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Biomedical subjects

E J MacDonald

Publications and source records attributed to E J MacDonald.

12 recordsLinked to original sources
PubMed2006

The use of an alternative light source to detect semen in clinical forensic medical practice.

One of the primary aims of forensic examination in sexual offences is to detect and recover biological material that will link the offender with the complainant. One potentially valuable method by which trace biological evidence may be identified in other forensic settings is via the use of an Alternate Light Source (ALS). The aim of this study was to determine whether or not there was any potential benefit in using an ALS as an adjunct in sexual assault examinations to aid the detection of forensically relevant areas on the body which are not identifiable on visual inspection for sampling. We present two case reports, which illustrate the potential value of using an ALS in clinical forensic medical practice as an adjunct in sexual assault examinations to detect potentially forensically useful areas of skin to sample for semen. Prior to introducing the ALS into our clinical forensic medical practice, we undertook a number of simple laboratory studies to determine a protocol for its use. Semen is known to fluoresce using an ALS at a wavelength of 450 nm. Although we did not conduct a rigorous scientific evaluation of the technique, we evaluated the use of an ALS to detect semen on a range of inanimate surfaces as well as human skin. On all surfaces, visibility of fluorescence was increased by reduced distance of light source from the surface and increased concentration of semen on the surface, but was not noticeably affected by the angle at which the light source was held in relation to the surface.

Adult↗
PubMed2006

Effects of feeding grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of laying hens, turkey poults, and broiler breeder hens.

Three experiments were conducted to compare the effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of laying hens, turkey poults, and broiler breeder hens. In Experiment 1, thirty-six 45-wk-old laying hens were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA). Concentrations of brain neurotransmitters and metabolites were analyzed in pons, hypothalamus, and cortex by HPLC with electrochemical detection. Neurotransmitters and the metabolites measured included dopamine, 3,4-dihydroxylphenyacetic acid, homovanillic acid, serotonin [5-hydroxytryptamine (5-HT)], 5-hydroxyindolacetic acid, epinephrine, and norepinephrine. The feeding of contaminated grains significantly increased concentrations of 5-HT and decreased the 5-hydroxyindolacetic acid:5-HT in the pons region in the brain stem. Dietary supplementation with GMA prevented these effects. There was no effect of diet on concentrations of other neurotransmitters or metabolites in the pons, hypothalamus, or cortex. In Experiment 2, thirty-six 1-d-old turkey poults were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. Hypothalamic, pons, and cortex neurotransmitter concentrations were not affected by diet. In Experiment 3, forty-two 26-wk-old broiler breeder hens were fed diets including the following for 15 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. There was no effect of diet on neurotransmitter concentrations in the pons, hypothalamus, or cortex. It was concluded that differences in intraspecies effects of these mycotoxins on brain neurotransmitter concentrations might explain the intraspecies differences in the severity of Fusarium mycotoxin-induced reductions in feed intake.

Animal Feed↗
PubMed2004

Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens.

Two experiments were conducted to compare the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens. A polymeric glucomannan mycotoxin adsorbent (GM polymer) was also tested for its efficacy in preventing Fusarium mycotoxicoses. In Exp. 1, a total of 150 starter pigs (initial weight = 9.3+/-1.1 kg) were fed five diets (six pens of five pigs per diet) for 21 d. Diets (as-fed basis) included control, 17% contaminated grains, 24.5% contaminated grains, 24.5% contaminated grains + 0.2% GM polymer, and a pair-fed control for comparison with pigs receiving 24.5% contaminated grains. In Exp. 2,360 1-d-old male broiler chicks were fed for 56 d one of four diets containing the same source of contaminated grains as was fed to pigs. The diets included control, 37% contaminated grains, 58% contaminated grains, and 58% contaminated grains + 0.2% GM polymer (as fed). Neurotransmitter concentrations in the cortex, hypothalamus, and pons were analyzed by HPLC. The following brain neurotransmitter alterations (P < or = 0.05) were observed. In pigs, inclusion of contaminated grains in the diet 1) linearly increased cortex 5-hydroxytryptamine (5HT, serotonin) concentrations, while linearly decreasing hypothalamic tryptophan concentrations; 2) quadratically increased hypothalamic and pons 5-hydroxyindoleacetic acid (5HIAA):5HT ratios, whereas the ratio decreased linearly in the cortex; and 3) linearly increased the ratio of hypothalamic 3,4-dihydroxyphenylacetic acid:dopamine (DA) concentrations, whereas hypothalamic norepinephrine (NRE) and pons DA and homovanillic acid (HVA) concentrations linearly decreased. In broiler chickens, inclusion of contaminated grains in the diet 1) linearly increased concentrations of 5HT and 5HIAA in the pons and 5HT concentrations in the cortex; 2) linearly decreased 5HIAA:5HT ratio; and 3) linearly increased pons NRE, 3-methoxy-4-hydroxyphenylethylene glycol, DA, and HVA concentrations. Supplementation of GM polymer to the contaminated diet decreased (P < 0.05) 5HT and 5HIAA concentrations in the cortex of pigs. It was concluded that the differences in alterations of brain neurochemistry might explain the species differences in the severity of Fusarium mycotoxin-induced feed refusal.

