ライフサイエンスコーパス: hemophilic

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 d failure load suggests the negative role of hemophilic arthropathy in bone density loss.

9 Hemophilic arthropathy occurs in all patients with sever

10 contribute to end-stage joint degeneration (hemophilic arthropathy), the major morbidity of hemophil

11 n time, a debilitating, crippling arthritis, hemophilic arthropathy, develops.

12 er wounding as it had been proposed to do in hemophilic arthropathy.

13 Hemophilic bleeding into joints causes synovial and micr

14 se of the experiment than in normal blood or hemophilic blood with factor VIII replaced, but signific

15 erformed on the plasma of more patients with hemophilic C-domain mutations, prediction of surface bin

16 tion in the two strains of mice; 100% of the hemophilic CD-1 mice formed antibodies to human factor I

17 Finally, hemophilic dogs given Solulin had improved clot strength

18 As a control, a fourth group of hemophilic dogs received 50 IU/kg of a high purity, plas

19 Three groups of hemophilic dogs received either 50, 100, or 200 IU/kg of

20 a method of treating the disease in mice and hemophilic dogs through intramuscular injection of a rec

21 F.IX) expression at a range of doses, and in hemophilic dogs we observed approximately 50-fold higher

22 In hemophilic dogs, a dose of rAAV that was approximately 1

23 plete correction of the bleeding disorder in hemophilic dogs.

24 se strategies are currently being applied to hemophilic dogs.

25 uce tolerance in both naive and fVIII-primed hemophilic (E16 fVIII(-/-)) mice.

26 To confirm in vitro results, hemophilic E17 knockout mice were pretreated with antibo

27 ies and loss of tolerance to both native and hemophilic factor VIII proteins.

28 ars to be more critical than his endogenous, hemophilic factor VIII to his developing high-titer anti

29 t-specific alphaIIb promoter in platelets of hemophilic (FVIIInull) mice to create 2bF8trans mice.

30 lytic properties of Solulin are exhibited in hemophilic human (in vitro) and dog (in vivo/ex vivo) bl

31 T(H)17/T(H)1-polarized cells play a role in hemophilic immune responses to FVIII.

32 Often hemophilic inhibitor plasmas were partially neutralized

33 joint-directed gene transfer may ameliorate hemophilic joint destruction, even in the absence of cir

34 uld play a major role in the pathogenesis of hemophilic joint disease (HJD).

35 ole in the proliferative changes observed in hemophilic joint disease and that aberrant expression of

36 tality, we studied a cohort comprised of all hemophilic males identified by a six-state surveillance

37 of hepatitis C virus (HCV) was studied in 21 hemophilic men coinfected with HCV and human immunodefic

38 progression was assessed in a cohort of 109 hemophilic men infected with HIV-1 for a median of 12.7

39 HIV and HCV virus loads were examined in hemophilic men, as were risks of HIV and HCV transmissio

40 In macrovascular injury models, hemophilic mice administered mFVIIa-FMR exhibited superi

41 own to be T-cell dependent by its absence in hemophilic mice also deficient for the T-cell costimulat

42 iants exhibited improved pharmacokinetics in hemophilic mice and rabbits.

43 Unexpectedly, hemophilic mice developed twice as many blood vessels in

44 l littermate controls, whereas the untreated hemophilic mice exhibited heavy blood loss and prolonged

45 ferent bleeding-time techniques, the treated hemophilic mice gave values identical to normal litterma

46 of hFVIII rescued the bleeding diathesis of hemophilic mice lacking endogenous FVIII.

47 ul for gene transfer studies, while the CD-1 hemophilic mice may be of greater utility in studying th

48 We previously found that oral delivery to hemophilic mice of cholera toxin B subunit-coagulation f

49 Hemophilic mice treated with lentiviral vectors showed e

50 These data suggest that the C57B1/6 hemophilic mice will be more useful for gene transfer st

51 nses to fVIII could be achieved in immunized hemophilic mice with existing anti-fVIII titers.

52 ocked the primary response to factor VIII in hemophilic mice with intact B7 function.

