戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 uces IL-22-dependent dermal inflammation and acanthosis.
2 opment of pustules and a partial decrease in acanthosis.
3 ficant reductions in CD4(+) cell numbers and acanthosis.
4 +, and CD45RO+ cells at 24 h, accompanied by acanthosis.
5 in these mice and correlated with attenuated acanthosis.
6  disease severity, epidermal hyperplasia and acanthosis.
7 urine epidermis developed hyperkeratosis and acanthosis 4 d after an adenoviral vector containing a h
8                          We report epidermis acanthosis and a preferential occlusion of the precapill
9 owth factor-beta, demonstrate less epidermal acanthosis and dermal inflammation than wild-type (WT) S
10    Furthermore, IL-22 mediates IL-23-induced acanthosis and dermal inflammation through the activatio
11  KO mice showed significantly less epidermal acanthosis and dermal influx of mast cells, macrophages,
12 o, the addition of IL-1beta and OSM promoted acanthosis and destructuring of reconstructed epidermis.
13                         Skin biopsy revealed acanthosis and focal lymphocytes with moderate perivascu
14 gous for a truncated keratin 10 gene exhibit acanthosis and hyperkeratosis as seen in the human disea
15 ate controls, marked epidermal papillomatous acanthosis and hyperkeratosis in the skin, with a notabl
16                        Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail ep
17 rophil infiltration, it did not protect from acanthosis and hyperkeratosis, demonstrating that neutro
18 y of the histologic features of HLP, such as acanthosis and hyperproliferation.
19  associated with enhanced reactive epidermal acanthosis and inflammatory KC hyperproliferation in the
20 m dendritic cell and T-cell infiltration and acanthosis and introduce targeting nerve-immunocyte/KC i
21  parchment-like scales and histologically by acanthosis and marked hyperkeratosis.
22 s at 1 week of age with underlying epidermal acanthosis and orthohyperkeratosis as well as a CD4+ T-c
23 ed a thickened ventral epidermis with marked acanthosis and papillomatosis, hyperplastic sebaceous gl
24 (CGRP) signaling reversed the improvement in acanthosis and prevented denervated-mediated decreases i
25 inhibits their hyperproliferation, decreases acanthosis and reduces the disease severity in psoriasis
26 istological analysis showed marked epidermal acanthosis and spongiosis, neovascularization, and eleva
27  mice alleviates imiquimod-induced psoriatic acanthosis and type 17 inflammation to the same extent a
28 y scale, parakeratosis, elongated rete pegs, acanthosis, and dermal angiogenic reaction.
29  epithelium typified by mild hyperkeratosis, acanthosis, and elongation and isolated anastamoses of r
30 ivo led to epidermal microabscess formation, acanthosis, and increased IL-1alpha and chemokine expres
31 le, hyperkeratosis, parakeratosis, epidermal acanthosis, and inflammatory infiltrates.
32  epidermal neutrophils, reduced keratinocyte acanthosis, and less dermal edema.
33 uation of the epidermal granular layer, mild acanthosis, and orthokeratotic hyperkeratosis.
34 cacy studies in mouse models of IL-23-driven acanthosis, anti-CD40-induced colitis, and spontaneous l
35 ased by 40% followed by a 30% improvement in acanthosis at 7 days and a 30% decrease in CD4(+) T-cell
36 otic hyperkeratosis, with papillomatosis and acanthosis being mild or absent.
37 ked hyperkeratosis with focal parakeratosis, acanthosis, dermal and epidermal lymphocytic and neutrop
38 sional human skin models was associated with acanthosis, disorganized epidermal architecture, and dow
39  of epithelial cells, which is indicative of acanthosis, higher collagen deposition, and angiogenesis
40 hronic skin barrier disease characterized by acanthosis, hyperkeratosis, and immune cell accumulation
41 ed by basal keratinocyte hyperproliferation, acanthosis, hyperkeratosis, intraepidermal neutrophil mi
42       The skin phenotype is characterized by acanthosis, hyperkeratosis, the presence of a mixed infl
43 ession of CARD14(E138A) rapidly induced skin acanthosis, immune cell infiltration and expression of p
44 biopsy specimen showed a slight psoriasiform acanthosis in association with spongiosis and infiltrati
45 ta and OSM synergistically induced epidermal acanthosis in mice.
46        The underlying cause of the epidermal acanthosis in psoriasis is still largely unknown.
47 trophil recruiting chemokine expression, and acanthosis in psoriasis-like skin inflammation induced b
48 d that IL-19, IL-20, IL-22, and IL-24 induce acanthosis in reconstituted human epidermis (RHE) in a d
49 arks of human psoriasis, including extensive acanthosis, increases in dermal CD4(+) T cells, infiltra
50 ly produced by T(H)17 cells and mediates the acanthosis induced by IL-23.
