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1 rols, the mast cells that lack FAK were less metachromatic and by electron microscopy had granules th
2 major criterion for assessing the lineage of metachromatic cells of hematopoietic origin.
3                                     Immature metachromatic cells with mono- and multi-lobular nuclei
4 acteristic staining of the same tissues with metachromatic dyes such as crystal violet or with the co
5 synovium were embedded in cartilage-specific metachromatic extracellular matrix and costained positiv
6  muscle that normally contain heparin lacked metachromatic granules and failed to store appreciable a
7 cluding proliferative responsiveness to SCF, metachromatic granules, mRNA expression for mast cell pr
8 ngliosidosis (Tay-Sachs and Sandhoff forms), metachromatic leucodystrophy, mucolipidosis type IV, Nie
9 e-infantile (456, 201-854) or early-juvenile metachromatic leukodystrophy (291.0, 104-445) and those
10 d blood (n = 92) samples of 40 patients with metachromatic leukodystrophy (aged 0-42 years) with 38 n
11 V) in individuals affected by late-infantile metachromatic leukodystrophy (LI-MLD).
12                                Patients with metachromatic leukodystrophy (MLD) and multiple sulfatas
13                      Krabbe disease (KD) and metachromatic leukodystrophy (MLD) are caused by accumul
14 A (ASA) causes the lysosomal storage disease metachromatic leukodystrophy (MLD) characterized by mass
15                                              Metachromatic leukodystrophy (MLD) is a lysosomal storag
16                                              Metachromatic leukodystrophy (MLD) is a lysosomal storag
17                                              Metachromatic leukodystrophy (MLD) is a rare, inherited,
18                                              Metachromatic leukodystrophy (MLD) is an ultrarare, seve
19                      Effective treatment for metachromatic leukodystrophy (MLD) remains a substantial
20 uction of the myelin sheath and resulting in metachromatic leukodystrophy (MLD), a neurodegenerative
21 tase A (ASA) activity found in patients with metachromatic leukodystrophy (MLD), a progressive neurod
22 ilable during the last 20 years for juvenile metachromatic leukodystrophy (MLD), reported with variab
23 changes in brain tissues of a mouse model of metachromatic leukodystrophy (MLD).
24 rovement of cerebral white matter changes in metachromatic leukodystrophy after treatment with hemato
25 e seen in single-sulfatase disorders such as metachromatic leukodystrophy and mucopolysaccharidoses I
26 ApoE-derived peptide appears useful to treat metachromatic leukodystrophy and possibly other neurolog
27  progressive multifocal leukoencephalopathy, metachromatic leukodystrophy and subacute infarct.
28 developed for X-linked adrenoleukodystrophy, metachromatic leukodystrophy and Zellweger syndrome and
29 h correction is possible in a mouse model of metachromatic leukodystrophy by the transplantation of h
30 T with cord blood in 1 patient with juvenile metachromatic leukodystrophy diagnosed before frank dege
31                                              Metachromatic leukodystrophy is a lethal metabolic leuko
32 iminated between healthy subject samples and metachromatic leukodystrophy patient samples, and, there
33                                              Metachromatic leukodystrophy subtype was determined base
34 he first to document neurological outcome of metachromatic leukodystrophy treated by umbilical cord b
35                          Three siblings with metachromatic leukodystrophy underwent umbilical cord bl
36 is; Fabry, Gaucher, and Krabbe diseases; and metachromatic leukodystrophy).
37 ylsulfatase A (ARSA), a gene responsible for metachromatic leukodystrophy, a lysosomal storage disord
38  stem cell transplant, if performed early in metachromatic leukodystrophy, can not only stabilize but
39                      APCs from patients with metachromatic leukodystrophy, who accumulate sulfatides
40 lidation of a new assay for the diagnosis of metachromatic leukodystrophy.
41 present in humans with phenotypes resembling metachromatic leukodystrophy.
42 efficacious gene therapy in a mouse model of metachromatic leukodystrophy.
43 d in KcsA tetramers, but not in monomers, by metachromatic reaction to o-toluidine blue stain on SDS-
44                                       Slight metachromatic reaction with toluidine blue is indicative
45 nterfere dramatically with these assays; the metachromatic response was also clearly influenced by di
46 nflammatory cells (lymphocytes, eosinophils, metachromatic staining cells, and neutrophils) in bronch
47 ted by higher proteoglycan content, stronger metachromatic staining, and altered ultrastructure in co
48 hat the absence of Ctr2 results in increased metachromatic staining, the latter indicating an impact
49 ositive cells (lymphocytes, eosinophils, and metachromatic-staining cells) in the group treated with
50 ut half were immunoreactive for tryptase and metachromatic with toluidine blue.