Song of Exile: A Cultural History of Brazil’s Most Popular Poem, 1846–2018

Song of Exile: A Cultural History of Brazil’s Most Popular Poem, 1846–2018 is the first comprehensive study of the influence of Antônio Gonçalves Dias’s “Canção do exílio.” Written in Coimbra, Portugal, in 1843 by a homesick student longing for Brazil, “Song of Exile” has inspired thousands of parodies and pastiches, and new variations continue to appear to this day. Every generation of Brazilian writers has adapted the poem’s Romantic verses to glorify the wonders of the nation or to criticize it via parody, exposing a litany of issues that have plagued the country’s progress over the years. Based on a core of five hundred texts painstakingly gathered over a five-year span, this book catalogs the networks of the poem’s reinvention as pastiche and parody in Brazilian print culture from nineteenth-century periodicals to new media. Mapping the reoccurrences of the original’s keywords and phrases over time, the book uncovers how the poem has been used by successive generations to write and rewrite the nation’s history. This process of reinvention has guaranteed the permanency of “Song of Exile” in Brazilian culture, making it not only the nation’s most popular poem, but one of the most imitated in the world.https://docs.lib.purdue.edu/psrl/1000/thumbnail.jp

Selective connection to Wi-Fi networks

Devices such as mobile phones, tablets, wearables, head mounted displays, and computers auto-connect to a wireless network (e.g., a Wi-Fi network) regardless of the speed or quality of the connection offered by the network. In some instances, a Wi-Fi network can deliver lower speed and can be less reliable than a cellular data connection. In such instances, the cellular data connection can be preferable to the Wi-Fi connection. Testing connection speeds of various available connections require connecting to the network first, can cause delays in connection, and requires extra network usage and battery power. This disclosure describes techniques that utilize prior information about the comparative quality of available Wi-Fi and cellular networks, and automatically connects the user device to a preferred network. The prior information includes, e.g., scores for various Wi-Fi networks and expected cellular speed at locations

Organization and post-transcriptional processing of focal adhesion kinase gene

BACKGROUND: Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase critical for processes ranging from embryo development to cancer progression. Although isoforms with specific molecular and functional properties have been characterized in rodents and chicken, the organization of FAK gene throughout phylogeny and its potential to generate multiple isoforms are not well understood. Here, we study the phylogeny of FAK, the organization of its gene, and its post-transcriptional processing in rodents and human. RESULTS: A single orthologue of FAK and the related PYK2 was found in non-vertebrate species. Gene duplication probably occurred in deuterostomes after the echinoderma embranchment, leading to the evolution of PYK2 with distinct properties. The amino acid sequence of FAK and PYK2 is conserved in their functional domains but not in their linker regions, with the absence of autophosphorylation site in C. elegans. Comparison of mouse and human FAK genes revealed the existence of multiple combinations of conserved and non-conserved 5'-untranslated exons in FAK transcripts suggesting a complex regulation of their expression. Four alternatively spliced coding exons (13, 14, 16, and 31), previously described in rodents, are highly conserved in vertebrates. Cis-regulatory elements known to regulate alternative splicing were found in conserved alternative exons of FAK or in the flanking introns. In contrast, other reported human variant exons were restricted to Homo sapiens, and, in some cases, other primates. Several of these non-conserved exons may correspond to transposable elements. The inclusion of conserved alternative exons was examined by RT-PCR in mouse and human brain during development. Inclusion of exons 14 and 16 peaked at the end of embryonic life, whereas inclusion of exon 13 increased steadily until adulthood. Study of various tissues showed that inclusion of these exons also occurred, independently from each other, in a tissue-specific fashion. CONCLUSION: The alternative coding exons 13, 14, 16, and 31 are highly conserved in vertebrates and their inclusion in mRNA is tightly but independently regulated. These exons may therefore be crucial for FAK function in specific tissues or during development. Conversely pathological disturbance of the expression of FAK and of its isoforms could lead to abnormal cellular regulation

