ライフサイエンスコーパス: CVP

1 CVP significantly decreased, while RV afterload remained

2 CVP was measured in the same manner by maintaining PPP a

3 d less frequently in patients who achieved a CVP <8 mm Hg (p = 0.01).

4 I, 1.4-4.6]; pooled specificity, 76%), but a CVP greater than the threshold made fluid responsiveness

5 alysis of MR patients, minimal disease after CVP was a favorable prognostic factor.

6 However, SOX2 is variably expressed among CVP epithelial cells, suggesting that their progenitor p

7 e correlations were observed between AWP and CVP and between PPP and CVP (P < 0.001).

8 BP and CVP were not significantly different between the 2 pacin

9 were higher in COI patients, whereas BP and CVP were similar in the two groups.

10 During tilt, BP did not change and CVP fell by the same extent in the 2 groups; the increas

11 0 min) also significantly increased PCWP and CVP, and abolished the beneficial preload effect of L-NM

12 rved between AWP and CVP and between PPP and CVP (P < 0.001).

13 The mean difference between PVP and CVP was 0.4 mm Hg and between PVP and pulmonary capillar

14 PVP and CVP were found to be highly correlated (r=0.947), while

15 inimum CSA with tidal breathing at baseline (CVP nl) were intermediate.

16 er three conditions of CVP: (1) at baseline (CVP nl) with patients lying supine; (2) at decreased CVP

17 s were combined, the overall r value between CVP and PCWP was 0.92.

18 regulator of cardiovascular progenitor cell (CVP) specification.

19 All 30 patients enrolled completed CVP as well as tositumomab and (131)I-tositumomab therap

20 -anthracycline-containing regimen comprising CVP followed by one cycle of tositumomab and (131)I-tosi

21 est that in the assessed thermal conditions, CVP appropriately tracks left ventricular filling pressu

22 In contrast, CVP neuronal inhibition blocked cocaine-primed, but not

23 patients lying supine; (2) at decreased CVP (CVP-) by inflating blood pressure cuffs to 40 mm Hg on b

24 m Hg on both legs; and (3) at increased CVP (CVP+) by elevating both legs to 33 degrees.

25 FDA-approved NNRTI, bear a cyanovinylphenyl (CVP) group.

26 with patients lying supine; (2) at decreased CVP (CVP-) by inflating blood pressure cuffs to 40 mm Hg

27 but 80% of genes most highly induced during CVP development have reduced expression, suggesting adop

28 With the legs elevated (CVP+), neither mean nor minimum CSA showed any significa

29 tion factor KLF2; fish CCM and the embryonic CVP lesion failed to form in klf2a null fish indicating

30 rgic receptor (adrb1) prevents the embryonic CVP lesion, we proposed that adrb1 plays a role in CCM p

31 hat adrb1(-/-) zebrafish exhibited 86% fewer CVP lesions and 87% reduction of CCM lesion volume relat

32 ssion (median 32 months versus 15 months for CVP; P < .0001).

33 CHOP, 20.7% v G-CHOP, 7.0%; R-CVP, 21.7% v G-CVP, 9.4%).

34 esponse technology to eight cycles of GP2013-CVP or R-CVP (combination phase), followed by monotherap

35 phamide, vincristine, and prednisone (GP2013-CVP) with rituximab-CVP (R-CVP) in patients with follicu

36 e and 23 [10%] of 231 patients in the GP2013-CVP group and 13 [6%] of 231 patients in the R-CVP group

37 enia (55 [18%] of 312 patients in the GP2013-CVP group and 65 [21%] of 315 patients in the R-CVP grou

38 enia (80 [26%] of 312 patients in the GP2013-CVP group and 93 [30%] of 315 patients in the R-CVP grou

39 se and 17 [7%] of 231 patients in the GP2013-CVP group and nine [4%] of 231 patients in the R-CVP gro

40 ups (289 [93%] of 312 patients in the GP2013-CVP group had an adverse event and 71 [23%] of 312 patie

41 ups (five [2%] of 268 patients in the GP2013-CVP; three [1%] in the R-CVP group).

