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1                                              CVF attenuated the development of AHR by O3.
2                                              CVF depleted both systemic and brain C3 by the time of s
3                                              CVF elafin in early pregnancy was modestly predictive of
4                                              CVF plus NK cell depletion further prolonged survival (>
5                                              CVF treatment, when given in the period immediately befo
6                                              CVF was given daily until rejection.
7                                              CVF was injected i.v., and neutrophil sequestration and
8                                              CVF was measured with a multistage treadmill test and wa
9                                              CVF-dependent C3 cleavage in the deficient serum require
10  2, p = .009); PEEP-CVF (24 +/- 1, p = .01); CVF-PLV (30 +/- 2, p = .03); and CVF-PEEP (37 +/- 1, p =
11                                     Adjusted CVF cathelicidin and HNE concentrations (but not elafin)
12            Platelet depletion did not affect CVF-induced up-regulation of lung vascular P-selectin, i
13 , p = .01); CVF-PLV (30 +/- 2, p = .03); and CVF-PEEP (37 +/- 1, p = .04).
14  TIMP-2 along with upregulation of MMP-2 and CVF-I in the atrium is associated with the development o
15 er, the combination of high-dose GPI 562 and CVF resulted in a significant decrease in intragraft pla
16 re overexpressed in endocervical+BVAB CM and CVF from women with BV and were capable of disrupting en
17 esis of xenograft rejection and that CyA and CVF suppress xenograft rejection by preventing exposure
18                       Combination of CyA and CVF, which we have previously shown to overcome rejectio
19                                   Plasma and CVF concentrations for both drugs fell rapidly after rin
20                               In SP, RF, and CVF, baseline HIV-1 RNA was >40 copies/mL in 12/15, 13/1
21                               In SP, RF, and CVF, the baseline HIV-1 RNA was >40 copies/mL in 12/15,
22 hile unbound RPV exceeded the EC50 in RT and CVF but not in SP.
23  Unbound CAB exceeded the EC50 in SP, RT and CVF while unbound RPV exceeded the EC50 in RT and CVF bu
24 nd bictegravir concentrations in SP, RT, and CVF highly exceeded the EC50 value (1.1 ng/mL).
25 in-unbound BIC concentrations in SP, RT, and CVF highly exceeded the half-maximal effective concentra
26 al bictegravir concentrations in SP, RT, and CVF were 65.5 (20.1-923) ng/mL, 74.1 (6.0-478.5) ng/g, a
27 dian total BIC concentrations in SP, RT, and CVF were 65.5 (20.1-923) ng/mL, 74.1 (6.0-478.5) ng/g, a
28 investigated the effects of various sCR1 and CVF regimens, and combinations thereof, in the discordan
29 pha Gal) antibody, and a slower rise in anti-CVF antibody.
30   Cervical 3TCtp was not correlated with any CVF cytokines.
31 T=32 hr), although not to the same extent as CVF.
32 moderate PA, would be associated with better CVF and lower %BF.
33 d to CVF from women experiencing term birth, CVF from women who subsequently experienced preterm birt
34             Systemic complement depletion by CVF prevented the induction of anterior uveitis by anti-
35       These fevers were totally prevented by CVF (10 U/mouse, i.v.) pretreatment.
36 es of C3 and factor B activation in vitro by CVF demonstrated that in factor D-deficient serum the al
37         This study investigated the Cheoeum (CVF) and MIRAE-2 (M2VF) vent fields in the 12-16 degrees
38  cobra venom factor-dependent C5 convertase (CVF, Bb) made with CVF purified from the venom of Naja n
39              By activating C3/C5 convertase, CVF depletes complement while additionally generating C5
40      Moreover, 30-35% of xenografts from CsA/CVF rats survived long term and accommodated in the seco
41                          Xenografts from CsA/CVF-treated rats survived significantly longer upon retr
42          Long-term xenograft survival in CsA/CVF-treated recipients was associated with an ongoing Th
43 ly in the control group, whereas, in the CsA/CVF-treated group, IgG EXA were totally suppressed.
