ライフサイエンスコーパス: VAC

1 VAC and VAI or VIE with surgery (with or without RT), ar

2 VAC events were associated with significantly increased

3 VAC is an objective measure which can be readily obtaine

4 VAC is defined by increases in fraction of inspired oxyg

5 VAC may be a useful surveillance tool.

6 VAC signals were most often caused by volume overload an

7 VAC, like other poxviruses, has a linear, double-strande

8 VAC-treated wounds were characterized by the formation o

9 in (2.9 +/- 2.0 vs. 1.6 +/- 2.8; p < 0.002), VAC (-0.21 +/- 0.17 vs. -0.09 +/- 0.15; p < 0.0001), and

10 .5 mg/m(2), and cyclophosphamide 2.2 g/m(2) (VAC) and vincristine 1.5 mg/m(2), topotecan 0.75 mg/m(2)

11 Allocated treatment was either 7 VAC courses with 1.5 g/m(2) of cyclophosphamide or seven

12 We found that disrupting a VAC-localized cysteine protease compromised VAC digestiv

13 factor for development of hepatopathy after VAC therapy was age.

14 ied by derangements of contractile state and VAC.

15 ide (VAC) or vincristine, melphalan (VM) and VAC.

16 We analyzed the association between VAC and clinical diagnoses, ICU length of stay, duration

17 ur strategy to construct a nearly 200,000-bp VAC-bacterial artificial chromosome (BAC) was based on c

18 sion along with mechanical forces exerted by VAC therapy was associated with the formation of more ph

19 intracellular acidic compartments per cell (VAC), and we show here that inhibition of the increase i

20 terminate in the ventral association center (VAC).

21 mechanisms by which vacuum assisted closure (VAC) modulates wound angiogenesis are still largely unkn

22 livered through the Vacuum Assisted Closure (VAC) Therapy System.

23 d resembled the vacuolar apical compartment (VAC) previously observed in epithelial cells that lose c

24 n intracellular vacuolar apical compartment (VAC) when prevented from polarizing.

25 ogenesis of the virion assembly compartment (VAC), increased secretion of noninfectious particles, an

26 ies a newly recognized vacuolar compartment (VAC) that undergoes dynamic fragmentation during T. gond

27 -like vacuole (PLV) or vacuolar compartment (VAC).

28 in the total volume of acidic compartments (VAC), mainly constituted by lysosomes, is a common event

29 Ventilator-associated complications (VAC) is a simple, objective measure of respiratory deter

30 VAC-localized cysteine protease compromised VAC digestive function and markedly reduced chronic infe

31 definition, ventilator-associated condition (VAC), identifies patients with a period of sustained res

32 n-related) ventilator-associated conditions (VAC, IVAC) and VAP.

33 ctile reserve, ventriculo-arterial coupling (VAC) reserve, and chronotropic response to the progressi

34 ication, vibration assisted crystallization (VAC) that produces superior films, which approach the fu

35 cristine, dactinomycin and cyclophosphamide (VAC) during weeks 6 to 41 (VTC/VAC).

36 ristine, dactinomycin, and cyclophosphamide (VAC) or vincristine, melphalan (VM) and VAC.

37 and dactinomycin (VA) and cyclophosphamide (VAC, n = 235), or VA and ifosfamide (VAI, n = 222), or v

38 incristine, topotecan, and cyclophosphamide (VAC/VTC).

39 ristine, dactinomycin, and cyclophosphamide (VAC; total cumulative cyclophosphamide dose, 26.4 g/m(2)

40 vincristine, dactinomycin, cyclophosphamide (VAC), and XRT did not significantly improve survival in

41 ristine, dactinomycin, and cyclophosphamide [VAC] v vincristine, dactinomycin, and ifosfamide [VAI])

42 ial were randomly assigned to receive either VAC alone or VAC alternating with vincristine, topotecan

43 The engineered VAC genomes can then be used to produce clonally pure re

44 icial chromosome (BAC) containing the entire VAC genome can be engineered in Escherichia coli by homo

45 Stable plasmids containing the entire VAC genome, with an intact concatemer junction sequence,

46 e 3.9 (95% confidence interval, 2.9-5.3) for VAC, 2.5 (1.5-4.1) for IVAC, 2.0 (1.1-3.6) for VAE-VAP,

47 or the inhibition of TNF-induced increase in VAC and cell death.

