ライフサイエンスコーパス: acanthosis

1 in these mice and correlated with attenuated acanthosis.

2 uces IL-22-dependent dermal inflammation and acanthosis.

3 opment of pustules and a partial decrease in acanthosis.

4 ficant reductions in CD4(+) cell numbers and acanthosis.

5 +, and CD45RO+ cells at 24 h, accompanied by acanthosis.

6 urine epidermis developed hyperkeratosis and acanthosis 4 d after an adenoviral vector containing a h

7 We report epidermis acanthosis and a preferential occlusion of the precapill

8 owth factor-beta, demonstrate less epidermal acanthosis and dermal inflammation than wild-type (WT) S

9 Furthermore, IL-22 mediates IL-23-induced acanthosis and dermal inflammation through the activatio

10 KO mice showed significantly less epidermal acanthosis and dermal influx of mast cells, macrophages,

11 o, the addition of IL-1beta and OSM promoted acanthosis and destructuring of reconstructed epidermis.

12 gous for a truncated keratin 10 gene exhibit acanthosis and hyperkeratosis as seen in the human disea

13 ate controls, marked epidermal papillomatous acanthosis and hyperkeratosis in the skin, with a notabl

14 Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail ep

15 rophil infiltration, it did not protect from acanthosis and hyperkeratosis, demonstrating that neutro

16 y of the histologic features of HLP, such as acanthosis and hyperproliferation.

17 associated with enhanced reactive epidermal acanthosis and inflammatory KC hyperproliferation in the

18 m dendritic cell and T-cell infiltration and acanthosis and introduce targeting nerve-immunocyte/KC i

19 parchment-like scales and histologically by acanthosis and marked hyperkeratosis.

20 s at 1 week of age with underlying epidermal acanthosis and orthohyperkeratosis as well as a CD4+ T-c

21 ed a thickened ventral epidermis with marked acanthosis and papillomatosis, hyperplastic sebaceous gl

22 (CGRP) signaling reversed the improvement in acanthosis and prevented denervated-mediated decreases i

23 inhibits their hyperproliferation, decreases acanthosis and reduces the disease severity in psoriasis

24 istological analysis showed marked epidermal acanthosis and spongiosis, neovascularization, and eleva

25 y scale, parakeratosis, elongated rete pegs, acanthosis, and dermal angiogenic reaction.

26 epithelium typified by mild hyperkeratosis, acanthosis, and elongation and isolated anastamoses of r

27 ivo led to epidermal microabscess formation, acanthosis, and increased IL-1alpha and chemokine expres

28 epidermal neutrophils, reduced keratinocyte acanthosis, and less dermal edema.

29 uation of the epidermal granular layer, mild acanthosis, and orthokeratotic hyperkeratosis.

30 ased by 40% followed by a 30% improvement in acanthosis at 7 days and a 30% decrease in CD4(+) T-cell

31 otic hyperkeratosis, with papillomatosis and acanthosis being mild or absent.

32 ked hyperkeratosis with focal parakeratosis, acanthosis, dermal and epidermal lymphocytic and neutrop

33 sional human skin models was associated with acanthosis, disorganized epidermal architecture, and dow

34 ed by basal keratinocyte hyperproliferation, acanthosis, hyperkeratosis, intraepidermal neutrophil mi

35 The skin phenotype is characterized by acanthosis, hyperkeratosis, the presence of a mixed infl

36 biopsy specimen showed a slight psoriasiform acanthosis in association with spongiosis and infiltrati

37 ta and OSM synergistically induced epidermal acanthosis in mice.

38 The underlying cause of the epidermal acanthosis in psoriasis is still largely unknown.

39 trophil recruiting chemokine expression, and acanthosis in psoriasis-like skin inflammation induced b

40 d that IL-19, IL-20, IL-22, and IL-24 induce acanthosis in reconstituted human epidermis (RHE) in a d

41 arks of human psoriasis, including extensive acanthosis, increases in dermal CD4(+) T cells, infiltra

42 ly produced by T(H)17 cells and mediates the acanthosis induced by IL-23.

