ライフサイエンスコーパス: wound

1 s, corresponding to cell loss at the primary wound.

2 nd back of the cells on the two sides of the wound.

3 hold temperature associated with an infected wound.

4 anscription can influence MPhi plasticity in wounds.

5 n fibrin sloughs from patients with infected wounds.

6 reatment of chronic inflammation in diabetic wounds.

7 enic enhancers that distinguish cancers from wounds.

8 ty in the treatment of non-healing radiation wounds.

9 onalized management and treatment of chronic wounds.

10 quired for innate immune cell recruitment to wounds.

11 PTH2R) in extracellular matrix production in wounds.

12 capacity to replace dying cells and to heal wounds.

13 e growth of bacteria associated with chronic wounds.

14 easingly recognized to be capable of healing wounds.

15 to track ASCs after transplantation to skin wounds.

16 lls were present in the regenerated gingival wounds.

17 ic triggers of pathological scarring in skin wounds.

18 assess the effects of 0.5% PVI on acute skin wounds.

19 istance contribute to persistent, nonhealing wounds.

20 was performed on days 3, 7, 10, and 14 after wounding.

21 a similar manner in both genotypes following wounding.

22 lts in reduced proliferation in neonatal and wounded adult epidermis.

23 n the abilities to prevent infection of burn wound, aid healing, and an anti-inflammatory dressing ma

24 ellipodia, focal adhesions, and repair after wounding, along with impaired H2O2 responses after expos

25 ely purified from intact nerves and from the wound and distal regions of severed nerves.

26 in is compromised, bacteria can colonize the wound and impair wound healing.

27 d substance P-positive nerve density in both wounded and unwounded eyes compared with vehicle-treated

28 o comprise approximately 28% of all surgical wounds and are frequently complex to manage.

29 nvestigation of botanical folk medicines for wounds and infections led us to study Schinus terebinthi

30 mass index of 28 kg/m, 77% had contaminated wounds, and 84% completed 24-months follow-up.

31 gly reduced in fibroblasts of human gingival wounds, and blocking Cx43 function in cultured human gin

32 roperties of cells surrounding a single-cell wound are investigated during closure of the defect.

33 Chronic wounds are typically polymicrobial, with Staphylococcus

34 lar matrix proteins are deposited within the wound area, resulting in persistent inflammation and res

35 iated stimulation of cell migration over the wounded area by altering the subcellular distribution of

36 nnective tissue matrix components within the wound beds compared to wounds treated with chitosan scaf

37 ch ES affects repair, microarray analysis of wound biopsy samples was performed on days 3, 7, 10, and

38 ults, and clinical outcome for foodborne and wound botulism patients confirmed by laboratory testing,

39 n favor of LC but with an increased perineal wound breakdown rate.

40 on that can result in delayed wound healing, wound breakdown, fistula formation, and compromised tiss

41 l fibroblasts are recruited into the clotted wound by a concentration gradient of platelet-derived gr

42 tive variables (eg, age, comorbidities, ASA, wound classification), procedure type (eg, laparoscopic

43 ty, induced necroptosis, and delayed culture wound closing in three types of immortalized cancer cell

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

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

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

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

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

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

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

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

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

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

54 Wound closure requires the activation of keratinocyte mi

55 Wound closure was clinically evaluated.

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

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

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

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

60 was required for optimal intestinal mucosal wound closure.

61 Hsp90alpha as a potential driver for normal wound closure.

62 ly, localized microinjection of PMN-MPs into wounded colonic mucosa was sufficient to impair epitheli

63 are developed with the aims to fight against wound colonization.

64 Superficial wound complication was the most common wound event, 2.24

65 5%, P = 0.26) rates favored LC with perineal wound complications (38.3% vs 50.0%, P = 0.26) in favor

66 Perineal wound complications frequently occur after eAPR with pre

67 ease in 30-day hospital readmission rates or wound complications when compared with discharge 1 or 2

68 otic administration and in simulated shallow wounds conditions.

69 e induction of cellular migration by scratch-wounding confluent cell cultures, culturing under subcon

70 chitosan scaffolds containing control DNA or wounded controls.

71 ge Mertk deficiency led to decreased cardiac wound debridement, increased infarct size, and depressed

72 done with a clear temporal or clear superior wound, does not affect intraocular pressure, bleb morpho

73 atio, 2.19; 95% CI, 1.00-4.82], performing a wound dressing [odds ratio, 8.35; 95% CI, 2.07-33.63] an

74 ctors of wound infection identified standard wound dressings as the only significant predictor of SSI

75 oward developing electronically controllable wound dressings that can deliver drugs with desired temp

76 of application, including tissue adhesives, wound dressings, and tissue repair.

