289 research outputs found

    A Working Model for the Rehabilitation of Juvenile Delinquents

    Full text link
    During the last decade, institutional treatment of delinquents has shifted decidedly toward community based programs designed around a family unit model. Throughout the country, various state and local agencies have acquired large, older homes in well-established neighborhoods and turned them into residences for delinquent adolescents. These homes are similar to half-way houses in their size and operation. House parents, usually a young married couple, live in the house and provide supervision for five or ten juveniles. During the day, these residents either go to school or work, and during the evening they engage in various recreational and school related activities. Each resident has clearly delineated household responsibilities and specific input into decisions made regarding how the house is to be run. These group homes are different than half-way houses in that juveniles go to the home, instead of a correctional facility.before rather than after institutionalization. They serve as an alternative to the large training school or correctional facility

    A study of the relationship between the financial status and the certificated personnel of selected secondary school districts of San Joaquin County

    Get PDF
    The problem for this study consists of a question: Is there a relationship between the financial status and the academic preparation and experience of teachers in selected secondary school districts of San Joaquin County? The purpose of this study will, therefore, be to determine the relationship between financial status of the school district and the academic preparation of employed certificated personnel in selected secondary schools of San Joaquin County

    Methylmercury photodemethylation in Kajimkujik lakes

    Get PDF
    Methylmercury (MeHg) concentration in surface waters is a key variable regulating mercury availability to food webs. Few studies have quantified the seasonal importance of photodemethylation reactions and the influence of chromophoric dissolved organic matter (DOM) properties on these relationships. To address this research gap we have used numerous controlled experiments that focused primarily on the quantification of the relationships between solar radiation exposures, DOM, and MeHg within six freshwater lakes in Kejimkujik National Park and National Historic Site in Nova Scotia. The concentration of DOM was found to strongly control the photoreactivity of DOM in these study lakes across sampling seasons (RÂČ=0.94). The effect of DOM photoreactivity on MeHg photodemethylation was directly tested using photochemically manipulated water from one lake collected in three different months. Photodemethylation rate constants and efficiencies tended to be higher in water collected during June, when in-situ DOM concentration was lower, than in water collected in August and October. Experiments that included water from all six lakes in summer and fall showed that DOM concentration could explain 76% of variation in photodemethylation rate constants. The outcomes from this combination of studies and experiments provide insight for prediction of photodemethylation potential in our study system and for comparison with MeHg concentrations in corresponding food webs. Methylmercury is associated with DOM (DOM-MeHg) in complexes, however in high DOM waters the proportion of DOM that is associated with MeHg (DOM-MeHg) will decrease and this MeHg-free DOM may be critical in regulating photodemethylation reactions. Photodemethylation will still occur in high DOM waters but at a limited rate because a smaller proportion of the photoreactions will involve DOM-MeHg complexes. This is the first study to test and quantify a competitive interaction between MeHg photodemethylation and DOM phototransformations (both photomineralization and photobleaching) to support the conceptual idea that higher dissolved organic carbon systems will have slower rates of photodemethylation. Overall, this compiled body of work yielded a method for predicting seasonal and spatial changes to MeHg concentrations in surface waters depending on environmental and physicochemical factors

    Morphologic and functional correlates of synaptic pathology in the cathepsin D knockout mouse model of congenital neuronal ceroid lipofuscinosis

    Get PDF
    Mutations in the cathepsin D (CTSD) gene cause an aggressive neurodegenerative disease (congenital neuronal ceroid lipofuscinosis) that leads to early death. Recent evidence suggests that presynaptic abnormalities play a major role in the pathogenesis of CTSD deficiencies. To identify the early events that lead to synaptic alterations, we investigated synaptic ultrastructure and function in pre-symptomatic CTSD knock-out (Ctsd(−/−)) mice. Electron microscopy revealed that there were significantly greater numbers of readily releasable synaptic vesicles present in Ctsd(−/−) mice than in wild-type control mice as early as postnatal day 16. The size of this synaptic vesicle pool continued to increase with disease progression in the hippocampus and thalamus of the Ctsd(−/−) mice. Electrophysiology revealed a markedly decreased frequency of miniature excitatory postsynaptic currents (EPSCs) with no effect on pair-pulse modulation of the evoked EPSPs in the hippocampus of Ctsd(−/−) mice. The reduced miniature EPSC frequency was observed before the appearance of epilepsy or any morphological sign of synaptic degeneration. Taken together, the data indicate that CTSD is required for normal synaptic function, and that a failure in synaptic trafficking or recycling may be an early and important pathological mechanism in Ctsd(−/−) mice; these presynaptic abnormalities may initiate synaptic degeneration in advance of subsequent neuronal loss

    Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the R6/2 Mouse Model of HD

    Get PDF
    Huntington's disease (HD) is caused by the expansion of a CAG repeat in the huntingtin (HTT) gene. The R6/2 mouse model of HD expresses a mutant version of exon 1 HTT and develops motor and cognitive impairments, a widespread huntingtin (HTT) aggregate pathology and brain atrophy. Despite the vast number of studies that have been performed on this model, the association between the molecular and cellular neuropathology with brain atrophy, and with the development of behavioral phenotypes remains poorly understood. In an attempt to link these factors, we have performed longitudinal assessments of behavior (rotarod, open field, passive avoidance) and of regional brain abnormalities determined through magnetic resonance imaging (MRI) (whole brain, striatum, cortex, hippocampus, corpus callosum), as well as an end-stage histological assessment. Detailed correlative analyses of these three measures were then performed. We found a gender-dependent emergence of motor impairments that was associated with an age-related loss of regional brain volumes. MRI measurements further indicated that there was no striatal atrophy, but rather a lack of striatal growth beyond 8 weeks of age. T2 relaxivity further indicated tissue-level changes within brain regions. Despite these dramatic motor and neuroanatomical abnormalities, R6/2 mice did not exhibit neuronal loss in the striatum or motor cortex, although there was a significant increase in neuronal density due to tissue atrophy. The deposition of the mutant HTT (mHTT) protein, the hallmark of HD molecular pathology, was widely distributed throughout the brain. End-stage histopathological assessments were not found to be as robustly correlated with the longitudinal measures of brain atrophy or motor impairments. In conclusion, modeling pre-manifest and early progression of the disease in more slowly progressing animal models will be key to establishing which changes are causally related. © 2013 Rattray et al

    Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington\u27s disease

    Get PDF
    Neurons in Huntington\u27s disease exhibit selective morphological and subcellular alterations in the striatum and cortex. The link between these neuronal changes and behavioral abnormalities is unclear. We investigated relationships between essential neuronal changes that predict motor impairment and possible involvement of the corticostriatal pathway in developing behavioral phenotypes. We therefore generated heterozygote mice expressing the N-terminal one-third of huntingtin with normal (CT18) or expanded (HD46, HD100) glutamine repeats. The HD mice exhibited motor deficits between 3 and 10 months. The age of onset depended on an expanded polyglutamine length; phenotype severity correlated with increasing age. Neuronal changes in the striatum (nuclear inclusions) preceded the onset of phenotype, whereas cortical changes, especially the accumulation of huntingtin in the nucleus and cytoplasm and the appearance of dysmorphic dendrites, predicted the onset and severity of behavioral deficits. Striatal neurons in the HD mice displayed altered responses to cortical stimulation and to activation by the excitotoxic agent NMDA. Application of NMDA increased intracellular Ca(2+) levels in HD100 neurons compared with wild-type neurons. Results suggest that motor deficits in Huntington\u27s disease arise from cumulative morphological and physiological changes in neurons that impair corticostriatal circuitry

    Ebullition of methane from peatlands: Does peat act as a signal shredder?

    Get PDF
    Bubbling (ebullition) of greenhouse gases, particularly methane, from peatlands has been attributed to environmental forcings, such as changes in atmospheric pressure. However, observations from peat soils suggest that ebullition and environmental forcing may not always be correlated and that interactions between bubbles and the peat structure may be the cause of such decoupling. To investigate this possibility, we used a simple computer model (Model of Ebullition and Gas storAge) to simulate methane ebullition from a model peat. We found that lower porosity peat can store methane bubbles for lengthy periods of time, effectively buffering or moderating ebullition so that it no longer reïŹ‚ects bubble production signals. Our results suggest that peat structure may act as a “signal shredder” and needs to be taken into account when measuring and modeling ebullition

    The effect of sampling effort on estimates of methane ebullition from peat

    Get PDF
    We investigated the effect of sample size and sampling duration on methane bubble flux (ebullition) estimates from peat using a computer model. A field scale (10 m), seasonal (> 100 days) simulation of ebullition from a two-dimensional structurally-varying peat profile was modelled at fine spatial resolution (1 mm × 1 mm). The spatial and temporal scale of this simulation was possible because of the computational efficiency of the reduced complexity approach that was implemented, and patterns of simulated ebullition were consistent with those found in the field and laboratory. The simulated ebullition from the peat profile suggested that decreases in peat porosity – which cause increases in gas storage – produce ebullition that becomes increasingly patchy in space and erratic in time. By applying different amounts of spatial and temporal sampling effort it was possible to determine the uncertainty in ebullition estimates from the peatland. The results suggest that traditional methods to measure ebullition can equally overestimate and underestimate flux by 20% and large ebullition events can lead to large overestimations of flux when sampling effort is low. Our findings support those of field studies, and we recommend that ebullition should be measured frequently (hourly to daily) and at many locations (n > 14)
    • 

    corecore