44                              Thus, under CyA/CVF treatment, complement activation by hamster cells wa
45 the administration of cobra venom factor; d) CVF-PLV group, animals received partial liquid ventilati
46 enom factor (CVF), or splenectomy plus daily CVF.
47 uid ventilation after cobra venom factor; e) CVF-PEEP group, animals received PEEP after cobra venom
48 cantly decreased by administration of either CVF or Crry-Ig.
49 eturn, and when combined with blood exchange/CVF/CyA facilitated long-term survival of grafts.
50 ) or in combination with cobra venom factor (CVF) (DXR model).
51 ts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days, a time when the ant
52 mplement-depleting agent cobra venom factor (CVF) 24 hr before HI lesioning and evaluated both acute
53 tion of complement using cobra venom factor (CVF) accelerates pulmonary xenograft failure.
54 ombination with systemic cobra venom factor (CVF) administration to deplete complement when delayed x
55 complement inhibition by cobra venom factor (CVF) and sustained T-cell immunosuppression by cyclospor
56 rprisingly, injection of cobra venom factor (CVF) caused a profound and reproducible reduction in ser
57                          Cobra venom factor (CVF) depletes complement and may therefore be of use in
58 y into rats treated with cobra venom factor (CVF) develop disease over 72 hours.
59 zation by treatment with cobra venom factor (CVF) diminished serum anti-PPS14 concentrations after pr
60 estigate the efficacy of cobra venom factor (CVF) in preventing hyperacute rejection (HAR) after pig-
61                          Cobra venom factor (CVF) induces lung injury through oxidant- and neutrophil
62 ment by i.v. infusion of cobra venom factor (CVF) is known to be P-selectin dependent.
63 mplement depletion using cobra venom factor (CVF) markedly reduced the efficacy of rituximab and 1F5
64 ivation of complement by cobra venom factor (CVF) or after intrapulmonary deposition of IgG immune co
65 aperitoneal injection of cobra venom factor (CVF) or complement receptor-related gene y (Crry)-Ig, a
66 ed using either CsA plus cobra venom factor (CVF) or CsA plus rapamycin.
67 ent of athymic rats with cobra venom factor (CVF) partially reverses this effect.
68 mplement inhibition with cobra venom factor (CVF) plus daily and continuing cyclosporin A (CyA) preve
69 aperitoneal injection of cobra venom factor (CVF) reduced C3 levels in the cornea approximately 40%,
70 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regeneration following ca
71 it was preincubated with cobra venom factor (CVF) to deplete C3.
72 aft dysfunction by using cobra venom factor (CVF) to deplete recipient complement and transgenic swin
73        Administration of cobra venom factor (CVF), 1 day before and at the time of transplantation, r
74 toneal injection of 35 U cobra venom factor (CVF), 24 hours before antibody injection.
75 d to immobilized C3b and cobra venom factor (CVF), a C3b analogue.
76 ft recipients as well as cobra venom factor (CVF), a complement blocker, treatment.
77 thout heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus interferon-gamma treatm
78  daily administration of cobra venom factor (CVF), or splenectomy plus daily CVF.
79 noclonal antibody (mAb), cobra venom factor (CVF), pig hematopoietic growth factors (interleukin-3 (p
80  by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was significantly increased.
81 rther investigated using cobra venom factor (CVF), which systemically depleted the rats of complement
82  susceptibilities to the cobra venom factor (CVF)-dependent convertase.
83 ft survival was 62 hr in cobra venom factor (CVF)-treated controls versus 108 hr (DSG), 129 hr (LEF),
84 yclosporine (CsA) and/or cobra venom factor (CVF).
85 us injection of purified cobra venom factor (CVF).
86  of complement (C) using cobra venom factor (CVF).
87 ion of lung injury using cobra venom factor (CVF); b) PLV-CVF group, animals received partial liquid
88 y (p < 0.001) delayed by cobra venom factor (CVF; 11 +/- 8 h in four of five cases) but was still mor
89 depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]).