77 o include patients of different gender, age, wound duration and type of surgery (general, vascular an

78 activation of Toll a few cell diameters from wound edges is reminiscent of local activation of Toll i

79 nvestigated the ability of components of the wound environment to modulate interactions between P. ae

80 requires dynamic cellular adaptation to the wound environment.

81 a2 in cultured keratinocytes in vitro and in wound epidermis in vivo.

82 icial wound complication was the most common wound event, 2.24% in neoadjuvant-treated versus 2.45% i

83 Here, we used a mouse wound excisional model to characterize the infection dyn

84 tes the rise of cytosolic calcium across the wound field.

85 TCPs of about 11 kDa are present in acute wound fluids as well as in fibrin sloughs from patients

86 Although the wound H2O2 gradient reaches deep into the tissue, it lik

87 with a concentration-dependent incidence of wound healing adverse events (WHAE).

88 PGE2 production is essential for intestinal wound healing after colonic surgery, possibly via its ef

89 Perineal wound healing after eAPR with preoperative radiotherapy

90 ferentiation, and migration and in epidermal wound healing and barrier repair.

91 ys, and cell behaviors to those activated in wound healing and identifies a repertoire of potential t

92 -derived exosomes may be involved in corneal wound healing and neovascularization, and thus, may serv

93 d for proteins involved in defense response, wound healing and protein phosphorylation when compared

94 his Review presents current understanding in wound healing and regeneration as two distinct aspects o

95 f FZD4 signaling on alveolar epithelial cell wound healing and repair, as well as on expression of el

96 ng axons, while in adult tissues they aid in wound healing and the maintenance of intestinal cell pop

97 anonical WNT-driven alveolar epithelial cell wound healing and transdifferentiation in vitro.

98 The wound healing assay reveals that inhibiting either BCL2L

99 All cell migration and wound healing assays are based on the inherent ability o

100 Furthermore, cell invasion and wound healing assays together with qRT-PCR determination

101 mputation-free survival by 18%, and improved wound healing by 59%, without affecting mortality.

102 sms of glucocorticoid (GC) downregulation of wound healing by interaction with the membrane bound GC

103 solving mediators of inflammation accelerate wound healing by preventing chronic inflammation and all

104 Wound healing complications were more prevalent in the b

105 point was the rate of uncomplicated perineal wound healing defined as a Southampton wound score of le

106 ay play a key role in tissue homeostasis and wound healing during Th2-mediated immune responses, such

107 Although the wound healing effects of nitric oxide (NO) are known, th

108 tions demonstrated clearance of bacteria and wound healing following repeated i.v. administration of

109 rosis and myofibroblast formation in corneal wound healing have not been fully elucidated.

110 gnized as a central clinical issue for RDEB, wound healing impairment has been only marginally invest

111 effects and mechanism of AS II on intestinal wound healing in both in vitro and in vivo models.

112 rove beneficial in the treatment of impaired wound healing in diabetes.

113 angiotensin system is implicated in abnormal wound healing in diabetic and older adults.

114 evaluating antiretroviral effects on genital wound healing in future clinical trials.

115 Here, using an in vivo model of cutaneous wound healing in mice, we provide evidence that GPNMB is

116 langiocyte cell line and demonstrated potent wound healing in mice.

117 blation of epidermal caspase-8 as a model of wound healing in Mus musculus, we analyzed the signaling

118 r occludin, down-regulation had no impact on wound healing in normal scratch assays, but after subjec

119 Compared to skin, wound healing in oral mucosa is faster and produces less

120 s the method can be readily applied to image wound healing in other injured or diseased tissues, or t

121 We concluded that corneal endothelial wound healing in rabbits has different outcomes dependin

122 elial cells (ATII) are instrumental in early wound healing in response to lung injury, restoring epit

123 c mucosa was sufficient to impair epithelial wound healing in vivo.

124 come was assessment of wound healing using a wound healing index (WHI).

125 Wound healing is a biological process directed towards r

126 Epithelial wound healing is an evolutionarily conserved process tha

127 IL-10-induced HA synthesis for regenerative wound healing is demonstrated by inhibition of HA synthe

128 hese findings are novel in understanding how wound healing is regulated.

