ライフサイエンスコーパス: wound closure

1 accelerated, whereas HIF1alpha shRNA delayed wound closure.

2 ) and ectocervix (ECX) significantly delayed wound closure.

3 then monthly until week 20 or occurrence of wound closure.

4 n-chaperone function of Hsp90alpha in normal wound closure.

5 eta abolished the effect of PVI treatment on wound closure.

6 acute drug treatment accelerates actin-based wound closure.

7 working to promote rapid cell migration and wound closure.

8 nflammatory response, poor angiogenesis, and wound closure.

9 migration of SCC cells, leading to decreased wound closure.

10 to predict the hierarchy of factors driving wound closure.

11 le tools to identify the mechanical basis of wound closure.

12 e impairs re-epithelialization and efficient wound closure.

13 panied with persistent inflammation and slow wound closure.

14 d wound re-epithelialization and kinetics of wound closure.

15 tion, supports angiogenesis, and accelerates wound closure.

16 t correlation to the observed differences in wound closure.

17 um spp.) significantly prolonged the time to wound closure.

18 consequence, there is a significant delay in wound closure.

19 essential for wound edge actin assembly and wound closure.

20 actin accumulation around wounds and slower wound closure.

21 coordinates cellular movements and promotes wound closure.

22 osin cable, and these actin structures drive wound closure.

23 nt role for mitochondria in skin quality and wound closure.

24 expression and improved capability to induce wound closure.

25 of vimentin impairs repair cell function and wound closure.

26 a model to screen for factors implicated in wound closure.

27 g further dermal tissue growth and enhancing wound closure.

28 he eyelids and ocular annexes at the time of wound closure.

29 pha transcription factor is a key feature of wound closure.

30 laboration of vimentin-rich protrusions, and wound closure.

31 otential as exogenous contaminant at time of wound closure.

32 Abelson (Abl) contributes to rapid embryonic wound closure.

33 ce were found to have an accelerated rate of wound closure.

34 antly diminished the PMA-induced increase in wound closure.

35 applications involving neurite extension and wound closure.

36 ophage recruitment, bacterial clearance, and wound closure.

37 s well as reduced proliferation and impaired wound closure.

38 ECs and plays an important role in promoting wound closure.

39 sin cable, a structure that is essential for wound closure.

40 ell-matrix associations, cell migration, and wound closure.

41 esis, and, ultimately, tissue remodeling and wound closure.

42 enty-four of these underwent lower extremity wound closure.

43 presumably to facilitate cell migration and wound closure.

44 EGF and LXA4 increased corneal epithelial wound closure.

45 inase DAPK-1 acts as a negative regulator of wound closure.

46 esulting in increased rates of migration and wound closure.

47 esulted in a significant delay in epithelial wound closure.

48 and ensures appropriate timing of excisional wound closure.

49 ty of a microRNA-based therapy for promoting wound closure.

50 pithelization and, consequently, accelerates wound closure.

51 the wound site and significantly accelerated wound closure.

52 egative pressure wound therapy or a standard wound closure.

53 PF-573228 prevented ZINC40099027-stimulated wound closure.

54 und care and assessment for the potential of wound closure.

55 of MCs restored both bacterial clearance and wound closure.

56 e their inhibition leads to marked delays in wound closure.

57 migrate into the wound, resulting in faster wound closure.

58 was no effect on the total time required for wound closure.

59 al in the management of burn wounds is early wound closure.

60 R2, both significantly inhibited endothelial wound closure.

61 vacuum-treated honey trended towards faster wound closure.

62 l innate immune contributor to IL-10-induced wound closure.

63 s during tissue repair, resulting in delayed wound closure.

64 was required for optimal intestinal mucosal wound closure.

65 Hsp90alpha as a potential driver for normal wound closure.

66 resulted in significantly increased rates of wound closure (72.3 +/- 14.7% with XAV-939; and 52.1 +/-

67 application of InsP4 accelerate the speed of wound closure, a finding that has potential implications

68 During wound closure, a supracellular actomyosin cable at the w

69 ayers resulted in 5.8+/-0.7-fold increase in wound closure after 24 hours.

