ライフサイエンスコーパス: epithelialization

1 amniotic membrane grafting to facilitate re-epithelialization.

2 atinocyte migration is critical for wound re-epithelialization.

3 and require debridement and AMT for rapid re-epithelialization.

4 mal fibroblasts are recruited only during re-epithelialization.

5 ta-catenin, allowing them to progress toward epithelialization.

6 antiseptic therapy significantly accelerated epithelialization.

7 local inflammatory response and promoting re-epithelialization.

8 esses, including cell migration and wound re-epithelialization.

9 irs keratinocyte migration and skin wound re-epithelialization.

10 xposure to estrogen markedly delays wound re-epithelialization.

11 sed macrophage recruitment and delayed wound epithelialization.

12 GA on activation of the GR and inhibition of epithelialization.

13 quired to compete a particular step of wound epithelialization.

14 isional wounds enhanced the rate of wound re-epithelialization.

15 uggested a function during the process of re-epithelialization.

16 ssing improves wound macrophage function and epithelialization.

17 sure, reduced contraction and accelerated re-epithelialization.

18 strated that beta-AR agonists delay wound re-epithelialization.

19 eas before (original) and after (regrown) re-epithelialization.

20 nd ultimately accelerate human skin wound re-epithelialization.

21 y leukocyte emigration appears to promote re-epithelialization.

22 satrienoic acid, had no impact on corneal re-epithelialization.

23 h neutralizing VEGFR-1 antibodies delayed re-epithelialization.

24 delineate the functions of CaSR in wound re-epithelialization.

25 Ephrin signaling in the regulation of somite epithelialization.

26 nd dramatically impairs cell motility and re-epithelialization.

27 outcome measure was time to complete corneal epithelialization.

28 e potential of mouse keratinocytes for wound epithelialization.

29 sPCM accelerated wound re-epithelialization.

30 d expression of paraxis implicated in somite epithelialization.

31 shed to near undetectable levels after wound epithelialization.

32 ed that they supported multi-layered surface epithelialization.

33 sion of MMP9 also contributes to impaired re-epithelialization.

34 ances keratinocyte migration and promotes re-epithelialization.

35 nduced AD-like lesions, there was delayed re-epithelialization.

36 to the control group at the time of complete epithelialization.

37 otes wound edge IGF1R phosphorylation and re-epithelialization.

38 SMA and TGF beta, neovascularization and re-epithelialization.

39 ts of genes and molecules affecting wound re-epithelialization.

40 th AT-RvD3, which also promoted cutaneous re-epithelialization.

41 icient mice completely restores bronchial re-epithelialization.

42 leading to increased proliferation during re-epithelialization.

43 ing extracellular matrix proteins to promote epithelialization.

44 tic penetrating keratoplasty; and time to re-epithelialization.

45 or NPD1 (1 microg) increased the rate of re-epithelialization (65-90%, n = 6-10, p < 0.03) and atten

46 e were examined by IF at times up to full re-epithelialization (96 hours).

47 Post epithelialization adjuvant topical chemotherapy was give

48 licular fibroblasts would accelerate skin re-epithelialization after injury faster than interfollicul

49 n vivo, TIMP-1 deficiency enhanced airway re-epithelialization after naphthalene injury.

50 ient for paraxis, a gene required for somite epithelialization, also display defects in the axial ske

51 ncreased keratinocyte migration and hence re-epithelialization, although the mechanisms responsible f

52 , and eplerenone) rescues GC-induced delayed epithelialization and accelerates wound closure in diabe

53 Of note, topical mevastatin stimulated epithelialization and angiogenesis in vivo Mevastatin al

54 Epithelialization and Best Corrected Snellen Visual Acui

55 MP signaling, whereas N-cadherin inhibits de-epithelialization and BMP signaling.

56 nhancing tensile stiffness and/or increasing epithelialization and collagen deposition, as well as by

57 is and provide a framework for understanding epithelialization and complex tissue formation.

58 hanced wound closure, vascularization and re-epithelialization and confirmed that DRP1 has a vital ro

59 stroma both express Wnt4, where it regulates epithelialization and controls smooth muscle fate, respe

60 port the child's clinical progress, tracheal epithelialization and costs over the 4 years.

