Sialyl oligosaccharides from milk.
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Biomedical subjects
Publications and source records attributed to D F Smith.
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Inbred strains of male mice (C3H, DBA, BALB, C57) were used to determine whether genetic factors play a role in lithium toxicity. Significant differences in the LD50 for LiCl were observed between the mouse strains after a subcutaneous injection of 37 degrees isotonic LiCl. The LD50 values in the C3H, DBA, BALB and C57 strains were 17.4, 17.6, 18.2, and 19.4 mmol/kg, respectively. Significant differences were also observed between the mouse strains in the concentrations of lithium in plasma, heart, liver, kidney and brain 2 hrs. after a subcutaneous injection of 15.1 or 18.2 mmol/kg LiCl, but the lithium concentrations were not related in an obvious manner to LiCl toxicity. The results show that genetic factors can influence the toxicity and pharmacodynamics of lithium.
Retrospective radiological documentation of a growing Wilms's tumour in rare. Considered to be a relatively rapidly growing tumour, we present a case where there was adequate radiological evidence of a Wilms's tumour 4 years before the clinical metastatic presentation.
Excretion of lithium in urine was studied in 2 healthy males while recumbent and while upright, either walking or standing quietly. An oral dose of 24.3 mmol of Lit was taken as three lithium carbonate tablets 13 h before clearance tests. Renal lithium clearance decreased and lithium fractional reabsorption increased while upright. Standing immersed to the neck in water, which prevents the fall in plasma volume upon changing posture from recumbent to upright, prevented the fall in renal lithium clearance as well as the rise in lithium fractional reabsorption while upright. Oral doses of guanethidine (total dose of 200 mg) or oxprenolol (total dose of 140 mg) taken to prevent high levels of sympathetic nervous system activity and plasma renin, respectively, failed to prevent the fall in renal lithium clearance or the rise in lithium fractional reabsorption upon changing posture from recumbent to upright. The findings indicate that the fall in renal lithium clearance and the rise in lithium fractional reabsorption upon changing posture from recumbent to upright is related to the fall in plasma volume but not to high levels of sympathetic nervous system activity or plasma renin activity.
Samples of saliva were collected from healthy subjects given a test dose of lithium carbonate. Lithium clearance in saliva was well related to salivary potassium clearance but not to salivary sodium clearance. Stimulation of adrenocortical activity by changing from the recumbent to the upright posture caused salivary sodium clearance to fall, but failed to affect the clearance of lithium and potassium in saliva. The findings show that the secretion of lithium in saliva resembles potassium secretion more than sodium secretion.
Heinz body formation was induced in calf erythrocytes by a daily dose of 8 mg phenylhydrazine/kg body weight. Body weights and feed intakes were not affected, the glutathione content of erythrocytes was reduced, but the hemolysis rate of erythrocytes was not changed. Morphological changes in erythrocytes were shown by light and high resolution scanning microscopy. The appearance of Heinz bodies may have value as an indicator of oxidative stress under conditions such as copper toxicity or deficiency of selenium-vitamin E.
Rats given a subcutaneous injection of beta-phenylethyl-amine (PEA) (30 or 60 mg/kg) showed stereotyped behavior and autonomic effects which were suppressed by LiCl. Inhibition of Type A MAO by clorgyline or Lilly 51641 (2 or 8 mg/kg) or of Type B MAO by l-deprenyl (2 or 8 mg/kg) counteracted the suppressant effects of LiCl on PEA-behavior. The findings suggest that both Type A MAO and Type B MAO play a role in the effects of LiCl on PEA-behavior.
The pathophysiology, diagnostic evaluation and medical management of the horse with intestinal obstruction is outlined. Emphasis is on early and accurate determination of the need for surgery and on providing optimal preoperative medical support.
A rapid and specific assay has been developed for UDPglucose-collagen glucosyltransferase (UDPglucose: 5-hydroxylysine-collagen glucosyltransferase, EC 2.4.1.66) using galactosylhydroxylysine (Gal-Hyl) as acceptor. Studies with intact human platelets and isolated plasma membranes indicated that about 5--10% of the total activity was surface bound and the rest was of cytoplasmic origin. The two forms of the enzyme had similar broad pH optima (6.5--8.0), Km values for UDPglucose (5 muM) and Gal-Hyl (approx. 4 mM) and for optimal manganese concentrations (25 mM). The soluble form of the enzyme was purified 80-fold. The reaction mechanism was determined as being rapid equilibrium random BiBi + dead end complex or ordered BiBi with UDPglucose being the first substrate to bind. Using Gal-Hyl bound in purified alpha 1 chain of chick skin collagen, a Km value three orders of magnitude less (2 muM) was found than for free Gal-Hyl and the manganese requirement decreased to 2 mM. These results suggest that the binding to the enzyme of Gal-Hyl in the collagen molecule is enhanced by the presence of the protein portion so that the enzyme may be capable of recognizing not only the carbohydrate side chains but also the primary structure of collagen.
A branchial cyst in a heifer was removed surgically. Diagnosis was based on clinical signs, analysis of cyst contents, and histologic examination of the cyst wall. Biochemically, the cyst fluid resembled a transudate. The cyst lining consisted of nonciliated, pseudostratified columnar epithelium and pigmented, keratinized, stratified squamous epithelium. The embryologic origin was thought to be endoderm of the 2nd pharyngeal pouch and adjacent ectoderm.
