Toxin production in marine microalgae was previously shown to be tightly coupled with cellular stoichiometry. The highest values of cellular toxin are in fact mainly associated with a high carbon to nutrient cellular ratio. In particular, the cellular accumulation of C-rich toxins (i.e., with C:N > 6.6) can be stimulated by both N and P deficiency. Dinoflagellates are the main producers of C-rich toxins and may represent a serious threat for human health and the marine ecosystem. As such, the development of a numerical model able to predict how toxin production is stimulated by nutrient supply/deficiency is of primary utility for both scientific and management purposes. In this work we have developed a mechanistic model describing the stoichiometric regulation of C-rich toxins in marine dinoflagellates. To this purpose, a new formulation describing toxin production and fate was embedded in the European Regional Seas Ecosystem Model (ERSEM), here simplified to describe a monospecific batch culture. Toxin production was assumed to be composed by two distinct additive terms; the first is a constant fraction of algal production and is assumed to take place at any physiological conditions. The second term is assumed to be dependent on algal biomass and to be stimulated by internal nutrient deficiency. By using these assumptions, the model reproduced the concentrations and temporal evolution of toxins observed in cultures of Ostreopsis cf. ovata, a benthic/epiphytic dinoflagellate producing C-rich toxins named ovatoxins. The analysis of simulations and their comparison with experimental data provided a conceptual model linking toxin production and nutritional status in this species. The model was also qualitatively validated by using independent literature data, and the results indicate that our formulation can be also used to simulate toxin dynamics in other dinoflagellates. Our model represents an important step towards the simulation and prediction of marine algal toxicity.
HPB-surgeon to resect liver malignancies invading the hepatic veins/inferior vena cava. Single-center experience with ante-situm liver resection over the past 10 years is presented. Methods: Retrospective analysis on patients receiving ante situm liver resection comprising demographical and basic clinical data as well as perioperative courses. Results: Ante situm liver resection was performed on 7 patients suffering from primary (n=5) or secondary (n=2) liver tumors. Patients received trisegmentectomy (n=4), extended left hemihepatectomy (n=1) or atypical liver resection (segments 8/4a; n=2) combined with dissection of the suprahepatic vena cava/liver veins. Venous reconstruction was performed as reinsertion of liver veins (n=3) or vascular replacement with allogeneic donor veins (n=3) or PTFE-graft (n=1) in total vascular occlusion (mean of 29.6 min.). Severe morbidity defined as Dindo Clavien >3a was found in 3 patients; one patient died due to small-forsize syndrome. Mean length of stay at ICU and hospital were 9.0 and 34.3 days, respectively. R0-resection was achieved in 5 cases (twice a R1-situation). Disease-free survival was 24.6 months with an overall survival of 34.4 months. Conclusion: Ante situm liver resection offers the opportunity to achieve surgical cure in otherwise unresectable tumors. Nevertheless, this approach remains challenging with need for complex vascular reconstruction.
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