61 lular matrix signalling, these cells undergo epithelialization and create an apical surface in contac

62 demonstrate a beta2-AR-mediated delay in re-epithelialization and decrease in wound-induced epiderma

63 i-adhesive properties and is felt to promote epithelialization and decrease inflammation, neovascular

64 that abrogation of this response impairs re-epithelialization and efficient wound closure.

65 an AM lumican to cultured medium promoted re-epithelialization and enhanced cell proliferation of wil

66 Re-epithelialization and epithelial cell division were both

67 These alterations in epithelialization and fusion apparently lead to a loss o

68 e pluripotent state is required for epiblast epithelialization and generation of the pro-amniotic cav

69 , in vivo overexpression of miR-21 inhibited epithelialization and granulation tissue formation in a

70 influencing multiple processes including re-epithelialization and granulation tissue matrix depositi

71 nd closure resulted primarily from faster re-epithelialization and increased formation of granulation

72 ound closure was associated with improved re-epithelialization and increased neovascularization; and

73 ion (decreased pain and inflammation with re-epithelialization and infiltrate resolution) of 46.9 +/-

74 of these cells resulted in delayed wound re-epithelialization and kinetics of wound closure.

75 naling system for wound repair, promoting re-epithelialization and modulating the maturation of the s

76 mental gastric ulcer healing and promoted re-epithelialization and muscle restoration.

77 t mice exhibited a defect in both corneal re-epithelialization and neutrophil recruitment that correl

78 s corneal ulcers by promoting faster corneal epithelialization and overall better recovery of the VA.

79 l disturbances converge to result in delayed epithelialization and persistent inflammation.

80 accelerated wound closure, with improved re-epithelialization and reductions in inflammation and fib

81 l wound-healing is characterized by rapid re-epithelialization and remodeling, with minimal scar form

82 oth muscle cells, which are essential for re-epithelialization and restoration of muscular structures

83 to repair corneal defects that drive proper epithelialization and stromal remodeling of the wounded

84 wound-healing interventions that enhance re-epithelialization and the formation of granulation tissu

85 ysically attaches to the duct during de novo epithelialization and tubulogenesis.

86 vity to the pharynx and anterior epidermis ("Epithelialization"), and (3) a concomitant movement of t

87 a cadherin 6B and BMP signaling-mediated de-epithelialization, and a subsequent delamination through

88 ith inflammatory responses, wound healing re-epithelialization, and altered differentiation.

89 feration, keratinocyte proliferation with re-epithelialization, and angiogenesis compared with dermal

90 ealing by stimulating cell proliferation, re-epithelialization, and angiogenesis in a diabetic mice e

91 g wound closure by stimulating angiogenesis, epithelialization, and collagen deposition.

92 g diagnoses, previous treatments, days to re-epithelialization, and complications for subsequent anal

93 ual acuity, infiltrate/scar size, time to re-epithelialization, and corneal perforation.

94 ng kinetics, including wound contraction, re-epithelialization, and microscopic metrics such as cell

95 limbus of abraded corneas contributes to re-epithelialization, and P-selectin provides a necessary s

96 cts of exogenous IGF-1 on cell migration, re-epithelialization, and proliferation-essential component

97 tion showed decreased wound widths, enhanced epithelialization, and reduced numbers of neutrophils an

98 treatment, durability of the neosquamous re-epithelialization, and safety of the procedure were dete

99 nic skin wounds are characterized by poor re-epithelialization, angiogenesis and granulation.

100 Surprisingly, wound re-epithelialization, angiogenesis, and collagen synthesis

101 exhibited lower skin AGE deposits, increased epithelialization, angiogenesis, inflammation, granulati

102 ling characterized by impaired or delayed re-epithelialization are a serious medical problem.

103 we reveal that IGF-1-mediated effects on re-epithelialization are directly mediated by IGF-1R.

104 Impaired cell adhesion and epithelialization are indicated by decreased E-cadherin

105 h HoxD3-treated wounds also show improved re-epithelialization as compared to control db/db wounds, t

106 hat papc is an important regulator of somite epithelialization associated with segmentation.

