戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 herapeutic that prevents complement-mediated intravascular hemolysis.
2  as therapeutics for patients with excessive intravascular hemolysis.
3 ributes to these processes without affecting intravascular hemolysis.
4 eased mortality and morbidity resulting from intravascular hemolysis.
5  the disease result from complement-mediated intravascular hemolysis.
6 PI)-linked membrane proteins, which leads to intravascular hemolysis.
7 n in SCD, and potentially other disorders of intravascular hemolysis.
8 hemoglobin released into blood plasma during intravascular hemolysis.
9  of red cells in PNH patients, manifested by intravascular hemolysis.
10 iated with extravascular hemolysis than with intravascular hemolysis.
11  vaso-occlusive crisis associated with acute intravascular hemolysis.
12 iciency state and vasculopathy consequent to intravascular hemolysis, (2) chronic pulmonary thromboem
13                                              Intravascular hemolysis, a hallmark of SCD, results in t
14 cells results in chronic complement-mediated intravascular hemolysis, a process central to the morbid
15 ransfusion with old but not new blood led to intravascular hemolysis, acute hypertension, vascular in
16                                        Acute intravascular hemolysis after infusions of intravenous R
17                                Low levels of intravascular hemolysis after transfusion of aged stored
18 Infusion of a low dose of hemin caused acute intravascular hemolysis and autoamplification of extrace
19 blood cells (RBCs) to complement, leading to intravascular hemolysis and hemoglobinuria.
20 and thus consistent with the hypothesis that intravascular hemolysis and increased endogenous erythro
21 ages to remove senescent erythrocytes led to intravascular hemolysis and increased expression of the
22 ickle cell disease (SCD) is characterized by intravascular hemolysis and inflammation coupled to a 40
23                       However, the degree of intravascular hemolysis and microparticle formation in h
24  LDH may represent a convenient biomarker of intravascular hemolysis and NO bioavailability, characte
25 (PNH) are susceptible to complement-mediated intravascular hemolysis and thrombosis.
26 re simultaneous damage to endothelial cells, intravascular hemolysis, and activation of platelets lea
27 or 2 hours after transfusion by 50%, reduced intravascular hemolysis, and lowered the levels of compl
28 ssociated with Hb levels </=6 g/dL at onset, intravascular hemolysis, and previous splenectomy.
29 loantibodies, which fixed complement, led to intravascular hemolysis, and resulted in decreased level
30 ations are consistent with NO depletion from intravascular hemolysis, and they indicate that the path
31 imed at controlling extravascular as well as intravascular hemolysis are also examined.
32 s with sickle cell disease (SCD) suffer from intravascular hemolysis-associated vascular injury and t
33 PNH) is characterized by complement-mediated intravascular hemolysis because of the lack from erythro
34                                This explains intravascular hemolysis but does not explain the mechani
35                                              Intravascular hemolysis can be inhibited in patients by
36                                              Intravascular hemolysis can impair NO bioavailability an
37                              In PNH, chronic intravascular hemolysis causes an increase in morbidity
38 es, the development of PH is associated with intravascular hemolysis, cutaneous leg ulceration, renal
39                                              Intravascular hemolysis describes the relocalization of
40 PNH) is characterized by complement-mediated intravascular hemolysis due to the lack of CD55 and CD59
41 ing erythrocytic sickling, vascular ectasia, intravascular hemolysis, exuberant hematopoiesis, cardio
42  inhibition is highly effective for treating intravascular hemolysis from PNH and virtually eliminate
43          However, when it is released during intravascular hemolysis from the cell into blood plasma,
44  low titer of DL antibody can mediate severe intravascular hemolysis given its propensity to sensitiz
45     Although a role of free heme released by intravascular hemolysis has been suspected, the mechanis
46 exes on red blood cells (RBC) and subsequent intravascular hemolysis, heme cytotoxicity, and acute ki
47 ainst terminal complement protein C5 reduces intravascular hemolysis, hemoglobinuria, and the need fo
48 acquired stem cell disorder characterized by intravascular hemolysis, hypercoagulability, and relativ
49             We experimentally produced acute intravascular hemolysis in a canine model in order to te
50                                       During intravascular hemolysis in human disease, vasomotor tone
51 henylhydrazine (PHZ), as well as the role of intravascular hemolysis in increasing the stress oxidati
52 relation between priapism and high levels of intravascular hemolysis in men with SCD.
