The diversity and abundance of small arthropods in onion, Allium cepa, seed crops, and their potential role in pollination.

Onion, Allium cepa L. (Asparagales: Amaryllidaceae), crop fields grown for seed production require arthropod pollination for adequate seed yield. Although many arthropod species visit A. cepa flowers, for most there is little information on their role as pollinators. Small flower visiting arthropods (body width < 3 mm) in particular are rarely assessed. A survey of eight flowering commercial A. cepa seed fields in the North and South Islands of New Zealand using window traps revealed that small arthropods were highly abundant among all except one field. Insects belonging to the orders Diptera and Thysanoptera were the most abundant and Hymenoptera, Collembola, Psocoptera, Hemiptera, and Coleoptera were also present. To test whether small arthropods might contribute to pollination, seed sets from umbels caged within 3 mm diameter mesh cages were compared with similarly caged, hand-pollinated umbels and uncaged umbels. Caged umbels that were not hand-pollinated set significantly fewer seeds (average eight seeds/umbel, n = 10) than caged hand-pollinated umbels (average 146 seeds/umbel) and uncaged umbels (average 481 seeds/umbel). Moreover, sticky traps placed on umbels within cages captured similar numbers of small arthropods as sticky traps placed on uncaged umbels, suggesting cages did not inhibit the movement of small arthropods to umbels. Therefore, despite the high abundance of small arthropods within fields, evidence to support their role as significant pollinators of commercial A. cepa seed crops was not found.

2,3,7,8-tetrachlorodibenzo-p-dioxin increases reactive oxygen species production in human endothelial cells via induction of cytochrome P4501A1.

Studies in our laboratory have demonstrated that subchronic 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) exposure of adult mice results in hypertension, cardiac hypertrophy, and reduced nitric oxide (NO)-mediated vasodilation. Moreover, increased superoxide anion production was observed in cardiovascular organs of TCDD-exposed mice and this increase contributed to the reduced NO-mediated vasodilation. Since cytochrome P4501A1 (CYP1A1) can contribute to some TCDD-induced toxicity, we tested the hypothesis that TCDD increases reactive oxygen species (ROS) in endothelial cells by the induction of CYP1A1. A concentration-response to 24h TCDD exposure (10pM-10nM) was performed in confluent primary human aortic endothelial cells (HAECs). Oxidant-sensitive fluorescent probes dihydroethidium (DHE) and 2',7'-dichlorofluorescin diacetate (DCFH-DA), were used to measure superoxide anion, and hydrogen peroxide and hydroxyl radical, respectively. NO was also measured using the fluorescent probe diaminofluorescein-2 diacetate (DAF-2DA). These assessments were conducted in HAECs transfected with siRNA targeting the aryl hydrocarbon receptor (AhR), CYP1A1, or CYP1B1. TCDD concentration-dependently increased CYP1A1 and CYP1B1 mRNA, protein, and enzyme activity. Moreover, 1nM TCDD maximally increased DHE (Cont=1.0+/-0.3; TCDD=5.1+/-1.0; p=0.002) and DCFH-DA (Cont=1.0+/-0.2; TCDD=4.1+/-0.5; p=0.002) fluorescence and maximally decreased DAF-2DA fluorescence (Cont=1.0+/-0.4; TCDD=0.68+/-0.1). siRNA targeting AhR and CYP1A1 significantly decreased TCDD-induced DHE (siAhR: Cont=1.0+/-0.1; TCDD=1.3+/-0.2; p=0.093) (siCYP1A1: Cont=1.0+/-0.1; TCDD=1.1+/-0.1; p=0.454) and DCFH-DA (siAhR: Cont=1.0+/-0.2; TCDD=1.3+/-0.3; p=0.370) (siCYP1A1: Cont=1.0+/-0.1; TCDD=1.3+/-0.2; p=0.114) fluorescence and increased DAF-2DA fluorescence (siAhR: Cont=1.00+/-0.03; TCDD=0.97+/-0.03; p=0.481) (siCYP1A1: Cont=1.00+/-0.03; TCDD=0.92+/-0.03; p=0.034), while siRNA targeting CYP1B1 did not. These data suggest that TCDD-induced increase in ROS is AhR-dependent and may be mediated, in part, by CYP1A1 induction.