107 onocyte infiltration, neovascularization and epithelialization at days 3, 5, 7, and 10 postwounding.

108 ocytes undergo many changes that engender an epithelialization behavior.

109 ded microbiologic cure at 6 days, rate of re-epithelialization, best-corrected visual acuity and infi

110 ogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammati

111 obilization is a critical aspect of wound re-epithelialization, but the mechanisms that control its p

112 h factors and chemokines to promote wound re-epithelialization by increasing migration of skin cells

113 at TIMP-1 overexpression restricts airway re-epithelialization by inhibiting matrilysin activity, con

114 xia component of ischemia may limit wound re-epithelialization by stabilizing HIF-1alpha, which induc

115 s, activated parietal cells mediated tuft re-epithelialization by two distinct mechanisms.

116 data suggest that differing propensities for epithelialization can sort cell types into distinct comp

117 Mean time to complete (>/=95%) epithelialization (CE) for patients that did and did not

118 l redistribution of beta-catenin, aspects of epithelialization characteristic of cells at somite boun

119 ects of the wound healing cascade, including epithelialization, collagen deposition, and cell migrati

120 does not significantly alter the rate of re-epithelialization, collagen deposition, or tensile stren

121 ed epidermal cellular migration and wound re-epithelialization compared with vehicle-treated STZ-diab

122 ntegrins show enhanced wound healing with re-epithelialization complete several days earlier than in

123 Inhibition of Wnt signalling after re-epithelialization completely abrogates this wounding-ind

124 Wound healing consists of re-epithelialization, contraction and formation of granulat

125 D1-deficient mice exhibited delayed wound re-epithelialization correlated with a reduced proliferatio

126 delay in wound healing with insufficient re-epithelialization, decreased inflammatory reaction, and

127 ound healing as a consequence of complete re-epithelialization, diminished inflammation, and enhanced

128 beta1 is crucial for efficient and proper re-epithelialization during cutaneous wound healing.

129 fish, neural progenitors undergo progressive epithelialization during neurulation, and thus provide a

130 Cell migration is an integral part of re-epithelialization during skin wound healing, a complex p

131 in regulating keratinocyte migration and re-epithelialization during wound healing.

132 Keratinocyte migration is a key aspect of re-epithelialization during wound healing.

133 ates cell migration and proliferation and re-epithelialization during wound healing.

134 OR 2AT4 is involved in human keratinocyte re-epithelialization during wound-healing processes.

135 healing by rapid wound closure, improved re-epithelialization, enhanced extracellular matrix remodel

136 ectionally into the wound bed to initiate re-epithelialization, essential for wound repair and restor

137 nd are thereby inhibited from undergoing the epithelialization event that culminates in the formation

138 f tarsal conjunctiva trauma with lamellar de-epithelialization, followed by re-epithelialization to f

139 epithelial T cells (DETCs), which promote re-epithelialization following injury.

140 nts, or DETCs are silenced in young skin, re-epithelialization following wounding is perturbed.

141 d prohealing functions by promoting wound re-epithelialization, formulation of granulation tissue, an

142 , redox response, inflammation, epidermis re-epithelialization, granulation formation, and proper wou

143 Healing was induced by rapid re-epithelialization, granulation tissue formation, and acc

144 animals, they coacted to accelerate wound re-epithelialization, granulation tissue formation, and syn

145 These studies show that re-epithelialization, granulation tissue formation, includi

146 er MIC was associated with slower time to re-epithelialization (hazards ratio, 0.92; 95% CI, .86-.97;

147 ng that beta-AR antagonists promote wound re-epithelialization in a "chronic" human skin wound-healin

148 skin explant culture system to better assess epithelialization in a wound-like environment.

149 hich blocks FPP formation, not only promotes epithelialization in acute wounds but also reverses the

150 Both miR-21 and miR-130a delayed epithelialization in an acute human skin wound model.

151 pithelialization in pig burn wounds (100% re-epithelialization in antagonist-treated wounds vs. appro

152 The significant impairment in corneal re-epithelialization in AQP3-deficient mice results from di

153 nist-treated wounds vs. approximately 70% re-epithelialization in control wounds on postburn day 26)

154 inflammation and significantly increased re-epithelialization in corneal wounds.

