arXiv subjects

Thomas M. Michelitsch

Publications and source records attributed to Thomas M. Michelitsch.

28 records · Page 2Linked to original sources

arXiv2019

Generalized space-time fractional dynamics in networks and lattices

We analyze generalized space-time fractional motions on undirected networks and lattices. The continuous-time random walk (CTRW) approach of Montroll and Weiss is employed to subordinate a space fractional walk to a generalization of the time-fractional Poisson renewal process. This process introduces a non-Markovian walk with long-time memory effects and fat-tailed characteristics in the waiting time density. We analyze `generalized space-time fractional diffusion' in the infinite $\it d$-dimensional integer lattice $\it \mathbb{Z}^d$. We obtain in the diffusion limit a `macroscopic' space-time fractional diffusion equation. Classical CTRW models such as with Laskin's fractional Poisson process and standard Poisson process which occur as special cases are also analyzed. The developed generalized space-time fractional CTRW model contains a four-dimensional parameter space and offers therefore a great flexibility to describe real-world situations in complex systems.

cond-mat.stat-mech↗

arXiv2018

The high osmotic pressure in a lens fiber as a driving force for the development of senile cortical cataract

In lens cataract, the clouding change in lens leads to a decline of transparency of part of the lens. There are three types of senile cataract: cortical cataract, nuclear cataract, and posterior/anterior sub-capsular cataract. The most common senile cataract is cortical cataract. For understanding cortical cataract, the pathology and the causing factors in cortical cataract are analyzed. The clouding change in senile cortical cataract begins from the edge of the lens and develops progressively to lens centre. The pathology of clouding change in cortical cataract is characterized by disruption of some lens fibers, swelling of some other fibers, and deposition of water between fibers. Based on the property of a lens fiber, we propose here a hypothesis on the mechanism of development of senile cortical cataract. I. Cortical cataract is triggered by disruption of a cortical lens fiber as a result of injury. The disrupted fiber will release water and crystallin proteins. II. Neighbor fibers can absorb this water due to high intracellular osmotic pressure (IOP) and become swollen. Swelling makes a fiber be stiff and have increased risk to disrupt when it is curved during the accommodation of the lens. These fibers will release water again when they disrupt, and the water will make more local fibers swelling. In this way, the local fibers become swollen and then disrupt successively. III. The successive swellings and disruptions of local fibers result in enlargement of a clouding change in lens. Since the fibers on the outer part of lens cortex have higher risk to be injured than that in the inner part, a clouding change starts from the edge of the lens. In conclusion, the progressive development of senile cortical cataract is a result of successive swellings and disruptions of local lens fibers, and this is driven by the high IOP in a lens fiber.

q-bio.TO↗

arXiv2017

Misrepair mechanism in the development of atherosclerotic plaques

Atherosclerosis is a disease characterized by the development of atherosclerotic plaques (APs) in arterial endothelium. The APs in part of an arterial wall are inhomogeneous on size and on distribution. In order to understand this in-homogeneity, the pathology of APs is analyzed by Misrepair mechanism, a mechanism proposed in our Misrepair-accumulation aging theory. I. In general, development of an AP is a result of repair of injured endothelium. Because of infusion and deposition of lipids beneath endothelial cells, the repair has to be achieved by altered remodeling of local endothelium. Such a repair is a Misrepair. During repair, smooth muscular cells (SMCs) are clustered and collagen fibers are produced to the lesion of endothelium for reconstructing an anchoring structure for endothelial cells and for forming a barrier to isolate the lipids. II. Altered remodeling (Misrepair) makes the local part of endothelium have increased damage-sensitivity and reduced repair-efficiency. Thus, this part of endothelium will have increased risk for injuries, lipid-infusion, and Misrepairs. Focalized accumulation of Misrepairs and focalized deposition of lipids result in development of a plaque. III. By a viscous circle between lipid-infusion and endothelium-Misrepair, growing of an AP is self-accelerating. Namely, once an AP develops, it grows in an increasing rate with time and it does not stop growing. Within part of an arterial wall, older APs grow faster than younger ones. The oldest and the biggest AP is the most threatening one in narrowing local vessel lumen. Therefore, the self-accelerated growing of an AP is a fatal factor in atherosclerosis. In conclusion, development of APs is focalized and self-accelerating, because it is a result of accumulation of Misrepairs of endothelium.

