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1 nd-healing and reduce hair loss in acid-burn skin injury.
2 3A controls TLR3-mediated inflammation after skin injury.
3 orum sensing allows coordinated responses to skin injury.
4 e treatment to prevent or mitigate radiation skin injury.
5 g mechanisms of and treatments for radiation skin injury.
6 ry hair germ that proliferate in response to skin injury.
7 igh levels of autoreactive Ig contributes to skin injury.
8 The lag of stem cell activity is reversed by skin injury.
9 get for agents designed to block UVA-induced skin injury.
10 porcine normal and impaired animal models of skin injury.
11 repairing vasculature in areas of brain and skin injury.
12 n dose can reduce the likelihood and type of skin injury.
13 ted eyelids were examined daily for signs of skin injury.
14 re monitored daily for onset and duration of skin injury.
15 nocyte activation that occurs in response to skin injury.
16 n site, substantially reducing the extent of skin injury.
17 set of skin injury and the total duration of skin injury.
18 CD28 also downregulated IFN-I response upon skin injury.
19 s in immune complex-mediated peritonitis and skin injury.
20 mice display delayed wound healing following skin injury, a defect partly related to impaired keratin
21 oxorubicin cotreatments delayed the onset of skin injury and decreased the total duration of injury t
22 tential of CRF to prevent the development of skin injury and eyelid soreness after local doxorubicin
23 ide in the murine epidermis where they sense skin injury and serve as regulators and orchestrators of
24 models and emphasizes the role of mechanical skin injury and skin barrier dysfunction in eliciting al
25 ut their role in UV radiation (UVR)-mediated skin injury and subsequent tissue regeneration is less c
26 ings establish CCN1 as a critical opsonin in skin injury and suggest a therapeutic potential for CCN1
27 epidermal innate immune responses induced by skin injury and the involvement of EGFR for distinct AMP
30 role in the progression of radiation-induced skin injury, and that the injury can be mitigated by app
31 F signaling axis is activated in response to skin injury, and treatment of dermal wounds with isoxazo
32 been used in the treatment of full-thickness skin injuries as an allogenic dermal substitute providin
35 ies demonstrated that lupus serum IgG causes skin injury by involving the TNFR1 signaling pathway and
38 e first barrier exposed to radiation, though skin injury can progress over days to years following ex
40 CAR Tregs alleviated the alloimmune-mediated skin injury caused by transferring allogeneic peripheral
48 perienced severe respiratory distress and/or skin injury following cleaning operation of home aquaria
49 perienced severe respiratory distress and/or skin injury following cleaning operation of home aquaria
52 that TNFRI is involved in the expression of skin injury in MRL/lpr mice with lupus and that p60 PLAD
53 oural hypersensitivity that follows neonatal skin injury in rats and for the prolonged sensory change
56 xidative stress in delayed radiation-induced skin injury, including impaired wound healing, we tested
57 Here, we determined that TCR stimulation and skin injury induces IL-17A production by a subset of DET
61 leukin (IL)-1alpha, which are produced after skin injury, modulate bacterial adherence and the initia
62 th mild trauma with no evidence of overlying skin injury, no bony injury, and minimum cytokine respon
63 n, swelling, infection, risks of anesthesia, skin injury, nonresolution or worsening of symptoms, and
72 s changes in sensory neuropeptides following skin injury, thereby promoting vasodilation and wound he
73 uting, and granulation tissue formation upon skin injury, these activities were abrogated following p
75 1 cases of excessive swelling, nine cases of skin injury, two patients with infection, and two with p
76 he kinetics of wound closure following acute skin injury was similar in control and IR/IGF-1R(MKO) mi
77 eorganization of keratin filaments following skin injury, we propose that altered K16 expression affe
79 e directly recruited to polymer films within skin injuries, where they home to a perivascular niche a
82 oting the recruitment of MSCs to the site of skin injury, which in turn modulates inflammatory respon
84 ted with locoregional anatomical changes and skin injury, with the optimal antibiotic regimen introdu
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