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S J Mason

Publications and source records attributed to S J Mason.

14 recordsLinked to original sources
PubMed1992

Regulation of Cl- channels in normal and cystic fibrosis airway epithelial cells by extracellular ATP.

The rate of Cl- secretion by human airway epithelium is determined, in part, by apical cell membrane Cl- conductance. In cystic fibrosis airway epithelia, defective regulation of Cl- conductance decreases the capability to secrete Cl-. Here we report that extracytosolic ATP in the luminal bath of cultured human airway epithelia increased transepithelial Cl- secretion and apical membrane Cl- permeability. Single-channel studies in excised membrane patches revealed that ATP increased the open probability of outward rectifying Cl- channels. The latter effect occurs through a receptor mechanism that requires no identified soluble second messengers and is insensitive to probes of G protein function. These results demonstrate a mode of regulation of anion channels by binding ATP at the extracellular surface. Regulation of Cl- conductance by external ATP is preserved in cystic fibrosis airway epithelia.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Adenosine receptors on human airway epithelia and their relationship to chloride secretion.

1. We have characterized an adenosine receptor subtype present in human airway epithelial cells by measuring the changes in the intracellular levels of adenosine 3':5'-cyclic monophosphate (cyclic AMP) and the rate of transepithelial Cl- secretion. 2. Primary cultures of human nasal epithelium obtained from excised surgical airway epithelial tissues and the cell lines BEAS39 and CF/T43 derived from human airway epithelium were grown on plastic dishes and labelled with [3H]-adenine for measurement of intracellular cyclic AMP accumulation. Primary cultures were loaded with the calcium indicator fura-2 to measure [Ca2+]i and studied as polarized, ion transporting epithelia on collagen matrix supports for measurement of Cl- secretion. 3. Adenosine analogues stimulated cyclic AMP accumulation with a rank order of potency characteristic of an A2-receptor: 5-N-ethyl-carboxamidoadenosine (NECA) greater than adenosine greater than R-phenylisopropyladenosine (R-PIA), 6-N-cyclopentyladenosine (CPA) greater than S-PIA. NECA increased cyclic AMP accumulation in normal and cystic fibrosis (CF) primary cells as well as in the CF/T43 and BEAS39 cell lines with K0.5 values ranging from 0.3 to 3 microM. Preincubation with NECA resulted in the homologous desensitization of airway epithelial cells. The effect of NECA was specifically inhibited by the adenosine receptor antagonist, aminophylline, in a competitive manner. 4. The A1-adenosine receptor agonists CPA and R-PIA did not inhibit isoprenaline-stimulated cyclic AMP accumulation in CF/T43 cells, and potentiating effects of the adenosine analogues were observed on forskolin-stimulated cyclic AMP accumulation. Adenosine analogues did not cause significant changes in intracellular Ca2+ ([Ca2+]i) in airway epithelium.5. Adenosine analogues, applied to either the serosal or mucosal side of the polarized amiloride pretreated primary cultures, induced changes in I,, with a rank order of potency of agonists similar to that observed for stimulation of cyclic AMP accumulation. Intracellular microelectrode studies indicated that the locus of action was the apical membrane Cl- conductance. Adenosine failed to stimulate C1- secretion in CF airway epithelium.6. These results provide evidence for the existence of an A2-adenosine receptor that modulates intracellular levels of cyclic AMP in human airway epithelium. Activation of this receptor might lead to stimulation of Cl- secretion in amiloride pretreated normal but not CF cells.

Adenosine↗
PubMed1992

Effects of bradykinin on Na+ and Cl- transport in human nasal epithelium.

Human nasal epithelium (HNE) is a Na+ absorptive epithelium but establishes a baseline Cl- secretory current in the presence of amiloride (10(-4) M, luminal). We compared the effects of an inflammatory mediator, bradykinin (BK), on ion transport in primary cultures of HNE using double-barreled Cl(-)-selective microelectrodes. In untreated HNE, BK (10(-5) M) transiently increased the equivalent short-circuit current (Ieq). Maximal Ieq occurred with hyperpolarization of the transepithelial potential difference (Vt), which was associated with hyperpolarization and decreased resistance of the basolateral membrane; a subsequent depolarization of Vt was observed that was associated with depolarization and decreased resistance of the apical membrane. Removal of bath Cl- did not affect the BK-induced Ieq response. In amiloride-treated HNE, the electrical pattern of the BK-induced response was identical, but the magnitude of the Ieq was reduced by 54% and the change in Ieq could be abolished by removal of bath Cl-. Equivalent-circuit analysis of the response in amiloride-treated tissues indicated activation of a hyperpolarizing conductance in the basolateral membrane, followed 20-30 s later by activation of an apical Cl- conductance. We conclude that BK stimulates both Na+ absorption in untreated HNE and Cl- secretion in amiloride-treated HNE by activating a basolateral (K+) conductance. Analysis of the entire Ieq response under both conditions also suggested that BK induces a delayed activation of apical membrane Na+ and Cl- conductances.

Adult↗
PubMed1991

Regulation of transepithelial ion transport and intracellular calcium by extracellular ATP in human normal and cystic fibrosis airway epithelium.