155 ation in human skin wounds and a delay in re-epithelialization in murine tail-clip wounds.

156 keratinocyte cell line and enhances wound re-epithelialization in ob/ob mice.

157 anted into rabbit corneas to determine their epithelialization in organ culture.

158 a synthetic TGF-b antagonist accelerates re-epithelialization in pig burn wounds (100% re-epithelial

159 les of hair follicle regeneration and for re-epithelialization in response to wounding.

160 brane (AM) transplantation facilitates rapid epithelialization in severe neurotrophic corneal ulcers.

161 2.20 weeks (p = 0.01) and achieved complete epithelialization in significantly more patients (72.7%

162 spreading of the ectoderm and persistent de-epithelialization in the endoderm also arise during loca

163 LIMK1 induces de-epithelialization in the neural tube and dominant negati

164 cytes to stimulate cell proliferation and re-epithelialization in the skin, whereas IL-27 leads to su

165 and ZGA inhibited keratinocyte migration and epithelialization in vitro and ex vivo.

166 dition, a deficiency of TNF-alpha delayed re-epithelialization in vivo and this correlated with reduc

167 iation, which recapitulates the hallmarks of epithelialization in vivo in a synchronized rather than

168 Time to corneal re-epithelialization in vivo was significantly delayed in A

169 tes in vitro, we found no effect on wound re-epithelialization in vivo.

170 cial part in the pathogenesis of retarded re-epithelialization in wound.

171 way mediates non-canonical BMPRII induced de-epithelialization, in response to either cadherin-6B or

172 a subset of the transcripts associated with epithelialization, including Pax8, cyclin D1 (Ccnd1) and

173 e VEGF-treated wounds demonstrated increased epithelialization, increased matrix deposition, and enha

174 ytes from the adjacent epidermis and make re-epithelialization independent of keratinocyte proliferat

175 lation deficient mutated cofilin inhibits de-epithelialization induced by cadherin-6B as well as LIMK

176 Furthermore, de-epithelialization induced by cadherin-6B was found to be

177 ube and dominant negative LIMK1 decreases de-epithelialization induced by either cadherin-6B or BMP.

178 Impaired re-epithelialization is a hallmark of these wounds, which i

179 Rescue of epithelialization is accompanied by restoration of kerat

180 ogenous "wound current" upon injury until re-epithelialization is complete.

181 cytes late in the regenerative phase when re-epithelialization is completed and matrix maturation ens

182 ompatible with metazoans, but the absence of epithelialization is consistent only with a stem-metazoa

183 ed; bone histolysis does not occur, wound re-epithelialization is inhibited and the blastema does not

184 We now find that de-epithelialization is mediated by non-canonical BMP signa

185 kewed immune response directed at bladder re-epithelialization is observed, with limited capacity to

186 asticity of keratinocytes (KCs) during wound epithelialization is one of the major goals in epithelia

187 l role of keratinocyte alpha9beta1 during re-epithelialization is unknown and analysis has been precl

188 xpression is up-regulated following vascular epithelialization, is required to prevent the disassembl

189 These nonautonomous aspects of epithelialization may involve interplay of EphA4 with ot

190 On re-epithelialization, MCT3 was detected in chick and hfRPE

191 e A (PKA), through PKA-2, in a specific post-epithelialization morphogenetic step (conversion of the

192 ectionally into the wound bed to initiate re-epithelialization, necessary for wound closure and resto

193 associated with increased proliferation, re-epithelialization, neovascularization, and blood flow.

194 Re-epithelialization, neutrophil influx, and platelet accum

195 Re-epithelialization occurred in 17 of 20 eyes.

196 Re-epithelialization of 5- to 6-mm-wide rabbit corneal epit

197 ced flap with CT graft resulting from the de-epithelialization of a free gingival graft.

198 K) migration plays a critical role in the re-epithelialization of acute skin wounds.

199 epithelial repair and is required for the re-epithelialization of airway wounds by facilitating cell

200 the expression of MCT3 after wounding and re-epithelialization of chick RPE explant and human fetal (

201 MCT expression after scratch wounding and re-epithelialization of chick RPE/choroid explant cultures

202 a signaling would be predicted to enhance re-epithelialization of cutaneous wounds and reduce scarrin

203 Re-epithelialization of cutaneous wounds in adult mammals t

204 ocytes in intact skin and is required for re-epithelialization of human skin wounds.

