Theoretical Biology Forum最新文献

At present a wave of obscurantism is spreading over Western countries affecting both science and art in a deadly way. It becomes mandatory to stave off this movement by defining precisely the way science and art are created and to clarify the basic principles on which they are established. The scientific community has already reacted to this situation but the problem continues to be treated marginally. The reason may lie in the fact that modern technology has been most successful in transforming our daily lives and in allowing us to conquer outer space. These impressive achievements have, to a large extent, made us dumb, making it difficult to perceive the danger that lies ahead. Hence, there is a pressing need to bring forward the original sources in which, leading scientists and renowned artists, explained the principles that they followed in their discovery of novel phenomena and in the creation of unique works of art. It turns out that both types of minds speak the same language. There is a basic denominator that unites the human endeavour.

Cancer is still the growing global public health problem. There are many theories about carcinogenesis but none of them can explain carcinogenesis clearly. We have developed a cancer theory based on stem cells, chaos and adaptation ten years ago (Chaotic Adaptation Theory – CAT). Additionally, we think that, this theory is first Lamarckian view of carcinogenesis. In this article, we have revised CAT based on new literature findings.

In 1967 Lynn (Sagan) Margulis proposed that mitochondria, photosynthetic plastids and cilia were acquired prokaryotes and evolved symbiotically to form anaerobic bacteria, photosynthetic bacteria and eventually algae. Although most of this theory is well-accepted now, the hypothesis that endosymbiotic spirochaetes developed into eukaryotic flagella and cilia, and the following proposals of an endosymbiotic origin of other eukaryotic organelles such as peroxisomes, glyoxysomes, etc. have not received much acceptance, since evidence suggests they lack a genome and do not show ultrastructural similarities to bacteria or archaea. Nevertheless, the idea that over millennia mitochondria, plastids, prokaryotic and eukaryotic cells and even flagella and peroxisomes, as either primary or secondary endosymbionts, transferred some or all of their own DNA to the host cell’s nucleus through a process called «endogenosymbiosis» (i.e. a symbiotic gene transfer, such as the internalisation of the endosymbiont’s DNA with lateral transfer) has been recently suggested. This endogenosymbiosis could take place during the evolutionary transition from the symbiotic interacting community, invoked by Margulis, to a fully-integrated (either prokaryotic or eukaryotic) cell. This process could explain the missing evidence of the presence of DNA in flagella and peroxisomes whose ancestor endosymbionts, during the long endogenosymbiotic evolution, could have transferred their whole genome to the host cell that subsequently integrated it in its own genome, directly controlling its expression. Furthermore, the endogenosymbiosis hypothesis could be the explanation of the transition between an RNA to a DNA world and of some cases of true sympatric evolution of species, apparently inexplicable by the canonical speciation processes. Here, after an introduction to the theoretical basis of endogenosymbiosis and a discussion of the empirical confirming evidence, I show a graphical summary of the integration between this and the former endosymbiosis theories. The Serial Endosymbiosis Theory and the Secondary Endosymbiosis are merged with the Endogenosymbiosis Theory in a Unified Symbiogenetic Theory (UST).

The origin of life out of molecular disorder represents an extraordinary transition in the local fabric of the cosmos. The result can only be described by language that is imbued with echoes of purpose and agency. The «codescript» information stored in genes cannot be adequately understood in terms of Shannon’s syntactical measure. Biology requires a molecular-level explanation of the origin and maintenance of meaning, not just the emergence of functionally integrated nano-machinery. The highly ordered, autonomously maintained structure and functional organisation inside cells would be impossible without the precision afforded by information stored in read-only memory. Genetic information provides patterned boundary conditions that constrain the outcome of a biological system’s mechanically determined stochastic dynamics so that it is maintained in a continual state of self-construction. The evolution of genetic coding is the key to understanding how biological systems have reflexively embedded a representation of their own chemistry in DNA molecules. From the point of view of chemistry the genetic code is rule based, providing a map of very deep aspects of the physical phenomena an organism must control in order to exist. The map from genetic information onto functional molecular machinery that interprets genetic information reflects information onto its meaning and vice versa. It is the means whereby mechanical causation is commandeered and controlled by self-constructing semantic structures that unfold their own existence upon a material substrate.

Angiogenesis is a physiological process required for embryonic vascular development and involved in the pathophysiological progress of diseases such as atherosclerosis. In fact, hypoxia, ischemia and oxidative stress are common events in atherosclerotic plaque that stimulate angiogenesis, leading to the formation of a neovascularization in the intima of atherosclerotic lesions. The presence of these capillaries favours the progression of the plaque instability. Several studies indicate oxidized low-density lipoprotein (ox-LDL) and its endothelial receptor lectin-like oxidized low-density lipoprotein (LOX-1) as the major responsible for the occurrence and progression of atherosclerosis through apoptosis. At the same time, some authors showed that moderate concentrations of ox-LDL stimulate angiogenesis via LOX-1 activation of NADPH oxidase, MAPKs-NF-KB pathways and the generation of low levels of reactive oxygen species (ROS). Thyroid hormones have well documented effects on angiogenesis through genomic and non-genomic action and increased levels of ROS have been reported in hyperthyroidism. Moreover, by in vitro studies triiodothyronine (T3) and L-thyroxine (T4) significantly increased the intracellular ROS production based on the oxidation of 2',7'-dichloro dihydrofluorescein to a fluorescent 2',7'-dichlorofluoresein. Previous findings showed that ROS directly increase LOX-1 production in microvascular endothelial cells. New in vitro studies demonstrated the capability of T3 at supra-physiological doses to upregulate the LOX-1 expression in human microvascular endothelial cells. Thus, we can speculate the existence of a crosstalk between LOX-1-ROS and high levels of T3, suggesting that high levels of T3, as in hyperthyroidism, could cause a worsening of plaque vulnerability inducing angiogenesis.