**4. Conclusions**

This is the first demonstration that SAB is present in PMN, a constituent cell of the human body. While SAB has been shown in human spermatozoa (Brugger, et. al., 2002), sperm cells are required to function in the world exterior to the body, while PMN are not.

The apparent strengthening of SAB in the long-legged forced-turn T-maze compared to the standard forced-turn maze, may be partially attributable to the higher n in the former and natural variation in data, but observation of hundreds of PMN in the maze environments suggests it might also result from a sort of practice effect of "frustrated" turn attempts in the channel, in a dose-response like paradigm. Length of time/distance spent in foiled attempts to turn may then serve as an order parameter. The persistence of SAB in this condition may also suggest multiple time scale, memory-like mechanisms operating in PMN.

There are, in fact, established physiological mechanisms and behavior that are consistent with this speculation and with my qualitative microscopic. PMNs are known to oscillate on multiple temporal and spatial scales, from 7sec, 70sec, and 260sec membrane potential fluctuations (Jäger, et al., 1988) and 25sec calcium flux oscillations, to the ~8sec G-F-actin oscillations (Marks and Maxfield, 1990), to 21.6sec and 230sec glycolytic cycles that produce NAD(P)H oscillations (Jäger, et al., 1988), and 10sec and 20sec pericellular proteolysis fluctuations (Marks and Maxfield, 1990), among many others. The time series in my recent study of PMN morphodynamics demonstrated scaling, board band power spectra with multiple resonances, suggesting a constellation of motility times (Selz, 2011). While there is debate over the specific fitness value(s) and mechanism(s) underlying SAB, it is clearly a phylogentically highly conserved behavior (Richman, et al.1986), and so, is assumed to be valuable. It follows that multiple mechanistically diverse time scales of function could be recruited to its service. This suggests the possibility of decentralized control in a highly interconnected, living dynamical system through local feedback. The necessary and sufficient conditions for a stable macro-system composed of multiple smaller systems operating on a variety of temporal and spatial scales are known in non-biological contexts (Ramakrishna and Viswanadham, 1982). Work is currently underway, adapting these constraints to a PMN model.

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Because, with the prior forced turn, systems statistically deviate from equiprobability in a later choice circumstance, SAB represents a reduction in population behavioral entropy, and a situation in which a reduction in the behavior degrees of freedom and reduced statistical behavioral entropy is favored evolutionarily. This finding is contrary to some findings of increased entropic states being associated with greater biological health and/or function (e.g. Mandell, 1987; Paulus et al., 1980).

#### **Author details**

Karen A. Selz *Franklin-Fetzer Laboratory, Cielo Institute, Asheville, NC, USA* 

#### **5. References**


constraints to a PMN model.

Mandell, 1987; Paulus et al., 1980).

*Franklin-Fetzer Laboratory, Cielo Institute, Asheville, NC, USA* 

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**Author details** 

Karen A. Selz

**5. References** 

325-8.

Springer.

There are, in fact, established physiological mechanisms and behavior that are consistent with this speculation and with my qualitative microscopic. PMNs are known to oscillate on multiple temporal and spatial scales, from 7sec, 70sec, and 260sec membrane potential fluctuations (Jäger, et al., 1988) and 25sec calcium flux oscillations, to the ~8sec G-F-actin oscillations (Marks and Maxfield, 1990), to 21.6sec and 230sec glycolytic cycles that produce NAD(P)H oscillations (Jäger, et al., 1988), and 10sec and 20sec pericellular proteolysis fluctuations (Marks and Maxfield, 1990), among many others. The time series in my recent study of PMN morphodynamics demonstrated scaling, board band power spectra with multiple resonances, suggesting a constellation of motility times (Selz, 2011). While there is debate over the specific fitness value(s) and mechanism(s) underlying SAB, it is clearly a phylogentically highly conserved behavior (Richman, et al.1986), and so, is assumed to be valuable. It follows that multiple mechanistically diverse time scales of function could be recruited to its service. This suggests the possibility of decentralized control in a highly interconnected, living dynamical system through local feedback. The necessary and sufficient conditions for a stable macro-system composed of multiple smaller systems operating on a variety of temporal and spatial scales are known in non-biological contexts (Ramakrishna and Viswanadham, 1982). Work is currently underway, adapting these

Because, with the prior forced turn, systems statistically deviate from equiprobability in a later choice circumstance, SAB represents a reduction in population behavioral entropy, and a situation in which a reduction in the behavior degrees of freedom and reduced statistical behavioral entropy is favored evolutionarily. This finding is contrary to some findings of increased entropic states being associated with greater biological health and/or function (e.g.

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Solomon RL. (1948). The influence of work on behavior. *Psychol Bull*;45:1–40.502; R.N. Hughes (2004)*Neuroscience and Biobehavioral Reviews* 28, 497–505

**Chapter 9** 

© 2012 Moschandreou, licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2012 Moschandreou, licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

and reproduction in any medium, provided the original work is properly cited.

**RBC-ATP Theory of Regulation for** 

It is known that red blood cells release ATP when blood oxygen tension decreases. ATP has an effect on microvascular endothelial cells to form a retrospective conducted vasodilation to the upstream arteriole. Local metabolic control of coronary blood flow due to vasodilation in microvascular units where myocardial oxygen extraction is relatively high occurs due to ATP.[5] Arterioles dilate or constrict in response to changing intravascular

"It is well known that myogenic responses, ow-dependent vasodilation, local metabolic effects, and propagation all contribute to blood ow regulation. Primarily responsible for carrying oxygen in blood, red blood cells (RBCs) may also act as oxygen sensors and thus play a role in the communication of metabolic demand" [3,7]. The mechanisms for release of ATP from the RBC in response to lowered oxygen saturation have been studied. [8]. Jagger et al. [9] measured the ATP release at low O2 levels in the presence and absence of CO to demonstrate that the release of ATP from RBCs may be connected to the change of the hemoglobin molecule from its relaxed state to its deoxygenated state. Upon release, ATP binds to P2Y purinergic receptors on the luminal surface of the endothelium, starting the conducted response [10].An in vitro microfluidic experimental study to investigate the dynamics of shear-induced ATP release from human RBCs with millisecond resolution was conducted by Wan et al. [11].Conclusively it was shown that there is a sizable delay time between the onset of increased shear stress and the release of ATP. "It was seen that this response time decreases with shear stress, but does not depend significantly on membrane rigidity. It was shown that even though the RBCs deform significantly in short constrictions

(duration of increased stress <3 ms), no measurable ATP is released."[11]

**Tissue Oxygenation-ATP** 

Additional information is available at the end of the chapter

**Concentration Model** 

Terry E. Moschandreou

http://dx.doi.org/10.5772/48580

**1. Introduction** 

pressure.[6]


**Chapter 9** 