Adsorption↗
PubMed2003

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

An experiment was conducted to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological parameters of starter pigs. A polymeric glucomannan mycotoxin adsorbent (GM polymer, Alltech Inc., Nicholasville, KY) was also tested for its efficacy in preventing Fusarium mycotoxicoses. A total of 150 starter pigs (initial weight of 9.3 +/- 1.1 kg) were fed one of five treatment diets (six pens of five pigs per diet) for 21 d. Diets included control, low level of contaminated grains, high level of contaminated grains, high level of contaminated grains + 0.20% GM polymer, and pair-fed control for comparison with pigs receiving the high level of contaminated grains. Feed intake and cumulative weight gain of pigs decreased linearly with the inclusion of contaminated grains in the diet throughout the experiment (P < 0.0001). Weight gains recovered, however, during wk 3 (P > 0.05). There was no difference between the pair-fed group and the pigs fed the diet containing the high level of contaminated grains in terms of weight gain or feed efficiency (P > 0.05). Feeding contaminated grains linearly increased the serum albumin:globulin ratio (P = 0.01), whereas serum urea concentrations and gamma-glutamyltransferase activities responded in a quadratic fashion (P = 0.02). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were decreased in pigs fed the diet containing the high level of contaminated grains. The feeding of contaminated diets did not significantly alter organ weights expressed as a percentage of BW, serum immunoglobulin concentrations, percentages of peripheral blood lymphocyte subsets, contact hypersensitivity to dinitrochlorobenzene, or primary antibody response to sheep red blood cells (P > 0.05). It was concluded that most of the adverse effects of feeding Fusarium mycotoxin-contaminated grains to starter pigs were caused by reduced feed intake. Although supplementation of GM polymer to the contaminated diet prevented some toxin-induced changes in metabolism, it did not prevent the mycotoxin-induced growth depression under the current experimental conditions.

Adsorption↗
PubMed2002

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on swine performance, brain regional neurochemistry, and serum chemistry and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

The co-occurrence of Fusarium mycotoxins in contaminated swine diets has been shown to result in synergistic toxicity beyond that observed for individual toxins. An experiment was conducted, therefore, to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth, brain regional neurochemistry, serum immunoglobulin (Ig) concentrations, serum chemistry, hematology, and organ weights of starter pigs. Three levels of glucomannan polymer (GM polymer, extract of yeast cell wall, Alltech Inc.) were also tested for its efficacy to overcome Fusarium mycotoxicoses. A total of 175 starter pigs (initial weight of 10 +/- 1.1 kg) were fed five diets (seven pens of five pigs per diet) for 21 d. Diets included (1) control, (2) blend of contaminated grains, (3) contaminated grains + 0.05% GM polymer (4) contaminated grains + 0.10% GM polymer and (5) contaminated grains + 0.20% GM polymer. Diets containing contaminated grains averaged 5.5 ppm deoxynivalenol, 0.5 ppm 15-acetyldeoxynivalenol, 26.8 ppm fuuric acid, and 0.4 ppm zearalenone. Feed intake and weight gain of all pigs fed contaminated grains was significantly reduced compared to controls throughout the experiment. The weights of liver and kidney, expressed as a percentage of body weight, were lower in pigs fed the contaminated diet than in those fed the control diet. The feeding of contaminated grains significantly reduced concentrations of dopamine in the hypothalamus and pons and concentrations of dihydroxyphenylacetic acid and norepinephrine in the pons. The ratios of 5-hydroxyindoleacetic acid to serotonin, however, were elevated in the hypothalamus and pons. The feeding of contaminated grains increased serum IgM and IgA concentrations, while serum IgG concentrations were not altered. The supplementation of GM polymer prevented some of the mycotoxin-induced alterations in brain neurotransmitter and serum Ig concentrations. In summary, the feeding of grains naturally contaminated with Fusarium mycotoxins reduced growth, altered brain neurochemistry, increased serum Ig concentrations, and decreased organ weights in starter pigs. Some of the Fusarium mycotoxin-induced changes in neurochemistry and serum Ig concentrations can be prevented by the feeding of yeast cell wall polymer at appropriate concentrations, although this was not reflected in increased growth rate under these experimental conditions.

Adsorption↗
PubMed1991

Effect of fusaric acid on brain regional neurochemistry and vomiting behavior in swine.

