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  1. Book ; Online: Distributed Reinforcement Learning for Robot Teams

    Wang, Yutong / Damani, Mehul / Wang, Pamela / Cao, Yuhong / Sartoretti, Guillaume

    A Review

    2022  

    Abstract: Purpose of review: Recent advances in sensing, actuation, and computation have opened the door to multi-robot systems consisting of hundreds/thousands of robots, with promising applications to automated manufacturing, disaster relief, harvesting, last- ... ...

    Abstract Purpose of review: Recent advances in sensing, actuation, and computation have opened the door to multi-robot systems consisting of hundreds/thousands of robots, with promising applications to automated manufacturing, disaster relief, harvesting, last-mile delivery, port/airport operations, or search and rescue. The community has leveraged model-free multi-agent reinforcement learning (MARL) to devise efficient, scalable controllers for multi-robot systems (MRS). This review aims to provide an analysis of the state-of-the-art in distributed MARL for multi-robot cooperation. Recent findings: Decentralized MRS face fundamental challenges, such as non-stationarity and partial observability. Building upon the "centralized training, decentralized execution" paradigm, recent MARL approaches include independent learning, centralized critic, value decomposition, and communication learning approaches. Cooperative behaviors are demonstrated through AI benchmarks and fundamental real-world robotic capabilities such as multi-robot motion/path planning. Summary: This survey reports the challenges surrounding decentralized model-free MARL for multi-robot cooperation and existing classes of approaches. We present benchmarks and robotic applications along with a discussion on current open avenues for research.

    Comment: Preprint of the paper submitted to Springer's Current Robotics Reports
    Keywords Computer Science - Robotics ; Computer Science - Artificial Intelligence ; Computer Science - Machine Learning ; Computer Science - Multiagent Systems
    Subject code 629
    Publishing date 2022-04-07
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: An electron paramagnetic resonance study of the affinity of nitrite for methemoglobin.

    Goetz, Bradley I / Shields, Howard W / Basu, Swati / Wang, Pamela / King, S Bruce / Hogg, Neil / Gladwin, Mark T / Kim-Shapiro, Daniel B

    Nitric oxide : biology and chemistry

    2009  Volume 22, Issue 2, Page(s) 149–154

    Abstract: Recent data suggests that reactions of nitrite with ferric hemoglobin are potentially important in heme-protein dependent NO signaling. Our group and others are evaluating the role of reductive nitrosylation reactions in the generation of N(2)O(3) as a ... ...

    Abstract Recent data suggests that reactions of nitrite with ferric hemoglobin are potentially important in heme-protein dependent NO signaling. Our group and others are evaluating the role of reductive nitrosylation reactions in the generation of N(2)O(3) as a signaling molecule. The latter reaction is hypothesized to involve reactions on NO, nitrite and methemoglobin to form N(2)O(3) in an anhydrase reaction. Of potential importance to these reactions is the affinity of methemoglobin for nitrite and the reactivity of nitrite-bound methemoglobin with nitric oxide. In this paper, we review work related to the electronic structure of nitrite-bound methemoglobin and its dissociation constant. We present new data using electron paramagnetic resonance spectroscopy which confirm that methemoglobin has a much higher affinity for nitrite, under certain conditions, than reported in classical observations. Interestingly the affinity is greatest at lower pH and low nitrite:methemoglobin ratios. These data suggest additional interesting chemistry in the reaction of nitrite with ferric and ferrous heme species. Moreover, this reaction could serve as a paradigm for ferric heme reactions with nitrite.
    MeSH term(s) Electron Spin Resonance Spectroscopy ; Methemoglobin/chemistry ; Methemoglobin/metabolism ; Nitrites/chemistry ; Nitrites/metabolism
    Chemical Substances Nitrites ; Methemoglobin (9008-37-1)
    Language English
    Publishing date 2009-11-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1362794-6
    ISSN 1089-8611 ; 1089-8603
    ISSN (online) 1089-8611
    ISSN 1089-8603
    DOI 10.1016/j.niox.2009.10.009
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  3. Article ; Online: Bradykinin inducible receptor is essential to lipopolysaccharide-induced acute lung injury in mice.

    Campanholle, Gabriela / Landgraf, Richardt G / Borducchi, Erica / Semedo, Patricia / Wang, Pamela H M / Amano, Mariane T / Russo, Momtchilo / Pacheco-Silva, Alvaro / Jancar, Sonia / Camara, Niels O S

    European journal of pharmacology

    2010  Volume 634, Issue 1-3, Page(s) 132–137

    Abstract: Lipopolysaccharides from gram-negative bacteria are amongst the most common causative agents of acute lung injury, which is characterized by an inflammatory response, with cellular infiltration and the release of mediators/cytokines. There is evidence ... ...

