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1 d by the NO scavenger hemoglobin, but not by methemoglobin.
2 ake rate, but did not reduce the activity of methemoglobin.
3 iled studies of this reaction of low NO with methemoglobin.
4 roid hormone metabolism and the reduction of methemoglobin.
5 result in conversion of plasma hemoglobin to methemoglobin.
6 generates NO and oxidizes deoxyhemoglobin to methemoglobin.
7 ed by Sartor, Mayer, and Johari for hydrated methemoglobin.
8 ccurs during the reaction of hydroxyurea and methemoglobin.
9  by an assay for conversion of hemoglobin to methemoglobin.
10 radation products (intra- and extra-cellular methemoglobin), 3.lipid-containing lesions (lipoma, derm
11                                For instance, methemoglobin A in solution is, as expected, nearly indi
12 on reaction that also oxidizes hemoglobin to methemoglobin, a non-oxygen-binding form of hemoglobin t
13                                Using a human methemoglobin alpha beta dimer, it has been shown that a
14          In the detoxication of cyanide with methemoglobin, an intermediate dicyanhemimethemoglobin w
15 methemoglobin and nitrite/nitrate or between methemoglobin and any other clinical variable.
16 circulation, whereas controlled infusions of methemoglobin and cyanomethemoglobin, which do not consu
17                                              Methemoglobin and denatured hemoglobin binding to the RB
18 idation and suppress oxidation of Hb to form methemoglobin and ferryl hemoglobin were pH-dependent.
19 emoglobin, the differences between deoxy-Hb, methemoglobin and HbCO are smaller than the correspondin
20 ht help prevent the detrimental formation of methemoglobin and hemichrome in vivo, insofar as this is
21 nown to result in oxidation of hemoglobin to methemoglobin and hemichrome.
22 nce (EPR) spectroscopy, DHA oxidized HbNO to methemoglobin and liberated NO from HbNO as determined b
23  reaction with oxyhemoglobin, which produces methemoglobin and nitrate (NO 3 (-)).
24                                  Circulating methemoglobin and nitrite/nitrate concentrations are inc
25                                  Circulating methemoglobin and nitrite/nitrate concentrations were si
26 n study entry and every 6 hrs for 72 hrs for methemoglobin and nitrite/nitrate determinations.
27 re were no significant relationships between methemoglobin and nitrite/nitrate or between methemoglob
28                 A strong correlation between methemoglobin and plasma nitrate formation was observed,
29 anidine-hydrochloride-induced disassembly of methemoglobin and previous measurements of apohemoglobin
30 that hydroxyurea oxidizes deoxyhemoglobin to methemoglobin and reduces methemoglobin to deoxyhemoglob
31 droxy group react with oxyhemoglobin to form methemoglobin and variable amounts of nitrite/nitrate.
32 modynamic, gas exchange, pulmonary function, methemoglobin, and nitrite/nitrate measurements were obt
33 ra indicated that hemoglobin was oxidized to methemoglobin, and the addition of catalase demonstrated
34  estimate blood levels of carboxyhemoglobin, methemoglobin, and total hemoglobin (SpHb), as well as t
35                 With donor, only nitrate and methemoglobin are formed, stoichiometric with the amount
36                                              Methemoglobin assay confirmed these results and demonstr
37 encountered with persistently high levels of methemoglobin associated with a left-shift in the oxygen
38 e pH 7.1 and 5.4 crystal structures of horse methemoglobin at 1.6 and 2.1 A resolution, respectively,
39 cells produced almost complete conversion to methemoglobin, but no detectable lipid extraction.
40                                              Methemoglobin, but not heme-stabilized cyanomethemoglobi
41 tion, blood pressure, oxygen saturation, and methemoglobin concentration.
