73 research outputs found

    Eliciting Risk Preferences using Choice Lists

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    We study the effect of embedding pairwise choices between lotteries within a choice list on measured risk attitude. Using an experiment with online workers, we find that subjects choose the risky lottery rather than a sure payment significantly more often when responding to a choice list. This behavior can be rationalized by the interaction between non-expected utility and the random incentive system, as suggested by Karni and Safra (1987)

    A Century and a Half of Research on the Stable Fly, \u3ci\u3eStomoxys calcitrans\u3c/i\u3e (L.) (Diptera: Muscidae), 1862-2011: An Annotated Bibliography

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    The stable fly, Stomoxys calcitrans, is a cosmopolitan pest of livestock, wild animals, pets, and humans. It is a primary pest of cattle in the United States, estimated to cause more than $1 billion in economic losses annually. It also causes dissension at the rural-urban interface and is a problem in recreation areas such as Florida beaches and the Great Lakes. Due to its pestiferous nature and painful bite, methods to control stable flies have been investigated for over a century. A large amount of research has been reported on stable fly biology, ecology, genetics, physiology, and vector competence. For this bibliography, literature has been gathered from journals and other resources available to the authors, and a selected number of articles have been annotated. This bibliography represents an update of literature published since 1980; literature from pre-1980 was included if copy could be ascertained

    A Century and a Half of Research on the Stable Fly, \u3ci\u3eStomoxys calcitrans\u3c/i\u3e (L.) (Diptera: Muscidae), 1862-2011: An Annotated Bibliography

    Get PDF
    The stable fly, Stomoxys calcitrans, is a cosmopolitan pest of livestock, wild animals, pets, and humans. It is a primary pest of cattle in the United States, estimated to cause more than $1 billion in economic losses annually. It also causes dissension at the rural-urban interface and is a problem in recreation areas such as Florida beaches and the Great Lakes. Due to its pestiferous nature and painful bite, methods to control stable flies have been investigated for over a century. A large amount of research has been reported on stable fly biology, ecology, genetics, physiology, and vector competence. For this bibliography, literature has been gathered from journals and other resources available to the authors, and a selected number of articles have been annotated. This bibliography represents an update of literature published since 1980; literature from pre-1980 was included if copy could be ascertained

    Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis.

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    Molecular, genetic and pathological evidence suggests that deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition. Although the factors that trigger these deficits are diverse, there is increasing evidence that they converge on a common pathological hub that involves NMDA receptor hypofunction and oxidative stress. These factors have been separately linked to schizophrenia pathogenesis, but evidence now suggests that they are mechanistically interdependent and contribute to a common schizophrenia-associated pathology

    Mutations in the RNA Granule Component TDRD7 Cause Cataract and Glaucoma

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    The precise transcriptional regulation of gene expression is essential for vertebrate development, but the role of posttranscriptional regulatory mechanisms is less clear. Cytoplasmic RNA granules (RGs) function in the posttranscriptional control of gene expression, but the extent of RG involvement in organogenesis is unknown. We describe two human cases of pediatric cataract with loss-of-function mutations in TDRD7 and demonstrate that Tdrd7 nullizygosity in mouse causes cataracts, as well as glaucoma and an arrest in spermatogenesis. TDRD7 is a Tudor domain RNA binding protein that is expressed in lens fiber cells in distinct TDRD7-RGs that interact with STAU1-ribonucleoproteins (RNPs). TDRD7 coimmunoprecipitates with specific lens messenger RNAs (mRNAs) and is required for the posttranscriptional control of mRNAs that are critical to normal lens development and to RG function. These findings demonstrate a role for RGs in vertebrate organogenesis

    A Dominant-Negative Mutation of Mouse Lmx1b Causes Glaucoma and Is Semi-lethal via LBD1-Mediated Dimerisation

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    Mutations in the LIM-homeodomain transcription factor LMX1B cause nail-patella syndrome, an autosomal dominant pleiotrophic human disorder in which nail, patella and elbow dysplasia is associated with other skeletal abnormalities and variably nephropathy and glaucoma. It is thought to be a haploinsufficient disorder. Studies in the mouse have shown that during development Lmx1b controls limb dorsal-ventral patterning and is also required for kidney and eye development, midbrain-hindbrain boundary establishment and the specification of specific neuronal subtypes. Mice completely deficient for Lmx1b die at birth. In contrast to the situation in humans, heterozygous null mice do not have a mutant phenotype. Here we report a novel mouse mutant Icst, an N-ethyl-N-nitrosourea-induced missense substitution, V265D, in the homeodomain of LMX1B that abolishes DNA binding and thereby the ability to transactivate other genes. Although the homozygous phenotypic consequences of Icst and the null allele of Lmx1b are the same, heterozygous Icst elicits a phenotype whilst the null allele does not. Heterozygous Icst causes glaucomatous eye defects and is semi-lethal, probably due to kidney failure. We show that the null phenotype is rescued more effectively by an Lmx1b transgene than is Icst. Co-immunoprecipitation experiments show that both wild-type and Icst LMX1B are found in complexes with LIM domain binding protein 1 (LDB1), resulting in lower levels of functional LMX1B in Icst heterozygotes than null heterozygotes. We conclude that Icst is a dominant-negative allele of Lmx1b. These findings indicate a reassessment of whether nail-patella syndrome is always haploinsufficient. Furthermore, Icst is a rare example of a model of human glaucoma caused by mutation of the same gene in humans and mice
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