体育、运动场与国家表征 ——英国国家体育场的政治学诠释 (Sport, Place and Nationhood - The Politics of the National Stadia of the United Kingdom)

In order to fully understand the social and cultural significance of sporting places and the national identities it carries, the article draws on the path of the Chicago School of Urban Ecology and Symbolic Interaction Theory, and analyses the interaction among the sports events, the so-called national stadia and national identities in the multi-national United Kingdom. The author underlines the political role of the stadia as the urban landscape and the national symbols, and highlights the analytical value of the sporting place

Embracing city life: physical activities and the social integration of the new generation of female migrant workers in urban China

Drawing on empirical data from interviews with young Chinese female rural-urban migrant workers in the Pearl River Delta of China’s Guangdong province, this article explores the ways in which physical activities help to fulfil the ‘urban dream’ of this new generation of female migrant workers and promote their social integration. The article demonstrates that physical activities exert their influence and facilitate the young female migrant workers’ social integration into cities through four dimensions: ‘space’, ‘network’, ‘identity’ and ‘image’. Participating in sport and exercise expands the scale of workers’ living spaces and contributes to building social networks and selfidentification. It also enhances female migrant workers’ individualistic values, as opposed to family-oriented ones. These new values allow them to enjoy recreational life and to change the stereotypical image of rural-urban migrant workers

BACE1 Aptamer-Modified Tetrahedral Framework Nucleic Acid to Treat Alzheimer’s Disease in an APP-PS1 Animal Model

Alzheimer’s disease is a neurodegenerative disease caused by excessive amyloid β protein-induced neurotoxicity. However, drugs targeting amyloid β protein production face many problems, such as the low utilization rate of drugs by cells and the difficulty of drugs in penetrating the blood–brain barrier. A tetrahedral framework nucleic acid is a new type of nanonucleic acid structure that functions as a therapy and drug carrier. Here, we synthesized a BACE1 aptamer-modified tetrahedral framework nucleic acid and tested its therapeutic effect on Alzheimer’s disease in vitro and in vivo. Our results demonstrated that the tetrahedral framework nucleic acid could be used as a carrier to deliver the BACE1 aptamer to the brain to reduce the production of amyloid β proteins. It also played an antiapoptotic role by reducing the production of reactive oxygen species. Thus, this nanomaterial is a potential drug for Alzheimer’s disease

Canine Spontaneous Head and Neck Squamous Cell Carcinomas Represent Their Human Counterparts at the Molecular Level

<div><p>Spontaneous canine head and neck squamous cell carcinoma (HNSCC) represents an excellent model of human HNSCC but is greatly understudied. To better understand and utilize this valuable resource, we performed a pilot study that represents its first genome-wide characterization by investigating 12 canine HNSCC cases, of which 9 are oral, via high density array comparative genomic hybridization and RNA-seq. The analyses reveal that these canine cancers recapitulate many molecular features of human HNSCC. These include analogous genomic copy number abnormality landscapes and sequence mutation patterns, recurrent alteration of known HNSCC genes and pathways (e.g., cell cycle, PI3K/AKT signaling), and comparably extensive heterogeneity. Amplification or overexpression of protein kinase genes, matrix metalloproteinase genes, and epithelial–mesenchymal transition genes <i>TWIST1</i> and <i>SNAI1</i> are also prominent in these canine tumors. This pilot study, along with a rapidly growing body of literature on canine cancer, reemphasizes the potential value of spontaneous canine cancers in HNSCC basic and translational research.</p></div

RNA-seq analysis reveals dog-human homology in sequence mutations.

<p>(A) The fractions (the Y-axis) of base substitution types in the canine samples (the X-axis) detected by RNA-seq when compared to the dog reference genome [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref033" target="_blank">33</a>]. (B) Base transversions are significantly more prevalent in CPV-negative tumors than CPV-positive tumors at CpG sites. (C) Synonymous (green dots) and non-synonymous (yellow dots) substitutions, and a nonsense mutation (red star) uncovered in the <i>RELN</i> gene in tumor 404.</p

Pilot HNSCC driver–passenger discrimination via human–dog comparison.

