100,481 research outputs found
Jon Huseby, \u2701, appointed Magistrate Judge for the District of MN
No full textMichael J. Davis, Chief U.S. District Judge, is pleased to announce the appointment of Jon T. Huseby to the position of Part-Time United States Magistrate Judge for the District of Minnesota. Magistrate Judge Huseby took the oath of office in the U.S. Courthouse in Minneapolis on February 25, 2015. A formal investiture ceremony will be held at a later date.
The U.S. District Judges of the District of Minnesota appointed an eight-member Merit Selection Panel to review applications, interview prospective candidates, and recommend to the District Judges the candidates they deemed best qualified for the position. The Honorable Donovan W. Frank, U.S. District Judge, chaired the Panel.
Huseby graduated from the University of North Dakota School of Law in 2001, after earning a B.A. from the University of Minnesota and attending the Norwegian University of Science and Technology in Trondheim, Norway. Before attending school, Huseby served in the U.S. Army. After law school, Huseby moved to the Bemidji area where he worked as an associate attorney at Hazelton and Rodgers from 2001 to 2006 and as a staff attorney for the Legal Services of Northwestern Minnesota from 2006-2008. Since 2008, Huseby has worked at the firm of Fuller, Wallner, Cayko, Pederson & Huseby in Bemidji, where he is currently a partner, specializing in the areas of worker’s compensation, social security disability appeals, and personal injury.
Part-Time U.S. Magistrate Judges are appointed by the U.S. District Court for a four-year term and are eligible for reappointment to successive terms. The Part-Time Magistrate Judge position serves the U.S. District Court, District of Minnesota in the Bemidji area. The primary duties performed by the Part-Time U.S. Magistrate Judge include reviewing and issuing warrants, presiding over initial appearance proceedings, and presiding over petty offense and misdemeanor proceedings
Investigating the Peptide-MHC Specificity of Alloreactive T Cells and Natural T Regulatory Cells Using a Self-peptide Display Library
Get PDFT cells use their highly variable T cell receptor (TCR) to engage major histocompatibility molecules (MHC) presenting peptides on the surface of antigen presenting cells during an immune response. The TCR repertoire of developing T cells is shaped by thymic selection, resulting in a self-tolerant and foreign peptide specific naïve T cell population. However, naive T cells are alloreactive and generate immune responses towards foreign MHC alleles in clinical settings involving transplantation. While T cell immune responses towards foreign pathogens are peptide specific, the overall specificity of allo-responses is still debated. Under normal circumstances, immune system homeostasis and self-tolerance is maintained by specialized natural T regulatory cells (nTregs) that develop in the thymus. nTregs respond to self-peptide MHC they encountered in peripheral tissues with immune-suppressive activities. However, the identify of self-peptides that stimulate nTregs, specificity towards these self-peptides, and the method nTreg TCRs engage self-peptide MHC molecules is not clear. Here, we built a library of defined MHC-linked self-peptides eluted from the I-Ab MHC molecule to screen alloreactive T cells and self-reactive nTregs for activating self-peptides. We used this library to show that negative selection shapes the TCR repertoire’s specificity to self-peptides. We also provide evidence that alloreactive T cells have degenerate self and foreign peptide recognition if the foreign MHC allele is largely different from the host’s MHC allele. Finally, we identified a self-peptide that activates an nTreg, and present protein crystal structures that reveal its TCR engages self and foreign peptide MHC complexes via fairly conventional mechanisms.Immunology and Microbiolog
Characterization of the Role of CD4 T Cell Help in Promoting Islet-specific CD8 T Cell Responses in Type 1 Diabetes Pathogenesis
Get PDFType 1 diabetes mellitus (T1D) is a chronic autoimmune disease characterized by CD8+ T cell-mediated destruction of the insulin-producing beta cells within the pancreatic islets. Although CD8+ T cells are thought to be the primary mediators of beta cell killing, strong genetic associations with homozygous expression of MHC-II alleles bearing beta chain polymorphisms suggest a central role for CD4+ T cells in disease pathogenesis. Despite these recognized associations, the mechanisms by which heterozygous expression of one high-risk and one protective allele abrogates disease risk remain unclear. Here, using the non-obese diabetic (NOD) mouse model, we demonstrate that heterozygous expression of the T1D-protective I-Ag7 Beta-56P/57D allele induces negative selection to the I-Ag7-restricted T cell repertoire, including high-affinity beta-islet-specific CD4+ T cells, resulting in a marked reduction in the islet-specific CD8+ T cell response. Further, we show that protected mice exhibit a dramatic loss of CXCR6+ islet-specific CD4+ T cells, specifically implicating a role for this population in supporting islet-directed CD8+ T cell responses. Finally, we characterize the functional contribution of CD4+ T cell help in promoting CD8+ T cell effector differentiation in the periphery using NOD mouse models with genetically limited CD4+ T cell help. We find that islet-specific CD8+ T cells receiving inadequate help signals undergo increased levels of apoptosis, but can be rescued with IL-2 complex treatment. Taken together, these studies provide mechanistic insights into how protective MHC-II molecules manifest T cell tolerance and reveal how CD4+ T cell help contributes to the expansion and survival of islet-specific CD8+ T cells.Immunology and Microbiology6 months2026-01-3
