ライフサイエンスコーパス: TVR

1 TVR and Peg-IFN accounted for 85% of costs.

2 TVR-resistant variants were detected in plasma, but not

3 TVR/PR efficiently inhibited V36M and R109K variants and

4 nce interval [CI]: 0.38 to 0.78; p = 0.001), TVR (RR: 0.77; 95% CI: 0.64 to 0.92; p = 0.004), and MI

5 I (HR, 0.063; 95% CI, 0.009-0.462; P=0.007), TVR (HR, 0.517; 95% CI, 0.323-0.826; P=0.006), and MACE

6 therapy for chronic C hepatitis genotype 1 (TVR, 1125 mg every 12 hours, pegylated interferon-alpha

7 A TVR greater than or equal to 25% allowed prediction of d

8 A TVR of greater than or equal to 25% was associated with

9 ditional 36 weeks of P/R after 12 weeks of a TVR triple regimen (total of 48 weeks).

10 After TVR administration was initiated, the TAC dosage was ski

11 0.04), TLR (71.4% vs. 15.3%, p < 0.0001) and TVR (78.6% vs. 23.7%, p = 0.0002).

12 t of lower MI (2.9% vs. 8.1%; p < 0.001) and TVR rates (5.9% vs.10.7%; p = 0.001) in the ZES group.

13 nfarction occurred in 5 patients (2.1%), and TVR was required in 26 patients (11.1%).

14 er restenosis (63.8% vs. 48.4% p = 0.13) and TVR (70.6% vs. 56.0%, p = 0.14) in diabetic versus nondi

15 ar restenosis (15.6% vs. 10.7% p = 0.33) and TVR (22.9% vs. 28.2% p = 0.41) rates.

16 er; lightweight cars from Lotus, Ferrari and TVR; and high-speed trains, speedboats, and racing yacht

17 Myocardial infarction and TVR were not different between the groups.

18 d similar rates of cardiac death/MI, MI, and TVR compared with other second-generation DP-DES but hig

19 d similar rates of cardiac death/MI, MI, and TVR compared with second-generation DP-DES but higher ra

20 reduction in 6-month rates of death, MI, and TVR compared with stent-placebo or balloon-abciximab the

21 tide reduced the composite of death, MI, and TVR from 14.5% to 6.0% in women versus 9.0% to 6.8% in m

22 At 9 months, death, MI, and TVR occurred in 2.2%, 2.0%, and 4.1%, respectively, of t

23 ACE) were defined as death, nonfatal MI, and TVR.

24 vely), MI (3.4% vs. 2.4%, respectively), and TVR (8.1% vs. 4.3%, respectively).

25 In the base-case analysis BOC-RVR and TVR-IL28B strategies were the most effective and cost-ef

26 o significant difference in tumor volume and TVR was found among the six MR imaging sequences (P = .9

27 was sustained at six months (death, MI, any TVR: 14.6% vs. 19.8%, HR = 0.71, p = 0.010), and this wa

28 and target vessel failure (TVF), defined as TVR, any death, or myocardial infarction (MI) of the tar

29 valuate the role of RTV in the bidirectional TVR and atazanavir (ATV) interactions.

30 VR and sustained virologic response, and BOC/TVR prices.

31 , p=0.002) and lowered the incidence of both TVR (11.4% vs. 15.4%, p=0.001) and non-TVR (8.0% vs. 10.

32 SOF was dominated by TVR in G1b patients even if, in clinical practice, this

33 l exposure was not substantially modified by TVR.

34 oup differences in baseline characteristics, TVR (hazard ratio [HR] 0.88, 95% confidence interval [CI

35 al, the addition of abciximab reduced 30-day TVR without increasing bleeding risk, and primary stenti

36 We defined TVR as repeat intervention for chest pain/positive stres

37 Angiographic restenosis and ischemia-driven TVR rates were higher in patients treated in the U.S.

38 l, predominantly by reducing ischemia-driven TVR.

39 hereby reducing the need for ischemia-driven TVR.

40 d efficient immunosuppressive regimen during TVR-based triple therapy.

41 tment for other baseline prognostic factors (TVR: OR = 0.95, 95% confidence interval [CI]: 0.71,1.29;

42 e BA, stent and RA groups (39%, 40%, 33% for TVR and 43%, 40%, 33% for MACE, p = NS).

43 omes than any percutaneous treatment (8% for TVR and 23% for MACE).

44 (TVR) in CHD; the expanding indications for TVR; and the technological obstacles to optimizing TVR.