70 that the PKCbetaII-mediated increase in IEC wound closure after PMA stimulation was mediated by incr

71 GF signalling, which are only required after wound closure, allowing the epidermis outside the wound

72 f coordinated cell movement during embryonic wound closure also drive tissue development and cancer m

73 Percentage wound closure and angiogenesis at 1 week was assessed us

74 rol and hesperetin formulation also improved wound closure and angiogenesis in diabetic mice.

75 le mice exhibited delayed corneal epithelial wound closure and attenuated polymorphonuclear (PMN) leu

76 a novel therapeutic strategy for increasing wound closure and augmenting angiogenesis, which is a ce

77 al precursor to collective cell migration in wound closure and cancer metastasis, respectively.

78 EGF-induced wound closure and cell migration rates of human corneal

79 and Tolvaptan, or V2R gene silencing reduced wound closure and cell viability of 786-O and Caki-1 hum

80 row to MFG-E8(+/+) mice resulted in impaired wound closure and compromised wound vascularization.

81 s, and local application of RvD1 accelerated wound closure and decreased accumulation of apoptotic ce

82 novel therapeutic agent to improve diabetic wound closure and demonstrate the primary mechanism of i

83 closure, whereas elevation of mtROS promotes wound closure and enhances survival of mutant animals de

84 pithelization leads to significantly delayed wound closure and excessive inflammation causes tissue d

85 esis in the wound tissues results in delayed wound closure and healing.

86 ceived wild-type bone marrow showed improved wound closure and improved wound vascularization.

87 AS II promoted wound closure and increased cell proliferation, L-argini

88 nock-out (Has1/3 null) mice show accelerated wound closure and increased numbers of fibroblasts in th

89 tions in cellular phenotype including slowed wound closure and increased transepithelial resistance.

90 Here, we show that S. aureus inhibits wound closure and induces miR-15b-5p in acute human and

91 TSG-6 plays an important role in regulating wound closure and inflammation during cutaneous wound re

92 with recombinant PDGF-AA rescued the delayed wound closure and lack of myofibroblast differentiation.

93 onsistent with normal tissue does not affect wound closure and may even lead to highly favorable long

94 VAP-1 enhanced stromal cell spreading and wound closure and modulated expression of profibrotic ge

95 pture the cellular events that contribute to wound closure and morphogenesis of regenerating legs wit

96 PTCH1 knockdown attenuated wound closure and mucous expression in airway epithelial

97 In the absence of IL-10 (IL-10(-/-) mice), wound closure and organization of collagen were normaliz

98 proliferation and migration that facilitate wound closure and recovery of the intestinal epithelial

99 hCVAM) has been shown to effectively promote wound closure and reduce wound-related infections.

100 rast, at older ages, Sod2 deficiency delayed wound closure and reduced epidermal thickness, accompani

101 of YAP and TAZ markedly delayed the rate of wound closure and reduced the transforming growth factor

102 ted small interfering RNA (siRNA) to promote wound closure and regeneration.

103 ntraction (retraction) is thought to promote wound closure and secure hemostasis while preventing vas

104 y performing time-lapse imaging of planarian wound closure and sequential imaging over days of head r

105 We investigated how loss of TSG-6 affects wound closure and skin inflammation.

106 of dermal wounds with isoxazole accelerates wound closure and suppresses the inflammatory response.

107 TSG-6-null wounds rescues both the delay in wound closure and the aberrant neutrophil phenotype.

108 dictating cellular behaviors that facilitate wound closure and tissue repair.

109 FCs (p < 0.01 and p < 0.001), and defects in wound closure and tube formation were apparent in NP ECF

110 ion support tools (CDST) to decrease time to wound closure and wound failure rates.

