DIE ONTWIKKELING EN INHOUD VAN ’N MAATSKAPLIKE GROEPWERK-BEMAGTIGINGSPROGRAM VIR ALKOHOLAFHANKLIKE BEJAARDES

In hierdie artikel word gefokus op ’n maatskaplike groepwerk-bemagtigingsprogram, ooreenkomstig’n sterkteperspektief, wat ontwikkel en aangebied is vir alkoholafhanklike bejaardesverbonde aan ’n geregistreerde behandelingsentrum. Die voorgenoemde program is deur dienavorsers ontwikkel, gemik op die eiesoortige behoeftes, sterktes en uitdagings van diékliëntegroep

Do agreements between adolescent and parent reports on family socioeconomic status vary with household financial stress?

<p>Abstract</p> <p>Background</p> <p>Many studies compared the degree of concordance between adolescents' and parents' reports on family socioeconomic status (SES). However, none of these studies analyzed whether the degree of concordance varies by different levels of household financial stress. This research examines whether the degree of concordance between adolescents' and parent reports for the three traditional SES measures (parental education, parental occupation and household income) varied with parent-reported household financial stress and relative standard of living.</p> <p>Methods</p> <p>2,593 adolescents with a mean age of 13 years, and one of their corresponding parents from the Taiwan Longitudinal Youth Project conducted in 2000 were analyzed. Consistency of adolescents' and parents' reports on parental educational attainment, parental occupation and household income were examined by parent-reported household financial stress and relative standard of living.</p> <p>Results</p> <p>Parent-reported SES variables are closely associated with family financial stress. For all levels of household financial stress, the degree of concordance between adolescent's and parent's reports are highest for parental education (κ ranging from 0.87 to 0.71) followed by parental occupation (κ ranging from 0.50 to 0.34) and household income (κ ranging from 0.43 to 0.31). Concordance for father's education and parental occupation decreases with higher parent-reported financial stress. This phenomenon was less significant for parent-reported relative standard of living.</p> <p>Conclusions</p> <p>Though the agreement between adolescents' and parents' reports on the three SES measures is generally judged to be good in most cases, using adolescents reports for family SES may still be biased if analysis is not stratified by family financial stress.</p

The impact of maternal separation on adult mouse behaviour and on the total neuron number in the mouse hippocampus

The maternal separation paradigm has been applied to C57BL/6J mice as an animal developmental model for understanding structural deficits leading to abnormal behaviour. A maternal separation (MS) model was used on postnatal day (PND) 9, where the pups were removed from their mother for 24 h (MS24). When the pups were 10 weeks old, the level of anxiety and fear was measured with two behavioural tests; an open field test and an elevated plus maze test. The Barnes platform maze was used to test spatial learning, and memory by using acquisition trials followed by reverse trial sessions. The MS24 mice spent more time in the open arms of the elevated plus maze compared to controls, but no other treatment differences were found in the emotional behavioural tests. However, in the reverse trial for the Barnes maze test there was a significant difference in the frequency of visits to the old goal, the number of errors made by the MS24 mice compared to controls and in total distance moved. The mice were subsequently sacrificed and the total number of neurons estimated in the hippocampus using the optical fractionator. We found a significant loss of neurons in the dentate gyrus in MS mice compared to controls. Apparently a single maternal separation can impact the number of neurons in mouse hippocampus either by a decrease of neurogenesis or as an increase in neuron apoptosis. This study is the first to assess the result of maternal separation combining behaviour and stereology

Reduction of EEG Theta Power and Changes in Motor Activity in Rats Treated with Ceftriaxone

The glutamate transporter GLT-1 is responsible for the largest proportion of total glutamate transport. Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. In addition, physiological studies have shown that GLT-1 up-regulation strongly affects synaptic plasticity, and leads to an impairment of the prepulse inhibition, a simple form of information processing, thus suggesting that GLT-1 over-expression may lead to dysfunctions of large populations of neurons. To test this possibility, we assessed whether CEF affects cortical electrical activity by using chronic electroencephalographic (EEG) recordings in male WKY rats. Spectral analysis showed that 8 days of CEF treatment resulted in a delayed reduction in EEG theta power (7–9 Hz) in both frontal and parietal derivations. This decrease peaked at day 10, i.e., 2 days after the end of treatment, and disappeared by day 16. In addition, we found that the same CEF treatment increased motor activity, especially when EEG changes are more prominent. Taken together, these data indicate that GLT-1 up-regulation, by modulating glutamatergic transmission, impairs the activity of widespread neural circuits. In addition, the increased motor activity and prepulse inhibition alterations previously described suggest that neural circuits involved in sensorimotor control are particularly sensitive to GLT-1 up-regulation

Social disparities in exposures to bisphenol A and polyfluoroalkyl chemicals: a cross-sectional study within NHANES 2003-2006

