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  • 1
    Publication Date: 2022-05-25
    Description: Author Posting. © The Author(s), 2014. This is the author's version of the work. It is posted here by permission of Koninklijke Brill for personal use, not for redistribution. The definitive version was published in Journal of Crustacean Biology 34 (2014): 671-673, doi:10.1163/1937240X-00002268.
    Description: A northern range extension is presented here for the marsh fiddler crab Uca pugnax. In summer 2014, adult crabs were found as far north as Hampton, New Hampshire (42.924428, -70.820517), which is 80 km north of its previously established northern limit determined in 2003. Thus, the mean annual northern movement of U. pugnax is currently 7.2 km y-1. I hypothesize that crabs recruited to the most northern sites during 2012 or 2013 when ocean temperatures were up to 1.3 C higher than the average of the previous decade. In a scenario of continued warming oceans associated with climate change, the range of U. pugnax is thus predicted to continue to extend northward. Given that fiddler crabs are ecosystem engineers affecting coastal wetland productivity, biogeochemistry and sediment structure, the introduction of this species into northern salt marshes may have consequences for marsh structure and function.
    Description: This work was funded by NSF 1354494 and 1238212.
    Keywords: Marine invasion ; Climate velocity ; Decapod ; Uca
    Repository Name: Woods Hole Open Access Server
    Type: Preprint
    Format: application/pdf
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  • 2
    Publication Date: 2022-05-25
    Description: Author Posting. © The Author(s), 2014. This is the author's version of the work. It is posted here by permission of Koninklijke Brill for personal use, not for redistribution. The definitive version was published in Journal of Crustacean Biology 35 (2015): 105-110, doi:10.1163/1937240X-00002293.
    Description: Worldwide, climate-change is shifting species distributions poleward. Here I present recent (2012-2014) observations of the blue crab, Callinectes sapidus, in the Gulf of Maine (GoM), north of its historical range of Cape Cod, Massachusetts. To test the hypothesis of a climate-driven range expansion, I examined near-surface ocean temperatures. On average, ocean temperatures in the GoM in summer 2012 and 2013 were up to 1.3°C higher than the average of the previous decade, suggesting that warmer waters may have promoted the recruitment of C. sapidus to the GoM. Previous ephemeral populations of C. sapidus in the Gulf of Maine have been reported since the 1860's. Recent observations and continued warming in the northwest Atlantic may signal a permanent poleward expansion of C. sapidus into the GoM. If so, then a key goal for ecologists and managers will be to understand the effect of C. sapidus on GoM food-webs and fisheries.
    Description: This work was funded by NSF Grants No. 1354494 and 1238212. Additional support from the Northeast Climate Science Center, Grant No. DOI G12AC00001.
    Keywords: Callinectes ; Climate velocity ; Decapod ; Marine invasion
    Repository Name: Woods Hole Open Access Server
    Type: Preprint
    Format: application/pdf
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  • 3
    ISSN: 1432-1335
    Keywords: CM101 ; GBS toxin ; Cancer ; Inflammation ; Neovascularization ; Angiogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A polysaccharide toxin, GBS toxin, is produced by group BStreptococcus (GBS) isolates from neonates who died of “early-onset disease”. GBS toxin, named CM101 in the clinic, was hypothesized, on the basis of our previous in vivo studies, to induce inflammation in pulmonary neovasculature in neonates by crosslinking of embryonic receptors still expressed after birth and in tumor neovasculature in adults. Immunohistochemical in vitro analysis of human biopsies showed that tumor neovasculature is indeed a binding site for CM101. In vivo studies in mice have demonstrated that CM101 induced inflammatory responses in neoplastic tumor neovasculature causing inhibition of tumor growth and tumor cell necrosis. These experimental observations warranted a phase I clinical trial for CM101 as an anti-neovascularization agent in human cancer therapy. Cancer patients received one cycle of therapy consisting of three treatments during 1 week. CM101 was administered over 15 min by i.v. infusion. Dosages of 7.5 μg/kg (1 U/kg),n=3; 15 μg/kg (2 U/kg),n=6; 24.75 μg/kg (3.3 U/kg),n=3; and 37.5 μg/kg (5 U/kg),n=3 were used. Enzyme-linked