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1 s of high-sensitivity C-reactive protein and asymmetric dimethylarginine).
2 en the SPIN1 triple Tudor domain and histone asymmetric dimethylarginine.
5 n (angiopoietin-2, osteoprotegerin, ICAM-1), asymmetric dimethylarginine (ADMA) and impaired microvas
8 uanidino-methylated arginines (MA) including asymmetric dimethylarginine (ADMA) and N(G)-methyl-l-arg
9 eased concentrations of two methylarginines, asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-l
12 anidinomethylated arginines (MAs), including asymmetric dimethylarginine (ADMA) and NG-methyl-L-argin
13 and positive associations were found for the asymmetric dimethylarginine (ADMA) and symmetric dimethl
14 r (15)N-arginine intravenous infusion and on asymmetric dimethylarginine (ADMA) and symmetric dimethy
15 n mammalian cells: monomethylarginine (MMA), asymmetric dimethylarginine (ADMA) and symmetric dimethy
16 ndogenous arginine derivatives homoarginine, asymmetric dimethylarginine (ADMA) and symmetric dimethy
19 oth fibroblast growth factor 23 (FGF-23) and asymmetric dimethylarginine (ADMA) are associated with p
23 ) bioavailability, inflammation profile, and asymmetric dimethylarginine (ADMA) in patients undergoin
24 ncentrations of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in the hypoxia-induce
34 rculating concentrations of the uremic toxin asymmetric dimethylarginine (ADMA) were elevated in 2KO
35 ne, and the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) were measured with li
36 ork implicating the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormon
42 rogens regulate the metabolism or release of asymmetric dimethylarginine (ADMA), an endogenous inhibi
43 ffects in part by elevating plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibi
45 dy prospectively determined plasma levels of asymmetric dimethylarginine (ADMA), an endogenous nitric
46 l contributor to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous nitric
48 l contributor to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous NO syn
50 aw the next morning for soluble CD40 ligand, asymmetric dimethylarginine (ADMA), and nitrotyrosine le
51 1) strictly generates monomethylarginine and asymmetric dimethylarginine (ADMA), but not symmetric di
52 risk factors, total homocysteine (tHcy) and asymmetric dimethylarginine (ADMA), correlate with decre
53 Plasma was assayed for endothelin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesi
54 dogenous inhibitor of nitric oxide synthase, asymmetric dimethylarginine (ADMA), is elevated in patie
55 a levels of arginine, citrulline, ornithine, asymmetric dimethylarginine (ADMA), symmetric dimethylar
56 function and raised plasma concentrations of asymmetric dimethylarginine (ADMA), the endogenous inhib
67 e endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine [ADMA, via inhibition of dim
68 bin [TAT] complex), endothelial dysfunction (asymmetric dimethylarginine [ADMA]), and platelet-derive
70 vels of apolipoprotein AI and high levels of asymmetric dimethylarginine, an endogenous inhibitor of
71 lammation (C-reactive protein), or levels of asymmetric dimethylarginine, an endogenous inhibitor of
72 aminohydrolases (DDAHs) are known to degrade asymmetric dimethylarginine, an endogenous inhibitor of
74 that 3.7% of the molecules naturally contain asymmetric dimethylarginine and/or monomethylarginine.
75 Decompartmentalized hemoglobin, arginase 1, asymmetric dimethylarginine, and adenine nucleotides are
77 1(-/-) mice showed a significant increase of asymmetric dimethylarginine concentration in plasma (1.4
78 ferase 1 (PRMT1) catalyzing the formation of asymmetric dimethylarginines has been implicated in canc
83 atocrit levels were lower and plasma CFH and asymmetric dimethylarginine levels were higher in patien
89 eduction in the level of p-cresol sulfate or asymmetric dimethylarginine to significant reductions in
91 pending on the resulting methylated product: asymmetric dimethylarginine (Type I PRMT), symmetric dim
92 ients were characterized by higher levels of asymmetric dimethylarginine, tyramine, 2-hydroxybutyric
93 uremic milieu contains increased amounts of asymmetric dimethylarginine, we speculate that such accu
94 stable nitric oxide oxidation products, and asymmetric dimethylarginine were abnormal in patients wi
95 plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine were measured at serial time
97 h severe malaria, hematocrit and CFH but not asymmetric dimethylarginine were significant predictors.
98 il, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in uri