111 2 to 4 days after the injury coincided with wound closure, and by 8 days the expression reached near

112 njured patients, early surgical excision and wound closure, and general advances in the intensive car

113 tion and activation in wounded skin, delayed wound closure, and increased proinflammatory macrophage

114 nin-driven epithelial cell proliferation and wound closure, and it interfered with ATII-to-ATI cell t

115 This was associated with a reduced growth, wound closure, and migration capacity.

116 i.e., exocytotic glutamate release, in vitro wound closure, and proliferation), whereas Ca(2+) wave p

117 rected dermal-epidermal separation, improved wound closure, and reduced blister formation.

118 ufficient to mediate accelerated dorsal skin wound closure, and the effects are lost in mice that are

119 Cell-mediated remodeling and wound closure are critical for efficient wound healing,

120 ntin protein expression, cell migration, and wound closure are prevented by a pharmacological inhibit

121 expression in cultures caused inhibition of wound closure as a result of 60% to 75% decrease in epit

122 of Hsp90alpha-Delta mutant protein promoted wound closure as effectively as the full-length wild-typ

123 olon cancer (HT29) cells was assessed with a wound-closure assay in the presence of a mitotic inhibit

124 In a wound-closure assay, GRK6(-/-) mice showed enhanced myel

125 associated with decreased cell migration in wound closure assays, and the inhibitory effect of miR-1

126 EMD and P2 significantly promoted early wound closure at day 1 (P <0.001 and P = 0.004, respecti

127 0 from no suture group (nSG) showed complete wound closure at day 14 (P >0.05) and at 30 days, comple

128 on-to-treat, was proportion of patients with wound closure at week 20.

129 earning was used to estimate both successful wound closure (based on penultimate debridement biomarke

130 icant enhancement in the rate and quality of wound closure both clinically and histologically relativ

131 sPCM not only accelerated wound closure but also improved the quality of healing b

132 age depletion during this period resulted in wound closure but permanent failure of limb regeneration

133 facilitate nursing care and delayed primary wound closure but the evidence to support its use is poo

134 SMalphaA) and normally function to assist in wound closure, but have been implicated in pathological

135 We show that COL7A1 is instrumental for skin wound closure by 2 interconnected mechanisms.

136 hat mbGR inhibits keratinocyte migration and wound closure by activating a Wnt-like phospholipase (PL

137 -1 induced epithelial cell proliferation and wound closure by activating epithelial pro-proliferative

138 h GLO1 overexpression remarkably accelerated wound closure by enhancing angiogenesis compared with di

139 to a cutaneous wound, where they accelerate wound closure by inducing myofibroblast differentiation

140 mtROS can promote wound closure by local inhibition of Rho GTPase activity

141 ve surgical debridement as well as secondary wound closure by means of skin grafting.

142 conclude that topical mevastatin accelerates wound closure by promoting epithelialization via multipl

143 nalysis, and postulate that sAXL accelerates wound closure by promoting migration and inhibiting epit

144 WED accelerated functional wound closure by restoring skin barrier function.

145 nalysis of single-cell migration and scratch-wound closure clearly demonstrated that hERG1-expressing

146 The effect of miR-125b was analyzed in wound closure, colony formation, migration, and invasion

147 howed significantly accelerated and enhanced wound closure compared with a clinically approved collag

148 enhanced neutrophil recruitment, and faster wound closure compared with GRK6(+/+) animals.

149 sisted in the wound and facilitated diabetic wound closure compared with primary DFU fibroblasts.

150 Zeb1(+/-) mice exhibited compromised wound closure complicated by defective EMT and poor woun

151 tide that in preclinical studies accelerated wound closure, decreased inflammation and granulation ti

152 Poor wound closure due to diabetes, aging, stress, obesity, a

153 at keratinocyte-produced SCF is essential to wound closure due to the increased recruitment of a uniq

154 n PLGA nanoparticles (PLGA-LL37 NP) promotes wound closure due to the sustained release of both LL37

155 OSM treatment also improved wound closure during the early inflammatory phase of hea

156 We obtained promising results from mouse wound closure experiments; no visible signs of irritatio

157 ualizing the processes involved in cutaneous wound closure, facilitating the dissection of direct fro

158 Whereas the kinetics of wound closure following acute skin injury was similar in

159 ble protein, leading to potent inhibition of wound closure following PMN-MP binding to IECs.

