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M A Bayne

Publications and source records attributed to M A Bayne.

10 recordsLinked to original sources
PubMed1994

Cloning and expression of a cDNA for the human prostanoid FP receptor.

A cDNA clone coding for a functional human prostanoid FP receptor has been isolated from a uterus cDNA library. The human FP receptor consists of 359 amino acid residues with a predicted molecular mass of 40,060, and has the seven putative transmembrane domains characteristic of G-protein-coupled receptors. Challenge of Xenopus oocytes expressing the FP receptor with 10 nM of either prostaglandin (PG) F2 alpha or the selective FP-receptor agonist fluprostenol resulted in an elevation in intracellular Ca2+. Radioreceptor binding studies using membranes prepared from mammalian COS cells transfected with the FP receptor cDNA showed that the rank order of potency for prostaglandins and prostaglandin analogs in competition for [3H]PGF2 alpha specific binding sites was as predicted for the FP receptor, with PGF2 alpha approximately fluprostenol > PGD2 > PGE2 > U46619 > iloprost. In summary, we have cloned the human prostanoid FP receptor which is functionally coupled to the Ca2+ signalling pathway.

Amino Acid Sequence↗
PubMed1993

Cloning and expression of a cDNA for the human prostaglandin E receptor EP1 subtype.

A functional cDNA clone coding for the human prostaglandin E receptor EP1 subtype has been isolated from a human erythroleukemia cell cDNA library probed by low-stringency hybridization using a polymerase chain reaction fragment of the human thromboxane receptor. The human EP1 receptor is comprised of 402 amino acids with a predicted molecular mass of 41,858 and has the topography common to all G-protein-coupled receptors with seven predicted transmembrane spanning domains. Prostaglandin (PG) E2 challenge of Xenopus oocytes injected with EP1 cDNA resulted in an increase in intracellular Ca2+. In addition, the rank order of potency for prostaglandins in competition for [3H]PGE2 specific binding to membranes prepared from EP1 cDNA transfected COS cells was PGE2 > PGE1 > PGF2 alpha > PGD2. Furthermore, the EP1 receptor-selective antagonists AH 6809 and SC19220 were more potent than the EP2 receptor-selective agonist butaprost in these competition binding assays. In summary, therefore, we have cloned the human EP1 receptor subtype which is functionally coupled to an increase in intracellular Ca2+.

Amino Acid Sequence↗
PubMed1987

GGT test.

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Humans↗
PubMed1983

Absorption of zinc by the rat ileum: effects of histidine and other low-molecular-weight ligands.

The role of certain amino acids, dipeptides and organic acids as ligands to facilitate the intestinal absorption of zinc was investigated by using an in vivo procedure on ileal segments of adult rats. Ligand:zinc ratios equal to or less than 3:1 were optimal for amino acids and dipeptides such as L-glutamate, glycine, L-histidine, L-tryptophan and glycylglycine. An excess of ligand reduced zinc absorption. At a 130:1 L-histidine:zinc ratio the absorption of zinc was less than one-fourth that obtained at a 3:1 ratio. Picolinate was a less effective ligand. The kinetics of the complex L-histidine:zinc at a 2:1 ratio and at pH 7.5 were determined in the absence and presence of a 20 mM excess of amino acid in a zinc concentration range between 0.038 mM and 6.00 mM. In both cases the Vmax was 2200 pmol/(minute . cm), but the Kt increased from 0.54 mM to 1.46 mM in the presence of the L-histidine excess. These data suggest a competitive inhibition of the L-histidine:zinc complex by the amino acid. Such an effect was dependent on the stereoisomerism of histidine, since the unnatural D-isomer was far less effective than the natural L-isomer in facilitating zinc absorption. The presence of an intact protein (bovine serum albumin) sharply decreased the ileal absorption of the L-histidine:zinc complex.

Amino Acids↗
PubMed1983

Altered jejunal macromolecular barrier induced by alpha-dihydroxy deconjugated bile salts.

The effect of deconjugated bile salt hydroxy group position and numbers on the ability of these agents to alter the normal lumen-to-blood jejunal barrier to intact protein penetration was analyzed. Only in vivo jejunal perfusion with 0.5 mM alpha-dihydroxy deconjugated bile salts chenodeoxycholate and deoxycholate led to increased penetration of the 40,000-molecular-weight protein horseradish peroxidase (HRP). This increased absorption of HRP with 0.5 mM chenodeoxycholate and deoxycholate was detectable biochemically, as well as by light and electron microscopic cytochemistry, and occurred in the absence of demonstrable histological or ultrastructural damage to the epithelium. Conjugation of chenodeoxycholate with glycine, epimerization of chenodeoxycholate from 7 alpha-hydroxy to 7 beta-hydroxy as in ursodeoxycholate, or addition of a third hydroxyl group as in cholate all eliminated the increase in jejunal HRP penetration and led to HRP absorption levels like those in bile salt-free preparations. The effect of chenodeoxycholate and deoxycholate on HRP absorption was paralleled by their production of net jejunal water secretion. The observations suggest that the naturally occurring alpha-dihydroxy bile salts may lead to an increase in intact antigen or toxin absorption during bacterial stasis syndromes.

Animals↗
PubMed1983

Disaccharide feedings enhance rat jejunal macromolecular absorption.

