Grodsky S.M.,University of Wisconsin - Madison |
Behr M.J.,University of Wisconsin - Madison |
Behr M.J.,Wisconsin Veterinary Diagnostic Laboratory |
Gendler A.,University of Wisconsin - Madison |
And 4 more authors.
Journal of Mammalogy | Year: 2011
Wind turbine-associated bat mortality is occurring at unanticipated rates, yet our understanding of the causes of these fatalities is limited. The prominent proximate causes of bat deaths at wind turbines are direct collision (i.e., blunt-force trauma) and barotrauma. The objectives of this study were to use veterinary diagnostic procedures to determine the lesions associated with bats killed by wind turbines and investigate relationships between patterns of injuries and proximate causes of death. A majority of the bats (74%; 29 of 39) examined by radiology had bone fractures; most of these fractures were in the wings and none was in the hind limbs. Visual inspection resulted in 33% fewer detected bone fractures when compared with radiology results. Bats dropped from a turbine nacelle (91.44 m) to determine extent and type(s) of bone fracture did not show signs of significant bone damage. Approximately one-half (52%; 12 of 23) of bats whose ears were examined had mild to severe hemorrhaging in the middle or inner ears (or both). None of the bats found during this study had any pre-existing disease. It is difficult to attribute individual fatalities exclusively to either direct collision or barotrauma. Gross necropsy, histopathology, and radiology complement each others' deficiencies and together give the best insight into cause of death. Delayed lethal effects after nonlethal contact with wind turbines are poorly understood and difficult to quantify by mortality searches alone but can result in underestimating bat mortality caused by wind energy facilities. © 2011 American Society of Mammalogists.
Wang Y.,University of Wisconsin - Madison |
Zeng S.,University of Wisconsin - Madison |
Lin T.-M.,University of Wisconsin - Madison |
Krugner-Higby L.,University of Wisconsin - Madison |
And 3 more authors.
Pharmaceutical Research | Year: 2014
Purpose: Although Cu complexes have been investigated as anticancer agents, there has been no description of Cu itself as a cancer killing agent. A stealth liposomal Cu formulation (LpCu) was studied in vitro and in vivo.Methods: LpCu was evaluated in prostate cancer origin PC-3 cells by a metabolic cytotoxicity assay, by monitoring ROS, and by flow cytometry. LpCu efficacy was evaluated in vivo using intratumoral and intravenous injections into mice bearing PC-3 xenograft tumors. Toxicology was assessed by performing hematological and blood biochemistry assays, and tissue histology and Cu distribution was investigated by elemental analysis.Results: LpCu and free Cu salts displayed similar levels of cell metabolic toxicity and ROS. Flow cytometry indicated that the mechanisms of cell death were both apoptosis and necrosis. Animals injected i.t. with 3.5 mg/kg or i.v. with 3.5 and 7.0 mg/kg LpCu exhibited significant tumor growth inhibition. Kidney and eye were the main organs affected by Cu-mediated toxicities, but spleen and liver were the major organs of Cu deposition.Conclusions: LpCu was effective at reducing tumor burden in the xenograft prostate cancer model. There was histological evidence of Cu toxicity in kidneys and eyes of animals treated at the maximum tolerated dose of LpCu 7.0 mg/kg. © 2014 Springer Science+Business Media New York.
Appler K.K.,New York State Department of Health |
Brown A.N.,New York State Department of Health |
Brown A.N.,University at Albany |
Brown A.N.,Ordway Research Institute |
And 11 more authors.
