ライフサイエンスコーパス: epidermal hyperplasia

1 become dysregulated, resulting in sustained epidermal hyperplasia.

2 canoylphorbol-13-acetate (TPA), resulting in epidermal hyperplasia.

3 e epidermal morphology in an animal model of epidermal hyperplasia.

4 aced by hyperproliferative cells, leading to epidermal hyperplasia.

5 is sufficient to cause skin inflammation and epidermal hyperplasia.

6 N19 is an important mediator of regenerative epidermal hyperplasia.

7 nhibitor of NF-kappaB to intact skin induced epidermal hyperplasia.

8 d WEHV2 are the causative agents of discrete epidermal hyperplasia.

9 s in aged epidermis is sufficient to produce epidermal hyperplasia.

10 of HPV-16 E7 correlated with the severity of epidermal hyperplasia.

11 aring at 5 d, preceded by the development of epidermal hyperplasia.

12 resolve existing lesions in immune-mediated epidermal hyperplasia.

13 - mice, developed cutaneous inflammation and epidermal hyperplasia.

14 on, and these mice demonstrated only minimal epidermal hyperplasia.

15 of CDK4(D158N), but not of CDK2, resulted in epidermal hyperplasia.

16 h dermal angiogenesis and the development of epidermal hyperplasia.

17 led that CD34KO skin developed and sustained epidermal hyperplasia.

18 is, given the recent implication of IL-20 in epidermal hyperplasia.

19 n and selective autophagy in IL-17A-mediated epidermal hyperplasia.

20 ific antibodies strongly reduces tRA-induced epidermal hyperplasia.

21 sed proliferation of basal keratinocytes and epidermal hyperplasia.

22 o significantly inhibited the development of epidermal hyperplasia.

23 Severe epidermal hyperplasia, acanthosis, orthokeratosis, and h

24 at wa-1 mice exhibited only modest sustained epidermal hyperplasia after multiple treatments with TPA

25 After TPA treatment, all genotypes developed epidermal hyperplasia, although the labeling index was l

26 ated inflammatory response, characterized by epidermal hyperplasia and an acute dermal inflammatory c

27 domain of E7 are necessary for induction of epidermal hyperplasia and carcinogenesis in mouse skin a

28 t E6 induced cellular hyperproliferation and epidermal hyperplasia and caused skin tumors in adult mi

29 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperplasia and cell proliferation.

30 As the mice age, however, they display epidermal hyperplasia and chronic inflammation, typified

31 UV-induced epidermal hyperplasia and cutaneous angiogenesis were hi

32 This results in reversal of the epidermal hyperplasia and cutaneous inflammation charact

33 of C/EBPbeta-deficient mice revealed a mild epidermal hyperplasia and decreased expression of K1 and

34 eletion of the Notch1 gene results in marked epidermal hyperplasia and deregulated expression of mult

35 e production, inflammatory cell recruitment, epidermal hyperplasia and dermal fibrosis.

36 e induction of cell proliferation leading to epidermal hyperplasia and dermal sarcoma.

37 in/peptidase inhibitor 3), and modulation of epidermal hyperplasia and differentiation measures.

38 i-67, and cytokine expression, together with epidermal hyperplasia and diffuse inflammation, similar

39 ponses, including infiltrates of leukocytes, epidermal hyperplasia and epidermal necrosis.

40 resence of HPV-16 E7 is sufficient to induce epidermal hyperplasia and epithelial tumors in transgeni

41 of a cyclin D1 transgene with E2F1 augments epidermal hyperplasia and further disrupts hair follicle

42 The chronic epidermal hyperplasia and hyperkeratosis seen in these m

43 C transgenic mice also exhibited significant epidermal hyperplasia and hyperkeratosis, and developed

44 14.src(530) transgenic mice developed severe epidermal hyperplasia and hyperkeratosis, and did not su

45 amination of the skin from these mice showed epidermal hyperplasia and hyperkeratosis, marked thicken

