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Biomedical subjects

D L Hamilton

Publications and source records attributed to D L Hamilton.

At least 55 records · Page 3Linked to original sources
PubMed1984

Site-specific recombination by the bacteriophage P1 lox-Cre system. Cre-mediated synapsis of two lox sites.

The bacteriophage P1-encoded recombinase Cre forms a simple DNA-protein complex at the specific recognition site loxP. Furthermore, Cre is able to mediate a synaptic union of two loxP sites. When two loxP sites are on the same linear DNA molecule, Cre binds the two sites together to form a circular protein-DNA complex. These complexes can be resolved into a linear DNA molecule and a closed circular DNA molecule, the end products of site-specific recombination.

Base Sequence↗
PubMed1984

The agricultural use of municipal sewage.

The reuse of municipal sewage for agricultural purposes is becoming more prevalent. The literature concerning the impact of this practice is reviewed. It is readily apparent that agricultural reuse of municipal sewage is preferable to other common methods of disposal both from the point of view of ecological influence and economical waste utilization. There is a need to establish guidelines for the agricultural use of municipal sewage which will serve the variable conditions found in Canada and meet the public health concerns associated with an extensive agricultural use.

Agriculture↗
PubMed1984

Biointeraction of dietary T-2 toxin and zinc in mice.

The effect of varying dietary levels of zinc was evaluated in mice fed T-2 toxin. A semipurified diet was used to produce a low zinc (less than 2 parts per million (ppm], a zinc replete (100 ppm), and a high zinc (2500 ppm) diet. T-2 toxin was added to the three zinc diets at a concentration of 10 ppm. The mice were fed one of the six diets ad libitum for up to 28 days. Mice from each diet were submitted for necropsy after 14 and 28 days and after 14 days zinc absorption and retention was measured in mice from each of the low and replete zinc diets, with and without T-2 toxin. Animals receiving a low zinc diet with T-2 toxin had reduced weight gains. The high zinc diet did not depress growth and did not influence T-2 depression of growth. The diets produced significant hematological changes without evidence of a T-2 toxin - zinc interaction. While zinc absorption was greater in mice fed the low zinc diet than those fed the replete zinc diet, T-2 toxin decreased absorption of zinc in the low zinc group and increased absorption in the replete zinc group. T-2 toxin did not influence the biological half-life of retained zinc in either the low or replete zinc groups. The biological half-life of zinc was significantly increased in the mice fed the low zinc diet relative to the replete zinc diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Liver injury with alcoholiclike hyalin after gastroplasty for morbid obesity.

Hepatic damage resembling alcoholic hepatitis has been described after jejunoileal bypass surgery for morbid obesity, but has not been previously reported as a complication of gastric partitioning operations (gastric bypass and gastroplasty). A patient who developed an alcoholic hepatitislike clinical picture 8 mo after gastroplasty is described, suggesting that malnutrition superimposed on obesity may be responsible for the injury in both settings. Reversal of the gastroplasty was associated with clinical and biochemical improvement.

Adult↗
PubMed1981

Organic acid proton donors decrease intestinal secretion caused by enterotoxins.

The effects of several weak acids on the secretory actions of cholera toxin and the heat-stable enterotoxin of Escherichia coli (ST) have been examined in ligated jejunal loops in weanling pigs. Ascorbic and acetic acids had no effect, but L-lactic acid reduced the net fluid secretion caused by cholera toxin. Glutaric acid and p-aminobenzoic acid blocked net fluid secretion caused by cholera toxin or by ST. Antisecretory effects were pH dependent for p-aminobenzoic acid in this study and for nicotinic acid in a previous report (6). At a pH of 5.0, p-aminobenzoic acid treatment increased lumen-to-blood sodium flux and decreased the blood-to-lumen sodium flux caused by cholera toxin. These weak acid effects were more marked on fluid fluxes in enterotoxin-treated loops than in control loops and persisted for 20-30 min after acid removal from loops. These findings are discussed in terms of requirements for antisecretory activity and possible modes of action of antisecretory compounds.

Animals↗
PubMed1980

DNA translocation by the restriction enzyme from E. coli K.

The restriction endonuclease Eco K binds to a host specificity site and then proceeds to cleave the DNA at sites that may to several thousand bases away. It does this by translocating the DNA past the enzyme in an ATP-dependent reaction that results in the formation of highly twisted loop intermediates. DNA cleavage can occur on either side of the host specificity site.

Adenosine Triphosphate↗
PubMed1979

Failure to reverse cholera toxin induced intestinal secretion by agents which decrease mucosal cAMP.

The feasibility of reducing intestinal secretion by the use of agents which decrease intestinal mucosal cAMP concentration has been investigated in the weanling pig and the rabbit. Three different agents for decreasing mucosal cAMP concentration were studied. The cyclic nucleotide phosphodiesterase activator, imidazole, significantly reduced mucosal cAMP concentrations only in the weanling pig. Intraluminal 2'-deoxyadenosine-3'AMP inhibited adenylate cyclase and caused a decrease in mucosal cAMP concentration in both the pig and the rabbit. The introduction of the heat-stable enterotoxin of Escherichia coli into pig jejunal segments also gave lowered mucosal cAMP concentrations. While these three agents effectively reduced cAMP concentrations in intestinal mucosa, they were ineffective in reducing the net fluid secretory effects of cholera toxin. Secretion caused by cholera toxin apparently persists independent of the temporary changes in cAMP concentration which can be induced by pharmacological agents.

