The purpose of this thesis is to develop a testing environment for mobile robot experiments, to examine methods for multi-robot platooning through hostile environments, and test these algorithms on mobile robots. Such a system will allow us to rapidly address and test problems that arise concerning robot swarms and consequent interactions. In order to create this hardware simulation environment a test bed will be created using ROS or Robot Operating System. This platform is highly modular and extensible for future development. Trajectory generation for the robots will use smoothing splines, B-splines, and A* search. Each method has distinct properties which will be analyzed and rated with respect to its effectiveness with regards to robotic platooning. A few issues to be considered include: Is the optimal path taken with respect to distance and threats? Is the formation of the robots maintained or compromised during traversal of the path? And finally, what sorts of compromises or additions are needed to make each method effective? This work will be helpful for choosing route planning methods in future work and will provide a large code base for rapid prototyping.

Mémoire d'étude (DCB) : Ecole nationale supérieure des sciences de l'information et des bibliothèques : Villeurbanne (France) : 2001. / Notes bibliogr.

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Viena svarbiausių augalų genetikos problemų yra jų atsparumas abiotiniams veiksniams. Tokie veiksniai kaip šaltis, ozonas ar ultravioletinė spinduliuotė sukelia oksidacinį stresą ir ROS formavimąsi augalų ląstelėse. Visi augalai turi antioksidantines sistemas, vykdančias ROS detoksikaciją. Žalioji kreisvė (Crepis capillaris L.(Wallr.)) ir atsparūs šalnoms bulvių somatiniai asimetriniai hibridai buvo tiriami atsparumui abiotiniams veiksniams, įvertinant morfometrinius, biocheminius ir genetinius rodiklius po UV-B –(2, 4, 8 kJ/m2) ir ozono (40 ir 80 ppb) poveikio. Nustatyta, kad jautrūs stresiniams veiksniams yra morfometriniai parametrai- žalia ir sausa biomasė, lapų plotas ir skaičius. Biocheminiai parametrai, tirpių baltymų kiekis ir antioksidantinio fermento superoksido dismutazės (SOD) aktyvumas, tirtuose augaluose proporcingai didėjo priklausomai nuo dozės dydžio. Padidėjęs antioksidantinio SOD fermento aktyvumas po abiotinių veiksnių poveikio vertintinas kaip augalo adaptacinis atsakas į UV-B sukeltą oksidacinį stresą. Tiriant atsparumą šalčiui nustatyta, kad atsparus šalčiui bulvių hibridas H269, įgijo iš donoro Solanum commersonii DNR fragmentą, susijusį su padidinta mitochondrijų elektronų pernašos sistemos genų raiška, kuri siejama ROS koncentracijos reguliavimu ląstelėje ir šalčio atsako genų reguliavimu branduoliniame genome. Parodėme, kad atsparumai abiotiniams veiksniams- ozonui, UV-B ir šalčiui augaluose funkcionuoja kaip vientisa gynybos sistema, apimanti... [toliau žr. visą tekstą] / One of the major issues of plant genetics is their tolerance and resistance to abiotic factors. Low temperatures, ozone and ultraviolet radiation are the factors that increase ROS formation and oxidative stress in a plant cell. All plants have effective antioxidant systems to detoxify ROS. Researches were carried out to evaluate the resistance of Smooth Hawksbeard (Crepis capillaris L. (Wallr)) and frost resistant asymmetric somatic potato hybrids to abiotic stresses, estimating the morphometrical, biochemical and genetic data after treating the plants with UV-B (2, 4, 8 kJ/m2) and ozone (40 ir 80 ppb) doses. Test data shows, that morphometrical parameters such as fresh and dry weight along with leaf area and count are very sensitive to stress factors. Biochemical parameters such as soluble protein content and the activity of antioxidant enzyme superoxide dismutase (SOD) have risen pro rata from the dose given. The increment of SOD after treating the plants with simulated abiotic factors is annotated as adaptation to UV-B stress. Analysis of the cold acclimation has shown, that potato hybrid H269 has gained DNA fragment from the donor species Solanum commersonii. This fragment is associated with over-expressed genes of mitochondrial electron transfer system which regulates the concentration of ROS in the cell and controls the expression of nuclear genes related with cold-acclimation. With this analysis we have showed that plant resistance to abiotic factors such as ozone... [to full text]