Synergy between chemical and biological control in the IPM of currant-lettuce aphid (Nasonovia ribisnigri) in Canterbury, New Zealand.

Field trials were conducted at four Canterbury, New Zealand locations in 2005-06 to determine if the synergistic effects of biological control by natural enemies and standard drenching techniques controlled lettuce aphid populations throughout the entire growing season. Chemical usage significantly lowered aphid densities in the outer, wrapper and heart leaves compared to control plants at most times. However, in mid-summer, natural enemies, such as the brown lacewing (Micromus tasmaniae), 11-spotted ladybird beetle (Coccinella undecimpunctata) and small hoverfly larvae (Melanostoma fasciatum), were more than sufficient to control lettuce aphids without the use of insecticides. Drenching, in addition to natural enemy attack, appears to be required in early spring and late summer to maintain very low levels of lettuce aphid. Given the potential for imidacloprid resistance to develop, it may be advisable to restrict drenches to these key periods in order to allow populations of natural enemies to maintain control of prey populations. We recommend industry support the validation of action thresholds across different regions within New Zealand and focus on the seasonal biology of predators to assist growers with the sustainable long-term control of lettuce aphids. The inclusion of additional data into an economic model to compare pest damage with predator loading would be useful for growers in managing aphid problems. These results will assist in the continued improvement and development of a sustainable IPM strategy for lettuce aphids in New Zealand and elsewhere.

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on murine heart development: alteration in fetal and postnatal cardiac growth, and postnatal cardiac chronotropy.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related chemicals are potent cardiovascular teratogens in developing piscine and avian species. In the present study we investigated the effects of TCDD on murine cardiovascular development. Pregnant mice (C57Bl6N) were dosed with 1.5-24 microg TCDD/kg on gestation day (GD) 14.5. At GD 17.5, fetal mice exhibited a dose-related decrease in heart-to-body weight ratio that was significantly reduced at a maternal dose as low as 3.0 microg TCDD/kg. In addition, cardiocyte proliferation was reduced in GD 17.5 fetal hearts at the 6.0-microg TCDD/kg maternal dose. To determine if this reduction in cardiac weight was transient, or if it continued after birth, dams treated with control or 6.0 microg TCDD/kg were allowed to deliver, and heart weight of offspring was determined on postnatal days (P) 7 and 21. While no difference was seen on P 7, on P 21 pups from TCDD-treated litters showed an increase in heart-to-body weight ratio and in expression of the cardiac hypertrophy marker atrial natriuretic factor. Additionally, electrocardiograms of P 21 offspring showed that the combination of in utero and lactational TCDD exposure reduced postnatal heart rate but did not alter cardiac responsiveness to isoproterenol stimulation of heart rate. These results demonstrate that the fetal murine heart is a sensitive target of TCDD-induced teratogenicity, resembling many of TCDD-induced effects observed in fish and avian embryos, including reduced cardiocyte proliferation and altered fetal heart size. Furthermore, the combination of in utero and lactational TCDD exposure can induce cardiac hypertrophy and bradycardia postnatally, which could increase the risk of cardiovascular disease development.

Toxicogenomic profile of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the murine fetal heart: modulation of cell cycle and extracellular matrix genes.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and similar environmental contaminants have been demonstrated to be potent cardiovascular teratogens in developing piscine and avian species. In the present study, we investigated the effects of TCDD on gene expression during murine cardiovascular development. C57Bl6N pregnant mice were dosed with 1.5, 3.0, or 6.0 microg TCDD/kg on gestational day (GD) 14.5, and microarray analysis was used to characterize the global changes in fetal cardiac gene expression on GD 17.5. TCDD significantly altered expression of a number of genes involved in xenobiotic metabolism, cardiac homeostasis, extracellular matrix production/remodeling, and cell cycle regulation. Interestingly, while the AhR-responsive genes Cyp1A1, Cyp1B1, Ugt1a6, and Ahrr, were all induced by TCDD in the fetal murine heart, other AhR-responsive genes, Cyp1a2, Nqo1, and Gsta1, were not. Quantitative real-time polymerase chain reactions confirmed the changes in expression of several G1/S-type cyclins and extracellular matrix-related genes. These results demonstrate the global changes in cardiac gene expression that result from TCDD exposure of the fetal murine heart and implicate genes involved in cell cycle and extracellular matrix regulation in TCDD-induced cardiac teratogenicity and functional deficits.

