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1                                              LDV 90 mg is currently being investigated in combination
2                                              LDV aerosol emissions were predominantly carbonaceous, a
3                                              LDV and SOF were evaluated using a fully factorial exper
4                                              LDV-C-EPD infected mice as efficiently as did LDV-P, but
5                                              LDV-induced IFN-alpha had little effect on FV infection
6                                              LDV-permissive macrophages accumulated and supported the
7                                              LDV/SOF plus RBV was associated with a greater incidence
8                                              LDV/SOF without RBV is an effective and safe treatment o
9 veterans initiated therapy: 757 LDV/SOF, 138 LDV/SOF + RBV, 28 OPrD, and 73 OPrD + RBV.
10    Individual SVOC emissions from the Tier 2 LDVs and fuel technologies tested are substantially lowe
11 red with either treatment group (PrOD, 0.3%; LDV/SOF, 1.4%; untreated controls, 2.5%; P < .001).
12 rquartile range {IQR}, 0.08-0.30]; n = 372), LDV/SOF and TDF/PI (0.17 [IQR, 0.04-0.30]; n = 100), and
13 1-coinfected veterans initiated therapy: 757 LDV/SOF, 138 LDV/SOF + RBV, 28 OPrD, and 73 OPrD + RBV.
14 s contained a moderate number of LDVs (14.86 LDVs/microm2), some varicosities contained a large numbe
15 el ventilation air supply to derive accurate LDV source profiles incorporating three platinum group e
16                                           An LDV peptide-based small molecule that preferentially bin
17  to an ICAM-4-Fc construct is mediated by an LDV-inhibitable integrin on hemopoietic cells and an RGD
18 ilarity between the data we generated for an LDV ligand and published data for the RGD family support
19               Neither an unusual LETS nor an LDV motif in the first domain of ICAM-4 was critical for
20 he binding of a fluorescent derivative of an LDV peptide to several cell lines and leukocytes with al
21                         Injection of such an LDV-C pool into mice of various strains resulted in the
22 ery late antigen-4 (VLA-4), measured with an LDV-containing small molecule, varies with cellular avid
23 TDF/PI (0.17 [IQR, 0.04-0.30]; n = 100), and LDV/SOF without TDF (0.15 [IQR, 0.00-0.30]; n = 423).
24 mpared with LDV 90 mg for 12 weeks (54%) and LDV 30 mg for 24 weeks (48%).
25 coexist in most available pools of LDV-C and LDV-P.
26           Sofosbuvir (400 mg once daily) and LDV (90 mg once daily) plus ribavirin (RBV) were given f
27  FV alone, those coinfected with both FV and LDV had delayed CD8(+) T-cell responses, as measured by
28     With this assay, we found that LDV-P and LDV-C coexist in most available pools of LDV-C and LDV-P
29 ps given a fixed-dose combination of SOF and LDV, with RBV (n = 9) or without RBV (n = 10).
30 ohydrate recognition domain (CRD) as well as LDV and RGD recognition sequences for integrin binding.
31 d with SOF resistance were not detected; but LDV-resistant mutants were selected and mutant subpopula
32 f LDV-C by LDV-P as the predominant LDV, but LDV-C also persisted in the mice at a low level along wi
33  displacement in the circulation of LDV-C by LDV-P as the predominant LDV, but LDV-C also persisted i
34 iferation, the immunosuppression mediated by LDV increased both the severity and the duration of FV i
35 us, lactate dehydrogenase-elevating virus C (LDV-C), competed with the SHFV 3'(-)209 RNA in competiti
36     Recently peptides containing a consensus LDV sequence based on the connecting segment-1 (CS-1) of
37 us mouse-passaged FV isolates also contained LDV and that coinfection with LDV delayed FV-specific CD
38 s been reported in gp120 proteins containing LDV/I, and the precise determinants of gp120-alpha4beta7
39 ype 1, an interferon-free regimen containing LDV/VDV/TGV/RBV was well tolerated and led to SVR12 in u
40 DV-C-EPD infected mice as efficiently as did LDV-P, but its level of viremia during the persistent ph
41 e freed LDV-C of LDV-P by endpoint dilution (LDV-C-EPD).
