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1 sess changes in survival with treatments for Hutchinson-Gilford progeria syndrome.
2 ugs is now being tested for the treatment of Hutchinson-Gilford progeria syndrome.
3 luding Emery-Dreifuss muscular dystrophy and Hutchinson-Gilford progeria syndrome.
4 min A (LA) cause the premature aging disease Hutchinson-Gilford Progeria Syndrome.
5 ade in the most dramatic of these disorders, Hutchinson-Gilford progeria syndrome.
6 cular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome.
7 cular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome.
8 rexpressed in fibroblasts from patients with Hutchinson-Gilford progeria syndrome, a form of accelera
9 e absence of primary neurological disease in Hutchinson-Gilford progeria syndrome, a genetic disease
10 teoporosis, which are phenotypes shared with Hutchinson-Gilford progeria syndrome, a human disease ca
11 the biology of premature aging uncovered in Hutchinson-Gilford progeria syndrome and other accelerat
12 with vascular smooth muscle cell loss (e.g., Hutchinson-Gilford progeria syndrome) and experimental s
13 hologies, including some forms of cancer and Hutchinson-Gilford Progeria Syndrome, and often include
14 n wrinkling, and osteoporosis, patients with Hutchinson-Gilford progeria syndrome are affected by acc
15 the brain could explain why mouse models of Hutchinson-Gilford progeria syndrome are free of central
16 cell line for the accelerated aging disease Hutchinson-Gilford progeria syndrome caused by mutant la
19 hy diseases, restrictive dermopathy (RD) and Hutchinson Gilford progeria syndrome (HGPS), are charact
20 utosomal dominant premature ageing disorder--Hutchinson Gilford Progeria Syndrome (HGPS)-lead to redu
21 ure aging syndromes in humans, including the Hutchinson-Gilford Progeria Syndrome (HGPS) and Atypical
23 characterized DNA RT program alterations in Hutchinson-Gilford progeria syndrome (HGPS) and Rothmund
24 cytoplasmic Ran distribution is disrupted in Hutchinson-Gilford Progeria syndrome (HGPS) fibroblasts
55 Ran are reduced in cells from patients with Hutchinson-Gilford progeria syndrome (HGPS), a disease c
56 colon, and acute myeloid leukemia as well as Hutchinson-Gilford progeria syndrome (HGPS), a genetic d
58 is a mutant form of lamin A responsible for Hutchinson-Gilford progeria syndrome (HGPS), a premature
61 both accelerated in patients suffering from Hutchinson-Gilford progeria syndrome (HGPS), a rare gene
62 ffort to develop experimental treatments for Hutchinson-Gilford progeria syndrome (HGPS), an endeavor
63 s redundancy suggests that diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that are ca
64 w, we highlight these recent developments in Hutchinson-Gilford progeria syndrome (HGPS), Werner synd
71 arly half of the world's known patients with Hutchinson-Gilford progeria syndrome, in a comprehensive
72 s, we determined that progerin expression in Hutchinson-Gilford progeria syndrome inhibits the nucleo
81 rom two laminopathic mouse models, including Hutchinson-Gilford progeria syndrome (Lmna(L530P/L530P))
82 s that LMNA, a gene targeted for mutation in Hutchinson Gilford Progeria Syndrome, may control the on
85 y explains why "prelamin A diseases" such as Hutchinson-Gilford progeria syndrome spare the central n
86 responsible for the premature aging disease Hutchinson-Gilford progeria syndrome (termed progerin) a
87 rogerin (a toxic form of prelamin A found in Hutchinson-Gilford progeria syndrome), the levels of pro
89 responsible for the premature aging disorder Hutchinson-Gilford progeria syndrome, with its partners
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