Fusaric (5-butylpicolinic) acid is a phytotoxin produced especially by Fusarium moniliforme, a mold commonly found in Canadian-grown corn. Experiments were conducted to determine the effects of acute doses of fusaric acid on brain neurochemistry and behavior in swine. A total of 40 crossbred barrows (initial weight 10 kg) were orally dosed with 0 or 200 mg of fusaric acid/kg of BW and five animals from each treatment were killed 4.5, 9, 18, or 36 h after dosing. All brains were dissected, and concentrations of indoleamine and catecholamine neurotransmitters and metabolites were determined. Animals in the group killed 36 h after dosing were observed for behavioral changes. Vomiting was noted in 60% of the pigs dosed with fusaric acid. These pigs also seemed more lethargic than controls and appeared sedated. The major neurochemical changes due to exposure to fusaric acid were seen in the hypothalamus 18 h after dosing. Brain tryptophan, serotonin, and 5-hydroxyindoleacetic acid all tended to be elevated by the action of fusaric acid. Brain catecholamine concentrations were largely refractory to treatment. It was concluded that exposure to acute doses of fusaric acid can cause vomiting and neurochemical changes in swine. Fusaric acid may, therefore, be acting synergistically with trichothecene mycotoxins to cause vomiting and feed refusal in pigs consuming trichothecene-contaminated feedstuffs.

Administration, Oral↗
PubMed1988

Potential for dietary amino acid precursors of neurotransmitters to overcome neurochemical changes in acute T-2 toxicosis in rats.

Experiments were conducted to determine the potential for overcoming T-2 toxin-induced changes in brain neurotransmitter concentrations through dietary manipulation. Rats were fed either a tryptophan-deficient, gelatin-based diet or the same diet supplemented with a mixture of large neutral amino acids for 4 d. Rats were then dosed with 0 or 2.0 mg T-2 toxin/kg body weight and killed 4, 8 or 12 h after dosing. The large neutral amino acid supplements successfully reduced brain concentrations of tryptophan and serotonin in control rats, but this was not enough to overcome the acute effects seen in T-2 toxin-treated rats. A further experiment was then conducted to monitor the effect of T-2 toxin on the ratio of free to protein-bound tryptophan in plasma. Total plasma tryptophan increased in T-2 toxin-treated rats, although there were no significant differences in the ratio of free to protein-bound tryptophan. A final experiment was conducted to determine the specificity of the T-2 toxin effect on concentrations of plasma amino acids. Concentrations of amino acids that use the large neutral amino acid transport system into the brain were higher in T-2 toxin-treated animals. The only other amino acid that had a higher concentration was arginine. It was concluded that acute doses of T-2 toxin may selectively alter membrane transport of amino acids.

Amino Acids↗
PubMed1988

Effect of acute oral doses of T-2 toxin on tissue concentrations of biogenic amines in the rat.

T-2 toxin [3 alpha-hydroxy-4 beta, 15-diacetoxy-8 alpha-(3-methylbutyryloxy)-12,13-epoxytrichotec-9-ene] is an emetic Fusarium trichothecene mycotoxin known to cause lethargy, ataxia and feed refusal in economically important animals. Experiments were conducted to determine the effect of acute oral doses of T-2 toxin on tissue concentrations of neurotransmitters thought to play some role in regulation of feed consumption. Sixty-seven male weanling rats were intubated with a few grams of diet in a liquid slurry with or without 2.0 mg T-2 toxin per kilogram of body weight. At 1, 2, 4, 6, 8, 12, 24 and 48 h following dosing, rats were killed, and brains, spleens, hearts and adrenal glands were excised and analyzed for concentrations of neurotransmitters and metabolites using high-performance liquid chromatography with electrochemical detection. Administration of T-2 toxin caused increases in brain concentrations of tryptophan and serotonin at the early time intervals after dosing. Brain concentrations of dopamine increased, whereas concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) decreased at the later time interals following dosing. Concentrations of dopamine were increased in adrenal glands, whereas epinephrine concentrations decreased. Epinephrine was detected in spleen and heart after administration of T-2 toxin. It was concluded that the increase in brain indoleamines induced by T-2 toxin could contribute to feed refusal in animals suffering from T-2 toxicosis.

Administration, Oral↗
PubMed1977

ECT and the media.

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Communication↗
PubMed1975

Protective effect of tryptophan and 5-hydroxytryptophan on experimental phenylketonuria induced with phenylalanine+ p-cholorophenylalanine in rats.

An experimental phenylketonuria-like syndrome was produced in rats by oral administration of 1-phenylalanine (Phe, 500 mg/kg) and dl-p-chloro-phenylalanine (pCPA, 100-125 mg/kg) daily from the 2nd-3rd day of life to the age of 42 days. The effects of added dl-5-hydroxytryptohan (5HTP, 5 mg/kg) or 1-tryptophan (Trp, 100-125 mg/kg) were also studied. The groups receiving Phe+pCPA gained less weight than normal and less than the Phe controls. When tested during the last week of treatment the Phe+pCPA rats made more errors in the swim maze without changes in swimming times, and they showed significantly poorer learning of conditioned shock avoidance. These effects were partly antagonized by 5HTP or Trp. One to three weeks after the end of the treatments similar differences still remained in conditioned shock avoidance (and Trp and 5HTP prevented the effect of pCPA), but no more in maze learning, motor activity, or exploration on open field. Brain 5HT and 5-hydroxyindoleacetic acid (5HIAA) were lowered in all the pCPA treated rats during the treatment but returned to normal after it. Trp and 5HTP in the doses used only partly corrected the decrease of 5HT and 5HIAA. Brain noradrenaline did not change much.

5-Hydroxytryptophan↗