48 show here that inhibition of the increase in VAC due to PMCA4 deficiency not only reduced cell death

49 by inhibition of the TNF-induced increase in VAC.

50 in wild-type L929 cells, while increases in VAC due to genetic mutation, senescence, cell culture co

51 Rescue of infectious VAC was consistently achieved by transfecting the VAC-BA

52 M-VAC remains the standard of care for metastatic transiti

53 M-VAC was recycled every 21 days, with prophylactic recomb

54 treatment was five cycles of chemotherapy (M-VAC: methotrexate, vinblastine, doxorubicin, and cisplat

55 te, vincristine, adriamycin and cisplatin (M-VAC) chemotherapy has been the standard of therapy for o

56 , vinblastine, doxorubicin, and cisplatin (M-VAC) chemotherapy to assess an impact on long-term survi

57 , vinblastine, doxorubicin, and cisplatin (M-VAC) was performed in poor-risk patients with advanced u

58 , vinblastine, doxorubicin, and cisplatin (M-VAC) was superior to single-agent cisplatin in patients

59 , vinblastine, doxorubicin, and cisplatin (M-VAC), the standard chemotherapy regimen for locally adva

60 are unlikely to benefit significantly from M-VAC chemotherapy.

61 Assessment of dose-intense M-VAC as salvage treatment in patients who failed to respo

62 Dose-intense M-VAC is superior to gallium nitrate/5-FU in poor-risk pat

63 Dose-intense M-VAC was associated with a greater incidence of neutropen

64 receive either two courses of neoadjuvant M-VAC followed by surgery plus three additional cycles of

65 TCC, previously reported in five trials of M-VAC chemotherapy.

66 y assigned to treatment with either FAP or M-VAC.

67 tion of the intergroup trial confirms that M-VAC is superior to single-agent cisplatin in patients wi

68 term follow-up evaluation, survival in the M-VAC arm continues to be superior to cisplatin (P = .0001

69 d 5-FU arm was 19 versus 17 months for the M-VAC arm, with a median follow-up duration of 35 months (

70 e FAP arm and more myelosuppression in the M-VAC arm.

71 Thus, FAP is very likely to be inferior to M-VAC and is certainly no less toxic.

72 Only 3.7% of the patients randomized to M-VAC are alive and continuously disease-free at 6 years.

73 lium nitrate/5-FU combination responded to M-VAC as second-line therapy (42%; 95% CI, 15.2% to 72.3%)

74 nificantly different, patients assigned to M-VAC had a much better chance of responding to front-line

75 Among the patients assigned to M-VAC, 51 (59%) of 86 had an objective response, with comp

76 Sixteen of 17 patients treated with M-VAC (94%; 95% CI, 71.3% to 99.8%) demonstrated a major r

77 ate, the median survival for patients with M-VAC remained unsatisfactory.

78 Moreover, VAC-treated wounds displayed a well-oxygenated wound bed

79 rcularization of head-to-tail concatemers of VAC DNA.

80 All cases occurred after cycles of VAC (n = 16) or vincristine and cyclophosphamide with co

81 Therapy included four cycles of VAC followed by four cycles of VA over 22 weeks.

82 There was no difference in effect of VAC versus VAC/VTC across risk groups.

83 Incidences of VAC, IVAC, VAE-VAP, and VAP according to prospective sur

84 bition of lysosome exocytosis or increase of VAC by sucrose restored the sensitivity of PMCA(mut) cel

85 sis is also associated with the increases of VAC.

86 ncertainty surrounding the noninferiority of VAC compared with VAI remains at this stage.

87 events in the promoter and coding region of VAC-INVcis-QTL were also detected for ADP-glucose pyroph

88 The utility of VAC prevention bundles merits assessment.

89 ological analyses revealed that formation of VACs and endocytosis of TJ proteins was mediated by Rho-

90 The IFN-gamma dependent formation of VACs required ATPase activity of a myosin II motor but w

91 K-mediated, myosin II-dependent formation of VACs.

92 r progressive disease after TC received only VAC.