45 LYG for BOC-RVR and euro 11.455 per LYG for TVR-IL28B.

46 nts not receiving abciximab and the need for TVR among all patients.

47 as an independent predictor of the need for TVR at 1 year (hazard ratio, 0.62; 95% CI, 0.43 to 0.89;

48 nical restenosis as measured by the need for TVR.

49 clinical events including death and need for TVR.

50 of restenosis when measured by the need for TVR.

51 outcomes with both stents (8 registries for TVR and 7 registries for MACE), the likelihood of TVR (P

52 Clinical variables with increased risk for TVR included younger age; hypertension; diabetes mellitu

53 38 (12.2%) patients had TLR, 748 (14.3%) had TVR, and 848 (16.0%) had TVF, more than two-thirds highe

54 By contrast, during hyperthermia, TVR was low and CVA unit activity was absent.

55 ificant independent predictor of death and I-TVR at six months.

56 ischemic target vessel revascularization (I-TVR) (OR 15.0, 95% CI 8.68 to 26.0) at six months.

57 there was still no significant difference in TVR between the two groups (HR: 1.09; 95% CI: 0.84 to 1.

58 ing a decrease in the relative difference in TVR rates (ie, no effect of abciximab on reducing resten

59 Hypoxia evoked a graded fall in TVR indicating vasodilatation, but there were no consist

60 at the changes evoked by systemic hypoxia in TVR and sympathetic nerve activity to CVA are dependent

61 Systemic hypoxia evoked graded increases in TVR, indicating vasoconstriction, and in 8% O(2) there w

62 us is primarily attributable to reduction in TVR.

63 ductions in ST with concordant reductions in TVR and MI compared to non-EE-DES.

64 ite end point of death/myocardial infarction/TVR (RR, 1.26; 95% CI, 1.13 to 1.40, P<0.01).

65 Records of 147 patients who initiated TVR-based triple therapy at the Mount Sinai Medical Cent

66 Human intrahepatic TVR concentration, measured for the first time, was lowe

67 creased angiographic restenosis and ischemic TVR.

68 ng significantly reduced the 30-day ischemic TVR without increasing bleeding or stroke rates.

69 A total of 14% (n = 1,609) had ischemic TVR.

70 from 28.1% to 19.1% (P=0.01) and in ischemic TVR from 20.4% to 10.8% (P=0.002) compared with PTCA.

71 RESTO trial, we compared nine-month ischemic TVR after PCI in U.S.-treated patients (n = 5,026) with

72 riven largely by increased rates of ischemic TVR (19.1% vs. 9.1%, p < 0.001); no significant differen

73 significant increase in the risk of ischemic TVR at U.S. treatment sites.

74 were associated with lower risk of ischemic TVR.

75 Late TVR occurred in 29.8% of patients with no CK elevation,

76 a paradoxical decrease in the need for late TVR was present.

77 imal glycemic control had a rate of 12-month TVR similar to that of nondiabetic patients (15% vs. 18%

78 The 6-month TVR rate was 16.6% for stent-placebo, 18.4% for balloon-

79 We studied nine-month TVR in 11,484 patients enrolled in the PRESTO trial.

80 The risk of six-month TVR was independently associated with left anterior desc

81 he model to discriminate patients who needed TVR on follow-up.

82 both TVR (11.4% vs. 15.4%, p=0.001) and non-TVR (8.0% vs. 10.5%, p=0.017) compared with 40 mg pravas

83 arget vessel revascularization (TVR) and non-TVR during follow-up.

84 ratio: 0.74, p=0.015) while the odds of non-TVR did not (odds ratio: 0.92, p=0.55).

85 t vessel revascularizations [TVRs], four non-TVRs).

86 During modest hypothermia and normoxia, TVR was high and CVA unit activity was present, with mar

87 The coadministration of TVR and unboosted ATV results in increased exposure of b

88 ose fall-off zones was the best correlate of TVR and should become a standard analysis site in all va

89 implanted were the strongest determinants of TVR.

90 The boost effect of TVR on ATV exposure is higher than on RTV, despite its s

91 t valves has demonstrated the flexibility of TVR, while highlighting the need for devices to address

92 To understand the clinical impact of TVR-resistant variants, we analyzed samples from patient

93 our findings suggest that implementation of TVR, scheduled for 2014, risks exacerbating the TB probl

94 Incidence of TVR and MACE were similar in the BA, stent and RA groups

95 The reduction in the incidence of TVR was independent of low-density lipoprotein cholester

96 nd 7 registries for MACE), the likelihood of TVR (PES vs. SES) (OR 0.77, 95% CI 0.54 to 1.10, p = 0.1

97 P<0.01) and with an increased likelihood of TVR (RR, 1.27; 95% CI, 1.14 to 1.42, P<0.01), as well as

98 absorption phase or first-pass metabolism of TVR.