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The metabolism of 2-deoxy-D-galactose has been studied in AS-30D rat ascites hepatoma cells in suspension. Using 2-deoxy-D-(1-14C)galactose and an alkaline ethanol deproteinization procedure, the quantitatively identified metabolites included 2-deoxy-D-galactose 1-phosphate comprising 99.3%, and UDP-2-deoxy-D-galactose and UDP-2-deoxy-D-glucose, together amounting to 0.4% of the total metabolites. After incubation for 5 h in the presence of 2-deoxy-D-galactose (1 mmo1/1), the content of 2-deoxy-D-galactose 1-phosphate reached 35 mmo1x(kg cells)-1. The rate of phosphorylation of 2-deoxy-D-galactose was rapid during the first 30 min and decreased to approximately 20% of this rate during the subsequent hours. The rapid trapping of Pi in the form of 2-deoxy-D-galactose 1-phosphate resulted in a depression of free intracellular Pi in spite of a concomitant increase in net 32Pi uptake from the medium and a decrease of ATP and other 5'-nucleotides. The rates of glucose utilization and lactate production were depressed by more than 80% in the presence of 2-deoxy-D-galactose (1 mmo1/1). Interruption of Pi trapping by removal of 2-deoxy-D-galactose from the medium reversed the depressions of Pi and ATP and resulted in a rapid but incomplete relief of glycolysis inhibition. Crossover analysis of glycolytic intermediates indicated an inhibition at the 6-phosphofructokinase step. The depression of glucose utilization may be mediated by the increased level of glucose 6-phosphate, a potent inhibitor of hexokinase. An additional inhibitory effect of a metabolite of 2-deoxy-D-galactose at the 6-phosphofructokinase step was indicated by crossover analysis after reversal of Pi and ATP depressions in the presence of a high intracellular content of 2-deoxy-D-glactose 1-phosphate. The quantitative analysis of the metabolites of 2-deoxy-D-galactose demonstrated the predominance of the monophosphate and the negligible formation of UPD derivatives of this sugar analog in AS-30D hepatoma cells. This provides a system for the investigation of a galactose analog as a phosphate-trapping agent in the virtual absence of uridylate trapping.
Excretion of lithium in urine and saliva was studied in healthy males while recumbent and while upright, walking and standing quietly. An oral dose of 24.3 mEq of LI+ was taken as three lithium carbonate tablets 13 hr before clearance tests. Urinary lithium clearance decreased when posture was changed from recumbent to upright, but salivary lithium clearance was not affected by the abrupt change in posture. A correlation was observed while recumbent between lithium clearance in urine and saliva, but not while upright. The findings are related to the extrapolation of saliva lithium excretion data to urinary lithium clearance.
Studies on the effects of lithium on drinking, food intake, locomotor activity and aggression in rats are reviewed. Particular attention is paid to the dosage, concentration, route and schedule of lithium treatments. The effects of lithium on behavior are found to depend on the experimental methods. The main effects of lithium treatments on rat behavior are found to be prevention of the reoccurrence of certain behaviors, enhancement of intake of water and sodium chloride solutions, suppression of some types of spontaneous and drug-induced activity, production of hyperactivity when given together with MAO inhibitors, reduction of some types of aggressive behavior, enhancement of morphine analygesia and reduction of morphine intake. The relationship between the outcome of studies on behavior in rats given lithium and the use of lithium salts to treat human disorders is briefly discussed.
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Renal lithium clearance, tissue lithium levels, serum lithium concentration, and body temperature were determined in rats given lithium alone or combined with haloperidol (0.5-1 mg/kg). A slight increase in serum lithium concentration occurred in one of the three groups given lithium plus haloperidol. Haloperidol failed to affect renal lithium clearance, tissue lithium levels and body temperature. The data do not support the hypothesis that haloperidol exerts an action on lithium pharmacokinetics.
Hyperactivity, salivation, piloerection, exophthalmia and ejaculation occurred in rats given reserpine (5 mg/kg i.p.) 2 hr after an oral dose (5 mg/kg) of trans-dl-2-phenylcyclopropylamine (tranylcypromine, dl-Tcp). The same syndrome occurred in rats given the d-isomer (d-Tcp) plus reserpine but not in rats given the l-isomer (l-Tcp) lus reserpine. Neither alpha methyl-p-tyrosine (2 X 150 mg/kg s.c.) nor parachlorophenylalanine (200 mg/kg s.c.) pretreatment prevented the hyperactivity syndrome. The results suggest that mainly MAO inhibition and release of monoamines are involved in the hyperactivity syndrome produced by dl-Tcp plus reserpine.
Locomotor activity of male rats was studied in an open field after an i.p. injection (15 mg/kg) of the d- or l-isomers of tranylcypromine (d-Tc and l-Tc, respectively) or after s.c. injection of either clorgyline (0.5, 1 or 5 mg/kg) which selectively inhibits Type A MAO or deprenyl (0.5, 5 or 10 mg/kg) which selectively inhibits Type B MAO. The rats were fed a diet containing either no lithium (control group) or lithium chloride (lithium group) for at least 28 days prior to tests. In the control group, d-Tc increased ambulation while l-Tc, deprenyl and clorgyline failed to affect activity. In the lithium group, d-Tc and deprenyl increased ambulation, l-Tc increased ambulation and rearing, while clorgyline failed to affect activity. Lithium appeared to potentiate the behavioral effects of deprenyl and l-Tc. Symptoms of serotonin-dependent hyperactivity appeared in the control group and lithium group given d-Tc. The role of biogenic amines in the effects of the drugs on open field activity is discussed.