Sporting activity and hyperglycemia in middle-aged men.

OBJECTIVE: To assess the relationship between self-reported frequency of participation in sporting activity and the prevalence of hyperglycemia (nonfasting glucose level > or = 7.8 mM) in middle-aged men. RESEARCH DESIGN AND METHODS: We used a cross-sectional study of 7617 British middle-aged men, drawn from 24 general practices in England, Wales, and Scotland, who were participants in the British Regional Heart Study. The response rate was 78%. Patients with diabetes (physician-diagnosed) were excluded from our analysis. Frequency of participation in sporting activity was determined by the respondents and reported as none (61%), occasionally (12%), or frequently (27%). RESULTS: The age-adjusted prevalence odds ratio for hyperglycemia was 0.86 (95% confidence interval, 0.6-1.2) in those reporting occasional, and 0.62 (95% confidence interval, 0.4-0.85) in those reporting frequent sporting activity, compared with those reporting none. This effect of frequent sporting activity on the prevalence of hyperglycemia was independent of body mass index, occupational status, smoking status, systolic blood pressure, use of antihypertensive therapy, and time of sampling. CONCLUSIONS: Frequent sporting activity in middle-aged men is associated with a reduced prevalence of hyperglycemia and may reduce the risk of NIDDM.

Measurement of n-alkanals and hydroxyalkenals in biological samples.

A modified method was developed to measure nM levels of a range of n-alkanals and hydroxyalkenals in biological samples such as blood plasma and tissue homogenates and also in Folch lipid extracts of these samples. Butylated hydroxytoluene (BHT) and desferrioxamine (Desferal) were added to samples to prevent artifactual peroxidation. Aldehydes were reacted with 1,3-cyclohexanedione (CHD), cleaned up by solid-phase extraction on a Sep-Pak C18 cartridge and the fluorescent decahydroacridine derivatives resolved by reverse-phase high-performance liquid chromatography (HPLC) with gradient elution. A wider range of aldehydes was detected in lipid extracts of plasma and liver homogenate compared to whole (unextracted) samples. Human plasma contained nM levels of acetaldehyde, propanal, butanal, pentanal, hexanal, and heptanal. 4-Hydroxynonenal (0.93 nmol/g) and alkanals with two to six carbons (up to 7.36 nmol/g) were detected in rat liver. Recovery of aldehydes added to whole plasma or to lipid extracts of plasma was dependent on carbon chain length, varying from 95% for acetaldehyde to 8% for decanal. Recovery from biological samples was significantly less than that of standards taken through the Sep-Pak clean-up procedure, suggesting that aldehydes can bind to plasma protein and lipid components.

Food-allergic reactions in schools and preschools.

