ライフサイエンスコーパス: radiation injury

1 ween bone marrow and brain in the setting of radiation injury.

2 l metabolism and cytoprotective responses to radiation injury.

3 ept under extreme conditions of depletion or radiation injury.

4 t development and in normal lens response to radiation injury.

5 r selective normal tissue protection against radiation injury.

6 arrow (BM), which did not increase following radiation injury.

7 lenished by bone marrow precursors following radiation injury.

8 t part of the adaptation of keratinocytes to radiation injury.

9 lity to differentiate recurrent gliomas from radiation injury.

10 evels correlate with improved survival after radiation injury.

11 ization grade II-IV infiltrating gliomas and radiation injury.

12 regeneration, and are resistant to high-dose radiation injury.

13 is for distinguishing recurrent gliomas from radiation injury.

14 e eye is likely the most sensitive organ for radiation injury.

15 pendent compensatory proliferation following radiation injury.

16 tor of apoptosis) in apoptosis of HSCs after radiation injury.

17 nsible for long-term tissue damage following radiation injury.

18 ndin-1-null mice are remarkably resistant to radiation injury.

19 ased apoptosis alone and in combination with radiation injury.

20 equired for recovery of granulopoiesis after radiation injury.

21 vascular endothelium in the absence of acute radiation injury.

22 n(II) accumulation facilitates recovery from radiation injury.

23 l in tissue repair mechanisms resulting from radiation injury.

24 ructural, cellular, and molecular aspects of radiation injury.

25 aling pathways which is acutely sensitive to radiation injury.

26 e regeneration of hematopoietic tissue after radiation injury.

27 em cell survival and proliferation following radiation injury.

28 cal elements in the response of the brain to radiation injury.

29 ecialties to evaluate and manage large-scale radiation injuries.

30 After sublethal radiation injury (500 rad), the infusion of purified CD4

31 ecurrent tumors (all K-ratios >/= 1.70) from radiation injury (all K-ratios < 1.50) (100% sensitivity

32 mice showed minimal histological evidence of radiation injury and near full retention of mitochondria

33 jury is a prominent feature of normal tissue radiation injury and plays a critical role in both acute

34 tion of rhIL-11 ameliorates early intestinal radiation injury and support further development of rhIL

35 a offer new insight into the mechanism(s) of radiation-injury and suggest that CCR2 is a critical med

36 tors, such as dual oxidases, defense against radiation injuries, and novel proteins such as ZBP-89.

37 (e.g. bladder exstrophy, neurogenic bladder, radiation injury, and marked urethral dysfunction) or to

38 mors, the histologic changes associated with radiation injury, and the diagnostic and prognostic info

39 mal tissue or that facilitate the healing of radiation injury are being developed.

40 immune responses promote fibrosis following radiation injury, but the full spectrum of factors gover

41 ressed whether protection against intestinal radiation injury can be achieved by intraluminal adminis

42 Acute radiation injury can continue into a chronic phase or ch

43 imals, animals that received G-CSF following radiation injury exhibited enhanced functional brain rep

44 To protect against radiation injury from extravasation of therapeutic radio

45 PET has been used to differentiate radiation injury from malignancy on the basis of differe

46 crease) correctly differentiated tumors from radiation injury in all but 1 case (100% sensitivity and

47 arkedly decreases the deleterious effects of radiation injury in mesenchyme-derived tissues and prese

48 IL-17A as a hemopoietic response cytokine to radiation injury in mice and an inducible mechanism that

49 mediators has been proposed to contribute to radiation injury in normal tissues.

50 IL-11 to reduce manifestations of intestinal radiation injury in the clinic.

51 Radiation injury in the CNS has been linked to persisten

52 estinal morphology but are hypersensitive to radiation injury in the intestine compared with wild-typ

53 The cellular response to radiation injury in the intestine or bone marrow can be

54 2 (PGE2) synthesis modulates the response to radiation injury in the mouse intestinal epithelium thro

55 Radiation injury induced a dose-dependent decrease in th

56 Our results demonstrate that radiation injury induces early cytoskeletal remodeling,

57 treatment resulted in a 36% reduction in the radiation injury intestinal mucosal damage score, corres

58 Intestinal radiation injury is associated with overexpression of al

59 Intestinal radiation injury is dose limiting during abdominal and p

60 brain metastases (RPBM) from late or delayed radiation injury (LDRI).

61 ost interactions before and after small bowl radiation injury may eventually allow prediction of dise

62 of small intestinal epithelial cells in the radiation injury model.

63 eters were higher in tumors (n = 12) than in radiation injury (n = 10) (P </= 0.012 in all comparison

64 Radiation injury occurs in 5% to 37% of cases and can be

65 r (TbetaR-II) protein ameliorates intestinal radiation injury (radiation enteropathy).

66 We conclude that radiation injury results in increased Cox-1 levels in cr

67 stations of radiation enteropathy, including radiation injury score (6.5 +/- 0.6 in the vehicle group

68 Anterior thalamic radiation injury showed correlation with decreased proce

69 The overt pathologies of radiation injury such as white matter necrosis or vascul

70 Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes

71 trategy may be limited by the possibility of radiation injury, the results are consistent with the pa

72 mor efficacy of radiation without increasing radiation injury to normal tissue.

73 early diagnosis, and management of potential radiation injury to the liver and to other organs.

74 ECT biomarkers have the potential to predict radiation injury to the lungs before substantial functio

75 is unlikely to result in acute or long-term radiation injury to the patient or to a measurable incre

76 The acute phase of radiation injury to the rectum occurs during or up to 3

77 ies will be highly useful for characterizing radiation injury to the spinal cord and illuminate our u

78 Understanding how initial radiation injury translates into long-term effects is an

79 Marrow Transplantation have established the Radiation Injury Treatment Network (RITN), a voluntary c

80 Acute radiation injury typically occurs 2 weeks to 3 months af

81 rovide comprehensive evaluation and care for radiation injury victims.

82 Radiation injury was assessed at 6 weeks using quantitat

83 computerized image analysis, and structural radiation injury was assessed by quantitative histopatho

84 In the setting of radiation injury, we find dynamic fluctuations in marrow

85 ellular, and molecular aspects of intestinal radiation injury were assessed.

86 icacy of a single FSL-1 dose for alleviating radiation injury while protecting against adverse effect

87 Postn(-/-) mice recover faster from radiation injury with concomitant loss of primitive HSCs