ライフサイエンスコーパス: skin injury

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Skin injury is a deterministic effect of radiation.

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

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

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

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

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

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

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

70 Skin injury severely compromises the epidermal barrier a

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

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

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

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

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

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

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

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

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

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

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