The complexity of mobile robots increases as more parts are added to the system. Introducing microcontrollers into a mobile robot abstracts and modularises the system architecture, creating a demand for seamless microcontroller integration. The Robot Operating System (ROS) used by ABB’s new mobile robot, the mobile YuMi prototype (mYuMi), allows standardised robot software libraries and packages to simplify robotic creations. As ABB is porting over from ROS1 to ROS2, the ROS2 compatible Microcontroller Robot Operating System (micro-ROS) will be incorporated into the system to smoothly integrate microcontrollers into mYuMi. In order to display the validity of micro-ROS, this project used tracing and latency measurements with external applications to test the remote communication between mYuMi using ROS2 and microcontrollers using micro-ROS, with three different microcontrollers tested. The communication was evaluated in different scenarios with a test bench, using ping pong communication to get the round-trip time. A reinforcement of the test results was presented by demonstrating the use of micro-ROS live in a prototype developed, where mYuMi controlled a 1D rangefinder and an RC servo motor by utilising two microcontrollers. The results concluded that the micro-ROS delay could be analysed in theory with external applications, equivalent micro-ROS functionality should apply to most microcontrollers, and the test results and prototype displayed the potential of micro-ROS matching ROS2 in terms of delay and stability.

No description available.

Palmitate (PA), one of the most prevalent saturated fatty acids, causes myocardial dysfunction. However, the mechanisms by which PA induces cell apoptosis and autophagy remain to be elucidated. We showed that autophagy was induced in an mTORC1-dependent way and played a protective role against PA-induced apoptosis, which was verified by pretreatment with 3-methyladenine (3MA) and rapamycin. However, p62 began to accumulate after 18 h treatment with PA, suggesting prolonged exposure to PA lead to an impairment of autophagic flux. PA enhanced ROS production as well as activated p38-mitogen-activated protein kinase (p38 MAPK) and c-jun NH2 terminal kinases (JNKs). The antioxidant N-Acety-L-Cysteine (NAC) was found to attenuate the JNK and p38 MAPK activation with a concomitant reduction of PA-induced autophagy and apoptosis. Furthermore, both JNK and p38 MAPK inhibitors were shown to directly abrogate caspase 7 cleavage as well as the conversion of LC3BI to LC3BII. Thus, we demonstrate that PA stimulates autophagy and apoptosis via ROS-dependent JNK and p38 MAPK pathways.

According to the WHO, 38 million individuals were living with human immunodeficiency virus (HIV), 25.4 million of which were using antiretroviral therapy (ART) at the end of 2019. Despite ART-mediated suppression of viral replication, ART is not a cure and is associated with viral persistence, residual inflammation, and metabolic disturbances. Indeed, due to the presence of viral reservoirs, lifelong ART therapy is required to control viremia and prevent disease progression into acquired immune deficiency syndrome (AIDS). Successful ART treatment allows people living with HIV (PLHIV) to achieve a similar life expectancy to uninfected individuals. However, recent studies have illustrated the presence of increased comorbidities, such as accelerated, premature immune aging, in ART-controlled PLHIV compared to uninfected individuals. Studies suggest that both HIV-infection and ART-treatment lead to mitochondrial dysfunction, ultimately resulting in cellular exhaustion, senescence, and apoptosis. Since mitochondria are essential cellular organelles for energy homeostasis and cellular metabolism, their compromise leads to decreased oxidative phosphorylation (OXPHOS), ATP synthesis, gluconeogenesis, and beta-oxidation, abnormal cell homeostasis, increased oxidative stress, depolarization of the mitochondrial membrane potential, and upregulation of mitochondrial DNA mutations and cellular apoptosis. The progressive mitochondrial damage induced by HIV-infection and ART-treatment likely contributes to accelerated aging, senescence, and cellular dysfunction in PLHIV. This review discusses the connections between mitochondrial compromise and cellular dysfunction associated with HIV-and ART-induced toxicities, providing new insights into how HIV and current ART directly impact mitochondrial functions and contribute to cellular senescence and aging in PLHIV. Identifying this nexus and potential mechanisms may be beneficial in developing improved therapeutics for treating PLHIV.

