ライフサイエンスコーパス: dermal

1 Other exposure routes, for example, dermal absorption and drinking water, make a relatively

2 Dermal absorption data reveal systemic exposure of UV fi

3 data for certain UV filters including their dermal absorption data.

4 imated daily intakes of MEL and PFAS through dermal absorption from nylon clothes were three orders o

5 Dermal absorption of BPA from thermal paper receipts occ

6 Compared to dietary BPA exposure, dermal absorption of BPA leads to prolonged exposure and

7 Preliminary calculations found that dermal absorption via PCP use may be an important exposu

8 and single-cell RNA sequencing revealed that dermal adipocytes alter their fate and generate ECM-prod

9 Here, we isolated dermal adipocytes and characterized dermal fat at the ce

10 ervations unravel a surprising plasticity of dermal adipocytes and provide an explanation for the dyn

11 The fate of the mature dermal adipocytes and the origin of the rapidly reappear

12 ses to external stimuli, we established that dermal adipocytes are a distinct class of white adipocyt

13 Genetic mouse studies revealed that dermal adipocytes are necessary to initiate inflammation

14 es and the origin of the rapidly reappearing dermal adipocytes at different stages remain unclear.

15 Furthermore, mature dermal adipocytes dedifferentiate into migratory extrace

16 WAT highlighted an important role for mature dermal adipocytes for hair cycling and wound healing.

17 (2020) reveal that dermal adipocytes regulate skin wound repair via release

18 cell RNA sequencing, we observed that mature dermal adipocytes undergo dedifferentiation and rediffer

19 Dermal adipose tissue (also known as dermal white adipos

20 l fibroblasts functions as a key mediator of dermal aging.

21 asts (COL1A2-CCN1), display accelerated skin dermal aging.

22 Importantly, similar mechanisms drive human dermal aging.

23 The dermal albumin sensor consisted of 3',3'',5',5''-tetrach

24 s model was characterized by highly expanded dermal alphabeta T clonotypes that produce the type thre

25 These dermal alterations reflect reduced production of collage

26 To compare the pharmacokinetics of dermal and dietary BPA exposure, six male participants h

27 nodes involving Ag presentation by migratory dermal and lymph node-resident DC.

28 Changes in vascular barrier function in dermal and meningeal vessels were measured in real time

29 of how B. burgdorferi transmigrates through dermal and tissue vascular barriers and establishes diss

30 cipants provided information on respiratory, dermal, and eye irritation health.

31 to the dispersants and adverse respiratory, dermal, and eye irritation symptoms.

32 ir immediate relatives, the extinct jawless, dermal armor-encased osteostracans, which have conventio

33 es in horses with hereditary equine regional dermal asthenia (HERDA), an equine model of Ehlers-Danlo

34 pogenic differentiation of ADSCs, leading to dermal augmentation.

35 les, providing the necessary force to breach dermal barriers and enhance payload delivery.

36 n and soft tissue specimens for the study of dermal biology, wound healing and fibrotic pathologies.

37 eloped into MNAs and their effectiveness for dermal biosensing.

38 Here, minimally invasive, injectable dermal biosensors were developed for measuring pH, gluco

39 Here, we use matched donor-derived human dermal blood and lymphatic endothelial cells (BEC and LE

40 d expression of alpha-smooth muscle actin in dermal blood vessels and improve the impaired neovascula

41 t the origin of the fluorescence lies in the dermal bone of the head and back, visible through a part

42 carried by a cheekbone or a series of short dermal bones along the jaw edges, and teeth are added li

43 des show hybrid morphologies around the oral-dermal boundary, suggesting signal cross-communication.

44 acrophages was correlated with the number of dermal C-C chemokine receptor type 4(+) T helper type 2

45 en immunity is essential to control oral and dermal candidiasis.

46 vity across the entire skin reveals a latent dermal capacity to undergo spatially patterned self-orga

47 Mouse dermal capillary vessels lose pericyte coverage substant

48 Here, we examined the roles of dermal cDC1s and cDC2s during bacterial infection, notab

49 Neutrophil recruitment by dermal cDC1s was also observed during S. aureus, bacillu

50 These cells are transcriptionally similar to dermal cDC2 but are more efficient antigen-presenting ce

51 Concurrently, this dermal cell aggregation triggers the mechanosensitive ac

52 The absence of one single murine dermal cell type, the innate neonatal-derived IL-17 prod

53 and fewer cyclooxygenase 2 (Cox-2)-positive dermal cells than controls.

