Theoretical Biology Forum最新文献

The speciation phenomenon is the process used by the evolution to allow populations to become distinct species. The speciation is the primary cause of the complexity of the ecological network. Sympatric speciation concerns the rise of a new species from a surviving ancestral species while both continue to inhabit the same ecological niche or geographical region. In sympatric speciation, reproductive isolation evolves within a population in an ecological niche without the aid of geographic barriers. Different models have been proposed for alternative modes of sympatric speciation. The most popular was first put forward by John Maynard Smith in 1966 who suggested that in a given population homozygous individuals may, under particular environmental conditions, have a greater fitness than those with alleles heterozygous for a certain trait, eventually leading to speciation in the population. In this framework we assume an effective description of the speciation process based on a dynamical model for the populations in an ecological system. Our basic assumption is the existence of an ancestral population in an ecological niche that can express two phenotypes. In presence of certain environmental conditions one of the phenotypes has the propensity to separate from the original population in the reproduction process. Then new individuals may give rise to a new species in the ecosystem realizing a sympatric speciation. Due to the finite resources in the niche the populations are continuously competing each other's, and their numerousness fluctuates according to the changes of the environmental conditions. The effect of natural selection is introduced in the model by stochastic perturbations, that decrease the reproduction rate of the populations in the niche. We show some the dynamical properties of the system and we prove the existence of a threshold values in the environmental stress in order to observe the speciation process. We also discuss some biological implications of the model and the validation problem using empirical data.

Aging is a natural, time-dependent process characterized by irreversible changes in the molecules, cells, tissues, and organs. It occurs as a result of cumulative damage at different levels of the organization, in particular by damaging proteins and DNA. There is no single definition, nor a unique attitude about when and how age arises and what are its causes. The process is extremely complex and most likely a consequence of the effects of different mechanisms (not only genetic but also acquired) that lead to disrupt homeostasis, reduce stress resistance and the more frequent occurrence of the disease. There are many classifications of theories about aging and they often contradict one another. No one theory is sufficiently able to explain the process of aging. The aim of this work is to analyze the different aspects, main characteristics of the aging, individual differences in the speed of this process and theories about the mechanisms of aging.

To date, classical deterministic Newtonian physics has been used by biologists to describe living processes. However, it is increasingly appreciated that the probabilistic view offered by quantum mechanics more accurately describes the behavior of atoms and materials in all systems. Here, we discuss how the concepts of quantum mechanics can be applied to biological processes involved in cancer. We present a concise summary inspired by Heisenberg's Uncertainty Principle to describe our «Genetic Environmental Field Hypothesis». Combining the uncertainties of genetic changes as expressed by epigenetic changes and/or somatic mutations with the uncertainties of environmental changes, cells may become cancerous as a way to increase entropy. Throughout the paper we will utilize the H19 gene system as an example. Using the concepts of quantum mechanics to describe oncological processes may provide novel directions in our understanding of cancer.

We use recent insights from evolutionary biology and the principle of biological relativity to reveal the remarkable parallels between forms of cooperation in biology, business and economics. The principle of biological relativity states that there is no privileged level of causation. The creation of higher levels of organisation and regulation constrains the components of co-operation in a form of downward causation. The upward and downward forms of causation are not equivalent. Downward causation is an organising principle arising from the ordered creation of the 'initial' and 'boundary' conditions experienced by the lower level components. But the existence of the lower level components is also the necessary condition for the creation of the higher-level constraints. Very similar processes are at work in corporations. The restrictions imposed by the legal form of the corporation bind investors to the provision of permanent capital in a similar way to that of fusion of organisms in biological processes, creating a form of symbiogenesis. The higher order conditions imposed on the agents of the firm provide an organising principle and the existence of the lower level agents is a necessary condition for the creation of the higher-level constraints. Furthermore, the process of entry into new business environments resembles that of symbiosis or symbiogenesis in that the interaction is asymmetric; the subsequent process is dynamic, resulting in super-additivity. The dynamic processes can create higher levels of organisation, such as new business models involving cooperation between businesses, corporations, regulators and governments. These in turn constrain the entities forming the new process.

We construct a mathematical model considering the populations of multiple predators and one prey, with herd defense by the prey modelled by modifying the law of mass action with a single parameter. This modification introduces a novel bifurcation in the case where all the predators are specialists. When some predators may be generalists, the analysis is more complicated and we consider only the case of two predators of which one or two may be generalists. In this case, novel steady states occur via saddlenode bifurcation, and in some cases the coexistence steady state exhibits Hopf bifurcation to a stable limit cycle. We show that the phenomenon of finite time extinction of prey also occurs in this context. Finally, we extend the analysis from constant herding effect to a model where predator pressure increases the strength of herding.

Several inflammatory factors have been determined as indicators of coronary artery disease (CAD) and recently some studies showed neutrophyl to lymphocyte ratio (NLR) as a powerful predictor. The aim of this study was to evaluate NLR, comparing it with the consolidate inflammatory and oxidative stress marker in a group of control and CAD patients. Twenty healthy subjects and 47 patients, that were affected by 1-4 compromised coronary arteries, were enrolled in the study. All subjects were classified into 3 groups on the base of NLR tertile. The efficacy of NLR as indicator of the severity of CAD and its association with inflammatory markers were analyzed. According to the tertile of NLR, patients in the high NLR value had higher % of males, number of compromise coronary arteries, CRP levels, neutrophyl count, and low lymphocyte count. Moreover NLR and CRP levels showed to be independent predictors of 3-4 compromised coronary arteries. The ROC curve analysis showed that CRP and NLR markers had the largest area under the curve (AUC = 0,85, 95% CI: 0,74-0,96, p = 0,000; AUC = 0,81, 95% CI: 0,66-0,96, p = 0,001). In conclusion our data indicate that only NLR and CRP are independent predictors for 3-4 compromised coronary arteries.

Serum angiopoietin-2 level is elevated in several diseases suggesting its possible role as a mediator of angiogenesis and vascular network remodeling. Triiodothyronine and thyroxine have well documented effects on angiogenesis in vitro, but only few reports have studied angiopoietin-2 in thyroid-disease patients. The aim of the present study was to measure soluble angiopoietin-2 serum levels in a group of thyroid-disease patients with different levels of free triiodothyronine and thyroxine. Angiopoietin- 2 were quantified by ELISA in sera of fifteen healthy volunteers and forty-two thyroid ambulatory patients: nine with hyperthyroidism, four in therapy for hyperthyroidism, seven with subclinal hyperthyroidism, twelve with hypothyroidism, five with thyroiditis and five in therapy for thyroiditis. Median angiopoietin-2 level was significantly elevated in hyperthyroid patients (p < 0.01) and it was significantly increased vs all the other groups (p < 0.0001). In hyperthyroid patients anti thyroid therapy seems to reduce angiopoietin-2 level. A significant positive correlation was observed between Log angiopoietin-2 levels and serum concentration of Log free triiodothyronine (r = 0.4, P < 0.001) and Log free thyroxine (r = 0.4, P < 0.001) respectively. In conclusion, increased levels of angiopoietin-2 are present in hyperthyroid patients, and seems to correlate with free triiodothyronine and free thyroxine levels but not with anti-thyroid antibodies. These findings suggest angiopoietin-2 as a mediator of angiogenesis and vascular network remodeling in this disease, but further studies will be needed to determine the role of this biomarker in the pathophysiology and progression of hyperthyroidism.