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1 em, bleeding times were performed in normal, hemophilic, and adenoviral-treated hemophilic mice.
2                                              Hemophilic animals developed subcutaneous hematomas; nor
3 he protease state and restores hemostasis in hemophilic animals upon vascular injury.
4                       Moreover, treatment of hemophilic animals with a TLR9 agonist suppressed FVIII-
5 specific tolerance, but there are no data in hemophilic animals with pre-existing inhibitors.
6  liver of adeno-associated virus (AAV)-naive hemophilic animals.
7 nd no longer detectable at day 21 of life in hemophilic animals.
8          When bleeding occurs in the joints, hemophilic arthropathy (HA) may develop, resulting in he
9 erin deposition in the knee joint tissues of hemophilic arthropathy (HA) patients using quantitative
10  bleeding into joints in hemophilia leads to hemophilic arthropathy (HA), a debilitating joint diseas
11 interaction with EPCR in the pathogenesis of hemophilic arthropathy and its treatment with recombinan
12  be major contributors to the development of hemophilic arthropathy following hemarthrosis.
13 d failure load suggests the negative role of hemophilic arthropathy in bone density loss.
14                           The development of hemophilic arthropathy in EPCR-overexpressing FVIII-/- m
15                                              Hemophilic arthropathy occurs in all patients with sever
16  contribute to end-stage joint degeneration (hemophilic arthropathy), the major morbidity of hemophil
17  EPCR deficiency protects against developing hemophilic arthropathy, administration of a single dose
18 n time, a debilitating, crippling arthritis, hemophilic arthropathy, develops.
19  of endothelial protein C receptor (EPCR) in hemophilic arthropathy.
20 er wounding as it had been proposed to do in hemophilic arthropathy.
21                                              Hemophilic bleeding into joints causes synovial and micr
22 se of the experiment than in normal blood or hemophilic blood with factor VIII replaced, but signific
23 erformed on the plasma of more patients with hemophilic C-domain mutations, prediction of surface bin
24 tion in the two strains of mice; 100% of the hemophilic CD-1 mice formed antibodies to human factor I
25                                     Finally, hemophilic dogs given Solulin had improved clot strength
26              As a control, a fourth group of hemophilic dogs received 50 IU/kg of a high purity, plas
27                              Three groups of hemophilic dogs received either 50, 100, or 200 IU/kg of
28 a method of treating the disease in mice and hemophilic dogs through intramuscular injection of a rec
29 F.IX) expression at a range of doses, and in hemophilic dogs we observed approximately 50-fold higher
30                                           In hemophilic dogs, a dose of rAAV that was approximately 1
31 se strategies are currently being applied to hemophilic dogs.
32 plete correction of the bleeding disorder in hemophilic dogs.
33  induced pluripotent stem cells (iPSCs) of a hemophilic donor, results in 12% correction of the inver
34 uce tolerance in both naive and fVIII-primed hemophilic (E16 fVIII(-/-)) mice.
35                 To confirm in vitro results, hemophilic E17 knockout mice were pretreated with antibo
36 ies and loss of tolerance to both native and hemophilic factor VIII proteins.
37 ars to be more critical than his endogenous, hemophilic factor VIII to his developing high-titer anti
38 emained clinically meaningful to distinguish hemophilic from nonhemophilic FVIII activity levels.
39 t-specific alphaIIb promoter in platelets of hemophilic (FVIIInull) mice to create 2bF8trans mice.
40 lytic properties of Solulin are exhibited in hemophilic human (in vitro) and dog (in vivo/ex vivo) bl
41  T(H)17/T(H)1-polarized cells play a role in hemophilic immune responses to FVIII.
42                                        Often hemophilic inhibitor plasmas were partially neutralized
43  joint-directed gene transfer may ameliorate hemophilic joint destruction, even in the absence of cir
44 uld play a major role in the pathogenesis of hemophilic joint disease (HJD).
45 ole in the proliferative changes observed in hemophilic joint disease and that aberrant expression of
46 tality, we studied a cohort comprised of all hemophilic males identified by a six-state surveillance
47 of hepatitis C virus (HCV) was studied in 21 hemophilic men coinfected with HCV and human immunodefic
48  progression was assessed in a cohort of 109 hemophilic men infected with HIV-1 for a median of 12.7
49     HIV and HCV virus loads were examined in hemophilic men, as were risks of HIV and HCV transmissio
50              In macrovascular injury models, hemophilic mice administered mFVIIa-FMR exhibited superi
51 own to be T-cell dependent by its absence in hemophilic mice also deficient for the T-cell costimulat
52 iants exhibited improved pharmacokinetics in hemophilic mice and rabbits.
53                                Unexpectedly, hemophilic mice developed twice as many blood vessels in
54 1-/- mice were generated, with ST2-deficient hemophilic mice developing significantly reduced joint d
55 l littermate controls, whereas the untreated hemophilic mice exhibited heavy blood loss and prolonged
56 ferent bleeding-time techniques, the treated hemophilic mice gave values identical to normal litterma
57                                           In hemophilic mice injected with KP1-packaged recombinant A
58  of hFVIII rescued the bleeding diathesis of hemophilic mice lacking endogenous FVIII.
59 ul for gene transfer studies, while the CD-1 hemophilic mice may be of greater utility in studying th
60    We previously found that oral delivery to hemophilic mice of cholera toxin B subunit-coagulation f
61                                              Hemophilic mice treated with lentiviral vectors showed e
62          These data suggest that the C57B1/6 hemophilic mice will be more useful for gene transfer st
63 nses to fVIII could be achieved in immunized hemophilic mice with existing anti-fVIII titers.