129 Wound healing is significantly delayed in irradiated ski

130 ating TNFalpha and IL-1beta during the early wound healing phase and reduced inflammation by downregu

131 n by downregulating IL-1beta during the late wound healing phase.

132 othelial cellular traits associated with the wound healing process and may also be able to regulate t

133 s implies a potential regulatory role in the wound healing process and, thus highlights their potenti

134 the absence of LPA1 mitigates the epithelial wound healing process.

135 ion on CMR and increases in inflammation and wound healing proteins on post-MI day 7.

136 the mechanism by which NO modulates corneal wound healing remains unclear.

137 Lung fibrosis is an unabated wound healing response characterized by the loss and abe

138 and antiviral host defense during the normal wound healing response.

139 ted to stress responses and apoptosis at the wound healing stage, signaling pathways including Wnt an

140 Secondary outcome was assessment of wound healing using a wound healing index (WHI).

141 stress, which is normally present in wounds, wound healing was impaired.

142 ugh alpha3beta1 promotes this process during wound healing, alpha9beta1 has an inhibitory role, sugge

143 an impact allergic and autoimmune responses, wound healing, and anti-microbial defense.

144 elf-organization in biofilms, embryogenesis, wound healing, and cancer metastasis.

145 o been shown to favor embryonic development, wound healing, and even tumor growth, suggesting more co

146 Selective inhibition of cell adhesion, wound healing, and invasion are demonstrated; near-infra

147 T) is critical for embryonic development and wound healing, and occurs in fibrotic disease and carcin

148 revascularization are to relieve pain, help wound healing, and prevent limb loss.

149 erentiation of cells in stem cell therapies, wound healing, and the treatment of cancer.

150 During skin wound healing, CD26-positive cells accumulated over time

151 During the proliferative phase of cutaneous wound healing, dermal fibroblasts are recruited into the

152 through distinct, yet overlapping phases of wound healing, including hemostasis, inflammation, proli

153 on of gene expression, cellular homeostasis, wound healing, inflammation, allergy, autoimmunity, and

154 thy is characterized by proteins involved in wound healing, ongoing fibrosis, and inflammation.

155 ibrillogenesis, promoting corneal epithelial wound healing, regulating gene expression and maintainin

156 duction, the blinking reflex, and epithelial wound healing, resulting in loss of transparency and vis

157 cations, such as graft infection and delayed wound healing, were seen in 6 patients; 8 patients exper

158 HTS is the result of dysregulated wound healing, where excessive collagen and extracellula

159 whether Pseudomonas species directly impair wound healing, wild-type mice were infected with Pseudom

160 n resulted in significantly impaired scratch wound healing, with delayed migration and reduced prolif

161 ious complication that can result in delayed wound healing, wound breakdown, fistula formation, and c

162 (GFBLs) strongly regulated the expression of wound healing-related genes.

163 genesis of chronic inflammation, cancer, and wound healing.

164 s relevant to cancer, vascular diseases, and wound healing.

165 , bacteria can colonize the wound and impair wound healing.

166 Cre+) ) to determine the function of MLL1 in wound healing.

167 factors and conditions can lead to impaired wound healing.

168 host-pathogen defense, organ rejection, and wound healing.

169 did not interfere with skin development and wound healing.

170 lso reduced FPD development by promoting FPD wound healing.

171 erals (TM) play a role in skin integrity and wound healing.

172 are involved in developmental regulation and wound healing.

173 induced angiogenesis, especially in diabetic wound healing.

174 actor for osteoarthritis (OA) and diminished wound healing.

175 y a prolonged inflammatory phenotype in late wound healing.

176 the M2 polarization of macrophages in acute wound healing.

177 in vivo for their ability to promote dermal wound healing.

178 ely, progressive fashion promotes pathologic wound healing.

179 are shown to promote the corneal epithelial wound healing.

180 ation-related miRNAs with potential roles in wound healing.

181 ession during papilloma induction and during wound healing.

182 ave the potential to induce angiogenesis and wound healing.

183 ls and macrophages and play central roles in wound healing.

184 a key aspect of re-epithelialization during wound healing.

185 n regulating cellular traits associated with wound healing.

186 orly understood inputs for organogenesis and wound healing.

187 ion could promote fast and scarless gingival wound healing.

188 ant tissue loss), and are known as 'surgical wounds healing by secondary intention'.

189 tions, particularly to "unexpected" surgical wounds healing by secondary intention.

