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Biomedical subjects

G F Baker

Publications and source records attributed to G F Baker.

At least 19 recordsLinked to original sources
PubMed1992

The pH volume changes of human red cells in vitro due to the exchange of chloride and hydroxyl anions.

In glucose exit experiments measured photoelectrically, the excursions on the chart recorder were found to be larger for exits in media of alkaline pH. This was shown to be due to the addition of a pH volume effect to that of the osmotic shrinkage resulting from the glucose efflux. The pH-dependent volume change also occurred in glucose-free cells and was a linear function of the pH of the medium between pH 6.8 and 9.0. The effect is consistent with the loss (or gain) of chloride in exchange for hydroxyl anions on the band 3 anion transporter and with the buffering of the hydroxyl anions by haemoglobin. The implications for the working of the anion exchanger and for respiratory physiology are discussed.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1992

An hypothesis for a contractile protein based on the principles of submicroscopic physiology.

The discovery of the polyguanidinium ring complex and its various properties has emphasised the versatility of arginines in functional proteins. In an extension of these studies the possibility of formulating a polypeptide which could be the basis for a contractile element in muscle presented itself. Although hypothetical, the deduced molecular properties, based on the unique chemistry of arginine guanido groups are in keeping with known functional aspects of some muscles, and could form the foundation for a more detailed theory of muscular contraction. The structural requirements and the theoretical principles involved are briefly described in this paper.

Models, Molecular↗
PubMed1991

Infantile myofibromatosis.

Infantile myofibromatosis is part of a heterogeneous group of rare childhood fibromatoses characterized by the proliferation of myofibroblasts. It is not a common condition and is frequently misdiagnosed. We present an unusual patient who had small, depressed, atrophic, skin lesions uncharacteristic of infantile myofibromatosis.

Atrophy↗
PubMed1991

The polyguanidinium-ring-complex cation shield in the human red cell glucose transporter.

Widdas and Baker (1991) have described a possible structure and functioning of the human erythrocyte glucose transporter, based on its amino acid sequence. It was noted that eight positively charged side chains surrounded the proposed transfer cleft on the inside. These could form a ring shield which prevented the loss of K+ ions. Theoretical and model-making considerations point to this shield being made up of a polyguanidinium-ring-complex cation with eight (or ten) positive charges distributed over two identical rings of hydrogen bonds and normal linkages.

Amino Acid Sequence↗
PubMed1991

The polyguanidinium complex of the glucose transporter: a possible basis for bistable cationic gates and anionic channels in biology.

The detailed molecular structure and mechanism of action of the red cell glucose transporter would endow it with the ability to transfer the less hydrated potassium ion. This is prevented by a polyguanidinium-ring-complex cation which provides an effective electrical energy barrier. The ring complex has structural features which could form a bistable state of ring charges; in one form the electrical repulsions would be fully effective (gate 'shut'), whereas in the other form they would be ineffective (gate 'open'). It is also suggested that the polyguanidinium linkages could form a linear complex which could be the basis for anionic channels in biology. The theoretical basis for both these hypotheses is described.

Biological Transport↗
PubMed1991

The role of the surface energy of water in the conformational changes of the human erythrocyte glucose transporter.

There is now strong experimental evidence that the red cell glucose transporter protein operates by a conformational change which has the effect of presenting a sugar binding site to the outside and inside medium of the cells in an alternating manner, but the way in which this is brought about is still unknown. Kinetic evidence that the conformational changes which create the inward and outward facing modes can occur in the absence of a sugar substrate has been put on a firmer experimental basis by Appleman and Lienhard (1989). Conformational changes of the magnitude envisaged are too large to be attributed only to spontaneous thermal agitation in the protein. Theoretical considerations show that the surface energy of water could be an alternative source of energy which, in a suitable reciprocating cycle of activity, could sustain the conformational changes throughout the existence of the transporter.

Alcohols↗
PubMed1988

Parameters for 3-O-methyl glucose transport in human erythrocytes and fit of asymmetric carrier kinetics.

1. Equilibrium exchanges in the range of 2-40 mM-3-O-methyl glucose at 16 degrees C suggested that the half-saturation concentration for exchange was 22 mM and that the maximum velocity (Vmax) was ca. 149 mmol l-1 min-1. 2. Initial rates of exchange influx from 1, 2, 4 and 8 mM into 76 mM solution gave a half-saturation value of 3.6 mM and a Vmax of 122 mmol-1 min-1. 3. The non-transportable inhibitor 4,6-O-ethylidene-alpha-D-glucopyranose (ethylidene glucose) acting on the outside of the cells inhibited 3-O-methyl glucose exchanges at 16 degrees C with an inhibition constant (KI) of ca. 11 mM. 4. Sen-Widdas exit experiments gave the half-saturation for 3-O-methyl glucose at 16 degrees C as only ca. 2 mM and the KI for ethylidene glucose as ca. 4 mM. 5. Efflux inhibitions by ethylidene glucose are satisfactorily predicted by the asymmetric carrier kinetics of Regen & Tarpley (1974) when using the parameters derived from the exchange experiments but not with parameters from Sen-Widdas exits. 6. Uphill transfer by counterflow experiments and Sen-Widdas exits cannot be fitted by the Regen and Tarpley kinetics (using the same parameters) unless the kinetics are modified to provide for an extra exchange element which replaces some of the net exit component in the equations. 7. At present the modification to the kinetics is only possible in computer simulations and data handling, but with it the fit to experimental results is good. The nature of the modification is described and in the light of it a revised interpretation of the significance of the Km derived from Sen-Widdas exits is discussed.

