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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
3           In 1927, two neurologists, Bernard Sachs (American, 1858-1944) and Otto Marburg (Austrian,
4 RT groups, and a model recently developed by Sachs and Brenner proposed a mechanism for repopulation
5         In 1928, an introductory letter from Sachs went out to the international community and, in 19
6 or disease (osteoarthritis, Bankart and Hill-Sachs lesions, subchondral cysts), and evidence of prior
7                    In this issue of the JCI, Sachs and colleagues provide experimental confirmation o
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
10                                          Tay-Sachs and Sandhoff diseases are caused by mutations in t
11                                          Tay-Sachs and Sandhoff diseases are lysosomal storage disord
12                                          Tay-Sachs disease (TSD) is a classical glycosphingolipid (GS
13                                          Tay-Sachs disease (TSD) is an autosomal recessive, neurodege
14                                          Tay-Sachs disease is an inborn lysosomal disease characteriz
15                                          Tay-Sachs disease, an inborn lysosomal disease featuring a b
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
18 M1 gangliosidosis, Sandhoff disease, and Tay-Sachs disease brains.
19 al storage disorders, namely Gaucher and Tay-Sachs disease.
20 lysaccharidosis type IIIB, MPSIIIB), and Tay-Sachs.
21  found in lipid storage diseases such as Tay-Sachs [8].
22  nuclei) reminiscent of the asymptomatic Tay-Sachs model mice.
23          The mouse model of human type B Tay-Sachs disease recently engineered by the targeted disrup
24 atabolic pathway for GM2 in human type B Tay-Sachs patients.
25 A) causes the lysosomal storage disorder Tay-Sachs disease (TSD).
26 n the severe neurodegenerative disorder, Tay-Sachs disease.
27  Mouse models of the GM2 gangliosidoses [Tay-Sachs, late onset Tay-Sachs (LOTS), Sandhoff] and GM1 ga
28                  The GM2 gangliosidoses, Tay-Sachs and Sandhoff diseases, are caused by mutations in
29  GM1 gangliosidosis, GM2 gangliosidosis (Tay-Sachs and Sandhoff forms), metachromatic leucodystrophy,
30 orrected the metabolic defect in a human Tay-Sachs fibroblasts cell line in vitro.
31  behavioral manifestations seen in human Tay-Sachs patients.
32 nidase and that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redunda
33        Furthermore, as loss of GM2-AP in Tay-Sachs disease prevents degradation of GM2 gangliosides a
34 at a level reported to be therapeutic in Tay-Sachs disease.
35 eurodegenerative conditions that include Tay-Sachs disease, Sandhoff disease, and the GM2 activator d
36            GM2 gangliosidoses, including Tay-Sachs and Sandhoff diseases, are neurodegenerative lysos
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
43  such as brains from this mouse model of Tay-Sachs and Sandhoff disease.
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
47 mycin, was evaluated in a mouse model of Tay-Sachs disease.
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
52  platforms are implemented to detect the Tay-Sachs genetic disorder mutant.
53                      However, unlike the Tay-Sachs mice, the Gm2a -/- mice displayed significant stor
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
57                                    Thus, Tay-Sachs disease can be caused by the deficiency of either
58 ficiency (also known as the AB variant), Tay-Sachs disease, and Sandhoff disease are the major forms
59                                     When Tay-Sachs mice were treated with N-butyldeoxynojirimycin, th
60 imulation, and our model further implies the Sachs Canalization Hypothesis and resolves a dilemma reg

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