Eglė Meškauskaitė. Cognitive maturity for school of preschool-aged children with defective sight in the context of integrated education. Scientific adviser: prof. habil.dr. Vytautas Gudonis. Vilnius Pedagogical University, Faculty of Pedagogy and Psychology, Department of Pedagogy, Branch of special education. – Vilnius, 2005. In order to determine cognitive maturity for school of preschool-aged children with defective sight in the context of integrated education 50 children with defective sight from the kindergartens of Kaunas and Vilnius, in respect of whom integrated education is applied, and 50 children with good sight from the kindergartens of Kaunas, Kulautuva and Raudondvaris have been examined. The research is based on a questionnaire which has been developed in accordance with the “General Programmes and Education Standards. Preschool Education” (2003). The data processing has revealed that the maturity of children with defective sight for school in the context of having an interest in the self, the own body, adults, knowledge of the close natural environment and the world, performance of practical tasks is not only lower than the one of children with good sight, but even higher. No differences between children with good sight and children with defective sight have been established as regards other principal capacities connected with children’s cognitive maturity for school, as set out in the general programmes and education standards. It has been established that... [to full text]

Rapid evolution of RNA viruses with mRNA-sense genomes is a major concern to health and economic welfare due to the devastating diseases these viruses inflict on humans, animals and plants. Rapid viral RNA evolution is frequently due to RNA recombination, which can be facilitated by recombination signals present in viral RNAs. Among such signals are short sequences with high AU contents that constitute recombination hot spots in Brome mosaic virus (BMV) and retroviruses. We have demonstrated that a defective interfering (DI) RNA, a model template associated with Tomato bushy stunt virus (TBSV), a tombusvirus, undergoes frequent recombination in plants and protoplast cells when it carries the AU-rich hot spot sequence from BMV. Similar to the situation with BMV, most of the recombination junction sites in the DI RNA recombinants were found within the AU-rich region. Our results support the idea that common AU-rich recombination signals might promote interviral recombination between unrelated viruses. To test if host genes can affect the evolution of RNA viruses, we used a Saccharomyces cerevisiae single-gene deletion library, which includes ~80% of yeast genes, in RNA recombination studies based on a small viral replicon RNA derived from TBSV. The genome-wide screen led to the identification of five host genes, whose absence resulted in rapid generation of novel viral RNA recombinants. Thus, these genes normally suppress viral RNA recombination, but in their absence hosts become viral recombination hotbeds. Four of the five recombination suppressor genes are likely involved in RNA degradation, suggesting that RNA degradation could play a role in viral RNA recombination. Overall, our results demonstrate for the first time that a set of host genes have major effect on RNA virus recombination and evolution. Replication of the non-segmented, plus-stranded RNA genome of Cucumber necrosis tombusvirus (CNV) requires two essential overlapping viral-coded replication proteins, the p33 replication co-factor and the p92 RNA-dependent RNA polymerase. We have demonstrated that p33 is phosphorylated in vivo and in vitro by a membrane-bound plant kinase. Based on in vitro studies with purified recombinant p33, we show evidence for phosphorylation of threonine and serine residues adjacent to the essential RNA-binding site in p33. Our findings suggest that phosphorylation of threonine/serine residues adjacent to the essential RNA-binding site in the auxiliary p33 protein likely plays a role in viral RNA replication and subgenomic RNA synthesis during tombusvirus infections.

