Equine Melanocytic Tumors: A Retrospective Study of 53 Horses (1988 to 1991)

A study of 57 cutaneous melanocytic tumors from 53 horses revealed 4 distinct clinical syndromes: melanocytic nevus, dermal melanoma, dermal melanomatosis, and anaplastic malignant melanoma. Melanocytic nevus and anaplastic melanoma each had histopathologic features that distinguished them from dermal melanoma and dermal melanomatosis. Dermal melanoma and dermal melanomatosis were histologically similar but could be differentiated by their clinical features. Melanocytic nevi were diagnosed in 29 horses with an average age of 5 years; they were solitary, superficial masses that occurred in both grey and nongrey horses, and in which surgical excision was generally curative. Dermal melanomas were diagnosed in 20 horses with an average age of 13 years; all horses of known coat color were grey. Eight horses with an average age of 7 years had 1 or 2 discrete dermal melanomas. Follow-up information was available for 6 horses; metastases occurred in 2 horses, and surgical excision was apparently curative in 4 horses. Dermal melanomatosis was diagnosed in 12 grey horses with an average age of 17 years; all 6 of these horses evaluated had internal metastases. In 2 aged nongrey horses with anaplastic malignant melanoma, the tumors metastasized within 1 year of diagnosis. Two tumors with features of both melanocytic nevus and dermal melanoma remained unclassified.     

Soil saturation effects on forest dynamics: scaling across a southern boreal/northern hardwood landscape

Patch modeling can be used to scale-up processes to portray landscape-level dynamics. Via direct extrapolation, a heterogeneous landscape is divided into its constituent patches; dynamics are simulated on each representative patch and are weighted and aggregated to formulate the higher level response. Further extrapolation may be attained by coarsening the resolution of or lumping environmental data (e.g., climatic, edaphic, hydrologic, topographic) used to delimit a patch.Forest patterns at the southern boreal/northern hardwood transition zone are often defined by soil heterogeneity, determined primarily by the extent and duration of soil saturation. To determine how landscape-level dynamics predicted from direct extrapolation compare when coarsening soil parameters, we simulated forest dynamics for soil series representing a range of drainage classes from east- central Maine. Responses were aggregated according to the distribution of soil associations comprising a 600 ha area based on local- (1:12,000), county- (1:120,000) and state- (1:250,000) scale soil maps. At the patch level, simulated aboveground biomass accumulated more slowly in poorer draining soils. Different soil series yielded different communities comprised of species with various tolerances for soil saturation. When aggregated, removal of waterlogging caused a 20–60% increase in biomass accumulation during the first 50 years of simulation. However, this early successional increase and the maximum level of biomass accumulation over a 200 year period varied by as much as 40% depending on the geospatial data. This marked discrepancy suggests caution when extrapolating with forest patch models by coarsening parameters and demonstrates how rules used to rescale environmental data need to be evaluated for consistency.     

The 5‐lipoxygenase inhibitor tepoxalin induces oxidative damage and altered PTEN status prior to apoptosis in canine osteosarcoma cell lines

The 5‐lipoxygenase (5‐LOX) inhibitor tepoxalin has been shown to slow canine osteosarcoma (OSA) tumour xenografts growth, yet the mechanisms are poorly elucidated. Further examination of tepoxalin in canine OSA cell lines shows that tepoxalin treated cells undergo apoptosis through caspase‐3 activation and annexin staining. Interestingly, apoptosis is superseded by an increase in reactive oxygen species (ROS), as measured by activation of dihydrorhodamine 123 and mitosox. This increase in ROS appears to be related to the 5‐LOX inhibitor regardless of cellular 5‐LOX status, and was not observed after treatment with the tepoxalin metabolite RWJ20142. Additionally, 5‐LOX inhibition by tepoxalin appears to increase phosphatase and tensin (PTEN) homolog activity by preventing its alkylation or oxidation. PTEN modification or inhibition allows phosphoinositide‐3 (PI3) kinase activity thereby heightening activation of protein kinase B (AKT) phosphorylation. Our data suggest that off target oxidation and LOX inhibition play roles in the apoptotic response.