ライフサイエンスコーパス: severe burn

1 ery contractility and relaxation following a severe burn.

2 muscle catabolism and osteopenia induced by severe burn.

3 ty and, hence, the survival of patients with severe burns.

4 potential utility in treating patients with severe burns.

5 that increases morbidity and mortality after severe burns.

6 intensive care unit, including patients with severe burns.

7 anding of the acute phase pathophysiology of severe burns.

8 tic fibrosis, compromised immune systems, or severe burns.

9 ned patients receiving delayed treatment for severe burns.

10 iture and muscle catabolism in patients with severe burns.

11 ity or corneal clarity in either moderate or severe burns.

12 ls and can improve bacterial clearance after severe burn, an injury that increases susceptibility to

13 Catabolism is associated with severe burn and leads to erosion of lean mass, impaired

14 Patients with severe burn and/or smoke inhalation injury suffer both s

15 Management of combat casualties with severe burns and associated traumatic injuries requires

16 the criterion standard for the treatment of severe burns and of late sequels after ingestion of corr

17 therapy, which can be expanded to treat less severe burns and other skin defects, such as chronic dia

18 Following severe burns and trauma injuries, the changes of neutrop

19 fter transplantation, a curative therapy for severe burns and, recently, diseases with epidermal loss

20 Severe burns are associated with a persistent hypermetab

21 Patients with severe burns are highly susceptible to bacterial infecti

22 Burn injuries, particularly severe burns, are accompanied by an immune and inflammat

23 Severe burn causes exaggerated muscle protein catabolism

24 Severe burn causes metabolic disturbances that can last

25 holamine-mediated hypermetabolic response to severe burns causes increased energy expenditure and mus

26 Presence of severe burns (common in high-voltage electrical injury),

27 d to resuscitate 32 subsequent patients with severe burns (computer decision support system group) an

28 acts the recovery of lean tissue following a severe burn, contributing to prolonged frailty in burn s

29 d artery dysfunction occurs within 6 h after severe burn, demonstrating decreased sensitivity to adre

30 orests helps meet evaporative demands unless severe burns disrupt internal tree structure and deplete

31 We hypothesize that severe burns disturb arterial contractility through acut

32 In this study, while some children surviving severe burns had lingering physical disability, most had

33 rstand the long-term systemic effects of non-severe burns in children, targeted mass spectrometry ass

34 are differentially regulated in response to severe burns in young animals.

35 ly important in patients, such as those with severe burns, in whom preserved renal concentrating abil

36 n expect patients younger than 55 years with severe burn injuries and inhalation injury to survive th

37 Immunodeficient patients with severe burn injuries are extremely susceptible to infect

38 simplest, effective anabolic strategies for severe burn injuries are: early excision and grafting of

39 The patient with severe burn injuries offers significant challenges to th

40 Thirteen patients were studied after severe burn injury (>60% total body surface area).

41 of 211 adult patients (age >= 18 years) with severe burn injury (>= 20% total body surface area) to g

42 cell responsiveness that occur subsequent to severe burn injury are not merely the result of global o

43 events intestinal barrier loss in a model of severe burn injury in which injury was associated with d

44 Severe burn injury induces satellite cell proliferation

45 Severe burn injury induces skeletal muscle regeneration

46 Severe burn injury is associated with vitamin D deficien

47 Patient survival after severe burn injury is largely determined by burn size.

48 A severe burn injury leads to marked hypermetabolism and c

49 for clinical studies to improve the care of severe burn injury patients.

50 Severe burn injury predisposes patients to burn wound in

51 Severe burn injury seriously affects multiple aspects of

52 e a key driver of immune cell dysfunction in severe burn injury through hyperinflammatory neutrophili

53 o injury could be selectively assessed after severe burn injury using humanized mice.

54 rone can ameliorate the muscle catabolism of severe burn injury with normal feedings.

55 etiology of lean tissue recovery following a severe burn injury.

56 could be a new predictor of sepsis onset in severe burn injury.

57 , as well as stimulating tissue repair after severe burn injury.

58 creased the early inflammatory response to a severe burn injury.

59 uginosa wound infection in a rodent model of severe burn injury.

60 on for treating insulin resistance following severe burn injury.

61 cted patients may help children survive very severe burn injury.

62 mortality in patients that have sustained a severe burn injury.

63 roves hepatic structure and function after a severe burn injury; insulin also restores hepatic homeos

64 The hypermetabolic response to severe burn is associated with increased energy expendit

65 cells, satellite cells, acutely following a severe burn is unknown and may contribute to the recover

66 Severe burns lead to insulin resistance, which is associ

67 h autograft-allograft closure is standard in severe burn management.

68 Critically ill patients or those with severe burns may have higher requirements.

69 A total of 1209 patients with severe burns (mean burn size, 33% of total body-surface

70 Twenty-five children with acute and severe burns (more than 40 percent of total body-surface

71 Severe burning of organic soils shifted tree dominance f

72 critical and life-threatening cases, such as severe burns on >30% of total body surface area and EB.

73 benefit in improving re-epithelialization in severe burns or visual acuity or corneal clarity in eith

74 ted disfigurements due to neurofibromatosis, severe burns, or ballistic trauma and had no relevant co

75 ents with paralysis, traumatic brain injury, severe burns, or trauma.

76 When given to children for 1 year after a severe burn, oxandrolone significantly improves lean bod

77 autosomal dominant disorder characterized by severe burning pain in response to mild warmth, has been

78 Severe burn patients are some of the most challenging cr

79 nty-first-century characteristics of IFDs in severe burn patients confirming known risk factors with

80 ografts represents a lifesaving strategy for severe burn patients, but their ultimate rejection limit

81 factors and outcomes in a 10-year cohort of severe burn patients.

82 t respiratory distress syndrome seen in some severe burn patients.

83 ose of insulin administered to patients with severe burns promoted skeletal muscle glucose uptake and

84 emonstrates the resilience of these soils to severe burning, providing important implications for pos

85 Severe burns result in cardiovascular dysfunction, but r

86 Severe burns result in profound skeletal muscle atrophy

87 ABSTRACT: Severe burns result in profound skeletal muscle atrophy;

88 Severe burns result in profound skeletal muscle atrophy;

89 KEY POINTS: Severe burns result in significant skeletal muscle cache

90 Severe burn results in muscle wasting affecting quality

91 Severe skin damage caused by severe burns, skin cancer, chemical accidents, and indus

92 In patients with severe burns, supplemental glutamine did not reduce the

93 ly first-line treatment in the management of severe burns that would not preclude subsequent use of a

94 After a severe burn, the liver plays a pivotal role by modulatin

95 in organ transplant rejection, major trauma, severe burns, the antiphospholipid syndrome, preeclampsi

96 Severe burn trauma is generally followed by a catabolic

97 at the pathophysiological stress response to severe burn trauma persists for several years after inju

98 s a sustained immunometabolic imprint of non-severe burn trauma, potentially linked to long-term immu

99 changes that occur in skeletal muscle after severe burn trauma.

100 for improving resistance to infections after severe burn trauma.

101 Severe burns trigger a hypermetabolic response that pers

102 e 'ecological catastrophes.' Landscape-scale severe burning was catastrophic from a tree overstory pe

103 Hypermetabolism associated with severe burns was thought to cease with wound healing and

104 or immediate wound coverage in children with severe burns without the associated risks of cadaver ski

105 nogenic strategy to improve clinical care of severe burn wounds.