Pink (1/f) noise is one of the most common behaviours of biosystems. Our present paper is devoted to clarify the origin of this interesting phenomenon. It is shown that the stationary random stochastic processes under self-similar conditions (as we have in living objects) generate pink noise independently of the kind and number of variables.

The classical hyperthermia effect is based on well-focused energy absorption targeting the malignant tissue. The treatment temperature has been considered as the main technical parameter. There are discussions about the mechanism and control of the process because of some doubts about the micro-mechanisms. The main idea of the extracellular hyperthermia is to heat up the targeted tissue by means of electric field, keeping the energy absorption in the extracellular liquid. This produces a temperature gradient and connected heat flow through the cell membrane, which initializes numerous nonequilibrium thermal microprocesses to destroy the cell membrane. Furthermore, before the heat shock activates the intracellular heat shock protein (HSP) mechanisms, the cell membrane has been already compromised, therefore the HSP synthesis in the cells starts secondarily only after the membrane damage. The process could explain why the nonuniform and basically unsatisfactorily high temperature locoregional hyperthermia could be effective.

Comparison of thermal noise limits and the effects of low frequency electromagnetic fields (LFEMF) on the cellular membrane have important implications for the study of bioelectro-magnetism in this regime. Over a decade ago, Weaver and Astumian developed a model to show that thermal noise can limit the efficacy of LFEMF. A recent report by Kaune [Kaune (2002) Bioelectromagnetics 23:622-628], however, contradicted their findings. Kaune assumes that the conductance noise current of cell membrane can be decomposed into two components, where one of them is identical regarding all segments (coherent), while the other is different (incoherent). Besides, this decomposition is not unequivocal and contradicts to the statistical independence of the segment noise currents, and therefore to the second law of thermodynamics as well. We suggest the procedure based on the method of symmetrical components, by the means of which we can re-interpret the result of Kaune in a correct way.

We shall assume, of course, that the objective of hyperthermia is to destroy the malignant cells. Destruction definitely needs energy. Description and quality assurance of hyperthermia use the Pennes heat equation to describe the processes. However the energy balance of the Pennes-equation does not contain the hyperthermic cell-destruction energy, which is a mandatory factor of the process. We propose a generalization of the Pennes-equation, inducing the entire energy balance. The new paradigm could be a theoretical basis of the till now empirical dose-construction for oncological hyperthermia. The cell destruction is a non-equilibrium thermodynamical process, described by the equations of chemical reactions. The dynamic behavior (time dependence) has to be considered in this approach. We are going to define also a dose concept that can be objectively compared with other oncological methods. We show how such empirical dose as CEM43oC could be based theoretically as well.

No abstract

No abstract

We studied the homeostatic equilibrium of the healthy organism. The homeostasis is controlled by oppositely effective physiologic feedback signal-pairs in various timescales. We show the entropy of every signal in this state is identical and constant: SE = 1.8. The controlling physiological signals fluctuate around their average values. The fluctuation is time-fractal, (pink-noise), which characterizes the homeostasis. The aging is the degradation of the competing pairs of signals, decreasing the complexity of the organism. This way, the color of the noise gradually changes to brown. A special scaling process occurs during the aging: the exponent of the frequency dependence of the power density function grows in this process from 1 to 2, but the homeostasis of the system is unchanged.

Despite experimental evidence supporting ICR-like interactions in biological systems, to date there is no reasonable theoretical explanation for this phenomenon. The parametric resonance approach introduced by Lednev has enjoyed limited success in predicting the response as a function of the ratio of AC magnetic intensity to that of the DC field, explaining the results in terms of magnetically induced changes in the transition probability of calcium binding states. In the present work, we derive an expression for the velocity of a damped ion with arbitrary q/m under the influence of the Lorentz force. Series solutions to the differential equations reveal transient responses as well as resonance-like terms. One fascinating result is that the expressions for ionic drift velocity include a somewhat similar Bessel function dependence as was previously obtained for the transition probability in parametric resonance. However, in the present work, not only is there an explicit effect due to damping, but the previous Bessel dependence now occurs as a subset of a more general solution, including not only the magnetic field AC/DC ratio as an independent variable, but also the ratio of the cyclotronic frequency Omega to the applied AC frequency omega. In effect, this removes the necessity to explain the ICR interaction as stemming from ion-protein binding sites. We hypothesize that the selectively enhanced drift velocity predicted in this model can explain ICR-like phenomena as resulting from increased interaction probabilities in the vicinity of ion channel gates.