q-bio.TO↗

arXiv2017

Tissue fibrosis: a principal proof for the central role of Misrepair in aging

Tissue fibrosis is the phenomenon that a tissue has progressive deposition of collagen fibers with age. Tissue fibrosis is associated with aging of most of our organs, and it is the main pathology in arteriosclerosis, chronic bronchitis/emphysema, and benign prostatic hyperplasia. The causes and characteristics of fibrosis are analyzed with Misrepair mechanism, a mechanism proposed in Misrepair-accumulation aging theory. Tissue fibrosis is known to be a result of repairs of tissue by collagen fibers. A repair with collagen fibers is a manner of "Misrepair". The collagen fibers are used for replacing dead cells or disrupted extracellular matrixes (ECMs) including elastic fibers, myofibers, and basement membrane. The progressive tissue fibrosis with age manifests the essential role of Misrepair in aging, because it reveals three facts: A. a process of Misrepair exists; B. Misrepairs are unavoidable; and C. Misrepairs accumulate. As a result of accumulation of Misrepairs of tissue with collagen fibers, tissue fibrosis is focalized and self-accelerating, appearing as growing of spots of hyaline degeneration. Fibrosis results in stiffness or atrophy of an organ and progressive failure of the organ. In arteriosclerosis, the deposition of collagen fibers in arterial wall is for replacing disrupted elastic fibers or myofibers, however results in hardness of the wall. Wrinkle formation is part of skin fibrosis, and it may be a result of accumulation of collagen fibers of different lengths. Senile hair-loss and hair-whitening are probably consequence of dermal fibrosis. In conclusion, tissue fibrosis is a result of accumulation of Misrepairs of tissue with collagen fibers, and the phenomenon of fibrosis is a powerful proof for the central role of Misrepair in aging.

q-bio.TO↗

arXiv2017

Premature aging as a consequence of Mis-construction of tissues and organs during body development

Hutchinson-Gilford Progeria syndrome, Werner syndrome, and Cockayne syndrome are three genetic disorders, in which the children have premature aging features. To understand the phenomenon of premature aging, the similarity of aging features in these syndromes to that in normal aging is investigated. Although these three syndromes have different genetic backgrounds, all the patients have abnormal structures of tissues/organs like that in normal aging. Therefore, the abnormality in tissue structure is the common point in premature aging and normal aging. This abnormality links also a defective development and a defective repair, the Misrepair. Defective development is a result of Mis-construction of the structure of tissues and organs as consequence of genetic mutations. Aging is a result of Mis-reconstructions, the Misrepairs, for maintaining the structure of tissues/organs. Construction-reconstruction of the structure of an organism is thus the coupling point of development and aging. Mis- construction and Mis-reconstruction (Misrepair) are the essential processes for the development of aging-like feathers. In conclusion, premature aging is a result of Mis- construction of tissues and organs during body development as consequence of genetic disorders.

q-bio.TO↗

arXiv2017

Cell transformation in tumor-development: a result of accumulation of Misrepairs of DNA through many generations of cells

Development of a tumor is known to be a result of accumulation of DNA changes in somatic cells. However, the processes of how DNA changes are produced and how they accumulate in somatic cells are not clear. DNA changes include two types: point DNA mutations and chromosome changes. However, point DNA mutations (DNA mutations) are the main type of DNA changes that can remain and accumulate in cells. Severe DNA injuries are the causes for DNA mutations. However, Misrepair of DNA is an essential process for transforming a DNA injury into a survivable and inheritable DNA mutation. In somatic cells, Misrepair of DNA is the main source of DNA mutations. Since the surviving chance of a cell by Misrepair of DNA is low, accumulation of DNA mutations can take place only possibly in the cells that can proliferate. Tumors can only develop in the tissues that are regenerable. The accumulation of Misrepairs of DNA needs to proceed in many generations of cells, and cell transformation from a normal cell into a tumor cell is a slow and long process. However, once a cell is transformed especially when it is malignantly transformed, the deficiency of DNA repair and the rapid cell proliferation will accelerate the accumulation of DNA mutations. The process of accumulation of DNA mutations is actually the process of aging of a genome DNA. Repeated cell injuries and repeated cell regenerations are the two preconditions for tumor-development. For cancer prevention, a moderate and flexible living style is advised.

q-bio.TO↗

arXiv2017

Misrepair mechanism: a mechanism essential for individual adaptation, species adaptation and species evolution