42 19-35 Mt/y in 2040 (2.5-4.7% of total direct LDV CO2 emissions).
43 l tracers of PM derived from gasoline-driven LDVs.
44 and NO2 anthropogenic increments, and either LDVs or area sources, the smallest.
45  (LDV) and SOF (LDV/SOF; LONESTAR, ELECTRON [LDV/SOF arms], ION1, ION2, and ION3), using deep sequenc
46 s as a technique to more accurately estimate LDVs' contributions to airborne PM.
47 he mechanism of this impairment, we examined LDV-induced innate immune responses and found LDV-specif
48                                     Existing LDVs would see more advanced spark timing and more effic
49 in HCV genotype-1 (GT-1) patients who failed LDV/SOF-containing therapy.
50                                       First, LDV-induced IFN-gamma signaling indirectly modulated FV-
51         Recently, we described a fluorescent LDV-containing small molecule that was used to monitor V
52         Recently, we described a fluorescent LDV-containing small molecule, which we used to monitor
53       SVR rates were 91.3% (3,191/3,495) for LDV/SOF and 92.0% (527/573) for LDV/SOF+RBV (P = 0.65).
54 1/3,495) for LDV/SOF and 92.0% (527/573) for LDV/SOF+RBV (P = 0.65).
55 e glide paths provide long-term guidance for LDV powertrain/fuel development.
56 nt phase was only 1/10,000 that observed for LDV-P.
57 odified cost and performance projections for LDV technologies are adapted from the National Research
58 DV-induced innate immune responses and found LDV-specific induction of IFN-alpha and IFN-gamma.
59                                We have freed LDV-C of LDV-P by endpoint dilution (LDV-C-EPD).
60 conomy, and CO2 emission benefits for future LDVs through higher compression ratios for different ass
61 the conditions under which EDVs achieve high LDV market penetration in the U.S. and quantify the asso
62  to BAU, OPT gives 16% and 36% reductions in LDV greenhouse gas (GHG) emissions for 2030 and 2050, re
63                                  Ledipasvir (LDV)/sofosbuvir (SOF) has demonstrated high efficacy, sa
64 entify drug interactions between ledipasvir (LDV) and sofosbuvir (SOF) against a genotype 1b replicon
65 25) and 5 studies of combination ledipasvir (LDV) and SOF (LDV/SOF; LONESTAR, ELECTRON [LDV/SOF arms]
66 ir (SOF) with the NS5A inhibitor ledipasvir (LDV) or the NS5B non-nucleoside inhibitor GS-9669 in pat
67 uctural protein (NS)5A inhibitor ledipasvir (LDV), NS3 protease inhibitor vedroprevir (VDV), non-nucl
68 essed the efficacy and safety of ledipasvir (LDV) and sofosbuvir (SOF) for 12 weeks in HCV genotype-1
69 ssess the efficacy and safety of ledipasvir (LDV)-SOF plus RBV in patients with genotype 1 hepatitis
70 uated the safety and efficacy of ledipasvir (LDV)-sofosbuvir (SOF) in treating HCV genotype-4 infecte
71 arly the use of sofosbuvir (SOF)/ledipasvir (LDV) without RBV in this patient population.
72 tic acid-valine-proline (BIO1211) as a model LDV-containing ligand to study alpha4beta1 integrin-liga
73 V2) of gp120, including the tripeptide motif LDV/I, are thought to mediate gp120-alpha4beta7 binding.
74 iffers about 60% between the neuropathogenic LDV-C and the nonneuropathogenic LDV-P, we have develope
75          Therefore, although neuropathogenic LDVs possess the unique ability to infect anterior horn
76 e and others have found that neuropathogenic LDVs fail to retain their neuropathogenicity during pers
77 opathogenic LDV-C and the nonneuropathogenic LDV-P, we have developed a reverse transcription-PCR ass
78                       We have freed LDV-C of LDV-P by endpoint dilution (LDV-C-EPD).
79 the rapid displacement in the circulation of LDV-C by LDV-P as the predominant LDV, but LDV-C also pe
80 ost-effective was 13 and the maximum cost of LDV/SOF therapy at which treatment before LT is cost-eff
81                                   Effects of LDV operating conditions and ambient temperature (-7 and
82    Use of RBV did not impact the efficacy of LDV/SOF regimens in the ION phase III studies.
83 ple, various plasma pools of 10(9.5) ID50 of LDV-C/ml contained about 10(5) ID50 of LDV-P/ml.
