct ligation anima
23 ase or heme oxygenase-1 inhibitors (1400W or tin protoporphyrin IX).
24                 MGd used in combination with tin protoporphyrin IX, an inhibitor of HO1, resulted in
25                         HO-1 inhibition with tin-protoporphyrin IX and silencing with RNA interferenc
26 y bilirubin and abolished by incubation with tin protoporphyrin-IX and knock down of nuclear factor-E
27 s potentiated by the HO inhibitors, zinc and tin protoporphyrin-IX as well as by the CO scavenger, he
28                Treatment of the animals with tin protoporphyrin-IX, a global HO inhibitor, or HO-1 sm
29 ent of sheared SMCs with the HO-1 inhibitor, tin protoporphyrin-IX, blocked the antiaggregatory effec
30 th DHCR24 and HO-1 small interfering RNA and tin-protoporphyrin-IX treatment abolished these effects.
31 al cells with HO-1 small interfering RNA and tin-protoporphyrin-IX treatment did not inhibit the (A-I
32 CR24 and HO-1 and systemic administration of tin-protoporphyrin-IX, an HO inhibitor, abolished these
33 acological inhibition of HO-1 activity using tin protoporphyrin or knockdown of HO-1 prevents the ind
34  the induction of HO-1 and was attenuated by tin protoporphyrin (SnPP) IX, an inhibitor of HO-1 activ
35                        Inhibition of HO-1 by tin protoporphyrin (SnPP) or siRNA downregulated Pax3/7-
36 O inhibitors (zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP)) suppressed the channel in a m
37 proliferation was inhibited by ZnPP, whereas tin protoporphyrin (SnPP), another equally potent HO-1 i
38 sing a competitive inhibitor of HO activity, tin protoporphyrin (SnPP), in protocols affording a comp
39             The effects of the HO inhibitor, tin protoporphyrin (SnPP), on brain electrical activity
40 ondiabetic and diabetic animals treated with tin protoporphyrin (SnPP, a heme oxygenase-1 enzyme inhi
41   When HO-1 enzymatic activity is blocked by tin protoporphyrin (SnPPIX) or the action of CO is inhib
42 decreased in the presence of HO-1 inhibitor, tin protoporphyrin (SnPPIX).
43 n vitro with the heme oxygenase-1 inhibitor, tin protoporphyrin, substantially decreased survival and
44                                              Tin protoporphyrin treatment normalized carboxyhemoglobi

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