99 reactive protein concentrations, the odds of TVR with high-dose statin therapy remained significant (

100 The potential of TVR has not been fully realized, but holds promise in tr

101 % was a significant independent predictor of TVR (odds ratio 2.87, 95% confidence interval 1.13 to 7.

102 index was the only independent predictor of TVR (p = 0.02).

103 ization (TVR) and to determine predictors of TVR from clinical and angiographic variables available i

104 h A1c >7% had a significantly higher rate of TVR than those with A1c <7% (34% vs. 15%, p = 0.02).

105 < or =7%) is associated with a lower rate of TVR, cardiac rehospitalization, and recurrent angina.

106 Higher rates of TVR (18% vs. 11%), and angiographic restenosis (65% vs.

107 5.4%; p = 0.49) but markedly lower rates of TVR (3.4% vs. 20.3%; p = 0.0004), MACE (5.6% vs. 25.4%;

108 The rates of TVR after percutaneous revascularization procedures, and

109 ry angiographic follow-up increases rates of TVR among patients receiving both BMS and PES and overes

110 larization (TVR) than BMS and lower rates of TVR than fast-release zotarolimus-eluting stents.

111 an BMS, with SES also showing lower rates of TVR than PES.

112 to determine the frequency and retention of TVR-resistant variants in patients who did not achieve s

113 The best angiographic surrogate of TVR was the 50% follow-up DS obtained from the ribbon+ma

114 The threshold of TVR associated with myometrial invasion was assessed by

115 Patients were randomized to 12 weeks of TVR (750 mg q8h) plus peginterferon (180 mug/week) and r

116 109K variant were treated with 8-24 weeks of TVR and peginterferon-alpha2a (P) with or without ribavi

117 lpha/RBV treatment, and RGT with 12 weeks of TVR, Peg-IFN-alpha/RBV followed by 12 weeks of Peg-IFN-a

118 nd the technological obstacles to optimizing TVR.

119 fference in myocardial infarction, death, or TVR between the CrCl groups.

120 The composite of death, MI, or TVR after one year occurred in 24.5% of women compared w

121 e (death, reinfarction, disabling stroke, or TVR) was greater after optimal PTCA than routine stentin

122 easured viral kinetics, resistance patterns, TVR concentrations, and host transcription profiles.

123 st-effectiveness ratios of 4,678 dollars per TVR avoided and 47,798 dollars/quality-adjusted life yea

124 cost-effectiveness ratios of 760 dollars per TVR event avoided and $5,105/QALY gained.

125 inical and angiographic variables to predict TVR is modest.

126 of each section, and the tumor volume ratio (TVR) was calculated.

127 rred in 74% (28 in 38) of patients receiving TVR plus PEG-IFN-alpha2a-ribavirin and 45% (10 in 22) of

128 occurred in 5% (2 in 38) of those receiving TVR plus PEG-IFN-alpha2a-ribavirin and 0% (0 in 22) of t

129 The DES significantly reduce TVR compared with BMS, without an increase in death, MI,

130 The PES reduced TVR by 12.2 events per 100 patients treated, resulting i

131 Because PES reduced TVR by approximately 60% regardless of type of follow-up

132 and wild-type viral sequence showed reduced TVR sensitivity in our assay.

133 Compared with BMS, DES significantly reduced TVR (relative risk [RR]: 0.44; 95% confidence interval [

134 ries (N = 26,521), DES significantly reduced TVR (RR: 0.54; 95% CI: 0.40 to 0.74) without an increase

135 Nonetheless, PES substantially reduces TVR regardless of assignment to mandatory angiographic f

136 Test-vaccinate/remove (TVR) is a novel approach that entails testing individual

137 ndependent predictors of the need for repeat TVR were side branch diameter >2.3 mm, longer lesion len

138 ients died, 1% had Q-wave MI, 17% had repeat TVR, and the overall rate of major adverse cardiac event

139 the-art for transcatheter valve replacement (TVR) in CHD; the expanding indications for TVR; and the

140 Tricuspid valve replacement (TVR) with allograft mitral valve also is briefly discuss

141 ing tail blood flow and vascular resistance (TVR) from the CVA, under conditions of modest hypothermi

