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 se (SCD) by inhibiting the polymerization of sickle hemoglobin.
2 ffened by polymerized fibers of deoxygenated sickle hemoglobin.
3 hemia in a transgenic mouse expressing human sickle hemoglobin.
4 ttempt to alter the solubility properties of sickle hemoglobin.
5 s was achieved after correction of the human sickle hemoglobin allele by gene-specific targeting.
6 er some protection against polymerization of sickle hemoglobin and exert a reversible antiplatelet ef
7 olymerization by laser photolysis of carboxy sickle hemoglobin and observing stochastic variation of
8                     The binding of CO to the sickle hemoglobin and the simultaneous melting of the he
9   Recognizing the qualitative abnormality of sickle hemoglobin as a prototype, Pauling & Castle estab
10 le RBC ROS generation has been attributed to sickle hemoglobin auto-oxidation and Fenton chemistry re
11 that affects the heterogeneous nucleation of sickle hemoglobin by using convex particle theory.
12 homozygous sickle cell anemia (HbSS), 7 with sickle hemoglobin C (HbSC), 7 with sickle/beta-thalassem
13 beta degrees -thalassemia (S beta degrees ), sickle-hemoglobin C disease (SC), or sickle-beta(+)-thal
14                We tested the hypothesis that sickle hemoglobin disrupts cdB3-based regulatory protein
15                         In experiments using sickle hemoglobin droplets suspended in oil, it has been
16 ated 70 kDa dextran lowers the solubility of sickle hemoglobin, due to molecular crowding, and provid
17 utation plus the natural genetic mutation of sickle hemoglobin, E6V(beta).
18                                           If sickle hemoglobin fibers fail to depolymerize fully duri
19 of a very significant material anisotropy in sickle hemoglobin fibers, as might arise from the differ
20  entire class of linear aggregates, not just sickle hemoglobin fibers.
21  studied the variations of twist and bend in sickle hemoglobin fibers.
22                                              Sickle hemoglobin forms long, multistranded polymers tha
23 el method for measuring the microrheology of sickle hemoglobin gels, based on magnetically driven com
24   Given the recently determined stiffness of sickle hemoglobin gels, the observed obstruction seen in
25  by a variant of the beta-globin gene called sickle hemoglobin (Hb S).
26           Three novel recombinant mutants of sickle hemoglobin (Hb S, beta 6Glu-->Val) have been cons
27  homogeneous and heterogeneous nucleation on sickle hemoglobin (HbS beta 6 Glu-->Val) additionally mo
28  on the sites that promote polymerization of sickle hemoglobin (HbS) after formation of the initial h
29 hemoglobin (HbF) decreases polymerization of sickle hemoglobin (HbS) and improves outcomes in sickle
30 rstanding of intracellular polymerization of sickle hemoglobin (HbS) and subsequent interaction with
31 n standard treatment (N = 66) maintained 30% sickle hemoglobin (HbS) and tolerated deferasirox at 28.
32 n red blood cell (RBC) polymorphisms such as sickle hemoglobin (HbS) are known to protect against mal
33 s may be acting to prevent polymerization of sickle hemoglobin (HbS) by binding to and stabilizing li
34 kle cell anemia has been that replacement of sickle hemoglobin (HbS) by fetal hemoglobin (HbF) would
35 ed healthy hemoglobin A (HbA) and homozygous sickle hemoglobin (HbS) containing RBCs using whole bloo
36 (HbF) expression while coordinately reducing sickle hemoglobin (HbS) expression.
37        We apply this analysis to a system of sickle hemoglobin (HbS) fibers that laterally attract on
38 ical trials that led to approval either were sickle hemoglobin (HbS) gene homozygotes (sickle cell an
39 ous and heterogeneous nucleation kinetics of sickle hemoglobin (HbS) have been studied for various de
40 y-free paper-based test capable of detecting sickle hemoglobin (HbS) in newborn blood samples with a
41 ene of hemoglobin that leads to synthesis of sickle hemoglobin (HbS) in red blood cells (RBCs).
42 lity, is driven by polymerization of mutated sickle hemoglobin (HbS) in red blood cells (RBCs).
43                                              Sickle hemoglobin (HbS) is a point mutation of the two b
44                            Polymerization of sickle hemoglobin (HbS) is the primary pathogenic event
45 een on transfusions aimed at maintaining the sickle hemoglobin (HbS) level below 30%.
46 sing blood samples from 25 SCD patients with sickle hemoglobin (HbS) levels varying from 64 to 90.1%,
47 idative stress and oxidative modification of sickle hemoglobin (HbS) play a role in sickle cell disea
48 at possesses the beta6 Glu-->Val mutation of sickle hemoglobin (HbS) plus beta73 Asp-->Asn.
49                                 Deoxygenated sickle hemoglobin (HbS) polymerization drives the pathop
50                                              Sickle hemoglobin (HbS) polymerization occurs when the c
51 intense interest given the HbF inhibition of sickle hemoglobin (HbS) polymerization.
52 pe of sickle cell anemia by inhibiting deoxy sickle hemoglobin (HbS) polymerization.
53 located at axial and lateral contacts of the sickle hemoglobin (HbS) polymers and strongly inhibit de
54 d comparatively little toxicity, and reduced sickle hemoglobin (HbS) synthesis as well as sickling of
55 ification agents that reduce the tendency of sickle hemoglobin (HbS) to aggregate represents an impor
56                                              Sickle hemoglobin (HbS), as a result of its polymer-rela
57 atments directly targeting polymerization of sickle hemoglobin (HbS), the proximate event in the path
58  To create mice expressing exclusively human sickle hemoglobin (HbS), transgenic mice expressing huma
59  nitrite reductase activity of unpolymerized sickle hemoglobin (HbS), whose oxygen affinity and coope
60 ion results on the self-assembly behavior of sickle hemoglobin (HbS).
