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Biomedical subjects

P Baker

Publications and source records attributed to P Baker.

At least 145 records · Page 8Linked to original sources
PubMed1979

An in vitro evaluation of clavulanic acid, a potent, broad-spectrum beta-lactamase inhibitor.

The in vitro efficacy of clavulanic acid, a new broad-spectrum inhibitor of enterobacterial beta-lactamases, was investigated. In conventional agar dilution tests, the presence of a sub-inhibitory level of clavulanic acid (8 microgram/ml) lowered the minimum inhibitory concentration of ampicillin for many resistant enterobacteria to therapeutically achievable levels. When tested against dense populations of Escherichia coli and klebsiella strains in a static turbidimetric system and in an in vitro model of the treatment of bacterial cystitis, clavulanic acid plus ampicillin suppressed bacterial growth for periods far exceeding the normal interdose interval at concentrations at which neither agent alone was effective. In addition to its activity as a beta-lactamase inhibitor, clavulanic acid may interact with other beta-lactam antibiotics in a second, distinct way. Because of this synergic interactions may occur with non-beta-lactamase producing organisms, and the overall synergic effect obtained with beta-lactamase producers may be compounded of two separate elements.

Ampicillin↗
PubMed1978

Coma in the Wernicke-Korsakoff syndrome.

Four comatose patients were found to have the Wernicke-Krosakoff syndrome. All had a history of alcoholism, previous alcoholic neurological disease, and poor nutrition. Intravenous or nasogastric tube feeding without vitamin supplements precipitated coma in three. Examination showed a diffuse encephalopathy with intact pupillary light reflexes, no focal neurological signs, and absent doll's eye and caloric responses. The tendon reflexes were uniformly absent. Two patients were hypothermic and one was hypotensive. Although the level of consciousness improved in all after parenteral thiamine, three died and one was left disabled. The Wernicke-Korsakoff syndrome merits wider recognition as a cause of coma and empirical treatment with thiamine in cases of coma of unknown cause is recommended.

Coma↗
PubMed1977

Increased tissue concentrations of 5-hydroxytryptamine in the duodenal mucosa of patients with coeliac disease.

Tissue concentrations of 5-HT have been measured in the duodenal mucosa of adults and children with coeliac disease and were found to be significantly higher than those from a control group. This finding may be associated with hyperactivity or hyperplasia of enterochromaffin (EC) cells in the duodenum of patients with coeliac disease and could also be directly related to described abnormalities of 5-HT metabolism in this disease.

Adult↗
PubMed1975

Time to talk.

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Communication↗
PubMed1975

Studies on the inhibition of C56-initiated lysis (reactive lysis). III. Characterization of the inhibitory activity C567-INH and its mode of action.

An activity in serum which inhibits reactive lysis has recently been shown to do so by preventing the attachment of C567 complexes to cells, and hence has been designated C567-INH. This report describes certain physiochemical characteristics of the inhibitory activity. It behaves as a heat-stable pseudoglobulin, soluble in 20 per cent Na2SO4, and having alpha1 mobility on Pevikon block electrophoresis. It is excluded from CM cellulose at pH 6-0, RSC Equals 0.007 M, is retained by an XM-100 membrane and is heterogenous on Sephadex G-200, eluting in at least two peaks. The combined active materials from the Sephadex column elute from DE-52 in at least four peaks. The mechanism of action of material from each of these four peaks is shown to involve prevention of attachment of C567 complexes to membranes, and this is shown to involve an effect on C567 complexes in solution rather than an effect on the membrane. A less dramatic effect on the lysis of EC567 by limited quanities of C8 and C9 can be demonstrated. Haemolytic studies using cell-bound C567 suggest that the interaction of C567-INH with C567 involves a loose reversible association. It is therefore postulated that C567-INH inhibits reactive lysis primarily by reversibly associating with the nascent C567 complex in solution, increasing its bulk and decreasing its diffusion capacity so that it is unable to reach a cell membrane before its haemolytic potential decays.

Animals↗
PubMed1975

Studies on the inhibition of C56-initiated lysis (reactive lysis). V. The roleof C567-INH in the regulation of complement-dependent haemolysis initiated by cobravenom factor.

Activation of the alternative pathway of complement by a factor from cobra venom (CVF) can lead to lysis of unsensitized erythrocytes (E) of some species. In these studies we observed that alterations in CVF-induced lysis could be produced by manipulation of C567-INH, a naturally occurring inhibitory activity which acts on fluid phase C567 complexes. Venom lysis of sheep and guinea-pig E was markedly inhibited by serum fractions having C567-INH activity. Microgram quantities of poly-L-lysine (PLL), molecular weight 180,000, a polycation which is a functional antagonist to C567-INH in serum, potentiated CVF lysis of sheep and guinea-pig E, and permitted the lysis of human E, which are otherwise not suscepticle to CVF lysis. The potentiation of venom lysis by PLL seemed not to be due to alterations in the target cell membrane; furthermore, it in turn was reversed by substances with C567-INH activity. This suggests that the generation of fluid phase C567 complexes contributes to the CVF-induced lysis of erythrocytes of these species, and that the haemolytic potential of fluid phase C567 generated during alternative pathway activation by this means is regulated by C567-INH.

Ammonium Sulfate↗
PubMed1975

Studies of the inhibition of C56-initiated lysis (reactive lysis). IV. Antagonism of the inhibitory activity c567-INH by poly-L-lysine.

The stable intermediate complex C56 can initiate the lysis (reactive lysis) of unsensitized erythrocytes (E) by the membrane attack machanism of complement. Certain serum constituents designated C567-INH inhibit reactive lysis by preventing the C567 complex, once formed, from attaching to a membrane surface. It is shown here that microgram quantities of poly-L-lysine (PLL), a synthetic polycation of molecular weight 180,000, can reverse the effests of C567-INH, and thereby potentiate formation of EC567 by erythrocytes, C56 and C7 in whole serum. Erythrocytes exposed to PLL in a preincubation step did not show either increased susceptibility to C567 or resistance to C567-INH, and reversal of C567-IHN by given amounts of PLL was not diminished as cell concentrations were greatly increased, indicating that the effect of PLL was predominantly directed against fluid phase rather than against erythrocyte membrane substrates. The effects of PLL and C567-INH were quantitatively reciprocal. Thus, PLL-induced potentiation of C56-induced lysis is a solute effect which seems to involve direct neutralization of naturally occurring serum inhibitors of the C567 trimolecular complex of complement. The use of PLL thus provides a suitable antagonist for C567-INH in reaction mixtures, and allows evaluation of the role of C567 and C567-INH in a variety of situations involving C-mediated lysis.

Alpha-Globulins↗