64 ocked the primary response to factor VIII in hemophilic mice with intact B7 function.
65 r increases in antifactor VIII when given to hemophilic mice with low antifactor VIII antibody titers
66  cells can efficiently restore hemostasis to hemophilic mice with preexisting inhibitory antibodies u
67  coagulation capacity in MiniAdFVIII-treated hemophilic mice, as determined by tail clipping observat
68                       Using this approach in hemophilic mice, BDD-F8 was expressed in liver cells as
69                        In bleeding models of hemophilic mice, PEGylated FVIII not only exhibited prol
70 n normal, hemophilic, and adenoviral-treated hemophilic mice.
71  R338L-Padua after AAV-based gene therapy in hemophilic mice.
72 cantly ameliorated joint damage during HA in hemophilic mice.
73 aptive immune responses in immune-competent, hemophilic mice.
74 tive in correcting the coagulation defect in hemophilic mice.
75 m tolerance to FVIII in different strains of hemophilic mice.
76 f did not reduce the severity of bleeding in hemophilic mice.
77 rsistence of ferric iron was also greater in hemophilic mice.
78  and prophylactic dose-dependent efficacy in hemophilic monkeys.
79                      We used a new humanized hemophilic mouse model to identify FVIII peptides presen
80                         To explore this in a hemophilic mouse model, we characterized 2 variants of m
81                   Evaluation of experimental hemophilic mouse models with or without functional IDO1
82 ained higher activities as compared with the hemophilic mutant FVIII forms.
83 12.3; P=0.04), despite a similar spectrum of hemophilic mutations and degree of severity of illness i
84 ophageal echocardiogram (TEE), revealed in a hemophilic patient, and diagnosed with cardiac CT.
85  The zeolite nanoparticles can be adapted to hemophilic patients (hemophilia A (F-VIII deficient) and
86                                   Of the 178 hemophilic patients (mean age, 29 years), TTV-DNA was fo
87                    All 1816 HCV-seropositive hemophilic patients at 16 centers were followed for up t
88                                              Hemophilic patients were screened for factor VIII C-doma
89           To clarify these relationships, 42 hemophilic patients who developed ESLD and random sample
90  genotypes, the distribution of genotypes in hemophilic patients who had been treated with nonvirally
91 o developed ESLD and random samples from 164 hemophilic patients with HCV infection alone and 146 wit
92                                    From 3993 hemophilic patients with hepatitis C, 257 sibling pairs,
93 far indicates that the use of factor VIIa in hemophilic patients with inhibitors is both safe and eff
94 for the treatment of hemorrhagic episodes in hemophilic patients with inhibitors to factors VIII and
95 o offer a more objective measure of both the hemophilic phenotype as well as the response to treatmen
96 n of the vector to FVIII-deficient dogs, the hemophilic phenotype was corrected, based on determinati
97 cient endothelial-KO models display a severe hemophilic phenotype with no detectable plasma FVIII act
98 y is less than 1% and the mouse exhibits the hemophilic phenotype.
99                              Clots formed in hemophilic plasma in the presence of a plasminogen activ
100                                           In hemophilic plasma, FXa(I16L) and FXa(V17A) have prolonge
101 of clotting times and thrombin generation in hemophilic plasma.
102 inhibitors were present in 71% (24 of 34) of hemophilic plasmas, but only 33% (7 of 21) of autoantibo
103 s pattern was found in only 15% (5 of 34) of hemophilic plasmas.
104 tion may facilitate thrombin generation in a hemophilic setting.
105                                              Hemophilic siblings provide a unique population to explo
106 nd suggest novel strategies for ameliorating hemophilic states through drugs that disrupt the ZPI-PZ
107                               In conclusion, hemophilic subjects coinfected with chronic HBV and thos
108 of local and systemic angiogenic response in hemophilic subjects with recurrent hemarthroses suggesti
109  of HCV, we studied a cohort of HCV-infected hemophilic subjects without human immunodeficiency virus
110  pairs to those expected for randomly paired hemophilic subjects.
111 flammatory and proliferative disorder termed hemophilic synovitis (HS).
112 lted in pathologic changes observed in human hemophilic synovitis and a marked increase in synovial c
113 od and the molecular changes responsible for hemophilic synovitis are not known.
114 t to fully prevent the development of milder hemophilic synovitis in EPCR-/-FVIII-/- mice.
115 cking monoclonal antibodies markedly reduced hemophilic synovitis in FVIII-/- mice subjected to joint
116 d 3 doses of rFVIIa partly protected against hemophilic synovitis in these mice.
117                                              Hemophilic synovitis was evaluated by monitoring joint b
118 icrovascular proliferation and inflammation (hemophilic synovitis) that contribute to end-stage joint
119 thin the joint space can protect joints from hemophilic synovitis, we established a hemophilia B mous
120 - mice significantly reduced the severity of hemophilic synovitis.
121 ers to identify the onset and progression of hemophilic synovitis.
122 in cell proliferation and the development of hemophilic synovitis.
123 s in a chronic inflammatory condition termed hemophilic synovitis.
124 pothesized that iron plays a similar role in hemophilic synovitis.
125 ity, survival is significantly greater among hemophilics who receive medical care in HTCs.

 
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