ライフサイエンスコーパス: skin injury

1 aprophyticus, also prevent S. aureus-induced skin injury.

2 temporal stages of clinical and pathological skin injury.

3 dies that seek to mitigate radiation-induced skin injury.

4 the potential for negative impact, including skin injury.

5 ic approach for preventing radiation-induced skin injury.

6 g is required in the induction of AVPs after skin injury.

7 last fate during the physiologic response to skin injury.

8 nd-healing and reduce hair loss in acid-burn skin injury.

9 CD28 also downregulated IFN-I response upon skin injury.

10 3A controls TLR3-mediated inflammation after skin injury.

11 orum sensing allows coordinated responses to skin injury.

12 e treatment to prevent or mitigate radiation skin injury.

13 g mechanisms of and treatments for radiation skin injury.

14 ry hair germ that proliferate in response to skin injury.

15 igh levels of autoreactive Ig contributes to skin injury.

16 The lag of stem cell activity is reversed by skin injury.

17 get for agents designed to block UVA-induced skin injury.

18 porcine normal and impaired animal models of skin injury.

19 repairing vasculature in areas of brain and skin injury.

20 n dose can reduce the likelihood and type of skin injury.

21 ted eyelids were examined daily for signs of skin injury.

22 re monitored daily for onset and duration of skin injury.

23 nocyte activation that occurs in response to skin injury.

24 n site, substantially reducing the extent of skin injury.

25 set of skin injury and the total duration of skin injury.

26 s in immune complex-mediated peritonitis and skin injury.

27 .g., by COVID-19 healthcare workers leads to skin injuries.

28 onged durations, resulting in device-induced skin injuries.

29 ) had status epilepticus, 20 of 99 (20%) had skin injuries, 53 of 99 (54%) underwent neurosurgical in

30 mice display delayed wound healing following skin injury, a defect partly related to impaired keratin

31 Skin injuries across the body continue to disrupt everyd

32 other skin simulants to assess the onset of skin injuries and the ability of padding to prevent them

33 LL37 is produced by skin injury and bacterial infection and plays an importa

34 oxorubicin cotreatments delayed the onset of skin injury and decreased the total duration of injury t

35 tential of CRF to prevent the development of skin injury and eyelid soreness after local doxorubicin

36 aluronan (HA) catabolism is activated during skin injury and fibroblast-to-adipocyte differentiation

37 d the induction and regulation of AVPs after skin injury and identified a key role of TRPV1 in this p

38 ide in the murine epidermis where they sense skin injury and serve as regulators and orchestrators of

39 Skin injury and several diseases elicit fibrosis and ind

40 models and emphasizes the role of mechanical skin injury and skin barrier dysfunction in eliciting al

41 ut their role in UV radiation (UVR)-mediated skin injury and subsequent tissue regeneration is less c

42 ings establish CCN1 as a critical opsonin in skin injury and suggest a therapeutic potential for CCN1

43 epidermal innate immune responses induced by skin injury and the involvement of EGFR for distinct AMP

44 injection site to determine day of onset of skin injury and the total duration of skin injury.

45 cluded the total number of dressing changes, skin injury, and CVC failure.

46 tral HPA axes in the context of homeostasis, skin injury, and inflammatory skin disorders.

47 role in the progression of radiation-induced skin injury, and that the injury can be mitigated by app

48 proliferation, and differentiation following skin injury, and thereby reexamine the canonical phases

49 F signaling axis is activated in response to skin injury, and treatment of dermal wounds with isoxazo

50 been used in the treatment of full-thickness skin injuries as an allogenic dermal substitute providin

51 is the development of acute inflammation and skin injury at the injection site.

52 lls in hair follicles can be activated after skin injury by fatty acids released from adipocytes.

53 ediated protection against radiation-induced skin injury by inhibiting ROS production.

54 ies demonstrated that lupus serum IgG causes skin injury by involving the TNFR1 signaling pathway and

55 derlying amplification of ROS and consequent skin injury by radiation.

56 Overall, the results show that skin injury can be reduced by using softer mask material

57 These results show that early skin injury can cause prolonged changes in central senso

58 e first barrier exposed to radiation, though skin injury can progress over days to years following ex

59 ch significantly attenuate lewisite-mediated skin injury, can serve as potent antidotes.

60 characterized the molecular pathogenesis of skin injury caused by additionally structurally distinct

61 th epidermal barrier defects, dysbiosis, and skin injury caused by scratching.

62 CAR Tregs alleviated the alloimmune-mediated skin injury caused by transferring allogeneic peripheral

63 The major mechanism of skin injury common to these exposures is radiation-induc

64 f Doxil resulted in significant reduction of skin injury compared with doxorubicin alone.

65 This treatment did not result in increased skin injury compared with doxorubicin alone.

66 e systems entail risks of causing iatrogenic skin injuries, complicating clinical care and impeding s

67 Following skin injury, DETC-derived IL-17A induced expression of m

68 In contrast, following neonatal skin injury, dorsal horn cell receptive field sizes were

69 Taken together, skin injury, dysbiosis, and filaggrin deficiency trigger

70 ht to determine the mechanisms through which skin injury, dysbiosis, and increased epidermal IL-1alph

71 mation (15 [24%] vs 48 [55%]), and radiation skin injury (eight [13%] vs 27 [31%]).