142 (IC50 ) correlating with clinical response (TVR IC50 for genotype (G)1 was 0.042 +/- 0.003 vs. 0.117

143 0.0001) and target vessel revascularization (TVR) (70.6% vs. 22.9%, p < 0.0001) rates in diabetic pat

144 timates for target vessel revascularization (TVR) (PES: 5.8%, 95% CI 3.9% to 8.5%; SES: 7.2%, 95% CI

145 ferences in target vessel revascularization (TVR) after percutaneous coronary intervention (PCI) in t

146 infarction, target vessel revascularization (TVR) and a combined end point of these major adverse car

147 ncidence of target vessel revascularization (TVR) and non-TVR during follow-up.

148 he rates of target vessel revascularization (TVR) and to determine predictors of TVR from clinical an

149 her rate of target vessel revascularization (TVR) at 1 year (adjusted hazard ratio [HR] 1.46; p = 0.0

150 arction, or target vessel revascularization (TVR) at 1 year (adjusted hazard ratio, 0.73; 95% CI, 0.5

151 Target vessel revascularization (TVR) at 3 years was one of the secondary outcomes.

152 Ischemic target vessel revascularization (TVR) at 30 days occurred more frequently after optimal P

153 , or urgent target vessel revascularization (TVR) at 30 days, compared with 4.2% in those patients wi

154 r elective) target vessel revascularization (TVR) at 6 months by intention-to-treat (ITT) analysis.

155 events, and target vessel revascularization (TVR) at 6 to 9 months.

156 n (MI), and target vessel revascularization (TVR) at 9 months.

157 tenosis and target vessel revascularization (TVR) at follow-up was determined.

158 nd 30 days, target vessel revascularization (TVR) beyond 30 days, and target vessel failure (TVF), de

159 al cost per target vessel revascularization (TVR) event avoided and was analyzed separately among coh

160 ates repeat target-vessel revascularization (TVR) in approximately 20% of patients during this time p

161 ncidence of target vessel revascularization (TVR) in diabetic patients undergoing elective percutaneo

162 p = 0.36), target vessel revascularization (TVR) rate at nine-month follow-up was significantly high

163 n (TLR) and target vessel revascularization (TVR) rates were similar in the two groups.

164 I), MI, and target vessel revascularization (TVR) than BMS and lower rates of TVR than fast-release z

165 s of 1-year target vessel revascularization (TVR) than BMS, with SES also showing lower rates of TVR

166 o the first target vessel revascularization (TVR) was 173 +/- 127 days after the index procedure and

167 ncidence of target vessel revascularization (TVR) was 53% in the PTCA group as compared with 28% in t

168 arction, or target vessel revascularization (TVR) was analyzed as time-to-first event within 9 months

169 ction (MI), target vessel revascularization (TVR), and definite stent thrombosis.

170 onfatal MI, target vessel revascularization (TVR), and procedure costs.

171 ction (MI), target vessel revascularization (TVR), and stent thrombosis in randomized trials of ST-se

172 MI), urgent target vessel revascularization (TVR), and unplanned GP IIb/IIIa use, occurred in 10.5% o

173 ed for late target vessel revascularization (TVR), is unknown.

174 bosis (ST), target vessel revascularization (TVR), myocardial infarction (MI), and cardiac death in r

175 emia-driven target-vessel revascularization (TVR), or disabling stroke at 30 days (4.6% versus 7.0%;

176 ction (MI), target vessel revascularization (TVR), stent thrombosis, and follow-up angiographic reste

177 ally driven target vessel revascularization (TVR).

178 rction, and target vessel revascularization (TVR).

179 on (MI), or target vessel revascularization (TVR).

180 predicting target vessel revascularization (TVR).

181 on (MI), or target-vessel revascularization (TVR).

182 subsequent target vessel revascularization (TVR, 21% versus 38%, P=.0823).

183 ), ischemic target-vessel revascularization (TVR; 16.7% versus 12.1%, P=0.006), and major adverse car

184 , or urgent target vessel revascularization [TVR]) was lower among clopidogrel-pretreated patients (6

185 f 78% (six target vessel revascularizations [TVRs], four non-TVRs).

186 ) telaprevir IL28B genotype-guided strategy (TVR-IL28B).