46 skin of Ctsl(nkt)/Ctsl(nkt) mice showed mild epidermal hyperplasia and hyperkeratosis, severe hyperpl

47 all, or homeotic)-like (Drosophila)] develop epidermal hyperplasia and impaired epidermal stratificat

48 ransgenic mice, including the development of epidermal hyperplasia and increased malignant progressio

49 the keratin 5 promoter (K5CDK4 mice) develop epidermal hyperplasia and increased susceptibility to sq

50 inflammatory skin disease, characterized by epidermal hyperplasia and infiltration of leukocytes int

51 is cascade, if sustained, signals downstream epidermal hyperplasia and inflammation.

52 , it mediates keratinocyte proliferation and epidermal hyperplasia and is thought to play a central r

53 ching, induces an IL-22 response that drives epidermal hyperplasia and keratinocyte proliferation in

54 regulate features of the disease, including epidermal hyperplasia and neutrophil infiltrating respon

55 aft associated with pathological findings of epidermal hyperplasia and neutrophil infiltration.

56 acetate)-induced keratinocyte proliferation, epidermal hyperplasia and onset of papillomas compared w

57 Fgfr2+/Y394C mice exhibited epidermal hyperplasia and premature closure of cranial s

58 -kappaB and MAP kinase signalling and caused epidermal hyperplasia and psoriatic skin inflammation.

59 " of ultraviolet-B also produced significant epidermal hyperplasia and resulted in complete loss of h

60 AG is effective in prevention of UVR-induced epidermal hyperplasia and SCC.

61 reveal their increased susceptibility toward epidermal hyperplasia and skin tumor formation.

62 In these mice, E5 induced epidermal hyperplasia and spontaneous skin tumors.

63 novel DLX3-dependent network that constrains epidermal hyperplasia and squamous tumorigenesis.

64 Steroids (particularly clobetasol) restored epidermal hyperplasia and terminal differentiation versu

65 of rhino mice with PADMA 28 failed to induce epidermal hyperplasia and was completely non-irritating.

66 noting how defective skin barrier function, epidermal hyperplasia, and abnormal immune responses fav

67 -20 and IL-22, including neonatal lethality, epidermal hyperplasia, and abnormality in keratinocyte d

68 y changes (swelling, leukocyte infiltration, epidermal hyperplasia, and accumulation of proinflammato

69 eased in the context of ErbB-driven reactive epidermal hyperplasia, and decreased in the context of h

70 asis, including robust scratching, extensive epidermal hyperplasia, and dramatic changes in gene expr

71 antly inhibited: (a) TPA-induced skin edema, epidermal hyperplasia, and proliferating cell nuclear an

72 role of EGFR activation in retinoid-induced epidermal hyperplasia, and suggest that EGFR inhibitors

73 In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T

74 tis, septic shock, intestinal neoplasia, and epidermal hyperplasia, as well as in cellular signaling

75 ng in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis.

76 KGF signaling pathway might account for the epidermal hyperplasia associated with psoriasis.

77 due to AFC treatment was seen in TPA-induced epidermal hyperplasia at 24 hours.

78 ions are not required for the development of epidermal hyperplasia but contribute to the striking mye

79 wed weak CXCR4 expression in areas of severe epidermal hyperplasia, but strong CXCR4 expression in no

80 ed induction of basal cell proliferation and epidermal hyperplasia by all-trans RA (tRA).

81 ing (p < 0.001, all p values versus saline), epidermal hyperplasia by histology (p < 0.001) and confo

82 tion of EGFR activation by genistein reduces epidermal hyperplasia caused by topical retinoid treatme

83 inhibitors, all-trans retinoic acid induced epidermal hyperplasia comparable to that induced in inta

84 UVR-induced epidermal hyperplasia could also be detected and quantif

85 However, the marked epidermal hyperplasia, cutaneous inflammation, and incre

86 aviolet-B irradiation of the skin results in epidermal hyperplasia, degradation of extracellular matr

87 n, whereas GPx4 loss in the epidermis caused epidermal hyperplasia, dermal inflammatory infiltrate, d

88 ice appeared normal, without any evidence of epidermal hyperplasia, despite the fact that Cav-1 null

89 ment of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and

90 -22, but not IL-17A, mediates psoriasis-like epidermal hyperplasia following recombinant murine (rm)I

91 optotic cell death, and delayed the onset of epidermal hyperplasia following UV irradiation.

