A general model for multiple substrate biodegradation, application to co-metabolisms of non structurally analogous compounds.

The availability of multiple carbon/energy sources, as is common in wastewater treatment plants, often enhances the biodegradation of recalcitrant compounds. In this paper, we classify and model different modes of multiple substrate utilization in a systematic way, using the concept of synthesizing unit. According to this concept, substrates can be substitutable or complementary; their uptake (or processing) can be sequential or parallel. We show how the different modes of multiple substrate interaction can be described by a single general model. From the general model, we derive simple expressions for co-metabolism of substrates that are not structurally analogous. Both the general and the specific co-metabolism model have the advantage that they can be used in combination with any microbial growth model. To test the co-metabolism model's realism, we confront it with experimental data. The results attained with the co-metabolism model support that the general model constitutes a useful framework for modeling aspects of multiple substrate utilization. © 2003 Elsevier Ltd. All rights reserved

Correction: A DHODH inhibitor increases p53 synthesis and enhances tumor cell killing by p53 degradation blockage (Nature Communications (2018) DOI: 10.1038/s41467-018-03441-3)

10.1038/s41467-018-04198-5Nature Communications91207

A DHODH inhibitor increases p53 synthesis and enhances tumor cell killing by p53 degradation blockage

10.1038/s41467-018-03441-3Nature Communications91110

A mathematical model that accounts for the effects of caloric restriction on body weight and longevity.

Several aspects of energy dynamics, such as energy expenditure and caloric intake, are known to affect the aging process. In this article we therefore model the aging process within a mathematical framework describing the energy dynamics of an organism. The resulting model comprises food intake, body growth and survival. The equation for the mortality rate accounts for food consumption and is suited to describe caloric restriction data. For non-growing animals, the expression for the mortality rate reduces to the well-known Gompertz equation. We successfully applied our model to growth and survival data on mice exposed to different food levels

Modelling microbial adaptation to changing availability of substrates.

In their natural environment microorganisms encounter changes in substrate availability, involving either nutrient concentrations or nutrient types. They have to adapt to the new conditions in order to survive. We present a model for slow microbial adaptation, involving the synthesis of new enzymes, in response to changes in the availability of substitutable substrates. The model is based on reciprocal (or mutual) inhibition of expression of both the substrate-specific carriers and the associated assimilatory machinery. The inhibition kinetics is derived from the kinetics of synthesizing units. An interesting property of the adaptation model is that the presence of a single limiting resource results in a constant maximum specific substrate consumption rate for fully adapted microorganisms. Because the maximum specific consumption rate is not a function of substrate concentration, for growth on one substrate, the Monod and Pirt models for instance are still valid. Other adaptation models known to us do not fulfil this property. The simplest version of our model describes adaptation during diauxic growth, using only one preference parameter and one initial condition. The applicability of the model is exemplified by fitting it to published data from diauxic growth experiments. © 2003 Elsevier Ltd. All rights reserved

Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib

10.1371/journal.pone.0195956PLoS ONE134e019595