28,804 research outputs found
Letter from Carl Hayden to Henry F. Ashurst
No full textLetter describing three enclosures, a letter from F. M. Gold, Carl T. Hayden's reply to Gold's letter, and a copy of a bill introduced by Cameron
Letter from A. F. Potter to Carl Hayden
No full textLetter from A. F. Potter to Carl T. Hayden describing John H. Page's request to build a railway for the Canyon Copper Company as "impractical"
DNA fusion gene vaccination mobilizes effective anti-leukemic cytotoxic T lymphocytes from a tolerized repertoire
No full textThe majority of known human tumor-associated antigens derive from non-mutated self proteins. T cell tolerance, essential to prevent autoimmunity, must therefore be cautiously circumvented to generate cytotoxic T cell responses against these targets. Our strategy uses DNA fusion vaccines to activate high levels of peptide-specific CTL. Key foreign sequences from tetanus toxin activate tolerance-breaking CD4+ T cell help. Candidate MHC class Ibinding tumor peptide sequences are fused to the C terminus for optimal processing and presentation. To model performance against a leukemia-associated antigen in a tolerized setting, we constructed a fusion vaccine encoding an immunodominant CTL epitopederived from Friend murine leukemia virus gag protein (FMuLVgag) and vaccinated tolerant FMuLVgag-transgenic (gag-Tg) mice. Vaccination with the construct induced epitopespecificIFN-c-producing CD8+ T cells in normal and gag-Tg mice. The frequency and avidity of activated cells were reduced in gag-Tg mice, and no autoimmune injury resulted. However, these CD8+ T cells did exhibit gag-specific cytotoxicity in vitro and in vivo. Also, epitope-specific CTL killed FBL-3 leukemia cells expressing endogenous FMuLVgag antigen and protected against leukemia challenge in vivo. These results demonstrate a simple strategy to engage anti-microbial T cell help to activate epitope-specific polyclonal CD8+ T cell responses from a residual tolerized repertoire
Reply to comment by K. Gajewski on Abrupt environmental change in Canada\u27s northernmost lake
No full textWe welcome the opportunity to respond to Gajewski\u27s [2008] comments on our study [Antoniades et al., 2007, hereinafter referred to as A07]. We demonstrate here that his assertions are not supported by the evidence and that the conclusions in A07 are based on a sound interpretation of the data. Copyright 2008 by the American Geophysical Union
Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8α+ dendritic cells
No full textDespite lack of tumor control in many models, spontaneous T cell priming occurs frequently in response to a growing tumor. However, the innate immune mechanisms that promote natural antitumor T cell responses are undefined. In human metastatic melanoma, there was a correlation between a type I interferon (IFN) transcriptional profile and T cell markers in metastatic tumor tissue. In mice, IFN-b was produced by CD11c(+) cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacking IFN-a/bR or Stat1. IFN signaling was required in the hematopoietic compartment at the level of host antigen-presenting cells, and selectively for intratumoral accumulation of CD8a(+) dendritic cells, which were demonstrated to be essential using Batf3(-/-) mice. Thus, host type I IFNs are critical for the innate immune recognition of a growing tumor through signaling on CD8alfa(+) DCs.Fil: Fuertes, Mercedes Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University Of Chicago; Estados UnidosFil: Kacha, Aalok K. . University Of Chicago; Estados UnidosFil: Kline, Justin . University Of Chicago; Estados UnidosFil: Woo, Seng Ryong . University Of Chicago; Estados UnidosFil: Kranz, David M. . University Of Illinois; Estados UnidosFil: Murphy, Kenneth M. . Washington University in St. Louis; Estados UnidosFil: Gajewski, Thomas F. . University Of Chicago; Estados Unido
Innate immune sensing of cancer: clues from an identified role for type I IFNs
No full textA subset of patients with a variety of cancers shows evidence of a natural adaptive immune response against their tumor, as evidenced by spontaneous T-cell infiltration, circulating anti-tumor T cells, or antibody responses. Evidence has indicated that such natural immune responses have positive prognostic import in early stage disease and may be predictive of clinical response to immunotherapeutics in advanced disease. However, these observations raise a new critical fundamental question?what innate immune signals might be generated in the context of non-pathogen-induced cancers that drive productive antigen presentation toward induction of an adaptive immune response? Gene expression profiling