In Misrepair-accumulation theory, we have proposed a Misrepair mechanism for interpreting aging. However, Misrepair mechanism is also important in biological adaptation. Misrepair is a strategy of repair for increasing the surviving chance of an organism when it suffers from severe injuries. As a surviving strategy, Misrepair mechanism plays also an important role in individual adaptation, species survival, and species differentiation. Firstly, Misrepair of an injury is one of the manners of individual adaptation; and Misrepair mechanism gives an organism a great potential in adapting to changeable and destructive environment. Secondly, Misrepair mechanism is important in maintaining and enlarging the diversity of genome DNAs of a species; and a large diversity of genome DNAs is essential for the adaptation and the differentiation of a species in different environments. On one hand, somatic Misrepairs are essential for maintaining the sufficient number of individuals in a species, which are the vectors of different genome DNAs. On the other hand, Misrepair of DNA is a source of DNA mutations and the DNA Misrepairs in germ cells may contribute to the diversity of genome DNAs in a species. In conclusion, Misrepair mechanism is a mechanism essential for individual adaptation, species adaptation, and species evolution.

q-bio.TO↗

arXiv2017

Misrepair accumulation theory: a theory for understanding aging, cancer development, longevity, and adaptation

Misrepair accumulation theory is a novel theory in interpreting aging phenomena. With a new concept of Misrepair, this theory reaches a unified understanding of aging: aging of an organism is a result of accumulation of Misrepairs of its structure. Misrepair accumulation theory (MA theory) is distinct and it can improve our understanding of life on several aspects. I. MA theory is fundamentally different from other theories by: A. proposing a generalized concept of Misrepair; B. pointing out the evolutionary advantage of aging mechanism; and C. distinguishing between aging of a cell and aging of a tissue. II. MA theory overcomes the limitations of traditional theories on interpreting the phenomena of tissue fibrosis and cancer development. Tissue fibrosis, as a result of accumulation of Misrepairs with collagen fibers, is a powerful evidence for demonstrating the central role of Misrepairs in aging. Cancer development is a result of accumulation of DNA Misrepairs in somatic cells, which needs to proceed over many generations of cells in a regenerable tissue. III. MA theory improves also our understanding on longevity, premature aging, adaptation, and species evolution. The potential of longevity of an organism is hidden in the complexity of its structure. IV. MA theory suggests that for retarding aging, the most important is to reduce the opportunity of damage-exposure.

q-bio.TO↗

arXiv2009

Relations de dispersion pour chaînes linéaires comportant des interactions harmoniques auto-similaires

Many systems in nature have arborescent and bifurcated structures such as trees, fern, snails, lungs, the blood vessel system, etc. and look self-similar over a wide range of scales. Which are the mechanical and dynamic properties that evolution has optimized by choosing self-similarity? How can we describe the mechanics of self-similar structures in the static and dynamic framework? Physical systems with self-similarity as a symmetry property require the introduction of non-local particle-particle interactions and a (quasi-) continuous distribution of mass. We construct self-similar functions and linear operators such as a self-similar variant of the Laplacian and of the D'Alembertian wave operator. The obtained self-similar linear wave equation describes the dynamics of a quasi-continuous linear chain of infinite length with a spatially self-similar distribution of nonlocal inter-particle springs. The self-similarity of the nonlocal harmonic particle-particle interactions results in a dispersion relation of the form of a Weierstrass-Mandelbrot function which exhibits self-similar and fractal features. We deduce a continuum approximation that links the self-similar Laplacian to fractional integrals and which yields in the low-frequency regime a power law frequency dependence for the oscillator density. For details of the present model we refer to our recent paper (Michelitsch et al., Phys. Rev. E 80, 011135 (2009)).

math-ph↗

arXiv2009

Dispersion Relations and Wave Operators in Self-Similar Quasi-Continuous Linear Chains

We construct self-similar functions and linear operators to deduce a self-similar variant of the Laplacian operator and of the D'Alembertian wave operator. The exigence of self-similarity as a symmetry property requires the introduction of non-local particle-particle interactions. We derive a self-similar linear wave operator describing the dynamics of a quasi-continuous linear chain of infinite length with a spatially self-similar distribution of nonlocal inter-particle springs. The self-similarity of the nonlocal harmonic particle-particle interactions results in a dispersion relation of the form of a Weierstrass-Mandelbrot function which exhibits self-similar and fractal features. We also derive a continuum approximation which relates the self-similar Laplacian to fractional integrals and yields in the low-frequency regime a power law frequency-dependence of the oscillator density.

math-ph↗