ライフサイエンスコーパス: burn wound

1 in both murine full-thickness excisional and burn wounds.

2 strategy to improve clinical care of severe burn wounds.

3 this study focused on shock wave effects in burn wounds.

4 zation and skin regeneration in third-degree burn wounds.

5 re them to combat infections in contaminated burn wounds.

6 t microbial organisms isolated from infected burn wounds.

7 pathogenesis of P. aeruginosa infections in burn wounds.

8 nt role of the soxR gene in the infection of burn wounds.

9 activity in wound fluid obtained from acute (burn) wounds.

10 nist accelerates re-epithelialization in pig burn wounds (100% re-epithelialization in antagonist-tre

11 e treatment to the superficial second-degree burn wound after debridement/topical antiseptic therapy

12 shown the abilities to prevent infection of burn wound, aid healing, and an anti-inflammatory dressi

13 s study, we utilize a panel of P. aeruginosa burn wound and cystic fibrosis (CF) lung isolates to dem

14 mited bacterial growth and spread within the burn wounds and a decrease in systemic dissemination of

15 ximize therapeutic success for patients with burn wounds and chronic wound disorders.

16 appeared in the dermis of skin bordering the burn wound, and further increased in response to wound i

17 slands of regenerating epithelium within the burn wound, and in the duct and proximal tubules of eccr

18 uscitation, respiratory support, care of the burn wound, and long range evacuation.

19 iety of diseases, including cystic fibrosis, burn wounds, and chronic suppurative otitis media.

20 maintain tissue perfusion, early excision of burn wounds, and rapid wound coverage.

21 Burn wounds are prone to infection by Pseudomonas aerugi

22 efficiently on burn wounds, suggesting that burn wounds are purine-deficient environments.

23 en-activated protein kinase inhibitor to the burn wound attenuated pulmonary neutrophil infiltration

24 opolymers, can facilitate closure of massive burn wounds by increasing the availability of autologous

25 guidelines along with the standardization of burn wound care and continued provider education have re

26 g represents a breakthrough in second-degree burn wound care.

27 d to provide an extended period of temporary burn wound coverage.

28 ing the use of this technology with standard burn wound coverage.

29 d December 2007 to receive standard therapy (burn wound debridement/topical antiseptic therapy) with

30 Here we demonstrate that the presence of a burn wound dramatically affects expression of both human

31 An adhesive yet easily removable burn wound dressing represents a breakthrough in second-

32 Current second-degree burn wound dressings absorb wound exudate, reduce bacter

33 MMP-1 accumulates in the fluid phase of the burn wound environment within 2 d of injury and reaches

34 RON protein was markedly upregulated in burn wound epidermis and accessory structures, in prolif

35 The primary endpoint, time to complete burn wound epithelialization, was determined by independ

36 Finally, early burn wound excision and coverage with new biodegradable

37 Standard burn care with early burn wound excision and grafting.

38 eparin-binding growth factors was studied in burn wound fluid (BWF) from 45 pediatric patients who ha

39 nsepidermal water loss every 12 hours on the burn wounds for 72 hours postburn.

40 Infection of the burn wound has always been a major factor in retardation

41 e data support a role for PDGF and HB-EGF in burn wound healing and suggest that the response to inju

42 Hydrogel treatment accelerated third-degree burn wound healing by rapid wound closure, improved re-e

43 cells (ASCs) accelerates the process of acid burn wound-healing.

44 he mechanism of EPO action on the healing of burn wounds in the skin of pigs with experimentally indu

45 lg not only accelerates the healing of acute burn wounds in wild-type mice, but also improves the hea

46 cutoff values were determined for mortality, burn wound infection (at least two infections), sepsis (

47 insulin improves outcome following a lethal burn wound infection are not known, the data suggest tha

48 Resistance to burn wound infection could also be conferred to recipien

49 hGSTA4 expression negatively correlates with burn wound infection episodes per patient.

50 ort a fatal case of S. erythrospora invasive burn wound infection in a 26-year-old male injured durin

51 se the resistance of mice to a P. aeruginosa burn wound infection through both stimulation of dendrit

52 tion to increase the resistance of mice to a burn wound infection with Pseudomonas aeruginosa, a comm

53 cial role in the pathogenesis of PA14 during burn wound infection, most likely by contributing to PA1

54 to the pathogenesis of P. aeruginosa during burn wound infection.

55 acteria in a model of Pseudomonas aeruginosa burn wound infection.

56 of neutrophils in FL-mediated resistance to burn wound infection.

57 critical role in FL-mediated resistance to a burn wound infection.

58 the outcome of rats in response to a lethal burn wound infection.

59 nontreated mice did not confer resistance to burn wound infection.

60 icantly increased survival upon a subsequent burn wound infection.

61 determine the effect of fluid group on AKI, burn wound infections (BWIs), and pneumonia.

62 useful tool in studying the pathogenicity of burn wound infections and in evaluating the efficacy of

63 d (FL) significantly increases resistance to burn wound infections in a DC-dependent manner that is c

64 Severe burn injury predisposes patients to burn wound infections that can disseminate, lead to unco

65 ual involvement in nosocomial and especially burn wound infections.

66 al p38 MAPK inhibition significantly reduced burn wound inflammatory signaling and subsequent systemi

67 We hypothesized that topical attenuation of burn wound inflammatory signaling will control the derma

68 We propose that the depth of a burn wound is a sum of the thermal energy applied and of

69 es of severely burned patients with infected burn wounds is not known.

70 Failure to close a massive burn wound leads to sepsis and multiple system organ fai

71 sight into the local effects of Flt3L at the burn wound, localization of Langerhans cells was examine

72 Full-thickness paravertebral burn wounds measuring 36 cm2 were created on 11 farm swi

73 n limited because of their susceptibility to burn wound microorganisms as a result of their lack of a

74 terial infection in an in vivo second-degree burn wound model.

75 We first developed a procedure to treat burn wounds on mice with dextran hydrogels.

76 ical inhibition of inflammatory signaling in burn wounds reduced systemic inflammatory response and b

77 uginosa is extremely efficient at colonizing burn wounds, spreading systemically, and causing sepsis,

78 inosa was unable to replicate efficiently on burn wounds, suggesting that burn wounds are purine-defi

79 on of the ptrA during the infection of mouse burn wound suggests that P. aeruginosa has evolved tight

80 By day 21, burn wounds treated with hydrogel developed a mature epi

81 opportunities to simplify the management of burn wound treatment.

82 g opportunities to improve the management of burn wound treatment.

83 Approaches to optimise healing potential of burn wounds use targeted wound care and surgery to minim

84 Edema in the burn wound was not affected by treatment, while hyperton

85 ithelialization of partial thickness porcine burn wounds was blocked following treatment with EGFR in

86 HB-EGF in the surface epithelium of burn wounds was uniformally distributed, whereas it was

87 ten used as a disinfectant and treatment for burn wounds, we present here an important fitness factor

88 Burn wounds were topically inoculated with a lethal dose

89 Adult burn wounds, which lack hyaluronan (HA), often undergo e

90 Inflammatory source control in burn wounds with topical p38 mitogen-activated protein k

91 Therefore, adding a HA derivative to burn wounds would better mimic the fetal extracellular m