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1 d repair, due to the paucity of cells at the wound site.
2 ytosis of intracellular vesicles next to the wound site.
3 y, and low bioavailability of factors at the wound site.
4 increased leptin production at the ischemic wound site.
5 sponse and increased matrix deposited at the wound site.
6 ence sufficient to withstand the rigors of a wound site.
7 ates of PDL cells and GF to fill an in vitro wound site.
8 the concentration profile of TGF-beta at the wound site.
9 he abilities of these 2 cell types to fill a wound site.
10 ele cells to factors present in serum at the wound site.
11 ions of tissue constituents distant from the wound site.
12 y pro-inflammatory mediators released at the wound site.
13 on was localised to a few cells close to the wound site.
14 ) rise in cytosolic Ca2+ was detected at the wound site.
15 the onset of keratinocyte migration into the wound site.
16 of HB-EGF in the surface epithelium near the wound site.
17 fusion of intracellular compartments at the wound site.
18 un N-terminal kinase (JNK) signaling, at the wound site.
19 er involving local cell proliferation at the wound site.
20 local production of mtROS superoxide at the wound site.
21 tro, and deliver them as MSCs on FMBs at the wound site.
22 nt of coe(+) and sim(+) progenitors near the wound site.
23 KC, MIP-2, and MCP-1 chemokine levels at the wound site.
24 i, rapidly melanizes after collection from a wound site.
25 re down-regulated, even far-removed from the wound site.
26 that repopulate the wound and the RPE at the wound site.
27 neutrophil and macrophage recruitment to the wound site.
28 e delivering autologous keratinocytes to the wound site.
29 ioactive form of JA, in leaves distal to the wound site.
30 yo's developmental stage and the subcellular wound site.
31 d fusion of lipid vesicles trafficked to the wound site.
32 zed with fluorescein-labeled fetuin A at the wound site.
33 cruitment of antimicrobial leukocytes to the wound site.
34 of the cell in membranes extending over the wound site.
35 an endogenous antiangiogenic factor from the wound site.
36 ly of phenolic compounds released from plant wound sites.
37 ice had reduced IGF-1 receptor activation at wound sites.
38 2 months (12/24; 50%) compared with baseline wound sites.
39 pidly deposit callose, a beta-1,3-glucan, at wound sites.
40 inhibiting tumor cell implantation in trocar wound sites.
41 n fibrin gel, a likely provisional matrix at wound sites.
42 es--interleukin 1alpha and interleukin 8--at wound sites.
43 nt petioles and unfertilized flowers, and at wound sites.
44 ds and monosaccharides, synthesized at plant wound sites.
45 ry tract, indwelling catheters, and surgical wound sites.
46 r deplete the influx of eosinophils into the wound sites.
47 ea, and led to more normalized tissue in the wound sites.
48 ChvE and monosaccharides released from plant wound sites.
49 onse to chemical signals released from plant wound sites.
50 esponse genes in epidermal cells surrounding wound sites.
51 itored HF formation at small circular (2 mm) wound sites.
52 ns in response to natural enzymes present at wound sites.
53 ling macrophages, and better angiogenesis at wound sites.
54 extracellular proteases highly expressed at wound sites.
55 g small GTPase translation in neutrophils at wound sites.
56 nst S. aureus infection and its clearance at wound sites.
57 ctin filaments (F-actin) and myosin-2 around wound sites.
58 signals that are thought to be released from wound sites.
59 and subsequent macrophage infiltration into wound sites.
60 e insect-derived elicitor, at a mechanically wounded site.
61 they respond by developing tumors along the wounded site.
