We address the issue of visual saliency from three perspectives. First, we consider saliency detection as a frequency domain analysis problem. Second, we achieve this by employing the concept of nonsaliency. Third, we simultaneously consider the detection of salient regions of different size. The paper proposes a new bottom-up paradigm for detecting visual saliency, characterized by a scale-space analysis of the amplitude spectrum of natural images. We show that the convolution of the image amplitude spectrum with a low-pass Gaussian kernel of an appropriate scale is equivalent to an image saliency detector. The saliency map is obtained by reconstructing the 2D signal using the original phase and the amplitude spectrum, filtered at a scale selected by minimizing saliency map entropy. A Hypercomplex Fourier Transform performs the analysis in the frequency domain. Using available databases, we demonstrate experimentally that the proposed model can predict human fixation data. We also introduce a new image database and use it to show that the saliency detector can highlight both small and large salient regions, as well as inhibit repeated distractors in cluttered images. In addition, we show that it is able to predict salient regions on which people focus their attention.
The activation of cytokine genes in response to antigenic stimulation of T cells is mediated by NF-AT proteins. Previous studies have identified two NF-AT proteins, NF-ATp and NF-ATc, that are homologous within a 290 aa domain distantly related to the Rel domain. We have isolated two additional members of this gene family, NF-AT3 and NF-AT4, which encode proteins 65% identical to the other NF-AT proteins within the Rel domain. The four NF-AT genes are transcribed in different sets of tissues that included many sites of expression outside the immune system. The Rel homology domain is sufficient for DNA recognition and cooperative binding interactions with AP-1. Although other members of the Rel family bind DNA as dimers, NF-AT proteins are monomers in solution or bound to DNA. Transfection assays indicate that each of the four NF-AT proteins can activate the IL-2 promoter in T cells.
STAT proteins (signal transducers and activators of transcription) activate distinct target genes despite having similar DNA binding preferences. The transcriptional specificity of STAT proteins was investigated on natural STAT binding sites near the interferon-gamma gene. These sites are arranged in multiple copies and required cooperative interactions for STAT binding. The conserved amino-terminal domain of STAT proteins was required for cooperative DNA binding, although this domain was not essential for dimerization or binding to a single site. Cooperative binding interactions enabled the STAT proteins to recognize variations of the consensus site. These sites can be specific for the different STAT proteins and may function to direct selective transcriptional activation.
The advent of mammalian gene engineering and genetically modified mouse models has led to renewed interest in developing resources for referencing and quantitative analysis of mouse brain anatomy. In this study, we used diffusion tensor imaging (DTI) for quantitative characterization of anatomical phenotypes in the developing mouse brain. As an anatomical reference for neuroscience research using mouse models, this paper presents DTI based atlases of ex vivo C57BL/6 mouse brains at several developmental stages. The atlas complements existing histology and MRI-based atlases by providing users access to three-dimensional, high-resolution images of the developing mouse brain, with distinct tissue contrasts and segmentations of major gray matter and white matter structures. The usefulness of the atlas and database was demonstrated by quantitative measurements of the development of major gray matter and white matter structures. Population average images of the mouse brain at several postnatal stages were created using large deformation diffeomorphic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Author ManuscriptNeuroimage. Author manuscript; available in PMC 2012 January 1.
NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript metric mapping and their anatomical variations were quantitatively characterized. The atlas and database enhance our ability to examine the neuroanatomy in normal or genetically engineered mouse strains and mouse models of neurological diseases.
IMPORTANCE Microglia, the resident immune cells of the central nervous system, play an important role in the brain's response to injury and neurodegenerative processes. It has been proposed that prolonged microglial activation occurs after single and repeated traumatic brain injury, possibly through sports-related concussive and subconcussive injuries. Limited in vivo brain imaging studies months to years after individuals experience a single moderate to severe traumatic brain injury suggest widespread persistent microglial activation, but there has been little study of persistent glial cell activity in brains of athletes with sports-related traumatic brain injury. OBJECTIVE To measure translocator protein 18 kDa (TSPO), a marker of activated glial cell response, in a cohort of National Football League (NFL) players and control participants, and to report measures of white matter integrity.
DESIGN, SETTING, AND PARTICIPANTSThis cross-sectional, case-control study included young active (n = 4) or former (n = 10) NFL players recruited from across the United States, and 16 age-, sex-, highest educational level-, and body mass index-matched control participants. This study was conducted at an academic research institution
Signal transducer and activator of transcription (Stat)4 is a signaling molecule required for normal responses to interleukin-12 (IL-12) and is critically involved in in¯ammatory responses. We have isolated an alternatively spliced isoform of Stat4, termed Stat4b, which lacks 44 amino acids at the C-terminus, encompassing the putative transcriptional activation domain. To assess the in vivo roles of these Stat4 isoforms, we generated transgenic Stat4-de®cient mice expressing Stat4a or Stat4b. Our results indicate that T-cell-speci®c expression of Stat4a or Stat4b can mediate many aspects of IL-12 signaling including the differentiation of Th1 cells. However, Stat4a is required for normal levels of IL-12-induced interferon-g production from Th1 cells. Microarray analysis identi®ed 98 genes induced by both Stat4 isoforms, 32 genes induced only by Stat4a and 29 genes induced only by Stat4b. Some induced genes correlate with speci®c functions including the ability of Stat4b, but not Stat4a, to mediate IL-12-stimulated proliferation. Thus, Stat4a and Stat4b have distinct roles in mediating responses to IL-12.
Objectives. To examine the extent to which the phrases, “COVID-19” and “Chinese virus” were associated with anti-Asian sentiments. Methods. Data were collected from Twitter’s Application Programming Interface, which included the hashtags “#covid19” or “#chinesevirus.” We analyzed tweets from March 9 to 23, 2020, corresponding to the week before and the week after President Donald J. Trump’s tweet with the phrase, “Chinese Virus.” Our analysis focused on 1 273 141 hashtags. Results. One fifth (19.7%) of the 495 289 hashtags with #covid19 showed anti-Asian sentiment, compared with half (50.4%) of the 777 852 hashtags with #chinesevirus. When comparing the week before March 16, 2020, to the week after, there was a significantly greater increase in anti-Asian hashtags associated with #chinesevirus compared with #covid19 (P < .001). Conclusions. Our data provide new empirical evidence supporting recommendations to use the less-stigmatizing term “COVID-19,” instead of “Chinese virus.” (Am J Public Health. Published online ahead of print March 18, 2021: e1–e9. https://doi.org/10.2105/AJPH.2021.306154 )
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