No Arabic abstract
The delayed luminescence of biological tissues is an ultraweak reemission of absorbed photons after exposure to external monochromatic or white light illumination. Recently, Wang, Bokkon, Dai and Antal (Brain Res. 2011) presented the first experimental proof of the existence of spontaneous ultraweak biophoton emission and visible light induced delayed ultraweak photon emission from in vitro freshly isolated rats whole eye, lens, vitreous humor and retina. Here, we suggest that the photobiophysical source of negative afterimage can also occur within the eye by delayed bioluminescent photons. In other words, when we stare at a colored (or white) image for few seconds, external photons can induce excited electronic states within different parts of the eye that is followed by a delayed reemission of absorbed photons for several seconds. Finally, these reemitted photons can be absorbed by nonbleached photoreceptors that produce a negative afterimage. Although this suggests the photobiophysical source of negative afterimages is related retinal mechanisms, cortical neurons have also essential contribution in the interpretation and modulation of negative afterimages.
In this paper we argue that, in addition to electrical and chemical signals propagating in the neurons of the brain, signal propagation takes place in the form of biophoton production. This statement is supported by recent experimental confirmation of photon guiding properties of a single neuron. We have investigated the interaction of mitochondrial biophotons with microtubules from a quantum mechanical point of view. Our theoretical analysis indicates that the interaction of biophotons and microtubules causes transitions/fluctuations of microtubules between coherent and incoherent states. A significant relationship between the fluctuation function of microtubules and alpha-EEG diagrams is elaborated on in this paper. We argue that the role of biophotons in the brain merits special attention.
In this paper we briefly discuss the necessity of using quantum mechanics as a fundamental theory applicable to some key functional aspects of biological systems. This is especially relevant to three important parts of a neuron in the human brain, namely the cell membrane, microtubules (MT) and ion channels. We argue that the recently published papers criticizing the use of quantum theory in these systems are not convincing.
We present the novel approach to mathematical modeling of information processes in biosystems. It explores the mathematical formalism and methodology of quantum theory, especially quantum measurement theory. This approach is known as {it quantum-like} and it should be distinguished from study of genuine quantum physical processes in biosystems (quantum biophysics, quantum cognition). It is based on quantum information representation of biosystems state and modeling its dynamics in the framework of theory of open quantum systems. This paper starts with the non-physicist friendly presentation of quantum measurement theory, from the original von Neumann formulation to modern theory of quantum instruments. Then, latter is applied to model combinations of cognitive effects and gene regulation of glucose/lactose metabolism in Escherichia coli bacterium. The most general construction of quantum instruments is based on the scheme of indirect measurement, in that measurement apparatus plays the role of the environment for a biosystem. The biological essence of this scheme is illustrated by quantum formalization of Helmholtz sensation-perception theory. Then we move to open systems dynamics and consider quantum master equation, with concentrating on quantum Markov processes. In this framework, we model functioning of biological functions such as psychological functions and epigenetic mutation.
Six thermo-activated transient receptor potential (TRP) channels are the molecular basis of the thermosensation for mammals. But the molecular source of their gating remains unknown. In the Letter, we suggest a physically based model for the TRP channels and show that the temperature dependence of the internal friction can be a key factor governing the ion channels gating. Results of the computer modeling allowed us to successfully reproduce the experimental data for the open probability Popen of the TRPV1 and TRPM8 channels at different temperatures and voltages.
In this work, we study the dynamic range in a neuronal network modelled by cellular automaton. We consider deterministic and non-deterministic rules to simulate electrical and chemical synapses. Chemical synapses have an intrinsic time-delay and are susceptible to parameter variations guided by learning Hebbian rules of behaviour. Our results show that chemical synapses can abruptly enhance sensibility of the neural network, a manifestation that can become even more predominant if learning rules of evolution are applied to the chemical synapses.