63 ing at 3 months (21 intact graft sites of 24 wound sites; 87%), 6 months (16/24; 67%), and 12 months
65 pair perfectly without a remnant scar at the wound site, adult tissue repair always leads to formatio
66 , at least in part, to the protection of the wound site against oxidative/nitrosative damage and prev
68 e number of SDF-1-bearing macrophages in the wound sites amplifying the "pull" of mobilized stem cell
69 ation-an initial localized response near the wound site and a subsequent systemic response that varie
70 ed expression of NFIA, SOX9 and GLAST at the wound site and in the ventricular zone (VZ) of the injur
71 njury, F4/80(+) myeloid cells infiltrate the wound site and induce smooth muscle actin (SMA) expressi
72 s calcium flash inhibits H2O2 release at the wound site and leads to a reduction in the number of imm
73 JAK/STAT signaling becomes activated at the wound site and promotes regenerative cell proliferation
74 ) such as hydrogen peroxide are generated at wound sites and act as long-range signals in wound heali
75 homologs are necessary for cell migration to wound sites and for the establishment of migratory cell
76 d in response to wounding can be detected at wound sites and in distal leaf veins within 1 hr after w
77 l known to cause crown gall tumours at plant wound sites and to benefit from this plant association b
78 abscess formation at S. aureus-infected skin wound sites and were also more susceptible to horizontal
80 ymes can inadvertently serve as reporters of wounded sites and constitute an "Achilles heel," allowin
81 athogens, clear tissue debris present at the wound site, and orchestrate aspects of tissue remodeling
82 healing, cells collectively migrate into the wound site, and the converging tissue fronts collide and
85 rocyte marker, GFAP, was up-regulated at the wound site, around necrotic areas and cysts, plus in usu
86 hed in this study showed that GF fill in the wound site at a significantly (P <0.0025) faster rate th
89 ifference in fibroblast proliferation at the wound site but Wnt signalling was highly upregulated in
90 y a critical role in leukocyte emigration to wound sites, but differences are evident in different va
91 egation contributes to arresting bleeding at wound sites, but may cause occlusion of atherosclerotic
94 ndard wound care) were randomly allocated to wound sites by a computer generated randomisation scheme
95 tudies suggest that IGF-I can concentrate at wound sites by binding to fibrin-immobilized IGFBP-3, an
96 EC monolayers, EPCs showed clustering at the wound site, compared with untreated regions (P < 0.001);
97 om the contralateral side of the limb to the wound site concomitantly with nerve deviation, the ectop
98 receptor CX3CR1 were both highly induced at wound sites; CX3CL1 colocalized with macrophages and end
99 lation) phenotype and a heightened basal and wound site DNA damage/repair response that is also commo
100 that excessive and prolonged TGFbeta1 at the wound site does not benefit wound healing, which is part
101 ) three-dimensional scaffold into an in vivo wound site effectively blocks the majority of organized
103 sis factor alpha, and IL-1beta) was lower at wound sites following marital conflicts than after socia
106 the technical difficulties in preparing the wound site for morphologic studies, and the postnatal ph
108 We found that epithelial cells near the wound site fuse to form a giant syncytium, which sends l
109 owth factor-beta (TGF-beta) signaling at the wound site has been implicated in re-epithelization, inf
110 ing of how platelets localize coagulation to wound sites has come mainly from studies of a subpopulat
111 emonstrated accumulation of m-calpain at the wound site in association with the membrane repair prote
113 RhoA and Cdc42 are rapidly activated around wound sites in a calcium-dependent manner and segregate
114 uitment of these inflammatory blood cells to wound sites in both Drosophila and vertebrates [1, 2].
115 led systemin is a primary signal released at wound sites in response to herbivory that systemically s
116 ith 5 mCi of (64)Cu-PTSM, whereas 96% of the wound sites in the group treated with saline had macrosc
117 Direct effects of CX3CR1 disruption at the wound site included marked reduction of macrophages and
118 he growth factor and cytokine profile at the wound site is changed, cell death is reduced, and dying
119 e resultant actomyosin array closes over the wound site, junctional F-actin and myosin-2 become mecha
120 in blast injuries, soft tissue injuries, >3 wound sites, loss of limb, abdominal trauma, and higher
127 We also show that hyperinnervation of the wound site, previously believed to be a consequence of i
129 on of proinflammatory cytokines at an actual wound site, providing in vivo data on the development of
130 e recruitment is restricted to the immediate wound site rather than spilling extensively into the adj
131 eutrophils and macrophages, recruited to the wound site, release reactive oxygen species by respirato
132 rmal wounding, tissue-bound cells around the wound site remain sessile and unresponsive, whereas circ
133 ha then recruits these EPCs to the cutaneous wound site, resulting in accelerated wound healing.
134 g in live mice to monitor macrophage flux at wound sites revealed that macrophage accumulation was pr
135 Histologic analysis of thrombospondin 2-null wound sites revealed the presence of an irregularly orga
136 issue injury, a fibrin network formed at the wound site serves as a scaffold supporting the early mig
137 lls, by cytokines present in the periodontal wound site, such as interleukin-1 (IL-1), may be an impo
138 ation and basement membrane breakdown at the wound site, suggest that MRL mice may share other featur
139 nted dentate gyrus and in macrophages at the wound site, suggesting a role in lesion-induced tissue r
140 ABA levels increased preferentially near the wound site, suggesting that ABA may have accumulated bec
141 wound-associated erythema, tenderness at the wound site, swelling at the site, purulent drainage, and
143 ision and apoptosis were not observed at the wound site, the needle puncture significantly enhanced D
144 atelets bind to exposed vascular matrix at a wound site through a highly specialized surface receptor
148 esulted in persistent PMN trafficking to the wound site via an IL-6-mediated mechanism, and this in t
153 e back of guinea pigs with a 4 mm punch, and wound sites were collected at different time points duri
156 ages, or their equivalents, are drawn to the wound site where they engulf cell and matrix debris and
157 ecruits these cells from the follicle to the wound site, where downstream Hh signal transduction is d
158 and CRK peptides, selectively accumulated at wound sites, where they partially co-localized with bloo
159 evokes Ca(2+)-regulated exocytosis near the wound site, which is essential for membrane resealing.
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