ライフサイエンスコーパス: epidermal hyperplasia

1 erized by intense inflammation and prominent epidermal hyperplasia.

2 sed proliferation of basal keratinocytes and epidermal hyperplasia.

3 o significantly inhibited the development of epidermal hyperplasia.

4 become dysregulated, resulting in sustained epidermal hyperplasia.

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

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

7 aced by hyperproliferative cells, leading to epidermal hyperplasia.

8 N19 is an important mediator of regenerative epidermal hyperplasia.

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

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

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

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

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

14 bone resorption, hair follicle atrophy, and epidermal hyperplasia.

15 contributes to immune cell infiltration and epidermal hyperplasia.

16 overy of skin barrier function and decreased epidermal hyperplasia.

17 rized by abnormal inflammatory responses and epidermal hyperplasia.

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

19 is sufficient to cause skin inflammation and epidermal hyperplasia.

20 resolve existing lesions in immune-mediated epidermal hyperplasia.

21 e characterized by aberrant inflammation and epidermal hyperplasia.

22 - mice, developed cutaneous inflammation and epidermal hyperplasia.

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

24 contributes to immune cell infiltration and epidermal hyperplasia.

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

26 h dermal angiogenesis and the development of epidermal hyperplasia.

27 led that CD34KO skin developed and sustained epidermal hyperplasia.

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

29 ific antibodies strongly reduces tRA-induced epidermal hyperplasia.

30 Severe epidermal hyperplasia, acanthosis, orthokeratosis, and h

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

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

33 e model of PsO ameliorates disease severity, epidermal hyperplasia and acanthosis.

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

35 ch increased IL-22 expression contributes to epidermal hyperplasia and barrier defects.

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

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

38 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperplasia and cell proliferation.

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

40 UV-induced epidermal hyperplasia and cutaneous angiogenesis were hi

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

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

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

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

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

46 clinical features of AD, exhibiting reduced epidermal hyperplasia and dermal thickening, less skin i

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

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

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

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

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

52 ukin (IL)-17(+) gammadelta T cell expansion, epidermal hyperplasia and host resistance against S. man

53 The chronic epidermal hyperplasia and hyperkeratosis seen in these m

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

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

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

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

58 reatment significantly inhibited UVB-induced epidermal hyperplasia and hyperproliferation and reduced

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

60 ilumab established significant inhibition of epidermal hyperplasia and improvement in epidermal diffe

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

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

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

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

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

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

67 -7 in the pathogenesis of psoriasis, in both epidermal hyperplasia and keratinocyte-mediated inflamma

68 also more compromised in POAD, with greater epidermal hyperplasia and lower expression of markers re

69 logical examination displayed a reduction of epidermal hyperplasia and macrophage infiltration by the

70 duced inflammation, fibrosis, and subsequent epidermal hyperplasia and molecularly abolished TGF-beta

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

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

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

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

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

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

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

78 Basophils and IL-4 promoted epidermal hyperplasia and skin barrier dysfunction by ac

79 r, galectin-7-deficient mice showed enhanced epidermal hyperplasia and skin inflammation in response

80 eatment of Skiv2l-deficient mice ameliorated epidermal hyperplasia and skin inflammation.

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

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

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

84 Cellular markers of epidermal hyperplasia and T-cell/dendritic cell infiltra

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

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

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

88 -20 and IL-22, including neonatal lethality, epidermal hyperplasia, and abnormality in keratinocyte d

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

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

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

92 characterized by intense local inflammation, epidermal hyperplasia, and leukocyte infiltration.

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

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

95 ation of genes associated with inflammation, epidermal hyperplasia, and Th2 and Th22 immune responses

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

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

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

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

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

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

102 Mutant embryos display epidermal hyperplasia, but also apical cell extrusions,

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

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

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

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

107 RS1C2) better represented by tape-strips and epidermal hyperplasia changes (KRT16, MKI67) better dete

108 eduction in psoriasis lesions as measured by epidermal hyperplasia, characteristic gross skin lesion,

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

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

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

112 Es) and changes from baseline in biomarkers (epidermal hyperplasia/cytokines) at days 29 and 71.

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

114 sponse than wild-type mice, with exacerbated epidermal hyperplasia, dermal inflammatory cell infiltra

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

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

117 a]anthracene treatment alone but reduced the epidermal hyperplasia during 12-O-tetradecanoylphorbol-1

118 High SATB1 expression was associated with epidermal hyperplasia, eosinophil infiltration, less lar

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

120 -22, but not IL-17A, mediates psoriasis-like epidermal hyperplasia following recombinant murine (rm)I

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

122 Cluster 2 was enriched for markers of epidermal hyperplasia, glycolytic enzymes, and actin fil

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

124 Epidermal hyperplasia, hair follicle cysts, and odontoma

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

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

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

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

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

130 pin E1 inhibitor reduced MC903-induced itch, epidermal hyperplasia, immunocyte infiltration, and resu

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

132 utophagy, attenuates imiquimod (IMQ)-induced epidermal hyperplasia in adult mice as well as naturally

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

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

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

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

137 scle actin(+) fibroblasts before attenuating epidermal hyperplasia in K5.TGFbeta1 skin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 by keratinocytes and results in decreases in epidermal hyperplasia, inflammatory cytokine release, im

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

160 mmation (matrix metalloproteinase [MMP]-12), epidermal hyperplasia (keratin-16 [KRT16]), T-helper 2 (

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

162 zed HS tunnels recapitulate the psoriasiform epidermal hyperplasia morphology of the overlying epider

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

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

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

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

167 Histologic examination revealed epidermal hyperplasia overlying infected dermis four day

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

169 < 0.001, versus IL-23-injected WT mice) and epidermal hyperplasia (p < 0.001 by histology and p < 0.

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

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

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

173 cluding T(H)2 and T(H)17/T(H)22 pathways and epidermal hyperplasia/proliferation.

174 We demonstrate that IL-17A and IL-22 induce epidermal hyperplasia, promote neutrophil recruitment, a

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

176 Epidermal hyperplasia represents a morphologic hallmark

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

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

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

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

181 mmatory skin disease characterized mainly by epidermal hyperplasia, scaling, and erythema; T helper 1

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

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

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

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

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

187 e symptoms of psoriasis lesion and inhibited epidermal hyperplasia through induction of cell apoptosi

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

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

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

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

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

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

194 Epidermal hyperplasia was documented by 48 h and reached

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

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

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

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

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

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

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

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

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

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

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

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

207 inflammatory skin disorder characterized by epidermal hyperplasia, which is primarily driven by IL-1

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

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

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