42                            Four patients had methemoglobin concentrations >5%.
43                                      Maximum methemoglobin concentrations were greater in patients tr
44 aramagnetic behavior that deoxyhemoglobin or methemoglobin containing RBCs experience when suspended
45 throcytes and hemoxidizing the hemoglobin to methemoglobin, cystalysin was also capable of removing t
46 2.8 angstrom and ~3.2 angstrom structures of methemoglobin demonstrate that distinct conformational s
47 s to ferrous hemoglobin, thus completing the methemoglobin-dependent sulfide oxidation cycle.
48                                              Methemoglobin-dependent sulfide oxidation in mammals is
49 ion with the alternate crystal structures of methemoglobin establish that the solution structure of w
50 e soluble protein that reduces cytochrome c, methemoglobin, ferricyanide, and molecular oxygen in vit
51 n vivo or in vitro, involves autoxidation to methemoglobin, followed by cofactor loss and globin unfo
52 ve been associated with vascular reactivity, methemoglobin formation and development of antibodies.
53   T1 relaxation time was related to thrombus methemoglobin formation and further processing.
54 cibly; (ii) the speed of the reaction limits methemoglobin formation by autooxidation; (iii) there is
55 e membranes exerted an exaggerated effect on methemoglobin formation in solution, an effect completel
56                  Major findings include that methemoglobin formation mediated by the lipophilic t-BuB
57 table contrast enhancement and extracellular methemoglobin formation occurs within 24 hours of the co
58   Significantly, Ap44mSe limited deleterious methemoglobin formation, highlighting its usefulness in
59 globin (oxyHb) (96%), which was converted to methemoglobin (>95%) after treatment with 150 microM NO.
60 es a redox cycle between deoxyhemoglobin and methemoglobin has been forwarded to explain these result
61            Consistent with this formation of methemoglobin, human plasma was found to consume approxi
62 scopy shows that the formation of a low-spin methemoglobin-hydroxyurea complex is critical for iron n
63 ied the pathway involved in the reduction of methemoglobin in the family, thereby describing the firs
64 y have been associated with metmyoglobin and methemoglobin in the lesions.
65 in seven patients because of the presence of methemoglobin in the tumor bed.
66  deoxyhemoglobin, and high-spin and low-spin methemoglobins in each spectrum collected as the reactio
67 oxyheme of hemoglobin (producing nitrate and methemoglobin) is extremely rapid, it has been proposed
68 ted snakes indicated by a 50-60% increase in methemoglobin levels and a 40% decrease in oxyhemoglobin
69 ed normal 2,3-bisphosphoglycerate (2,3-BPG), methemoglobin levels and intracellular pH.
70                                      Because methemoglobin levels are modified by several mechanisms
71  TAK-242 resulted in mild increases in serum methemoglobin levels but was otherwise well tolerated.
72 ic oxide at doses of < or =20 ppm maintained methemoglobin levels of <3.0% and circuit concentrations
73         Transient, dose-related increases in methemoglobin levels were observed with TAK-242 treatmen
74 tients with HbE beta thalassemia showed that methemoglobin levels were significantly increased and th
75 on, a highly significant correlation between methemoglobin levels, splenectomy, and factors that modi
76 d not cause systemic hypotension or increase methemoglobin levels.
77  no clinically significant increase in blood methemoglobin levels.
78  the reactions of hydroxyurea and deoxy- and methemoglobin likely proceed by inner-sphere mechanisms.
79 oposed a global disassembly scheme for human methemoglobin, linking hemin (ferric protoporphyrin IX)
80                                  Circulating methemoglobin measurements are not superior to plasma ni
81 s was investigated through the evaluation of methemoglobin (MetHb) and malondialdehyde (MDA) levels.
82 t IsdX2 NEAT domains only scavenge heme from methemoglobin (metHb) and that autoxidation of oxyhemogl
83 in dissociation occurs much faster from fish methemoglobin (metHb) compared to mammalian metHb yet th
84           We determined total hemoglobin and methemoglobin (MetHb) concentrations, cytochrome b(5) re
85  studies have demonstrated that 3-AP induces methemoglobin (metHb) formation and hypoxia in patients,
86 yanide toxicity can be reduced by the use of methemoglobin (MetHb) formers, and antidotal dosage is b
87 ectrons in the four heme groups of deoxy and methemoglobin (metHb) gives these species paramagnetic p
88 d as nitrosylhemoglobin (HbNO) in an aqueous methemoglobin (MetHb) solution.
