Brief communication: Comparison of the performance of thermistors and digital temperature sensors in a mountain permafrost borehole

Monitoring mountain-permafrost temperatures in boreholes is challenging regarding the resilience and long-term temperature stability of the sensor systems. Whilst resistance thermistors boast a high accuracy, they are prone to drift when exposed to moisture, pressure or cable strain. Supplementing or replacing them with digital bandgap temperature sensors requires careful analysis of the sensor performance. We carry out a first comparison of two temperature sensor systems under field conditions in mountain permafrost at 15 identical depths in 1 borehole. Temperature values, sensing delays and noise levels are compared and discussed.</p

Learning of Closed-Loop Motion Control

Learning motion control as a unified process of designing the reference trajectory and the controller is one of the most challenging problems in robotics. The complexity of the problem prevents most of the existing optimization algorithms from giving satisfactory results. While model-based algorithms like iterative linear-quadratic-Gaussian (iLQG) can be used to design a suitable controller for the motion control, their performance is strongly limited by the model accuracy. An inaccurate model may lead to degraded performance of the controller on the physical system. Although using machine learning approaches to learn the motion control on real systems have been proven to be effective, their performance depends on good initialization. To address these issues, this paper introduces a two-step algorithm which combines the proven performance of a model-based controller with a model-free method for compensating for model inaccuracy. The first step optimizes the problem using iLQG. Then, in the second step this controller is used to initialize the policy for our PI$^2$-01 reinforcement learning algorithm. This algorithm is a derivation of the PI$^2$ algorithm enabling more stable and faster convergence. The performance of this method is demonstrated both in simulation and experimental results

Bandwidth Allocation and Reservation - End-to-End Specification

The Bandwidth Allocation and Reservation (BAR) activity within JRA4 of the EGEE project specified and implemented the necessary components and interfaces to enable the EGEE Grid middleware to request and use guaranteed bandwidth services. This report describes the components and interfaces required for an end-to-end BAR service and how they interact

Direct Interrogation of Viral Peptides Presented by the Class I HLA of HIV-Infected T Cells

Identification of CD8+ cytotoxic T lymphocyte (CTL) epitopes has traditionally relied upon testing of overlapping peptide libraries for their reactivity with T cells in vitro. Here, we pursued deep ligand sequencing (DLS) as an alternative method of directly identifying those ligands that are epitopes presented to CTLs by the class I human leukocyte antigens (HLA) of infected cells. Soluble class I HLA-A*11:01 (sHLA) was gathered from HIV-1 NL4-3-infected human CD4+ SUP-T1 cells. HLA-A*11:01 harvested from infected cells was immunoaffinity purified and acid boiled to release heavy and light chains from peptide ligands that were then recovered by size-exclusion filtration. The ligands were first fractionated by high-pH high-pressure liquid chromatography and then subjected to separation by nano-liquid chromatography (nano-LC)–mass spectrometry (MS) at low pH. Approximately 10 million ions were selected for sequencing by tandem mass spectrometry (MS/MS). HLA-A*11:01 ligand sequences were determined with PEAKS software and confirmed by comparison to spectra generated from synthetic peptides. DLS identified 42 viral ligands presented by HLA-A*11:01, and 37 of these were previously undetected. These data demonstrate that (i) HIV-1 Gag and Nef are extensively sampled, (ii) ligand length variants are prevalent, particularly within Gag and Nef hot spots where ligand sequences overlap, (iii) noncanonical ligands are T cell reactive, and (iv) HIV-1 ligands are derived from de novo synthesis rather than endocytic sampling. Next-generation immunotherapies must factor these nascent HIV-1 ligand length variants and the finding that CTL-reactive epitopes may be absent during infection of CD4+ T cells into strategies designed to enhance T cell immunity

An inflammatory checkpoint regulates recruitment of graft-versus-host reactive T cells to peripheral tissues