160 wounds were induced, and careful analysis of wound closure, granulation tissue formation, and angioge

161 ilage regeneration (H2=26%; P=0.006) and ear wound closure (H2=53%; P<0.00001) were significantly her

162 Although applying adhesive strips to a wound closure has been shown to have outcomes equivalent

163 tial advantages over sutures and staples for wound closure, hemostasis, and integration of implantabl

164 tive clinical improvement, including sternal wound closure, improved liver function, and substantial

165 ted third-degree burn wound healing by rapid wound closure, improved re-epithelialization, enhanced e

166 rimental and theoretical model for epidermal wound closure in 3D, negating the previously proposed co

167 also found to accelerate corneal epithelial wound closure in an in vivo murine model without affecti

168 netic deletion of IL-17A resulted in delayed wound closure in animals.

169 Th2 cytokines also impaired wound closure in BEC monolayers.

170 eting the fragment-5 region disrupted normal wound closure in both wild-type Hsp90alpha and Hsp90alph

171 ed delayed epithelialization and accelerates wound closure in diabetic animals by targeting epithelia

172 We validate MEDUSA by quantifying wound closure in Drosophila embryos, and we show that th

173 ecretion of a neutrophil chemokine and slows wound closure in HBE cells.

174 In addition, we observed modestly delayed wound closure in Il1r1(-/-) mice associated with higher

175 nd infection and found significantly delayed wound closure in infected skin wounds.

176 the Toll/NF-kappaB pathway is essential for wound closure in late Drosophila embryos.

177 administration of synthetic NATs accelerates wound closure in mice and stimulates repair-associated r

178 n of F-5 peptide promoted acute and diabetic wound closure in mice far more effectively than did PDGF

179 ound edges enhanced inflammation and delayed wound closure in mice.

180 sts were also functionally less effective at wound closure in nude mice.

181 nduced healing defects and restored youthful wound closure in old, sedentary mice.

182 ulfate dressing versus a control dressing on wound closure in patients with neuroischaemic diabetic f

183 s transfected with PTP1B siRNA showed faster wound closure in response to VEGF.

184 Consistent with these findings, wound closure in T cell- and B cell-deficient Rag1-/- mi

185 Although rescue of epidermal wound closure in the absence of macrophages promotes bla

186 During wound closure in the embryonic epidermis, the cells arou

187 Wnt/beta-catenin activator CHIR99021 reduced wound closure in the iAEC2 cultures but not pAEC2 cultur

188 ously added TGF-beta3 accelerated epithelial wound closure in type 2 rat and type 1 mouse DM corneas

189 application of glycomimetic improved scratch wound closure in vitro in patient ECFCs (p < 0.01), most

190 Accelerated wound closure in vitro induced by anti-miR-200c was asso

191 Additionally, Erdr1 accelerates scratch-wound closure in vitro, increases Lgr5(+) intestinal ste

192 n, tight junction stabilization and impaired wound closure in vitro.

193 dification as well as a delay in the rate of wound closure in vitro.

194 ion to fibronectin, and an increased rate of wound closure in vitro.

195 opographical features can alter the speed of wound closure in vitro.

196 Inhibition of GC synthesis accelerated wound closure in vivo, providing the evidence that modul

197 ng that CD301b-depleted mice exhibit delayed wound closure in vivo, which could be rescued by topical

198 ivery vehicle, and this resulted in enhanced wound closure in vivo.

199 -19b alone in mice keratinocytes accelerated wound closure in vivo.

200 , in young mice, Sod2 deficiency accelerated wound closure, increasing epidermal differentiation and

201 not stimulate proliferation, and stimulated wound closure independently of proliferation.