Prenatal stressors have been reported to affect postnatal cognitive, metabolic, reproductive and immune functions. This study examined immune indices and function in Brahman calves prenatally stressed by transportation of their dams on d 60, 80, 100, 120 and 140 ± 5 d of gestation. Based on assessment of cow’s temperament and their reactions to repeated transportation it was evident that temperamental cows displayed greater pre-transport cortisol (P < 0.0001) and glucose (P < 0.03) concentrations, and habituated slower to the stressor compared to cows of calm and intermediate temperament. Serum concentration of cortisol at birth was greater (P < 0.03) in prenatally stressed versus control calves. Total and differential white blood cell counts and serum cortisol concentration in calves from birth through the age of weaning were determined. We identified a sexual dimorphism in neutrophil cell counts at birth (P = 0.0506) and cortisol concentration (P < 0.02) beginning at 14 d of age, with females having greater amounts of both. Whether weaning stress differentially affected cell counts, cortisol concentrations and neutrophil function of prenatally stressed and control male calves was examined. At 2 d post weaning, all calves had increased cortisol concentration (P < 0.0001) and neutrophil cell counts (P < 0.0001). However, in vitro production of reactive oxidative species by neutrophils was decreased (P = 0.0002) 2 d post weaning. Moreover, prenatally stressed calves demonstrated a larger (P = 0.0203) decrease in their immune function relative to control calves at 2 d post-weaning. Importantly, prenatally stressed calves took longer than controls to recover from the weaning stress. Additional studies are needed to clarify if prenatally stressed calves are more susceptible than control calves to pathogens during the post weaning period. Management practices to improve animal welfare and livestock production may need modification if follow-up studies demonstrate that prenatal stress also affects reproductive development, growth, performance and meat quality.

Liver fatty acid binding protein has been reported to possess antioxidant properties in the liver. The aim of this study was to investigate the effect of this protein in a nonalcoholic fatty liver disease (NAFLD) cell culture model. Rat hepatoma cells were treated with an oleate:palmitate (2:1) mixture for either 1 and 2 days, or further treated with 500 µM clofibrate to induce L-FABP expression. Intracellular lipid accumulation was quantitated by Nile Red. Lipotoxicity was determined using the WST-1 assay. Dichlorofluorescein (DCF) was utilized to assess intracellular reactive oxidative species (ROS) level. Measurement of lipotoxicity showed statistical decreases in cell viability as lipid concentrations increased in a dose-dependent manner. NAFLD cell cultures showed characteristic cellular damage from increased ROS levels in fatty acid treated cells. All groups treated with clofibrate showed statistically increased intracellular L-FABP levels and reduced ROS levels. The results lead to the conclusion that clofibrate induces L-FABP expression and in this manner suppresses hepatocellular ROS generation.

Atherosclerosis is a complex inflammation condition involving the accumulation of lipid-filled macrophages within the artery wall. Progression of the initial fatty streak to an advanced atherosclerotic plaque is characterized by the development of a necrotic core region containing cholesterol and dead cells. The oxidation of low-density lipoprotein (LDL) to oxidized LDL (oxLDL) and its subsequent uptake by macrophages to form foam cells are the key process in plaque formation. OxLDL is found within atherosclerotic plaque, and it is cytotoxic to a range of cells including macrophages through the generation of reactive oxygen species (ROS) and induction of oxidative stress. The aim of this study was to examine the cytotoxic effects of oxLDL to U937 human monocyte-like cells. OxLDL caused a rapid concentration-dependent cell viability loss in U937 cells within 6 hours. The progression of oxLDL-induced cell death was found to be strongly correlated with the intracellular ROS production and intracellular glutathione (GSH) loss. OxLDL also caused a rapid loss of intracellular aconitase activity, indicating the impairment of the cellular metabolic function. The cytosolic calcium ion (Ca²⁺) level was also elevated by oxLDL, which could be from both intra- and extra-cellular sources. OxLDL also activated plasma membrane superoxide generation complex NADPH oxidase (NOX), and the progression of oxLDL-induced NOX activation was correlated with oxLDL-mediated ROS production, suggesting NOX is the major source of ROS. Further investigations using NOX inhibitors apocynin or diphenyleneiodonium (DPI) found that inhibition of NOX prevented oxLDL-induced cell viability loss, ROS production, GSH loss and aconitase activity decrease. The cytosolic Ca²⁺ elevation caused by oxLDL was also suppressed slightly by inhibiting NOX activity. These results clearly show that NOX is the major site of oxidative stress upon oxLDL activation, contributing to the oxLDL-induced cell death. This study also examined the protective effect of 7,8-dihydroneopterin (7,8-NP) on oxLDL-induced oxidative stress. 7,8-NP dramatically protected cells from oxLDL-induced cell viability loss, ROS generation and aconitase activity loss. 7,8-NP also inhibited oxLDL-induced cytosolic Ca²⁺ influx particularly after 3 hours. 7,8-NP did not inhibited mitochondrial aconitase activity decrease caused by oxLDL, nor inhibited mitochondrial ROS production. This indicates the protective effect of 7,8-NP against oxLDL damage could primarily in cytoplasm. The failure of 7,8-NP protection from oxLDL activating NOX suggests that the protection of 7,8-NP against oxLDL-induced oxidative stress was not due to the inhibition of NOX activation, but by radical scavenging activity of the NOX products.

