Generalized Communicating P Systems Working in Fair Sequential Model

In this article we consider a new derivation mode for generalized communicating P systems (GCPS) corresponding to the functioning of population protocols (PP) and based on the sequential derivation mode and a fairness condition. We show that PP can be seen as a particular variant of GCPS. We also consider a particular stochastic evolution satisfying the fairness condition and obtain that it corresponds to the run of a Gillespie's SSA. This permits to further describe the dynamics of GCPS by a system of ODEs when the population size goes to the infinity.Comment: Presented at MeCBIC 201

Minimization Strategies for Maximally Parallel Multiset Rewriting Systems

Maximally parallel multiset rewriting systems (MPMRS) give a convenient way to express relations between unstructured objects. The functioning of various computational devices may be expressed in terms of MPMRS (e.g., register machines and many variants of P systems). In particular, this means that MPMRS are computationally complete; however, a direct translation leads to quite a big number of rules. Like for other classes of computationally complete devices, there is a challenge to find a universal system having the smallest number of rules. In this article we present different rule minimization strategies for MPMRS based on encodings and structural transformations. We apply these strategies to the translation of a small universal register machine (Korec, 1996) and we show that there exists a universal MPMRS with 23 rules. Since MPMRS are identical to a restricted variant of P systems with antiport rules, the results we obtained improve previously known results on the number of rules for those systems.Comment: This article is an improved version of [1

Method of Construction of Specialized Algorithms for Solving Differential Equations

Considered the problem of optimization of the process of constructing specialized algorithms for the given form nonlinear ordinary differential equations systems’ numerical solution. The problem is reduced to the determination and use of approximating representations of the numerical integration errors by the chosen basic metho

(Tissue) P Systems with Vesicles of Multisets

We consider tissue P systems working on vesicles of multisets with the very simple operations of insertion, deletion, and substitution of single objects. With the whole multiset being enclosed in a vesicle, sending it to a target cell can be indicated in those simple rules working on the multiset. As derivation modes we consider the sequential mode, where exactly one rule is applied in a derivation step, and the set maximal mode, where in each derivation step a non-extendable set of rules is applied. With the set maximal mode, computational completeness can already be obtained with tissue P systems having a tree structure, whereas tissue P systems even with an arbitrary communication structure are not computationally complete when working in the sequential mode. Adding polarizations (-1, 0, 1 are sufficient) allows for obtaining computational completeness even for tissue P systems working in the sequential mode.Comment: In Proceedings AFL 2017, arXiv:1708.0622

A Note on the Probabilistic Evolution for P Systems

In this note we propose a method that permits to describe in a uniform man- ner variants of probabilistic/stochastic P systems. We give examples of such a description for existing models of P systems using probabilities

Second Buckingham-effect virial coeffcients of non-dipolar molecules

Master of Science in physics in the School of Chemistry and Physics,University of KwaZulu-Natal .Pietermaritzburg campus,2019.A molecular-tensor theory of the second electric-field-gradient-induced birefringence (EFGIB) virial coeffcient BQ, which describes the effects of molecular pair interactions on the molar Buckingham constant mQ, is developed for non-dipolar molecules with axial and higher symmetry. The resulting expressions for contributions to BQ are evaluated numerically for the molecules CO2, C2H4 and C2H6. These molecules were chosen since previously developed molecular-tensor theories of the second light-scattering virial coeffcient Bp and the second Kerr-effect virial coeffcient BK have yielded calculated values for these species which are in close agreement with the available measured data. The BQ values calculated for CO2, C2H4 and C2H6 reveal that, for the uids behaving as gases, the pair-interaction contributions to mQ are generally at or below the threshold of resolution of the EFGIB apparatus, so that the measured mQ values reported in the literature have not been contaminated by pair-interaction effects. In addition, it is seen that if the precision of measured mQ data can be increased by around an order of magnitude, it should in principle become possible to resolve BQ contributions, particularly for higher gas densities

Enrollment in Kansas high school subjects with special emphasis on social science

Call number: LD2668 .R4 1955 S53

The Role of Cardiotrophin-Like Cytokine Factor 1 on the Development of Atherosclerosis

