5 research outputs found

    Review of Major Crop and Animal Arthropod Pests of South Texas

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    The Lower Rio Grande Valley is an area in Texas that consists of the four southern-most counties. This area contains a diverse range of agriculture and land-use including vegetable, row-crop and livestock production. The year-around cool to hot subtropical climate means that green vegetation is continually present, including many crops. Geographically, it shares an international border, making it a region vulnerable to new invasive species and the re-introduction of pests that have been previously eliminated in the United States. These combined factors lead to an array of arthropod pests that may have serious impacts on the crops, animals, and people in the region. This review focuses on arthropod pests that have historically, currently, or have the potential to significantly impact vegetables, row-crops, livestock, and humans in the LRGV. This is not an all-inclusive re-view but aims to focus on many of the arthropods that have been significant in the last 20 years

    Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.

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    Many mutations confer one or more toxic function(s) on copper/zinc superoxide dismutase 1 (SOD1) that impair motor neuron viability and cause familial amyotrophic lateral sclerosis (FALS). Using a conformation-specific antibody that detects misfolded SOD1 (C4F6), we found that oxidized wild-type SOD1 and mutant SOD1 share a conformational epitope that is not present in normal wild-type SOD1. In a subset of human sporadic ALS (SALS) cases, motor neurons in the lumbosacral spinal cord were markedly C4F6 immunoreactive, indicating that an aberrant wild-type SOD1 species was present. Recombinant, oxidized wild-type SOD1 and wild-type SOD1 immunopurified from SALS tissues inhibited kinesin-based fast axonal transport in a manner similar to that of FALS-linked mutant SOD1. Our findings suggest that wild-type SOD1 can be pathogenic in SALS and identify an SOD1-dependent pathogenic mechanism common to FALS and SALS

    Disruption

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    of muscle membrane and phenotype divergence in two novel mouse models of dysferlin-deficienc
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