    Abstract Lipopolysaccharides from gram-negative bacteria are amongst the most common causative agents of acute lung injury, which is characterized by an inflammatory response, with cellular infiltration and the release of mediators/cytokines. There is evidence that bradykinin plays a role in lung inflammation in asthma but in other types of lung inflammation its role is less clear. In the present study we evaluated the role of the bradykinin B1 receptor in acute lung injury caused by lipopolysaccharide inhalation and the mechanisms behind bradykinin actions participating in the inflammatory response. We found that in C57Bl/6 mice, the bradykinin B1 receptor expression was up-regulated 24h after lipopolysaccharide inhalation. At this time, the number of cells and protein concentration were significantly increased in the bronchoalveolar lavage fluid and the mice developed airway hyperreactivity to methacholine. In addition, there was an increased expression of tumor necrosis factor-alpha, interleukin-1 beta and interferon-gamma and chemokines (monocytes chemotactic protein-1 and KC) in the bronchoalveolar lavage fluid and in the lung tissue. We then treated the mice with a bradykinin B1 receptor antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin), 30 min after lipopolysaccharide administration. We observed that this treatment prevented the airway hyperreactivity as well as the increased cellular infiltration and protein content in the bronchoalveolar lavage fluid. Moreover, R-954 inhibited the expression of cytokines/chemokines. These results implicate bradykinin, acting through B1 receptor, in the development of acute lung injury caused by lipopolysaccharide inhalation.
    MeSH term(s) Acute Lung Injury/chemically induced ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/prevention & control ; Administration, Inhalation ; Animals ; Bradykinin/administration & dosage ; Bradykinin/analogs & derivatives ; Bradykinin/therapeutic use ; Bradykinin B1 Receptor Antagonists ; Bronchoalveolar Lavage Fluid ; Cytokines/analysis ; Cytokines/biosynthesis ; Disease Models, Animal ; Inflammation Mediators/administration & dosage ; Inflammation Mediators/metabolism ; Inflammation Mediators/physiology ; Lipopolysaccharides/administration & dosage ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Receptor, Bradykinin B1/administration & dosage ; Receptor, Bradykinin B1/biosynthesis ; Receptor, Bradykinin B1/physiology
    Chemical Substances Ac-Orn-(Oic2, alpha-MePhe5, D-betaNal7, Ile8)desArg9-bradykinin ; Bradykinin B1 Receptor Antagonists ; Cytokines ; Inflammation Mediators ; Lipopolysaccharides ; Receptor, Bradykinin B1 ; Bradykinin (S8TIM42R2W)
    Language English
    Publishing date 2010-05-25
    Publishing country Netherlands
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2010.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 522: Show issues Location:
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  4. Article ; Online: Transglutaminase is essential for IgA nephropathy development acting through IgA receptors.

    Berthelot, Laureline / Papista, Christina / Maciel, Thiago T / Biarnes-Pelicot, Martine / Tissandie, Emilie / Wang, Pamela H M / Tamouza, Houda / Jamin, Agnès / Bex-Coudrat, Julie / Gestin, Aurelie / Boumediene, Ahmed / Arcos-Fajardo, Michelle / England, Patrick / Pillebout, Evangéline / Walker, Francine / Daugas, Eric / Vrtosvnik, François / Flamant, Martin / Benhamou, Marc /
    Cogné, Michel / Moura, Ivan C / Monteiro, Renato C

    The Journal of experimental medicine

    2012  Volume 209, Issue 4, Page(s) 793–806

    Abstract: IgA nephropathy (IgAN) is a common cause of renal failure worldwide. Treatment is limited because of a complex pathogenesis, including unknown factors favoring IgA1 deposition in the glomerular mesangium. IgA receptor abnormalities are implicated, ... ...

    Abstract IgA nephropathy (IgAN) is a common cause of renal failure worldwide. Treatment is limited because of a complex pathogenesis, including unknown factors favoring IgA1 deposition in the glomerular mesangium. IgA receptor abnormalities are implicated, including circulating IgA-soluble CD89 (sCD89) complexes and overexpression of the mesangial IgA1 receptor, TfR1 (transferrin receptor 1). Herein, we show that although mice expressing both human IgA1 and CD89 displayed circulating and mesangial deposits of IgA1-sCD89 complexes resulting in kidney inflammation, hematuria, and proteinuria, mice expressing IgA1 only displayed endocapillary IgA1 deposition but neither mesangial injury nor kidney dysfunction. sCD89 injection into IgA1-expressing mouse recipients induced mesangial IgA1 deposits. sCD89 was also detected in patient and mouse mesangium. IgA1 deposition involved a direct binding of sCD89 to mesangial TfR1 resulting in TfR1 up-regulation. sCD89-TfR1 interaction induced mesangial surface expression of TGase2 (transglutaminase 2), which in turn up-regulated TfR1 expression. In the absence of TGase2, IgA1-sCD89 deposits were dramatically impaired. These data reveal a cooperation between IgA1, sCD89, TfR1, and TGase2 on mesangial cells needed for disease development. They demonstrate that TGase2 is responsible for a pathogenic amplification loop facilitating IgA1-sCD89 deposition and mesangial cell activation, thus identifying TGase2 as a target for therapeutic intervention in this disease.
    MeSH term(s) Animals ; Antigens, CD/physiology ; GTP-Binding Proteins/physiology ; Glomerulonephritis, IGA/etiology ; Humans ; Immunoglobulin A/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Fc/physiology ; Receptors, Transferrin/metabolism ; Transglutaminases/physiology
    Chemical Substances Antigens, CD ; Fc(alpha) receptor ; IgA receptor ; Immunoglobulin A ; Receptors, Fc ; Receptors, Transferrin ; Tfrc protein, mouse ; transglutaminase 2 (EC 2.3.2.-) ; Transglutaminases (EC 2.3.2.13) ; GTP-Binding Proteins (EC 3.6.1.-)
    Language English
    Publishing date 2012-03-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20112005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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