285,363 research outputs found
George R. Baker Letter - June 7, 1864
A letter written by George R. Baker to Catharine Hardenbergh Baker, sister of Solomon Hardenbergh. Solomon Hardenbergh joined the Company C, Michigan 1st Engineer Regiment in January 1864. He died on June 7, 1864 in Chattanooga, TN
Cross-orientation masking is speed invariant between ocular pathways but speed dependent within them
In human (D. H. Baker, T. S. Meese, & R. J. Summers, 2007b) and in cat (B. Li, M. R. Peterson, J. K. Thompson, T. Duong, & R. D. Freeman, 2005; F. Sengpiel & V. Vorobyov, 2005) there are at least two routes to cross-orientation suppression (XOS): a broadband, non-adaptable, monocular (within-eye) pathway and a more narrowband, adaptable interocular (between the eyes) pathway. We further characterized these two routes psychophysically by measuring the weight of suppression across spatio-temporal frequency for cross-oriented pairs of superimposed flickering Gabor patches. Masking functions were normalized to unmasked detection thresholds and fitted by a two-stage model of contrast gain control (T. S. Meese, M. A. Georgeson, & D. H. Baker, 2006) that was developed to accommodate XOS. The weight of monocular suppression was a power function of the scalar quantity ‘speed’ (temporal-frequency/spatial-frequency). This weight can be expressed as the ratio of non-oriented magno- and parvo-like mechanisms, permitting a fast-acting, early locus, as befits the urgency for action associated with high retinal speeds. In contrast, dichoptic-masking functions superimposed. Overall, this (i) provides further evidence for dissociation between the two forms of XOS in humans, and (ii) indicates that the monocular and interocular varieties of XOS are space/time scale-dependent and scale-invariant, respectively. This suggests an image-processing role for interocular XOS that is tailored to natural image statistics—very different from that of the scale-dependent (speed-dependent) monocular variety
Book review: El Sistema: orchestrating Venezuela’s youth, by Geoffrey Baker
Book review of: El Sistema: orchestrating Venezuela’s youth, by Geoffrey Baker.
New York, NY: Oxford University Press, 2014; ISBN: 9780199341559
($35.00)Publisher PD
Baker City Notice of Adopted Amendment (2012-03-19)
10 pp. Adopted 2012-03-19. Department of Land Conservation and Development Notice of Adopted AmendmentThe Comprehensive Plan "Land Suitability Map" and Baker City "Zone Map" have been amended to change the zone designation of four parcels, approximately 1 acre in size, from high-density residential (R-HD) to general commercial (C-G) located between Cedar Street and Oak Street, north of Campbell Street
No.215, William R. Murdoch, interview by Tim Larson
Transcript (35 pages) of interview by Tim Larson with William R. Murdoch, executive vice president and general manager of KSL, on July 11, 1988. This interview is no. 215 in the Everett L. Cooley Oral History Project, and tape no. 805Murdoch (b. 1931) recalls his early life and schooling; his family, especially his father Lennox Murdoch, KSL television station manager in the late 1940s; his involvement in promotion and management of KSL television; and many individuals who worked at KSL, 1940s-1980s. Interviewer: Tim Larso
tim-peterson/R-graphing-statistics: v1
<p>Creating v1 to prepare the ATRAID manuscript for its publication.</p>
[Letter from John R. Baker to John J. Herrera - January 27, 1977]
Letter from John R. Baker to John J. Herrera, dated January 27, 1977, regarding E & J Travel dba Arizona Bank Travel Service vs. League of United Latin American Citizens. The receipt, dated January 18, 1977, totals $58 and is from the Maricopa County Clerk for reproduction of a file
The Trail, 1922, The Yearbook of Daniel Baker College, Published Annually by the Senior Class
Yearbook for Daniel Baker College in Brownwood, Texas includes photos of and information about the college, student body, professors, and organizations
Personal performance: the resistant confessions of Bobby Baker
An analysis of the confessional performances of performance artist, Bobby Baker, in particular 'Box Story'
Upregulation of the Tim-3/galectin-9 pathway of T cell exhaustion in chronic hepatitis B virus infection.
The S-type lectin galectin-9 binds to the negative regulatory molecule Tim-3 on T cells and induces their apoptotic deletion or functional inactivation. We investigated whether galectin-9/Tim-3 interactions contribute to the deletion and exhaustion of the antiviral T cell response in chronic hepatitis B virus infection (CHB). We found Tim-3 to be expressed on a higher percentage of CD4 and CD8 T cells from patients with CHB than healthy controls (p<0.0001) and to be enriched on activated T cells and those infiltrating the HBV-infected liver. Direct ex vivo examination of virus-specific CD8 T cells binding HLA-A2/peptide multimers revealed that Tim-3 was more highly upregulated on HBV-specific CD8 T cells than CMV-specific CD8 T cells or the global CD8 T cell population in patients with CHB (p<0.001) or than on HBV-specific CD8 after resolution of infection. T cells expressing Tim-3 had an impaired ability to produce IFN-γ and TNF-α upon recognition of HBV-peptides and were susceptible to galectin-9-triggered cell death in vitro. Galectin-9 was detectable at increased concentrations in the sera of patients with active CHB-related liver inflammation (p = 0.02) and was strongly expressed by Kupffer cells within the liver sinusoidal network. Tim-3 blockade resulted in enhanced expansion of HBV-specific CD8 T cells able to produce cytokines and mediate cytotoxicity in vitro. Blocking PD-1 in combination with Tim-3 enhanced the number of patients from whom functional antiviral responses could be recovered and/or the strength of responses, indicating that these co-inhibitory molecules play a non-redundant role in driving T cell exhaustion in CHB. Patients taking antivirals able to potently suppress HBV viraemia continued to express Tim-3 on their T cells and respond to Tim-3 blockade. In summary, both Tim-3 and galectin-9 are increased in CHB and may contribute to the inhibition and deletion of T cells as they infiltrate the HBV-infected liver
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