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1 B-12 function (vitamin B-12 <200 pmol/L and methylmalonic acid >0.27 micromol/L) in the total group
3 tus [ie, plasma vitamin B-12 < 148 pmol/L or methylmalonic acid (MMA) > 210 nmol/L] with respect to a
4 racteristics of metabolic biomarkers such as methylmalonic acid (MMA) and holotranscobalamin II, whos
5 exists at which the relation between plasma methylmalonic acid (MMA) and SB-12 changes slope to diff
6 al, cognitive, routine diagnostic, and serum methylmalonic acid (MMA) and total homocysteine (tHcy) t
7 olate, serum vitamin B-12, homocysteine, and methylmalonic acid (MMA) concentrations in US children b
12 anscobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA) were measured before and after
13 B(12) status, total homocysteine (tHcy) and methylmalonic acid (MMA), among adult participants in ph
14 min B-12, holotranscobalamin (holoTC), tHcy, methylmalonic acid (MMA), and folate with the use of lin
15 amin B-12, plasma total homocysteine (tHcy), methylmalonic acid (MMA), and holotranscobalamin into on
16 However, diagnostic algorithms using Cbl, methylmalonic acid (MMA), and homocysteine (HCys) measur
17 tus used in past NHANES--serum vitamin B-12, methylmalonic acid (MMA), and total homocysteine (tHcy)-
18 parison of baseline serum cobalamin, folate, methylmalonic acid (MMA), total homocysteine (tHcy), and
23 the use of vitamin B-12 than with the use of methylmalonic acid (MMA; 3-26% and 2-6%, respectively).
24 vels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homoc
25 in the brain was evident from the increased methylmalonic acid (P<0.01-0.04), homocysteine (P<0.01),
26 th higher concentrations of homocysteine and methylmalonic acid and higher odds ratios for cognitive
28 the C-H and C-N modulated CSA experiments on methylmalonic acid and N-tBoc-glycine, respectively.
29 e highest concentrations of homocysteine and methylmalonic acid and the lowest concentration of holot
30 eficiency who received treatment (15 of 21), methylmalonic acid and total homocysteine levels decreas
31 sorders characterized by the accumulation of methylmalonic acid and/or homocysteine in blood and urin
33 ry results were significantly raised urinary methylmalonic acid compared with age-matched controls (p
34 n B-12 concentration < 148 pmol/L or a serum methylmalonic acid concentration > 210 nmol/L-the maximu
35 n B-12 concentration <148 pmol/L or a plasma methylmalonic acid concentration > or =210 nmol/L, the p
36 re, each 2-fold increment in homocysteine or methylmalonic acid concentration was associated with a d
44 ither vitamin B-12 or folate deficiency, and methylmalonic acid for detection of vitamin B-12 deficie
46 depression, had a significantly higher serum methylmalonic acid level and a nonsignificantly lower se
47 2 level less than 221 pmol/L and an elevated methylmalonic acid level; 2) a serum vitamin B12 level l
48 The higher serum cobalamin and lower serum methylmalonic acid levels at 4 months posttreatment in t
49 alization of elevated total homocysteine and methylmalonic acid levels may prevent the development of
51 ene of Pseudomonas aeruginosa, which encodes methylmalonic acid semialdehyde dehydrogenase (MSDH) and
54 f folate, cobalamin, total homocysteine, and methylmalonic acid with cognitive performance at 2 occas
55 elderly population as documented by elevated methylmalonic acid with or without elevated total homocy
56 The use of serum vitamin B-12 and plasma methylmalonic acid would provide continuity with past NH
57 lasma total vitamin B-12, 3 studies measured methylmalonic acid, and 6 studies measured total homocys
58 rum and red blood cell folate, vitamin B-12, methylmalonic acid, and homocysteine concentrations amon
59 ean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively,
60 the amount of B12 bound to TCII (holoTCII), methylmalonic acid, and homocysteine, in 128 healthy old
61 elevation of the metabolites, homocysteine, methylmalonic acid, and the ligand, transcobalamin II, i
62 serum concentrations of total vitamin B-12, methylmalonic acid, and total homocysteine are all effec
65 n status (defined by low cobalamin, elevated methylmalonic acid, and/or elevated homocysteine concent
67 using markers such as holotranscobalamin and methylmalonic acid, it has been found that cognition is
68 ne, kynurenine, leucine, lysine, methionine, methylmalonic acid, ornithine, phenylalanine, proline, s
69 , show failure to thrive, and show increased methylmalonic acid, propionylcarnitine, odd chain fatty
70 rum vitamin B-12, total homocysteine (tHcy), methylmalonic acid, serum folic acid, and 5-methyltetrah
71 ion test and measurement of homocysteine and methylmalonic acid, to cobalamin status has identified t
73 as associated with elevated homocysteine and methylmalonic acid, which were reduced by folate and vit
78 born error of cobalamin metabolism, combined methylmalonic acidemia and hyperhomocysteinemia, cblC ty
79 enetic basis of an X-linked form of combined methylmalonic acidemia and hyperhomocysteinemia, designa
80 nction occur in a tissue-specific fashion in methylmalonic acidemia and suggest treatment approaches
82 parallel, the liver from a patient with mut methylmalonic acidemia was studied in a similar fashion.
83 Two adult brothers, one documented to have methylmalonic acidemia with homocystinuria, or cobalamin
84 mimicking the human diseases propionic- and methylmalonic acidemia, in which the canonical B12-depen
85 of patients suffering from the mut- form of methylmalonic acidemia, resulting from defective AdoCbl
90 compound heterozygotes for mutations in the methylmalonic aciduria and homocystinuria type C (MMACHC
91 ficient for its interaction with MMADHC (the methylmalonic aciduria and homocystinuria type C protein
94 east two biologically compelling candidates, methylmalonic aciduria cblB type (MMAB) and mevalonate k
95 he missense mutations in MMAA that result in methylmalonic aciduria have been mapped onto MeaB and, i
97 n humans, deficiencies in the mutase lead to methylmalonic aciduria, a rare disease that is fatal in
98 in the human homolog of MeaB, MMAA, lead to methylmalonic aciduria, an inborn error of metabolism th
99 ions in the human ortholog of MeaB result in methylmalonic aciduria, an inborn error of metabolism.
100 n the human homologue of MeaB, MMAA, lead to methylmalonic aciduria, an inborn error of metabolism.
101 mutation, D180X, described in a patient with methylmalonic aciduria, and characterized the associated
102 7 days of age with poor feeding, hypotonia, methylmalonic aciduria, and elevated plasma homocysteine
103 cts in the human homologue of MeaB result in methylmalonic aciduria, but the role of this protein in
113 carboxylic acids, such as oxalic, malonic, 3-methylmalonic, and cyclobutanedicarboxylic acid, was uti
114 ts for the thermal decomposition of malonic, methylmalonic, and dimethylmalonic anhydrides were measu
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