BACKGROUND: Food allergies may affect up to 6% of school-aged children. OBJECTIVES: To conduct a telephone survey to characterize food-allergic reactions in children (defined as those aged 3-19 years in this study) with known food allergies in schools and preschools and to determine mechanisms that are in place to prevent and treat those reactions. DESIGN: The parents of food-allergic children were contacted by telephone and asked about their child's history of food-allergic reactions in school. The schools the children attended were contacted, and the person responsible for the treatment of allergic reactions completed a telephone survey. RESULTS: Of 132 children in the study, 58% reported food-allergic reactions in the past 2 years. Eighteen percent experienced 1 or more reactions in school. The offending food was identified in 34 of 41 reactions, milk being the causative food in 11 (32%); peanut in 10 (29%); egg in 6 (18%); tree nuts in 2 (6%); and soy, wheat, celery, mango, or garlic in 1 (3%) each. In 24 reactions (59%), symptoms were limited to the skin; wheezing occurred in 13 (32%), vomiting and/or diarrhea in 4 (10%), and hypotension in 1 (2%). Also, 15 (36%) of the 41 reactions involved 2 or more organ systems, and 6 (15%) were treated with epinephrine. Fourteen percent of the children did not have a physician's orders for treatment, and 16% did not have any medications available. Of the 80 participating schools, 31 (39%) reported at least 1 food-allergic reaction within the past 2 years and 54 (67%) made at least 1 accommodation for children with a food allergy, such as peanut-free tables, a peanut ban from the classroom, or alternative meals. CONCLUSIONS: It is common for food-allergic children to experience allergic reactions in schools and preschools, with 18% of children having had at least 1 school reaction within the past 2 years. Thirty-six percent of the reactions involved 2 or more organ systems, and 32% involved wheezing. Every effort should be made to prevent, recognize, and appropriately treat food-allergic reactions in schools.

Correlation of cardiotoxicity mediated by halogenated aromatic hydrocarbons to aryl hydrocarbon receptor activation.

In mammals, the toxicity of halogenated aromatic hydrocarbons (HAH) correlates with their ability to activate the aryl hydrocarbon receptor (AHR). To test this correlation in an avian model, we selected six HAHs based on their affinity for the mammalian AHR, including: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PCDD); 2,3,7,8-tetrachlorodibenzofuran (TCDF); 2,3,4,7,8-pentachlorodibenzofuran (PCDF); 3,3',4,4'-tetrachlorobiphenyl (PCB 77); and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153). We determined the ability of these compounds to induce cardiotoxicity, as measured by an increase in heart wet weight on incubation day 10 in the chick embryo (Gallus gallus) and formation of the avian AHR/ARNT/DNA binding complex in chicken hepatoma cells. Relative potency values (RPs) were calculated by dividing the TCDD EC(50) (AHR/ARNT/DNA binding) or ED(50) (15% increase in day-10 heart wet weight) by the HAH congeners EC(50) or ED(50), respectively. The rank order of potencies for inducing cardiotoxicity were TCDD > PCDD = PCDF = TCDF > PCDF > PCB77, PCB 153, no effect. The RP values for inducing AHR/ARNT DNA binding were then correlated with those for inducing cardiotoxicity (the RP values of PCDD were determined to be statistical outliers). This correlation was found to be highly significant (r = 0.94, p = 0.017). The ability of PCDD to act as an AHR agonist was verified using luciferase reporter assays and analysis of cytochrome P4501A1 protein levels. These results indicate that the ability of HAHs to activate the avian AHR signaling pathway, in general, correlates with their ability to mediate cardiotoxicity in the chick embryo.

Insulin regulation in AhR-null mice: embryonic cardiac enlargement, neonatal macrosomia, and altered insulin regulation and response in pregnant and aging AhR-null females.

The aryl hydrocarbon receptor (AhR) was originally characterized because of its high affinity binding of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin. However, studies using AhR-null mice have demonstrated the importance of this protein in normal physiology and development. Here we demonstrate that AhR-null embryos develop cardiac enlargement, and that this phenotype is dependent, at least in part, on the maternal genotype. Neonates born to AhR-null females had increased heart weights regardless of the neonatal genotype, an outcome also observed in gestational diabetes. The cardiac hypertrophy markers, beta-myosin heavy chain and atrial natriuretic factor, and the cardiac proliferative index were increased in AhR-null embryos, indicating that the cardiac enlargement is associated with myocyte hypertrophy and hyperplasia, which begin prior to birth. Importantly, two- to three-month-old pregnant and seven-month-old nonpregnant females, but not nonpregnant three-month-old AhR-null females had significantly decreased fasting plasma insulin levels and a reduced ability to respond to exogenous insulin compared to controls. Despite these alterations in insulin regulation and responsiveness, pregnant AhR females did not have abnormal glucose tolerance tests and did not develop hyperglycemia, classic characteristics of gestational diabetes. However, twenty-three percent of seven-month-old AhR-null females did have altered glucose tolerance tests, but did not show hyperglycemia or increased hemoglobin A1C concentration under normal feeding conditions. While the ultimate cause of the neonatal phenotype remains unclear, these studies establish that the AhR is required for normal insulin regulation in pregnant and older mice and for cardiac development in embryonic mice.

