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Biomedical subjects

P F Daniel

Publications and source records attributed to P F Daniel.

28 records · Page 2Linked to original sources
PubMed1984

Swainsonine-induced oligosaccharide excretion in sheep. Time-dependent changes in the oligosaccharide profile.

Urinary oligosaccharides isolated from locoweed-intoxicated sheep were separated and quantified by reversed-phase high pressure liquid chromatography of the perbenzoylated alditols. Mannose-containing oligosaccharides were elevated as early as day 3 of feeding, but maximum levels (approx. 1 mumol/ml) were not attained until after 6 weeks of feeding. The relative abundance of individual oligosaccharides changed over the course of the feeding period. Man3GlcNAc2 reached a peak on day 3 and then rapidly declined. Two isomers were shown to be present in this fraction and the relative proportions altered with the duration of locoweed treatment. The major isomer present at early time points (less than 8 days) co-eluted with synthetic Man(alpha 1-3)[Man(alpha 1-6)]Man(beta 1-4)GlcNAc(beta 1-4)GlcNAc, was digested by endo-beta-N-acetyl-glucosaminidase D, and is probably derived from the trimannosyl core of complex glycoproteins synthesized prior to locoweed treatment. Man3GlcNAc2 isolated from day 53 urine was resistant to endo-beta-N-acetylglucosaminidase D digestion but was cleaved by endo-beta-N-acetylglucosaminidase H. This isomer has the probable structure Man(alpha 1-3)Man(alpha 1-6)Man(beta 1-4)GlcNAc(beta 1-4)GlcNAc, indicative of its origin from hybrid or high-mannose glycoproteins. Man5GlcNAc2 reached a peak on day 13 and then slowly declined, whereas Man4GlcNAc2 increased concomitantly. The rapid increase in Man5GlcNAc2 can probably be attributed to the breakdown of hybrid glycans produced as a result of swainsonine inhibition of Golgi alpha-D-mannosidase II. The onset of observable clinical signs on day 38 closely correlated with the time point at which the level of Man4GlcNAc2 exceeded Man5GlcNAc2. After locoweed feeding was discontinued, the amount of urinary oligosaccharides declined rapidly and reached baseline levels within 12 days.

Acetylglucosaminidase↗
PubMed1983

Induced mannosidosis-excretion of oligosaccharides by locoweed-intoxicated sheep.

Daily urine samples were collected from a locoweed-fed sheep, and the oligosaccharide content examined by thin-layer and liquid chromatography. An unusual pattern of urine oligosaccharides was observed, which appears to be characteristic of loco intoxication. Changes in the pattern could be correlated with the onset of visible disease, which occurred approximately 5 weeks after the typical urine sugars were first detected. HPLC showed that these sugars consisted of two homologous series of oligosaccharides containing one and two residues of 2-acetamido-2-deoxy-D-glucose, respectively.

Animals↗
PubMed1983

Characterization of oligosaccharides from the urine of loco-intoxicated sheep.

Two major oligosaccharides were isolated by preparative HPLC from the urine of a locoweed-fed sheep. Analysis by gas-liquid chromatography and mass-spectrometry indicated compositions of (Man)4(GlcNAc)2 and (Man)5(GlcNAc)2, respectively. Structures were determined by digestion with alpha-D-mannosidase and endo-beta-N-acetylglucosaminidases D and H, and comparison of the products by HPLC with synthetic standards, and oligosaccharides isolated from human mannosidosis urine. Incubation with an exo-beta-N-acetylglucosaminidase was without effect.

Acetylglucosamine↗
PubMed1981

Mannosidosis: isolation and comparison of mannose-containing oligosaccharides from gingiva and urine.

Excessive gingival hyperplasia with storage of mannose-rich oligosaccharides appears to be a unique feature present in a 31-year-old mannosidosis patient. Fractionation and analysis of the gingiva established the presence of (Man)2GlcNAc (2.2 mumol/g), (Man)3GlcNAc (3.5 mumol/g), (Man)4GlcNAc (2.8 mumol/g) and higher oligomers (Man)5GlcNAc--(Man)8GlcNAc (0.5 mumol/g); (Man, mannose; GlcNAc, N-acetylglucosamine). Eight characteristic oligosaccharides were isolated from the patient's urine by thin-layer chromatography. The most abundant was (Man)2GlcNAc (161--558 mumol/l); decreasing amounts of higher homologues up to a dekasaccharide, (Man)9GlcNAc (1--4 mumol/l) were also present. In contrast to urine, in which the trisaccharide was predominant, tetrasaccharides and pentasaccharides were more abundant in gingiva.

Acetylglucosamine↗
PubMed1981

Serum and urinary trisaccharides in mannosidosis.