Adenylyl Cyclases↗
PubMed1979

Permeability properties of swine small intestine: effect of a heat stable Escherichia coli enterotoxin.

The permeability of weanling swine small intestine was estimated using measurements of filtration coefficients and equivalent pore size. Hypertonic solutions of mannitol, erythritol and urea were used to calculate reflection coefficients in the duodenum, mid jejunum and distal jejunum. Estimated effective pore radius was 6.4-7.4, 5.6-7.2 and 4.7-4.9A degrees in the three respective regions. Similarly the filtration coefficient induced by hypertonic solutions of mannitol decreased significantly in the distal jejunal segments. The results show an aboral gradient of decreasing permeability along the small intestine of the weanling pig. In situ incubation of loops in the proximal jejunum with a heat stable Escherichia coli enterotoxin for one hour did not significantly change the effective pore size as calculated from reflection coefficients of hypertonic solutions of erythritol and urea. However, the filtration coefficients of loops exposed to the enterotoxin were significantly greater than control loops with hypertonic solutions of erythritol and urea but not mannitol. This suggests the occurrence of a slight reduction in epithelial porosity. The results support the hypothesis that intestinal secretion induced by heat stable E. coli enterotoxin is not the result of an increased mucosal permeability.

Animals↗
PubMed1978

Cholera toxin effects on fluid secretion, adenylate cyclase, and cyclic AMP in porcine small intestine.

The effects of cholera toxin on mucosal cyclic nucleotide concentrations and on net fluid secretion in the porcine small intestine are reported. Cholera toxin causes net secretion of fluid into the small intestine of weanling pigs, and secretory rates are dependent on the dose of the toxin placed in intestinal loops. Intestinal secretion due to cholera toxin exposure was not consistently accompanied by elevated concentrations of mucosal cyclic AMP or cyclic GMP. Net fluid fluxes in individual loops did not correlate with mucosal cyclic AMP concentration in the same loop. Jejunal adenylate cyclase was activated to a lesser extent in pigs, compared with rabbits, after in vivo treatment with cholera toxin. In vitro activation in cell-free homogenates was similar for both species. Papaverine was similar to cholera toxin in causing fluid secretion without cyclic AMP accumulations, but 3-isobutyl-1-methyl xanthine significantly increased cyclic AMP concentration and induced fluid secretion in pigs. Weanling pigs appeared to differ from rabbits in having a secretory response to cholera toxin which was independent of elevations in total mucosal cyclic AMP concentration.

1-Methyl-3-isobutylxanthine↗
PubMed1978

Some comparative properties and localization of porcine jejunal adenylate cyclase.

Cholera toxin is thought to cause intestinal secretion by activating adenylate cyclase and increasing intracellular 3',5'-cyclic AMP concentrations in intestinal mucosa. Cholera toxin causes profuse secretion of fluid into ligated intestinal loops of both pigs and rabbits, but cholera toxin-induced increases in 3',5'-cyclic AMP concentration are much lower in the pig than in the rabbit. Porcine jejunal adenylate cyclase was examined for unusual properties which might account for a lack of 3'-5'-cyclic AMP accumulation after treatment with cholera toxin. The divalent cation requirements, the pH optimum, and the stimulation by fluoride ion were unremarkable. The Km for ATP was 0.11 mM with negative cooperativity indicated by a Hill coefficient of 0.83. Triton X-100 was inhibitory and guanosine diphosphate methylenephosphate stimulated enzyme activity. Adenylate cyclase activity was highest in the basal and lateral membrane fractions of jejunal mucosa and relatively low in brush-border preparations. Pretreatment of pig jejunum with cholera toxin caused a 30-40% activation of the crude and of the partly purified enzyme. A relatively low activation of adenylase cyclase in pig jejunal mucosa, compared with rabbit, may account for the absence of 3',5'-cyclic AMP accumulation after cholera-toxin treatment in the pig.

Adenylyl Cyclases↗
PubMed1978

Zinc, cadmium, and iron interactions during intestinal absorption in iron-deficient mice.

Zinc absorption from a test dose of (65Zn) zinc chloride was increased in mice with a high capacity to absorb iron induced by a low-iron diet. When radiolabelled zinc chloride in concentrations varying from 0.025 to 0.30 mM was perfused through open-ended duodenal loops of mice fed this diet, the proportion of zinc taken up from the lumen and transferred to the body was greater from lower than from higher doses. The addition of iron to the perfusate inhibited zinc uptake and transfer, and zinc had a similar effect on iron absorption. Cadmium, a potent inhibitor of iron uptake in mice fed a low-iron diet, impaired zinc uptake under these dietary conditions. These results suggest that in dietary-induced iron deficiency there are analogous mucosal binding sites for the uptake of iron and zinc. There also appear to be mutually exclusive binding sites for the absorption of these metals: radiolabelled iron absorption from an intragastric test dose was enhanced in mice with a high capacity to absorb iron produced by bleeding, whereas the absorption of zinc was not increased.

Animals↗