42 Median PVP was 9.5 (6-17) mm Hg, CVP was 8.5 (6-18) mm Hg, and pulmonary capillary wedge

43 88.9% of those with low, moderate, and high CVP levels, respectively (P<0.0001), at the 18-month con

44 riance (ANOVA) indicated that alterations in CVP were associated with changes in mean CSA (p = 0.03)

45 At FRC, changes in CVP had no significant effect on either mean or minimum

46 y was to test the hypothesis that changes in CVP reflect those in left ventricular filling pressure,

47 These results indicate that changes in CVP significantly alter the response of the upper airway

48 The decrease in CVP with LBNP was correlated with the reduction in PCWP

49 FS+ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and

50 There were no differences in CVP among all pacing modes (P:=0.27).

51 the heart and eliminating the blood flow in CVP by administration of 2,3-BDM suppressed the CVP lesi

52 rend for a decrease in BP and an increase in CVP (P=0.02).

53 ses in SBP, DBP, and MAP and the increase in CVP were significantly less during long-RP tachycardia (

54 strated an abrupt fall in BP, an increase in CVP, and an increase in SNA regardless of the AV interva

55 evidence for a role of Src family kinases in CVP development.

56 40 mm Hg on both legs; and (3) at increased CVP (CVP+) by elevating both legs to 33 degrees.

57 Eyes with increased CVP after more severe CRVO demonstrate significantly red

58 However, after leg-cuff inflation (CVP-), highly significant increases in both mean (163 +/

59 better baseline LV and RV function and lower CVP.

60 significantly higher in patients with lower CVP at all time points (P<0.0001).

61 male piglets and maintaining PPP at 25 mmHg, CVP was measured 3 times at each of 9 levels of airway p

62 ents with the bundle completed received more CVP/Scvo2 monitoring (100.0 vs. 64.8%, p < .01), more an

63 e taste bud cells (TBCs) purified from mouse CVP.

64 While normothermic, CVP was 6.3 +/- 0.2 mmHg and PCWP was 9.5 +/- 0.3 mmHg.

65 Furthermore, the ability of CVP to stratify risk for development of WRF was apparent

66 inspiration (VTei) under three conditions of CVP: (1) at baseline (CVP nl) with patients lying supine

67 domly assigned to receive either 8 cycles of CVP plus rituximab (R-CVP; n = 162) or CVP (n = 159).

68 eas of CNP that correlate with the degree of CVP elevation.

69 ncreased significantly with higher levels of CVP and progressed with time.

70 red by FTT was reduced with higher levels of CVP.

71 Spontaneous lowering of CVP had beneficial effects on BCVA, although this dimini

72 At each study visit, measurements of CVP, best-corrected visual acuity (BCVA), area of CNP, r

73 ous non-invasive point-of-care monitoring of CVP, without restricting patients to limited postures.

74 did not add significantly to the toxicity of CVP.

75 se values provides confidence for the use of CVP in studies assessing ventricular preload during ther

76 signed to eight cycles of R-CVP (n = 159) or CVP alone (n = 162).

77 es of CVP plus rituximab (R-CVP; n = 162) or CVP (n = 159).

78 t reduction in ventral extension and overall CVP area.

79 (RVP), but not the caudal ventral pallidum (CVP), were robustly Fos activated during cue-induced rei

80 n the posterior circumvallate taste papilla (CVP) of mice.

81 hich is expressed by circumvallate papillae (CVP) of the mouse tongue, has been implicated in oro-gus

82 ingly failed to form the caudal vein plexus (CVP).

