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D L Martin

Publications and source records attributed to D L Martin.

At least 109 records · Page 6Linked to original sources
PubMed1986

Contaminated produce--a common source for two outbreaks of Shigella gastroenteritis.

Simultaneous outbreaks of Shigella sonnei gastroenteritis occurred in October 1983 at two Texas university campuses 60 miles (96 km) apart. There were no common food handlers, recreational activities, water sources or swimming areas to explain the introduction of Shigella at both campuses. However, tossed salads were found to be associated with illness at both campuses. The investigation disclosed that both schools had received produce shipments from the same company during the week preceding these outbreaks. Shigella isolates from cases at both universities, sent to the Centers for Disease Control for plasmid analysis and colicin typing, were found to be identical. The same organism was evidently not a frequent cause of shigellosis within a 160-mile (256 km) radius of these universities since only 19% of control isolates chosen from this area were identical to the type which caused these outbreaks. This is the first report of two related outbreaks of shigellosis that were caused by a contaminated food source and not by a food handler. Simultaneous foodborne outbreaks of shigellosis should trigger a search for potential contamination at every step of food handling from farm to kitchen.

Disease Outbreaks↗
PubMed1986

Activation of beta-adrenergic receptors stimulates release of an inhibitory transmitter from astrocytes.

Activation of beta-adrenergic receptors on astrocytes in primary cell culture results in the release of taurine, an inhibitory transmitter. Taurine release occurs via a cyclic AMP-mediated intracellular pathway, because (a) taurine release and intracellular cyclic AMP accumulation have similar pharmacologies and time courses of activation and (b) N6,O2'-dibutyryl cyclic AMP stimulates release with a time course similar to that observed with the beta-adrenergic agonist isoproterenol. These results describe a previously unrecognized physiological function of astrocytes in the CNS-receptor-mediated release of the neuroactive amino acid taurine. This observation indicates that astrocytes may function as local regulators of neuronal activity.

Alprenolol↗
PubMed1986

Exogenous glutamate is metabolized to glutamine and exported by rat primary astrocyte cultures.

Rat cortical astrocytes in primary culture were examined for their capacity to transport and metabolize exogenous L-[U-14C]glutamate. After incubation for time periods up to 120 min, cells and incubation media were analyzed for labelled and endogenous glutamate and its metabolic products by HPLC coupled with fluorescence detection and liquid scintillation counting. Glutamine was the major labelled metabolite after 120 min, accounted for 38% of the original glutamate label, and was found primarily in the incubation medium. A further 13.5% of the label was recovered in deaminated metabolites of glutamate, 1.2% was associated with aspartate, 23% remained in glutamate, and 10.2% was found in an acid-precipitated cell fraction. More than 84% of the label was recovered in these fraction. suggesting that the maximum possible formation and loss of 14CO2 was 16%. The rate of total glutamine synthesis was 1.1 nmol X mg protein-1 X min-1 when 9 microM exogenous glutamate was present. The total amount of glutamine synthesized greatly exceeded the consumption of glutamate, indicating that a substantial proportion of glutamine was synthesized from other carbon sources. Almost all of the newly formed glutamine was exported into the medium. These results indicate that astrocytes in primary culture, by accumulating glutamate, producing glutamine, and exporting it, are capable of carrying out the glial component of the glutamine cycle.

Animals↗
PubMed1986

Activation of glutamate apodecarboxylase by succinic semialdehyde and pyridoxamine 5'-phosphate.

Glutamate apodecarboxylase was activated by incubation with succinic semialdehyde and pyridoxamine 5'-phosphate. Activation required both compounds and was highly selective for succinic semialdehyde. Of 18 analogs tested, only glyoxylate, pyruvate, oxaloacetate, and 2-oxoglutarate activated the apoenzyme significantly, but much higher concentrations of these compounds than of succinic semialdehyde were required. In the presence of pyridoxamine 5'-phosphate, the concentration of succinic semialdehyde giving half-maximal activation of apoenzyme was 7 microM. In contrast, the Ki for succinic semialdehyde as a competitive inhibitor of glutamate decarboxylation was 1.2 mM, indicating that apoenzyme with bound pyridoxamine 5'-phosphate has a much higher affinity for succinic semialdehyde than does holoenzyme. The concentration of pyridoxamine 5'-phosphate giving half-maximal activation was 17 microM, which is more than an order of magnitude greater than the corresponding value for pyridoxal 5'-phosphate.

Apoenzymes↗
PubMed1985

Chelidonic acid and other conformationally restricted substrate analogues as inhibitors of rat brain glutamate decarboxylase.

