Unlinked anonymous HIV prevalence among New Zealand sexual health clinic attenders: 2005-2006.

This unlinked anonymous study aimed at determining the prevalence of HIV among sexual health clinic attenders having blood samples taken for syphilis and/or hepatitis B serology in six major New Zealand cities over a 12-month period in 2005-2006. Overall, seroprevalence was five per 1000 (47/9439). Among men who have sex with men (MSM), the overall prevalence and that of previously undiagnosed HIV were 44.1 and 20.1 per 1000, respectively. In heterosexual men, the overall prevalence was 1.2 per 1000 and in women 1.4 per 1000. HIV remains to be concentrated among homosexual and bisexual men. Comparison with a previous survey in 1996-1997 suggests an increase in the prevalence of undiagnosed HIV among MSM and also an increase in the number of MSM attending sexual health clinics. The low prevalence of HIV among heterosexuals suggests no extensive spread into the groups identified at risk of other sexually transmitted infections.

Effects of feedborne fusarium mycotoxins on brain regional neurochemistry of turkeys.

An experiment was conducted to investigate the effects of feeding grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of turkeys. The possible preventative effect of a poly-meric glucomannan mycotoxin adsorbent (GMA) was also determined. Forty-five 1-d-old male turkey poults were fed wheat-, corn-, and soybean meal-based diets up to wk 6, formulated with control grains, contaminated grains, or contaminated grains + 0.2% GMA. Deoxynivalenol was the major contaminant, and the concentrations were 2.2 and 3.3 mg/kg of feed during starter and grower phases, respectively. Concentrations of brain monoamine neurotransmitters and metabolites were measured in discrete regions of the brain including the pons, hypothalamus, and cortex by HPLC with electrochemical detection. Neurotransmitters and metabolites analyzed included norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid, serotonin (5-hydroxytryptamine, 5-HT), and 5-hydroxyindoleacetic acid (5-HIAA). The concentration of 5-HIAA and the 5-HIAA:5-HT-ratio were significantly decreased in pons after feeding contaminated grains. Dietary supplementation with GMA prevented these effects. In the pons, a significant positive correlation (r = 0.52, P < 0.05) was observed between the concentration of 5-HT and BW gain after feeding contaminated diets. The feeding of contaminated diet had no significant effects on the concentrations of neurotransmitters and metabolites in hypothalamus and cortex. It was concluded that consumption of grains naturally contaminated with Fusarium mycotoxins adversely altered the pons serotonergic system of turkeys. Supplementation with GMA partially inhibited these effects.

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.

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.

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.

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.

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.

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.

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.

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.

Demographic variation in cancer in relation to industrial and environmental influence.

Mortality data (183,064 deaths in a 30-year period, 1940-1969) by sex and three ethnic groups (white excluding Spanish-surnamed, nonwhite, and Spanish-surnamed) in 15 regions within the city (Houston), grouped around the air pollution sample collection stations have been analyzed. Valid contrast studies were possible in only one region within the city for all three groups and in six regions for white excluding Spanish-surnamed and nonwhite. There is evidence that the environmental factors of exposure over time to air and industrial pollutants in Houston has had a demonstrable effect in increasing regional mortality from cancer of the respiratory tract as well as from all other diseases and conditions of the respiratory tract and heart disease. This study points out the need for mutually sustained collaboration of effort of the scientific and industrial communities to redirect their attention and research efforts to the exploration of the carcinogenic potential of the microchemical environment.

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.