Distinct roles of c-Jun N-terminal kinase isoforms in neurite initiation and elongation during axonal regeneration

c-Jun N-terminal kinases (JNKs) (comprising JNK1-3 isoforms) are members of the MAPK (mitogen-activated protein kinase) family, activated in response to various stimuli including growth factors and inflammatory cytokines. Their activation is facilitated by scaffold proteins, notably JNK-interacting protein-1 (JIP1). Originally considered to be mediators of neuronal degeneration in response to stress and injury, recent studies support a role of JNKs in early stages of neurite outgrowth, including adult axonal regeneration. However, the function of individual JNK isoforms, and their potential effector molecules, remained unknown. Here, we analyzed the role of JNK signaling during axonal regeneration from adult mouse dorsal root ganglion (DRG) neurons, combining pharmacological JNK inhibition and mice deficient for each JNK isoform and for JIP1. We demonstrate that neuritogenesis is delayed by lack of JNK2 and JNK3, but not JNK1. JNK signaling is further required for sustained neurite elongation, as pharmacological JNK inhibition resulted in massive neurite retraction. This function relies on JNK1 and JNK2. Neurite regeneration of jip1(-/-) DRG neurons is affected at both initiation and extension stages. Interestingly, activated JNKs (phospho-JNKs), as well as JIP1, are also present in the cytoplasm of sprouting or regenerating axons, suggesting a local action on cytoskeleton proteins. Indeed, we have shown that JNK1 and JNK2 regulate the phosphorylation state of microtubule-associated protein MAP1B, whose role in axonal regeneration was previously characterized. Moreover, lack of MAP1B prevents neurite retraction induced by JNK inhibition. Thus, signaling by individual JNKs is differentially implicated in the reorganization of the cytoskeleton, and neurite regeneration

Meningococcus Hijacks a β2-Adrenoceptor/β-Arrestin Pathway to Cross Brain Microvasculature Endothelium

SummaryFollowing pilus-mediated adhesion to human brain endothelial cells, meningococcus (N. meningitidis), the bacterium causing cerebrospinal meningitis, initiates signaling cascades, which eventually result in the opening of intercellular junctions, allowing meningeal colonization. The signaling receptor activated by the pathogen remained unknown. We report that N. meningitidis specifically stimulates a biased β2-adrenoceptor/β-arrestin signaling pathway in endothelial cells, which ultimately traps β-arrestin-interacting partners, such as the Src tyrosine kinase and junctional proteins, under bacterial colonies. Cytoskeletal reorganization mediated by β-arrestin-activated Src stabilizes bacterial adhesion to endothelial cells, whereas β-arrestin-dependent delocalization of junctional proteins results in anatomical gaps used by bacteria to penetrate into tissues. Activation of β-adrenoceptor endocytosis with specific agonists prevents signaling events downstream of N. meningitidis adhesion and inhibits bacterial crossing of the endothelial barrier. The identification of the mechanism used for hijacking host cell signaling machineries opens perspectives for treatment and prevention of meningococcal infection.PaperFlic

PTEN controls glandular morphogenesis through a juxtamembrane β-Arrestin1/ARHGAP21 scaffolding complex

PTEN controls three-dimensional (3D) glandular morphogenesis by coupling juxtamembrane signalling to mitotic spindle machinery. While molecular mechanisms remain unclear, PTEN interacts through its C2 membrane-binding domain with the scaffold protein β-Arrestin1. Because β-Arrestin1 binds and suppresses the Cdc42 GTPase-activating protein ARHGAP21, we hypothesize that PTEN controls Cdc42-dependent morphogenic processes through a β-Arrestin1-ARHGAP21 complex. Here we show that PTEN knockdown (KD) impairs β-Arrestin1 membrane localization, β-Arrestin1-ARHGAP21 interactions, Cdc42 activation, mitotic spindle orientation and 3D glandular morphogenesis. Effects of PTEN-deficiency were phenocopied by β-Arrestin1 KD or inhibition of β-Arrestin1-ARHGAP21 interactions. Conversely, silencing of ARHGAP21 enhanced Cdc42 activation and rescued aberrant morphogenic processes of PTEN-deficient cultures. Expression of the PTEN C2 domain mimicked effects of full-length PTEN but a membrane-binding defective mutant of the C2 domain abrogated these properties. Our results show that PTEN controls multicellular assembly through a membrane-associated regulatory protein complex composed of β-Arrestin1, ARHGAP21 and Cdc42