72 After skin injury, endothelial cells and fibroblasts provision

73 IL-33 is released after mechanical skin injury, enhances IgE-mediated MC degranulation, and

74 istopathology reveals that radiation-induced skin injury features temporally unique inflammatory chan

75 perienced severe respiratory distress and/or skin injury following cleaning operation of home aquaria

76 from S. felis significantly reduced necrotic skin injury from MRSP infection.

77 In response to skin injury, hair-follicle stem cells (HFSCs), normally

78 Our findings suggest that upon skin injury, HFSCs establish a temporary protective netw

79 In an excisional skin injury in a diet-induced diabetic murine model, we

80 tigate whether TNFR PLAD limits inflammatory skin injury in a mouse model of SLE.

81 otherapy-related adverse event was radiation skin injury in both groups (five [6%] of 89 in the NBTXR

82 Furthermore, we show that on acute skin injury in both human and murine settings, this tran

83 AVPs, including Oas2, Oasl2, and Isg15 after skin injury in mice.

84 that TNFRI is involved in the expression of skin injury in MRL/lpr mice with lupus and that p60 PLAD

85 oural hypersensitivity that follows neonatal skin injury in rats and for the prolonged sensory change

86 th SLE, yet the etiology and pathogenesis of skin injury in SLE remains unclear.

87 D (p80 PLAD) protein significantly inhibited skin injury in the MRL/lpr mouse model of lupus.

88 xidative stress in delayed radiation-induced skin injury, including impaired wound healing, we tested

89 profiling of cutaneous wounds revealed that skin injury induces high levels of AVPs in both mice and

90 Here, we determined that TCR stimulation and skin injury induces IL-17A production by a subset of DET

91 s related to blood flow along with an ABM of skin injury, inflammation, and ulcer formation.

92 3 by cutaneous MCs in response to mechanical skin injury inhibits the T(H)1 cell response to cutaneou

93 eriments in mice that adipocytes adjacent to skin injury initiate lipid release necessary for macroph

94 Radiation-induced skin injury is a common side effect of radiotherapy and

95 Skin injury is a deterministic effect of radiation.

96 shows that timely tissue regeneration after skin injury is dependent on endothelial TLR2 for robust

97 ath on Ripk3(-/-) background in a mechanical skin injury model in mice.

98 results in enhanced angiogenesis in a mouse skin injury model.

99 ocalize to activated complement in a primate skin injury model.

100 scaffolds facilitated tissue repair in large skin injury models.

101 leukin (IL)-1alpha, which are produced after skin injury, modulate bacterial adherence and the initia

102 th mild trauma with no evidence of overlying skin injury, no bony injury, and minimum cytokine respon

103 n, swelling, infection, risks of anesthesia, skin injury, nonresolution or worsening of symptoms, and

104 ut only 14% of those cages with fighting had skin injuries observable from cage-side.

105 No bruising, ulceration, or other skin injuries occurred, even after a third injection reg

106 Three skin injuries occurred: one in the intervention (blister

107 Skin injury of ft/ft mice induced chronic skin inflammat

108 Skin injury of wild-type, ft/ft, and myeloid differentia

109 ulated form of doxorubicin did not result in skin injury or ulceration.

110 s of localized inflammation, discomfort, and skin injury over the injection site.

111 In mouse models of COPD, lung fibrosis and skin injury, reduced expression of PRMT7 associates with

112 espite the technological advances, radiation skin injury remains a significant problem.

113 In conclusion, ultraviolet skin injury results in increased production and depositi

114 phagia (20 [32%] vs 36 [40%]), and radiation skin injury (seven [11%] vs 21 [24%]).

115 Skin injury severely compromises the epidermal barrier a

116 Child abuse may manifest as skin injuries, skeletal trauma, head injury, or many oth

117 Corroborating these findings, F-PRT reduced skin injury, stem cell depletion, and inflammation, miti

118 zing sentinel injuries, all of them included skin injuries, such as bruises, hematoma, or burns, but

119 When we performed skin injuries that are known to mobilize young HFSCs to

120 In a mouse model of skin injury that shares some features of cutaneous lupus

121 regulating Il17a expression after mechanical skin injury, thereby counteracting the adverse effect of

122 s changes in sensory neuropeptides following skin injury, thereby promoting vasodilation and wound he

123 uting, and granulation tissue formation upon skin injury, these activities were abrogated following p

124 Also, bulge Brg1 is activated by skin injury to facilitate early epidermal repair.

125 1 cases of excessive swelling, nine cases of skin injury, two patients with infection, and two with p

126 tion is the holy grail of tissue repair, but skin injury typically yields fibrotic, non-functional sc

127 he kinetics of wound closure following acute skin injury was similar in control and IR/IGF-1R(MKO) mi

128 eorganization of keratin filaments following skin injury, we propose that altered K16 expression affe

129 Signs of skin injury were minimal; there were small or no adverse

130 e directly recruited to polymer films within skin injuries, where they home to a perivascular niche a

131 Pressure ulcers (PUs) are serious skin injuries whereby the wound healing process is frequ

132 Local skin injury, which constituted the portal entry, was pre

133 oting the recruitment of MSCs to the site of skin injury, which in turn modulates inflammatory respon

134 nfection that can result in inflammation and skin injury with highly variable and unpredictable clini

135 grow as a result of the aberrant healing of skin injuries, with no effective treatment.

136 Scarring is a lifelong consequence of skin injury, with scar stiffness and poor appearance pre

137 ted with locoregional anatomical changes and skin injury, with the optimal antibiotic regimen introdu