190 hort-lived, transplanted ASCs can accelerate wound-healing and reduce hair loss in acid-burn skin inj

191 sis and help delineate an altered profile in wound-healing markers during ONJ development.

192 ated to FHs promote tissue regeneration in a wound-healing model of mouse submandibular glands (mSMGs

193 The cutaneous wound-healing program is a product of a complex interpla

194 ent second messenger and master regulator of wound-healing programs, it is unknown what initiates the

195 ponses may alter the homeostatic balance and wound-healing response of gingival connective tissues af

196 lly, PTX3 mediated the hepatic stellate cell wound-healing response.

197 promote tissue regeneration in which classic wound-healing responses predominate.

198 ly, generating myofibroblasts and associated wound-healing responses.

199 (ASCs) accelerates the process of acid burn wound-healing.

200 ation in hyphal tips and lesion expansion on wounded hosts, but significantly promoted germ tube elon

201 After diabetic mice were wounded in the right eye and treated in both eyes with P

202 ows that epithelial cells respond to minimal wounds in a collective fashion by increased contractilit

203 kin to organogenesis in adult mammals, large wounds in mice lead to de novo morphogenesis of hair fol

204 mice showed impaired healing of superficial wounds in the colon and impaired mucosal innate immune r

205 ion factor c-Myc (a biomarker of non-healing wounds), in porcine and human wound models.

206 e same effect was observed for a single-cell wound induced by laser ablation and during closure of a

207 Robust activation of wound-induced transcription from ple and Ddc requires To

208 e a mouse model for investigating E faecalis wound infection determinants, and suggest that both immu

209 Analysis of predictors of wound infection identified standard wound dressings as t

210 Secondary endpoints were postoperative wound infection, intra-abdominal abscess, reoperation, l

211 ween the timing of surgery and postoperative wound infection, intra-abdominal abscess, reoperation, o

212 vent, prolonged hospital length of stay, and wound infection/dehiscence).

213 Wound infections are a critical healthcare concern world

214 ith spontaneous chronic multi drug-resistant wound infections demonstrated clearance of bacteria and

215 lays an important role in sepsis, pneumonia, wound infections, and cystic fibrosis (CF), which is cau

216 coexist for long periods together in chronic wound infections.

217 re susceptible to horizontal transmission of wound infections.

218 spatial and temporal monitoring of potential wound infections.

219 hese two miRNAs are prominently expressed in wound-infiltrated neutrophils and macrophages and play c

220 ence interval (CI): 1.27, 2.71; for infected wounds, IRR = 3.04, 95% CI: 1.54, 5.98); exposure during

221 IRR = 3.28, 95% CI: 1.95, 5.51; for infected wounds, IRR = 4.96, 95% CI: 2.18, 11.29).

222 The healing of cutaneous wounds is dependent on the progression through distinct,

223 n = 3; 6.8%), endophthalmitis (n = 1; 2.3%), wound leak (n = 1; 2.3%), and choroidal detachment (n =

224 of the epithelial NADPH oxidase Duox at the wound margin is required early during this response.

225 iers only within approximately 30 mum of the wound margin.

226 However, some wounds may be left open to heal (if there is a risk of i

227 Detecting and healing these hidden wounds may help prevent and treat psychopathology emergi

228 The loss of wound melanization in T. anophthalmus was an apomorphy a

229 The speed of wound melanization was uncorrelated with a difference in

230 smosis (LRO) and reverse osmosis (RO) spiral-wound membranes showed LRO membrane to be very efficient

231 his study provides evidence that the dynamic wound microbiome is indicative of clinical outcomes and

232 unreported temporal dynamics of the chronic wound microbiome.

233 ure to systemic antibiotics destabilized the wound microbiota, rather than altering overall diversity

234 ue, Scl1 adhesin specifically recognizes the wound microenvironment, promotes adhesion and biofilm fo

235 ed by inhibition of HA synthesis in a murine wound model by administering 4-methylumbelliferone.

236 Furthermore, in a skin excisional wound model, we found the effects of succinate-pretreate

237 nduces miR-15b-5p in acute human and porcine wound models and in chronic DFUs.

238 of non-healing wounds), in porcine and human wound models.

239 In contrast, wounded mSMGs treated with FHs alone or in the absence o

240 xpression could be observed in both aged and wounded mutant tissues.

241 w that ES treatment of human acute cutaneous wounds (n = 40) increased reinnervation.

