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Contribution of villous atrophy to reduced intestinal maltase in infants with malnutrition.
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BACKGROUND
It has been known for many years that small intestinal maltase activities are reduced in malnourished infants and in other patients with villous atrophy. The recent availability of human maltase-glucoamylase cDNA provides the opportunity to test the hypothesis that villous atrophy
[Adult form of acid maltase deficiency presenting as progressive spinal muscular atrophy].
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As far as could be elucidated, a sporadic manifestation of a slowly progressing muscular weakness and atrophy had commenced in a female patient symmetrically in the pelvic girdle and thigh region at the age of about 22 years. Only at the age of 55 years a precise neurological examination was done.
Aneurysms and vacuolar degeneration of cerebral arteries in late-onset acid maltase deficiency.
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We present a case of late-onset acid maltase deficiency (AMD) with pronounced involvement of the liver and skeletal muscles. In addition, and in contrast to other adult cases of AMD, the case presented here shows CNS pathology with hypodense and hyperintense white matter areas on CT and MRI scans,
Maltose deterioration approach: Catalytic behavior optimization and stability profile of maltase from Bacillus licheniformis KIBGE-IB4.
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Maltase is an economically valuable enzyme that is used to catalyze the hydrolytic process of maltose and yields d-glucose as a product. In this study, the catalytic behavior of maltase was optimized under various physicochemical condition. Results indicated that bacterial maltase exhibited maximum
Selective vacuolar myopathy with atrophy of type II fibers. Occurrence in a childhood case of acid maltase deficiency.
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A 12-year-old boy being examined for vague chest pains was found to be suffering from acid maltase deficiency. Unlike previously reported cases in which vacuolization was most commonly noted in type I fibers, type II fibers were selectively involved in this patient and were atrophic Type I fibers
The transcription factors Atf1 and Pcr1 are essential for transcriptional induction of the extracellular maltase Agl1 in fission yeast.
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The fission yeast Schizosaccharomyces pombe secretes the extracellular maltase Agl1, which hydrolyzes maltose into glucose, thereby utilizing maltose as a carbon source. Whether other maltases contribute to efficient utilization of maltose and how Agl1 expression is regulated in response to
Childhood acid maltase deficiency. A clinical, biochemical, and morphologic study of three patients.
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Three children, including two siblings and a patient with sporadic glycogenosis type II (childhood form of acid maltase deficiency [AMD] ), were studied clinically, biochemically, and morphologically. In addition to a delay in developmental milestones and mild generalized muscle weakness, nasal
Human intestinal disaccharidase activities: correlations with age, biopsy technique, and degree of villus atrophy.
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The relationship between intestinal morphology, disaccharidase activity, and disaccharide absorption is controversial. A retrospective study of 798 consecutive biopsies was performed to determine whether disaccharidase activities varied by subject age, biopsy technique, and degree of villus atrophy.
Malabsorption and villous atrophy in patients receiving enteral feeding.
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BACKGROUND
The purpose of this study was to assess the structure and function of the small intestine before and after enteral feeding given via a percutaneous feeding gastrostomy (PEG). It is not known whether this method of feeding provides a good luminal drive to the small
Intravenous administration of nucleosides and a nucleotide mixture diminishes intestinal mucosal atrophy induced by total parenteral nutrition.
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Total parenteral nutrition (TPN) is associated with atrophic changes in the structure and function of the intestinal mucosa. Because rapidly renewing intestinal mucosal cells may require an external source of purines and pyrimidines for their optimal growth, it can be assumed that supplementation of
Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding.
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Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight,
Human small intestinal maltase-glucoamylase cDNA cloning. Homology to sucrase-isomaltase.
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It has been hypothesized that human mucosal glucoamylase (EC 3.2.1. 20 and 3.2.1.3) activity serves as an alternate pathway for starch digestion when luminal alpha-amylase activity is reduced because of immaturity or malnutrition and that maltase-glucoamylase plays a unique role in the digestion of
Genotype-phenotype correlation in adult-onset acid maltase deficiency.
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We performed a clinical, biochemical, and genetic study in 16 patients from 11 families with adult-onset acid maltase deficiency. All patients were compound heterozygotes and carried the IVS1(-13T --> G) transversion on one allele; the second allele harbored either a deletion of a T at position 525
The dipeptide alanyl-glutamine prevents intestinal mucosal atrophy in parenterally fed rats.
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This study was performed to determine whether the addition of alanyl-glutamine (Ala-Gln) can prevent intestinal mucosal atrophy induced by standard solution of total parenteral nutrition (S-TPN). Forty-one male Sprague-Dawley rats weighing 250 g were randomly divided into four groups: group I was
Neural regulation of acid maltase in an unusual adult onset deficiency.
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In a 48-year-old female, the first symptoms apparently manifested themselves 18 years before, with occasional tripping and weakness in both legs. During the next 18 years, weakness progressed and the patient developed a waddling gait; she became unable to rise from a lying or seated position
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