54 ly unsuspected population of Bmp4-expressing dermal cells.

55 Dermal cellularity was increased in contrast-treated gre

56 d, with persistent blood vessels and reduced dermal collagen at 10 days.

57 onfirmed by apple-green birefringence within dermal collagen, sweat glands, and arrector pili that en

58 ngs demonstrated objective thickening of the dermal collagen.

59 riously alters the structure and function of dermal collagen.

60 The hair follicle (HF) dermal condensate (DC) is a cluster of cells critical fo

61 and 4D microscopy, unclustered precursors of dermal condensates (DC), signaling niches for epithelial

62 Formula: see text] (95% CI: 1.22, 1.92)] and dermal contact [[Formula: see text] (95% CI: 1.22, 1.78)

63 However, discriminating between dermal contact and ingestion of drugs has never been ver

64 stimated daily intakes via hand-to-mouth and dermal contacts (for hands only) for PFOA were 0.83 and

65 indoor environment through hand-to-mouth and dermal contacts using hand wipes.

66 est exposure to adults via hand-to-mouth and dermal contacts, followed by PFOS.

67 IL-31 was released by dermal conventional type 2 dendritic cells (cDC2s) recru

68 Our results suggest that dermal CuV DNA carriage is associated with CTCL.

69 ies were shown to persist for >=20 years and dermal CuV DNA for 4 years.

70 The dermal CuV-DNA prevalence was significantly higher in CT

71 ing AhR, respectively, in LC and Langerin(+) dermal DC and in all CD11c(+) cells.

72 ion of Ag presentation to migratory CD103(-) dermal DC.

73 We demonstrate that dermal DCs engulf the intact granules exocytosed by MCs

74 TGF-beta1, which promotes wound healing, to dermal DCs in vitro was sufficient to induce Il31 expres

75 CD301b(+) dermal DCs respond to allergens encountered in vivo, but

76 tolerance induction, while talin1-deficient dermal DCs unexpectedly accumulated in the dermis despit

77 y ELISA; the percentage of migratory CD1a(+) dermal DCs was significantly decreased in the DSS patien

78 to draining lymph nodes of cross-presenting dermal DCs.

79 nst tumor-derived neo- and self-antigens via dermal DCs.

80 ial peptides (AMPs) as an effective chemical dermal defence.

81 ocytes, epidermal Langerhans cells (LC), and dermal dendritic cells (DC).

82 reveal that dermal dendritic cells produce interleukin-31, which act

83 Specifically, RUBCN deficiency in CD301b(+) dermal dendritic cells results in their increased antige

84 Langerhans cells in the dermis and CD11c(+) dermal dendritic cells were observed, corresponding to t

85 ls, including Langerhans cells, macrophages, dermal dendritic cells, mast cells, fibroblasts, and lym

86 yte-derived dendritic cells and interstitial dermal dendritic cells, yet the virus fully replicates o

87 ic cells, Langerhans cells, and interstitial dermal dendritic cells.

88 cells, basophils, substance P(+) cells, and dermal deposition of periostin and hemosiderin.

89 istologically, the ischaemic group exhibited dermal disorganization and inflammatory cell infiltratio

90 ed, with the increase being mainly caused by dermal emissions of mostly carbonyl compounds (57%).

91 Whole-body, breath, and dermal emissions were assessed.

92 We observed that dermal endothelial cells in rosacea had an increased exp

93 De novo infection of primary dermal endothelial cells with live and UV-inactivated KS

94 However, the impact of the aging dermal environment on female scalp hair follicles remain

95 natively activated phenotype despite the Th1 dermal environment required for their recruitment.

96 es, eosinophils induced separation along the dermal-epidermal junction of ex vivo skin.

97 ns as a cell-matrix adhesion molecule in the dermal-epidermal junction of the skin.

98 C3c deposition along the dermal-epidermal junction was partially or completely ab

99 zation, revealed recovery of function of the dermal-epidermal junction with no signs of blister forma

100 e main component of anchoring fibrils at the dermal-epidermal junction.

101 Dermal-epidermal separation by IL-5-activated eosinophil

102 ha-BP180 and BP230) and complement along the dermal-epidermal-junction is a hallmark of bullous pemph

103 regulated and differentiated by the oral and dermal epithelia.