202 ysis of protein localization dynamics during wound closure indicates that the rapid contraction of me

203 y facing the lesion participated directly in wound closure, indicating that closure is driven by move

204 angiogenesis was associated with compromised wound closure, insufficient granulation tissue formation

205 rmis is decreased in mouse models of delayed wound closure intended to mimic old age, obesity, and al

206 Throughout wound healing and after wound closure, InvEE macrophages demonstrated sustained

207 Based on our findings, epidermal wound closure is a process in which cell behavior is orc

208 Therefore, rapid wound closure is crucial for proper tissue function and

209 We find that wound closure is faster in early embryos, where, in addi

210 A key aspect of wound closure is the migration of keratinocytes across t

211 AS II to assess cell proliferation, scratch wound closure, L-arginine uptake, cationic amino acid tr

212 Effective wound closure mechanisms are essential for maintenance o

213 F within the wound significantly accelerated wound closure more effectively than an equal dosage of f

214 ell with these findings, revealing an active wound closure mostly completed by day seven after woundi

215 After 20 weeks, wound closure occurred in 60 patients (48%) in the sucro

216 sed in EM and CX epithelial cells even after wound closure occurred.

217 The fragmented mitochondria and accelerated wound closure of fzo-1 mutants are dependent on MIRO-1 f

218 these results can be exploited to accelerate wound closure of human skin in vivo.

219 octasulfate dressing significantly improved wound closure of neuroischaemic diabetic foot ulcers wit

220 guides, we achieve a full thickness (>10 mm) wound closure of porcine skin, which represents approxim

221 rms similarly to sutures and can be used for wound closure of the donor site of CTG.

222 A secondary outcome assessed wound closure of topically treated erosions.

223 n cell dynamics, including increased rate of wound closure on SPRY4-IT1 overexpression, suggest that

224 In contrast, TAF had no inhibitory effect on wound closure or tight junction formation following inju

225 increased bacterial colonization and delayed wound closure over time compared with young mice.

226 To follow airway-epithelial wound closure over time, we lesioned small areas of the

227 The EE group achieved earlier wound closure (P <0.001) and epithelialization (P <0.05;

228 repair mechanisms for treating patients with wound-closure pathologies.

229 Wounds were harvested upon complete wound closure (postoperative day 15) for histological ex

230 own of beta-catenin underwent evaluation for wound closure, proliferation, and bleomycin-induced cyto

231 alized increases in cellular crowding during wound closure promote the extrusion of nonapoptotic cell

232 Hsp90alpha-Delta mutant mice showed similar wound closure rate as the wild-type Hsp90alpha mice.

233 loss of HF neogenesis did not correlate with wound closure rate but with a reduction in Lrig1-positiv

234 We observed that macroscopic wound closure rate is accelerated in the absence of comm

235 Wound closure rate was not affected in the KO or KI mice

236 ation of GF mice with CV microbiota restored wound closure rate, neutrophil and macrophage accumulati

237 rming units, [CFU]), wound area measurement, wound closure rate, wound strength, and histological and

238 Wound closure rates are significantly delayed in TSG-6-n

239 Although many reports suggest that wound closure rates depend on isolated cell speed and/or

240 Wound closure rates were measured in human corneal epith

241 Wound closure rates, capillary density, and the recruitm

242 lication of recombinant SDF-1alpha increases wound closure rates, neovascularization, and endothelial

243 iogenesis, granulation tissue thickness, and wound closure rates, whereas local delivery of miR-135a-

244 sufficient for increased cell-migration and wound-closure rates.

245 Largest adherence gains were seen in wound closure re-gowning/re-gloving (24.0% vs. 62.0%, P

246 tinocytes in a hydrogel carrier showed rapid wound closure, reduced contraction and accelerated re-ep

247 The wound closure, reepithelialization, and collagen deposit

248 cellular and molecular mechanisms of SCF in wound closure remain poorly understood.