Depletion of alpha-tocopherol in human atherosclerotic lesions.

Estimations of alpha-tocopherol content were made on a series of human necropsy samples of normal arterial wall and of atherosclerotic lesions. The results were compared with stage of lesion, shown by histology, and with the amounts of cholesterol and hydroxycholesterols in the same lesions. The ratio of alpha-tocopherol to cholesterol levels varied widely in normal arterial wall but was consistently low in lesions, especially in lesions rich in macrophage foam cells. The results suggested that significant accumulation of hydroxycholesterols, found almost exclusively in lesions, only occurred when alpha-tocopherol levels were low in relation to the cholesterol content. This suggests that oxidative activity in the lesion may lead to significant oxidation of constituents of low-density lipoprotein only after alpha-tocopherol has been depleted.

Aryl hydrocarbon receptor null mice develop cardiac hypertrophy and increased hypoxia-inducible factor-1alpha in the absence of cardiac hypoxia.

The aryl hydrocarbon receptor (AhR) is a member of the basic helix loop helix PAS (Per-ARNT-SIM) transcription family, which also includes hypoxiainducible factor-1alpha (HIF-1alpha) and its common dimerization partner AhR nuclear translocator (ARNT). Following ligand activation or hypoxia, AhR or HIF-1alpha, respectively, translocate into the nucleus, dimerize with ARNT, and regulate gene expression. Mice lacking the AhR have been shown previously to develop cardiac enlargement. In cardiac hypertrophy, it has been suggested that the myocardium becomes hypoxic, increasing HIF-1alpha stabilization and inducing coronary neovascularization, however, this mechanism has not been demonstrated in vivo. The purpose of this study was to investigate the cardiac enlargement reported in AhR(-/-) mice and to determine if it was associated with myocardial hypoxia and subsequent activation of the HIF-1alpha pathway. We found that AhR(-/-) mice develop significant cardiac hypertrophy at 5 mo. However, this cardiac hypertrophy was not associated with myocardial hypoxia. Despite this finding, cardiac hypertrophy in AhR(-/-) mice was associated with increased cardiac HIF-1alpha protein expression and increased mRNA expression of the neovascularization factor vascular endothelial growth factor (VEGF). These data demonstrate that the development of cardiac hypertrophy in AhR(-/-) mice not associated with myocardial hypoxia, but is correlated with increased cardiac HIF-1alpha protein and VEGF mRNA expression.

Failed back surgery syndrome: 5-year follow-up in 102 patients undergoing repeated operation.

The indications for repeated operation in patients with persistent or recurrent pain after lumbosacral spine surgery are not well established. Long-term results have been reported infrequently, and in no case has mean follow-up exceeded 3 years. We report 5-year mean follow-up for a series of repeated operations performed between 1979 and 1983. Patient characteristics and modes of treatment have been assessed as predictors of long-term outcome. One hundred two patients with "failed back surgery syndrome" (averaging 2.4 previous operations), who underwent a repeated operation for lumbosacral decompression and/or stabilization, were interviewed by a disinterested third party a mean of 5.05 years postoperatively. Successful outcome (at least 50% sustained relief of pain for 2 years or at last follow-up, and patient satisfaction with the result) was recorded in 34% of patients. Twenty-one patients who were disabled preoperatively returned to work postoperatively; 15 who were working preoperatively became disabled or retired postoperatively. Improvements in activities of daily living were recorded, overall, as often as decrements. Loss of neurological function (strength, sensation, bowel and bladder control) was reported by patients more often than improvement. Most patients reduced or eliminated analgesic intake. Statistical analysis (including univariate and multivariate logistic regression) of patient characteristics as prognostic factors showed significant advantages for young patients and for female patients. Favorable outcome also was associated with a history of good results from previous operations, with the absence of epidural scar requiring surgical lysis, with employment before surgery, and with predominance of radicular (as opposed to axial) pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Focal microinjection of carbachol into the periaqueductal gray induces seizures in the forebrain of the rat.