104 ts occurs but BPA pharmacokinetics following dermal exposure is not understood.

105 osures related to air concentrations such as dermal exposure.

106 d healing process, eCRT induces abundant neo-dermal extracellular matrix (ECM) formation by 3 days po

107 r birth, leading to an age-dependent loss of dermal fat and a decrease in adipogenesis and cathelidic

108 isolated dermal adipocytes and characterized dermal fat at the cellular and molecular level.

109 s enriched with adipogenic dFBs and immature dermal fat that highly expressed cathelicidin.

110 In addition, P311 induced dermal fibroblast activation and proliferation.

111 n (aged 19-81 years) and primary cultures of dermal fibroblast and dermal sheath cells.

112 dipocytes) secrete factors that affect human dermal fibroblast behavior.

113 PNIPAAm-conjugated PCL allowed human dermal fibroblast cells (HDF) and mesenchymal stem cells

114 cytotoxic effects on SHSY5Y, MRC5, and human dermal fibroblast cells compared with the dissolved PhIP

115 ed in vitro studies on the response of human dermal fibroblast cells toward pristine titania nanotube

116 Primary dermal fibroblast cultures confirmed that matrix metallo

117 re assessed ex-vivo in primary human-derived dermal fibroblast cultures.

118 d scRNA-seq and exome-seq data from 32 human dermal fibroblast lines, identifying hundreds of differe

119 Specifically, an increase in 5-HETE enhanced dermal fibroblast migration and collagen deposition.

120 g mouse embryonic fibroblast Balb/3T3, human dermal fibroblast NHDF cell lines, and on neoplastic cel

121 to provide insights into the utility of SSc dermal fibroblast primary cells for therapeutic target d

122 an increase in dermal sheath proteins in the dermal fibroblast secretome with aging.

123 c mice, with selective expression of CCN1 in dermal fibroblasts (COL1A2-CCN1), display accelerated sk

124 Dermal fibroblasts (dFBs) resist infection by locally di

125 We exposed human dermal fibroblasts (HDFs) to the drug-eluting scaffold a

126 cal and cell attachment activity using human dermal fibroblasts (HDFs).

127 In vitro, primary dermal fibroblasts (pDFs) from KI mice showed substantia

128 s ROS induced carbonylation profile in human dermal fibroblasts along with A498 primary site and ACHN

129 Both EZH2 and H3K27me3 were elevated in SSc dermal fibroblasts and endothelial cells compared with h

130 delivery of either autologous or allogeneic dermal fibroblasts and epidermal keratinocytes directly

131 its individual components on matched primary dermal fibroblasts and epidermal keratinocytes from huma

132 al wounds bioprinted with layered autologous dermal fibroblasts and epidermal keratinocytes in a hydr

133 ll as in lung cancer-associated fibroblasts, dermal fibroblasts and hepatic stellate cells.

134 that TLY012 selectively blocks activation of dermal fibroblasts and induces DR-mediated apoptosis in

135 down the expression of 285 lncRNAs in human dermal fibroblasts and quantified cellular growth, morph

136 Instead, dermal fibroblasts are both necessary and sufficient to

137 These results suggest that synthetic dermal fibroblasts are plastic, and that CCN2 is require

138 liferative phase of cutaneous wound healing, dermal fibroblasts are recruited into the clotted wound

139 In skin homeostasis, dermal fibroblasts are responsible for coordinating the

140 trated the value of carefully-phenotyped SSc dermal fibroblasts as a platform for SSc target and drug

141 t, P4HA1 protein level and C-P4H activity in dermal fibroblasts compared to age-matched control sampl

142 Here we show that senescent dermal fibroblasts express the non-classical MHC molecul

143 We show here that cellular defects in dermal fibroblasts from affected individuals are complem

144 peripheral myelin protein 22) protein and in dermal fibroblasts from patients with CMT1A, PMP22 aggre

145 re, we demonstrate unexpectedly that primary dermal fibroblasts from pre-symptomatic mutation carrier

146 Primary dermal fibroblasts from R258C patients exhibited increas

147 onstrate that elevated expression of CCN1 by dermal fibroblasts functions as a key mediator of dermal

148 ciated matricellular protein, is elevated in dermal fibroblasts in aged human skin.