Twenty conformationally restricted analogues of glutamate including benzoic acids, hydroxy-benzoic acids, pyridine dicarboxylic acids, and pyran dicarboxylic acids were tested as inhibitors of glutamate decarboxylase from rat brain. Chelidonic acid, 2,6-pyridine dicarboxylic acid, chelidamic acid, gallic acid, and 3,4-dihydroxybenzoic acid were the most potent inhibitors of the enzyme, and generally the aromatic analogues were much more potent inhibitors than their aliphatic counterparts. An intercarboxylate distance of 0.75 nm appears optimal for substrate competition, indicating that glutamate binds to the active site in an extended conformation. At least one carboxyl group can be replaced by a phenolic hydroxyl without greatly affecting inhibition. The degree of inhibition was also influenced by the aromatic structure, particularly with respect to the atom bridging the dicarboxylate carbons. Kinetic analysis of the inhibition by chelidonic acid and chelidamic acid showed that these compounds were competitive with glutamate with Ki values of 1.2 and 33 microM respectively. Consistent with this result, chelidonic acid also inhibited the glutamate-dependent formation of apoenzyme. Chelidonic acid itself did not promote formation of apoenzyme and did not react with free pyridoxal-P. The effects of different classes of glutamate decarboxylase inhibitors are discussed in relation to the formation of apoenzyme and its reactivation by pyridoxal-P. As one of the most potent inhibitors of glutamate decarboxylase known, chelidonic acid may be of value in studies of the regulation of gamma-aminobutyric acid synthesis.

Animals↗
PubMed1985

Characterization of three kinetically distinct forms of glutamate decarboxylase from pig brain.

Pig brain contains three forms of glutamate decarboxylase with pI values of 5.3, 5.5 and 5.8, referred to as the alpha-, beta- and gamma-forms respectively. These forms were purified and kinetically characterized. The major synaptic form of glutamate decarboxylase (the beta-form) migrated as a single band on electrophoresis in sodium dodecyl sulphate/polyacrylamide gels with an apparent Mr of 60 000. Sodium dodecyl sulphate/polyacrylamide gel electrophoresis followed by immunoblotting with an affinity-purified antibody to the enzyme indicated a subunit Mr of 60 000 for the alpha- and gamma-forms as well. An extensive kinetic analysis, aided by an integrated equation that describes the inactivation and re-activation cycle of the enzyme, revealed that the three forms of the enzyme differ markedly in kinetic properties. The Km values for L-glutamate were 0.17, 0.45 and 1.24 mM respectively for the alpha-, beta- and gamma-forms. The Ki for 4-aminobutyrate, the first-order rate constants for inactivation by L-glutamate and 4-aminobutyrate, the rate constant for re-activation of the apoenzyme by pyridoxal 5'-phosphate and the dissociation constant for pyridoxal 5'-phosphate also differed in a similar way among the three forms; the values were in the order alpha-form less than beta-form less than gamma-form.

Animals↗
PubMed1985

Transaminations catalysed by brain glutamate decarboxylase.

In addition to normal decarboxylation of glutamate to 4-aminobutyrate, glutamate decarboxylase from pig brain was shown to catalyse decarboxylation-dependent transamination of L-glutamate and direct transamination of 4-aminobutyrate with pyridoxal 5'-phosphate to yield succinic semialdehyde and pyridoxamine 5'-phosphate in a 1:1 stoichiometric ratio. Both reactions result in conversion of holoenzyme into apoenzyme. With glutamate as substrate the rates of transamination differed markedly among the three forms of the enzyme (0.008, 0.012 and 0.029% of the rate of 4-aminobutyrate production by the alpha-, beta- and gamma-forms at pH 7.2) and accounted for the differences among the forms in rates of inactivation by glutamate and 4-aminobutyrate. Rates of transamination were maximal at about pH 8 and varied in parallel with the rate constants for inactivation from pH 6.5 to 8.0. Rates of transamination of glutamate and 4-aminobutyrate were similar, suggesting that the decarboxylation step is not entirely rate-limiting in the normal mechanism. The transamination was reversible, and apoenzyme could be reconstituted to holoenzyme by reverse transamination with succinic semialdehyde and pyridoxamine 5'-phosphate. As a major route of apoenzyme formation, the transamination reaction appears to be physiologically significant and could account for the high proportion of apoenzyme in brain.

Aminobenzoates↗
PubMed1985

A mysterious cluster of deaths and cardiopulmonary arrests in a pediatric intensive care unit.

