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1 t for the growth advantage of blood cells in paroxysmal nocturnal hemoglobinuria.
2 esistance in a small number of patients with paroxysmal nocturnal hemoglobinuria.
3 d proteins on blood cells from patients with paroxysmal nocturnal hemoglobinuria.
4 for their clonal dominance in patients with paroxysmal nocturnal hemoglobinuria.
5 d proteins on blood cells from patients with paroxysmal nocturnal hemoglobinuria.
6 ng the mutant phenotype of the human disease paroxysmal nocturnal hemoglobinuria.
7 procedures, 3 of whom carried a diagnosis of paroxysmal nocturnal hemoglobinuria, a relative contrain
8 CD4(+) and CD8(+) lymphocyte pool; in AA and paroxysmal nocturnal hemoglobinuria, a seemingly random
9 ty, deficiency of GPI has been recognized as paroxysmal nocturnal hemoglobinuria, an acquired clonal
10 mAb approved for treatment of patients with paroxysmal nocturnal hemoglobinuria and atypical hemolyt
11 he alternative pathway of complement such as paroxysmal nocturnal hemoglobinuria and other diseases.
12 cation in patients with sickle cell disease, paroxysmal nocturnal hemoglobinuria, beta-thalassemia ma
13 from other TMAs based on the hypothesis that paroxysmal nocturnal hemoglobinuria cells are more sensi
14 te antigen (HLA)-DR2 and those with expanded paroxysmal nocturnal hemoglobinuria clones showed more s
15 ease we demonstrated that FB28.4.2 protected paroxysmal nocturnal hemoglobinuria erythrocytes from co
16 lysis of red blood cells from patients with paroxysmal nocturnal hemoglobinuria in either the acidif
17 tients with chronic hemolysis suffering from paroxysmal nocturnal hemoglobinuria in which the acquire
18 physiology of other hemolytic states such as paroxysmal nocturnal hemoglobinuria, in which plasma hem
22 most accurate technique for the diagnosis of paroxysmal nocturnal hemoglobinuria; it is clearly more
23 mias, plasma cell neoplasms, acute leukemia, paroxysmal nocturnal hemoglobinuria, mast cell disease,
24 ells with mutated PIG-A genes in humans with paroxysmal nocturnal hemoglobinuria may be subject to co
25 ically relevant AP-mediated disease model of paroxysmal nocturnal hemoglobinuria, mini-FH largely out
26 develop a secondary clonal disorder, such as paroxysmal nocturnal hemoglobinuria, myelodysplastic syn
27 a 5-fold-enhanced complement regulation on a paroxysmal nocturnal hemoglobinuria patient's erythrocyt
28 s harbor granulocytes with the PIG-A mutant (paroxysmal nocturnal hemoglobinuria) phenotype at a medi
29 -cytometry we have examined 19 patients with paroxysmal nocturnal hemoglobinuria (PNH) (18 with activ
30 5 monoclonal antibody (mAb) for treatment of paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
31 predisposes individuals to disorders such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical h
32 , has been shown to prevent complications of paroxysmal nocturnal hemoglobinuria (PNH) and improve qu
33 uding the clonal PIGA(-) cells in 2 cases of paroxysmal nocturnal hemoglobinuria (PNH) and some myelo
34 servations related to the natural history of paroxysmal nocturnal hemoglobinuria (PNH) and to review
37 of 15 patients in the Cy arm had evidence of paroxysmal nocturnal hemoglobinuria (PNH) at diagnosis,
42 Peripheral blood T cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise a mix
43 Peripheral blood B cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise varia
45 ed by the alternative complement pathway, of paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes i
70 he mechanism of bone marrow failure (BMF) in paroxysmal nocturnal hemoglobinuria (PNH) is not yet kno
72 The most frequent and feared complication of paroxysmal nocturnal hemoglobinuria (PNH) is thrombosis.
74 e pathophysiology of myelodysplasia (MDS) or paroxysmal nocturnal hemoglobinuria (PNH) occurring as a
75 vivo measurements of complement activity in paroxysmal nocturnal hemoglobinuria (PNH) patients on ec
76 ric marrow biopsies of 35 AA, 37 MDS, and 21 paroxysmal nocturnal hemoglobinuria (PNH) patients, in w
77 ttings: when absent from the erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH) patients, who
80 ate that the erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH) undergoing ecu
81 lood, Krawitz et al report on a patient with paroxysmal nocturnal hemoglobinuria (PNH) who does not h
82 nulocytes, and platelets of 54 patients with paroxysmal nocturnal hemoglobinuria (PNH) with antibodie
83 study of the first patient to be treated for paroxysmal nocturnal hemoglobinuria (PNH) with syngeneic
84 hrocytes causes complement-mediated lysis in paroxysmal nocturnal hemoglobinuria (PNH), a disease tha
88 umber of patients with aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysp
89 e syndromes, including aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and some form
91 ly mutated in blood cells from patients with paroxysmal nocturnal hemoglobinuria (PNH), leading to de
98 ctivation on erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNH); the authors d
99 omide-treated erythrocytes that recapitulate paroxysmal nocturnal hemoglobinuria, PspCN enhanced prot
100 lications of human hemolytic anemias such as paroxysmal nocturnal hemoglobinuria, sickle cell disease
102 ssociated with the hemolytic anemia syndrome paroxysmal nocturnal hemoglobinuria, the in vivo biology
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