immunosorbent sandwich assays (ELISA) of the patients' sera showed a marked elevation of soluble E-selectin with a peak concentration observed at 8–12 h after each CM101. infusion. The average baseline value for soluble E-selectin prior to the first treatment was 97.3±23.4 ng/ml (mean±SEM,n=15) and the average peak level at 8 h was 441.6±62.4 (mean±SEM,n=15;P〈0.001). Subsequent treatments gave average maximum soluble E-selectin levels again at 8 h of 466.9±87.6 and 412.0±67.8 ng/ml, for treatment 2 and 3 respectively. Baseline values for treatment 2 and 3 were 192.3±26.4 and 226.4±26.1 ng/ml respectively (p〈0.01 versus treatment 1). Out of 15 patients, 5 showed tumor reduction or stabilization and were given additional cycles of therapy. CM101 induced an increase in soluble E-selectin levels, which remained elevated over baseline at the start of the following treatment cycles. The baseline remained elevated for several weeks after the final treatment, i.e.,P〈0.01 for levels before treatment 1 compared to those at week 4 after treatment. Elevated soluble E-selectin is considered proof of endothelial engagement in an inflammatory process. Our data support the contention that the inflammatory response observed in these cancer patients is targeting the tumor neovasculature and that measurement of soluble E-selectin levels in patients treated with CM101 can provide important information on the magnitude of CM101-mediated neovascular endothelial activation and tumor cell damage in cancer of endothelial origin, or cancer with a major neo-angiogenic component.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1335
    Keywords: Key words CM101 ; GBS toxin ; Cancer ; Inflammation ; Neovascularization ; Angiogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A polysaccharide toxin, GBS toxin, is produced by group B Streptococcus (GBS) isolates from neonates who died of “early-onset disease”. GBS toxin, named CM101 in the clinic, was hypothesized, on the basis of our previous in vivo studies, to induce inflammation in pulmonary neovasculature in neonates by crosslinking of embryonic receptors still expressed after birth and in tumor neovasculature in adults. Immunohisto chemical in vitro analysis of human biopsies showed that tumor neovasculature is indeed a binding site for CM101. In vivo studies in mice have demonstrated that CM101 induced inflammatory responses in neoplastic tumor neovasculature causing inhibition of tumor growth and tumor cell necrosis. These experimental observations warranted a phase I clinical trial for CM101 as an anti-neovascularization agent in human cancer therapy. Cancer patients received one cycle of therapy consisting of three treatments during 1 week. CM101 was administered over 15 min by i.v. infusion. Dosages of 7.5 μg/kg (1 U/kg), n=3; 15 μg/kg (2 U/kg), n=6; 24.75 μg/kg (3.3 U/kg), n=3; and 37.5 μg/kg (5 U/kg), n=3 were used. Enzyme-linked immunosorbent sandwich assays (ELISA) of the patients’ sera showed a marked elevation of soluble E-selectin with a peak concentration observed at 8–12 h after each CM101 infusion. The average baseline value for soluble E-selectin prior to the first treatment was 97.3±23.4 ng/ml (mean±SEM, n=15) and the average peak level at 8 h was 441.6±62.4 (mean±SEM, n=15; P〈0.001). Subsequent treatments gave average maximum soluble E-selectin levels again at 8 h of 466.9±87.6 and 412.0±67.8 ng/ml, for treatments 2 and 3 respectively. Baseline values for treatments 2 and 3 were 192.3±26.4 and 226.4±26.1 ng/ml respectively (p〈0.01 versus treatment 1). Out of 15 patients, 5 showed tumor reduction or stabilization and were given additional cycles of therapy. CM101 induced an increase in soluble E-selectin levels, which remained elevated over baseline at the start of the following treatment cycles. The baseline remained elevated for several weeks after the final treatment, i.e., P〈0.01 for levels before treatment 1 compared to those at week 4 after treatment. Elevated soluble E-selectin is considered proof of endothelial engagement in an inflammatory process. Our data support the contention that the inflammatory response observed in these cancer patients is targeting the tumor neovasculature and that measurement of soluble E-selectin levels in patients treated with CM101 can provide important information on the magnitude of CM101-mediated neovascular endothelial activation and tumor cell damage in cancer of endothelial origin, or cancer with a major neo-angiogenic component.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
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