A valuable analytical tool to understand the event of ruin is a Gerber-Shiu discounted penalty function. It acts as a unified means of identifying ruin-related quantities which may help insurers understand their vulnerability ruin. This thesis provides an introduction to the basic concepts and common techniques used for the Gerber-Shiu analysis. Chapter 1 introduces the insurer's surplus process in the ordinary Sparre Andersen model. Defective renewal equations, the Dickson-Hipp transform, and Lundberg's fundamental equation are reviewed. Chapter 2 introduces the classical Gerber-Shiu discounted penalty function. Two framework equations are derived by conditioning on the first drop in surplus below its initial value, and by conditioning on the time and amount of the first claim. A detailed discussion is provided for each of these conditioning arguments. The classical Poisson model (where interclaim times are exponentially distributed) is then considered. We also consider when claim sizes are exponentially distributed. Chapter 3 introduces the Gerber-Shiu function in the delayed renewal model which allows the time until the first claim to be distributed differently than subsequent interclaim times. We determine a functional relationship between the Gerber-Shiu function in the ordinary Sparre Andersen model and the Gerber-Shiu function in the delayed model for a class of first interclaim time densities which includes the equilibrium density for the stationary renewal model, and the exponential density. To conclude, Chapter 4 introduces a generalized Gerber-Shiu function where the penalty function includes two additional random variables: the minimum surplus level before ruin, and the surplus immediately after the claim before the claim causing ruin. This generalized Gerber-Shiu function allows for the study of random variables which otherwise could not be studied using the classical definition of the function. Additionally, it is assumed that the size of a claim is dependant on the interclaim time that precedes it. As is done in Chapter 2, a detailed discussion of each of the two conditioning arguments is provided. Using the uniqueness property of Laplace transforms, the form of joint defective discounted densities of interest are determined. The classical Poisson model and the exponential claim size assumption is also revisited.

RNA:protein interactions are central in many cellular processes, including activation of innate immune responses against microbial infection. Their study is essential to better understand the diverse biological events that occur within cells. However, isolation of RNA:protein complexes is often laborious and requires specialized techniques. This thesis is concerned with attempts to develop an improved purification protocol to isolate specific RNA:protein complexes. Taking advantage of the specific interaction of the Pseudomonas aeruginosa PP7 protein with its cognate RNA binding site, termed the PP7 recognition sequence (PRS), the aim was to identify cellular proteins involved in activating cell-signalling pathways, including the interferon-induction cascade, following viral infection with stocks of parainfluenza virus 5 (PIV5) rich in copyback defective interfering (DI) particles. Copyback DI genomes are powerful inducers of IFN and, here, I show they also activate the induction of IL-6, IL-8 and TNFα; cytokines that also have antiviral properties. Following the successful cloning of the PRS into a copyback DI genome, we investigated conditions for optimal in vitro capture of DI-PRS:protein complexes by PP7 on Dynabeads. When tested, the protocol led to the successful capture of ILF3 and PKR, two dsRNA binding proteins induced by IFN. We further developed a tap-tagging system to minimize the presence of non-specifically bound proteins to Dynabeads that may interfere with future mass spectrometry analysis. To isolate DI-PRS RNA:protein complexes from infected cells, attempts were made to rescue replicating DI-PRS genomes in the context of wild type PIV5. Similarly, efforts were made to isolate influenza A virus RNPs that contained the PRS in the neuraminidase (NA) gene from infected cells using the PP7-based protocol developed. However, for reasons discussed, unfortunately RNA:proteins complexes were not successfully purified from infected cells in either case.

Avec le développement de l’économie mondiale et du libre-échange dans le commerce, les consommateurs disposent de tout ce dont ils ont besoin et envie dans la société de consommation. Ils sont face à des produits surs et d'autres qui le sont moins. Les exigences des consommateurs portent non seulement sur la conformité des produits, mais également sur leur sécurité. C’est pourquoi, en Europe comme aux Etats Unis, il existe des lois spéciales pour encadrer la responsabilité des produits défectueux. L’analyse de l’approche Euro-Américaine dans le droit des produits défectueux, objet de cette thèse, permet non seulement d’aborder le régime dans ce domaine actuellement, mais également d’amener à une réflexion sur une protection plus efficace des consommateurs. / With the development of the world economy and the international trade, consumers find their pleasures in this consumer society and also insecurities sometimes. Consumer requirements do not only rely on compliance but also product safety. This is why in both Europe and the United States, there are special laws in product liability. This thesis based in the comparison of European and American laws of defect products, not only analyze the system in this area currently, but also to reflect on a more effective protection for consumers.