93 omly assigned to receive either VAC alone or VAC alternating with vincristine, topotecan, and cycloph

94 somal organelle (the vacuolar compartment or VAC) in turnover of autophagosomes and persistence durin

95 rofiles for patients who received VTC/VAC or VAC alone were comparable.

96 ruary 2000 and March 2010 (n = 431 receiving VAC and n = 425 receiving VAI).

97 modifications for younger children receiving VAC therapy are recommended.

98 Cells were infected with a recombinant VAC containing inserted sequences for plasmid replicatio

99 vations that chemical inhibitors that reduce VAC also reduced the plasma membrane disruption induced

100 For intermediate-risk RMS, VAC/VTC does not significantly improve FFS compared with

101 rhabdomyosarcoma (RMS) treated with standard VAC (vincristine, dactinomycin, and cyclophosphamide) ch

102 of Toxoplasma persistence and suggests that VAC proteolysis is a prospective target for pharmacologi

103 NPWT delivered by the VAC Therapy System seems to be a safe and effective trea

104 ions were significantly less frequent in the VAC arm (< 1%) than in the VAI arm (7%), mainly resultin

105 ienced more frequent thrombocytopenia in the VAC arm (45% v 35%) but fewer grade 2 to 4 acute tubular

106 Death of parasites lacking the VAC protease was preceded by accumulation of undigested

107 ne secretion and facilitate formation of the VAC for efficient infectious virus production.

108 poxia limited to the direct proximity of the VAC-foam interface, where higher VEGF levels were found.

109 ganization into structures that resemble the VAC and a decrease in cytokine release.

110 as consistently achieved by transfecting the VAC-BAC plasmids into mammalian cells that were infected

111 We also provide evidence that within the VAC or late endosome this protease mediates the proteoly

112 uminal compartment that is distinct from the VACs of MDCK cells.

113 264 were randomly assigned to VAC and 252 to VAC/VTC; 101 PME patients were nonrandomly treated with

114 nto the study: 264 were randomly assigned to VAC and 252 to VAC/VTC; 101 PME patients were nonrandoml

115 fit was apparent from the addition of DOX to VAC chemotherapy in patients with gross residual EOE.

116 r luminal compartment in Par1b-MDCK cells to VACs characteristic of control MDCK cells, indicating a

117 re was no difference in effect of VAC versus VAC/VTC across risk groups.

118 The large capacity of vaccinia virus (VAC) for added DNA, cytoplasmic expression and broad hos

119 he ability to manipulate the vaccinia virus (VAC) genome, as a plasmid in bacteria, would greatly fac

120 ophosphamide (VAC) during weeks 6 to 41 (VTC/VAC).

121 icity profiles for patients who received VTC/VAC or VAC alone were comparable.

122 rs, 4-year FFS was 73% with VAC and 68% with VAC/VTC (P = .3).

123 low-up of 4.3 years, 4-year FFS was 73% with VAC and 68% with VAC/VTC (P = .3).

124 increase in 5-year FFS from 64% to 75% with VAC/VTC.

125 not significantly improve FFS compared with VAC.

126 lication (IVAC), requires that patients with VAC also have an abnormal temperature or white blood cel

127 We assessed 153 patients with VAC and 390 without VAC.

128 ion and nonoverlapping toxicity profile with VAC makes this combination an attractive candidate for f

129 Three-year FFS rates with VAC, VAI, and VIE were 75%, 77%, and 77%, respectively (

130 topotecan received continuation therapy with VAC alone.

131 Nonresponders were treated with VAC alone.

132 hemotherapy to that of patients treated with VAC alternating with vincristine, topotecan, and cycloph

133 tracranial extension (PME) were treated with VAC and immediate x-ray therapy.

134 mpared with that of 24 patients treated with VAC and XRT without DOX (65% alive at 10 years, P = .93)

135 1 PME patients were nonrandomly treated with VAC.

136 ed myosin II was observed to colocalize with VACs after IFN-gamma exposure.

137 sessed 153 patients with VAC and 390 without VAC.