90 g predictors of confirmed virologic failure (CVF) with cabotegravir + rilpivirine long-acting (CAB +
91 >=50 copies/mL, confirmed virologic failure (CVF; 2 consecutive HIV-1 RNA >=200 copies/mL), safety an
92 L, incidence of confirmed virologic failure (CVF; 2 consecutive measurements >=200 copies/mL), safety
93  are associated with cardiovascular fitness (CVF) and percentage of body fat (%BF) in adolescents.
94 e method, referred to as covariance fitting (CVF), couples Q-matrix calculations with a maximum likel
95 d casing pressure (SCP) or casing vent flow (CVF)-two indicators of compromised well integrity.
96 rectal fluid (RF), and cervicovaginal fluid (CVF) at baseline, at days 3, 7, 14, and 28, and at weeks
97 rectal fluid (RF), and cervicovaginal fluid (CVF) at baseline; Days 3, 7, 14, and 28; and Weeks 12 an
98 d glycomic analyses of cervicovaginal fluid (CVF) from 36 pregnant women at high risk of preterm birt
99 l+BVAB CM), as well as cervicovaginal fluid (CVF) from women with BV, disrupted epithelial polarizati
100 od HIV-1 DNA load, and cervicovaginal fluid (CVF) HIV-1 DNA load were determined using quantitative r
101 vaginal microbiota and cervicovaginal fluid (CVF) immunophenotype data collected from 133 women at hi
102                  Human cervicovaginal fluid (CVF) is a complex, functionally important and glycan ric
103 measured in over 1,000 cervicovaginal fluid (CVF) samples (10 to 24 weeks' gestation).
104 e evaluated in plasma, cervicovaginal fluid (CVF), and cervical tissue samples.
105 ectal tissue (RT), and cervicovaginal fluid (CVF).
106 kines were measured in cervicovaginal fluid (CVF).
107 or MK-2048) and similar AUCs across arms for CVF samples.
108                           A higher index for CVF was associated with higher amounts of moderate and v
109        The cardiac collagen volume fraction (CVF) and cardiac myocyte apoptosis index in aFGF-NP+UTMD
110  in the LA, type I collagen volume fraction (CVF-I) increased significantly in the PmAF group followe
111  dilution as high as 1:32, while plasma from CVF-treated animals displays anti-HSV activity at lower
112                           In the PsAF group, CVF-I/CVF-III ratio was significantly correlated with AF
113 3 for histologic neutrophil counting): a) GV-CVF group, animals received gas ventilation (GV) with th
114 d with the cobra venom factor only group (GV-CVF 47 +/- 2 neutrophils/high-power field), reductions i
115 4, p = .01) groups when compared with the GV-CVF group (0.62 +/- 0.07).
116                    When compared with the GV-CVF group, a trend toward a reduction in myeloperoxidase
117  the Q8W arm and 2 (0.4%) in the Q4W arm had CVF.
118 rall, 1.4% (n = 23/1651) of participants had CVF through 152 weeks.
119 ing data beyond week 48, 18 participants had CVF; those in the higher BMI group (n = 8) all had at le
120                         We conclude that (i) CVF prevents HAR, (ii) the addition of Spx + IS delays r
121                     In the PsAF group, CVF-I/CVF-III ratio was significantly correlated with AF durat
122 as correlated with IL-10, IL-7, and IL-17 in CVF.
123                 Immunohistologic analysis in CVF-treated nude recipients with or without splenectomy
124 l an extremely rich and complex N-glycome in CVF of pregnant and non-pregnant women, abundant in pauc
125 that the apparent role of these molecules in CVF-induced lung injury depends on the method used to bl
126 els of complement deposition were present in CVF-treated recipients.
127 All women achieved undetectable HIV-1 RNA in CVF at Day 14.
128 All women achieved undetectable HIV-1 RNA in CVF at day 14.The median total bictegravir concentration
129 to determine the degree to which variance in CVF and %BF was explained by PA, after control for age,
130 ex >=30 kg/m2) was associated with increased CVF risk, consistent with prior analyses.
