Viking orbiter system primary mission

An overview of Viking Orbiter (VO) system and subsystem performances during the primary mission (the time period from VO-1 launch on August 20, 1975, through November 15, 1976) is presented. Brief descriptions, key design requirements, pertinent historical information, unique applications or situations, and predicted versus actual performances are included for all VO-1 and VO-2 subsystems, both individually and as an integrated system

Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62LloFoxP3+CD4+ T cells with limited suppressor activity

IL-2 plays a critical role in the induction and maintenance of FoxP3-expressing regulatory T cells (FoxP3+Treg). Reduced expression of IL-2 is linked to T cell-mediated autoimmune diseases such as Type 1 diabetes (T1D), in which an imbalance between FoxP3+Treg and pathogenic T effectors exists. We investigated the contribution of IL-2 to dysregulation of FoxP3+Treg by comparing wildtype NOD mice with animals congenic for a C57BL/6-derived disease resistant Il2 allele and in which T cell secretion of IL-2 is increased (NOD.B6Idd3). Whereas NOD mice exhibited a progressive decline in the frequency of CD62LHIFoxP3+Treg due to an increase in CD62LLOFoxP3+Treg, CD62LHIFoxP3+Treg were maintained in the pancreatic lymph nodes and islets of NOD.B6Idd3 mice. Notably, the frequency of proliferating CD62LHIFoxP3+Treg was elevated in the islets of NOD.B6Idd3 versus NOD mice. Increasing levels of IL-2 in vivo also resulted in larger numbers of CD62LHIFoxP3+Treg in NOD mice. These results demonstrate that IL-2 influences the suppressor activity of the FoxP3+Treg pool by regulating the balance between CD62LLO and CD62LHI FoxP3+Treg. In NOD mice reduced IL-2 expression leads to an increase in nonsuppressive CD62LLOFoxP3+Treg, which in turn correlates with a pool of CD62LHIFoxP3+Treg with limited proliferation

Quantitative conversations: the importance of developing rapport in standardised interviewing

© 2014, The Author(s). When developing household surveys, much emphasis is understandably placed on developing survey instruments that can elicit accurate and comparable responses. In order to ensure that carefully crafted questions are not undermined by ‘interviewer effects’, standardised interviewing tends to be utilised in preference to conversational techniques. However, by drawing on a behaviour coding analysis of survey paradata arising from the 2012 UK Poverty and Social Exclusion Survey we show that in practice standardised survey interviewing often involves extensive unscripted conversation between the interviewer and the respondent. Whilst these interactions can enhance response accuracy, cooperation and ethicality, unscripted conversations can also be problematic in terms of survey reliability and the ethical conduct of survey interviews, as well as raising more basic epistemological questions concerning the degree of standardisation typically assumed within survey research. We conclude that better training in conversational techniques is necessary, even when applying standardised interviewing methodologies. We also draw out some theoretical implications regarding the usefulness of the qualitative–quantitative dichotomy

Human Cord Blood Stem Cell-Modulated Regulatory T Lymphocytes Reverse the Autoimmune-Caused Type 1 Diabetes in Nonobese Diabetic (NOD) Mice

Background: The deficit of pancreatic islet b cells caused by autoimmune destruction is a crucial issue in type 1 diabetes (T1D). It is essential to fundamentally control the autoimmunity for treatment of T1D. Regulatory T cells (Tregs) play a pivotal role in maintaining self-tolerance through their inhibitory impact on autoreactive effector T cells. An abnormality of Tregs is associated with initiation of progression of T1D. Methodology/Principal Findings: Here, we report that treatment of established autoimmune-caused diabetes in NOD mice with purified autologous CD4 + CD62L + Tregs co-cultured with human cord blood stem cells (CB-SC) can eliminate hyperglycemia, promote islet b-cell regeneration to increase b-cell mass and insulin production, and reconstitute islet architecture. Correspondingly, treatment with CB-SC-modulated CD4 + CD62L + Tregs (mCD4CD62L Tregs) resulted in a marked reduction of insulitis, restored Th1/Th2 cytokine balance in blood, and induced apoptosis of infiltrated leukocytes in pancreatic islets. Conclusions/Significance: These data demonstrate that treatment with mCD4CD62L Tregs can reverse overt diabetes

Cellular Islet Autoimmunity Associates with Clinical Outcome of Islet Cell Transplantation

Islet cell transplantation can cure type 1 diabetes (T1D), but only a minority of recipients remains insulin-independent in the following years. We tested the hypothesis that allograft rejection and recurrent autoimmunity contribute to this progressive loss of islet allograft function.Twenty-one T1D patients received cultured islet cell grafts prepared from multiple donors and transplanted under anti-thymocyte globulin (ATG) induction and tacrolimus plus mycophenolate mofetil (MMF) maintenance immunosuppression. Immunity against auto- and alloantigens was measured before and during one year after transplantation. Cellular auto- and alloreactivity was assessed by lymphocyte stimulation tests against autoantigens and cytotoxic T lymphocyte precursor assays, respectively. Humoral reactivity was measured by auto- and alloantibodies. Clinical outcome parameters--including time until insulin independence, insulin independence at one year, and C-peptide levels over one year--remained blinded until their correlation with immunological parameters. All patients showed significant improvement of metabolic control and 13 out of 21 became insulin-independent. Multivariate analyses showed that presence of cellular autoimmunity before and after transplantation is associated with delayed insulin-independence (p = 0.001 and p = 0.01, respectively) and lower circulating C-peptide levels during the first year after transplantation (p = 0.002 and p = 0.02, respectively). Seven out of eight patients without pre-existent T-cell autoreactivity became insulin-independent, versus none of the four patients reactive to both islet autoantigens GAD and IA-2 before transplantation. Autoantibody levels and cellular alloreactivity had no significant association with outcome.In this cohort study, cellular islet-specific autoimmunity associates with clinical outcome of islet cell transplantation under ATG-tacrolimus-MMF immunosuppression. Tailored immunotherapy targeting cellular islet autoreactivity may be required. Monitoring cellular immune reactivity can be useful to identify factors influencing graft survival and to assess efficacy of immunosuppression.Clinicaltrials.gov NCT00623610