83 esion in the embryonic caudal venous plexus (CVP) caused by obstruction of blood flow by intraluminal

84 and prevents embryonic caudal venous plexus (CVP) lesions in zebrafish that follow mosaic inactivatio

85 e report that chemical vapor polymerization (CVP) of aminomethyl[2.2]paracyclophane into nematic liqu

86 clophosphamide, vincristine, and prednisone (CVP) followed by tositumomab and iodine-131 ((131)I) -to

87 clophosphamide, vincristine, and prednisone (CVP) in patients with newly diagnosed advanced-stage fol

88 clophosphamide, vincristine, and prednisone (CVP) is one of several standard treatment options for ad

89 clophosphamide, vincristine, and prednisone [CVP]) plus rituximab.

90 clophosphamide, vincristine, and prednisone [CVP]), every 3 weeks during induction, then rituximab ma

91 A low central venous pressure (CVP) (mean threshold <8 mm Hg) was associated with fluid

92 ct right atrial and central venous pressure (CVP) abnormalities in cardio-vascular diseases (CVDs) di

93 d WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p

94 fects of changes in central venous pressure (CVP) on upper airway size.

95 Central venous pressure (CVP) provides information regarding right ventricular fi

96 muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside i

97 lood pressure (BP), central venous pressure (CVP), and heart rate were recorded during 3 minutes of n

98 pressure (BP), ECG, central venous pressure (CVP), and muscle sympathetic nerve activity (MSNA) were

99 lood pressure (BP), central venous pressure (CVP), and peripheral muscle sympathetic nerve activity (

100 rgitation, elevated central venous pressure (CVP), and preserved right ventricular (RV) function were

101 lood pressure (BP), central venous pressure (CVP), and SNA were recorded during 3 minutes of right at

102 pressure (PVP) with central venous pressure (CVP), as well as other invasive hemodynamic measurements

103 ), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plas

104 pressure (PCWP) and central venous pressure (CVP).

105 rtment: a) initiate central venous pressure (CVP)/central venous oxygen saturation (Scvo2) monitoring

106 Under low airway pressure, CVP did not increase or often decreased when PPP was hig

107 Under high airway pressure, CVP was persistently higher than pneumoperitoneum pressu

108 alyses were performed among airway pressure, CVP, and pneumoperitoneum pressure.

109 RD-positive (R-CHOP, 20.7% v G-CHOP, 7.0%; R-CVP, 21.7% v G-CVP, 9.4%).

110 overall safety profiles of BR, R-CHOP, and R-CVP were as expected; no new safety data were collected

111 tter long-term disease control than R-CHOP/R-CVP and should be considered as a first-line treatment o

112 BR treatment group and 55.8% in the R-CHOP/R-CVP group.

113 ent end points for either the BR or R-CHOP/R-CVP study treatment groups by study completion.

114 e overall response rates for BR and R-CHOP/R-CVP were 97% and 91%, respectively (P = .0102).

115 BR was noninferior to R-CHOP/R-CVP, as assessed by the primary end point of complete re

116 e BR (n = 224) or standard therapy (R-CHOP/R-CVP, n = 223) for 6 cycles; 2 additional cycles were per

117 y) also favored the BR regimen over R-CHOP/R-CVP.

118 Purpose The FOLL05 trial compared R-CVP (rituximab plus cyclophosphamide, vincristine, and p

119 rednisone (GP2013-CVP) with rituximab-CVP (R-CVP) in patients with follicular lymphoma.

120 response rates were 88%, 93%, and 91% for R-CVP, R-CHOP, and R-FM, respectively (P=.247).

121 were registered during follow-up: four in R-CVP, five in R-CHOP, and 14 in R-FM.

122 were randomly assigned to eight cycles of R-CVP (n = 159) or CVP alone (n = 162).

123 echnology to eight cycles of GP2013-CVP or R-CVP (combination phase), followed by monotherapy mainten

124 ophosphamide, vincristine, and prednisone (R-CVP).

125 ophosphamide, vincristine, and prednisone [R-CVP]) for treatment-naive patients with indolent non-Hod

126 ailure was 27 months in patients receiving R-CVP and 7 months in the CVP arm (P < .0001).

127 nificantly prolonged in patients receiving R-CVP versus CVP (P < .0001).

128 ive either 8 cycles of CVP plus rituximab (R-CVP; n = 162) or CVP (n = 159).

