Vision based localization of mobile robots

Mobile robotics is an active and exciting sub-field of Computer Science. Its importance is easily witnessed in a variety of undertakings from DARPA\u27s Grand Challenge to NASA\u27s Mars exploration program. The field is relatively young, and still many challenges face roboticists across the board. One important area of research is localization, which concerns itself with granting a robot the ability to discover and continually update an internal representation of its position. Vision based sensor systems have been investigated [8,22,27], but to much lesser extent than other popular techniques [4,6,7,9,10]. A custom mobile platform has been constructed on top of which a monocular vision based localization system has been implemented. The rigorous gathering of empirical data across a large group of parameters germane to the problem has led to various findings about monocular vision based localization and the fitness of the custom robot platform. The localization component is based on a probabilistic technique called Monte-Carlo Localization (MCL) that tolerates a variety of different sensors and effectors, and has further proven to be adept at localization in diverse circumstances. Both a motion model and sensor model that drive the particle filter at the algorithm\u27s core have been carefully derived. The sensor model employs a simple correlation process that leverages color histograms and edge detection to filter robot pose estimations via the on board vision. This algorithm relies on image matching to tune position estimates based on a priori knowledge of its environment in the form of a feature library. It is believed that leveraging different computationally inexpensive features can lead to efficient and robust localization with MCL. The central goal of this thesis is to implement and arrive at such a conclusion through the gathering of empirical data. Section 1 presents a brief introduction to mobile robot localization and robot architectures, while section 2 covers MCL itself in more depth. Section 3 elaborates on the localization strategy, modeling and implementation that forms the basis of the trials that are presented toward the end of that section. Section 4 presents a revised implementation that attempts to address shortcomings identified during localization trials. Finally in section 5, conclusions are drawn about the effectiveness of the localization implementation and a path to improved localization with monocular vision is posited

Procoagulant microparticles promote coagulation in a factor XI-dependent manner in human endotoxemia

Human endotoxemia is characterized by acute inflammation and activation of coagulation, as well as increased numbers of circulating microparticles (MPs). Whether these MPs directly promote coagulation and through which pathway their actions are mediated, however, has not been fully explored

Microparticle analysis in disorders of hemostasis and thrombosis.

Microparticles (MPs) are submicron vesicles released from the plasma membrane of eukaryotic cells in response to activation or apoptosis. MPs are known to be involved in numerous biologic processes, including inflammation, the immune response, cancer metastasis, and angiogenesis. Their earliest recognized and most widely accepted role, however, is the ability to promote and support the process of blood coagulation. Consequently, there is ongoing interest in studying MPs in disorders of hemostasis and thrombosis. Both phosphatidylserine (PS) exposure and the presence of tissue factor (TF) in the MP membrane may account for their procoagulant properties, and elevated numbers of MPs in plasma have been reported in numerous prothrombotic conditions. To date, however, there are few data on true causality linking MPs to the genesis of thrombosis. A variety of methodologies have been employed to characterize and quantify MPs, although detection is challenging due to their submicron size. Flow cytometry (FCM) remains the most frequently utilized strategy for MP detection; however, it is associated with significant technological limitations. Additionally, pre-analytical and analytical variables can influence the detection of MPs by FCM, rendering data interpretation difficult. Lack of methodologic standardization in MP analysis by FCM confounds the issue further, although efforts are currently underway to address this limitation. Moving forward, it will be important to address these technical challenges as a scientific community if we are to better understand the role that MPs play in disorders of hemostasis and thrombosis

Gramscian Perspectives on Populism

Increasingly liberal states are facing challenges from populist movements. This paper argues that the prison writings of Antonio Gramsci can provide important insights into the phenomenon and how to counteract it. The first two sections outline a set of Gramscian analytical tools: hegemony, non-hegemony, passive revolution, and Caesarism. These theoretical tools are then applied to different periods of the Third Republic of France, 1870-1940. This paper looks at this French example because it features unique relationships between populism, ideology, and the experience of liberalism prior to World War II. The third section demonstrates the implications of non-hegemony within international society, and how it affects and shapes states\u27 domestic lives and inter-state relations