131                                           LA CVF-I significantly correlated with LA dimension and TIM
132                        Analysis of lesioned, CVF-treated animals demonstrated minimal neuronal C3 dep
133               WBI, ATG, MMF, anti-CD40L mAb, CVF, pIL3, pSCF, and PGI2 had no effect on purified babo
134  diabetes group showed similar results (MCD, CVF and cardiac myocyte apoptosis index) to other aFGF t
135 ke conventional sum-of-squares minimization, CVF fits both the magnitude of the recorded current and
136 ated data generated using a consensus model, CVF leads to reasonable parameter estimates and accurate
137 H2 was found similarly to inhibit CP but not CVF convertase activation, and the effects of alanine su
138 vel, distal binding site for the CP, but not CVF convertase.
139                      The concerted action of CVF and CPA significantly increases the life span of ath
140                   However, administration of CVF abolishes the tolerance induction.
141 onatal rat brain, systemic administration of CVF does not eliminate complement deposition within inju
142 ystemic injection and topical application of CVF reduced local C3 levels >60%, which eliminated MAb-m
143 ever, whereas the core temperature (T(c)) of CVF vehicle-treated controls rose approximately 1 degree
144 e dose of CVF, or sCRI plus a single dose of CVF (MST=64 hr), had similar xenograft survival times.
145 Grafts in rats treated with a single dose of CVF (MST=67 hr) or repetitive doses of CVF (MST=69 hr) s
146 ed that addition of sCR1 to a single dose of CVF resulted in decreased macrophage activation and redu
147        Animals treated with a single dose of CVF, or sCRI plus a single dose of CVF (MST=64 hr), had
148 se of CVF (MST=67 hr) or repetitive doses of CVF (MST=69 hr) survived significantly longer than those
149               When we examined the effect of CVF on HIV-1 transmigration through endocervical epithel
150 re near normal, and the enhancing effects of CVF treatment on the secondary anti-PPS14 antibody respo
151          In the current studies, infusion of CVF caused the appearance in plasma of C5a (as revealed
152 in a time-dependent manner after infusion of CVF.
153 oons studied, the intramuscular injection of CVF (0.25 mg/kg) was followed by a marked reduction in s
154  and lung injury in response to injection of CVF occurs through alternative pathways in mice with gen
155          A second intramuscular injection of CVF on day 14 was ineffective in reducing C3, CH50, and
156  of extravascular albumin after injection of CVF when compared to wild-type mice.
157                 The major oligosaccharide of CVF is known to contain alpha Gal residues, which we sug
158  quartile) did not improve the prediction of CVF beyond the presence of a combination of >=2 baseline
159 inetic covariates as potential predictors of CVF.
160 m2 were associated with an increased risk of CVF (P < .05 adjusted incidence rate ratio), with partic
161 ese baseline factors having a higher risk of CVF.
162 o active enzyme conformational transition of CVF-bound factor B.
163 onded with statewide increases in SCP and/or CVF occurrence in Colorado and Pennsylvania.
164 d a wider range (0.3 to 26.5%) of SCP and/or CVF occurrence than previously reported, highlighting th
165 wells were more likely to exhibit SCP and/or CVF than vertical wells in Colorado and Pennsylvania, an
166 inetic models with up to 11 free parameters, CVF leads to reasonable parameter estimates.
167 r field): PLV-CVF (20 +/- 2, p = .009); PEEP-CVF (24 +/- 1, p = .01); CVF-PLV (30 +/- 2, p = .03); an
168 he PLV-CVF (0.29 +/- 0.08, p = .02) and PEEP-CVF (0.34 +/- 0.04, p = .01) groups when compared with t
169 before the induction of lung injury; c) PEEP-CVF group, animals received positive end-expiratory pres
170   VCV and MK-2048 were detectable in plasma, CVF, and cervical tissue samples, and drug release and p
171                  The combination of CsA plus CVF, the latter given for either 2 days or 11 days, resu
172 njury using cobra venom factor (CVF); b) PLV-CVF group, animals received partial liquid ventilation b
173 l groups (neutrophils/high-power field): PLV-CVF (20 +/- 2, p = .009); PEEP-CVF (24 +/- 1, p = .01);
174 ntent was significantly decreased in the PLV-CVF (0.29 +/- 0.08, p = .02) and PEEP-CVF (0.34 +/- 0.04
175                        In C6-deficient rats, CVF infusion caused the same level of lung injury (measu
176                                 Two received CVF+/-Spx, which extended survival to 5 and 6 days, resp
177       Using multivariable linear regression, CVF IL-17, tissue dATP, plasma estradiol, and plasma ten
178  attendant toxicity associated with repeated CVF administration.