Le syndrome métabolique représente un problème majeur de la santé publique mondiale ; le taux augmente constamment en dépit de la technologie médicale innovante et des avancées thérapeutiques. Les maladies cardiovasculaires associées à la dyslipidémie demeurent la principale cause de décès et de morbidité à l'échelle mondiale en dépit d'une vaste recherche médicale et d'un large éventail de médicaments ciblant l'athérosclérose, l'obésité, le diabète, et autres. Des recherches récentes suggèrent l'existence et la persistance d'une inflammation de faible intensité dans la pathogenèse des pathologies comme l'athérosclérose et l'obésité. La « symbiose » entre le système métabolique et le système immunitaire est substantielle et toute perturbation contribue au développement des conditions métaboliques altérées qui aboutissent finalement à des troubles tels que l'obésité et l'athérosclérose. L'objectif général de ma maîtrise était de caractériser l'effet de la cardiotrophin-like cytokine factor 1 sur le développement de l'athérosclérose et de valider le dérivé de cardiotrophin-like cytokine factor 1 couplé avec le fragment Fc de l’immunoglobuline G qui possède une longue durée de vie. Cardiotrophin-like cytokine factor 1 est une cytokine du système immunitaire avec activité immunorégulatrice. Cardiotrophin-like cytokine factor 1 appartient à la famille d’interleukine 6. Cardiotrophin-like cytokine factor 1 est efficacement sécrétée en présence de cytokine receptor like factor 1, un récepteur soluble de la cytokine. Cardiotrophin-like cytokine factor 1 possède des activités neurotrophiques médiées par le récepteur du ciliary neurotrophic factor. Cardiotrophin-like cytokine factor 1 est également un ligand à haute affinité pour la sortiline. Des variantes du gène Sort1 codant pour ce récepteur ont été associés à l’hyperlipidémie et au risque d’infarctus du myocarde dans plusieurs études d’associations génomiques. Il a été observé que la cardiotrophin-like cytokine factor 1 lie et active les transfectants co-expriment de la sortiline et récepteur du leukemia inhibitory factor. Les deux récepteurs sont exprimés par les cellules myéloïdes et le récepteur du leukemia inhibitory factor est un puissant inducteur de la polarisation des macrophages de type M2 (anti-inflammatoire). L'objectif général du projet était d'étudier si la cardiotrophin-like cytokine factor 1 ou la cardiotrophin-like cytokine factor 1 couplée avec le fragment Fc interagiraient avec des macrophages des plaques d’athéroscléroses et réduirait la formation de cellules spumeuses et le développement de la plaque. Nos travaux montrent que l'expression de cardiotrophin-like cytokine factor 1 dans le modèle murin d’athérosclérose LDLR-/- ne diminue pas le développement de la plaque. Cependant, certains résultats ont révélé une contribution significative de la cardiotrophin-like cytokine factor 1 dans le gain de masse corporelle sans modification de l'apport calorique.Metabolic syndrome represents a major global health problem. Its rate is constantly increasing. Cardiovascular diseases emerging from dyslipidemia conditions are a worldwide leading cause of death and morbidity, despite extensive medical research and wide range of drugs targeting atherosclerosis, obesity, diabetes etc. Recent findings suggest the existence and persistence of low-grade inflammation in pathogenesis atherosclerosis and obesity. The “symbiosis” between metabolic and immune system is substantial and any perturbation contribute to the development of altered metabolic conditions that ultimately culminate in such disorders as obesity and atherosclerosis. The overall goal of my Master internship was to characterise the effect of cardiotrophin-like cytokine factor 1 on development of atherosclerosis and validate a long half-life derivative of cardiotrophin-like cytokine factor 1 coupled with Fc fragment of immunolglobulin G. Cardiotrophin-like cytokine factor 1 is a cytokine of the immune system with immunoregulatory activity. Cardiotrophin-like cytokine factor 1 belongs to the interleukin 6 family of monomeric cytokines. Cardiotrophin-like cytokine factor 1 is efficiently secreted in the presence of cytokine receptor like factor 1, a soluble cytokine receptor. Cardiotrophin-like cytokine 1 possesses neurotrophic activities mediated through the receptor of ciliary neurotrophic factor. Cardiotrophin-like cytokine factor 1 is a high affinity ligand for sortilin. Genome-wide association studies indicated that plasma low-density lipoprotein cholesterol levels and cardiovascular disease are associated with single nucleotide polymorphisms variants regulating sortilin expression. It was observed that cardiotrophin-like cytokine factor 1 binds and activates transfectants co-expressing sortilin and receptor of leukemia inhibitory factor. Both receptors are expressed by myeloid cells and leukemia inhibitory factor is a potent inducer of anti-inflammatory M2 macrophage differentiation. The overall objective was to investigate if the interaction of cardiotrophin-like cytokine factor 1 or cardiotrophin-like cytokine factor 1 coupled with Fc fragment of immunoglobulin G with atherosclerotic plaque macrophages will reduce the foam cell formation and development of plaque. Our work shows that cardiotrophin-like cytokine 1 expression in mice on LDLR-/- atherosclerosis model does not decrease the development of plaque. However, some results revealed a significant contribution of cardiotrophin-like cytokine factor 1 in gain of body mass without changes in food intake