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1 ceptionally clear review article by Brux and Sachs clarified the two-hit model of TRALI pathogenesis.
2 ch as those given by Hofmeister, Errera, and Sachs are developed and evaluated against observed cell
4 RT groups, and a model recently developed by Sachs and Brenner proposed a mechanism for repopulation
6 or disease (osteoarthritis, Bankart and Hill-Sachs lesions, subchondral cysts), and evidence of prior
8 tion, the Nishiyama-Wassermann and Kurdjumov-Sachs relationships between the face-centred cubic and b
9 in films, which demonstrate that the Lyddane-Sachs-Teller relation between the optical-phonon eigenfr
16 A message in lymphoblasts derived from a Tay-Sachs disease patient homozygous for the common frameshi
17 ssion profiles in cerebral cortex from a Tay-Sachs patient, a Sandhoff disease patient and a pediatri
27 Mouse models of the GM2 gangliosidoses [Tay-Sachs, late onset Tay-Sachs (LOTS), Sandhoff] and GM1 ga
29 GM1 gangliosidosis, GM2 gangliosidosis (Tay-Sachs and Sandhoff forms), metachromatic leucodystrophy,
32 nidase and that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redunda
35 eurodegenerative conditions that include Tay-Sachs disease, Sandhoff disease, and the GM2 activator d
37 t lysosomal storage disorders, including Tay-Sachs disease and Gaucher disease, can be accounted for
38 leukocytes from patients with infantile Tay-Sachs disease, including a patient with thermolabile hex
39 xb genes disrupted through interbreeding Tay-Sachs (Hexa-/-) and Sandhoff (Hexb-/-) disease model mic
40 ted with the development of another LSD, Tay-Sachs disease, thus suggesting general applicability of
41 reviously have described mouse models of Tay-Sachs (Hexa -/-) and Sandhoff (Hexb -/-) diseases with v
42 n of the hexb gene (hexb-/-), a model of Tay-Sachs and Sandhoff disease, versus the functionally norm
44 in GM2-AP result in an atypical form of Tay-Sachs disease known as variant AB GM2 gangliosidosis.
45 issues of an asymptomatic mouse model of Tay-Sachs disease, a severe human gangliosidosis, indicating
46 e observed results of the mouse model of Tay-Sachs disease, we have purified mouse liver Hex A and He
48 d applied for the amplified detection of Tay-Sachs genetic disorder mutant, with a detection limit of
49 M2 gangliosidoses [Tay-Sachs, late onset Tay-Sachs (LOTS), Sandhoff] and GM1 gangliosidosis have been
50 ographic distribution of the two primary Tay-Sachs disease mutations, with the first being more commo
51 ystic fibrosis CFDelta508 allele and the Tay-Sachs disease TSD 1278 allele from single heterozygous c
54 nition sequence for the analyte DNA (the Tay-Sachs mutant gene), a complementary sequence to the Mg(2
55 ccharidosis phenotype is not seen in the Tay-Sachs or Sandhoff disease model mice or in the correspon
56 ickle cell anemia (SCA) mutations, three Tay-Sachs mutations, eight Gaucher mutations, four mutations
58 ficiency (also known as the AB variant), Tay-Sachs disease, and Sandhoff disease are the major forms
60 imulation, and our model further implies the Sachs Canalization Hypothesis and resolves a dilemma reg
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