Efficient Model Learning for Human-Robot Collaborative Tasks

We present a framework for learning human user models from joint-action demonstrations that enables the robot to compute a robust policy for a collaborative task with a human. The learning takes place completely automatically, without any human intervention. First, we describe the clustering of demonstrated action sequences into different human types using an unsupervised learning algorithm. These demonstrated sequences are also used by the robot to learn a reward function that is representative for each type, through the employment of an inverse reinforcement learning algorithm. The learned model is then used as part of a Mixed Observability Markov Decision Process formulation, wherein the human type is a partially observable variable. With this framework, we can infer, either offline or online, the human type of a new user that was not included in the training set, and can compute a policy for the robot that will be aligned to the preference of this new user and will be robust to deviations of the human actions from prior demonstrations. Finally we validate the approach using data collected in human subject experiments, and conduct proof-of-concept demonstrations in which a person performs a collaborative task with a small industrial robot

The Impact of Advocacy Organizations on Low-Income Housing Policy in U.S. Cities

Financial support for affordable housing competes with many other municipal priorities. This work seeks to explain the variation in support for affordable housing among U.S. cities with populations of 100,000 or more. Using multivariate statistical analysis, this research investigates political explanations for the level of city expenditures on housing and community with a particular interest in the influence of housing advocacy organizations (AOs). Data for the model were gathered from secondary sources, including the U.S. Census and the National Center for Charitable Statistics. Among other results, the analysis indicates that, on average, the political maturity of AOs has a statistically significant, positive effect on local housing and community development expenditures

Concurrent Proinflammatory and Apoptotic Activity of a Helicobacter pylori Protein (HP986) Points to Its Role in Chronic Persistence

Helicobacter pylori induces cytokine mediated changes in gastroduodenal pathophysiology, wherein, the activated macrophages at the sub-mucosal space play a central role in mounting innate immune response against the antigens. The bacterium gains niche through persistent inflammation and local immune-suppression causing peptic ulcer disease or chronic gastritis; the latter being a significant risk factor for the development of gastric adenocarcinoma. What favors persistence of H. pylori in the gastric niches is not clearly understood. We report detailed characterization of a functionally unknown gene (HP986), which was detected in patient isolates associated with peptic ulcer and gastric carcinoma. Expression and purification of recombinant HP986 (rHP986) revealed a novel, ∼29 kDa protein in biologically active form which associates with significant levels of humoral immune responses in diseased individuals (p<0.001). Also, it induced significant levels of TNF-α and Interleukin-8 in cultured human macrophages concurrent to the translocation of nuclear transcription factor-κB (NF-κB). Further, the rHP986 induced apoptosis of cultured macrophages through a Fas mediated pathway. Dissection of the underlying signaling mechanism revealed that rHP986 induces both TNFR1 and Fas expression to lead to apoptosis. We further demonstrated interaction of HP986 with TNFR1 through computational and experimental approaches. Independent proinflammatory and apoptotic responses triggered by rHP986 as shown in this study point to its role, possibly as a survival strategy to gain niche through inflammation and to counter the activated macrophages to avoid clearance

Partially glycosylated dendrimers block MD-2 and prevent TLR4-MD-2-LPS complex mediated cytokine responses.

The crystal structure of the TLR4-MD-2-LPS complex responsible for triggering powerful pro-inflammatory cytokine responses has recently become available. Central to cell surface complex formation is binding of lipopolysaccharide (LPS) to soluble MD-2. We have previously shown, in biologically based experiments, that a generation 3.5 PAMAM dendrimer with 64 peripheral carboxylic acid groups acts as an antagonist of pro-inflammatory cytokine production after surface modification with 8 glucosamine molecules. We have also shown using molecular modelling approaches that this partially glycosylated dendrimer has the flexibility, cluster density, surface electrostatic charge, and hydrophilicity to make it a therapeutically useful antagonist of complex formation. These studies enabled the computational study of the interactions of the unmodified dendrimer, glucosamine, and of the partially glycosylated dendrimer with TLR4 and MD-2 using molecular docking and molecular dynamics techniques. They demonstrate that dendrimer glucosamine forms co-operative electrostatic interactions with residues lining the entrance to MD-2's hydrophobic pocket. Crucially, dendrimer glucosamine interferes with the electrostatic binding of: (i) the 4'phosphate on the di-glucosamine of LPS to Ser118 on MD-2; (ii) LPS to Lys91 on MD-2; (iii) the subsequent binding of TLR4 to Tyr102 on MD-2. This is followed by additional co-operative interactions between several of the dendrimer glucosamine's carboxylic acid branches and MD-2. Collectively, these interactions block the entry of the lipid chains of LPS into MD-2's hydrophobic pocket, and also prevent TLR4-MD-2-LPS complex formation. Our studies have therefore defined the first nonlipid-based synthetic MD-2 antagonist using both animal model-based studies of pro-inflammatory cytokine responses and molecular modelling studies of a whole dendrimer with its target protein. Using this approach, it should now be possible to computationally design additional macromolecular dendrimer based antagonists for other Toll Like Receptors. They could be useful for treating a spectrum of infectious, inflammatory and malignant diseases

North Beach, Anzac, looking towards Sulva [picture] /

Part of collection: Gallipoli Peninsula, Turkey, 1915.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn3072055

North Beach, Anzac, looking south [picture] /

Part of collection: Gallipoli Peninsula, Turkey, 1915.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn3072048. "1st Casualty Clearing Hospital in right hand distance. Range of hills is where Australians charged on day of landing."--Inscription on reverse

Rest Gully, Anzac, showing terraces of dug outs [picture] /

Part of collection: Gallipoli Peninsula, Turkey, 1915.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn3072008. Inscription: "Subsequently 2nd Australian Divisional Headquarters were here."--In pencil on reverse

Piccadilly, Lonesome Pine firing line [picture] /

Part of collection: Gallipoli Peninsula, Turkey, 1915.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn3072016. Inscription: "This was only 20 yards from the Turks. In left hand corner can be seen tunnel going under the Turks."--In pencil on reverse

[Warships at Gallipoli Peninsula, 1915] [picture] /

Title devised by cataloguer.; Part of collection: Gallipoli Peninsula, Turkey, 1915.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn3072083