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 CI: 1.74-4.56, P < .001, Gray test) with all VOD/SOS events.

4 the near-linear relationship between CWC and VOD and reduces the consistency in diurnal variation.

5 rtant driver of diurnal variation in CWC and VOD over tropical ecosystems and therefore should be acc

6 ermine the association between sirolimus and VOD.

7 ow LW(s) influenced the relationship between VOD and CWC.

8 nts were anicteric and 42% (n = 8) classical VOD patients presented with refractory thrombocytopenia,

9 ss than half met EBMT criteria for classical VOD in adults, highlighting gaps in real-world diagnosti

10 Log-rank; P = 0.81) comparable to classical VOD.

11 We compared VOD data from the Advanced Microwave Scanning Radiometer

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

13 remote sensing of vegetation optical depth (VOD) has been proposed as an important measure of vegeta

14 atellite microwave vegetation optical depth (VOD) observations.

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

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

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

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

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

20 (64%) of 14 with prior GO exposure developed VOD compared with 4 (8%) of 48 without prior GO exposure

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

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

23 splantation increases the risk of developing VOD.

24 stration are at increased risk of developing VOD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 to the development of venoocclusive disease (VOD).

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

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

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

47 ied 27 patients treated with Defibrotide for VOD/SOS diagnosis, where detailed data were available fo

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

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

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

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

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

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

54 en inferring plant diurnal water stress from VOD measurements.

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

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

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

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

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

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

61 one with persistent histological changes of VOD.

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

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

64 eived GO prior to SC transplantation died of VOD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 om a large UK transplant center reporting on VOD/SOS in consecutive HSCT adult patients (n = 530), tr

80 fibrotide access for treatment of late-onset VOD in current treatment guidelines.

81 Twenty percent (n = 2/8) of late-onset VOD patients were anicteric and 42% (n = 8) classical VO

82 (n = 8/27) of cases classified as late-onset VOD presenting at median of 46 (22-93) days but with D10

83 iled to recognize the syndrome of late-onset VOD.

84 and 1.80 g cm(-3)), detonation performance (VOD = 7505 and 8257 m s(-1), DP = 23.47 and 24.41 GPa),

85 egrees C), excellent detonation performance (VOD: 8592-9361 ms(-1), DP: 27.1-33.8 GPa), and acceptabl

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

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

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

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

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

91 achman-Diamond syndrome who developed severe VOD.

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

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

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

95 transplant was not a risk factor for severe VOD.

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

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

98 arly Defibrotide for the treatment of severe VOD/SOS in adults regardless of time of onset.

99 treatment-related death secondary to severe VOD.

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

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

102 ive disease/sinusoidal obstruction syndrome (VOD/SOS) is a serious complication post allogeneic hemat

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

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

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

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

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

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

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

110 s that while CWC is strongly correlated with VOD (R(2) = 0.62 across all sites), LW(s) accounts for 6

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