205 e motility plays an important role in the re-epithelialization of human skin wounds.

206 yte migration in vitro and accelerates wound epithelialization of human wounds ex vivo.

207 igated the effect of Smad2 overexpression on epithelialization of incision wounds.

208 We previously showed that epithelialization of incisional wounds is accelerated in

209 e that L. rhamnosus GG lysate accelerates re-epithelialization of keratinocyte scratch assays, potent

210 Deficits in the epithelialization of mesenchymal cells were evidenced by

211 er cells in the brain by facilitating the re-epithelialization of metastatic breast cancer cells and

212 that PAM induced senescence and impaired re-epithelialization of oral mucosa.

213 Re-epithelialization of partial- or full-thickness skin wou

214 Cadherin 6B selectively induces the de-epithelialization of PMNCCs, which is mediated by stimul

215 segmentation by altering the CDH2-dependent epithelialization of PSM cells.

216 s neovascularization, resulting in faster re-epithelialization of skin wounds in diabetic mice.

217 estigated the role of keratin IFs during the epithelialization of skin wounds using a keratin 6alpha

218 progenitor epithelial cells contribute to re-epithelialization of the airway and re-establishment of

219 erely affected embryos have abnormalities in epithelialization of the blastoderm, resulting in loss o

220 rovided evidence that cadherin-6B induces de-epithelialization of the neural crest prior to delaminat

221 implantation, graft dissolution at 3 weeks, epithelialization of the ocular surface and symblepharon

222 Epithelialization of the ocular surface without primary

223 nd 4 weeks after surgery for the complete re-epithelialization of the palatal wound (CWE), the altera

224 for maximal cell aspect ratio and thus full epithelialization of the posterior somite.

225 ads to loss of Six2 expression and premature epithelialization of the progenitors.

226 led wounds while simultaneously promoting re-epithelialization of the remaining provisional wound.

227 e mean best-corrected visual acuity after re-epithelialization of the shield ulcer was 20/30, 20/30,

228 Somite morphogenesis involves the epithelialization of the somite border cells around a co

229 AlloSLET helps in faster epithelialization of the surface, thus reducing the need

230 mmation and by enhancing angiogenesis and re-epithelialization of the wound, thereby reversing the pa

231 it was not sufficient to induce appropriate epithelialization of these cells.

232 Re-epithelialization of treated monolayers was compared to

233 unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3(-/-) and gal3(+

234 Exogenous galectin-3 accelerated re-epithelialization of wounds in gal3(+/+) mice but, surpr

235 cles (HFs) are able to contribute to this re-epithelialization of wounds in vivo.

236 uggest a potential mechanism for enhanced re-epithelialization of wounds under low oxygen tensions.

237 ifferent models of corneal wound healing, re-epithelialization of wounds was significantly slower in

238 The extent of acceleration of re-epithelialization of wounds with both galectin-3 and gal

239 te-binding proteins galectins-3 and -7 in re-epithelialization of wounds.

240 medical therapy does not accelerate corneal epithelialization or affect final visual acuity in sever

241 chieved earlier wound closure (P <0.001) and epithelialization (P <0.05; P = 0.03) at 7 and 14 days a

242 hicle and P=0.14 vs. cyclosporine A) but not epithelialization (P>0.2 vs. vehicle).

243 after injury (28 +/- 5% versus 79 +/- 14% re-epithelialization, P < 0.005).

244 ed by a masked investigator for lesion size, epithelialization, pain, infection, inflammation, and sc

245 Epithelialization, pain, infection, inflammation, and sc

246 Re-epithelialization, patterns of neutrophil influx and CXC

247 rotubule defects are associated with altered epithelialization/polarity in renal cells and with prone

248 ture, null keratinocytes exhibit an enhanced epithelialization potential due to increased migration.

249 uccessfully detect increases or decreases in epithelialization potential, and can be useful in the ch

250 the dermal compartment to synchronize the re-epithelialization process.

