628 research outputs found

    Pseudo noun incorporation is M-Merger: evidence from Balinese

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    In this paper, I argue that adjacency alone can license a nominal by demonstrating that properties of Balinese PNI are incompatible with either (covert) Head Movement (Baker 2012) or with a bare NP analysis (Massam 2001). The Balinese data are compatible with a scenario in which the nominal head happens to be adjacent to the verb. In this configuration, head-head adjacency licenses the nominal via M(orphological)-Merger (Marantz 1984). Under the proposed analysis, Balinese PNI is a last resort strategy, which vacuously satisfies the Case Filter

    Case and agreement in Cupeno: Morphology obscures a simple syntax

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    Quality of life measurement clarifies the cost-effectiveness of Helicobacter pylori eradication in peptic ulcer disease and uninvestigated dyspepsia 1

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    Previous economic studies of Helicobacter pylori eradication in dyspepsia and peptic ulcer disease have not measured quality of life using utilities (preference probabilities), which are needed to compare the cost-effectiveness of such treatment to other health care interventions. The goals of this study were to measure quality of life in patients with dyspepsia or peptic ulcer and apply these measurements to published models of disease management to determine cost-effectiveness in dollars per quality-adjusted life year (QALY) gained. Methods : Utilities for dyspepsia and peptic ulcer disease were measured in adult patients (n = 73) on chronic acid suppression for peptic ulcer or ulcer-like dyspepsia. Median utility values were applied to the results of published cost-effectiveness analyses and a previously validated dyspepsia model. Cost-utility ratios for early H. pylori eradication in uninvestigated dyspepsia and peptic ulcer disease were then computed. Results : The total disutility, or lost quality of life, for an ulcer was 0.11 QALY, of which 0.09 QALY was attributed to dyspeptic symptoms. After these results were incorporated into published studies, cost-utility ratios for ulcer treatment varied from 3,100to3,100 to 12,500 per QALY gained, whereas estimates for uninvestigated dyspepsia management ranged from 26,800to26,800 to 59,400 per QALY. Sensitivity analyses indicated a range of 1,300to1,300 to 27,300 per QALY for management of duodenal ulcer and 15,000to15,000 to 129,700 per QALY for dyspepsia. Conclusions: Strategies that emphasize early H. pylori eradication were cost-effective for patients with peptic ulcer and possibly cost-effective for patients with uninvestigated dyspepsia, relative to other medical interventions. Dyspeptic symptoms cause significant disutility that should be incorporated in future cost-effectiveness analyses of treatment strategies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73031/1/j.1572-0241.2001.03516.x.pd

    Developmental Exposure of Rats to Chlorpyrifos Leads to Behavioral Alterations in Adulthood, Involving Serotonergic Mechanisms and Resembling Animal Models of Depression

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    Developmental exposure to chlorpyrifos (CPF) causes persistent changes in serotonergic (5HT) systems. We administered 1 mg/kg/day CPF to rats on postnatal days 1–4, a regimen below the threshold for systemic toxicity. When tested in adulthood, CPF-exposed animals showed abnormalities in behavioral tests that involve 5HT mechanisms. In the elevated plus maze, males treated with CPF spent more time in the open arms, an effect seen with 5HT deficiencies in animal models of depression. Similarly, in an anhedonia test, the CPF-exposed group showed a decreased preference for chocolate milk versus water. Developmental CPF exposure also has lasting effects on cognitive function. We replicated our earlier finding that developmental CPF exposure ablates the normal sex differences in 16-arm radial maze learning and memory: during acquisition training, control male rats typically perform more accurately than do control females, but CPF treatment eliminated this normal sex difference. Females exposed to CPF showed a reduction in working and reference memory errors down to the rate of control males. Conversely, CPF-exposed males exhibited an increase in working and reference memory errors. After radial-arm acquisition training, we assessed the role of 5HT by challenging the animals with the 5HT(2) receptor antagonist ketanserin. Ketanserin did not affect performance in controls but elicited dose-dependent increases in working and reference memory errors in the CPF group, indicating an abnormal dependence on 5HT systems. Our results indicate that neonatal CPF exposures, classically thought to be subtoxic, produce lasting changes in 5HT-related behaviors that resemble animal models of depression

    Comparative Developmental Neurotoxicity of Organophosphate Insecticides: Effects on Brain Development Are Separable from Systemic Toxicity

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    A comparative approach to the differences between systemic toxicity and developmental neurotoxicity of organophosphates is critical to determine the degree to which multiple mechanisms of toxicity carry across different members of this class of insecticides. We contrasted neuritic outgrowth and cholinergic synaptic development in neonatal rats given different organophosphates (chlorpyrifos, diazinon, parathion) at doses spanning the threshold for impaired growth and viability. Animals were treated daily on postnatal days 1–4 by subcutaneous injection so as to bypass differences in first-pass activation to the oxon or catabolism to inactive products. Evaluations occurred on day 5. Parathion (maximum tolerated dose, 0.1 mg/kg) was far more systemically toxic than was chlorpyrifos or diazinon (maximum tolerated dose, 1–5 mg/kg). Below the maximum tolerated dose, diazinon impaired neuritic outgrowth in the forebrain and brainstem, evidenced by a deficit in the ratio of membrane protein to total protein. Diazinon also decreased choline acetyltransferase activity, a cholinergic neuronal marker, whereas it did not affect hemicholinium-3 binding to the presynaptic choline transporter, an index of cholinergic neuronal activity. There was no m(2)-muscarinic acetylcholine receptor down-regulation, as would have occurred with chronic cholinergic hyper-stimulation. The same pattern was found previously for chlorpyrifos. In contrast, parathion did not elicit any of these changes at its maximum tolerated dose. These results indicate a complete dichotomy between the systemic toxicity of organophosphates and their propensity to elicit developmental neurotoxicity. For parathion, the threshold for lethality lies below that necessary for adverse effects on brain development, whereas the opposite is true for chlorpyrifos and diazinon
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