<p>(A) Driver-passenger discrimination of human 8q. Human 8q is broken into dog chromosomes 29 (chr29) and 13 (chr13), with the numbers indicating the sequence coordinates. In human HNSCCs, the entire human 8q and all genes encoded (398 total) are recurrently amplified, as represented by a broken lined bar. In canine tumors, however, only chr13 is significantly amplified resulting in 125 genes being amplified and 85 genes unchanged, compared to only 2 genes amplified and 186 genes unchanged for chr29. The 125 amplified genes on chr13, including <i>MYC</i>, are considered as driver candidate genes (DCGs; in green), whereas the 186 unchanged genes on chr29 are deemed passenger candidate genes (PCGs; in red). The p-value shown is obtained with Fisher’s exact test; see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.s001" target="_blank">S1H Table</a>. (B) The 10Mb amplicon on chromosome 16 in tumor 240 (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.g002" target="_blank">Fig 2B</a>) is broken into three distinct regions in the human genome as shown. Only one region is significantly amplified in human HNSCC according to TCGA [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref001" target="_blank">1</a>], and the amplified genes encoded there, including known driver <i>FGFR1</i> [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref001" target="_blank">1</a>], are considered as driver candidate based on our dog-human comparison strategy [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref030" target="_blank">30</a>]. The p-value shown is obtained with Fisher’s exact test, see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.s001" target="_blank">S1H Table</a>. (C) The correlation between copy number status, represented by a gene’s </p><p></p><p></p><p></p><p></p><p></p><p><mi>log</mi></p><p><mn>2</mn></p><p></p><p></p><mo>⁡</mo><p></p><p></p><p><mi>T</mi><mi>u</mi><mi>m</mi><mi>o</mi><mi>r</mi></p><p><mi>N</mi><mi>o</mi><mi>r</mi><mi>m</mi><mi>a</mi><mi>l</mi></p><p></p><p></p><p></p><p></p><p></p> value, and mRNA expression level, represented by a gene’s log₂(<i>FPKM</i>) from RNA-seq or log₂(<i>intensity</i>) from SNP arrays. The data are from TCGA [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref001" target="_blank">1</a>]. The p-values shown are obtained with Hotelling's t-squared tests, see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.s001" target="_blank">S1H Table</a>.<p></p

Representative H&E stained images of canine normal squamous epithelium and SCC of the oral cavity.

<p>(A) Normal squamous epithelium of the oral mucosa (from case 240). Epithelium is between the arrow and the arrowhead. The arrow indicates the basal layer, while the arrowhead designates the stratum corneum. (B) SCC of the oral mucosa (from case 240). The arrow points to an area with loss of a distinct basal layer and basement membrane. The arrowhead indicates keratinizing squamous cells. The images are at 100X magnification.</p

The proposed carcinogenic mechanisms of canine oSCCs investigated.

<p>The cells of origin in these tumors are hypothesized as indicated, with oval cells representing the basal stem cells. Alterations at various levels are shown. For individual gene alterations, red represents gene amplification or overexpression, while green represents gene deletion or underexpression.</p

aCGH analysis reveals extensive CNAs in the majority of canine HNSCCs.

<p>(A) CNAs found in canine HNSCCs. Each tumor genome, with the tumor ID and location indicated on the top, is shown as a continuous line consisting of 38 canine autosomes separated by vertical black lines, with the chromosome numbers indicated. Within each chromosome, red/blue vertical lines above/below the chromosome indicate amplifications (red) or deletions (blue) respectively, with the line height representing the log2-ratio of the amplified or deleted segment. Tumors 419 and 419_2 are from the same case (ID 419), with 419_2 being less advanced. Notable amplified (red) or deleted (blue) genes, e.g., <i>MYC</i>, etc. are indicated.(B) Chromosome 16 of tumor 240 is enlarged to show a focal amplification, located at 20.8–30.7 Mb of chromosome 16 and harboring 63 genes as indicated, to exemplify that many of the amplified genes are also overexpressed and associated with tumor-promoting function. (C) Integration of genes’ copy number status and mRNA expression level. Genes (11,821 total) with FPKM (fragments per kilobase of exon per million mapped fragments) of ≥ 1 in at least one of the tumors subjected to RNA-seq were sorted into three groups based on the analysis indicated in (A): deleted (Del), unchanged, or amplified (Amp) as shown on the X-axis. Then, each group of genes was further divided into three subgroups based on the mRNA expression level: low, normal, and high determined as described [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.ref002" target="_blank">2</a>], with the percentages shown in the Y-axis. See also <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005277#pgen.1005277.s002" target="_blank">S2B Table</a>.</p