84 50 of LDV-C/ml contained about 10(5) ID50 of LDV-P/ml.
85  little as 10 50% infectious doses (ID50) of LDV.
86 aim of this study was to model the impact of LDV/SOF (ledipasvir/sofosbuvir), the first Peg-IFN- and
87 2) was higher in patients receiving 90 mg of LDV for 24 weeks (63%), compared with LDV 90 mg for 12 w
88 n part to a more efficient neutralization of LDV-C than LDV-P by antibodies to the primary envelope g
89 and LDV-C coexist in most available pools of LDV-C and LDV-P.
90 C(50) for HUTS-21 binding in the presence of LDV was identical to a previously reported ligand equili
91 mpare the safety and tolerability profile of LDV-SOF with and without RBV.
92                  The specific suppression of LDV-C replication in persistently infected mice is proba
93 assess sustained virologic response (SVR) of LDV/SOF+/-ribavirin (RBV) in routine medical practice.
94 eceived the fixed-dose combination tablet of LDV-SOF once-daily plus weight-based RBV (1,000 or 1,200
95  but also maximizing the clinical utility of LDV and SOF combination regimens.
96                              Twelve weeks of LDV-SOF plus RBV was an effective and safe treatment for
97  for relapse between 8 weeks and 12 weeks of LDV/SOF (relative risk = 0.99, 95% confidence interval 0
98 1-coinfected veterans initiating 12 weeks of LDV/SOF +/- RBV or OPrD +/- RBV.
99 rds on patients taking 8, 12, or 24 weeks of LDV/SOF +/- ribavirin (RBV).
100 to determine the effectiveness of 8 weeks of LDV/SOF treatment, examine variables associated with rel
101 the effectiveness of 8 weeks and 12 weeks of LDV/SOF treatment.
102  fibrosis who previously failed 4-6 weeks of LDV/SOF with GS-9669 and/or GS-9451 received LDV/SOF for
103 ho were randomized to 8, 12, and 24 weeks of LDV/SOF with or without RBV.
104 e a high SVR rate in response to 12 weeks of LDV/SOF, even for patients with NS5A resistance-associat
105  varicosities contained a moderate number of LDVs (14.86 LDVs/microm2), some varicosities contained a
106 ome varicosities contained a large number of LDVs, whereas others contained very few.
107  We identified 1473 persons on PrOD, 5497 on LDV/SOF, and 6970 propensity score-matched untreated per
108             Renal function did not worsen on LDV/SOF regimens with TDF.
109  weeks (N = 654) with LDV/SOF (N = 1,080) or LDV/SOF+RBV (N = 872).
110  LDV 30 mg once daily (QD; Arm 1; n = 46) or LDV 90 mg QD (Arm 2; n = 94); patients in both arms also
111                       Treatment with PrOD or LDV/SOF and SVR are associated with a significant mortal
112 ed HCV-infected persons initiated on PrOD or LDV/SOF, excluding those with human immunodeficiency vir
113 ulation of LDV-C by LDV-P as the predominant LDV, but LDV-C also persisted in the mice at a low level
114 imen with very high viral eradication rates (LDV/SOF) would translate to annual productivity loss sav
115 received LDV/SOF with RBV and 1,080 received LDV/SOF alone) were analyzed.
116 ta from 1,952 patients (of whom 872 received LDV/SOF with RBV and 1,080 received LDV/SOF alone) were
117 LDV/SOF with GS-9669 and/or GS-9451 received LDV/SOF for 12 weeks.
118                            Patients received LDV/SOF (90-400 mg) once daily for 12 to 24 weeks with o
119            The majority of patients received LDV/SOF with or without ribavirin (91%) and were treated
120 ange did not differ among patients receiving LDV/SOF and tenofovir disoproxil fumarate (TDF) without
121                           Patients receiving LDV/SOF regimens showed significant improvement of PRO s
122 concomitant medications than those receiving LDV/SOF alone.