The tumor suppressor p53 has a close relation with reactive oxygen species (ROS). As an indispensable component of the cellular redox system, ROS not only have been established to be involved in p53-dependent apoptosis, but also regulate p53 activity. Recent studies revealed several novel actions of p53, such as transactivation of antioxidative proteins, mitochondria translocation and inhibition of glycolysis. The fate of cells where p53 signaling pathways are initiated is either survival or death. In this review, we examine the hypothesis that ROS regulate cell fate through p53, in a way that physiological ROS levels trigger the protective pathways, while p53 behaves more like a cell killer under cytotoxic oxidative stress.

Liver fatty acid binding protein has been reported to possess antioxidant properties in the liver. The aim of this study was to investigate the effect of this protein in a nonalcoholic fatty liver disease (NAFLD) cell culture model. Rat hepatoma cells were treated with an oleate:palmitate (2:1) mixture for either 1 and 2 days, or further treated with 500 µM clofibrate to induce L-FABP expression. Intracellular lipid accumulation was quantitated by Nile Red. Lipotoxicity was determined using the WST-1 assay. Dichlorofluorescein (DCF) was utilized to assess intracellular reactive oxidative species (ROS) level. Measurement of lipotoxicity showed statistical decreases in cell viability as lipid concentrations increased in a dose-dependent manner. NAFLD cell cultures showed characteristic cellular damage from increased ROS levels in fatty acid treated cells. All groups treated with clofibrate showed statistically increased intracellular L-FABP levels and reduced ROS levels. The results lead to the conclusion that clofibrate induces L-FABP expression and in this manner suppresses hepatocellular ROS generation.

Development in multicellular organisms requires a strict balance between cell division and differentiation. The simple architecture of the Arabidopsis thaliana root makes it an ideal model for studying molecular mechanisms controlling both the transition from cell division to cell differentiation and cell fate determination. The class III Homeodomain-Leucine Zipper (HD-ZIP III) transcription factors (TFs) are well known developmental regulators, controlling important aspects of embryogenesis, shoot meristem activity, leaf polarity and vascular patterning. The HD-ZIP III TFs are under post-transcriptional control of microRNA165 (miR165) and miR166. In this thesis, I present a cell-to-cell signalling pathway underlying root vascular patterning and describe signaling pathways downstream of the HD-ZIP III TFs in their control of root development. The TF SHORTROOT (SHR), moves from the vascular stele cells to the surrounding endodermal cell layer. We show that SHR acts here to transcriptionally activate MIR165A and MIR166B, and the miR165/6 produced in the endodermis act non-cell autonomously to post-transcriptionally restrict HD-ZIP III mRNA levels in the peripheral stele. The resulting graded HD-ZIP III activity domain in the radial stele dose-dependently determines vascular cell type; high levels of HD-ZIP III in the central stele result in metaxylem formation while lower levels in the peripheral stele result in protoxylem. We provide evidence that the HD-ZIP III factors act as de novo xylem specifiers, because the quintuple mutant lacking all five HD-ZIP III genes forms no xylem. Furthermore, reducing the plasmodesmatal aperture through callose accumulation inhibits the bi-directional mobility of both signalling molecules, providing evidence that both SHR and miR165/6 move cell-to-cell via plasmodesmata to control root development. I present downstream components of the miR165/HD-ZIP III TFs in the root meristem, identified through a time-course induction of miR165 coupled to transcriptome analyses. This experiment revealed novel roles for HD-ZIP III TFs in vascular patterning and meristem size control. I show that HD-ZIP III directed repression of auxin hormone signalling in the xylem axis is essential for proper xylem differentiation. Furthermore, I provide data to show that they also control the balance of reactive oxygen species in the root meristem, thereby directing meristem size and ultimately controlling root growth.