In the period April 1981 through June 1982, there was an unusual increase in the number of deaths and cardiopulmonary arrests in the pediatric intensive care unit at a large medical center hospital in San Antonio, Texas. During this period, 34 of 42 deaths (81 per cent) occurred in the evening work shift, as compared with 36 of 106 (34 per cent) during the previous four years (P less than 0.0001). Reviews of records of patients revealed no association between death in this 15-month epidemic period and a variety of demographic, historical, medical, and admission characteristics; medical or surgical procedures; or the severity of illness. The findings of a blinded clinical consultant support the conclusion that the increase in deaths and cardiopulmonary arrests could not be explained on the basis of the clinical status of the patients, and the consultant concluded that during the epidemic period, there were more deaths and cardiopulmonary arrests that were either unexpected in timing or inconsistent with the previous clinical course. The presence of one nurse was associated with the increased numbers of deaths (relative risk, 10.7; 95 per cent confidence limits, 6.4 to 17.9), cardiopulmonary arrests (relative risk = 25.5, confidence limits = 16.8 to 38.6), and unexpected clinical events, (relative risk, infinite; confidence limits, 33.7 to infinity). Although the cause of the epidemic remains unclear, the findings illustrate that surveillance of deaths and cardiopulmonary resuscitation may allow early recognition of similar problems in other hospitals.

Child↗
PubMed1985

A cluster of true appendicitis cases.

A cluster of cases of appendicitis occurred primarily in school-age boys in a small Texas town. The expected rate of appendicitis is 1.5 cases per 1,000 persons, or about 1 case per month in that town. However, in the spring of 1984, 13 cases, 10 in school-age boys, occurred. In eight of these patients, the initial onset of abdominal pain occurred over a 15 day period. A case controlled study of school-age patients indicated that sweets in the diet and consumption of local farm eggs may have been associated with the appendicitis. We hypothesize that a group of young male patients who were susceptible to appendicitis because of the high sugar content of their diets were exposed to a bacterium or virus that precipitated this outbreak of appendicitis.

Acute Disease↗
PubMed1985

Application of the median method to the determination of kinetic constants for competitive enzyme inhibition.

A procedure was developed to determine kinetic constants for competitive inhibition (Km, Ki, Vmax) by the median method. Simulated experiments were used to compare the accuracy and precision of kinetic constants determined by the median method with unweighted and weighted least-squares analysis. The median method was superior to unweighted least-squares analysis. The weighted least-squares method was superior to the median method when the error was normally distributed but the median method was superior when two or more outliers were present. The dependence of the accuracy and precision of kinetic constants obtained by the median method on several experimentally important parameters, including the number of experimental points, the number and range of substrate concentrations, and the number and range of inhibitor concentrations, was determined.

Binding, Competitive↗
PubMed1985

Clinical and laboratory features of an outbreak of Vibrio cholerae O1 infections in the United States.

A point source outbreak of Vibrio cholerae O1 El Tor Inaba infections occurred aboard an oil rig south of Port Arthur, Texas, in September 1981. Sixteen crew members had V. cholerae O1 infections as determined by serology or stool specimens; 15 were symptomatic. The high percentage of symptomatic infections was attributed in part to the ingestion of a large number of V. cholerae O1 organisms by susceptible individuals. Symptoms included diarrheal stools (100%), weakness (60%), abdominal cramps (53%), nausea (40%), and vomiting (27%). Only one of the three patients who sought medical attention was diagnosed by his physician as having cholera. Physicians who treat patients who live near or travel to the Gulf Coast should consider cholera in patients with watery stools. If cholera is suspected, laboratories should use thiosulfate-citrate-bile salts-sucrose (TCBS) agar in addition to routine enteric media for processing stool specimens.

Adult↗
PubMed1985

Beta-receptor-stimulated and cyclic adenosine 3',5'-monophosphate-mediated taurine release from LRM55 glial cells.

Adrenergic stimulation of LRM55 glial cells results in the release of the neuroactive amino acid taurine. The present study characterizes the receptors involved in taurine release and shows that taurine release is mediated by cyclic adenosine 3',5'-monophosphate (cAMP). beta-Receptors in LRM55 cells were first characterized by [125I]iodohydroxybenzylpindolol binding. Binding was stereospecific and saturable with time and ligand concentration. Kinetic analysis of equilibrium binding at 37 degrees C revealed a single component of high affinity (Km = 113 pm; Bmax = 52.1 +/- 5.0 fmol/mg of protein). The pharmacologies of the stimulation of cAMP accumulation and taurine release were similar. The agonists isoproterenol (IPR), epinephrine (E) and norepinephrine (NE) showed a rank order of potency characteristic of a beta-adrenergic system (IPR greater than E greater than or equal to NE). The beta-antagonists alprenolol and propranolol inhibited the IPR stimulation of both processes; the alpha-antagonist phentolamine did not. The dependence of taurine release on cAMP was further suggested by the similarity of the two time courses and was demonstrated by the stimulation of taurine release by the cAMP analogue dibutyryl cAMP. Thus, one physiological response of glial cells to beta-adrenergic stimulation is the release of taurine. Receptor-activated release of taurine from glia represents a previously undescribed neuronal-glial interaction by which glia may actively regulate neuronal excitability.

Animals↗