Chemotactic effects in reaction-diffusion equations for inflammation.

Predator-prey systems are used to model time-dependent virus and lymphocyte population during a liver infection and to discuss the influence of chemotactic behavior on the chronification tendency of such infections. Therefore, a model family of reaction-diffusion equations is presented, and the long-term behavior of the solutions is estimated by a critical value containing the reaction strength, the diffusion rate, and the extension of the liver domain. Fourier techniques are applied to evaluate the influence of chemotactic behavior of the immune response to the long-term behavior of locally linearized models.

Modeling the Chronification Tendency of Liver Infections as Evolutionary Advantage.

Here, we discuss how the tendency of a liver infection to chronify can be seen as an evolutionary advantage for infected individuals. For this purpose, we present a set of reaction-diffusion equations as a mathematical model of viral liver infections, which allows chronic and acute courses of the liver infection. We introduce a cumulative wealth function, and finally, we show that an immune response favoring the chronification is evolutionary advantageous at the same time.

LTP or LTD? Modeling the Influence of Stress on Synaptic Plasticity.

In cognitive memory, long-term potentiation (LTP) has been shown to occur when presynaptic and postsynaptic activities are highly correlated and glucocorticoid concentrations are in an optimal (i.e., low normal) range.

Genetics of metabolic resistance.

Herbicide resistance has become a major issue for many weeds. Metabolic resistance refers to the biochemical processes within organisms that degrade herbicides to less toxic compounds, resulting in a shift of the dose response curve. This type of resistance involves polygenic inheritance.

Modelling and analysis of a gene-regulatory feed-forward loop with basal expression of the second regulator.

Efficient adaptation strategies to changing environmental conditions are essential for bacteria to survive and grow. Fundamental restructuring of their metabolism is usually mediated by corresponding gene regulation. Here, often several different environmental stimuli have to be integrated into a reasonable, energy-efficient response.

Energy allocation between brain and body during ontogenetic development.

Objective: We here studied how energy is allocated between brain and body both during the ontogenetic development from a child to an adult and during weight loss.

Methods: We investigated 180 normal weight female and male children and adolescents (aged 6.1-19.

The corpulent phenotype-how the brain maximizes survival in stressful environments.

The reactivity of the stress system may change during the life course. In many-but not all-humans the stress reactivity decreases, once the individual is chronically exposed to a stressful and unsafe environment (e.g.

Multi-gene-loci inheritance in resistance modeling.

The ability of an organism to degrade harmful substances to less toxic compounds is referred to as metabolic resistance. The biochemical processes result in a shift of dose-response curves associated with the toxic substances. Hence, the development of metabolic resistance may cause great problems of managing pests and diseases by pesticides.

The brain's supply and demand in obesity.

During psychosocial stress, the brain demands extra energy from the body to satisfy its increased needs. For that purpose it uses a mechanism referred to as "cerebral insulin suppression" (CIS). Specifically, activation of the stress system suppresses insulin secretion from pancreatic beta-cells, and in this way energy-particularly glucose-is allocated to the brain rather than the periphery.

Effect of constitution on mass of individual organs and their association with metabolic rate in humans--a detailed view on allometric scaling.

Resting energy expenditure (REE)-power relationships result from multiple underlying factors including weight and height. In addition, detailed body composition, including fat free mass (FFM) and its components, skeletal muscle mass and internal organs with high metabolic rates (i.e.

The selfish brain: stress and eating behavior.

The brain occupies a special hierarchical position in human energy metabolism. If cerebral homeostasis is threatened, the brain behaves in a "selfish" manner by competing for energy resources with the body. Here we present a logistic approach, which is based on the principles of supply and demand known from economics.

Why doesn't the brain lose weight, when obese people diet?

Objective: As has been shown recently, obesity is associated with brain volume deficits. We here used an interventional study design to investigate whether the brain shrinks after caloric restriction in obesity. To elucidate mechanisms of neuroprotection we assessed brain-pull competence, i.

Stress and eating behavior.

How stress, the stress response, and the adaptation of the stress response influence our eating behavior is a central question in brain research and medicine. In this report, we highlight recent advances showing the close links between eating behavior, the stress system, and neurometabolism.

Systemic investigation of a brain-centered model of the human energy metabolism.

The regulation of the human energy metabolism is crucial to ensure the functionality of the entire organism. Deregulations may lead to severe pathologies such as diabetes mellitus and obesity. The decisive role of the brain as active controller and heavy consumer in the complex whole-body energy metabolism is the object of recent research.

Compact energy metabolism model: brain controlled energy supply.

The regulation of the energy metabolism is crucial to ensure the functionality of the entire organism. Deregulations may lead to severe pathologies such as obesity and type 2 diabetes mellitus. The decisive role of the brain as the active controller and heavy consumer in the complex whole body energy metabolism is the matter of recent research.

Unbuffered and buffered supply chains in human metabolism.

The investigation of very complex dynamical systems like the human metabolism requires the comprehension of important subsystems. The present paper deals with energy supply chains as subsystems of the metabolism on the molecular, cellular, and individual levels. We form a mathematical model of ordinary differential equations and we show fundamental properties by Fourier techniques.

Deductive functional assignment of elements in appetite regulation.

This paper presents a simple mathematical model for energy transport from the body into the brain and for appetite regulation. Particular properties in appetite regulation are deduced from the general observation of cyclic food intake. These particular properties are the importance of a push component, however small it may be, from the body into the brain, the dependence of the appetite activation on the energy supply level in the brain and a necessary condition for the sensitivity of this dependence.

Build-ups in the supply chain of the brain: on the neuroenergetic cause of obesity and type 2 diabetes mellitus.

Obesity and type 2 diabetes have become the major health problems in many industrialized countries. A few theoretical frameworks have been set up to derive the possible determinative cause of obesity. One concept views that food availability determines food intake, i.

Making sense of AMPA receptor trafficking by modeling molecular mechanisms of synaptic plasticity.

Synaptic plasticity involves a complex molecular machinery with various protein interactions but it is not yet clear how its components give rise to the different aspects of synaptic plasticity. Here we ask whether it is possible to mathematically model synaptic plasticity by making use of known substances only. We present a model of a multistable biochemical reaction system and use it to simulate the plasticity of synaptic transmission in long-term potentiation (LTP) or long-term depression (LTD) after repeated excitation of the synapse.