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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.
15 bin in the plasma and prevented SRBC-induced hemoglobinuria and kidney injury.
16 y of complement such as paroxysmal nocturnal hemoglobinuria and other diseases.
17 anti-D-IGIV-associated hemoglobinemia and/or hemoglobinuria and provides pretreatment and posttreatme
18  mice at 14 days had severe pulmonary edema, hemoglobinuria, and glomerulonephritis.
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
30                         Paroxysmal nocturnal hemoglobinuria is an acquired hematopoietic stem cell (H
31                         Paroxysmal nocturnal hemoglobinuria is frequently associated with aplastic an
32 tic, defining defect in paroxysmal nocturnal hemoglobinuria is the somatic mutation of the PIG-A gene
33 hanism responsible for hemoglobinemia and/or hemoglobinuria is unexplained.
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
41 plement regulation on a paroxysmal nocturnal hemoglobinuria patient's erythrocytes.
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
49                  AA and paroxysmal nocturnal hemoglobinuria (PNH) are related clinically, and glycoph
50                         Paroxysmal nocturnal hemoglobinuria (PNH) arises from a somatic mutation of t
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
53                         Paroxysmal nocturnal hemoglobinuria (PNH) cells are partially (type II) or co
54                         Paroxysmal nocturnal hemoglobinuria (PNH) cells are susceptible to hemolysis
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
58                         Paroxysmal nocturnal hemoglobinuria (PNH) develops in patients who have had a
59  complement pathway, of paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes in human serum.
60 netic defect underlying paroxysmal nocturnal hemoglobinuria (PNH) has been shown to reside in PIGA, a
61           Patients with paroxysmal nocturnal hemoglobinuria (PNH) have blood cells deficient in glyco
62                         Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell
63                         Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell
64                         Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal stem cell disorder caus
65                         Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal stem cell disorder char
66                         Paroxysmal nocturnal hemoglobinuria (PNH) is a disorder of hematopoietic stem
67                         Paroxysmal nocturnal hemoglobinuria (PNH) is a nonmalignant clonal disease of
68                         Paroxysmal nocturnal hemoglobinuria (PNH) is a rare bone marrow failure disor
69                         Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal blood disorder tha
70                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired blood disease with d
71                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder of t
72                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematopoietic
73                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hematopoietic stem-c
74                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia cha
75                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia res
76                         Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired stem cell disorder c
77                         Paroxysmal nocturnal hemoglobinuria (PNH) is caused by phosphatidylinositol g
78                         Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-medi
79                         Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-medi
80                         Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by intravascular h
81                         Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by the presence in
82 he clinical hallmark of paroxysmal nocturnal hemoglobinuria (PNH) is chronic intravascular hemolysis
83            The syndrome paroxysmal nocturnal hemoglobinuria (PNH) is intimately related to aplastic a
84 marrow failure (BMF) in paroxysmal nocturnal hemoglobinuria (PNH) is not yet known.
85  distinctive feature of paroxysmal nocturnal hemoglobinuria (PNH) is that in each patient glycosylpho
86  feared complication of paroxysmal nocturnal hemoglobinuria (PNH) is thrombosis.
87           Patients with paroxysmal nocturnal hemoglobinuria (PNH) lack GPI proteins on the surface of
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
93                         Paroxysmal nocturnal hemoglobinuria (PNH) results from somatic mutations in t
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
100                      In paroxysmal nocturnal hemoglobinuria (PNH), acquired somatic mutations in the
101                      In paroxysmal nocturnal hemoglobinuria (PNH), an acquired mutation of the PIGA g
102 h aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysplasia (MDS).
103 g aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and some forms of myelodysplasia (
104                      In paroxysmal nocturnal hemoglobinuria (PNH), hematopoietic cells lacking glycos
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
107 PCs) from patients with paroxysmal nocturnal hemoglobinuria (PNH).
108 a is a major feature of paroxysmal nocturnal hemoglobinuria (PNH).
109 s a defining feature of paroxysmal nocturnal hemoglobinuria (PNH).
110 erated in patients with paroxysmal nocturnal hemoglobinuria (PNH).
111 c disorders, especially paroxysmal nocturnal hemoglobinuria (PNH).
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
114                              Paroxysmal cold hemoglobinuria requires aggressive supportive therapy, g
115 molytic anemias such as paroxysmal nocturnal hemoglobinuria, sickle cell disease, and thalassemia.
116  to complement lysis in paroxysmal nocturnal hemoglobinuria syndrome.
117 molytic anemia syndrome paroxysmal nocturnal hemoglobinuria, the in vivo biology of DAF is still poor
118                                  Episodes of hemoglobinuria were reduced by 96 percent (P<0.001), and
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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