242 The inevitable wounding of the roots caused by harvesting triggers an o

243 diated stimulation of endothelial cells, and wounds of epidermis-specific alpha9 knockout mice displa

244 tion of PRP accelerates healing of cutaneous wounds only as a controlled release formulation.

245 py for recurrence and those with non-healing wounds or active bleeding conditions were ineligible.

246 In cell monolayers with wounds oriented orthogonal to the force, nuclei were dis

247 nvolved in plant stress responses, including wounding, perhaps to evoke plant defense.

248 entation of tissue-engineered constructs for wound regeneration, perhaps the most significant hurdle

249 effectively promote wound closure and reduce wound-related infections.

250 gulating macrophage-mediated inflammation in wound repair and identify a potential target for the tre

251 o cell adhesion regulation during intestinal wound repair and the development of IBD.

252 w this interaction influences the process of wound repair are not well understood.

253 versus pathogenic microbial interactions in wound repair is important.

254 oV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth

255 Skin wound repair requires a coordinated program of epithelia

256 The process of wound repair requires the coordinated participation of m

257 idelity" recreates a state akin to transient wound repair that persists to maintain uncontrolled grow

258 the role of each cell type in the process of wound repair, the nature of the dynamic interplay betwee

259 show that lineage plasticity is critical in wound repair, where it operates transiently to redirect

260 linking innate immune activation to mucosal wound repair.

261 cellular responses are often required during wound repair.

262 option of a morphogen-responsive function in wound repair.

263 s normally associated with tissue injury and wound repair.

264 how they function in normal homeostasis and wound repair.

265 ion in human acute wounds, thus accelerating wound repair.

266 n, can induce decorin expression and enhance wound repair.

267 iched for genes involved in inflammation and wound repair.

268 skeletal remodeling processes in single cell wound repair.

269 were found to exhibit a significant delay in wound repair.

270 , barrier repair requires activation of many wound response genes in epidermal cells surrounding woun

271 ility of prosystemin to trigger the systemic wound response in vivo.

272 during the activation of macrophage cells or wound response in vivo.

273 ynamics of E faecalis and show that infected wounds result in 2 different states depending on the ini

274 d effective resolution of S. aureus-infected wounds, revealing a potential antibiotic-free strategy f

275 ineal wound healing defined as a Southampton wound score of less than 2 at 30 days postoperatively.

276 linical need exists for 63% to 65% of combat-wounded service members and 11% to 20% of civilians who

277 at three landmarks of pre-existing tissue at wounds set the location of anterior pole formation: a po

278 tion provides insight into the mechanisms of wound signaling in tomato.

279 ve distinct and specific regulatory roles in wound signalling and patterning to enable regeneration.

280 d repair, due to the paucity of cells at the wound site.

281 abscess formation at S. aureus-infected skin wound sites and were also more susceptible to horizontal

282 esponse genes in epidermal cells surrounding wound sites.

283 PUFAs were negatively correlated with OA and wound size, but positively correlated with adiponectin l

284 ayed calcium expansion event is predicted by wound size, indicating that a separate mechanism of calc

285 onsive enhancers during development and upon wounding suggests cooperation with distinct TFs in diffe

286 orbable (polydioxanone) suture material in a wound-suture ratio of minimum 1 : 4 was introduced in Ju

287 By using a stab wound telencephalic injury model, the impact of hypergly

288 enerative ability of adult brain, after stab wound telencephalic injury.

289 , salicylic acid, and gibberellic acid or by wounding, temperature, and light, factors known to affec

290 nerate lipid-filled adipocytes in large skin wounds that regenerate hair follicles, suggesting a new

291 in the abdomen and additionally showed that wounding the cuticle of the abdomen results in decreased

292 on and neural differentiation in human acute wounds, thus accelerating wound repair.

293 components within the wound beds compared to wounds treated with chitosan scaffolds containing contro

294 a quiescent cell cycle phase as assessed in wounds, tumors, and aorta.

295 onocytes migrating toward full-thickness ear wounds we found that Arpc2(-/-) monocytes maintain cell

296 10-mm full-thickness excisional wounds were also generated on the dorsal skin of rats tr

297 rats treated with 10 mg/kg SB431542 and all wounds were treated with 0.5% PVI for 5 days.

298 kin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and prom

299 hanical stress, which is normally present in wounds, wound healing was impaired.

300 ost frequently isolated bacterial species in wounds yet little is known about its pathogenic mechanis