4 research outputs found
Coupling langmuir with michaelis-menten-a practical alternative to estimate se content in rice?
Selenium plays an important, but vastly neglected role in human nutrition with a narrow gap between dietary deficiency and toxicity. For a potential biofortification of food with Se, as well as for toxicity-risk assessment in sites contaminated by Se, modelling of local and global Se cycling is essential. As bioavailability of Se for rice plants depends on the speciation of Se and the resulting interactions with mineral surfaces as well as the interaction with Se uptake mechanisms in plants, resulting plant Se content is complex to model. Unfortunately, simple experimental models to estimate Se uptake into plants from substrates have been lacking. Therefore, a mass balance of Se transfer between lithosphere (represented by kaolinite), hydrosphere (represented by a controlled nutrient solution), and biosphere (represented by rice plants) has been established. In a controlled, closed, lab-scale system, rice plants were grown hydroponically in nutrient solution supplemented with 0–10000 μgL¯¹ Se of either selenite or selenite. Furthermore, in a series of batch experiments, adsorption and desorption were studied for selenite and selenite in competition with each of the major nutrient oxy-anions, nitrate, sulfate and phosphate. In a third step, the hydroponical plants experiments were coupled with sorption experiments to study synergy effects. These data were used to develop a mass balance fitting model of Se uptake and partitioning. Adsorption was well-described by Langmuir isotherms, despite competing anions, however, a certain percentage of Se always remained bio-unavailable to the plant. Uptake of selenite or selenite by transporters into the rice plant was fitted with the non-time differentiated Michaelis-Menten equation. Subsequent sequestration of Se to the shoot was better described using a substrate-inhibited variation of the Michaelis-Menten equation. These fitted parameters were then integrated into a mass balance model of Se transfer
Application methods of tracers for N₂O source determination lead to inhomogeneous distribution in field plots
Source determination of N₂O has often been performed using stable isotope incubation experiments. In situ experiments with isotopic tracers are an important next step. However, the challenge is to distribute the tracers in the field as homogeneously as possible. To examine this, a bromide solution was applied as a stand-in tracer using either a watering can, a sprayer, or syringes to a relatively dry (25% gravimetric moisture content) or wet (30%) silt loam. After 1 h, samples were taken from three soil depths (0-10 cm), and analyzed for their water content and bromide concentration. The application with syringes was unsuccessful due to blocked cannulas. Therefore, further laboratory experiments were conducted with side-port cannulas. Despite a larger calculated gravimetric soil moisture difference with watering can application, more Br- tracer was recovered in the sprayer treatment, probably due to faster transport of Br- through macropore flow in the wetter conditions caused by the watering can treatment. The losses of Br- (33% for the watering can, 28% for the sprayer treatment) are equivalent to potential losses of isotopic tracer solutions. For application of 60 at% ¹⁵NHΚ₄+, this resulted in theoretical enrichments of 44-53 at% in the upper 2.5 cm and 7-48 at% in 5-10 cm. As there was hardly any NO₃- in the soil, extrapolations for ¹⁵NO₃- calculated enrichments were 57-59 at% in the upper 2.5 cm and 26-57 at% in 5-10 cm. Overall, no method, including the side-port cannulas, was able to achieve a homogeneous distribution of the tracer. Future search for optimal tracer application should therefore investigate methods that utilize capillary forces and avoid overhead pressure. We recommend working on rather dry soil when applying tracers, as tracer recovery was larger here. Furthermore, larger amounts of tracer lead to more uniform distributions. Further studies should also investigate the importance of plant surfaces
VEGF-ablation therapy reduces drug delivery and therapeutic response in ECM-dense tumors.
The inadequate transport of drugs into the tumor tissue caused by its abnormal vasculature is a major obstacle to the treatment of cancer. Anti-vascular endothelial growth factor (anti-VEGF) drugs can cause phenotypic alteration and maturation of the tumor's vasculature. However, whether this consistently improves delivery and subsequent response to therapy is still controversial. Clinical results indicate that not all patients benefit from antiangiogenic treatment, necessitating the development of criteria to predict the effect of these agents in individual tumors. We demonstrate that, in anti-VEGF-refractory murine tumors, vascular changes after VEGF ablation result in reduced delivery leading to therapeutic failure. In these tumors, the impaired response after anti-VEGF treatment is directly linked to strong deposition of fibrillar extracellular matrix (ECM) components and high expression of lysyl oxidases. The resulting condensed, highly crosslinked ECM impeded drug permeation, protecting tumor cells from exposure to small-molecule drugs. The reduced vascular density after anti-VEGF treatment further decreased delivery in these tumors, an effect not compensated by the improved vessel quality. Pharmacological inhibition of lysyl oxidases improved drug delivery in various tumor models and reversed the negative effect of VEGF ablation on drug delivery and therapeutic response in anti-VEGF-resistant tumors. In conclusion, the vascular changes after anti-VEGF therapy can have a context-dependent negative impact on overall therapeutic efficacy. A determining factor is the tumor ECM, which strongly influences the effect of anti-VEGF therapy. Our results reveal the prospect to revert a possible negative effect and to potentiate responsiveness to antiangiogenic therapy by concomitantly targeting ECM-modifying enzymes.Oncogene advance online publication, 6 June 2016; doi:10.1038/onc.2016.182