Standardization of microparticle enumeration across different flow cytometry platforms: results of a multicenter collaborative workshop

Microparticles are extracellular vesicles resulting from the budding of cellular membranes that have a high potential as emergent biomarkers; however, their clinical relevance is hampered by methodological enumeration concerns and a lack of standardization. Flow cytometry (FCM) remains the most commonly used technique with the best capability to determine the cellular origin of single MPs. However, instruments behave variably depending on which scatter parameter, (Forward (FSC) or Side scatter (SSC)), provides the best resolution to discriminate submicron particles. To overcome this problem, a new approach, based on two sets of selected beads adapted to FSC or SSC optimized instruments, was recently proposed to reproducibly enumerate platelet-derived MP counts among instruments with different optical systems

Should the Poor Foot the Bill

This article looks at the use of privatization to solve urban poverty under the auspices of the United Nations' Millennium Development Goals and the United States Agency for International Development's Urban Strategy. It questions whether the urban poor should be asked to pay their way out of poverty

Chemically diverse microtubule stabilizing agents initiate distinct mitotic defects and dysregulated expression of key mitotic kinases.

Microtubule stabilizers are some of the most successful drugs used in the treatment of adult solid tumors and yet the molecular events responsible for their antimitotic actions are not well defined. The mitotic events initiated by three structurally and biologically diverse microtubule stabilizers; taccalonolide AJ, laulimalide/fijianolide B and paclitaxel were studied. These microtubule stabilizers cause the formation of aberrant, but structurally distinct mitotic spindles leading to the hypothesis that they differentially affect mitotic signaling. Each microtubule stabilizer initiated different patterns of expression of key mitotic signaling proteins. Taccalonolide AJ causes centrosome separation and disjunction failure to a much greater extent than paclitaxel or laulimalide, which is consistent with the distinct defects in expression and activation of Plk1 and Eg5 caused by each stabilizer. Localization studies revealed that TPX2 and Aurora A are associated with each spindle aster formed by each stabilizer. This suggests a common mechanism of aster formation. However, taccalonolide AJ also causes pericentrin accumulation on every spindle aster. The presence of pericentrin at every spindle aster initiated by taccalonolide AJ might facilitate the maintenance and stability of the highly focused asters formed by this stabilizer. Laulimalide and paclitaxel cause completely different patterns of expression and activation of these proteins, as well as phenotypically different spindle phenotypes. Delineating how diverse microtubule stabilizers affect mitotic signaling pathways could identify key proteins involved in modulating sensitivity and resistance to the antimitotic actions of these compounds

Sequence dependent exposure of mammary carcinoma cells to Taxotere® and the MEK1/2 inhibitor U0126 causes enhanced cell killing in vitro

