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1 imidine levels were 10--25 times higher than pentosidine.
2 er than CML levels and 100-fold greater than pentosidine.
3 rmation of overall free fluorescent AGEs and pentosidine.
4 pecies scavengers decreased the formation of pentosidine.
5 rast to N(epsilon)-(carboxymethyl)lysine and pentosidine.
6 lycoxidation markers carboxymethyllysine and pentosidine.
7 ent decreased free and < 10,000 mol wt bound pentosidine.
8     Neither HD nor PD affected protein-bound pentosidine.
9 ar to the advanced glycosylation end product pentosidine.
10 ociated with 30-32% lower furosine, 9% lower pentosidine, 9-13% lower CML, 24% higher acid-soluble co
11                        We have also measured pentosidine, a fluorescent AGE derived from pentose suga
12                          We have quantitated pentosidine, a marker of glycoxidative stress in skin co
13 No analysed meat sample showed any traces of pentosidine above the instrumental determination limits.
14 ues within the nucleotide binding domain via pentosidine AGEs.
15 e by AGE-specific polyclonal antibodies, and pentosidine, an acid-stable fluorescent AGE.
16 ious results from our laboratory showed that pentosidine, an advanced glycation product, formed in sk
17 ecific advanced glycation end-products (anti-pentosidine and anti-pyrraline), protein modifications t
18 e sugars, and compared the concentrations of pentosidine and argpyrimidine.
19 related with the levels of renal and cardiac pentosidine and carboxymethyllysine and inversely correl
20             Blocking experiments showed that pentosidine and carboxymethyllysine formation was signif
21 onic renal failure enhances the formation of pentosidine and carboxymethyllysine via Fenton reaction
22 ohistochemical evidence for the formation of pentosidine and CML structures in human Bruch's membrane
23 centrations than the fluorescent cross-links pentosidine and dityrosine, identifying them as major Ma
24                                     Although pentosidine and glucosepane have been widely studied for
25 nd is structurally related to the other AGEs pentosidine and glucosepane.
26                                The fact that pentosidine and imidazolysine, formed from ribose and me
27 ollagen glycation (furosine), glycoxidation (pentosidine and N(epsilon)-[carboxymethyl]-lysine [CML])
28 erted similar antiglycative capacity against pentosidine and Nepsilon-carboxyethyl-lysine, although t
29         The renal and cardiac levels of UHP, pentosidine, and carboxymethyllysine in patients with CR
30 mine the carnosine, anserine, homocarnosine, pentosidine, and thiobarbituric acid-reactive substance
31                            A polyclonal anti-pentosidine antibody and a monoclonal antibody specific
32  dialysis (PD), yet plasma levels of the AGE pentosidine are significantly lower in PD than in hemodi
33 d AGEs, N(epsilon)-(carboxymethyl)lysine and pentosidine, are glycoxidation products, formed from glu
34 contained a 2-4 x greater content of the AGE pentosidine at all equilibrium time points.
35      However clearance of protein-associated pentosidine by the peritoneal membrane may explain lower
36                                              Pentosidine concentrations in serum and lens proteins we
37 ases in tissue fluorescence, absorbance, and pentosidine content (P < 0.001 for each comparison) by a
38 active free amine content, molecular weight, pentosidine content, and N-epsilon-carboxymethyl lysine
39 rformance liquid chromatography to determine pentosidine content.
40 (NS) whereas collagen glycation (P < 0.001), pentosidine cross-links (P < 0.001), and collagen fluore
41                                      Whereas pentosidine cross-links were significantly elevated in c
42 cert with Nepsilon-(carboxymethyl)lysine and pentosidine during glycoxidation of collagen in vitro, a
43 n levels of hemoglobin AGE, or tail collagen pentosidine, fluorescence, and thermal breaking time.
44 etween the accumulation of d-Asp and that of pentosidine for three normal collagenous tissues further
45 our findings, we propose a novel pathway for pentosidine formation on native proteins from glycated p
46 for a tissue-specific glycemic threshold for pentosidine formation, i.e., glycoxidation, in the lens.
47  of early glycation products are involved in pentosidine formation.
48 ere confirmed by lectin binding, and by anti-pentosidine immunoreactivity, an indicator of oxidative
49 tion products carboxymethyl-lysine (CML) and pentosidine, improved functional recovery, and increased
50   Incubation with the glycated gels produced pentosidine in a mixture of N-alpha-acetylarginine + N-a
51 r supports the idea that the accumulation of pentosidine in a particular tissue can, along with the r
52 ohistochemical evaluation showed evidence of pentosidine in Bruch's membrane, choroidal extracellular
53 anced glycation end products (AGEs) (namely, pentosidine in tail collagen and aorta, and Hb-AGE), ami
54  products Nepsilon-(carboxymethyl)lysine and pentosidine increase in skin collagen with age and at an
55 tional studies showing that its oxidation to pentosidine is both pH and oxygen dependent and is subst
56 hly acidic conditions typically employed for pentosidine isolation.
57                                              Pentosidine levels analyzed by HPLC also increased in a
58 hs, and both guanidines 1) normalized aortic pentosidine levels and renal collagenase-soluble collage
59 te levels of HbA1 (i.e., 8.0 +/- 0.4%), lens pentosidine levels were normal in this group and were el
60 reased glycated hemoglobin levels and aortic pentosidine levels.
61 /L-Asp ratios showed a good correlation with pentosidine levels.
62 tingly, previous reports have suggested that pentosidine may derive from pentosinane.
63 yl)lysine, N(epsilon)-(carboxyethyl)-lysine, pentosidine, N(d)-(5-hydro-5-methyl-4-imidazolon-2-yl)-o
64 nd that diabetic lens proteins produced more pentosidine on BLP than did aged lens proteins.
65 ns Maillard product 1 (LM-1) (P < 0.001) and pentosidine (P < 0.005) increased significantly with poo
66 ly NC-I and NC-II induced a 50% reduction in pentosidine (P = NS for NC-I; P = 0.035 for NC-II).
67  (3 or 5%) to pork stimulates glycoxidation (pentosidine, PEN), glycation (Maillard reaction products
68  N(epsilon)-(carboxymethyl)-lysine (CML) and pentosidine (PENT).
69 e that reached approximately 0.17 millimoles pentosidine per mole hydroxyproline in late life (r = 0.
70                          Immunoreactivity to pentosidine, pyrraline, and heme oxygenase-1 was seen in
71 0) showed a linear age-dependent increase in pentosidine that reached approximately 0.17 millimoles p
72                                              Pentosidine was also formed in BLP when incubated with w
73                We found urinary excretion of pentosidine was increased ca. twofold in patients with M
74 ents on PD and HD revealed that > 95% of the pentosidine was linked to proteins > 10,000 mol wt; < 1%
75 n-containing gel was incubated with BLP, and pentosidine was measured in the incubation mixtures.
76 ation products carboxymethyllysine (CML) and pentosidine were determined by GC/MS and HPLC, respectiv
77            Mean levels of the AGEs, CML, and pentosidine were markedly elevated in WS and WIS fractio
78 , Nepsilon-(1-carboxyethyl)lysine (CEL), and pentosidine were measured in plasma.
79 l)lysine, Nepsilon-(carboxyethyl)lysine, and pentosidine were measured with liquid chromatography.