Quantum Genetics and Quantum Automata Models of Quantum-Molecular Evolution Involved in the Evolution of Organisms and Species

Previous theoretical or general approaches to the problems of Quantum Genetics and Molecular Evolution are considered in this article from the point of view of Quantum Automata Theory first published by the author in 1971 and further developed in several recent articles. The representation of genomes and Interactome networks in categories of many-valued logic LMn –algebras that are naturally transformed during biological evolution, or evolve through interactions with the environment provide a new insight into the mechanisms of molecular evolution, as well as organismal evolution, in terms of sequences of quantum automata. Phenotypic changes are expressed only when certain environmentally-induced quantum-molecular changes are coupled with an internal re-structuring of major submodules of the genome and Interactome networks related to cell cycling and cell growth. Contrary to the commonly held view of `standard’ Darwinist models of evolution, the evolution of organisms and species occurs through coupled multi-molecular transformations induced not only by the environment but actually realized through internal re-organizations of genome and interactome networks. The biological, evolutionary processes involve certain epigenetic transformations that are responsible for phenotypic expression of the genome and Interactome transformations initiated at the quantum-molecular level. It can thus be said that only quantum genetics can provide correct explanations of evolutionary processes that are initiated at the quantum--multi-molecular levels and propagate to the higher levels of organismal and species evolution.

Biological evolution should be therefore regarded as a multi-scale process which is initiated by underlying quantum (coupled) multi-molecular transformations of the genomic and interactomic networks, followed by specific phenotypic transformations at the level of organism and the variable biogroupoids associated with the evolution of species which are essential to the survival of the species. The theoretical framework introduced in this article also paves the way to a Quantitative Biology approach to biological evolution at the quantum-molecular, as well as at the organismal and species levels. This is quite a substantial modification of the 'established’ modern Darwinist, and also of several so-called `molecular evolution’ theories

Quantum Genetics, Quantum Automata and Quantum Computation

The concepts of quantum automata and quantum computation are studied in the context of quantum genetics and genetic networks with nonlinear dynamics. In a previous publication (Baianu,1971a) the formal concept of quantum automaton was introduced and its possible implications for genetic and metabolic activities in living cells and organisms were considered. This was followed by a report on quantum and abstract, symbolic computation based on the theory of categories, functors and natural transformations (Baianu,1971b). The notions of topological semigroup, quantum automaton,or quantum computer, were then suggested with a view to their potential applications to the analogous simulation of biological systems, and especially genetic activities and nonlinear dynamics in genetic networks. Further, detailed studies of nonlinear dynamics in genetic networks were carried out in categories of n-valued, Lukasiewicz Logic Algebras that showed significant dissimilarities (Baianu, 1977) from Bolean models of human neural networks (McCullough and Pitts,1945). Molecular models in terms of categories, functors and natural transformations were then formulated for uni-molecular chemical transformations, multi-molecular chemical and biochemical transformations (Baianu, 1983,2004a). Previous applications of computer modeling, classical automata theory, and relational biology to molecular biology, oncogenesis and medicine were extensively reviewed and several important conclusions were reached regarding both the potential and limitations of the computation-assisted modeling of biological systems, and especially complex organisms such as Homo sapiens sapiens(Baianu,1987). Novel approaches to solving the realization problems of Relational Biology models in Complex System Biology are introduced in terms of natural transformations between functors of such molecular categories. Several applications of such natural transformations of functors were then presented to protein biosynthesis, embryogenesis and nuclear transplant experiments. Other possible realizations in Molecular Biology and Relational Biology of Organisms are here suggested in terms of quantum automata models of Quantum Genetics and Interactomics. Future developments of this novel approach are likely to also include: Fuzzy Relations in Biology and Epigenomics, Relational Biology modeling of Complex Immunological and Hormonal regulatory systems, n-categories and Topoi of Lukasiewicz Logic Algebras and Intuitionistic Logic (Heyting) Algebras for modeling nonlinear dynamics and cognitive processes in complex neural networks that are present in the human brain, as well as stochastic modeling of genetic networks in Lukasiewicz Logic Algebras

Frontiers in Pigment Cell and Melanoma Research

We identify emerging frontiers in clinical and basic research of melanocyte biology and its associated biomedical disciplines. We describe challenges and opportunities in clinical and basic research of normal and diseased melanocytes that impact current approaches to research in melanoma and the dermatological sciences. We focus on four themes: (1) clinical melanoma research, (2) basic melanoma research, (3) clinical dermatology, and (4) basic pigment cell research, with the goal of outlining current highlights, challenges, and frontiers associated with pigmentation and melanocyte biology. Significantly, this document encapsulates important advances in melanocyte and melanoma research including emerging frontiers in melanoma immunotherapy, medical and surgical oncology, dermatology, vitiligo, albinism, genomics and systems biology, epidemiology, pigment biophysics and chemistry, and evolution

Charge Transfer-oxy Radical Mechanism for Anti-cancer Agents

The proposal is advanced that anti-cancer drugs generally function by charge transfer resulting in formation of toxic oxy radicals which destroy the neoplasm. Electrochemical studies were performed with some of the main types of agents: iminium ions (adenine iminium from alkylating species, iminium metabolite of 6-mercaptopurine, nitidine, other polynuclear iminiums) and metal complexes (Pt(II)diaquodiammine-guanosine, copper salicylaldoximes). Reduction potentials ranged from -0.4 to -1.2 V. Literature data for quinones are presented and radiation is discussed. Based on the theoretical framework, a rationale is offered for the carcinogen-anti-cancer paradox and the role of antioxidants

Nonlinear Models of Neural and Genetic Network Dynamics:\ud \ud Natural Transformations of Łukasiewicz Logic LM-Algebras in a Łukasiewicz-Topos as Representations of Neural Network Development and Neoplastic Transformations \ud

A categorical and Łukasiewicz-Topos framework for Algebraic Logic models of nonlinear dynamics in complex functional systems such as Neural Networks, Cell Genome and Interactome Networks is introduced. Łukasiewicz Algebraic Logic models of both neural and genetic networks and signaling pathways in cells are formulated in terms of nonlinear dynamic systems with n-state components that allow for the generalization of previous logical models of both genetic activities and neural networks. An algebraic formulation of variable next-state/transfer functions is extended to a Łukasiewicz Topos with an N-valued Łukasiewicz Algebraic Logic subobject classifier description that represents non-random and nonlinear network activities as well as their transformations in developmental processes and carcinogenesis.\u

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

TGF-β signaling links E-cadherin loss to suppression of nucleotide excision repair.

E-cadherin is a cell adhesion molecule best known for its function in suppressing tumor progression and metastasis. Here we show that E-cadherin promotes nucleotide excision repair through positively regulating the expression of xeroderma pigmentosum complementation group C (XPC) and DNA damage-binding protein 1 (DDB1). Loss of E-cadherin activates the E2F4 and p130/107 transcription repressor complexes to suppress the transcription of both XPC and DDB1 through activating the transforming growth factor-β (TGF-β) pathway. Adding XPC or DDB1, or inhibiting the TGF-β pathway, increases the repair of ultraviolet (UV)-induced DNA damage in E-cadherin-inhibited cells. In the mouse skin and skin tumors, UVB radiation downregulates E-cadherin. In sun-associated premalignant and malignant skin neoplasia, E-cadherin is downregulated in association with reduced XPC and DDB1 levels. These findings demonstrate a crucial role of E-cadherin in efficient DNA repair of UV-induced DNA damage, identify a new link between epithelial adhesion and DNA repair and suggest a mechanistic link of early E-cadherin loss in tumor initiation