ライフサイエンスコーパス: severe burn

1 muscle catabolism and osteopenia induced by severe burn.

2 that increases morbidity and mortality after severe burns.

3 intensive care unit, including patients with severe burns.

4 anding of the acute phase pathophysiology of severe burns.

5 ned patients receiving delayed treatment for severe burns.

6 iture and muscle catabolism in patients with severe burns.

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

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

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

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

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

12 Severe burns are associated with a persistent hypermetab

13 Patients with severe burns are highly susceptible to bacterial infecti

14 Severe burn causes exaggerated muscle protein catabolism

15 Severe burn causes metabolic disturbances that can last

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Severe burn injury induces satellite cell proliferation

30 Severe burn injury induces skeletal muscle regeneration

31 Severe burn injury is associated with vitamin D deficien

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

33 A severe burn injury leads to marked hypermetabolism and c

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

35 Severe burn injury predisposes patients to burn wound in

36 Severe burn injury seriously affects multiple aspects of

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

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

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

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

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

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

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

44 on for treating insulin resistance following severe burn injury.

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

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

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

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

49 Severe burns lead to insulin resistance, which is associ

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

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

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

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

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

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

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

57 Severe burn patients are some of the most challenging cr

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

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

60 Severe burns result in profound skeletal muscle atrophy

61 Severe burns result in profound skeletal muscle atrophy;

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

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

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

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

66 Severe burn trauma is generally followed by a catabolic

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

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

69 for improving resistance to infections after severe burn trauma.

70 Severe burns trigger a hypermetabolic response that pers

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

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

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

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