89 that of Hb(III)NO formed when NO reacts with methemoglobin (MetHb), but is similar to metHb resulting
90 ransfer between the various couples of human methemoglobin (metHb), IsdA, IsdB, IsdC, and IsdE by spe
91 s well established and generates nitrate and methemoglobin (metHb).
92  reversibly bound O2, or paramagnetic ferric methemoglobin (metHb).
93    The effects of a lethal APAP oral dose on methemoglobin (MetHb, non-oxygen carrying form) levels a
94                                              Methemoglobin (Mhb) remained low in all subjects breathi
95 resistance index (SVRI), cardiac index (CI), methemoglobin, nitrite/nitrate, or lung pathology scores
96 s ascribed to a faster reaction of NO with a methemoglobin-nitrite complex.
97 conditions the product stoichiometry is 1:1 (methemoglobin:nitrosylhemoglobin), and unexpectedly, the
98 rhage by taking advantage of the short T1 of methemoglobin present in acute thrombus and intraplaque
99            OOPE5 was the most active against methemoglobin production (53.7% reduction), whereas OOPE
100 in-induced vaso-occlusion was blocked by the methemoglobin reducing agent methylene blue, haptoglobin
101 (HbA) tetramers or inhibit the activities of methemoglobin reductase and four selected glycolysis pat
102 een cytochrome b5 reductase 3, also known as methemoglobin reductase, and oxidized sGC.
103 dely distributed hemoglobins, and associated methemoglobin reductases, than dioxygen transport and st
104 olesterol biosynthesis, drug metabolism, and methemoglobin reduction.
105 hrocytes, soluble cytochrome b5 functions in methemoglobin reduction.
106  2 whereas the yield of trapping of NO(-) by methemoglobin remained unaffected.
107 he reactions of hydrogen peroxide with human methemoglobin, sperm whale metmyoglobin, and horse heart
108  protein, hemoglobin, which in the ferric or methemoglobin state binds H2S and oxidizes it to a mixtu
109   After all the oxyHb reacts with NO to form methemoglobin, the disappearance rate of NO slows greatl
110  nitric oxide or nitric dioxide or increased methemoglobin, the risk of complications with inhaled ni
111 s oxidized 85-90% of plasma oxyhemoglobin to methemoglobin, thereby inhibiting endogenous NO scavengi
112 deoxyhemoglobin to methemoglobin and reduces methemoglobin to deoxyhemoglobin.
113 at hydroxyurea reacts with oxy-, deoxy-, and methemoglobin to produce 2-6% of iron nitrosyl hemoglobi
114 d co-workers reported that crystalline horse methemoglobin undergoes a large lattice transition as th
115 ectron-transfer rate from cytochrome b(5) to methemoglobin using a formalism developed by Marcus.
116  form with NO exposure <2 microM, but plasma methemoglobin was detectable by paramagnetic resonance s
117  also associated with severity and fatality, methemoglobin was only modestly increased in patients wi
118 , PaCO2, pH, heart rate, blood pressure, and methemoglobin were recorded at baseline and after inhali
119 tilatory settings, arterial blood gases, and methemoglobin were recorded at each study period.
120 udying a complex between apo-HasAp and human methemoglobin were stymied by the rapid heme capture by
121  if infused hemoglobin was first oxidized to methemoglobin, which does not scavenge NO.
122 /HarA NEAT domains bind a single molecule of methemoglobin, while the distantly related NEAT domain f
123 tectable as a quintet at room temperature in methemoglobin with identical spectral features to those
124 mbus imaging (MRDTI) is capable of detecting methemoglobin within intraplaque hemorrhage.

 
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