123 pasvir/sofosbuvir with or without ribavirin (LDV/SOF +/- RBV) and ombitasvir/ paritaprevir/ritonavir
124  emissions and economic impacts for the U.S. LDV fleet are estimated based on a linear-programming re
125 rmationally sensitive antibodies and a small LDV-containing ligand to study the role of the inside-ou
126 ies of combination ledipasvir (LDV) and SOF (LDV/SOF; LONESTAR, ELECTRON [LDV/SOF arms], ION1, ION2,
127     Of TN patients receiving 6 weeks of SOF, LDV, and RBV, 17 of 25 (68%) achieved SVR12.
128 inally, a group of TN patients received SOF, LDV, and RBV for 6 weeks (n = 25).
129  SVR12-9 of 9 (100%) of those receiving SOF, LDV, and RBV and 10 of 10 (100%) of those receiving SOF,
130 y 25 of 25 (100%) TN patients receiving SOF, LDV, and RBV and 23 of 25 (92%) of those receiving SOF,
131 achieved by 9 (100%) of those receiving SOF, LDV, and RBV and 7 (70%) of those receiving SOF and LDVD
132                                          SOF/LDV without RBV was used for 12 weeks in patients with e
133 med to assess the efficacy and safety of SOF/LDV fixed-dose combination without RBV in patients with
134                       The combination of SOF/LDV without RBV for 12 or 24 weeks produced 100% SVR 12
135 ng a third DAA to ledipasvir and sofosbuvir (LDV/SOF) can result in high SVR rates in patients withou
136 ents treated with ledipasvir and sofosbuvir (LDV/SOF) with and without RBV.
137 ght weeks duration of ledipasvir/sofosbuvir (LDV/SOF) can be considered in genotype 1 hepatitis C vir
138         The uptake of ledipasvir/sofosbuvir (LDV/SOF) regimens across health care settings has been r
139  dasabuvir (PrOD) and ledipasvir/sofosbuvir (LDV/SOF) regimens upon mortality.
140 patients treated with ledipasvir/sofosbuvir (LDV/SOF) were significantly less likely to achieve cure
141 combination tablet of ledipasvir/sofosbuvir (LDV/SOF) with and without ribavirin (RBV) resulted in hi
142 g concomitant PPI and ledipasvir/sofosbuvir (LDV/SOF).
143  the efficient replication of superinfecting LDV-P.
144 00 ng/ml of SOF must be attained to suppress LDV-resistant subpopulations.
145  more efficient neutralization of LDV-C than LDV-P by antibodies to the primary envelope glycoprotein
146 s as well as concomitant medication use than LDV/SOF alone.
147               With this assay, we found that LDV-P and LDV-C coexist in most available pools of LDV-C
148                                          The LDV-induced suppression was not mediated by T regulatory
149 ve for the total replicon population and the LDV-resistant population, but a threshold concentration
150 hods, the L-type current was enhanced by the LDV but not LEV peptide and was blocked by PP2 or antibo
151 have little effect on GHG emissions from the LDV sector but are more effective in the electricity sec
152 wn to be located in similar positions in the LDV-C 3'(-)NCR and SHFV 3'(-)209 RNAs.
153   The structure/activity relationship of the LDV sequence is discussed and related to the recently pu
154 concentration of a peptide consisting of the LDV sequence of the fibronectin connecting segment, Ac-L
155   A series of cyclized peptides based on the LDV sequence of CS1 were synthesized and assayed for inh
156 er and mammary epithelial cells and that the LDV peptide represses PHSRN-stimulated MMP-1 production
157 nd to the SHFV 3'(-)209 RNA also bind to the LDV-C 3'(-)NCR RNA and equine arteritis virus 3'(-)NCR R
158              Patients were randomized 1:2 to LDV 30 mg once daily (QD; Arm 1; n = 46) or LDV 90 mg QD
159                        Adding a third DAA to LDV/SOF may result in a moderate SVR rate, lower than th
160  concentration-dependent vasoconstriction to LDV peptides but not to Leu-Glu-Val (LEV) control peptid
161 distinguishes between the genomes of the two LDVs and detects as little as 10 50% infectious doses (I
162 ction or immune responses, but unexpectedly, LDV-induced IFN-gamma production dampened Th1 adaptive i
163 om a societal perspective, HCV therapy using LDV/SOF with ribavirin before LT is the most cost-effect
164 in with peptides containing the Leu-Asp-Val (LDV) integrin--binding sequence, which is found in the C
165 rs of alpha4beta1, based on the Leu-Asp-Val (LDV) sequence from the alternatively spliced connecting
166 ntly described leucine-aspartic acid-valine (LDV)-based small molecule inhibitor of alpha4beta1 (BIO-
167 ion to meet growing U.S. light duty vehicle (LDV) demand.