Taxol (paclitaxel) and Taxotere (docetaxel) are considered as two of the most important anticancer chemotherapy drugs. The cytotoxic action of these drugs has been linked to their ability to inhibit microtubule depolymerization, causing growth arrest and subsequent cell death. Studies by a number of laboratories have also linked suppression of mitogen activated protein kinase (MAPK) signaling to enhanced Taxol toxicity. The present study examined the interactions of the semi-synthetic taxane Taxotere with MEK1/2 inhibitors in epithelial tumor cells. Concurrent treatment of MDA-MB-231 mammary and DU145 prostate carcinoma cells with Taxotere and MEK1/2 inhibitor resulted in protection from the anti-proliferative effects of Taxotere in MTT assays. In contrast, in MCF-7 mammary cells, concurrent Taxotere and MEK1/2 inhibitor treatment weakly enhanced the antiproliferative effects of the taxane. Sequential treatment of MDA-MB-231 and MCF-7 cells with Taxotere followed by MEK1/2 inhibitor also enhanced the anti-proliferative effects of the taxane in MTT assays. However, no enhancement was observed in DU145 or PC-3 cells. Colony formation assays, including isobologram analyses, provided a more definitive demonstration that MCF-7 and MDA-MB-231 cells were sensitized to the toxic effects of Taxotere by U0126. Similar data were observed using Laulimalide, which binds to tubulin at a different site to Taxotere. The enhancement in Taxotere anti-proliferative effects by U0126 correlated with increased cell killing, 48-72h after treatment of cells that was blocked by inhibition of caspase 9, but not caspase 8, function. This observation was associated with prolonged suppression of ERK1/2 and AKT activity, without alteration in either p38 or JNK1/2 activity. Collectively these findings demonstrate that sequential administration of Taxotere followed by MEK1/2 inhibition can lead to increased cell death and loss of reproductive capacity in some, but not all, human tumor cells. ©2003 Landes Bioscience.Fil: Yacoub, Adly. Virginia Commonwealth University; Estados UnidosFil: Han, Song Iy. Virginia Commonwealth University; Estados UnidosFil: Caron, Ruben Walter. Virginia Commonwealth University; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Gilfor, Donna. Virginia Commonwealth University; Estados UnidosFil: Mooberry, Susan. Southwest Foundation for Biomedical Research; Estados UnidosFil: Grant, Steven. Virginia Commonwealth University; Estados UnidosFil: Dent, Paul. Virginia Commonwealth University; Estados Unido

Identification and Characterization of a New Tubulin-Binding

We studied the mechanism of action of 3,5-dibromo-4-(3,4-dimethoxyphenyl)-1H-pyrrole-2-carboxylic acid ethyl ester (JG-03-14) and found that it is a potent microtubule depolymerizer. JG-03-14 caused a dose-dependent loss of cellular microtubules, formation of aberrant mitotic spindles, accumulation of cells in the G2/M phase of the cell cycle, and Bcl-2 phosphorylation. These events culminated in the initiation of apoptosis, as evidenced by the caspase 3-dependent cleavage of poly(ADP-ribose) polymerase (PARP). JG-03-14 has antiproliferative activity against a wide range of cancer cell lines, with an average IC50 value of 62 nM, and it is a poor substrate for transport by P-glycoprotein. JG-03-14 inhibited the polymerization of purified tubulin in vitro, consistent with a direct interaction between the compound and tubulin. JG-03-14 potently inhibited the binding of [3H]colchicine to tubulin, suggesting that it bound to tubulin at a site overlapping the colchicine site. JG-03-14 had antitumor effects in the PC3 xenograft model, in which it caused greater than 50% reduction in tumor burden after 14 days of treatment. Molecular modeling studies indicated that the dimethoxyphenyl group of JG-03-14 occupies a space similar to that of the trimethoxyphenyl group of colchicine. However, the 2,3,5-trisubstituted pyrrole group, which is connected to the dimethoxyphenyl moiety, interacted with both α and β tubulin in space not shared with colchicine, suggesting significant differences compared with colchicine in the mechanism of binding to tubulin. Our results suggest that this tetransubstituted pyrrole represents a new, biologically active chemotype for the colchicine site on tubulin

Standardization of pre-analytical variables in plasma microparticle determination: results of the International Society on Thrombosis and Haemostasis SSC Collaborative workshop

Microparticles (MP) are sub-micron sized vesicles released by activated or apoptotic cells. They are generally defined as 0.1 to 1 μm membrane particles that expose the anionic phospholipid phosphatidylserine (PS) and membrane antigens representative of their cellular origin [1]. It is now well recognized that MP behave as vectors of bioactive molecules, playing a role in blood coagulation, inflammation, cell activation and cancer metastasis. In clinical practice, circulating MP originating from blood and vascular cells are elevated in a variety of prothrombotic and inflammatory disorders, cardiovascular diseases, autoimmune conditions, infectious diseases and cancer [1-3