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1 pe of the human disease paroxysmal nocturnal hemoglobinuria.
2 ntage of blood cells in paroxysmal nocturnal hemoglobinuria.
3 ted HTRs, exemplified by rapid clearance and hemoglobinuria.
4 number of patients with paroxysmal nocturnal hemoglobinuria.
5 ment, leading to intravascular hemolysis and hemoglobinuria.
6 ells from patients with paroxysmal nocturnal hemoglobinuria.
7 for reported cases of hemoglobinemia and/or hemoglobinuria.
8 s from the pounding of feet on pavement, and hemoglobinuria.
9 inance in patients with paroxysmal nocturnal hemoglobinuria.
10 ells from patients with paroxysmal nocturnal hemoglobinuria.
11 carried a diagnosis of paroxysmal nocturnal hemoglobinuria, a relative contraindication for liver tr
12 phocyte pool; in AA and paroxysmal nocturnal hemoglobinuria, a seemingly random overrepresentation of
13 has been recognized as paroxysmal nocturnal hemoglobinuria, an acquired clonal disorder associated w
14 atment of patients with paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome.
17 anti-D-IGIV-associated hemoglobinemia and/or hemoglobinuria and provides pretreatment and posttreatme
19 protein C5 reduces intravascular hemolysis, hemoglobinuria, and the need for transfusion, with an as
20 th sickle cell disease, paroxysmal nocturnal hemoglobinuria, beta-thalassemia major, or thalassemia i
21 on the hypothesis that paroxysmal nocturnal hemoglobinuria cells are more sensitive to APC-activated
22 and those with expanded paroxysmal nocturnal hemoglobinuria clones showed more skewed VB repertoires.
23 that FB28.4.2 protected paroxysmal nocturnal hemoglobinuria erythrocytes from complement-mediated hem
24 ents who experienced acute hemoglobinemia or hemoglobinuria following anti-D IGIV administration for
25 DIC associated with acute hemoglobinemia or hemoglobinuria following anti-D IGIV administration for
26 received 15 reports of hemoglobinemia and/or hemoglobinuria following anti-D IGIV administration that
27 ells from patients with paroxysmal nocturnal hemoglobinuria in either the acidified serum or "sugar w
28 emolysis suffering from paroxysmal nocturnal hemoglobinuria in which the acquired mutation in the PIG
29 emolytic states such as paroxysmal nocturnal hemoglobinuria, in which plasma hemoglobin concentration
32 tic, defining defect in paroxysmal nocturnal hemoglobinuria is the somatic mutation of the PIG-A gene
34 ue for the diagnosis of paroxysmal nocturnal hemoglobinuria; it is clearly more specific, more quanti
35 plasms, acute leukemia, paroxysmal nocturnal hemoglobinuria, mast cell disease, myelodysplastic syndr
36 -A genes in humans with paroxysmal nocturnal hemoglobinuria may be subject to comparable pathophysiol
37 , anemia, elevated liver function tests, and hemoglobinuria-may be especially severe in asplenic or i
38 diated disease model of paroxysmal nocturnal hemoglobinuria, mini-FH largely outperformed FH and indi
39 lonal disorder, such as paroxysmal nocturnal hemoglobinuria, myelodysplastic syndrome, or leukemia.
40 e, cold agglutinin syndrome, paroxysmal cold hemoglobinuria, or autoimmune hemolytic anemia secondary
42 with the PIG-A mutant (paroxysmal nocturnal hemoglobinuria) phenotype at a median frequency (f) of a
43 amined 19 patients with paroxysmal nocturnal hemoglobinuria (PNH) (18 with active disease and 1 spont
44 (mAb) for treatment of paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndr
45 ls to disorders such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndr
46 revent complications of paroxysmal nocturnal hemoglobinuria (PNH) and improve quality of life and ove
47 (-) cells in 2 cases of paroxysmal nocturnal hemoglobinuria (PNH) and some myeloproliferative neoplas
48 the natural history of paroxysmal nocturnal hemoglobinuria (PNH) and to review new therapeutic strat
51 Cy arm had evidence of paroxysmal nocturnal hemoglobinuria (PNH) at diagnosis, with no substantial c
52 the genetic basis of a paroxysmal nocturnal hemoglobinuria (PNH) case without somatic mutations in P
55 has been proposed that paroxysmal nocturnal hemoglobinuria (PNH) cells may proliferate through their
56 cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise a mixture of residual norm
57 cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise variable mixtures of norma
60 netic defect underlying paroxysmal nocturnal hemoglobinuria (PNH) has been shown to reside in PIGA, a
82 he clinical hallmark of paroxysmal nocturnal hemoglobinuria (PNH) is chronic intravascular hemolysis
85 distinctive feature of paroxysmal nocturnal hemoglobinuria (PNH) is that in each patient glycosylpho
88 myelodysplasia (MDS) or paroxysmal nocturnal hemoglobinuria (PNH) occurring as a late complication of
89 complement activity in paroxysmal nocturnal hemoglobinuria (PNH) patients on eculizumab treatment.
90 f 35 AA, 37 MDS, and 21 paroxysmal nocturnal hemoglobinuria (PNH) patients, in whom specific CDR3 seq
91 rom the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) patients, who suffer from complemen
92 A 10-year-old girl with paroxysmal nocturnal hemoglobinuria (PNH) received an infusion of syngeneic b
94 ytes from patients with paroxysmal nocturnal hemoglobinuria (PNH) undergoing eculizumab treatment, wh
95 eport on a patient with paroxysmal nocturnal hemoglobinuria (PNH) who does not have a mutation of PIG
96 ets of 54 patients with paroxysmal nocturnal hemoglobinuria (PNH) with antibodies to glycosylphosphat
97 tient to be treated for paroxysmal nocturnal hemoglobinuria (PNH) with syngeneic bone marrow transpla
98 ement-mediated lysis in paroxysmal nocturnal hemoglobinuria (PNH), a disease that manifests after clo
99 clinical management of paroxysmal nocturnal hemoglobinuria (PNH), a rare but life-threatening hemato
103 g aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and some forms of myelodysplasia (
105 ells from patients with paroxysmal nocturnal hemoglobinuria (PNH), leading to deficiency of GPI-linke
106 rare hemolytic disease paroxysmal nocturnal hemoglobinuria (PNH), somatic mutations result in a defi
112 ytes from patients with paroxysmal nocturnal hemoglobinuria (PNH); the authors demonstrate that these
113 cytes that recapitulate paroxysmal nocturnal hemoglobinuria, PspCN enhanced protection of cells by FH
115 molytic anemias such as paroxysmal nocturnal hemoglobinuria, sickle cell disease, and thalassemia.
117 molytic anemia syndrome paroxysmal nocturnal hemoglobinuria, the in vivo biology of DAF is still poor
119 ytes from patients with paroxysmal nocturnal hemoglobinuria, which lack glycosylphosphatidylinositol-
120 , schistocytosis, free hemoglobin in plasma, hemoglobinuria with hemosiderinuria, and platelet activa
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