51 aracterized by hyperplasia of the epidermis (acanthosis), infiltration of leukocytes into both the de
52    Epidermal hyperproliferation resulting in acanthosis is an important clinical observation in patie
53 uced skin lesion model and the IL-23-induced acanthosis model.
54  of 268] vs 40.4% [19 of 47], P = .004), and acanthosis nigricans (AN) (36.9% [89 of 241] vs 20.0% [9
55                        Crouzon syndrome with acanthosis nigricans (CAN, a rare type of craniosynostos
56  achondroplasia with developmental delay and acanthosis nigricans (SADDAN), are associated with gluta
57 our individuals developed extensive areas of acanthosis nigricans beginning in early childhood, suffe
58                        Crouzon syndrome with acanthosis nigricans is a distinct disorder caused by a
59 gies for BSS and related conditions, such as acanthosis nigricans or craniosynostosis.
60 (d = -1.64 [95% CI, -2.87 to -0.41] cm), and acanthosis nigricans prevalence (d = -3.55% [95% CI, -6.
61 ofacial malformations, Crouzon syndrome with acanthosis nigricans results in characteristic cutaneous
62   The prevalence of overweight, obesity, and acanthosis nigricans was further reduced in communities,
63 n developmental syndromes achondroplasia and acanthosis nigricans with Crouzon Syndrome.
64  achondroplasia with developmental delay and acanthosis nigricans" (SADDAN) because it differs signif
65  achondroplasia with developmental delay and acanthosis nigricans) syndrome and thanatophoric dysplas
66            In Crouzon syndrome patients with acanthosis nigricans, a recurrent mutation occurs in the
67 R2 Y394C mutation evidenced by cutis gyrata, acanthosis nigricans, and craniosynostosis and provides
68 ory diseases (such as atopic dermatitis), in acanthosis nigricans, as an extension of epidermal nevus
69 r 3 (FGFR3), linked to Crouzon syndrome with acanthosis nigricans, as well as to bladder cancer.
70  paraneoplastic syndromes such as xanthomas, acanthosis nigricans, carcinoid syndrome, unusual erythe
71  the furrowed skin disorder of cutis gyrata, acanthosis nigricans, craniosynostosis, craniofacial dys
72 try; secondary outcomes were the presence of acanthosis nigricans, dietary intake derived from 2 days
73           Patients develop hyperinsulinemia, acanthosis nigricans, hypertriglyceridemia, diabetes mel
74       Features occasionally observed include acanthosis nigricans, hypogonadism, hypothyroidism, alop
75 and accompanied by other features, including acanthosis nigricans, organomegaly, hyperandrogenism, an
76  35, those of Hispanic ethnicity, those with acanthosis nigricans, those who had tried and failed die
77    All patients have widespread, early-onset acanthosis nigricans.
78  the mild phenotype in Crouzon syndrome with Acanthosis Nigricans.
79  the genetic cause for Crouzon syndrome with Acanthosis Nigricans.
80  facial features, and atypical and extensive acanthosis nigricans.
81 1Glu mutant, linked to Crouzon syndrome with acanthosis nigricans.
82 istance, diabetes mellitus, dyslipidemia and acanthosis nigricans.
83 ore, lack of running water, insulin use, and acanthosis nigricans.
84 kine expression, leukocyte infiltration, and acanthosis of mouse skin.
85 tosis of the forestomach, hyperkeratosis and acanthosis of the epidermis, and hypotrichosis associate
86 that received IFN-gamma+/+ T cells, although acanthosis of the skin was attenuated.
87 s developed hyperplasia, hyperkeratosis, and acanthosis of the skin with additional abnormalities in
88                Severe epidermal hyperplasia, acanthosis, orthokeratosis, and hyperkeratosis were only
89         Histopathology included hyperplasia, acanthosis, papillomatosis, increased cell size, and ost
90 p a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammat
91 1c(+) and CD4(+) cells, but had no effect on acanthosis; restoration of calcitonin gene-related pepti
92  inflammatory diseases with marked epidermal acanthosis, such as psoriasis.
93 evented the development of disease, reducing acanthosis (thickening of the skin), inflammatory infilt
94 ibited significant hyperplasia of epidermis (acanthosis), thickening of the cornified layer (hyperker
95                          Scale formation and acanthosis were aggravated, in correlation with increase
96  featuring hyperkeratosis, parakeratosis and acanthosis, with infiltration of lymphocytes and eosinop