Transfer of T cells to freshly irradiated allogeneic recipients leads to their rapid recruitment to nonlymphoid tissues, where they induce graft-versus-host disease (GVHD). In contrast, when donor T cells are transferred to established mixed chimeras (MCs), GVHD is not induced despite a robust graft-versus-host (GVH) reaction that eliminates normal and malignant host hematopoietic cells. We demonstrate here that donor GVH-reactive T cells transferred to MCs or freshly irradiated mice undergo similar expansion and activation, with similar up-regulation of homing molecules required for entry to nonlymphoid tissues. Using dynamic two-photon in vivo microscopy, we show that these activated T cells do not enter GVHD target tissues in established MCs, contrary to the dogma that activated T cells inevitably traffic to nonlymphoid tissues. Instead, we show that the presence of inflammation within a nonlymphoid tissue is a prerequisite for the trafficking of activated T cells to that site. Our studies help to explain the paradox whereby GVH-reactive T cells can mediate graft-versus-leukemia responses without inducing GVHD in established MCs

Identification of Class I HLA T Cell Control Epitopes for West Nile Virus

The recent West Nile virus (WNV) outbreak in the United States underscores the importance of understanding human immune responses to this pathogen. Via the presentation of viral peptide ligands at the cell surface, class I HLA mediate the T cell recognition and killing of WNV infected cells. At this time, there are two key unknowns in regards to understanding protective T cell immunity: 1) the number of viral ligands presented by the HLA of infected cells, and 2) the distribution of T cell responses to these available HLA/viral complexes. Here, comparative mass spectroscopy was applied to determine the number of WNV peptides presented by the HLA-A*11:01 of infected cells after which T cell responses to these HLA/WNV complexes were assessed. Six viral peptides derived from capsid, NS3, NS4b, and NS5 were presented. When T cells from infected individuals were tested for reactivity to these six viral ligands, polyfunctional T cells were focused on the GTL9 WNV capsid peptide, ligands from NS3, NS4b, and NS5 were less immunogenic, and two ligands were largely inert, demonstrating that class I HLA reduce the WNV polyprotein to a handful of immune targets and that polyfunctional T cells recognize infections by zeroing in on particular HLA/WNV epitopes. Such dominant HLA/peptide epitopes are poised to drive the development of WNV vaccines that elicit protective T cells as well as providing key antigens for immunoassays that establish correlates of viral immunity. © 2013 Kaabinejadian et al

‘How can I be post-Soviet if I was never Soviet?’ Rethinking categories of time and social change – a perspective from Kulob, southern Tajikistan

Based on anthropological fieldwork conducted in the Kulob region of southern Tajikistan, this paper examines the extent to which the existing periodization ‘Soviet/post-Soviet’ is still valid to frame scholarly works concerning Central Asia. It does so through an analysis of ‘alternative temporalities’ conveyed by Kulob residents to the author. These alternative temporalities are fashioned in especially clear ways in a relationship to the physical transformations occurring to two types of housing, namely flats in building blocks and detached houses. Without arguing that the categories ‘Soviet’ and ‘post-Soviet’ have become futile, the author advocates that the uncritically use of Soviet/post-Soviet has the unwanted effect of shaping the Central Asian region as a temporalized and specialized ‘other’

HLA class I molecules consistently present internal influenza epitopes

Cytotoxic T lymphocytes (CTL) limit influenza virus replication and prevent morbidity and mortality upon recognition of HLA class I presented epitopes on the surface of virus infected cells, yet the number and origin of the viral epitopes that decorate the infected cell are unknown. To understand the presentation of influenza virus ligands by human MHC class I molecules, HLA-B*0702-presented viral peptides were directly identified following influenza infection. After transfection with soluble class I molecules, peptide ligands unique to infected cells were eluted from isolated MHC molecules and identified by comparative mass spectrometry (MS). Then CTL were gathered following infection with influenza and viral peptides were tested for immune recognition. We found that the class I molecule B*0702 presents 3-6 viral ligands following infection with different strains of influenza. Peptide ligands derived from the internal viral nucleoprotein (NP418-426 and NP 473-481) and from the internal viral polymerase subunit PB1 (PB1 329-337) were presented by B*0702 following infection with each of 3 different influenza strains; ligands NP418-426, NP 473-481, and PB1329-337 derived from internal viral proteins were consistently revealed by class I HLA. In contrast, ligands derived from hemagglutinin (HA) and matrix protein (M1) were presented intermittently on a strain-by-strain basis. When tested for immune recognition, HLA-B*0702 transgenic mice responded to NP418-426 and PB1 329-337 consistently and NP473-481 intermittently while ligands from HA and M1 were not recognized. These data demonstrate an emerging pattern whereby class I HLA reveal a handful of internal viral ligands and whereby CTL recognize consistently presented influenza ligands