ライフサイエンスコーパス: pulmonary injury

1 uring S. aureus pneumonia, inducing necrotic pulmonary injury.

2 edical disorders such as cardiac failure and pulmonary injury.

3 cruitment of leukocytes, and immune-mediated pulmonary injury.

4 e clinical relevance of elevated histones in pulmonary injury.

5 ypoxia-reoxygenation-induced exacerbation of pulmonary injury.

6 atment was started 5-7 d after initiation of pulmonary injury.

7 role in regulating inflammatory responses to pulmonary injury.

8 ptase (TERT) deficiency in a murine model of pulmonary injury.

9 The dose-limiting toxicity was diffuse pulmonary injury.

10 ions, preserving systemic oxygenation during pulmonary injury.

11 provides potent protection against ischemic pulmonary injury.

12 mph duct ligation (LDL) before T/HS prevents pulmonary injury.

13 +) T cells in vivo abolishes the type 2-like pulmonary injury.

14 e aggregation, activation, and microvascular pulmonary injury.

15 ed to otherwise healthy animals resulting in pulmonary injury.

16 ctions, was tested for the ability to reduce pulmonary injury.

17 nto the plasma and by indices of gastric and pulmonary injury.

18 concomitant with attenuation of hepatic and pulmonary injury.

19 immunologic, infectious, ischemic, and toxic pulmonary injuries.

20 e first 8 patients had fatal regimen-related pulmonary injury, a complication not found among 11 subs

21 The evolution of BPD from a disorder of pulmonary injury affecting moderately preterm infants, t

22 of the role of proinflammatory cytokines in pulmonary injury after ARF, the anti-inflammatory cytoki

23 Lethal pulmonary injury after bleomycin treatment was higher in

24 contributes to the attenuation of HPV and to pulmonary injury after challenge with endotoxin.

25 accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating h

26 in impaired bacterial clearance and worsened pulmonary injury and death.

27 C and bacterial clearance, resulting in less pulmonary injury and decreased death.

28 were treated with bleomycin or vehicle, and pulmonary injury and fibrotic responses were compared.

29 In contrast, all of these pulmonary injury and inflammatory parameters were increa

30 quelae that contributes to radiation-induced pulmonary injury and IPF.

31 in reduction (P</=.05) of organism-mediated pulmonary injury and of pulmonary infiltrates detected b

32 We examined the role of CXCR3 in pulmonary injury and repair in vivo.

33 plays a central role in free radical-induced pulmonary injury and repair.

34 conclusion, radiation- and bleomycin-induced pulmonary injury and respiratory death are ameliorated b

35 close correlation between the development of pulmonary injury and TNF-alpha levels in this model of s

36 events correlate with evidence of histologic pulmonary injury and underscore the role of adhesion mol

37 alveolar lavage fluid after asbestos-induced pulmonary injury, and this response is markedly enhanced

38 Host mediated damage is also a culprit in pulmonary injury as both innate and adaptive immune cell

39 ith metastatic breast cancer, mice developed pulmonary injury as early as 1 day posttransplant.

40 Pulmonary injury, as defined by an increase in bronchoal

41 ective against permeability edema and remote pulmonary injury but not protective against histologic m

42 Arterial air emboli arising from severe pulmonary injury can cause ischaemic complications-espec

43 In murine intra-abdominal sepsis, pulmonary injury cannot be considered the etiology of de

44 Neurogenic vasoplegia exacerbates the pulmonary injury caused by brain death and primes the lu

45 ve in a rat model of sepsis-induced indirect pulmonary injury (cecal ligation and puncture).

46 rtment exhibited increased survival and less pulmonary injury compared with the appropriate wild-type

47 at neutrophil extracellular traps exacerbate pulmonary injury during influenza pneumonia.

48 ic effects of extracellular histones in that pulmonary injury during influenza was exacerbated.

49 ICAM-1 after the induction of AP ameliorates pulmonary injury, even in the face of severe pancreatic

50 esolution of established neutrophil-mediated pulmonary injury evoked by intratracheal instillation or

51 several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well a

52 pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorder

53 We have examined CD8(+) T cell-mediated pulmonary injury in a transgenic model in which adoptive

54 o be significant mediators of pancreatic and pulmonary injury in pancreatitis, and both the onset and

55 mphocytes (CTLs) produce lethal, progressive pulmonary injury in recipient mice expressing the viral

56 We have used the silica-induced model of pulmonary injury in the rat to study the pattern of coll

57 Ventilation of cadaver lungs with AG induces pulmonary injury in this model.

58 toxin challenge preserved HPV and attenuated pulmonary injury in wild-type mice but did not prevent t

59 acute absence of kidney function results in pulmonary injury independent of renal ischemia and highl

60 Pulmonary injury induced by isolated alpha-hemolysin or

61 on of oncogenic K-Ras in mouse lung elevated pulmonary injury, inflammation and tumorigenesis, but re

62 ocus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by expos

63 We hypothesized that pulmonary injury is associated with hepatic ischemia-rep

64 ting diseases such as human asthma, in which pulmonary injury is associated with the activity of IL-5

65 We also proposed that this remote pulmonary injury is attenuated through inactivation of c

66 We conclude that remote pulmonary injury is significantly decreased by concomita

67 We conclude that remote pulmonary injury is significantly influenced by the exte

68 es are complicated by the presence of severe pulmonary injury, massive blood loss, significant fluid

69 IAV, virus clearance, and the development of pulmonary injury, neutrophils can serve as APCs to anti-

70 CD4 T cells only, CD8 T cells only, or both, pulmonary injury occurs via different paths, depending o

71 .40; p = .02) and among subjects with direct pulmonary injury (OR, 1.75; 95% CI, 1.04-2.95; p = .04).

72 betes (ORadj 0.58, 95% CI 0.36-0.92), direct pulmonary injury (ORadj 3.78, 95% CI 2.45-5.81), hematol

73 eutic targets, since pancreatitis-associated pulmonary injury results in significant morbidity and is

74 bone marrow also confers protection against pulmonary injury, revealing that PPT-A gene expression i

75 In different models of pulmonary injury, SOD3 is reduced; however, it is unclea

76 rugs do not directly inhibit immune-mediated pulmonary injury that is a significant component of dise

77 ld-type newborn mice resulted in significant pulmonary injury that was prevented by deletion of TLR4

78 ssing NY1DD mice with Rag1(-/-) mice reduced pulmonary injury that was restored by adoptive transfer

79 important chemotherapy and radiation-induced pulmonary injuries, the pathologic mechanisms, where kno

80 4-5 day course of the development of lethal pulmonary injury, the effector CTLs, while necessary for

81 f p38 mitogen activated kinase decreases the pulmonary injury through attenuated production of TNF-al

82 Pulmonary injury was assessed at 24 hrs by histology and

83 Each of these variables of pulmonary injury was lessened in animals receiving CNI-1

84 Pancreatic and pulmonary injury was quantitated by histology, measureme

85 ose-dependent manner, and the pancreatic and pulmonary injuries were much severer in HTG mice than no