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1                                              HgCl2 did not modulate CD95 expression; however, it did
2                                              HgCl2 was not able to attenuate TNF-alpha-mediated apopt
3                                              HgCl2-induced cell death of macrophages resulted in the
4  A.SW mice (H-2s) received HgCl2 plus IL-12, HgCl2 alone, or IL-12 alone.
5 y incubation experiments using both Hg ((199)HgCl2 and CH3(201)Hg(+))- and hydrogen (CD3I)-stable iso
6 and spontaneous proliferation in vitro after HgCl2.
7 oromercuribenzoate (pCMB), mersalyl acid and HgCl2, but not by the stilbene anion exchange inhibitors
8 ibited by 2 water channel blockers, DMSO and HgCl2.
9 rane were different for HgO versus HgBr2 and HgCl2.
10 assay of osmotic water permeability (Pf) and HgCl2 inhibition dose-response.
11  in control (both F(A) and F(B) present) and HgCl2-treated (F(B)-less) PS I complexes from Synechococ
12 es of autoantibodies induced by pristane and HgCl2 were compared in SJL and BALB/c mice to examine wh
13 sibly inhibited by the water channel blocker HgCl2.
14 /s at 10 degrees C that was inhibited 95% by HgCl2.
15 d by the kinase inhibitor H7, and blocked by HgCl2, an inhibitor of aquaporin 1.
16  nitrous acid released from the S-NO bond by HgCl2 approaches 90-100% as documented by simultaneous a
17 ed a low activation energy, was inhibited by HgCl2 (0.1 mM), and exhibited a unit conductance of 3.2
18 ansport, glycerol transport was inhibited by HgCl2 and showed a low Ea (4.43 kcal/mol).
19               Pf was reversibly inhibited by HgCl2 in mutants S70C, G71C, G72C, H73C, and S189C but i
20  S) of the two root regions was inhibited by HgCl2.
21  energy, 4.5 kcal/mol), and not inhibited by HgCl2.
22 inhibition of GS activity in cell lysates by HgCl2 was reversed by the addition of dithiothreitol (DT
23      K1/2 values for 50% inhibition of Pf by HgCl2 were as follows (in millimolar): 0.40 (S70C), 0.36
24   The ADP-ribose bound to 30K was removed by HgCl2 but not by NH2OH, suggesting the modification of a
25 s were exposed to MeHg or mercuric chloride (HgCl2) for 1 or 6 h.
26 s mice, subtoxic doses of mercuric chloride (HgCl2) induce a complex autoimmune syndrome characterize
27 fer the ability to resist mercuric chloride (HgCl2)-induced autoimmunity.
28 ways in the development of mercury chloride (HgCl2)-induced autoimmune disease in mice, which is beli
29                     Different GOM compounds (HgCl2, HgBr2, and HgO) were found to have different affi
30                        Under wet conditions, HgCl2 (50 microM), which is known to block membrane wate
31  flowered, and set seed on medium containing HgCl2 concentrations of 25-100 microM (5-20 ppm), levels
32                                 In contrast, HgCl2 did not inhibit LP of the mid-root region under we
33                                 In contrast, HgCl2 produced a dose dependent decrease in astrocytic G
34 s (</=10 microM) of inorganic mercury (i.e., HgCl2) attenuated anti-CD95-mediated growth arrest and m
35 ibose bound to 80K was not removed by either HgCl2 or NH2OH, which is consistent with the modificatio
36 anges in GS protein or mRNA levels following HgCl2 exposure.
37    A predominant Th2-type response following HgCl2 treatment of wild-type B10.S mice was confirmed by
38 egans, focusing on inorganic and organic Hg (HgCl2 and MeHgCl) and Se (selenomethionine, sodium selen
39 salts, including CdCl2, ZnSO4, NiCl2, HgSO4, HgCl2, PbI2, and Pb(Ac)2.
40 t inhibited by the water transport inhibitor HgCl2.