149 on repressive function, causes conversion of dermal fibroblasts into CAFs.

150 KI mice displayed increased infiltration of dermal fibroblasts into the wound environment, increased

151 te and sebocyte differentiation, its role in dermal fibroblasts is unclear.

152 es have successfully demonstrated the use of dermal fibroblasts isolated from DPs as models for PDK4

153 argeted expression of CXCR2 in primary human dermal fibroblasts led to paracrine induction of nuclear

154 performed a non-integrative reprogramming of dermal fibroblasts obtained from two patients with radio

155 sion that also occur, to a lesser extent, in dermal fibroblasts of apparently unaffected skin.

156 SSc dermal fibroblasts retained most of the molecular diseas

157 Dermal fibroblasts showed splice-variant mediated skippi

158 es were undertaken by exposing primary human dermal fibroblasts to different concentrations of partic

159 ineered with iMyoD-hTERT-NHDFs, normal human dermal fibroblasts transduced with genes encoding human

160 olecular reprogramming trajectories of human dermal fibroblasts using single-cell transcriptomics.

161 f freshly isolated and in vitro cultured SSc dermal fibroblasts were characterized using whole transc

162 Human dermal fibroblasts were used as comparator cells.

163 CPyV is able to replicate within a subset of dermal fibroblasts, but MCPyV DNA has also been detected

164 rting cell population is combined with human dermal fibroblasts, encapsulated in a fibrin hydrogel an

165 ll metabolism for a healthy cell line (Human Dermal Fibroblasts, HDF) and a cervical cancer cell line

166 vation by various cells (e.g., primary human dermal fibroblasts, HMEC-1 endothelial cells), and unloc

167 to in vitro investigation of patient-derived dermal fibroblasts, laboratory engineered cell lines and

168 ) in keloid fibroblasts compared with normal dermal fibroblasts.

169 e cardiomyocytes compared to co-culture with dermal fibroblasts.

170 t of NF-kappaB to the MMP-1 promoter site in dermal fibroblasts.

171 EDA-dependent fibro-inflammatory response in dermal fibroblasts.

172 in different concentrations on primary human dermal fibroblasts.

173 lution (particulate matter) on human primary dermal fibroblasts.

174 quercetin alleviated cellular senescence of dermal fibroblasts.

175 educing the development of bleomycin-induced dermal fibrosis in mice in vivo.

176 t glycyrrhizin ameliorates bleomycin-induced dermal fibrosis through the inhibition of fibroblast act

177 ) into myofibroblasts in the pathogenesis of dermal fibrosis.

178 Moreover, we also show that the dermal field is characterized by a senescent phenotype.

179 hed only in areas overlying this multi-focal dermal field.

180 nt spine and tendon, aspiration biopsies and dermal fillers (DF).

181 rked by the origin of digits and the loss of dermal fin rays.

182 IL-1beta induces dermal gammadelta T cell proliferation and IL-17 product

183 IL-1 signaling in both dermal gammadelta T cells and other cells such as kerati

184 Migration of dermal gammadelta T cells to the dLN under steady-state

185 S1PR1 and CD69 are reciprocally expressed on dermal gammadelta T cells, with loss of CD69 associated

186 ic lesional skin, has increased IL-1beta and dermal gammadeltaT17 cell expansion.

187 is regulated by skin commensals to maintain dermal gammadeltaT17 homeostasis in mice.

188 The dermal glucose sensor consisted of glucose oxidase, 3,3'

189 in, alpha-smooth muscle actin in human adult dermal (HDFs) and neonatal fibroblasts (HFFs) mainly via

190 plasma and lesional CCL17 accounted for the dermal homing of CD8(+)CCR4(+) T-cells, that along with

191 ion, with 2 of the relatives presenting with dermal hyperneury, cutaneous lesions classically describ

192 DNA damage to skin causes epithelial and dermal hyperplasia, tissue expansion, and proliferation-

193 urfacing (AFR) within treated areas of focal dermal hypoplasia (FDH).

194 is pathogenesis via the direct regulation of dermal IL-17-producing cells and stimulation of keratino

195 In a strictly dermal infection model we found that mice, which were pr

196 The dermal infiltrate of cutaneous lesions of histiocytoid S

197 In SD lesions, dermal infiltrating IL-31(+) cells were increased in num

198 ng, enhanced epithelial cell activation, and dermal infiltration by T(h)1 effector T cells.