A trisaccharide, Man2glcNAc, was the most abundant urinary oligosaccharide (161-558 mumol per liter) in a patient with mannosidosis. By means of a newly developed high-performance liquid chromatography (HPLC) procedure, we were able to measure low levels of serum trisaccharide (0.1--0.4 nmol per milliliter). This is the first report of the measurements of serum oligosaccharides in mannosidosis. Our observations on the disparate relationship between serum and urinary concentrations of this trisaccharide suggest that a facilitated renal clearance of oligosaccharides may be related to the nonprogressive aspect of this disorder.

Adult↗
PubMed1976

Glycoprotein biosynthesis by organ cultures of hamster trachea.

Conditions have been developed for maintaining hamster tracheas in organ culture for at least 10 days. Secreted glycoproteins labelled with [14C]glucosamine and [3H]fucose were isolated from the spent medium and digested with papain, and the digest was fractionated on DEAE-Sephadex by stepwise elution with NaCl. The fractions eluted by 0.1 and 0.2 M NaCl and some of the products eluted with 0.4 M NaCl were shown to be derived from epithelial glycoproteins. Glycosaminoglycans were eluted by 0.4 M and by 1.25 M NaCl. Glycopeptides isolated from the epithelium by homogenization, ethanol precipitation and papain digestion, and defined as "intracellular", gave a very similar profile on DEAE-Sephadex. The 0.1 M glycopeptide peak was the major fraction of epithelial origin from both secreted and "intracellular" material; it labelled extensively with both glucosamine and fucose and had a molecular fraction was purified further by chromatography on Sephadex G-75 and DEAE-Sephadex; its amino acid and carbohydrate compositions were determined.

Amino Acids↗
PubMedDate not supplied

Incorporation of labeled glucosamine into glycoproteins by organ cultures of hamster trachea: adverse effects of HEPES buffer.

Hamster tracheas were cultured in serum-free CMRL 1066 medium buffered with either NaHCO3 alone or HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulphonic acid) plus NaHCO3 in an atmosphere of 95% O2 and 5% CO2. Afther 2 days in culture, tracheas maintained in HEPES plus NaHCO3-buffered medium showed an altered surface morphology. Histiological examination after 6 days of culture with HEPES plus NaHCO3 showed the presence of only scattered clumps of cilia. Incorporation of [14C]-glucosamine into intracellular glycoproteins was reduced by 75% and into secreted glycoproteins by 54% in cultures buffered with HEPES plus NaHCO3, compared to NaHCO3-buffered cultures. Incorporation of [H]fucose into intracellular glycoproteins was also reduced, although no effect was observed on secreted glycoproteins.

Animals↗
PubMedDate not supplied

Biochemical, ultrastructural and histochemical studies of cat placentae deficient in activity of lysosomal alpha-mannosidase.

Lysosomal alpha-mannosidase activity, oligosaccharide profiles, light and electron microscopy and lectin histochemistry studies were performed on full-term placentae obtained from five litters of cats. They resulted from breeding related cats who are obligate heterozygotes for lysosomal alpha-mannosidase deficiency. alpha-Mannosidase activity in placentae from affected kittens was less than 10 per cent of control, while in placentae from presumptive heterozygotes the activity was less than 50 per cent of control. High-pressure liquid chromatographic analysis of oligosaccharides revealed massive accumulation of undegraded oligosaccharides in placentae of affected kittens. A small elevation was found in placentae from presumptive heterozygous kittens, and none was detected in placentae of normal kittens. Light and electron microscopic examinations revealed vacuolization of fetal endothelial and mesenchymal cells only in placentae of affected kittens. Succinylated wheat germ agglutinin and concanavalin A stained the fetal fibroblasts only in placentae of affected kittens.

Animals↗
PubMedDate not supplied

Infantile sialic acid storage disease associated with renal disease.

A child with infantile sialic acid storage disease is reported. Ultrasonography demonstrated fetal ascites. At birth, the infant appeared hydropic and presented with numerous dysmorphic features, including sparse white hair, coarse facies, hypertelorism, epicanthal folds, anteverted nostrils, and a long philtrum. In addition, he had visceromegaly, bilateral inguinal hernias, and a slight gibbus deformity. Lymphocytes were vacuolated and bone marrow contained large numbers of foam cells. There were generalized vacuolations of both reticuloendothelial and parenchymal cells in the examined tissues. Neuropathologic studies revealed wide-spread neuronal storage, myelin loss, axonal spheroids, and gliosis. Neurons, endothelial cells, and Kupffer cells stained with wheat germ agglutinin indicated an accumulation of sialic acid. Free sialic acid was significantly increased in urine and serum, as well as in liver, heart, and brain tissues. The alpha-neuraminidase activity was normal. It is assumed that the basic defect of infantile sialic acid storage disease lies in impaired transport of sialic acid across the lysosomal membrane.

Brain↗