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1 ion in the respiratory cycle is dependent on S-nitrosohemoglobin.
2 nitric oxide (NO) to cysteinebeta93, forming S-nitrosohemoglobin.
3 iminates superoxide, increasing the yield of S-nitrosohemoglobin and nitrosylated hemes.
4                                              S-nitrosohemoglobin and plasma S-nitrosothiols did not c
5 he relative roles of adenosine triphosphate, S-nitrosohemoglobin, and nitrite as effectors.
6 terial vs. venous differences in nitrite and S-nitrosohemoglobin are diminished in sepsis and associa
7                         Systemic nitrite and S-nitrosohemoglobin consumption can be assessed by compa
8                                              S-nitrosohemoglobin contracts blood vessels and decrease
9 terial vs. venous red blood cell nitrite and S-nitrosohemoglobin differences were absent.
10  groups is a rapidly reversible process, and S-nitrosohemoglobin formation is probably not a primary
11                                           No S-nitrosohemoglobin forms during these reactions.
12 s accompanied by an allosteric transition in S-nitrosohemoglobin [from the R (oxygenated) to the T (d
13 issue oxygenation and is proportional to RBC S-nitrosohemoglobin (HbSNO) content (but not nitrosylhem
14  of hypotheses concerning the role played by S-nitrosohemoglobin in vivo.
15 sting systemic nitrite consumption), whereas S-nitrosohemoglobin levels are higher in venous vs. arte
16                                              S-nitrosohemoglobin levels were in the nanomolar range,
17 ologic paradigms contend that nitrite and/or S-nitrosohemoglobin mediate intravascular delivery of ni
18 nous vs. arterial blood (suggesting systemic S-nitrosohemoglobin production).
19 d relaxations during hypoxia correlated with S-nitrosohemoglobin (SNO-Hb) (R2=0.88) but not iron nitr
20                             In erythrocytes, S-nitrosohemoglobin (SNO-Hb) arises from S-nitrosylation
21                               We report that S-nitrosohemoglobin (SNO-Hb) concentrations declined rap
22 O-liganded Hb could support the chemistry of S-nitrosohemoglobin (SNO-Hb) formation.
23                                              S-Nitrosohemoglobin (SNO-Hb) is a vasodilator whose acti
24 s results run counter to the hypothesis that S-nitrosohemoglobin (SNO-Hb) serves as an in vivo reserv
25 sial, with separate roles for nitrite () and S-nitrosohemoglobin (SNO-Hb) widely contested given thei
26 itrosation of cysteine beta93 in hemoglobin (S-nitrosohemoglobin (SNO-Hb)) occurs in vivo, and transn
27 , RBC-dependent vasoregulatory function, and S-nitrosohemoglobin (SNO-Hb), through which hemoglobin (
28         Banked blood shows reduced levels of S-nitrosohemoglobin (SNO-Hb), which in turn impairs the
29  the blood is bound to thiols of Hb, forming S-nitrosohemoglobin (SNO-Hb), which releases the NO grou
30 ally, for S-nitrosation of betaCys93 to form S-nitrosohemoglobin (SNO-Hb).
31 ol, yielding a deficiency in the vasodilator S-nitrosohemoglobin (SNO-Hb).
32 nitrite, LMW-SNOs and HMW-SNOs, and red cell S-nitrosohemoglobin (SNO-Hb).
33 ation, and in transfer of the NO moiety from S-nitrosohemoglobin (SNO-HbS) to the RBC membrane.
34                      The mechanisms by which S-nitrosohemoglobin (SNOHb) stimulates vasodilation are
35 NO adducts were found in the RBCs, including S-nitrosohemoglobin (SNOHb).
36  the minority deoxyheme to subsequently form S-nitrosohemoglobin (SNOHb).
37                               Maintenance of S-nitrosohemoglobin was associated with improvements in
38                                 In contrast, S-nitrosohemoglobin was higher in venous compared to art
39 ing nitric oxide bioactivity (in the form of S-nitrosohemoglobin) was markedly diminished 10 hours af
40 te S-nitrosothiol content (reflecting mainly S-nitrosohemoglobin) was significantly higher for blood
41                                  Nitrite and S-nitrosohemoglobin were measured using tri-iodide-based
42 93 cysteine S-nitrosylated hemoglobin [SNOHb:S-nitrosohemoglobin], which has been shown to induce vas

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