199 ed on a topography that mimics the epidermal-dermal interface, spatial segregation of mean ERK activi

200 nvasive continuous sensing of lactate in the dermal interstitial fluid (ISF).

201 Dermal invasion is a hallmark of malignant melanoma.

202 and cytological information in epidermal and dermal layers while reducing the need for biopsies.

203 argets, previous data suggest post-kala-azar dermal leishmaniasis (PKDL) patients can act as an infec

204 Post Kala-azar dermal leishmaniasis (PKDL), caused by Leishmania donova

205 al treatment is available for post-kala-azar dermal leishmaniasis (PKDL), clinical sequela of viscera

206 aniasis (VL) and its sequela, post-kala-azar dermal leishmaniasis (PKDL), in a highly endemic communi

207 ted inflammation was associated with reduced dermal macrophage influx and production of reactive oxyg

208 Dermal macrophages (Mphi) are critical for the coordinat

209 Induction of BRP-39 was dominant in dermal macrophages.

210 n in normal subjects and it was expressed in dermal macrophages.

211 istry showed CXCL9 co-localized with CD68(+) dermal macrophages.

212 2 is indeed the dominant codeine receptor of dermal mast cells.

213 The long-term outcomes of acellular dermal matrix (ADM) for the treatment of isolated gingiv

214 MT) 1 year after treatment with an acellular dermal matrix (ADM).

215 t [CTG], collagen matrix [CM], and acellular dermal matrix [ADM]) resulted in a significant increase

216 t all investigated techniques (the acellular dermal matrix [ADM], collagen matrix [CM], connective ti

217 The use of a porcine dermal matrix at time of implant placement is effective

218 difference in GR reduction between acellular dermal matrix grafts (ADMG) + CAF and SCTG + CAF or betw

219 graft putty, and then covered with acellular dermal matrix membrane.

220 gival margin over time, while EMD, acellular dermal matrix, collagen matrix, and flap alone showed a

221 patients were assigned into group A (porcine dermal matrix, n = 24) or B (healing abutment used as te

222 hich agrees with the common usage of DMSO in dermal medicine.

223 mis and prominent clustering of the adjacent dermal mesenchymal cells.

224 We characterized the skin surface and dermal microbiota of 11 dogs affected by spontaneous mas

225 facilitates permeation of medicines into the dermal microcirculation.

226 for reducing fibrosis in the tumor-promoting dermal microenvironment of RDEB patients.

227 Human dermal microvascular ECs (HDMECs) treated with TLR3 [Pol

228 Cs), HUVEC-derived EA.hy926 cells, and human dermal microvascular endothelial cells (HDMECs), we foun

229 Human dermal microvascular endothelial cells 1, human platelet

230 However, in human dermal microvascular endothelial cells, P3 did not affec

231 these cells to induce adhesion molecules on dermal microvascular endothelial cells.

232 adhesion and transmigration of Tregs in the dermal microvasculature in a two-challenge model of cont

233 Tregs and assessed their interactions in the dermal microvasculature.

234 Functional assessment of gated individual dermal microvessels is therefore of outstanding interest

235 hogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly

236 Using a human dermal model of acute inflammation, we found that, altho

237 In summary, resident dermal Mphi are programmed locally, independently of bon

238 ERK was additionally required for TEM across dermal MVECs.

239 antitative PCR measurements of PMP22 mRNA in dermal nerves were performed using skin biopsies in huma

240 We propose that teeth and dermal odontodes are modifications of a single system, r

241 developmental relationship between teeth and dermal odontodes that is not evident from the adult morp

242 fluence on breath OH reactivity but enhanced dermal OH reactivity significantly.

243 branching tubules in three-dimensional human dermal organoid ex vivo culture.

244 oke exposures in firefighters susceptible to dermal PAH absorption when using personal protective equ

245 eets target lung CSCs but not normal primary dermal papilla (DP) stem cells.

246 trix metalloproteinase 1 was elevated in the dermal papilla and dermal sheath in situ.

247 supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocyte

248 nterior-posterior Wnt2b signaling within the dermal papilla controls barbule cell fates with spatiote

249 n wound closure, we found that hair follicle dermal papilla fibroblasts could accelerate closure of i

250 e used a cytokine array to determine how the dermal papilla fibroblasts were eliciting this effect an

251 ial compartment and androgen receptor in the dermal papilla of miniaturized hair.