179 analysis of N- and O-glycans revealed a rich CVF glycome.
180                                 Twenty-seven CVF Sprague-Dawley rats were subjected to OPW exposures,
181 ttreatment decubitus CTM examinations showed CVF resolution.
182 ir concentrations were quantified in BP, SP, CVF and rectal tissue (RT) at 24 hours postdose (C24h) o
183 s postdose (C24h) were quantified in BP, SP, CVF and rectal tissue (RT) on Day 28 and Week 12 using a
184                          Six underwent Spx + CVF therapy + IS; graft survival was 3 hr (technical com
185 ndocervical epithelium, we demonstrated that CVF samples with greater concentrations of BV-associated
186                       Both the basal and the CVF-inducible lung mRNA for inducible nitric oxide synth
187 the CVF-PLV (0.42 +/- 0.05, p = .07) and the CVF-PEEP (0.39 +/- 0.06, p = .07) groups.
188 preterm birth exhibited sharp changes in the CVF glycome shortly before delivery.
189                                       In the CVF model, intravenous infusion (but not intratracheal i
190 ction in myeloperoxidase was observed in the CVF-PLV (0.42 +/- 0.05, p = .07) and the CVF-PEEP (0.39
191 we thus show that the addition of CPA to the CVF treatment results in a significant increase in viral
192 Direct fibrin glue administration within the CVF may be one of the key factors for success.
193    C1-INH prevented factor B from binding to CVF-coated beads and dissociated bound factor B from suc
194 1-INH showed cross competition in binding to CVF-coated beads.
195                                  Compared to CVF from women experiencing term birth, CVF from women w
196 valuated to understand their contribution to CVF (alone or in combination).
197 aboon (n=3); group III, unmodified swine-to-(CVF treated) baboon (n=3); and group IV, hCD59/hDAF swin
198  (>7 days in four of five cases; p < 0.01 vs CVF only).
199 d 120 hr (DSG and LEF; all groups P<0.01 vs. CVF alone).
200              Similar results were found when CVF was injected in vivo during the early stages of CLP.
201  as 0.2 mug of antigen, and was maximal when CVF was administered within 2 days of immunization.
202 xenograft survival (2.2+/-0.4 days), whereas CVF alone led to minimal prolongation of survival (5.6+/
203                        LEF or DSG along with CVF can result in the longest prolongation of xenograft
204 east 1 other baseline factor associated with CVF (archived RPV resistance-associated mutations or HIV
205           Blood exchange in combination with CVF/CyA treatment dramatically decreased the level of pr
206  When blood HIV-1 DNA load was combined with CVF HIV-1 DNA load, the association with transmission in
207 on, and leukocyte infiltration compared with CVF alone.
208 ith heat inactivation and was corrected with CVF treatment.
209 plus mAb and with a human C3 derivative with CVF-like functions (HC3-1496) plus mAb was both superior
210 -dependent C5 convertase (CVF, Bb) made with CVF purified from the venom of Naja naja (CVFn) and Naja
211               Eight and 10 participants with CVF had treatment-emergent, resistance-associated mutati
212                            Pretreatment with CVF (group III) was ineffective in preventing xenograft
213 of the intragraft immune responses seen with CVF/sCR1 combination therapy may augment further therape
214 ompared with that in recipients treated with CVF alone.
215 at survive indefinitely in rats treated with CVF plus CyA express the anti-inflammatory gene heme oxy
216 f lymphoma-bearing mice after treatment with CVF plus mAb and with a human C3 derivative with CVF-lik
217                                      Without CVF, inhibition of cell infection by HSV is observed at

 
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