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1 r are candidate genes in the pathogenesis of alopecia areata.
2 lium, are similar to those observed in human alopecia areata.
3 n our understanding of the genetic basis for alopecia areata.
4 rthritis, juvenile idiopathic arthritis, and alopecia areata.
5 irst-line agent for limited patchy childhood alopecia areata.
6 a novel high-incidence model for spontaneous alopecia areata.
7 ivilege as a key step in the pathogenesis of alopecia areata.
8 a contributing factor in the development of alopecia areata.
9 elogen effluvium, androgenetic alopecia, and alopecia areata.
10 gous genes potentially associated with human alopecia areata.
11 gs regarding the use of these treatments for alopecia areata.
12 C57BL/6J mice do not develop alopecia areata.
13 supporting this locus as being important in alopecia areata.
14 eles of the IL-1RN and various phenotypes of alopecia areata.
15 er of skin grafts from mice with spontaneous alopecia areata.
16 ral chronic inflammatory diseases, including alopecia areata.
17 ma, 0.03% for decubitus ulcer, and 0.01% for alopecia areata.
18 areata, whereas 39 of 44 controls developed alopecia areata.
19 ndrogenetic alopecia (37.3 128.4, 46.1]) and alopecia areata (24.9 [17.2, 32.6]) were statistically s
23 t has long been appreciated that episodes of alopecia areata (AA) have occurred after severely stress
24 Alopecia universalis is an uncommon form of alopecia areata (AA) involving hair loss over the entire
44 nic stimulus, but only lymph node cells from alopecia areata affected mice displayed an increased res
45 is results, lymph node and spleen cells from alopecia areata affected mice injected into normal haire
46 ion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodie
48 a is a cell-mediated autoimmune disease, but alopecia areata affected skin graft hosts may resist alo
50 cia areata, only two of 22 receiving further alopecia areata affected skin grafts developed alopecia
51 utpatients clinic, 2 to 16 years of age with alopecia areata affecting at least 10% of scalp surface
54 ese therapeutic techniques for patients with alopecia areata and further refine which subtypes of the
55 heumatic disease, thyroid disease, vitiligo, alopecia areata and inflammatory bowel disease) were sel
58 acne," "vitiligo," "seborrheic dermatitis," "alopecia areata," and "lichen planus." Diverse study pop
59 e relatives of 110 patients and 45 controls: alopecia areata, ankylosing spondylitis, dermatomyositis
61 ation was observed between IL-1RN and patchy alopecia areata but it was not statistically significant
62 ed C3H/HeJ mouse skin to littermates induces alopecia areata, but high dietary soy oil reduces alopec
64 lated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-med
65 eczema, psoriasis, acne vulgaris, pruritus, alopecia areata, decubitus ulcer, urticaria, scabies, fu
66 onse towards the graft, it is suggested that alopecia areata develops as a consequence of an inapprop
71 characterize a new high-incidence model for alopecia areata in C57BL/6J mice, the first to our knowl
73 a(+)NKG2D(+) T effector memory cells mediate alopecia areata in part through Janus kinase (JAK) signa
86 ating question regarding the pathogenesis of alopecia areata is the potential linkage with the brain.
87 hrough Janus kinase (JAK) signaling and that alopecia areata might be treated with JAK inhibitors.
88 um (n = 30), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/un
90 In considering all patients with any form of alopecia areata, no association was found with IL-1RN.
92 a affected skin grafts but failed to develop alopecia areata, only two of 22 receiving further alopec
94 areata affected skin graft hosts may resist alopecia areata onset through active counter-regulatory
95 ainly to the contribution from mild cases of alopecia areata [OR 1.48 (0.96, 2.29)], suggesting that
97 an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting ant
104 1RN*2 allele was found to be associated with alopecia areata severity in a British case-control study
105 purported resistance locus) did not develop alopecia areata, supporting this locus as being importan
107 h telogen effluvium (50.1 [33.9, 66.33]) and alopecia areata totalis/universalis (52.3 [23.1, 81.5])
110 the case of dermatological diseases such as alopecia areata, vitiligo, psoriasis and atopic dermatit
111 o investigate the role of the IL-1 system in alopecia areata we examined three biallelic polymorphism
112 rticaria, pruritus, scabies, cellulitis, and alopecia areata were underrepresented in CDSR when match
114 opecia areata affected skin grafts developed alopecia areata, whereas 39 of 44 controls developed alo
115 is characterized by loss of hair in patches (alopecia areata) with progression in some individuals to
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