We consider a two-level supply chain involving a manufacturer and a retailer who serves as the quality gatekeeper. The manufacturer determines a wholesale price and a defective rate and announces his decisions to the retailer, who then makes her decisions on the retail price and identification rate that means the percent- age of the defects identified by the retailer and reflects the retailer’s gatekeeping effort on her quality assurance. We accordingly develop a leader-follower game and solve it to find Stackelberg equilibrium for the manufacturer and the retailer. In order to examine whether or not the supply chain benefits from the retailer's quality gatekeeping effort, we also develop and solve another leader-follower game where the manufacturer still announces its wholesale pricing and defective rate decisions but the retailer only decides on the retail price. We show that the manufacturer’s equilibrium defective rate for the game with the retailers gate-keeping is higher than that for the game without the retailer’s gatekeeping. The ratio of the manufacturers profit to the retailer’s profit is increased when the retailer serves as the gatekeeper. Moreover, the retailer reduces her price when she acts as the gatekeeper, if and only if the supply chain-wide cost decreases as a result of the retailer’s gatekeeping effort. We also perform sensitivity analysis of each parameter in our game models to further examine the impacts of the retailer’s gatekeeping on the manufacturer’s and the retailer’s decisions and profits. We find that the retailer’s penalty cost per defect has more significant impacts than the manufacturer’s unit penalty cost. The paper ends with a summary of managerial insights.

Leguminous plants are able to fix nitrogen by establishing a symbiotic relationship with soil dwelling bacteria, called rhizobia. The model plant Medicago truncatula forms a partnership with Sinorhizobium meliloti whereby the plant gains bioavailable nitrogen and in exchange the bacteria gains carbohydrates. This process occurs within nodules, which are structures produced on the roots of the plants within which nitrogen is fixed. M. truncatula incomplete root elongation (MtIRE) was localized to the infection zone, which is zone II of indeterminate nodules. It was shown to encode a signaling kinase so it was anticipated to play a role in nodulation. Mutants of MtIRE in the R108 background, mutagenized with the Tnt1 retrotransposon, were obtained from reverse screen, and were assessed to determine if a disrupted MtIRE gene was the cause of nitrogen fixation defective nodules. Mutant line NF1320, having a mutant phenotype, showed typical Mendelian segregation of 3:1 when backcrossed to R108. Experimental results show that MtIRE gene is not the cause of the mutant phenotype, but was linked to the causative locus. MtIRE co-segregated with the mutant phenotype 83%. Southern blot and the first version of the M. truncatula genome (version 3.5) reported a single MtIRE gene and this was shown to be on chromosome 5 but the latest version of the M. truncatula genome (version 4.0) showed a second copy of the gene on chromosome 4. The genome sequence is based on the A17 reference genome. Both genes are 99% identical. Genetic markers that originate from flanking sequence tags (FSTs) on both chromosome 4 and 5 were tested in an attempt to find an FST that co-segregated with the mutant phenotype 100%. An FST derived from a Tnt1 insertion in Medtr4g060930 (24F) co-segregated with the mutant phenotype closely, with 76% co-segregation. Medtr4g060930 (24F) is on chromosome 4, making it likely that the Tnt1 inserted in the MtIRE gene is also on chromosome 4, and thus the defective gene is on chromosome 4.

No description available.

Static Random Access Memory (SRAM) cells in ultra-low power Integrated Circuits (ICs) based on nanoscale Complementary Metal Oxide Semiconductor (CMOS) devices are likely to be the most vulnerable to large-scale soft errors. Conventional error correction circuits may not be able to handle the distributed nature of such errors and are susceptible to soft errors themselves. In this thesis, a distributed error correction circuit called Self-Healing Cellular Automata (SHCA) that can repair itself is presented. A possible way to deploy a SHCA in a system of SRAM-based embedded program memories (ePM) for one type of chip multi-processors is also discussed. The SHCA is compared with conventional error correction approaches and its strengths and limitations are analyzed.

The temptation of illiberal democracy in the postcommunist Europe Abstract This thesis deals with the concept of illiberal democracy. In the first half it sums up the debate from which the concept arose. It describes the difference between liberalism and democracy and it also explains how these two concepts are interconnected. It describes the concept of defective democracies as conceived by Wolfgang Merkel. I also outline the constitutional aspects of the debate about illiberal democracy. In the second half the text applies Merkel's theoretical framework to analyse the cases of Poland and Hungary. The period of time, that was chosen, starts with the moment when parties Law and Justice and Fidesz gained majorities large enough for profound institutional changes. The period ends with activation of article 7 of the Treaty on European union. The text follows the structure of the Merkel's criteria. It analyses, how the voting rights and free access to power were preserved in both countries, if the political decisions are taken by elected representants, if there is a mutual control between the institutions and to what degree can the state power intervene into the private sphere of the citizens. I conclude that both Poland and Hungary could not be called liberal democracies in the period under review. The Polish...