in melanoma revealed that tumors having high expression of T-cell markers also show evidence of a type I IFN transcriptional signature. Mechanistic experiments in mice have revealed that a spontaneous CD8+ T-cell response against transplantable tumors depends on host type I IFN signaling, through a mechanism dependent upon CD8α+ dendritic cells (DCs). The requirement for type I IFN production by host DCs has suggested a subset of innate immune sensing receptors and signaling pathways that might be involved with initiating this process. Elucidating further these innate immune mechanisms should provide new insights into cancer immunotherapy.Fil: Gajewski, Thomas F.. University Of Chicago; Estados UnidosFil: Fuertes, Mercedes Beatriz. University Of Chicago; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Woo, Seng Ryong. University Of Chicago; Estados Unido
Elaboration on Kwapien's theorem: Representing bounded mean zero functions f as coboundary f = g ◦ T − g
No full textIn [8] Kwapien proved that every mean zero function f ∈ L∞[0, 1] we can write as f = g ◦ T − g for some g ∈ L∞[0, 1] and some measure preserving transformation T of [0, 1]. However, as was discovered in [4] there is a gap in the proof for the case that f is not continuous. The aim of this bachelor thesis is filling in that gap in the proof. We first extend Kwapien’s proof for continuous functions to certain other measure spaces. Thereafter, we use the method of proof suggested by Kwapien, to proof the theorem for mean zero function f ∈ L∞[0, 1] for which λ(f−1({x})) = 0 for all x ∈ R. Using this result we then proof that every mean zero function f ∈ L∞[0, 1] can be written as a sum f =(g1 ◦ T1 − g1) + (g2 ◦ T2 − g2) where g1, g2 ∈ L∞[0, 1] and where T1, T2 are measure preserving transformations of [0, 1]. We finish this thesis with an application of Kwapien’s theorem in the study to singular traces Applied Mathematic
f(G,T) and its Cosmological Implications
No full textA coupled formulation of the Gauss-Bonnet invariant term G and the
energy momentum trace T term provide a modified f(G,T) gravity,
has been analyzed in this study. The functional form for the
f(G,T) gravity has been taken as f(G,T)=αT+ βGThe presentation of the authors' names and (or) special characters in the title of the pdf file of the accepted manuscript may differ slightly from what is displayed on the item page. The information in the pdf file of the accepted manuscript reflects the original submission by the author
Bianchi type-I universe in f(R, T) modified gravity with quark matter and Λ
No full text32nd International Physics Congress of Turkish-Physical-Society (TPS) -- SEP 06-09, 2016 -- Bodrum, TURKEYIn this study, we investigate homogeneous and anisotropic Bianchi type I universe in the presence of quark matter source in f (R, T) gravity (Harko et al. in Phys. Rev. D 84:024020, 2011) with cosmological constant A (where R is the Ricci scalar and T is the trace of the energy momentum tensor). For this aim we have used the anisotropy feature of Bianchi type I universe and equation of states (EoS) of quark matter. We explore the exact solution f(R, T)=R + 2f(T) model for Bianchi type I universe model. When t -> infinity, we get very small cosmological constant value, this result agrees with recent observations.Turkish Phys So
B7-1 but not B7-2 eficiently costimulates CD8(+) T lymphocytes in the P815 tumor system in vitro
No full textWe recently have developed a method to generate primary P815-specific CTL in vitro from normal syngeneic splenocytes by employing transfection of B7-1 combined with exogenous IL-12 and IL-6. Surprisingly, when the homologous costimulator molecule B7-2 was substituted for B7-1 in this system, no specific CTL activity was obtained, Similarly, B7-1- but not B7-2-transfected P815 cells generated alloantigen-specific CTL activity from C578L/6, accessory cell- and CD4(+)-depleted splenocytes, and costimulated proliferation of CD8(+) lymphocytes in the presence of low doses of anti-CD3 mAb. In all systems, combined expression of both B7-1 and B7-2 costimulated as effectively as B7-1 alone, arguing against delivery of a dominant negative signal by B7-2. Proliferation of allogeneic, CD4(+)-depleted splenocytes in response to P815 cells, which relies on costimulation by normal accessory cells, was inhibited by anti-B7-1 but not anti-B7-2 mAbs. Finally, indirect evidence suggested a higher avidity of B7-1(+) cells than B7-2(+) cells for CTLA4. Thus, at least in the context of primary stimulation by irradiated P815 transfectants, B7-1 appears to be superior to B7-2 at costimulation of CD8(+) T lymphocytes
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