3-O-Methylglucose↗
PubMed1988

Chronic fixed drug eruption caused by acetaminophen.

A case of chronic fixed drug eruption resembling parapsoriasis en plaques is reported, which presented with persistent, stable lesions that were present for seven months before the diagnosis was established. The patient's skin cleared totally with avoidance of acetaminophen and flared prominently with re-exposure. Distribution of the recurrence was different: some previous sites had apparently become refractory and remained clear, some involvement had recurred in the same site, and new areas of involvement had appeared, causing the eruption to "wander," as is often seen in acute fixed drug eruption due to acetaminophen.

Acetaminophen↗
PubMed1987

Wandering fixed drug eruption: a mucocutaneous reaction to acetaminophen.

Two patients are presented with a fixed drug eruption to acetaminophen characterized by recurring erythematous, circular plaques of the skin and oral mucosa along with multiple sites of deep (postinflammatory) hyperpigmentation clinically characteristic of fixed drug eruption. The involved sites did not necessarily flare with each exposure, nor did activity always appear in the same sites with each flare. Eventually some sites apparently became completely refractory. This caused the eruption to seem to "wander." Patch testing with 1% acetaminophen in alcohol (300 mg/30 ml alcohol) confirmed the causative agent in one patient. Although patch testing was negative in the other patient, oral reexposure caused a flare. Acetaminophen appears to be an uncommon cause of fixed drug eruption, with a tendency for lesions to appear at the same or at different sites in flares, perhaps because of a prolonged refractory period and the tendency to become completely refractory in some locations.

Acetaminophen↗
PubMed1987

Granular cell basal cell carcinoma.

Granular cell basal cell carcinoma (BCC) is a rare histologic variant of BCC. In this, the third reported case, the tumor consisted almost entirely of granular cells. By electron microscopy, these cells were filled with pleomorphic lysosome-like granules lined by unit membranes and containing homogeneous or granular electron-dense bodies, membranous debris and amorphous material. The epithelial origin of the tumor was suggested by the characteristic light microscopic appearance of tumor cell islands with some areas of peripheral palisading, and was confirmed by electron microscopic features of numerous well-formed pentalaminate desmosome junctions and sparse cytoplasmic tonofilament bundles, some of which showed attachments to the desmosomes. Histochemical immunoperoxidase stains for lysozyme showed no cytoplasmic lysozyme activity, in common with other granular cell tumors, but ultrastructural examination did not reveal angulate bodies, in contrast to findings in non-epithelial granular cell tumors.

Aged↗
PubMed1979

Evidence of multiple operational affinities for D-glucose inside the human erythrocyte membrane.

1. The Michaelis-Menten parameters of labelled D-glucose exit from human erythrocytes at 2 degrees C into external solution containing 50 mM D-galactose were obtained. The Km is 3.4 +/0 0.4 mM, V 17.3 +/- 1.4 MMOL . 1(-1) cell water . min-1 for this infinite-trans exit procedure. 2. The kinetic parameters of equilibrium exchange of D-glucose at 2 degrees C are Km = 25 +/- 3.4 mM, V 30 +/- 4.1 mmol . 1(-1) cell water . min-1. 3. The Km for net exit of D-glucose into solutions containing zero sugar is 15.8 +/- 1.7 mM, V 9.3 +/- 3.3 mmol . 1(-1) cell water . min-1. 4. This experimental evidence corroborates the previous finding of Hankin, B.L., Lieb, W.R. and Stein, W.D. [(1972) Biochim. Biophys. Acta 255, 126--132] that there are sites with both high and low operational affinities for D-glucose at the inner surface of the human erythrocyte membrane. This result is inconsistent with current asymmetric carrier models of sugar transport.

Biological Transport↗
PubMed1978

Asymmetry of the hexose transfer system in human erythrocytes. Experiments with non-transportable inhibitors.

1. The asymmetrical nature of sugar affinity for the hexose transfer system in human red cells has been demonstrated using purified 4,6-O-ethylidene-alpha-D-glucopyranose (ethylidene glucose) to inhibit the exchange of glucose, 3-O-methyl glucose and galactose. 2. The half-saturation concentration for ethylidene glucose inside the cell is estimated at ca. 110 mM whereas on the outside the value for exchange inhibition is ca 11mM. 3. The asymmetrics of affinities of two related non-transportable inhibitors 1,2-O-isopropylidene-D-glucofuranose and methyl-2,3-di-O-methyl-alpha-D-glucopyranoside have also been studied. 4. From experiments at varying concentrations and on theoretical grounds the half-saturation concentration for non-transportable inhibitors on the outside surface is shown to be over-estimated by measuring inhibition of exchange. In consequence the actual asymmetry of affinities may be greater than observed. 5. Experiments with ethylidene glucose also suggest that conformational changes redistributing components of the hexose transfer system between inward and outward facing modes may occur.

Biological Transport↗