Critical role of intracellular temperature

[Diokine]

People familiar with Dr. Peat and Dr. Ling's work shouldn't be as confused by common understanding of biological membranes. Commonly accepted understanding has obvious flaws, though a description of the physical structure of these fatty membranes is still relevant. These membranes can serve as mediators of signal transduction. Signals imply cause and effect, transduction conveys the physical medium of signal propagation and modification. Consider signals of excitation, relaxation, digestion, mitosis, differentiation. The common understanding of signal propagation through nerves relies on an electrical mechanism, mediated by ion concentration, charge gradients, and action potential. This understanding is useful, but incomplete. A more complete understanding of the physical processes includes the action of acoustic waves, which can exhibit very interesting effects.

A Comparison of the Hodgkin–Huxley Model and the Soliton Theory for the Action Potential in Nerves

“At physiological temperatures, the state of the biological membranes is fluid. The melting transition is linked to changes in enthalpy, entropy, but also to changes in volume, area, and thickness. This implies that the state of the membrane can be influenced not only by temperature but also by hydrostatic pressure and lateral pressure in the membrane plane. Due to the fluctuation–dissipation theorem, the fluctuations in enthalpy, volume, and area in the transition are at a maximum. Therefore, the heat capacity and the volume compressibility all reach maxima. Simultaneously, the relaxation timescale reaches a maximum. This implies that the lateral compression of a fluid membrane leads to an increase in compressibility. This effect is known as a nonlinearity. From experiment, it is known that the compressibility is also frequency dependent, an effect that is known as dispersion. These two phenomena are necessary conditions for the propagation of solitons. It can be shown that the features of lipid membranes slightly above a transition are sufficient to allow the propagation of mechanical solitons along membrane cylinders [21]. The solitons consist of a reversible compression of the membrane that is linked to a reversible release of heat, mechanical changes in the membrane. Furthermore, the soliton model also implies a mechanism for anesthesia that lies in the well-understood influence that anesthetics have on the lipid phase transition [38].”

​

These solitons offer the capacity for many more dimensions of encoding and complexity in signal propagation. This above statement also implies a critical role in the temperature of the spaces around cells and nerves. It is conceivable to imagine that this temperature is actually one of the most critically controlled variables in physiology, and is the determining factor in deciding outputs of various control mechanisms.

What are some of the factors influencing this temperature? The rate of blood delivery, the amount of oxygen present in the blood, and the amount of phosphorus in tissues appear to be the biggest factors. What effect does temperature have on the actions of the blood?

 

[Diokine]

Could misfolded low-complexity autocatalytic protein complexes (ie pathological prions) be sustained by critically low temperatures in tissue spaces?



Or. does a critical reduction of natural temperature swings in tissue lead to conditions that tend to generate pathological protein complexes?



Prion proteins exhibit substantial shifts in heat capacity and enthalpy upon conformational change.



//


Temperature-Dependent Structural Variability of Prion Protein Amyloid Fibrils

Heat stability of prion rods and recombinant prion protein in water, lipid and lipid–water mixtures

Thermostability as a highly dependent prion strain feature

Thermodynamic Characterization of the Unfolding of the Prion Protein