249 Wound closure requires a complex series of micro-environ

250 Wound closure requires the activation of keratinocyte mi

251 The accelerated wound closure resulted primarily from faster re-epitheli

252 e in vitro data were consistent with in vivo wound closure studies, and suggest that ANKRD1 is import

253 While sutures remain the common wound closure technique, they have many disadvantages.

254 After wound closure, the central corneal epithelium was comple

255 0.1%, while the cooked honey had incomplete wound closure, the vacuum-treated honey trended towards

256 release at tail fin wounds to initiate rapid wound closure through long-range activation of basal epi

257 ng model, i.p. MV administration accelerated wound closure through recruitment of PD-L1-expressing my

258 are independently regulated during embryonic wound closure, thus conferring robustness to the embryon

259 PGT inhibition shortened cutaneous wound closure time in diabetic mice from 22 to 16 days.

260 ality of wound healing without affecting the wound closure time likely due to an elevation of the ant

261 Wound closure timing was compared between IFI and non-IF

262 ared, there was no significant difference in wound closure timing.

263 lso given twice a week until complete socket wound closure up to 14 d.

264 ells) using a femtosecond laser and followed wound closure up to 6 hours by autofluorescence multipho

265 ffects of succinate-pretreated hMSC enhanced wound closure, vascularization and re-epithelialization

266 nced mitochondrial fragmentation accelerates wound closure via the upregulation of mtROS and Cytochro

267 The time to 50% wound closure was 11days, 16days, 14days, and 17days for

268 The defect in wound closure was accompanied by impaired removal of E-c

269 In the "suture" group, wound closure was achieved with standardized continuous

270 IFI wound closure was also assessed according to mold specie

271 Wound closure was associated with improved re-epithelial

272 Wound closure was clinically evaluated.

273 Corneal epithelial wound closure was delayed and re-innervation was slow an

274 nged, the formation of these junctions after wound closure was delayed.

275 ential of miR-10b and miR-21 in accelerating wound closure was demonstrated in in vitro assays and in

276 ines on TJ-mediated BEC barrier function and wound closure was examined by immunoblot, transepithelia

277 Wound closure was found to increase with substrate stiff

278 d an age-dependent expression pattern during wound closure was identified, including miR-31 and miR-2

279 The time to wound closure was longer for the IFI wounds (median, 16

280 oth equally impaired barrier function, while wound closure was more sensitive to TFV.

281 t in wound healing as assessed by percentage wound closure was observed only at the highest cell dose

282 In excisional wound-healing experiments, wound closure was significantly faster in Has1/3 null th

283 Fourteen days after treatment, wound closure was significantly more complete in AMD3100

284 Delayed wound closure was, in part, attributable to damage of th

285 how cell-cell junctions are regulated during wound closure (WC).

286 th in vitro and ex vivo models of human skin wound closure, we found that hair follicle dermal papill

287 sms by which AnxA2 promotes IEC movement and wound closure, we used a loss of function approach.

288 bpv(pic)) and LY294002 on cell migration and wound closure were investigated using time-lapse imaging

289 Overall, the times to wound closure were longest for the IFI wounds with Mucor

290 Among the IFI wounds, times to wound closure were significantly longer for wounds with

291 Cellular viability and wound closure were significantly promoted, and cytotoxic

292 n scaffold demonstrated increased percentage wound closure when compared with lower doses.

293 ide-specific antioxidants blocks actin-based wound closure, whereas elevation of mtROS promotes wound

294 expression of ANKRD1, and delayed excisional wound closure, which was characterized by decreased cont

295 C15 administration indirectly accelerates wound closure while altering fibroblast-mediated collage

296 dicted a relatively weak correlation between wound closure with proliferation, and the unexpectedly m

297 Smad7 on K5.TGFbeta1 skin wounds accelerated wound closure, with improved re-epithelialization and re

298 bsence of clinical BU specific features' or 'wound closure' within 6 months ("primary cure"), and 'ab

299 PKCdelta-infected SMCs increased endothelial wound closure without affecting their proliferation.

300 l rHDL application rescued diabetes-impaired wound closure, wound angiogenesis, and capillary density