61 abinoids in transgenic mice expressing human sickle hemoglobin (HbS).
62  by reducing intracellular polymerization of sickle hemoglobin (HbS).
63  (SCD) is the polymerization of deoxygenated sickle hemoglobin (HbS).
64             Adenine base editing can convert sickle hemoglobin (HbS, betaEpsilon6V) to G-Makassar hem
65 ing the solubilizing effect of iron nitrosyl sickle hemoglobin (HbS-NO).
66 ta-globin gene, leading to the expression of sickle hemoglobin (HbS; alpha(2)beta(S)(2)).
67 in of adult hemoglobin (HbA) that results in sickled hemoglobin (HbS).
68 in of adult hemoglobin (HbA) that results in sickled hemoglobin (HbS).
69 and F. A. Ferrone, in which up to 50% of the sickle hemoglobin is substituted by cross-linked hemoglo
70 moderate strength recommendation to maintain sickle hemoglobin levels of less than 30% prior to the n
71 all known free energies of polymerization of sickle hemoglobin measured in the presence of dextran.
72 BC deformability from both primary (host RBC sickle hemoglobin mediated) and secondary changes (Babes
73 ce between the association behavior of deoxy sickle hemoglobin molecules (HbS), which can polymerize
74                                              Sickle hemoglobin molecules assemble into polymers compo
75                                              Sickle hemoglobin nucleation occurs in solution as a hom
76 ar to but slightly greater than that seen in sickle hemoglobin nucleation.
77 emia [6 HbS/beta0, 1 HbS/beta+]), and 2 with sickle hemoglobin OArab (HbS/OArab).
78 cell anaemia codes for a variant hemoglobin, sickle hemoglobin or HbS, whose presence drives the path
79 s insight into the mechanism and kinetics of sickle hemoglobin polymer melting.
80 an effect mediated by its exclusion from the sickle hemoglobin polymer.
81 n hemoglobin (HBB) gene engineered to impede sickle hemoglobin polymerization (HBBAS3) to transduce h
82 n are both well described as consequences of sickle hemoglobin polymerization acting as a Brownian ra
83 of sickle cell disease, leading to increased sickle hemoglobin polymerization and decreased red blood
84 meliorate these manifestations by mitigating sickle hemoglobin polymerization and erythrocyte sicklin
85 meliorate these manifestations by mitigating sickle hemoglobin polymerization and erythrocyte sicklin
86  dissolution, and find that oxygen-dependent sickle hemoglobin polymerization and melting alone are s
87                                              Sickle hemoglobin polymerization exhibits a striking sen
88         We assessed the effect of GBT1118, a sickle hemoglobin polymerization inhibitor on bone loss
89                          We conclude that "a sickle hemoglobin polymerization inhibitor" might be eff
90                 Voxelotor is an inhibitor of sickle hemoglobin polymerization that is used to treat s
91  only drug approved by the FDA that inhibits sickle-hemoglobin polymerization.
92                                              Sickle hemoglobin polymerizes by two types of nucleation
93                                              Sickle hemoglobin polymerizes under hypoxic conditions,
94  a precise method of measuring the growth of sickle hemoglobin polymers by observing the time require
95 erstanding of the ligand binding kinetics of sickle hemoglobin polymers could have pathophysiological
96                            Polymerisation of sickle hemoglobin results in erythrocytes that are infle
97 ygous state of normal hemoglobin A (HbA) and sickle hemoglobin S (HbS), confers protection against ma
98 e rigidities are found to be consistent with sickle hemoglobin "single" fibers 20 nm in diameter, des
99 e evaluated children with SCD homozygous for sickle hemoglobin (SS disease) and controls (n = 65) and
100 travital microscopy in mice expressing human sickle hemoglobin (SS) that SS red blood cells (RBCs) bi
101                   By photolysing droplets of sickle hemoglobin suspended in oil we find that polymeri
102  effort to map the most important regions of sickle hemoglobin that are involved in polymerization, w
103             Although the molecular defect in sickle hemoglobin that produces sickle cell disease has
104                             In a solution of sickle hemoglobin, the molecules in the gel contribute n
105 n phenotype also reflects the instability of sickle hemoglobin, the release of heme, and the inductio
106 globin (HbF), which reduces the tendency for sickle hemoglobin to polymerize, thereby reducing the fr
107 trate abnormal (O2-dependent) association of sickle hemoglobin to RBC membrane that interferes with s
108 al NO synthase deletion (dNOS(-/-)) or human sickle hemoglobin transgenic expression (Sickle).
109                                            A sickle hemoglobin triple mutant with three amino acid su
110 nes on the rate of homogeneous nucleation in sickle hemoglobin, using preparations of open ghosts (OG
111 mutation (rd1) independent from that causing sickle hemoglobin was an incidental finding in some Berk
112                           On average, 43% of sickle hemoglobin was replaced by adult hemoglobin, ther
113    When transgenic mice that expressed human sickle hemoglobin were mated with mice having knockout m
114 e generated that expressed exclusively human sickle hemoglobin with 3 levels of HbF using their previ
115 ood vessels because of polymerization of the sickle hemoglobin within the red cells.

 
Page Top