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1 2) as a new profibrotic mediator in lung and skin fibrosis.
2 ell death, in 2 murine models of scleroderma skin fibrosis.
3 romote collagen accumulation and features of skin fibrosis.
4 hat fresolimumab rapidly reverses markers of skin fibrosis.
5 atosclerosis, a condition of excessive human skin fibrosis.
6 stroesophageal reflux, renal impairment, and skin fibrosis.
7 m SSc patients correlates with the extent of skin fibrosis.
8 17 signaling has been implicated in lung and skin fibrosis.
9 a significant reduction in fibrocytes and in skin fibrosis.
10 ibrocytes in the generation of IL-13-induced skin fibrosis.
11 s adenosine and adenosine A(2A) receptors to skin fibrosis.
12 that SFRP4 may modulate Wnt functions in Tsk skin fibrosis.
13 human disorder characterized by progressive skin fibrosis.
14 tient age, and correlates with the extent of skin fibrosis.
15 umulation of collagen and the development of skin fibrosis.
16 ify common and specific features of lung and skin fibrosis.
17 fficacy in rodent models of lung, liver, and skin fibrosis.
19 lerosis is a complex disease with widespread skin fibrosis and variable visceral organ involvement.
20 ) spontaneously developed severe dermatitis, skin fibrosis, and systemic T helper type 2 immunity, su
21 onstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 i
22 Skin wound healing and bleomycin-induced skin fibrosis are thought to reflect complex interaction
25 ate aberrant adiponectin pathway activity in skin fibrosis, identifying a novel function for this ple
26 ents, and the effects of anti-TGF-beta Ab on skin fibrosis, immune cell activation markers, and colla
28 These data indicate that the progression of skin fibrosis in IL-13-induced AD occurs via TSLP/TSLPR-
32 have suggested that Wnts might contribute to skin fibrosis in systemic sclerosis (SSc) by affecting t
35 issue disorders such as Marfan's syndrome or skin fibrosis in the tight skin mouse model of scleroder
37 It also suggests that MAGP-2 might mediate skin fibrosis in TSK mice and in patients with scleroder
39 l disruption of TLR4 signaling in vitro, and skin fibrosis induced by bleomycin in vivo was attenuate
41 1 as a key determinant in the development of skin fibrosis induced by bleomycin, and suggest that MCP
42 mad3-null (Smad3(-/-)) mice using a model of skin fibrosis induced by subcutaneous injections of bleo
43 ight-skin (Tsk) mouse, an animal model where skin fibrosis is caused by an in-frame duplication in fi
45 These findings were also confirmed using a skin fibrosis model in which multiple injections of fibr
46 emonstrated to induce impressive reversal of skin fibrosis, neoangiogenesis, improved functionality a
48 findings provide insight into the effects of skin fibrosis on DWAT ADSCs, identify a DC-ADSC survival
49 Skin fibrosis in the TSK mouse, a model of skin fibrosis seen in systemic sclerosis (SSc), is cause
50 tions in fibrillin-1 recapitulate aggressive skin fibrosis that is prevented by integrin-modulating t
53 ies have suggested that fibrillin 1 mediates skin fibrosis via its interface with associated microfib
54 foothold in the pathogenesis of pathological skin fibrosis, we studied stiff skin syndrome (SSS), a r
55 /-) mice were resistant to bleomycin-induced skin fibrosis, which suggests a key role for the inflamm
56 sorder leading to childhood onset of diffuse skin fibrosis with autosomal dominant inheritance and co
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