Previous studies have reported that the repetition of running-bouncing and tonic-clonic seizures mediated by brainstem structures eventually elicits seizure activity in the forebrain. The purpose of the present study was to determine if the periaqueductal gray (PAG) region is a component of the neural network through which brainstem seizures elicit forebrain seizures. Bilateral microinjection of 40 nmol carbachol into the PAG region of rats induced arrested, staring behavior accompanied by epileptiform electrocorticogram (ECoG) afterdischarge recorded from the parietal cortex. In two animals limbic seizure activity similar to kindled amygdala seizures was also induced. The carbachol effect was dose-related as the 40 nmol dose induced a significantly greater duration of ECoG afterdischarge than a 20 nmol dose. The carbachol effect was mediated by muscarinic receptors as bilateral 50 nmol atropine microinjection 1 min prior to 40 nmol carbachol microinjection inhibited all seizure activity. Immunohistochemical detection of the proto-oncogene c-fos was used to verify that seizure activity was induced in forebrain regions. Rats with seizures induced by PAG carbachol microinjections exhibited dense c-fos-like immunoreactivity in the dentate gyrus but not the CA(1) or CA(3) regions, amygdala, piriform cortex, perirhinal cortex or hypothalamus. In addition, PAG microinjection of 10 nmol N-methyl-D-aspartic acid (NMDA) induced wild-running convulsions while 400 pmol bicuculline induced clonic spasms, myoclonic activity or limbic seizures. These results indicate that stimulation of the PAG, a brainstem structure, is sufficient to induce forebrain seizures. Since the forebrain seizures were induced by a single carbachol administration, it is proposed that the PAG serves as a pathway for caudal-rostral seizure generalization.

Vitamin E analogues reduce the incidence of ventricular fibrillations and scavenge free radicals.

The aim of our study was to analyse the protective effects of different alpha-tocopherol analogues 1) against fibrillations induced by an ischemia-reperfusion sequence, and 2) to further investigate in vitro the radical scavenging properties of these analogues by two sensitive methods. Concerning 1: isolated rat hearts underwent 10 min of coronary ligation followed by reperfusion and the alpha-tocopherol analogues were infused 15 min before occlusion. Functional parameters including heart rate and fibrillations were recorded. Concerning 2: the beta-phycoerythrin assay was utilised to determine the oxygen radical absorbing capacity (ORAC) of these vitamin E analogues against peroxyl radicals. Electron paramagnetic resonance (EPR) was used to measure their scavenger abilities on hydroxyl radical and superoxide anion production. Concerning 1: ventricular fibrillation times were reduced for all analogues treated hearts at concentrations of 1 microM and 5 microM, with Trolox being the most efficacious. Concerning 2: in our experimental conditions of intense production of free radicals, scavenging IC50 values for hydroxyl radical were 1.15, 2.17 and 4.04 mM for Trolox, MDL 74270 and MDL 74366 respectively. Superoxide anion IC50 values were 1.0 and 6.75 mM for Trolox and MDL 74270. Our results show that water-soluble analogues of vitamin E are effective in the prevention of coronary ligation induced reperfusion arrhythmia, under our experimental conditions. Moreover, our data demonstrate that these vitamin E analogues are effective scavengers for a variety of radicals. Our studies support the view that compounds that can either inhibit the formation or scavenge free radicals can protect the heart against arrhythmia associated with ischemia-reperfusion.

Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction.

Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in association with thrombolytic therapy might be useful.

The influence of age and weight on women's body attitudes as measured by the Body Attitudes Questionnaire (BAQ).

The influence of age and weight on the body-related attitudes of a large sample of South Australian women were measured by the Ben-Tovim-Walker Body Attitudes Questionnaire (BAQ). Attitudes were found not to vary substantially with age, and only the Feeling Fat, Body Disparagement and Lower Body Fatness sub-scales of the BAQ were correlated with BMI. The effect of BMI on attitudes was independent of age. Obese subjects felt significantly less attractive than those with BMIs only slightly above average. However, they did not disparage their bodies more than did less overweight women. Body attitudes appear to be substantially independent of the current physical body.