92 PD-1KO mice showed severe epidermal hyperplasia, greater neutrophilic infiltration

93 Epidermal hyperplasia, hair follicle cysts, and odontoma

94 the basal layer of the epidermis resulted in epidermal hyperplasia, hyperkeratosis, and an increased

95 .cre/PTEN(flx/flx) keratinocytes resulted in epidermal hyperplasia/hyperkeratosis and novel 12-O-tetr

96 Similarly, wound-associated epidermal hyperplasia/hyperkeratosis, a hallmark of adul

97 tly delayed skin inflammation and associated epidermal hyperplasia/hyperkeratosis.

98 inase-4 (CDK4) in mouse epidermis results in epidermal hyperplasia, hypertrophy and severe dermal fib

99 ed human psoriasis and were characterized by epidermal hyperplasia, impaired epidermal differentiatio

100 vators resulted in a substantial decrease in epidermal hyperplasia in both the subacute and chronic m

101 ent of tumors, DMBA-treatment induced severe epidermal hyperplasia in Cav-1 null mice.

102 hese data indicate (i) that retinoid-induced epidermal hyperplasia in human skin proceeds through c-e

103 we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r(-/-)Rag1(-/-)- and Tcrdel

104 IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders.

105 sal skin tissues demonstrated a reduction in epidermal hyperplasia in mice treated with the antagonis

106 ced ERK hyperactivation in keratinocytes and epidermal hyperplasia in mouse skin.

107 logical analysis demonstrated that E7 causes epidermal hyperplasia in multiple transgenic lineages wi

108 s a strong correlation between inhibition of epidermal hyperplasia in organ culture and inhibition of

109 growth factor inhibited retinoid-stimulated epidermal hyperplasia in organ culture and reduced proli

110 onal epidermis might account in part for the epidermal hyperplasia in psoriasis.

111 gical inhibition of Ras-MAPK pathway impeded epidermal hyperplasia in Pten animals.

112 ermal neutrophilic inflammation and a strong epidermal hyperplasia in response to application of 12-O

113 r permeability; and neither angiogenesis nor epidermal hyperplasia in response to repeated tape strip

114 Genetic ablation of Egfr similarly delayed epidermal hyperplasia in response to UV exposure.

115 menting cell proliferation, and accelerating epidermal hyperplasia in response to UV.

116 The epidermal hyperplasia in the caspase 8 null skin is the

117 or IL-17A completely inhibited IL-23-induced epidermal hyperplasia in WT mice.

118 forms of AR and HB-EGF proteins, and induces epidermal hyperplasia, in human skin organ culture.

119 Ichthyosis samples showed increased epidermal hyperplasia (increased thickness and keratin 1

120 lasia, whereas involved skin exhibits robust epidermal hyperplasia, increased angiogenesis and leukoc

121 llar membrane structures, but they displayed epidermal hyperplasia, inflammation, and decreased (>50%

122 Ultraviolet radiation of mouse skin leads to epidermal hyperplasia, inflammation, and subsequent tumo

123 orchestrates a broad gene program promoting epidermal hyperplasia, inflammation, and the malignant p

124 Shh-induced epidermal hyperplasia is accompanied by continued cell p

125 C and western blotting revealed reduction in epidermal hyperplasia (Ki67) and in the dermal infiltrat

126 is is a severe skin disease characterized by epidermal hyperplasia, neutrophil-rich abscesses within

127 epresent a mechanism that contributes to the epidermal hyperplasia observed in patients with atopic d

128 to parental HK1 lines and exhibited neonatal epidermal hyperplasia or wound-associated hyperplasia in

129 istologic abnormalities of the skin or hair, epidermal hyperplasia, or developmental abnormalities of

130 Histologic examination revealed epidermal hyperplasia overlying infected dermis four day

131 genic mice exhibited a significantly reduced epidermal hyperplasia, oxidative skin damage, and photoc

132 < 0.001, versus IL-23-injected WT mice) and epidermal hyperplasia (p < 0.001 by histology and p < 0.