43 aracterized by hyperplasia of the epidermis (acanthosis), infiltration of leukocytes into both the de

44 Epidermal hyperproliferation resulting in acanthosis is an important clinical observation in patie

45 of 268] vs 40.4% [19 of 47], P = .004), and acanthosis nigricans (AN) (36.9% [89 of 241] vs 20.0% [9

46 achondroplasia with developmental delay and acanthosis nigricans (SADDAN), are associated with gluta

47 our individuals developed extensive areas of acanthosis nigricans beginning in early childhood, suffe

48 Crouzon syndrome with acanthosis nigricans is a distinct disorder caused by a

49 gies for BSS and related conditions, such as acanthosis nigricans or craniosynostosis.

50 ofacial malformations, Crouzon syndrome with acanthosis nigricans results in characteristic cutaneous

51 n developmental syndromes achondroplasia and acanthosis nigricans with Crouzon Syndrome.

52 achondroplasia with developmental delay and acanthosis nigricans" (SADDAN) because it differs signif

53 achondroplasia with developmental delay and acanthosis nigricans) syndrome and thanatophoric dysplas

54 In Crouzon syndrome patients with acanthosis nigricans, a recurrent mutation occurs in the

55 R2 Y394C mutation evidenced by cutis gyrata, acanthosis nigricans, and craniosynostosis and provides

56 ory diseases (such as atopic dermatitis), in acanthosis nigricans, as an extension of epidermal nevus

57 r 3 (FGFR3), linked to Crouzon syndrome with acanthosis nigricans, as well as to bladder cancer.

58 paraneoplastic syndromes such as xanthomas, acanthosis nigricans, carcinoid syndrome, unusual erythe

59 the furrowed skin disorder of cutis gyrata, acanthosis nigricans, craniosynostosis, craniofacial dys

60 Patients develop hyperinsulinemia, acanthosis nigricans, hypertriglyceridemia, diabetes mel

61 Features occasionally observed include acanthosis nigricans, hypogonadism, hypothyroidism, alop

62 and accompanied by other features, including acanthosis nigricans, organomegaly, hyperandrogenism, an

63 35, those of Hispanic ethnicity, those with acanthosis nigricans, those who had tried and failed die

64 All patients have widespread, early-onset acanthosis nigricans.

65 the mild phenotype in Crouzon syndrome with Acanthosis Nigricans.

66 the genetic cause for Crouzon syndrome with Acanthosis Nigricans.

67 facial features, and atypical and extensive acanthosis nigricans.

68 1Glu mutant, linked to Crouzon syndrome with acanthosis nigricans.

69 istance, diabetes mellitus, dyslipidemia and acanthosis nigricans.

70 kine expression, leukocyte infiltration, and acanthosis of mouse skin.

71 tosis of the forestomach, hyperkeratosis and acanthosis of the epidermis, and hypotrichosis associate

72 that received IFN-gamma+/+ T cells, although acanthosis of the skin was attenuated.

73 s developed hyperplasia, hyperkeratosis, and acanthosis of the skin with additional abnormalities in

74 Severe epidermal hyperplasia, acanthosis, orthokeratosis, and hyperkeratosis were only

75 Histopathology included hyperplasia, acanthosis, papillomatosis, increased cell size, and ost

76 1c(+) and CD4(+) cells, but had no effect on acanthosis; restoration of calcitonin gene-related pepti

77 inflammatory diseases with marked epidermal acanthosis, such as psoriasis.

78 evented the development of disease, reducing acanthosis (thickening of the skin), inflammatory infilt

79 ibited significant hyperplasia of epidermis (acanthosis), thickening of the cornified layer (hyperker

80 Scale formation and acanthosis were aggravated, in correlation with increase