ライフサイエンスコーパス: VOD

1 ere lower in the nonsirolimus arm (9% vs 21% VOD, P = .05; 1% vs 10% TMA, P = .06).

2 Mortality after VOD diagnosis was unaffected, and overall treatment-rela

3 ermine the association between sirolimus and VOD.

4 n six patients with histologically confirmed VOD who had progressive jaundice and ascites.

5 Alternatively, the vegetation optical depth (VOD) parameter from satellite passive microwave remote s

6 tions in microwave vegetation optical depth (VOD), which is directly related to leaf water potential.

7 Of 62 patients, 13 (21%) developed VOD; 9 (64%) of 14 with prior GO exposure developed VOD

8 total of 257 patients on TG (25%) developed VOD or disproportionate thrombocytopenia and switched to

9 of gemtuzumab ozogamicin; 6 (40%) developed VOD.

10 (64%) of 14 with prior GO exposure developed VOD compared with 4 (8%) of 48 without prior GO exposure

11 on 3.5 months or less following GO developed VOD compared with none of 4 patients who underwent SC tr

12 able analysis of risk factors for developing VOD, pretransplant HCV infection associated with elevate

13 splantation increases the risk of developing VOD.

14 stration are at increased risk of developing VOD.

15 Rates of veno-occlusive disease (VOD) and thrombotic microangiopathy (TMA) were lower in

16 ), previously called veno-occlusive disease (VOD) can be a difficult problem after hematopoietic cell

17 e noted an excess of veno-occlusive disease (VOD) in a clinical trial, and retrospectively reviewed t

18 Hepatic veno-occlusive disease (VOD) is a common complication of high-dose chemotherapy

19 Hepatic veno-occlusive disease (VOD) is one of the most serious complications following

20 Hepatic veno-occlusive disease (VOD) is the most common of the regimen-related toxicitie

21 Veno-occlusive disease (VOD) is the most common regimen-related toxicity accompa

22 Hepatic veno-occlusive disease (VOD) is the most serious regimen-related toxicity after

23 Veno-occlusive disease (VOD) is the third leading cause of mortality after bone

24 at 9 mg/m2 developed veno-occlusive disease (VOD) of the liver and defined the dose-limiting toxicity

25 incidence of hepatic veno-occlusive disease (VOD) was 5% for IV-BU and 1% with TBI (P < .001).

26 Hepatic veno-occlusive disease (VOD), also called sinusoidal obstruction syndrome (SOS),

27 nt of severe hepatic veno-occlusive disease (VOD), showing a 23% improvement in day +100 survival aft

28 cognition of hepatic veno-occlusive disease (VOD).

29 ity (DLT), including veno-occlusive disease (VOD).

30 rrence and severity of venocclusive disease (VOD); (2) the impact of HCV infection on liver dysfuncti

31 atitis (33%), hepatic venoocclusive disease (VOD) (5%), and pulmonary toxicity (4%).

32 Hepatic venoocclusive disease (VOD) is a common, life-threatening complication of bone

33 to the development of venoocclusive disease (VOD).

34 icity (one death from venoocclusive disease [VOD]) developed in 11 patients during CTCb, the interval

35 (SD), oven drying (OD), vacuum oven drying (VOD) and freeze drying (FD) for tomatoes (Solanum lycope

36 Patients had clinically established VOD and met risk criteria predicting progression and fat

37 ent with GO as a significant risk factor for VOD (odds ratio [OR], 21.6; 95% confidence interval [CI]

38 Risk factors for VOD are well established, but the biology of the syndrom

39 Treatment for VOD using rh-tPA and heparin was successful in 29% of pa

40 must balance the absolute risk of death from VOD against the risks of the underlying disease.

41 or the calculated probability of dying from VOD on the day treatment with rh-tPA and heparin was beg

42 lculated probability of a fatal outcome from VOD could discriminate responders from nonresponders.

43 had grade 3 or 4 hepatotoxicity, and two had VOD, without meeting DLT criteria.

44 brotide in patients with established hepatic VOD/SOS and advanced MOF.

45 as shown promising efficacy treating hepatic VOD/SOS with MOF in phase 2 studies.

46 Untreated hepatic VOD/SOS with multi-organ failure (MOF) is associated wit

47 ttempted for a few patients with intractable VOD, but this approach is limited by availability of a c

48 ents with venocclusive disease of the liver (VOD) after marrow transplantation using recombinant huma

49 one with persistent histological changes of VOD.

50 nts who underwent TIPS late in the course of VOD did not demonstrate any clinical improvement after T

51 inning a median of 6 days after diagnosis of VOD, DF was administered intravenously in doses ranging

52 eived GO prior to SC transplantation died of VOD.

53 The duration of VOD recovery to pre-burn conditions was also directly pr

54 es the pathogenesis and clinical features of VOD, with an emphasis on endothelial cell injury and ris

55 is associated with an increased incidence of VOD (OR 2.35, P = .005).

56 osystemic shunt (TIPS) for the management of VOD after BMT TIPS was performed in six patients with hi

57 gated the role of PAI-1 in a murine model of VOD produced by long-term nitric oxide synthase inhibiti

58 While the pathogenesis of VOD is uncertain, plasminogen activator inhibitor-1 (PAI

59 better understanding of the pathogenesis of VOD will lead to more effective prevention and treatment

60 rged as a diagnostic marker and predictor of VOD in humans.

61 e was associated with an even higher rate of VOD (OR 8.8, P = .008).

62 Resolution of VOD (bilirubin <2 mg/dL with improvement in other sympto

63 Complete resolution of VOD was seen in 36%, with 35% survival at day +100.

64 was not associated with an increased risk of VOD (OR 1.55, P = .33).

65 ived rh-tPA and heparin for the treatment of VOD between February 1991 and December 1995 were reviewe

66 al target in the prevention and treatment of VOD in humans.

67 analyzed a multi-year (2003-2010) satellite VOD record from the NASA AMSR-E (Advanced Microwave Scan

68 Severe VOD complicated by multisystem organ failure (MOF) remai

69 Severe VOD developed in 22 of 46 (48%) evaluable patients with

70 Nineteen patients who developed severe VOD after SCT were treated with DF on a compassionate-us

71 Eighty-eight patients who developed severe VOD after SCT were treated with DF under a defined treat

72 achman-Diamond syndrome who developed severe VOD.

73 vels is a significant risk factor for severe VOD after marrow transplant.

74 emic properties, in the treatment for severe VOD has suggested safety and activity.

75 spective evaluation of DF therapy for severe VOD should allow better definition of predictors of resp

76 transplant was not a risk factor for severe VOD.

77 minogen activator (t-PA) and heparin, severe VOD is almost uniformly fatal.

78 ) levels predicted the development of severe VOD (relative risk, 9.6; P =.0001).

79 treatment-related death secondary to severe VOD.

80 ustifiable approach in a patient with severe VOD post-BMT.

81 sing tPA and heparin in patients with severe VOD who have already developed multiorgan dysfunction.

82 V infection on liver dysfunction, other than VOD, occurring between 21 and 60 days after transplantat

83 The VOD lag was attributed to slower non-photosynthetic (woo

84 The VOD record indicated initial post-fire canopy biomass re

85 e optical-infrared remote sensing, while the VOD parameter enables more comprehensive assessments of

86 tely 25% may develop severe life threatening VOD with subsequent respiratory compromise and multiorga

87 gic approaches that clearly prevent or treat VOD have been identified.

88 uggest that sirolimus use is associated with VOD after TBI-based transplantation when used with metho

89 od for portal decompression in patients with VOD after BMT, and was associated with clinical improvem