Disaccharide feedings to post-weaning rats alters their jejunal barrier to macromolecular absorption. Penetration of horseradish peroxidase (HRP) across the jejunum was enhanced after short-term high concentration gavage (30 g . kg-1 . day-1) of lactose that produces weight loss, osmotic diarrhea, and jejunal mucosal damage. HRP absorption was also increased by longer term feedings of lower levels of disaccharide that did not produce body weight alterations, diarrhea, or cell damage. Rats without diarrhea and gavaged with 7.5 g . kg-1 . day-1 of either lactose or maltose showed an increase in lumen to blood HRP absorption after 21 days of feedings. Also, lactose or maltose in the solid food diet at 30 g . kg-1 . day-1 for 21 days did not lead to diarrhea but produced an increase in jejunal lumen to blood HRP absorption. Rats having no diarrhea and receiving 15 g . kg-1 . day-1 of lactose or maltose in the drinking water for 21 days, showed an increase in jejunal HRP absorption. When rats were fed either lactose or maltose for 21 days glucose absorption became totally dependent upon the sugar concentration in the perfusion medium. The kinetics of this glucose absorption are compatible with a decrease in the "unstirred" layer. Disaccharide-induced HRP absorption may be mediated by transport from endocytotic vesicles across the jejunal epithelium.

Animals↗
PubMed1981

Jejunal macromolecular absorption and bile salt deconjugation in protein-energy malnourished rats.

The combined stress of protein-energy malnutrition (PEM) and exposure of the jejunum to pathophysiological (0.5 mM) levels of a bacterial metabolite, deconjugated bile salts, led to alterations not apparent with either stress alone. Perfusion of the jejunum of PEM rats with 0.5 mM deoxycholate (DCh) and a 40,000 dalton macromolecular tracer, horseradish peroxidase, led to higher serum horseradish peroxidase levels than were seen in PEM rats not exposed to DCh or in well-nourished controls treated with DCh. Semiquantitative cytochemical analysis indicated an increased number of villi with horseradish peroxidase penetration in PEM rats treated with 0.5 mM DCh. DCh perfusion of PEM rats also produced fine structural damage to epithelial cells not apparent in other preparations. And, perfusion with 0.5 mM cholate only produced sodium secretion in PEM rats. These observations in an animal model of PEM suggest that malnourished children with a colonic type of bacterial overgrowth of the small bowel may attain increased levels of foreign antigens or toxins from the intestinal lumen.

Animals↗
PubMed1981

Bile salt-enhanced rat jejunal absorption of a macromolecular tracer.

Bile salt deconjugation may occur in the jejunum under conditions of fecal colonic overgrowth of the small intestine. We studied the effects of conjugated and deconjugated bile salts on rat jejunal absorption of a macromolecular tracer, horseradish peroxidase, in an in vivo perfusion system. At a 0.5 mM perfusion concentration, only the deconjugated bile salts, cholate and deoxycholate, produced a significant increase in horseradish peroxidase absorption into serum. At a 0.5 mM concentration of the conjugated salt, taurocholate, horseradish peroxidase-absorption was indistinguishable from that seen in bile salt-free preparations. At a higher 5 mM concentration, both the conjugated and deconjugated salts increased jejunal HRP absorption into serum over that seen in bile salt-free preparations; this absorption wa most marked with the deconjugated salts. At a 0.5 mM level, the bile salts induced minimal sodium and glucose transport alterations but did not produce evidence of morphologic damage to villi or absorptive epithelial cell organelles. At a 5 mM level, the deconjugated salts induced glucose and sodium transport abnormalities and appeared to damage cellular organelles. Our observations suggest that an alteration in the tight junctional barrier to macromolecular absorption may play a role in some of the enhanced horseradish peroxidase absorption seen with deoxycholic acid in these experiments. The process of an increased absorption of intact macromolecules induced by products of bacterial metabolism may be of pathologic significance in the etiology of immunologically related intestinal disease or in toxigenic processes.

Animals↗
PubMed1980

Zinc status and its relation to growth retardation in children with chronic inflammatory bowel disease.

Zinc status was studied in 30 patients with chronic inflammatory bowel disease (CIBD) as well as in 17 normal children, 13 primordial short stature, and 17 anorexia nervosa patients. Basal serum and urinary excretion levels of zinc were measured in all patients. In addition, a zinc loading test was performed in 16 CIBD patients, 21 normal and/or short stature children, and nine patients with anorexia nervosa. Eleven of 30 patients with CIBD had serum zinc values less than 0.7 microgram/ml, whereas none of the other patients had hypozincemia. In addition, the mean urinary zinc excretion of CIBD patients was significantly lower than that of patients with primordial short stature and with anorexia nervosa. An altered response to oral zinc load was the most frequent abnormality in CIBD patients. Those with moderate and severe clinical disease activity had a decreased serum rise of zinc after the oral load of this ion. Urinary excretion of zinc after oral load was also marked by deficiency in all CIBD patients. The abnormalities of zinc metabolism were more frequent among the CIBD patients with growth abnormalities, although they were also found in patients who had normal growth. Among the 14 patients with CIBD and growth abnormalities, seven were hypozincemic and four hypozincuric. Hypozincemia was only found in four patients who had normal height; however, the growth velocity was not known. The zinc tolerance test revealed abnormalities in four of five CIBD patients with short stature and in two of three patients with slow growth. On the other hand, similar alterations in zinc tolerance tests were seen in three of seven CIBD patients with normal height and growth.

Adolescent↗