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
A Parametric Class Of Production Strategies For Multi-Reservoir Production Optimization
No full textWhen a large oil or gas field is produced, several reservoirs often share the same processing facility. This facility is typically capable of processing only a limited amount of oil, gas and water per unit of time. In the present paper only single phase production, e.g., oil production, is considered. In order to satisfy the processing limitations, the production needs to be choked. That is, for each reservoir the production is scaled down by suitable choke factors between zero and one, chosen so that the total production does not exceed the processing capacity. Huseby & Haavardsson (2008) introduced the concept of a production strategy, a vector valued function defined for all points of time t ≥ 0 representing the choke factors applied to the reservoirs at time t. As long as the total potential production rate is greater than the processing capacity, the choke factors should be chosen so that the processing capacity is fully utilized. When the production reaches a state where this is not possible, the production should be left unchoked. A production strategy satisfying these constraints is said to be admissible. Huseby & Haavardsson (2008) developed a general framework for optimizing production strategies with respect to various types of objective functions. In the present paper we present a parametric class of admissible production strategies. Using the framework of Huseby & Haavardsson (2008) it can be shown that under mild restrictions on the objective function an optimal strategy can be found within this class. The number of parameters needed to span the class is bounded by the number of reservoirs. Thus, an optimal strategy within this class can be found using a standard numerical optimization algorithm. This makes it possible to handle complex, high-dimensional cases. Furthermore, uncertainty may be included, enabling robustness and sensitivity analysis
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CD4+ T cell tolerance to tissue-restricted self antigens
No full textSelf antigen-specific T cell development is influenced by how the self antigen is expressed. In this thesis, I explored this concept using a novel panel of mice in which a model self antigen is conditionally expressed in different tissues. We studied the steady state development of the unmanipulated endogenous self antigen-specific CD4+ T cell repertoire under these various conditions by using peptide:MHC II tetramers. We found that in some cases, self antigen-specific T cells were deleted efficiently in the thymus, while in others, they were partially deleted in peripheral lymphoid organs. Deletion specifically affected Foxp3- conventional T cells (Tconv), and was biased towards high avidity clones in the thymus but not periphery. In contrast, Foxp3+ regulatory T cell (Treg) numbers were elevated in the periphery, and were preferentially comprised of high avidity clones. Self antigen-specific T cells surviving deletion exhibited tolerance to antigen stimulation, with Tconv cells exhibiting greater functional impairment than Tregs. Acute ablation of Tregs partially restored the proliferative ability of self antigen-specific Tconv cells, which demonstrated that, in addition to Tconv deletion, Treg development is important in maintaining tolerance. Although functionally impaired in the absence of Tregs, self-antigen specific Tconv cells did not express FR4 and CD73, which mark anergic T cells undergoing transition into peripherally induced Tregs. Genetic deficiency of Aire did not affect the peripheral deletion of self antigen-specific T cells, indicating that this process can occur independently of this transcriptional regulator. Finally, we implemented the use of cutting edge single-cell RNA-seq technology to transcriptional profile tetramer-sorted self antigen-specific T cells, and our preliminary findings revealed the development of Foxp3- IL-10 expressing type 1 regulatory T cells (Tr1) in a gut self antigen-specific T cell population. Together, our results illustrate how steady state T cell recognition of tissue-restricted self antigens results in opposing effects on Tconv and Treg subset development, both of which contribute to self tolerance.Medical SciencesMedical Science
Handwritten biographical information on Paulina T. McClung Merritt
No full textA handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
Get PDFIFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
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