129 ete response rates were 81% and 41% in the R-CVP arm versus 57% and 10% in the CVP arm, respectively

130 se event; 288 [91%] of 315 patients in the R-CVP group had an adverse event and 63 [20%] had a seriou

131 group and 65 [21%] of 315 patients in the R-CVP group in the combination phase and 17 [7%] of 231 pa

132 group and 93 [30%] of 315 patients in the R-CVP group in the combination phase and 23 [10%] of 231 p

133 P group and 13 [6%] of 231 patients in the R-CVP group in the maintenance phase).

134 group and nine [4%] of 231 patients in the R-CVP group in the maintenance phase).

135 ients in the GP2013-CVP; three [1%] in the R-CVP group).

136 is study, R-CHOP and R-FM were superior to R-CVP in terms of 3-year TTF and PFS.

137 the respective treatment groups (R-CHOP v R-CVP, P=.003; R-FM v R-CVP, P=.006; R-FM v R-CHOP, P=.763

138 ent groups (R-CHOP v R-CVP, P=.003; R-FM v R-CVP, P=.006; R-FM v R-CHOP, P=.763).

139 udy end point, with R-CHOP and R-FM versus R-CVP and showed R-CHOP to have a better risk-benefit rati

140 FL International Prognostic Index 2 versus R-CVP was 0.73 for R-CHOP (95% CI, 0.54 to 0.98; P = .037)

141 d to lymphoma progression with R-FM versus R-CVP.

142 ade 3 to 4 neutropenia (64%) compared with R-CVP (28%) and R-CHOP (50%; P< .001).

143 Patients initially treated with R-CVP had a higher risk of lymphoma progression compared w

144 low-up of 30 months, patients treated with R-CVP had a very significantly prolonged time to progressi

145 4-year OS: 83% v 77%;) were achieved with R-CVP versus CVP alone.

146 es demonstrated an improvement in TTP with R-CVP versus CVP irrespective of the Follicular Lymphoma I

147 analyzed 91 untreated patients who received CVP chemotherapy (cyclophosphamide, vincristine, and pre

148 ar lymphoma) evaluable patients who received CVP were randomly assigned to OBS (n = 158) or MR (n = 1

149 ced heart rate and contractility and reduced CVP blood flow.

150 , and prednisone (GP2013-CVP) with rituximab-CVP (R-CVP) in patients with follicular lymphoma.

151 or often decreased when PPP was higher than CVP.

152 s embolism increases when PPP is higher than CVP.

153 used to design bicyclic replacements for the CVP group.

154 patients receiving R-CVP and 7 months in the CVP arm (P < .0001).

155 % in the R-CVP arm versus 57% and 10% in the CVP arm, respectively (P < .0001).

156 by administration of 2,3-BDM suppressed the CVP lesion.

157 The addition of rituximab to the CVP regimen significantly improves the clinical outcome

158 During the transition from mesoderm to the CVP, TMEM88 has a chromatin signature of genes that medi

159 Endothelial cells (ECs) within the CVP of bcar1-/- embryos produced fewer filopodial struct

160 -IV follicular lymphoma were assigned 1:1 to CVP plus intravenous infusions of 375 mg/m(2) CT-P10 or

161 se/complete response unconfirmed (CR/CRu) to CVP and making an anti-idiotype antibody are 2 independe

162 in patients with a partial response (PR) to CVP (P < .001).

163 uding OS, confirm the benefit of adding R to CVP in the front-line treatment of FL.

164 prolonged in patients receiving R-CVP versus CVP (P < .0001).

165 83% v 77%;) were achieved with R-CVP versus CVP alone.

166 ated an improvement in TTP with R-CVP versus CVP irrespective of the Follicular Lymphoma Internationa

167 on is correct during thermal challenges when CVP is elevated during skin-surface cooling or reduced d

168 sis iridis was significantly associated with CVP at all time points and was present in 5.6%, 27.9%, a

169 of PVP demonstrates a high correlation with CVP.