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Biomedical subjects

K Dawson

Publications and source records attributed to K Dawson.

At least 19 recordsLinked to original sources
PubMed1992

Thrombolysis in high risk patients.

The advent of intra-arterially administered thrombolytic agents of minimal antigenicity, together with small gauge good torque control catheters, enables thrombolysis to be used in patients that may previously have been deemed unsuitable for thrombolytic therapy. Thrombolysis may be used even in the presence of factors formerly and empirically considered to be contra-indications. The continued use of thrombolytic agent may also be warranted despite iatrogenic complications such as vessel wall perforation, particularly if the alternative is major amputation. We report on a series of eight patients in whom intra-arterial tissue plasminogen activator was used despite either recent vascular surgery, or iatrogenic vessel perforation. Suggestions for the use of thrombolysis in high risk patients and following iatrogenic complications are discussed.

Aged↗
PubMed1992

The management of acute laryngo-tracheo-bronchitis (croup): a consensus view.

The management of croup relies upon the traditional clinical skills of observation and examination. Parental involvement is essential and the appropriate reassurance of the patient is important. Endotracheal intubation is required only in a small percentage of children whose airway is compromised to such a degree as to produce fatigue and/or near occlusion.

Adrenal Cortex Hormones↗
PubMed1990

Runway malaria.

Explore the source record for details and available documents.

Aircraft↗
PubMed1990

Effect of BiTek agar on lysostaphin susceptibility of staphylococci.

Staphylococci which were considered to be lysostaphin susceptible on P agar containing Bacto-Agar showed different degrees of resistance to lysostaphin when tested on P agar made with BiTek agar. As a result, lysostaphin-susceptible strains were misidentified as lysostaphin-resistant strains.

Agar↗
PubMed1990

A nonenzymatic preparation of epithelial basolateral membrane for patch clamp.

A preparation has been developed that permits patch clamping of the basolateral membrane of Necturus gallbladder epithelial cells with a high success rate. The epithelium is separated from the underlying tissues mechanically, without enzymatic treatment. Its apical surface is attached to a plastic cover slip, and the basolateral surface, facing up, is cleaned with a suction pipette under microscopic observation. With this cleaning procedure, the success rate in obtaining gigaohm seals increases from less than 1% to approximately 10% of the attempts. The cells appear to retain their structural and functional integrity, as evidenced by electron-microscopic appearance and magnitude of cell membrane voltages. Major advantages of the preparation are that the basolateral membrane domain is preserved and that enzymatic treatment, which could potentially alter membrane proteins, is not necessary.

Animals↗
PubMed1990

Zinc blocks apical membrane anion exchange in gallbladder epithelium.

The effect of Zn2+ on Cl- transport across the apical membrane of Necturus gallbladder epithelium was studied with intracellular conventional and Cl(-)-selective microelectrodes and measurements of apparent base secretion. Most studies were done on tissues incubated in HEPES-buffered solutions; intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels were elevated by adding to the serosal bathing medium either theophylline or dibutyryl cAMP. Under these conditions, Zn2+ (added to mucosal solution) had no effect on membrane voltages, apparent cell membrane resistance ratio, or rapid depolarization induced by reducing mucosal solution [Cl-]. However, Zn2+ reduced the rate of cell membrane repolarization during exposure to the low-Cl- solution and decreased significantly the rate of fall of intracellular Cl- activity (alpha Cli) elicited by lowering mucosal solution [Cl-]. Both effects were time dependent, became significant after 10 min, and were slowly reversible. In tissues not stimulated by cAMP and incubated in a HCO3-CO2-buffered solution, Zn2+ also reduced the rate of fall of alpha Cli on lowering mucosal solution [Cl-]. Base secretion from cells to mucosal solution was assessed from changes in mucosal pH on stopping superfusion with a poorly buffered (1 mM HEPES) medium in the presence of 1 mM amiloride or a Na(+)-free medium, without cAMP stimulation. Exposure to Zn2+ reduced the alkalinization observed with both protocols. We conclude that Zn2+ has no effect on apical membrane Cl- conductance stimulated by cAMP and inhibits Cl(-)-HCO3- exchange. The slow onset and reversal of the effects suggests slow binding of Zn2+, a covalent modification of the exchanger, or an effect requiring Zn2+ transport to the cell interior.

Amiloride↗
PubMed1975

Potentiation by cocaine of relaxations of the guinea-pig colon caused by noradrenaline and by stimulation of adrenergic nerves.

The distal colon of the guinea-pig is relaxed by noradrenaline, by isoprenaline and by the stimulation of fibres running with the colonic nerves or intramurally. The relaxations in response to stimulation of the colonic nerves have a guanethidine-sensitive (adrenergic) and a guanethidine-insensitive (non-adrenergic) component. Cocaine causes a three-fold sensitization of the muscle to noradrenaline but no sensitization to isoprenaline. Cocaine increases the duration, but does not affect the amplitude, of the relaxation observed when adrenergic nerves are stimulated, and affects neither duration nor amplitude of the non-adrenergic response. The adrenergic nerve terminals lie in Auerbach's plexus, not in the longitudinal muscle. It is concluded that the sensitization to noradrenaline and the increases in durations of responses to adrenergic nerve stimulation are due to inhibition of catecholamine uptake into adrenergic nerves by cocaine. It appears that, even where the neuromuscular separation is large as it is in the colon, the concentration of exogenous noradrenaline at the receptors can be decreased by neuronal uptake, and the uptake mechanism can modify responses to nerve stimulation in vitro.

Animals↗