133 elatively little ear swelling (p < 0.09) and epidermal hyperplasia (p < 0.51 by histology and p < 0.7

134 -p53-/-, respectively) retained the neonatal epidermal hyperplasia phenotype, in adults, spontaneous

135 Interestingly, induction of epidermal hyperplasia prevented the appearance of senesc

136 Avicins inhibited epidermal hyperplasia, reduced p53 mutation, enhanced ap

137 Here we show that Fatp4 mutants exhibit epidermal hyperplasia resulting from an increased number

138 a chronic inflammatory skin disease in which epidermal hyperplasia results from skin infiltration by

139 activation of Erbb2 also resulted in milder epidermal hyperplasia, S-phase accumulation, and decreas

140 ld population and is mainly characterized by epidermal hyperplasia, scaling, and erythema.

141 ospho-ERK1/2 levels were up-regulated during epidermal hyperplasia, suggesting a possible mechanism f

142 PA for 11 weeks showed a similar increase in epidermal hyperplasia, suggesting that osteopontin does

143 The ability of oxysterols to reverse epidermal hyperplasia suggests that these agents could b

144 VEGF production, prominent angiogenesis, and epidermal hyperplasia, these results could provide a pot

145 l skin children showed comparable or greater epidermal hyperplasia (thickness and keratin 16) and cel

146 d whether the presence of HA is required for epidermal hyperplasia to occur in response to barrier in

147 ociated with WEH, designated here as walleye epidermal hyperplasia virus type 1 and type 2 (WEHV1 and

148 alignments of Gag-Pro-Pol from WDSV, walleye epidermal hyperplasia virus type 1, and walleye epiderma

149 dermal hyperplasia virus type 1, and walleye epidermal hyperplasia virus type 2 showed the P2 glutami

150 Walleye epidermal hyperplasia virus types 1 and 2 (WEHV1 and WEH

151 In each case, epidermal hyperplasia was accompanied by an increase in

152 Epidermal hyperplasia was documented by 48 h and reached

153 Marked epidermal hyperplasia was observed at TG wound edges, an

154 IL-23-dependent epidermal hyperplasia was observed in IL-19-/- and IL-24

155 barrier function developed, and emergence of epidermal hyperplasia was prevented; however, cytokine g

156 n imiquimod-induced model of immune-mediated epidermal hyperplasia, we found that mice lacking GRHL3

157 est whether HA may have a functional role in epidermal hyperplasia, we used Streptomyces hyaluronidas

158 Walleye dermal sarcoma (WDS) and walleye epidermal hyperplasia (WEH) are skin diseases of walleye

159 Walleye discrete epidermal hyperplasia (WEH) is a hyperproliferative skin

160 ss, myofibroblast content, angiogenesis, and epidermal hyperplasia were markedly reduced following ir

161 Both the abnormalities and the epidermal hyperplasia were reversed by co-applications o

162 vated S100A8/A9 expression (p < 0.05) but no epidermal hyperplasia, whereas involved skin exhibits ro

163 However, retinoids also induce epidermal hyperplasia, which can lead to excessive scali

164 as associated with quantitative reduction in epidermal hyperplasia, which correlated with quantitativ

165 beads induced hair follicle development and epidermal hyperplasia, while similar TGF-beta1 treatment

166 in eyelid opening, wavy fur, hair loss, and epidermal hyperplasia with increased levels of mammalian

167 trunk and extremities showing a distinctive epidermal hyperplasia with virus-laden keratinocytes con