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1 ng the mutant phenotype of the human disease paroxysmal nocturnal hemoglobinuria.
2 t for the growth advantage of blood cells in paroxysmal nocturnal hemoglobinuria.
3 at determine their efficacy in patients with paroxysmal nocturnal hemoglobinuria.
4 roliferative glomerulonephritis type II, and paroxysmal nocturnal hemoglobinuria.
5 d proteins on blood cells from patients with paroxysmal nocturnal hemoglobinuria.
6 for their clonal dominance in patients with paroxysmal nocturnal hemoglobinuria.
7 d proteins on blood cells from patients with paroxysmal nocturnal hemoglobinuria.
8 esistance in a small number of patients with paroxysmal nocturnal hemoglobinuria.
9 nd Drug Administration approval for treating paroxysmal nocturnal hemoglobinuria, a rare blood disord
10 procedures, 3 of whom carried a diagnosis of paroxysmal nocturnal hemoglobinuria, a relative contrain
11 CD4(+) and CD8(+) lymphocyte pool; in AA and paroxysmal nocturnal hemoglobinuria, a seemingly random
12 ty, deficiency of GPI has been recognized as paroxysmal nocturnal hemoglobinuria, an acquired clonal
13 mAb approved for treatment of patients with paroxysmal nocturnal hemoglobinuria and atypical hemolyt
14 e the MoA of pegcetacoplan and eculizumab in paroxysmal nocturnal hemoglobinuria and discuss the comp
15 he alternative pathway of complement such as paroxysmal nocturnal hemoglobinuria and other diseases.
16 cation in patients with sickle cell disease, paroxysmal nocturnal hemoglobinuria, beta-thalassemia ma
17 from other TMAs based on the hypothesis that paroxysmal nocturnal hemoglobinuria cells are more sensi
18 te antigen (HLA)-DR2 and those with expanded paroxysmal nocturnal hemoglobinuria clones showed more s
19 ical trials of complement inhibitors include paroxysmal nocturnal hemoglobinuria, cold agglutinin dis
20 ease we demonstrated that FB28.4.2 protected paroxysmal nocturnal hemoglobinuria erythrocytes from co
22 numerous organ-specific diseases, including paroxysmal nocturnal hemoglobinuria (erythrocytes), atyp
23 lysis of red blood cells from patients with paroxysmal nocturnal hemoglobinuria in either the acidif
24 tients with chronic hemolysis suffering from paroxysmal nocturnal hemoglobinuria in which the acquire
25 physiology of other hemolytic states such as paroxysmal nocturnal hemoglobinuria, in which plasma hem
29 most accurate technique for the diagnosis of paroxysmal nocturnal hemoglobinuria; it is clearly more
30 mias, plasma cell neoplasms, acute leukemia, paroxysmal nocturnal hemoglobinuria, mast cell disease,
31 ells with mutated PIG-A genes in humans with paroxysmal nocturnal hemoglobinuria may be subject to co
32 ically relevant AP-mediated disease model of paroxysmal nocturnal hemoglobinuria, mini-FH largely out
33 develop a secondary clonal disorder, such as paroxysmal nocturnal hemoglobinuria, myelodysplastic syn
34 a 5-fold-enhanced complement regulation on a paroxysmal nocturnal hemoglobinuria patient's erythrocyt
35 s harbor granulocytes with the PIG-A mutant (paroxysmal nocturnal hemoglobinuria) phenotype at a medi
36 -cytometry we have examined 19 patients with paroxysmal nocturnal hemoglobinuria (PNH) (18 with activ
37 rare, life-threatening clinical conditions: paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
38 5 monoclonal antibody (mAb) for treatment of paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
39 predisposes individuals to disorders such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
40 bophilia is one of the principal features of paroxysmal nocturnal hemoglobinuria (PNH) and constitute
41 , has been shown to prevent complications of paroxysmal nocturnal hemoglobinuria (PNH) and improve qu
42 uding the clonal PIGA(-) cells in 2 cases of paroxysmal nocturnal hemoglobinuria (PNH) and some myelo
43 servations related to the natural history of paroxysmal nocturnal hemoglobinuria (PNH) and to review
48 typical hemolytic uremic syndrome (aHUS) and paroxysmal nocturnal hemoglobinuria (PNH) as well as thr
49 of 15 patients in the Cy arm had evidence of paroxysmal nocturnal hemoglobinuria (PNH) at diagnosis,
54 Peripheral blood T cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise a mix
55 Peripheral blood B cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise varia
57 ed by the alternative complement pathway, of paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes i
86 he mechanism of bone marrow failure (BMF) in paroxysmal nocturnal hemoglobinuria (PNH) is not yet kno
88 The most frequent and feared complication of paroxysmal nocturnal hemoglobinuria (PNH) is thrombosis.
90 e pathophysiology of myelodysplasia (MDS) or paroxysmal nocturnal hemoglobinuria (PNH) occurring as a
91 tic exacerbation occurring in a patient with paroxysmal nocturnal hemoglobinuria (PNH) on treatment w
92 vivo measurements of complement activity in paroxysmal nocturnal hemoglobinuria (PNH) patients on ec
93 ric marrow biopsies of 35 AA, 37 MDS, and 21 paroxysmal nocturnal hemoglobinuria (PNH) patients, in w
94 ttings: when absent from the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) patients, who
99 ate that the erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH) undergoing ecu
100 lood, Krawitz et al report on a patient with paroxysmal nocturnal hemoglobinuria (PNH) who does not h
101 nulocytes, and platelets of 54 patients with paroxysmal nocturnal hemoglobinuria (PNH) with antibodie
102 study of the first patient to be treated for paroxysmal nocturnal hemoglobinuria (PNH) with syngeneic
103 hrocytes causes complement-mediated lysis in paroxysmal nocturnal hemoglobinuria (PNH), a disease tha
107 umber of patients with aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysp
108 e syndromes, including aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and some form
109 including age-related macular degeneration, paroxysmal nocturnal hemoglobinuria (PNH), atypical hemo
111 ly mutated in blood cells from patients with paroxysmal nocturnal hemoglobinuria (PNH), leading to de
113 ranging from the rare hematological disease paroxysmal nocturnal hemoglobinuria (PNH), to the common
121 ctivation on erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH); the authors d
122 omide-treated erythrocytes that recapitulate paroxysmal nocturnal hemoglobinuria, PspCN enhanced prot
123 lications of human hemolytic anemias such as paroxysmal nocturnal hemoglobinuria, sickle cell disease
125 ssociated with the hemolytic anemia syndrome paroxysmal nocturnal hemoglobinuria, the in vivo biology
127 treatments are challenges for patients with paroxysmal nocturnal hemoglobinuria who have received an