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1 ent specifically in injecting drug users and hemophiliacs.
2 the major cause of chronic liver disease in hemophiliacs.
3 els over time in a cohort of multitransfused hemophiliacs.
4 IV-infected blood transfusion recipients and hemophiliacs.
5 wo patients were classified as mild/moderate hemophiliacs.
6 o develop KS than AIDS-afflicted children or hemophiliacs.
8 luated end-stage liver disease (ESLD) in 157 hemophiliacs (85 HIV positive and 72 HIV negative) with
11 ster and trends in incidence in HIV-infected hemophiliacs and homosexual men (n=1218) were examined.
15 of FVIII pharmaceutical products, the use of hemophiliac dogs for gene therapy studies has several li
17 ting recombinant activated factor VII in non-hemophiliacs have been published as abstracts, supportin
21 al vector encoding hFVIII, and transplant to hemophiliac mouse recipients, results in the induction o
25 to human immunodeficiency virus infection in hemophiliacs rather than a susceptibility to hepatitis C
26 r among HIV-positive than among HIV-negative hemophiliacs (relative risk [RR], 3.72; 95% confidence i
27 munodeficiency virus type 1 (HIV-1)-infected hemophiliacs to define the relationship between the SDF1
29 of the blood-borne TT virus (TTV) in Italian hemophiliacs treated with different preparations of fact
30 st, the major inhibitors in 35% (8 of 23) of hemophiliacs treated with plasma fVIII were directed aga
31 indicate that TTV frequently infects Italian hemophiliacs treated with plasma-derived factor VIII con
32 f neovessels during angiogenesis but renders hemophiliacs vulnerable to hemorrhage during healing.
33 demonstrated that the inhibitor response in hemophiliacs was more complex and the epitope specificit
36 conclude that genotype changes are common in hemophiliacs with chronic HCV, particularly in those who
37 y of factor VIIa in the medical treatment of hemophiliacs with inhibitors is, in part, based on overc
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