251 c time-points for markers of interest in the epithelialization process.

252 The re-epithelialization rate was similar among treatment group

253 Open wound and epithelialization rates and angiogenesis significantly i

254 trate/scar size, corneal perforation, and re-epithelialization rates stratified by culture positivity

255 macrophage depletion resulted in delayed re-epithelialization, reduced collagen deposition, impaired

256 In addition, re-epithelialization requires long-range epithelial rearran

257 Collective processes such as wound re-epithelialization result from the integration of individ

258 y contribute to inflammation, histolysis, re-epithelialization, revascularization and cell proliferat

259 These findings suggest that the de-epithelialization step of the neural crest EMT by cadher

260 keratinocyte migration, proliferation or re-epithelialization, suggesting that the effect of berylli

261 inning, ulceration, and delayed conjunctival epithelialization; there is some evidence of increasing

262 h calcimimetic NPS-R568 accelerated wound re-epithelialization through enhancing the epidermal Ca(2+)

263 was to determine whether TIMP-1 inhibits re-epithelialization through matrilysin.

264 First, COL7A1 was required for re-epithelialization through organization of laminin-332 at

265 were sacrificed at day 3 before making a re-epithelialization time analysis with fluorescein stainin

266 Re-epithelialization time and best-corrected visual acuity.

267 main outcome measures: Re-epithelialization time and best-corrected visual acuity.

268 amellar de-epithelialization, followed by re-epithelialization to form an epithelialized tunnel as a

269 esponse to manual debridement wounds when re-epithelialization took more than 24 hours.

270 tubule induction and differentiation (i.e., epithelialization, tubular organization and elongation a

271 oRNAs may be implicated in limiting wound re-epithelialization under hypoxia, a major component of is

272 evidence revealed that DAMPs also trigger re-epithelialization upon kidney injury and contribute to e

273 tatin accelerates wound closure by promoting epithelialization via multiple mechanisms: modulation of

274 The mean time to complete epithelialization was 56.7 +/- 14.9, 22.0 +/- 10.2, and

275 Wound re-epithelialization was also significantly faster in betaa

276 QP3-facilitated cell migration to corneal re-epithelialization was assessed using an organ culture mo

277 UB cell epithelialization was augmented in the presence of MM ce

278 By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wou

279 Re-epithelialization was delayed with a deficient delineati

280 al of the corneal epithelium by scraping, re-epithelialization was followed by fluorescein staining.

281 In the grade 2 group, re-epithelialization was seen in 36 (88%) eyes that receive

282 In the grade 1 group, re-epithelialization was seen in 67 (94%) eyes.

283 In the grade 3 group, re-epithelialization was seen in only 1 (1.7%) eye that rec

284 Re-epithelialization was significantly delayed in mice with

285 Mean time to epithelialization was similar, and there was no signific

286 rimary endpoint, time to complete burn wound epithelialization, was determined by independent, blinde

287 f marapsin, which closely correlated with re-epithelialization, was virtually absent in a genetic mou

288 To address mechanisms of impaired re-epithelialization we examined MMP9 expression in vivo in

289 nt the most promising targets to engineer re-epithelialization, we examined collective and individual

290 e wound and a concomitant acceleration of re-epithelialization were identified as the underlying mech

291 Therefore, targeting re-epithelialization, which mainly involves keratinocytes,

292 onolayer scratch assay was used to assess re-epithelialization; which comprises keratinocyte prolifer

293 r wound closure, keratinocyte AR promoted re-epithelialization, while fibroblast AR suppressed it.

294 soft tissue wound opening and more rapid re-epithelialization with MaR1 delivery versus vehicle on s

295 from Smad7 tg mice exhibited accelerated re-epithelialization, with increased activation of extracel

296 uteri significantly increased the rate of re-epithelialization, with L. rhamnosus GG being the most e

297 ice displayed significantly delayed wound re-epithelialization, with the greatest delay at day 3 afte

298 of cryopreserved AM had significantly faster epithelialization within 3.56 +/- 1.78 weeks vs 5.87 +/-

299 Complete epithelialization without wound dehiscence was noted in

300 lization, proliferation, human skin wound re-epithelialization, wound-induced ERK phosphorylation, an