168 sion reductions from the light-duty vehicle (LDV) fleet consistent with stabilization of atmospheric
169 ric vehicles into the US light duty vehicle (LDV) sector.
170  1, light duty vehicle-low emission vehicle (LDV-LEV), light duty truck 2-LEV (LDT2-LEV), and Tier 2
171 y that is restricted to light-duty vehicles (LDVs) and (2) inverse dispersion model calculations.
172 ng advanced controls on light-duty vehicles (LDVs) and other sources.
173  emission compliance of Light Duty Vehicles (LDVs) around the world and to establish the reference ve
174                         Light-duty vehicles (LDVs) in the United States and elsewhere are required to
175 -fueled privately owned light duty vehicles (LDVs) operated in Tehran.
176 efits of designing U.S. light-duty vehicles (LDVs) to attain higher fuel economy by utilizing higher
177 inantly gasoline-driven light-duty vehicles (LDVs) traversing the Washburn Tunnel in Houston, Texas d
178 ted from three light-duty gasoline vehicles (LDVs) operating on gasoline (e0) and ethanol-gasoline fu
179 esicles (CLV) and large dense core vesicles (LDV).
180 ) and lactate dehydrogenase-elevating virus (LDV) are endemic mouse viruses that can cause long-term
181 es of lactate dehydrogenase-elevating virus (LDV) differ from nonneuropathogenic isolates in their un
182  with lactate dehydrogenase-elevating virus (LDV) impairs early adaptive immune responses to Friend v
183                                        While LDV did not alter the type of acute pathology induced by
184 1), 12 (N = 867), or 24 weeks (N = 654) with LDV/SOF (N = 1,080) or LDV/SOF+RBV (N = 872).
185 sisted in the mice at a low level along with LDV-P.
186 also contained LDV and that coinfection with LDV delayed FV-specific CD8(+) T-cell responses during a
187  mg of LDV for 24 weeks (63%), compared with LDV 90 mg for 12 weeks (54%) and LDV 30 mg for 24 weeks
188 not only in mice infected concomitantly with LDV but also in mice chronically infected with LDV 8 wee
189 V but also in mice chronically infected with LDV 8 weeks prior to infection with FV.
190                     Coinfection of mice with LDV and FV provides a well-defined, natural host model f
191  1 did not affect the treatment outcome with LDV/SOF.
192 uctivity, treatment of CHC GT1 patients with LDV/SOF-based regimens is likely to result in significan
193    In this real-world cohort, SVR rates with LDV/SOF+/-RBV nearly matched the rates reported in clini
194                  Patients receiving RBV with LDV/SOF were more likely to require dose modification, i
195              IFN- and RBV-free regimens with LDV/SOF result in early HCV suppression with simultaneou
196                     Of patients treated with LDV, SOF, and the NS3/4A protease inhibitor GS-9451 for
197 ment in HCV genotype 1 patients treated with LDV/SOF+/-RBV (ION-1, -2, and -3).
198 nt-naive, HCV-infected veterans treated with LDV/SOF+/-RBV.
199 1,979 patients with chronic HCV treated with LDV/SOF.
200        Intensification of SOF treatment with LDV reduced the emergence of L159F or V321A to 2% (1 of
201         An 8-week duration of treatment with LDV/SOF is highly effective in properly selected patient
202     On the other hand, during treatment with LDV/SOF+RBV, PRO scores declined (up to -5.5% regardless
203                                 PPI use with LDV/SOF +/- RBV did not affect SVR (89.7% [131/146] with
204        African American race or PPI use with LDV/SOF +/- RBV was not associated with lower SVR rates,
205 , 634 patients were treated for 8 weeks with LDV/SOF, of whom all had outcomes of cure or relapse wit

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