Le nombre de lymphocytes T (LT) présents dans l’organisme est contrôlé de manière étroite et maintenu constant. En réponse à une chute de ce nombre, par exemple suite à une infection, un traitement de chimiothérapie ou lors d’une greffe de moelle osseuse, les LT résiduels ou transférés se divisent activement et repeuplent les compartiments lymphoïdes, rétablissant ainsi un nombre «normal» de cellules immunes périphériques. Ce processus, appelé prolifération homéostatique, est soutenu par l’IL-7 ainsi que les signaux TCR et mène à la génération de LT effecteurs/mémoire. Ces cellules effectrices/mémoire peuvent favoriser le développement d’une réponse anti-tumorale mais sont aussi impliquées dans le développement de maladies auto-immunes et inflammatoires.Des changements métaboliques sont étroitement liés à la différenciation et aux fonctions des LT. De plus, un nombre grandissant de données suggère qu’une modulation du métabolisme permet d’influencer le cours d’une réponse immune. L’AMP-activated protein kinase (AMPK) est un senseurmajeur du stress métabolique qui régule l’homéostasie des mitochondries, la glycolyse et l’équilibre rédox. Si l’AMPK est activée lors de la stimulation du TCR, son implication dans la biologie des LT reste confuse.Au cours de cette thèse, nous avons entrepris une série d’expériences afin d’évaluer le rôle de l’AMPK sur la biologie des LT et plus particulièrement au cours de leur prolifération homéostatique. Grâce à différents modèles in vivo et in vitro, nous avons montré que l’AMPK, bien que dispensable pour les étapes précoces de l’activation du TCR, est requise pour soutenir la viabilité et l’expansion des LT au cours de proliférations de longues durées. L’AMPK promeut l’accumulation de LT effecteurs/ mémoire au cours d’une prolifération homéostatique. En accord avec ces données, la transplantation de LT AMPK-KO dans un hôte allogénique conduit au développement d’une réaction du greffon contre l’hôte de moindre gravité.D’un point de vue métabolique, l’AMPK soutient le potentiel de membrane mitochondrial, permet une plus grande flexibilité métabolique, limite la production de dérivés toxiques de l’oxygène (ROS) et protège les LT contre le stress oxydant. En outre, la neutralisation des ROS par un traitement antioxydant restaure partiellement la prolifération des LT AMPK-KO.Nos données suggèrent qu’en limitant l’accumulation de dégâts mitochondriaux et oxydatifs au cours de cycles de divisions prolongées, l’AMPK soutient la viabilité, la prolifération et les fonctions effectrices des LT. / Doctorat en Sciences / info:eu-repo/semantics/nonPublished

The aim of this thesis is the development and implementation of a controlled testing platform for the Robust Intelligent Sensing and Controls (RISC) Lab at Utah State University (USU). This will be an open source adaptable expandable robotics platform usable for both education and research. This differs from the many other platforms developed in that the entire platform software will be made open source. This open source software will encourage collaboration among other universities and enable researchers to essentially pick up where others have left off without the necessity of replicating months or even years of work. The expected results of this research will create a foundation for diverse robotics investigation at USU as well as enable attempts at novel methods of control, estimation and optimization. This will also contribute a complete software testbed setup to the already vibrant robotics open source research community. This thesis first outlines the platform setup and novel developments therein. The second stage provides an example of how this has been used in education, providing an example curriculum implementing modern control techniques. The third section provides some exploratory research in trajectory control and state estimation of the tip of an inverted pendulum atop a small unmanned aerial vehicle as well as bearing-only cooperative localization experimentation. Finally, a conclusion and future work is discussed.

Indiana University-Purdue University Indianapolis (IUPUI) / Self-driving is simply the capacity of a vehicle to drive itself without human intervention. To accomplish this, the vehicle utilizes mechanical and electronic parts, sensors, actuators and an AI computer. The on-board PC runs advanced programming, which permits the vehicle to see and comprehend its current circumstance dependent on sensor input, limit itself in that climate and plan the ideal course from point A to point B. Independent driving is not an easy task, and to create self-sufficient driving arrangements is an exceptionally significant ability in the present programming designing field. ROS is a robust and versatile communication middle ware (framework) tailored and widely used for robotics applications. This thesis work intends to show how ROS could be used to create independent driving programming by investigating self-governing driving issues, looking at existing arrangements and building up a model vehicle utilizing ROS. The main focus of this thesis is to develop and implement a one-tenth scale of an autonomous RACECAR equipped with Jetson Nano board as the on-board computer, PCA9685 as PWM driver, sensors, and a ROS based software architecture. Finally, by following the methods presented in this thesis, it is conceivable to build an autonomous RACECAR that runs on ROS. By following the means portrayed in this theory of work, it is conceivable to build up a self-governing vehicle.