53 relation between priapism and high levels of intravascular hemolysis in men with SCD.
54 cells and the lack of clinically significant intravascular hemolysis in patients with IGD.
55  against the complement protein 5, stops the intravascular hemolysis in PNH.
56                             We conclude that intravascular hemolysis in SCD releases heme that activa
57  reviews the current knowledge on mechanical intravascular hemolysis in valvular disease, before and
58 ant function in a murine model that displays intravascular hemolysis induced by phenylhydrazine (PHZ)
59                           Here we found that intravascular hemolysis, induced by injection of phenylh
60  had gastroenteritis followed by progressive intravascular hemolysis, initially attributed to acute p
61 othesized that plasma hemoglobin released by intravascular hemolysis initiates endothelial injury thr
62                                              Intravascular hemolysis is a frequent finding after PFA
63 n expanding body of research indicating that intravascular hemolysis is a pathological mechanism in s
64                                   Mechanical intravascular hemolysis is frequently observed following
65          Hp-depleted sera from patients with intravascular hemolysis is severalfold more trypanolytic
66 ion of ILY in ThCD59(RBC) mice induced acute intravascular hemolysis, leading to reduced nitric oxide
67                                              Intravascular hemolysis leads to impaired bioavailabilit
68                                      Chronic intravascular hemolysis leads to nitric oxide (NO) deple
69               We recently generated a unique intravascular hemolysis mouse model in which the membran
70                                              Intravascular hemolysis occurred in 5 patients, of which
71                                              Intravascular hemolysis occurs in patients on extracorpo
72 ervations confirm that the acute toxicity of intravascular hemolysis occurs secondarily to the accele
73 of inhibiting both the extravascular and the intravascular hemolysis of PNH.
74 e have investigated the impact of persistent intravascular hemolysis on liver dysfunction using the m
75 ' deposits on liver endothelium in mice with intravascular hemolysis or injected with heme as well as
76                                The degree of intravascular hemolysis post-transfusion and effects on
77 ell disease, ischemia-reperfusion injury and intravascular hemolysis produce endothelial dysfunction
78 sign, we demonstrate that free water-induced intravascular hemolysis produces dose-dependent systemic
79 GPI-AP expression gradually decreased, while intravascular hemolysis progressively increased.
80 e are no experimental studies that show that intravascular hemolysis promotes alterations in erectile
81                        Our results show that intravascular hemolysis promotes increased corpus cavern
82 olymerizes in hypoxic conditions, leading to intravascular hemolysis, release of free hemoglobin and
83                                              Intravascular hemolysis releases hemoglobin into the blo
84                                        Thus, intravascular hemolysis represents an intrinsic mechanis
85 lytic diseases are characterized by enhanced intravascular hemolysis resulting in heme-catalyzed reac
86 ries have discovered that even low levels of intravascular hemolysis severely disrupt nitric oxide bi
87                                              Intravascular hemolysis showed a positive correlation wi
88 0.58, P < .001) and to laboratory markers of intravascular hemolysis, such as reticulocyte count (r =
89 al nocturnal hemoglobinuria (PNH) is chronic intravascular hemolysis that is a consequence of unregul
90   Our previous studies suggested that during intravascular hemolysis the expression of HO-1 protein i
91  thrombotic microangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kid
92        However, direct contribution of acute intravascular hemolysis to fatal PAH has not been invest
93 icate that the pathophysiologic cascade from intravascular hemolysis to NO depletion and its cardiopu
94 rticles test fundamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pat
95 used on the complement protein C5 to prevent intravascular hemolysis using the monoclonal antibody ec
96                                              Intravascular hemolysis was simulated by infusion of pre
97                    A total of 7 instances of intravascular hemolysis were identified in 60 TIPS patie
98 laria (2.5 vs 1 g/dL; P = .0001), markers of intravascular hemolysis were not higher in severe diseas
99 nal hemoglobinuria (PNH) is characterized by intravascular hemolysis, which is effectively controlled
100                         Predictive tests for intravascular hemolysis with crossmatch-incompatible ser