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1 tion as a means to prevent pregnancy-induced megaloblastic anemia.
2 parable with those observed in patients with megaloblastic anemia.
3 en the S-phase accumulation and apoptosis in megaloblastic anemia.
4 thesis of thymidylate in the pathogenesis of megaloblastic anemia.
5  the metabolic disorder, thiamine-responsive megaloblastic anemia.
6 es explanations for the clinical findings in megaloblastic anemia.
7 festation of nutritional folate deprivation: megaloblastic anemia.
8           Imerslund-Grasbeck syndrome (I-GS, megaloblastic anemia 1) is an autosomal recessive disord
9  of vitamin B12 (a phenotype associated with megaloblastic anemia 1, MGA1; OMIM 261100; refs.
10 f folate or vitamin B(12) (cobalamin) causes megaloblastic anemia, a disease characterized by pancyto
11 Mutations in THTR-1 cause thiamin-responsive megaloblastic anemia, a tissue-specific disease associat
12                          Thiamine-responsive megaloblastic anemia, also known as "TRMA" or "Rogers sy
13                Vitamin B12 deficiency causes megaloblastic anemia and neurologic disorder in humans.
14 r de novo dTMP biosynthesis can lead to both megaloblastic anemia and SCID in MTHFD1 deficiency.
15 TRMA) is characterized by diabetes mellitus, megaloblastic anemia and sensorineural deafness.
16 inborn error of metabolism, characterized by megaloblastic anemia and/or pancytopenia, severe cerebra
17       B12 deficiency is the leading cause of megaloblastic anemia, and although more common in the el
18 itions (SF3B1-mutant and SF3B1-wildtype MDS, megaloblastic anemia, and iron deficiency anemia), Haemo
19             The proband presented with SCID, megaloblastic anemia, and neurologic abnormalities, but
20 c disease associated with diabetes mellitus, megaloblastic anemia, and sensorineural deafness.
21 data) for risk of deficiency on the basis of megaloblastic anemia as a hematologic indicator in perso
22 ary levels of the vitamin folate can lead to megaloblastic anemia, birth defects, impaired cognitive
23 normal erythropoiesis is a common feature of megaloblastic anemias, congenital dyserythropoietic anem
24       "Cyclin D1-only" mice developed severe megaloblastic anemia, "cyclin D2-only" mice presented ne
25          A mouse model of thiamin-responsive megaloblastic anemia (diabetes mellitus, deafness, megal
26 essive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and sensorineur
27 utosomal recessive syndrome characterized by megaloblastic anemia, diabetes, and sensorineural deafne
28                          Hereditary juvenile megaloblastic anemia due to vitamin B12 (cobalamin) defi
29 paired purine nucleotide metabolism, whereas megaloblastic anemia has been associated with impaired d
30 dies of impaired DNA synthesis and repair in megaloblastic anemia have concerned mainly the decreased
31         Clinical and experimental studies of megaloblastic anemia have demonstrated an impairment of
32  while prevalent in both iron deficiency and megaloblastic anemia, hyperlobulated neutrophils are lar
33 wed not only as a nutrient needed to prevent megaloblastic anemia in pregnancy but also as a vitamin
34 sm, the degree of uracil misincorporation in megaloblastic anemia is sufficient to increase the stead
35  been appreciated for decades in relation to megaloblastic anemia, it has been recently proposed that
36 blastic anemia (diabetes mellitus, deafness, megaloblastic anemia) lacking functional Slc19a2 has bee
37 -vitamin B12 receptor, results in hereditary megaloblastic anemia (MGA1), owing to vitamin B12 malabs
38                 Although rarely resulting in megaloblastic anemia, mild deficiency may be associated
39 amage, accounting for the pathophysiology of megaloblastic anemia observed in vitamin B12 and folate
40 ral tube defects, homocysteine imbalance and megaloblastic anemia, often associated with cobalamin de
41 However, in patients with thiamin-responsive megaloblastic anemia, plasma thiamin levels are within n
42 and symptoms of vitamin B12 deficiency, e.g. megaloblastic anemia, precise evaluation and treatment i
43 Cubulin mutations cause a hereditary form of megaloblastic anemia secondary to vitamin B(12) deficien
44                           Thiamin-responsive megaloblastic anemia syndrome (TRMA) is characterized by
45       Pernicious anemia is a common cause of megaloblastic anemia throughout the world and especially
46 isincorporated into the DNA of patients with megaloblastic anemia to levels detectable by nonradioact
47 lasts from patients with thiamine-responsive megaloblastic anemia (TRMA) syndrome with diabetes and d
48 y of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness.
49  described as a cause of thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive synd
50 iency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with sp
51  parents had diabetes mellitus, deafness, or megaloblastic anemia, which raised the possibility that
52 linical vitamin B12 deficiency can result in megaloblastic anemia, which results from the inhibition
53                             They suffer from megaloblastic anemia with or without some degree of neur
54 result in negative health outcomes including megaloblastic anemia, with additional neurocognitive imp