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 in 37 eyes (20 infants) was compared before and afte

3 TVR was not associated with measured increases in either

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

5 TVR/PR efficiently inhibited V36M and R109K variants and

6 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

7 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

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

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

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

11 haviours were examined prior to and during a TVR protocol in NI.

12 kly, or interrupting ART beyond 5 weeks in a TVR study.

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

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

15 0.04), TLR (71.4% vs. 15.3%, p < 0.0001) and TVR (78.6% vs. 23.7%, p = 0.0002).

16 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.

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

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

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

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

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

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

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

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

25 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

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

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

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

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

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

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

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

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

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

35 , 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.

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

37 l exposure was not substantially modified by TVR.

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

39 In placebo-controlled TVR studies, 120 participants are required in each arm t

40 Current TVR HIV cure studies are underpowered to detect statisti

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

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

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

44 l, predominantly by reducing ischemia-driven TVR.

45 hereby reducing the need for ischemia-driven TVR.

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

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

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

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

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

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

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

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

54 nical restenosis as measured by the need for TVR.

55 clinical events including death and need for TVR.

56 of restenosis when measured by the need for TVR.

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

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

59 38 (12.2%) patients had TLR, 748 (14.3%) had TVR, and 848 (16.0%) had TVF, more than two-thirds highe

60 However, little is known about how TVR affects the behaviour and movement of badgers within

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

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

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

64 No significant change in TVR was found before and after bevacizumab treatment wit

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

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

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

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

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

70 us is primarily attributable to reduction in TVR.

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

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

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

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

75 creased angiographic restenosis and ischemic TVR.

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

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

78 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.

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

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

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

82 were associated with lower risk of ischemic TVR.

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

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

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

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

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

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

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

90 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

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

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

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

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

95 Whether or not TVR may alter badger behaviours remains to be seen, but

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

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

98 implanted were the strongest determinants of TVR.

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

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

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

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

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

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

105 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

106 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

107 absorption phase or first-pass metabolism of TVR.

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

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

110 % was a significant independent predictor of TVR (odds ratio 2.87, 95% confidence interval 1.13 to 7.

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

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

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

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

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

116 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%;

117 The rates of TVR after percutaneous revascularization procedures, and

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

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

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

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

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

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

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

125 109K variant were treated with 8-24 weeks of TVR and peginterferon-alpha2a (P) with or without ribavi

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

127 nd the technological obstacles to optimizing TVR.

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

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

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

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

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

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

134 inical and angiographic variables to predict TVR is modest.

135 alculation of temporal vascularization rate (TVR) for each eye.

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

137 observed dynamics of time to viral rebound (TVR) post-ATI, we modelled estimates for optimal sample

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

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

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

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

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

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

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

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

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

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

148 Test, vaccinate or remove ('TVR') of bTB test-positive badgers, has been suggested t

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

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

151 h carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker.

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

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

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

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

156 0.0001) and target vessel revascularization (TVR) (70.6% vs. 22.9%, p < 0.0001) rates in diabetic pat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 ally driven target vessel revascularization (TVR).

191 rction, and target vessel revascularization (TVR).

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

193 predicting target vessel revascularization (TVR).

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

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

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

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

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

199 tion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 ory values were closely monitored during the TVR phase.

222 ed to detect a significant difference in the TVR between control and intervention groups.

223 %), respectively, without any changes in the TVR terminal half-life.

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

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

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

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

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

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

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

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

232 Using TVR, GA, and BW as predictors, a machine learning model

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

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

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

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

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

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

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

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

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

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

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

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

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

246 orrelated with increasing ROP severity, with TVR being 29% slower in group C eyes (n=50) than group A

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

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

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

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

251 A total of 1797 patients were treated with TVR.

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