1 The role of extracellular nucleotides in regulation of ion transport activities (short circuit current, Isc) of human respiratory epithelia was studied. 2 Application of nucleotides to the apical or basolateral membrane of human nasal epithelium induced a concentration-dependent increase in Isc. 3 The rank order of potency of purine- or pyrimidine-induced changes in Isc of normal human nasal epithelium when applied to the apical membrane (UTP greater than or equal to ATP greater than ATP gamma S greater than 2MeSATP greater than ADP beta S much greater than beta gamma MeATP greater than or equal to alpha beta MeATP) or basolateral membrane (2MeSATP greater than UTP greater than ATP greater than ATP gamma S greater than alpha beta MeATP greater than beta gamma MeATP) is consistent with involvement of a P2 purinoceptor. A similar rank order of potencies was observed for nucleotide effects on intracellular calcium measured by Fura-2 fluorescence using microspectrofluorimetry. 4 Similar nucleotide potency in the regulation of ion transport and intracellular calcium in cystic fibrosis (CF) airway epithelium (UTP greater than or equal to ATP) was observed, suggesting purinoceptors might be used to stimulate ion transport processes that would promote hydration of airway secretions and facilitate their clearance from CF lungs. 5 These data provide evidence for the regulation of ion transport by P2 purinoceptors in normal and cystic fibrosis human airway epithelium.

Adenosine Triphosphate↗
PubMed1991

HIV testing.

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AIDS Serodiagnosis↗
PubMed1977

The Duffy blood group determinants: their role in the susceptibility of human and animal erythrocytes to Plasmodium knowlesi malaria.

Duffy blood group negative erythrocytes from blacks are refractory to invasion by Plasmodium knowlesi merozoites in vitro, and blacks with this genotype are resistant to infection by P. vivax in vivo. In order to evaluate in a direct manner the role of Duffy blood group determinants in invasion by P. knowlesi merozoites, we studied erythrocytes from three rare non-black Duffy negative individuals, Fy(a-b-), in whom the Duffy negative phenotype probably represents a mutation and not the introduction of the black Fy gene. These cells were resistant to invasion by P. knowlesi in vitro indicating that resistance to invasion is mediated by the FyFy genotype and not another closely linked factor. The erythrocyte receptors for invasion, however, may not be the Fya or Fyb Duffy antigens themselves, or at least not restricted to these determinants, since refractory Duffy negative human erythrocytes were invaded after treatment with trypsin or neuraminidase although these enzyme-treated cells still lacked Fy a and Fy b determinants. Furthermore, new world monkey erythrocytes and chymotrypsinized chimpanzee and kra monkey erythrocytes were invaded, although there was no serologic evidence of Fya or Fyb determinants on these cells.

Animals↗
PubMed1977

Further evidence for the parasitic origin of the surface coat on Malaria merozoites.

It has been observed that a surface coat, 20 nm in thickness, extends from the plasma membrane of extracellular merozoites and that this coat contains strain-specific antigens. In the present study we determined the possible effect of protein in the culture medium on this structure. The surface coat on merozoites in culture medium devoid of protein was indistinguishable by transmission electron microscopy from the coat in a protein-containing medium. This supports the hypothesis that the surface coat originates from the parasite rather than from adsorbed serum protein.

Animals↗
PubMed1976

The resistance factor to Plasmodium vivax in blacks. The Duffy-blood-group genotype, FyFy.

Duffy-blood-group-negative human erythrocytes, FyFy, are resistant to invasion in vitro by Plasmodium knowlesi. The FyFy genotype is found predominantly in African and American blacks, who are the only groups completely resistant to infection by P. vivax. To determine if the FyFy genotype is the vivax resistance factor, we performed blood typing on 11 black and six white volunteers who had been exposed to the bites of P. vivax-infected mosquitoes. Only the five FyFy blacks were resistant to erythrocytic infection; the remaining six blacks and all whites had the Duffy-positive determinants (Fya or Fyb or both) and had contracted malaria. We conclude that Duffy determinants (Fya or Fyb or both) on the erythrocyte surface are required for invasion of erythrocytes by vivax merozoites.

Adult↗
PubMed1975

Erythrocyte receptors for (Plasmodium knowlesi) malaria: Duffy blood group determinants.

Duffy blood group negative human erythrocytes (FyFy) are resistant to infection by Plasmodium knowlesi, a simian malaria that infects Duffy positive human erythrocytes. The P. knowlesi resistance factor, Duffy negative erythrocytes, occurs in high frequency in West Africa, where the people are resistant to vivax malaria. This suggests that Duffy blood group determinants (Fya or Fyb) may be erythrocyte receptors for P. vivax.

Binding Sites↗
PubMedDate not supplied

The use of echocardiography for quantitative evaluation of left ventricular function.

Echocardiography is a valuable technique for the diagnosis and serial follow-up of patients with impaired cardiac function. It is subject to certain limitations due to the assumptions inherent in deriving ventricular volume from a one-dimensional measurement and must be interpreted with caution in cases of suspected regional abnormalities of contraction. Given these caveats, echocardiography is valuable in the quantitative assessment of cardiac size and the level of compensation in patients with primary myocardial disease, valvular heart disease, and left ventricular hypertrophy. It can detect abnormal contraction in some patients with ischemic heart disease and provides an accurate method to serially follow changes produced as a result of drug or surgical therapy. Finally, two-dimensional techniques promise to provide a new perspective on the evaluation of patients with regional wall motion abnormalities.

Cardiac Volume↗