Indiana University-Purdue University Indianapolis (IUPUI) / Type 1 diabetes (T1D) is a multifactorial disease involving genetic and environmental factors. One of the factors implicated in disease pathogenesis is early life viral infection. A typical immune response to viral infection includes production of type 1 interferons (IFN), such as IFN-α, which can induce stress in the pancreatic β-cells. Reactive oxygen species (ROS) accumulation occurs after exposure to other inflammatory cytokines, causing oxidative stress that may be linked to T1D pathogenesis. Therefore, we hypothesized that IFN-α may also elicit β-cell ROS accumulation. Our in vivo and in vitro experiments with human islets showed rapid and heterogenous ROS accumulation with IFN-α. Although T1D is characterized by autoimmune destruction of β-cells, some cells survive this persistent attack. We hypothesized that survival/ death of β-cells could be attributed to the ability to effectively mitigate ROS accumulation. One mechanism to mitigate ROS is autophagy, which degrades and recycles cellular components to promote cellular homeostasis. We observed an impairment in autophagy in β-cells of donors with T1D as well as in islets of diabetic non-obese diabetic (NOD) mouse model of autoimmune diabetes. Autophagic flux was also impaired in diabetic NOD mouse islets, further confirming impairment of autophagy. Interestingly, we observed an induction of autophagy after acute treatment with IFN-α both in vitro and in vivo, suggesting compensatory upregulation of autophagy to restore homeostasis. Similarly, we observed an increase in autophagosomes and telolysosomes in β-cells of normoglycemic autoantibody positive organ donors compared to nondiabetic organ donors. Together, these data implicate a defect in the final degradation step of autophagy involving lysosomes. Therefore, we analyzed the activity and expression of lysosomal cysteine protease Cathepsin H (CTSH, a T1D susceptibility locus), and found both to be increased in islets of pre-diabetic NOD mice. Together, these data support compensatory hyperactivation of lysosomal enzymes prior to overt diabetes, potentially to rid the cell of ROS and degradation-resistant oxidized proteins and lipids. We also observed that C57Bl/6J mice lacking a key autophagy enzyme, ATG7, in their β-cells, spontaneously developed hyperglycemia. Collectively, these data highlight the importance of -phagic degradation process in the pathogenesis of T1D. / 2022-12-28

No description available.

Oxidative stress (OS) occurs when DNA repair mechanisms are overcome by the amount of single and double strand DNA breaks caused by an accumulation of reactive oxygen species (ROS). Genomic instability (GI) by microsatellite instability (MSI) accumulation is characterized by changes in DNA single tandem repeats (STR) as a direct result of ROS. Deregulation of DNA repair and tumor suppressor pathways have been described as causes of tumor progression and metastasis. Studies in mammals have focused on GI and the implications of increased mutation frequency due to accumulation of MSI leading to development of diseases, including infertility and cancer. Ovarian cancer is a deadly disease displaying the highest mortality rate among gynecological cancers. Hereditary ovarian cancer displays GI that can be established early in primordial germinal cells (PCGs) development and migration across the genital ridge, where PGCs are exposed to ROS damage. The hypothesis of this study was ROS-induced GI is marked by the accumulation of MSI on repetitive sequences of DNA that override DNA repair, tumor suppressor and redox homeostasis pathways. In this study, we induced ROS in human ovarian cell lines by hydrogen peroxide (H2O2) exposure, as well as evaluated mouse PGCs to determine whether MSI occurs in specific regions of human and mouse genomes. Our results show that MSI was present in specific markers after ROS-induced damage in human ovarian cells and in mouse Sod1 knockout PGCs during cell migration, both of which accumulate specific mutations caused by free radical damage. Ovarian tumor cells and mouse PGCs showed an increase of MSI in 12 human and 5 mouse repetitive markers that are located near important genes related to DNA repair, tumor suppression, cell proliferation, apoptosis and differentiation. This could be a signal that leads to tumor initiation, formation and progression in adult ovarian cells due to improper DNA repair and tumor suppression mechanisms or in disruption of PGC migration that determines germinal cell pool selection during early embryonic development due to absence of cell antioxidant mechanisms. Therefore, these specific unstable STRs are novel biomarkers that could be useful in early diagnostics, prognosis, and successful therapy of ovarian tumorigenesis.