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1 mes involved in the lysosomal degradation of mucopolysaccharides.
2 ultiple organs demonstrating accumulation of mucopolysaccharides.
3 on of sphingolipids, phospholipids, and acid mucopolysaccharides.
4 containing phospholipids, sphingolipids, and mucopolysaccharides.
5 nd histochemical stains, including those for mucopolysaccharides (Alcian blue and/or colloidal iron).
6    The explanted cornea was stained for acid mucopolysaccharides (AMP) and periodic acid-Schiff stain
7  is occupied by membrane-spanning mucins and mucopolysaccharides densely tethered to the airway surfa
8                              All corneas had mucopolysaccharide deposition visible on hematoxylin-eos
9 lular matrix, resulting in cell aggregation, mucopolysaccharide deposition, and significant obstructi
10 manifestations, lysosomal storage disorders, mucopolysaccharide disorders, primary central nervous sy
11  an exosite that binds both factor X and the mucopolysaccharide, heparin.
12 analyses revealed co-deposits of Cochlin and mucopolysaccharide in human TM around Schlemm's canal, s
13 istributed throughout the lumen and the acid mucopolysaccharide localized in the central core.
14                                              Mucopolysaccharide (MPS) diseases are characterized by a
15 ally, the findings suggest that the capsular mucopolysaccharide of serogroup A strains of P. multocid
16 ), along with complete loss of intracellular mucopolysaccharide staining in the airway epithelium.
17 nt unexpected finding in a neurodegenerative mucopolysaccharide storage disease, the Sanfilippo syndr
18 erkeley, led me, rather improbably, to study mucopolysaccharide storage disorders in the intramural p
19       I have traced the path from studies of mucopolysaccharide turnover in cultured cells to the dev
20                    Interestingly, the acidic mucopolysaccharides were found increased in the PTK-indu
21  amphophilic collections of stromal granular mucopolysaccharides which are visible on hematoxylin-eos