53 r increases in antifactor VIII when given to hemophilic mice with low antifactor VIII antibody titers

54 cells can efficiently restore hemostasis to hemophilic mice with preexisting inhibitory antibodies u

55 coagulation capacity in MiniAdFVIII-treated hemophilic mice, as determined by tail clipping observat

56 In bleeding models of hemophilic mice, PEGylated FVIII not only exhibited prol

57 aptive immune responses in immune-competent, hemophilic mice.

58 m tolerance to FVIII in different strains of hemophilic mice.

59 tive in correcting the coagulation defect in hemophilic mice.

60 rsistence of ferric iron was also greater in hemophilic mice.

61 n normal, hemophilic, and adenoviral-treated hemophilic mice.

62 We used a new humanized hemophilic mouse model to identify FVIII peptides presen

63 To explore this in a hemophilic mouse model, we characterized 2 variants of m

64 Evaluation of experimental hemophilic mouse models with or without functional IDO1

65 ained higher activities as compared with the hemophilic mutant FVIII forms.

66 12.3; P=0.04), despite a similar spectrum of hemophilic mutations and degree of severity of illness i

67 ophageal echocardiogram (TEE), revealed in a hemophilic patient, and diagnosed with cardiac CT.

68 The zeolite nanoparticles can be adapted to hemophilic patients (hemophilia A (F-VIII deficient) and

69 Of the 178 hemophilic patients (mean age, 29 years), TTV-DNA was fo

70 All 1816 HCV-seropositive hemophilic patients at 16 centers were followed for up t

71 Hemophilic patients were screened for factor VIII C-doma

72 To clarify these relationships, 42 hemophilic patients who developed ESLD and random sample

73 genotypes, the distribution of genotypes in hemophilic patients who had been treated with nonvirally

74 o developed ESLD and random samples from 164 hemophilic patients with HCV infection alone and 146 wit

75 From 3993 hemophilic patients with hepatitis C, 257 sibling pairs,

76 far indicates that the use of factor VIIa in hemophilic patients with inhibitors is both safe and eff

77 for the treatment of hemorrhagic episodes in hemophilic patients with inhibitors to factors VIII and

78 o offer a more objective measure of both the hemophilic phenotype as well as the response to treatmen

79 n of the vector to FVIII-deficient dogs, the hemophilic phenotype was corrected, based on determinati

80 cient endothelial-KO models display a severe hemophilic phenotype with no detectable plasma FVIII act

81 y is less than 1% and the mouse exhibits the hemophilic phenotype.

82 Clots formed in hemophilic plasma in the presence of a plasminogen activ

83 In hemophilic plasma, FXa(I16L) and FXa(V17A) have prolonge

84 of clotting times and thrombin generation in hemophilic plasma.

85 inhibitors were present in 71% (24 of 34) of hemophilic plasmas, but only 33% (7 of 21) of autoantibo

86 s pattern was found in only 15% (5 of 34) of hemophilic plasmas.

87 tion may facilitate thrombin generation in a hemophilic setting.

88 Hemophilic siblings provide a unique population to explo

89 nd suggest novel strategies for ameliorating hemophilic states through drugs that disrupt the ZPI-PZ

90 In conclusion, hemophilic subjects coinfected with chronic HBV and thos

91 of local and systemic angiogenic response in hemophilic subjects with recurrent hemarthroses suggesti

92 of HCV, we studied a cohort of HCV-infected hemophilic subjects without human immunodeficiency virus

93 pairs to those expected for randomly paired hemophilic subjects.

94 flammatory and proliferative disorder termed hemophilic synovitis (HS).

95 lted in pathologic changes observed in human hemophilic synovitis and a marked increase in synovial c

96 od and the molecular changes responsible for hemophilic synovitis are not known.

97 icrovascular proliferation and inflammation (hemophilic synovitis) that contribute to end-stage joint

98 thin the joint space can protect joints from hemophilic synovitis, we established a hemophilia B mous

99 ers to identify the onset and progression of hemophilic synovitis.

100 in cell proliferation and the development of hemophilic synovitis.

101 s in a chronic inflammatory condition termed hemophilic synovitis.

102 pothesized that iron plays a similar role in hemophilic synovitis.

103 ity, survival is significantly greater among hemophilics who receive medical care in HTCs.