187 Of the 257 patients who had subsequent TVR after failed IRT, 68 (26%) underwent coronary artery

188 Telaprevir (TVR) has been approved for response-guided-therapy (RGT)

189 Telaprevir (TVR) plus peginterferon-alpha2a (PEG-IFN-alpha2a) and ri

190 Telaprevir (TVR), a hepatitis C virus (HCV) NS3/4A protease inhibito

191 pared with boceprevir (BOC)- and telaprevir (TVR)-based TT in untreated genotype 1 (G1) chronic hepat

192 esponse-guided therapy (RGT) for telaprevir (TVR) in combination with pegylated interferon-alpha and

193 We measured sensitivity of telaprevir (TVR) and alisporivir (AVR) in different genotypes, and s

194 bavirin, and boceprevir (BOC) or telaprevir (TVR) is more effective than peginterferon-ribavirin dual

195 confers low-level resistance to telaprevir (TVR) and boceprevir and confers high-level resistance (>

196 ined virologic response (SVR) to telaprevir (TVR) in genotype 1 patients with hepatitis C and prior p

197 ractions have been observed when telaprevir (TVR) and ritonavir (RTV)-boosted human immunodeficiency

198 tion trials, triple therapy with telaprevir (TVR), pegylated interferon (Peg-IFN), and ribavirin (RBV

199 ter response rates achieved with telaprevir (TVR)-based triple therapy have led to better graft and p

200 with genotype 1 HCV treated with telaprevir (TVR)/pegylated-interferon alpha/ribavirin.

201 We tested TVR-resistant viral isolates and identified changes in I

202 Multiple case series have demonstrated that TVR with the Melody transcatheter pulmonary valve in pro

203 itivity, and vaccine effectiveness mean that TVR would be expected to leave some infected and some su

204 Existing simulation models predict that TVR could reduce cattle TB if such small-scale culling c

205 The TVR arms were pooled for the purposes of this analysis.

206 uided (6.9% vs. 8.4%, p = 0.22) although the TVR was similar between two groups (6.0% vs. 6.0%, p = 0

207 ory values were closely monitored during the TVR phase.

208 %), respectively, without any changes in the TVR terminal half-life.

209 At 6- to 9-month follow-up, the TVR was significantly higher in the PPCP group compared

210 After RTV was withdrawn, the TVR AUC(0-12) (area under the concentration-time curve),

211 RVR); 4) telaprevir response-guided therapy (TVR-RGT); 5) telaprevir IL28B genotype-guided strategy (

212 etroviral regimens were randomly assigned to TVR plus PEG-IFN-alpha2a-ribavirin or placebo plus PEG-I

213 One patient with a poor clinical response to TVR and wild-type viral sequence showed reduced TVR sens

214 usal relationship with virologic response to TVR-based therapy than HOMA-IR.

215 incidence of death, reinfarction, or urgent TVR at all time points assessed (9.9% versus 3.3%, P=0.0

216 and 30 days) death, reinfarction, or urgent TVR.

217 In subjects with the R155K variant, TVR/PR provided greater antiviral activity than PR alone

218 We studied samples from a 2-week TVR monotherapy study in which 5 of 8 patients with G3 H

219 Total costs were TVR (61%), IFN (24%), RBV (4%), adverse event management

220 for the adverse interactions that occur when TVR and ATVr are administered together, possibly by infl

221 LYG was 4.04 with BOC-RVR and 4.42 with TVR-IL28B.

222 ients had on-treatment HCV breakthrough with TVR-resistant variants.

223 reshold of euro 25,000 per LYG compared with TVR in the entire population of untreated G1 patients.

224 In comparison with TVR-based strategies, SOF was cost-effective in IL28B CT

225 IFN-alpha/RBV (48 weeks), group A), FLT with TVR, Peg-IFN-alpha/RBV for 12 weeks with a long (+36 wee

226 nausea, rash, and dizziness were higher with TVR plus PEG-IFN-alpha2a-ribavirin during the first 12 w

227 and HIV-1, more adverse events occurred with TVR versus placebo plus PEG-IFN-alpha2a-ribavirin; these

228 restenosis occurred in 28% of patients with TVR of 26%.

229 Rapid HCV suppression was seen with TVR plus PEG-IFN-alpha2a-ribavirin (68% [26 in 38 patien

230 After failure to achieve SVR with TVR-based treatment, resistant variants are observed in

231 e rates were higher in patients treated with TVR versus placebo plus PEG-IFN-alpha2a-ribavirin.

232 Patients were treated with TVR, PEG-IFN, and RBV for 12 weeks, followed by 12 or 36

233 y to those in patients with HCV treated with TVR.

234 A total of 1797 patients were treated with TVR.

235 ng risk, and primary stenting reduced 1-year TVR and MACE rates compared with PTCA.