41                             In cell lysates, HgCl2 was three-times more potent than MeHg in inhibitin
42 itrosothiols in protein-containing mixtures, HgCl2-mediated release of nitrous acid in the presence o
43  permeability of SjAQP was inhibited by 1 mM HgCl2, 3 mM tetraethylammonium, 1 mM ZnCl2, and 1 mM CuS
44 l) and was reduced 70% upon addition of 1 mM HgCl2.
45 erved in the presence and absence of 0.18 mM HgCl2.
46 72% (reduced to 22+/-1 microm/sec) by 0.3 mM HgCl2 and was inhibited by 56% to 58% by coinjection wit
47                As a positive control, 0.3 mM HgCl2 inhibited AQP1 water permeability by >95%.
48                 Pf was not altered by 0.3 mM HgCl2 or 50 microM forskolin, but was increased to 31 x
49                    Apical addition of 0.5 mM HgCl2 elicited an 11-fold increase in paracellular condu
50               Pf was decreased 30% by 0.5 mM HgCl2 in < 1-d lungs and 44% in 4-d lungs.
51 t 23 degrees C and was reduced 54% by 0.5 mM HgCl2.
52 ed conditions in a hydroponic system (30 muM HgCl2) was compared with that of naturally occurring Hor
53                                       Murine HgCl2-induced autoimmunity (mHgIA) is a T cell-dependent
54 when either Hg-cysteine complexes or neutral HgCl2 dominated the speciation of Hg(II), demonstrating
55                            Administration of HgCl2 to naive BN rats induced marked autoantibody produ
56 d activated T cells before administration of HgCl2, and less autoreactivity and spontaneous prolifera
57 s able to routinely inject stable amounts of HgCl2 and HgBr2 into atmospheric mercury measurement sys
58 JL mice were neither those characteristic of HgCl2-treated SJL mice nor those associated with pristan
59 n certain strains of mice, subtoxic doses of HgCl2 (mercuric chloride; mercury) induce a complex auto
60  migration of fibrillarin in the presence of HgCl2.
61 ere similar in mice receiving HgCl2 alone or HgCl2 plus IL-12.
62          Groups of A.SW mice (H-2s) received HgCl2 plus IL-12, HgCl2 alone, or IL-12 alone.
63 ent FK506 immunosuppression before receiving HgCl2.
64 l Ig deposits were similar in mice receiving HgCl2 alone or HgCl2 plus IL-12.
65                      After 8 d of rewetting, HgCl2 decreased LP and L(R, S) of the distal region by 2
66               In this study, we observe that HgCl2 administration in susceptible mice results in the
67 rine externalization, directly verified that HgCl2 attenuated anti-CD95-mediated apoptosis.
68                     IL-12 also inhibited the HgCl2-induced serum IgG1 increase, but, in contrast, did
69 larin Abs with some of the properties of the HgCl2-induced anti-fibrillarin response.
70                       The sensitivity of the HgCl2-induced modification of fibrillarin to 2-ME, iodoa
71 d finding that IL-12 further potentiated the HgCl2-triggered IL-4 induction in this model.
72                                  Exposure to HgCl2 or Cu(acetate)2 resulted in release of nitric oxid
73 1C, G72C, H73C, and S189C but insensitive to HgCl2 in the other mutants.
74 sylhistone synthesized by Rt6 were stable to HgCl2 and HCl, but labile to NH2OH, consistent with ADP
75             This thiol linkage was stable to HgCl2.
76 ensitivity was as low as 5 microM RSNO using HgCl2.
77 h pathway were analyzed to determine whether HgCl2 could modulate them.
78           Both increases were abolished with HgCl2, and the mercurial inhibition was reversible with
79 e GS activity in cell lysates incubated with HgCl2 or MeHg.
80         In contrast, BN rats pretreated with HgCl2-resistant allogeneic Lewis bone marrow and transie
81  lysates from endothelial cells treated with HgCl2.
82 e bound label is resistant to treatment with HgCl2 but sensitive to NH2OH, characteristic of arginine

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