<p>Abstract</p> <p>Background</p> <p>Bisphenol A (BPA) and polyfluoroalkyl chemicals (PFCs) are suspected endocrine disrupting compounds known to be ubiquitous in people's bodies. Population disparities in exposure to these chemicals have not been fully characterized.</p> <p>Methods</p> <p>We analyzed data from the 2003-2006 National Health and Nutrition Examination Survey. Using multivariable linear regression we examined the association between urinary concentrations of BPA, serum concentrations of four PFCs, and multiple measures of socioeconomic position (SEP): family income, education, occupation, and food security. We also examined associations with race/ethnicity.</p> <p>Results</p> <p>All four PFCs were positively associated with family income, whereas BPA was inversely associated with family income. BPA concentrations were higher in people who reported very low food security and received emergency food assistance than in those who did not. This association was particularly strong in children: 6-11 year-olds whose families received emergency food had BPA levels 54% higher (95% CI, 13 to 112%) than children of families who did not. For BPA and PFCs we saw smaller and less consistent associations with education and occupation. Mexican Americans had the lowest concentrations of any racial/ethnic group of both types of chemicals; for PFCs, Mexican Americans not born in the U.S. had much lower levels than those born in the U.S.</p> <p>Conclusions</p> <p>People with lower incomes had higher body burdens of BPA; the reverse was true for PFCs. Family income with adjustment for family size was the strongest predictor of chemical concentrations among the different measures of SEP we studied. Income, education, occupation, and food security appear to capture different aspects of SEP that may be related to exposure to BPA and PFCs and are not necessarily interchangeable as measures of SEP in environmental epidemiology studies. Differences by race/ethnicity were independent of SEP.</p

Facing the Challenge of Data Transfer from Animal Models to Humans: the Case of Persistent Organohalogens

A well-documented fact for a group of persistent, bioaccumulating organohalogens contaminants, namely polychlorinated biphenyls (PCBs), is that appropriate regulation was delayed, on average, up to 50 years. Some of the delay may be attributed to the fact that the science of toxicology was in its infancy when PCBs were introduced in 1920's. Nevertheless, even following the development of modern toxicology this story repeats itself 45 years later with polybrominated diphenyl ethers (PBDEs) another compound of concern for public health. The question is why? One possible explanation may be the low coherence between experimental studies of toxic effects in animal models and human studies. To explore this further, we reviewed a total of 807 PubMed abstracts and full texts reporting studies of toxic effects of PCB and PBDE in animal models. Our analysis documents that human epidemiological studies of PBDE stand to gain little from animal studies due to the following: 1) the significant delay between the commercialisation of a substance and studies with animal models; 2) experimental exposure levels in animals are several orders of magnitude higher than exposures in the general human population; 3) the limited set of evidence-based endocrine endpoints; 4) the traditional testing sequence (adult animals – neonates – foetuses) postpones investigation of the critical developmental stages; 5) limited number of animal species with human-like toxicokinetics, physiology of development and pregnancy; 6) lack of suitable experimental outcomes for the purpose of epidemiological studies. Our comparison of published PCB and PBDE studies underscore an important shortcoming: history has, unfortunately, repeated itself. Broadening the crosstalk between the various branches of toxicology should therefore accelerate accumulation of data to enable timely and appropriate regulatory action

Neurexin-1 and Frontal Lobe White Matter: An Overlapping Intermediate Phenotype for Schizophrenia and Autism Spectrum Disorders

Background: Structural variation in the neurexin-1 (NRXN1) gene increases risk for both autism spectrum disorders (ASD) and schizophrenia. However, the manner in which NRXN1 gene variation may be related to brain morphology to confer risk for ASD or schizophrenia is unknown. Method/Principal Findings: 53 healthy individuals between 18–59 years of age were genotyped at 11 single nucleotide polymorphisms of the NRXN1 gene. All subjects received structural MRI scans, which were processed to determine cortical gray and white matter lobar volumes, and volumes of striatal and thalamic structures. Each subject’s sensorimotor function was also assessed. The general linear model was used to calculate the influence of genetic variation on neural and cognitive phenotypes. Finally, in silico analysis was conducted to assess potential functional relevance of any polymorphisms associated with brain measures. A polymorphism located in the 39 untranslated region of NRXN1 significantly influenced white matter volumes in whole brain and frontal lobes after correcting for total brain volume, age and multiple comparisons. Follow-up in silico analysis revealed that this SNP is a putative microRNA binding site that may be of functional significance in regulating NRXN1 expression. This variant also influenced sensorimotor performance, a neurocognitive function impaired in both ASD and schizophrenia. Conclusions: Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brai

3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings

RATIONALE: 3,4-Methylenedioxymethamphetamine (MDMA) is a widely abused illicit drug. In animals, high-dose administration of MDMA produces deficits in serotonin (5-HT) neurons (e.g., depletion of forebrain 5-HT) that have been interpreted as neurotoxicity. Whether such 5-HT deficits reflect neuronal damage is a matter of ongoing debate. OBJECTIVE: The present paper reviews four specific issues related to the hypothesis of MDMA neurotoxicity in rats: (1) the effects of MDMA on monoamine neurons, (2) the use of “interspecies scaling” to adjust MDMA doses across species, (3) the effects of MDMA on established markers of neuronal damage, and (4) functional impairments associated with MDMA-induced 5-HT depletions. RESULTS: MDMA is a substrate for monoamine transporters, and stimulated release of 5-HT, NE, and DA mediates effects of the drug. MDMA produces neurochemical, endocrine, and behavioral actions in rats and humans at equivalent doses (e.g., 1–2 mg/kg), suggesting that there is no reason to adjust doses between these species. Typical doses of MDMA causing long-term 5-HT depletions in rats (e.g., 10–20 mg/kg) do not reliably increase markers of neurotoxic damage such as cell death, silver staining, or reactive gliosis. MDMA-induced 5-HT depletions are accompanied by a number of functional consequences including reductions in evoked 5-HT release and changes in hormone secretion. Perhaps more importantly, administration of MDMA to rats induces persistent anxiety-like behaviors in the absence of measurable 5-HT deficits. CONCLUSIONS: MDMA-induced 5-HT depletions are not necessarily synonymous with neurotoxic damage. However, doses of MDMA which do not cause long-term 5-HT depletions can have protracted effects on behavior, suggesting even moderate doses of the drug may pose risks