252 ndrogenetic alopecia by interfering with the dermal papilla.

253 unravel new molecular landscapes within the dermal papilla.

254 ent bone marrow had a complete abrogation of dermal pathology.

255 anic acid ionic liquid (CAGE) to enhance its dermal penetration.

256 these strategies in enhancing epidermal and dermal penetration.

257 The dermal pH sensor was based on methyl red, bromothymol bl

258 approach, we previously demonstrated that a dermal premalignant field characterized by inflammatory

259 CCN2 is required for the differentiation of dermal progenitor cells into a myofibroblast/CAF phenoty

260 Failure of dermal protection or repair mechanisms might lead to vis

261 The evolution of dermal rays in crownward stem tetrapods reflects adaptat

262 ggests that cross-sectional asymmetry in the dermal rays of paired fins is plesiomorphic to crown gro

263 To address this knowledge gap, we study the dermal rays of the pectoral fins of 3 key tetrapodomorph

264 tion, the number of CD14(+) CD207(+) CCR6(+) dermal-resident monocytes that can differentiate into ep

265 example being the retrovirus causing walleye dermal sarcoma in fish.

266 quires a two-field composite consisting of a dermal senescent field driving the persistence of the ov

267 (PKDL), caused by Leishmania donovani is the dermal sequel of Visceral Leishmaniasis and importantly,

268 Thus, our study identifies the dermal sheath as smooth muscle that drives follicle regr

269 mRNA, MMP1, increased with aging, whereas in dermal sheath cells, hyaluronic acid synthase 2, HAS2, a

270 nd primary cultures of dermal fibroblast and dermal sheath cells.

271 ase 1 was elevated in the dermal papilla and dermal sheath in situ.

272 Proteomics revealed an increase in dermal sheath proteins in the dermal fibroblast secretom

273 Here, we identify the dermal sheath that lines the follicle as the key driver

274 g., sharks and skates) possess a postcranial dermal skeleton consisting of tooth-like "denticles" emb

275 dentine throughout the ancestral vertebrate dermal skeleton.

276 scular or subfascial implants, 440 (21%) had dermal sling implants, 42 (2%) had pre-pectoral implants

277 These regenerated tissues had a dermal structure and composition similar to healthy skin

278 Here we characterize the dermal T cell and epidermal Langerhans cell components o

279 -treated groups also had evidence of reduced dermal thickness and collagen fiber network organization

280 A decrease in dermal thickness was found to be positively associated w

281 At 12 months of age, reduced skin dermal thickness was observed in both MFS and control mi

282 n significantly increased wound vascularity, dermal thickness, collagen deposition and tensile streng

283 erved in both MFS and control mice, but only dermal thinning in MFS mice was rescued by doxycycline t

284 were enriched in epidermis from NLP, whereas dermal tissue responses and T-cell compositions were sim

285 rack perturbed glucose and lactate levels in dermal tissue with results in close agreement with stand

286 e reactive or spontaneous fibroproliferative dermal tumors characterized by the exaggerated and uncon

287 of interferon regulatory factor 4-dependent dermal type 2 conventional DC subsets and not by epiderm

288 Direct air-to-skin dermal uptake has been shown to be comparable to the inh

289 of BPA by BPS in thermal paper and the lower dermal uptake of BPS compared to BPA.

290 characterized by photosensitivity, abnormal dermal vascular behavior, inflammation, and enhanced exp

291 Notably, although both meningeal and dermal vessels were affected, intracerebral vessels, whi

292 Dermal white adipose tissue (dWAT) expansion is associat

293 Dermal adipose tissue (also known as dermal white adipose tissue and herein referred to as dW

294 recent progress in understanding the role of dermal white adipose tissue in immunity, both as an inna

295 Dermal white adipose tissue is a unique layer of adipocy

296 tantly, the tPA-MG53 mice display remarkable dermal wound healing capacity, enhanced muscle performan

297 nalyzed in vivo for their ability to promote dermal wound healing.

298 y regulates the angiogenic process in normal dermal wounds and thereby delays healing, whereas the st

299 administration of Myr-CBD7 peptide on mouse dermal wounds not only blocked CCR10-eNOS interaction, b

300 nt of angiogenesis to promote the healing of dermal wounds.