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1 as been identified as the candidate gene for dystrophic epidermolysis bullosa.
2 angiomas and bone marrow transplantation for dystrophic epidermolysis bullosa.
3 from the skin of two patients with recessive dystrophic epidermolysis bullosa.
4 res leads to the chronic blistering disease, dystrophic epidermolysis bullosa.
5 1, give rise to the blistering skin disease, dystrophic epidermolysis bullosa.
6 fore allelic with other variants of dominant dystrophic epidermolysis bullosa.
7 s syndrome is a clinical variant of dominant dystrophic epidermolysis bullosa.
8 VII collagen gene (COL7A1) in patients with dystrophic epidermolysis bullosa.
9 evated in tumours of patients with Recessive Dystrophic Epidermolysis Bullosa, a disease characterize
10 found in the skin of children with recessive dystrophic epidermolysis bullosa after allogeneic bone m
11 reening of COL7A1 mutations in patients with dystrophic epidermolysis bullosa and compared them with
13 n the overwhelming majority of patients with dystrophic epidermolysis bullosa, and most of them in th
15 CFB in invasive cSCCs (n = 71) and recessive dystrophic epidermolysis bullosa-associated cSCCs (n = 1
16 utations in cells of patients with recessive dystrophic epidermolysis bullosa can be corrected by hom
17 anchoring fibrils in patients with recessive dystrophic epidermolysis bullosa can be morphologically
18 tein replacement or cell-based therapies for dystrophic epidermolysis bullosa caused by genetic defic
19 ominant (DDEB) and recessive (RDEB) forms of dystrophic epidermolysis bullosa (DEB) and have subseque
26 tations in gene COL7A1 encoding for C7 cause dystrophic epidermolysis bullosa (DEB), a genetic mechan
30 with either systemic sclerosis or recessive dystrophic epidermolysis bullosa has led to the common f
31 obullous disease Hallopeau-Siemens recessive dystrophic epidermolysis bullosa (HS-RDEB) results from
33 n deficiency in generalised severe recessive dystrophic epidermolysis bullosa, in which blood and mar
38 defects (n = 3) or with autosomal recessive dystrophic epidermolysis bullosa (n = 4) were included a
39 ns in genomic DNA predicted severe recessive dystrophic epidermolysis bullosa or junctional epidermol
41 that the high caries experience in recessive dystrophic epidermolysis bullosa patients is probably re
42 of the three techniques we have screened 93 dystrophic epidermolysis bullosa patients yielding an ov
46 f keratinocytes from patients with recessive dystrophic epidermolysis bullosa (RDEB) and normal derma
47 he genetic skin blistering disease recessive dystrophic epidermolysis bullosa (RDEB) develop aggressi
60 s demonstrated in vivo utilizing a recessive dystrophic epidermolysis bullosa (RDEB) knockout mouse m
61 data suggest that individuals with recessive dystrophic epidermolysis bullosa (RDEB) only develop squ
62 man skin fragility disorder coined recessive dystrophic epidermolysis bullosa (RDEB) that is associat
63 trix, we explored their utility in recessive dystrophic epidermolysis bullosa (RDEB), a blistering di
64 Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering sk
65 observations of severe generalized recessive dystrophic epidermolysis bullosa (RDEB), a currently inc
67 eatment is currently available for recessive dystrophic epidermolysis bullosa (RDEB), a severe herita
68 ch as the blistering skin disorder recessive dystrophic epidermolysis bullosa (RDEB), caused by mutat
73 enetic analyses have revealed that recessive dystrophic epidermolysis bullosa results from mutations
74 n, M2798K, that is associated with recessive dystrophic epidermolysis bullosa, was unable to form ant
75 utions previously disclosed in patients with dystrophic epidermolysis bullosa, we studied how these a
77 we treated seven children who had recessive dystrophic epidermolysis bullosa with immunomyeloablativ
78 tations in 13 patients with severe recessive dystrophic epidermolysis bullosa yielding a detection se
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