Body image, disfigurement and disability.

The body-related attitudes of groups of women suffering from physical conditions that are commonly regarded as being disfiguring and/or disabling were studied by means of the Body Attitudes Questionnaire. Despite their conditions, the women did not necessarily disparage their bodies. They also seemed to worry less about small changes in weight and shape than did comparable women without physical difficulties, and to have an enhanced sense of their own robustness. There was an indication that development of negative body attitudes might be linked to emergence of a chronic physical condition during adolescence, rather than from birth or during adulthood. If our results are confirmed, they point to the need to pay special attention to the psychological needs of women whose bodies become dysfunctional at this sensitive time.

Event-related potentials and monoamines in autistic children on a clinical trial of fenfluramine.

In a double blind, crossover study of the response of autistic subjects to fenfluramine, event-related potentials (ERPs) were recorded from 7 subjects on an attention-demanding auditory choice reaction time task (ACRT). ACRT, IQ and biochemical measures were taken after 5 months placebo and 5 months fenfluramine treatment. After fenfluramine treatment blood serotonin levels fell, urinary catecholamine levels fell and the HVA/DA ratio rose. IQ and ACRT performance improved. On the ACRT subjects were asked to press a button to a rare target (500 Hz, P = 0.14) and to ignore higher pitched rare (2,000 Hz, P = 0.14) and frequent non-targets (1,000 Hz). After fenfluramine treatment N1 latencies increased. The scalp distribution of ERP maxima changes slightly with treatment. P3 maxima elicited by rare non-targets were recorded more rostrally after fenfluramine treatment. After rare non-targets N1 amplitudes at Fz decreased but P3 amplitudes at Pz increased. Early negativity after the rare non-target (particularly on the right side) was negatively correlated with the HVA/DA ratio. Subtraction of the P3 component elicited in a passive condition where no response was required from the active condition showed that P3 positivity to targets was halved with treatment. (In contrast Nd increased on fenfluramine treatment). Overall, N1 and P3 components showed greatest responsiveness to rare non-targets on fenfluramine. N1 but not P3 changes may represent slight improvement of attention-related function with treatment. Small changes in ERP latency and distribution, associated with the neuroleptic action of fenfluramine may be partly responsible for a mild improvement of IQ and ACRT performance on medication.

Event-related potentials in autistic and healthy children on an auditory choice reaction time task.

Event-related potentials (ERPs) were recorded from midline (Fz, Cz, Pz) and lateral sites (F3, F4, P3, P4) in autistic children (n = 7) and age-matched controls (n = 9) on an auditory choice reaction time task. Subjects were asked to press a button to an infrequent target (500 Hz, P = 0.14) and to ignore higher pitched infrequent (2000 Hz, P = 0.14) and frequent (1000 Hz) non-targets. Autistic subjects made twice as many errors of omission as controls and showed a higher criterion (beta) for targets. Maximum ERP peak amplitudes showed a more varied scalp distribution in the autistic group. N1 latencies were consistently shorter in the autistic group and in 3 subjects the target P3 latencies were markedly longer than for the controls. Compared to controls, the N1 amplitude of the autistic response was larger to the rare stimuli (particularly to non-targets). The amplitude of the P3 component was smaller in the autistic group (particularly to the target). The stimuli were also presented in a passive condition requiring no response. After subtraction of the waveform obtained in the passive condition from that obtained in the active condition or subtraction of the waveform elicited by the rare non-target from that elicited by the target, N1 target amplitude was larger in control than in autistic children. Autistic subjects showed more early negativity to the rare non-target at left frontal and a larger P3 to the target at right parietal sites. ERPs of autistic children are more responsive to stimulus features (e.g. high/rare non-target tone) and less responsive to their associations or meaningfulness (e.g. target P3). Attention-related ERPs of autistic children show signs of precocious (right dominance for P3) and delayed development (P3 not maximal at parietal sites).