PLoS ONE | Year: 2010
Most acute infections with RNA viruses are transient and subsequently cleared from the host. Recent evidence, however, suggests that the RNA virus, West Nile virus (WNV), not only causes acute disease, but can persist long term in humans and animal models. Our goal in this study was to develop a mouse model of WNV persistence. We inoculated immunocompetent ice subcutaneously (s.c.) with WNV and examined their tissues for infectious virus and WNV RNA for 16 months (mo) post-inoculation (p.i.). Infectious WNV persisted for 1 mo p.i. in all mice and for 4 mo p.i. in 12% of mice, and WNV RNA persisted for up to 6 mo p.i. in 12% of mice. The frequency of persistence was tissue dependent and was in the following order: skin, spinal cord, brain, lymphoid tissues, kidney, and heart. Viral persistence occurred in the face of a robust antibody response and in the presence of inflammation in the brain. Furthermore, persistence in the central nervous system (CNS) and encephalitis were observed even in mice with subclinical infections. Mice were treated at 1 mo p.i. with cyclophosphamide, and active viral replication resulted, suggesting that lymphocytes are functional during viral persistence. In summary, WNV persisted in the CNS and periphery of mice for up to 6 mo p.i. in mice with subclinical nfections. These results have implications for WNV-infected humans. In particular, immunosuppressed patients, organ transplantation, and long term sequelae may be impacted by WNV persistence. © 2010 Appler et al.
Springer D.J.,New York State Department of Health |
Springer D.J.,University at Albany |
Springer D.J.,Duke University |
Ren P.,New York State Department of Health |
And 12 more authors.
PLoS ONE | Year: 2010
Cryptococcus gattii, an emerging fungal pathogen of humans and animals, is found on a variety of trees in tropical and temperate regions. The ecological niche and virulence of this yeast remain poorly defined. We used Arabidopsis thaliana plants and plant-derived substrates to model C. gattii in its natural habitat. Yeast cells readily colonized scratch-wounded plant leaves and formed distinctive extracellular fibrils (40-100 nm diameter ×500-3000 nm length). Extracellular fibrils were observed on live plants and plant-derived substrates by scanning electron microscopy (SEM) and by high voltage-EM (HVEM). Only encapsulated yeast cells formed extracellular fibrils as a capsule-deficient C. gattii mutant completely lacked fibrils. Cells deficient in environmental sensing only formed disorganized extracellular fibrils as apparent from experiments with a C. gattii STE12α mutant. C. gattii cells with extracellular fibrils were more virulent in murine model of pulmonary and systemic cryptococcosis than cells lacking fibrils. C. gattii cells with extracellular fibrils were also significantly more resistant to killing by human polymorphonuclear neutrophils (PMN) in vitro even though these PMN produced elaborate neutrophil extracellular traps (NETs). These observations suggest that extracellular fibril formation could be a structural adaptation of C. gattii for cell-to-cell, cell-to-substrate and/or cell-to-phagocyte communications. Such ecological adaptation of C. gattii could play roles in enhanced virulence in mammalian hosts at least initially via inhibition of host PMN-mediated killing. © 2010 Springer et al.
Lorch J.M.,University of Wisconsin - Madison |
Muller L.K.,U.S. Geological Survey |
Russell R.E.,U.S. Geological Survey |
O'Connor M.,Wisconsin Veterinary Diagnostic Laboratory |
And 2 more authors.
Applied and Environmental Microbiology | Year: 2013
White-nose syndrome (WNS) is an emerging disease of hibernating bats caused by the recently described fungus Geomyces destructans. First isolated in 2008, the origins of this fungus in North America and its ability to persist in the environment remain undefined. To investigate the correlation between manifestation of WNS and distribution of G. destructans in the United States, we analyzed sediment samples collected from 55 bat hibernacula (caves and mines) both within and outside the known range of WNS using a newly developed real-time PCR assay. Geomyces destructans was detected in 17 of 21 sites within the known range of WNS at the time when the samples were collected; the fungus was not found in 28 sites beyond the known range of the disease at the time when environmental samples were collected. These data indicate that the distribution of G. destructans is correlated with disease in hibernating bats and support the hypothesis that the fungus is likely an exotic species in North America. Additionally, we examined whether G. destructans persists in infested bat hibernacula when bats are absent. Sediment samples were collected from 14 WNS-positive hibernacula, and the samples were screened for viable fungus by using a culture technique. Viable G. destructans was cultivated from 7 of the 14 sites sampled during late summer, when bats were no longer in hibernation, suggesting that the fungus can persist in the environment in the absence of bat hosts for long periods of time. © 2013, American Society for Microbiology.