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1 ignated this new variant type 2M:Milwaukee-1 vWD.
2 of this polymorphism in patients with type 1 vWD compared with normal individuals.
3 enotype in individuals diagnosed with type 1 vWD is about 0.5%.
4                The molecular basis of type 1 vWD is largely undefined.
5  low collagen receptor density, among type 1 vWD patients (807C =.71; 807T =.29) was significantly hi
6 nd normal multimerization, typical of type 1 vWD, but disproportionately-low agonist-mediated platele
7                                       Type 2 vWD is further divided into four subtypes (A, B, N, and
8 s-sense mutations account for most of type 2 vWD, whereas major disruptions in the vWF gene produce t
9 lopment of protease inhibitor therapy for 2A vWD.
10                                  The type 2A vWD mutation sites in the A2 domain correspond to buried
11 P mutation causes the characteristic type 2A vWD phenotype.
12 for developing specific treatment of type 2A vWD.
13                                  Two type 2B vWD A1 domain mutants, R1306Q and R1450E, converted catc
14 ion of the vWF gene in patients with type 2b vWD has resulted in identification of a panel of mutatio
15 hermore, expression of more than one type 2b vWD mutation in the same molecule (cis) or in different
16                     In contrast, the type 2B vWD mutation sites that are involved in upregulation of
17 ave expressed six of the most common type 2b vWD mutations in recombinant vWF and show that each muta
18 on" or "off" conformation, with most type 2b vWD mutations resulting in vWF locked in the on conforma
19                  We conclude that in type 2B vWD, prolonged lifetimes of vWF bonds with GPIbalpha on
20              von Willebrand disease type 2B (vWD-type 2B) is characterized by gain-of-function mutati
21                    Inspection of the type 2M vWD mutation sites that are involved in downregulation o
22 mong individuals with types 2A, 2B, 2M, or 3 vWD.
23 IIbbeta3 in platelets from mice expressing a vWD-type 2B-associated vWF (vWF/p.V1316M), platelets fro
24                                     Acquired vWD may also occur with certain medications.
25 is, but the estimated prevalence of acquired vWD (often termed von Willebrand syndrome or vWS) is now
26                             We show that all vWD domains of FCGBP with a GDPH sequence are cleaved an
27  B-fold, while the third EGF-like domain and vWD domain were predominantly random coils.
28 t is comprised of repeated von Willebrand D (vWD) domain assemblies, most of which have a GDPH amino
29 pes 2B, 2M, and 2A von Willebrand's disease (vWD) are located in the A1 and A2 domains.
30                    von Willebrand's disease (vWD) arises from abnormalities in von Willebrand factor
31 of moderately severe von Willebrand disease (vWD) characterized by low plasma von Willebrand factor a
32                      von Willebrand disease (vWD) is a common, autosomally inherited, bleeding disord
33              Type 2b von Willebrand disease (vWD) is a qualitative form of vWD resulting from enhance
34 % of the population, von Willebrand disease (vWD) is the most common hereditary bleeding diathesis, b
35 ound in some type 2A von Willebrand disease (vWD) patients was observed to undergo proteolysis in viv
36 n that cause type 2B von Willebrand disease (vWD) reduce the flow requirement for adhesion.
37 ociated with type 2B von Willebrand disease (vWD), a bleeding disorder that is due to the spontaneous
38 multimers in type 2A von Willebrand disease (vWD), and the results with tetracyclines and monoclonal
39  diathesis disorder, von Willebrand disease (vWD), on the structure and rheology of vWF A1 domain adh
40            In type 1 von Willebrand disease (vWD), platelet adhesive functions are impaired due to th
41 e 2A (phenotype IID) von Willebrand disease (vWD).
42 n connected via a disulfide bond within each vWD domain.
43 kely contributes to the bleeding tendency in vWD-type 2B.
44                  The laboratory diagnosis of vWD and its several variants is made on the basis of imm
45             The mainstay of the diagnosis of vWD is laboratory testing.
46 brand disease (vWD) is a qualitative form of vWD resulting from enhanced binding of vWF to platelets.
47 describe two families with a variant form of vWD where affected members of both families have borderl
48 uent in vivo analysis of additional forms of vWD and in the development of protease inhibitor therapy
49 s in symptomatic patients with five types of vWD (type 1, n = 78; type 2A, n = 25, type 2B, n = 14; t
50 vWF-platelet interactions, which affects the vWD functional phenotype and the severity of thrombocyto
51                 These data indicate that the vWD-type 2B mutation p.V1316M is associated with severe
52 e mainstay of therapy for most patients with vWD in desmopressin, a pharmacologic agent that stimulat
53                       Also, in patients with vWD type 1 and borderline to normal ristocetin-cofactor
54                                Patients with vWD-type 2B have a bleeding tendency that is linked to l