889 research outputs found

    Insta-Appropriation: Finding Boundaries for the Second Circuit’s Fair Use Doctrine After Campbell

    Get PDF
    Copyright law’s current fair use landscape is riddled with unclear standards and old considerations forced upon new media. This is especially problematic in the context of digital appropriation of art from online social media platforms—an issue highlighted by Richard Prince’s exhibit “New Portraits,” in which he appropriated strangers’ Instagram photos for his own profit. Unless this situation is remedied, digital content creators will effectively lose their statutory copyright protections. Thus, when considering digital appropriation cases, courts should require a transformation of content rather than purpose, should elevate the weight of the fourth statutory factor, and should reinstate the “comment upon” standard for works of parody and satire. Other scholars have proposed changes to the fair use doctrine, but none adequately protect first-order digital content creators. As such, this Note proposes a reinterpretation of the fair use factors in light of digital appropriation and social media

    Insta-Appropriation: Finding Boundaries for the Second Circuit’s Fair Use Doctrine After Campbell

    Get PDF
    Copyright law’s current fair use landscape is riddled with unclear standards and old considerations forced upon new media. This is especially problematic in the context of digital appropriation of art from online social media platforms—an issue highlighted by Richard Prince’s exhibit “New Portraits,” in which he appropriated strangers’ Instagram photos for his own profit. Unless this situation is remedied, digital content creators will effectively lose their statutory copyright protections. Thus, when considering digital appropriation cases, courts should require a transformation of content rather than purpose, should elevate the weight of the fourth statutory factor, and should reinstate the “comment upon” standard for works of parody and satire. Other scholars have proposed changes to the fair use doctrine, but none adequately protect first-order digital content creators. As such, this Note proposes a reinterpretation of the fair use factors in light of digital appropriation and social media

    Entscheidungen ĂŒber kĂŒnstliche ErnĂ€hrung und FlĂŒssigkeitsgabe bei Patienten mit fortgeschrittener Demenz

    Get PDF

    Conformational control of Bax localization and apoptotic activity by Pro168

    Get PDF
    In healthy cells, Bax resides inactive in the cytosol because its COOH-terminal transmembrane region (TMB) is tucked into a hydrophobic pocket. During apoptosis, Bax undergoes a conformational change involving NH2-terminal exposure and translocates to mitochondria to release apoptogenic factors. How this process is regulated remains unknown. We show that the TMB of Bax is both necessary and sufficient for mitochondrial targeting. However, its availability for targeting depends on Pro168 located within the preceding loop region. Pro168 mutants of Bax lack apoptotic activity, cannot rescue the apoptosis-resistant phenotype of Bax/Bak double knockout cells, and are retained in the cytosol even in response to apoptotic stimuli. Moreover, the mutants have their NH2 termini exposed. We propose that Pro168 links the NH2 and the COOH terminus of Bax and is required for COOH-terminal release and mitochondrial targeting once this link is broken

    High-Fat Diet Induces Unexpected Fatal Uterine Infections in Mice with aP2 -Cre-mediated Deletion of Estrogen Receptor Alpha

    Get PDF
    Estrogen receptor alpha (ERα) is a major regulator of metabolic processes in obesity. In this study we aimed to define the relevance of adipose tissue ERα during high-fat diet (HFD)-induced obesity using female aP2-Cre−/+/ERαfl/fl mice (atERαKO). HFD did not affect body weight or glucose metabolism in atERαKO- compared to control mice. Surprisingly, HFD feeding markedly increased mortality in atERαKO mice associated with a destructive bacterial infection of the uterus driven by commensal microbes, an alteration likely explaining the absence of a metabolic phenotype in HFD-fed atERαKO mice. In order to identify a mechanism of the exaggerated uterine infection in HFD-fed atERαKO mice, a marked reduction of uterine M2-macrophages was detected, a cell type relevant for anti-microbial defence. In parallel, atERαKO mice exhibited elevated circulating estradiol (E2) acting on E2-responsive tissue/cells such as macrophages. Accompanying cell culture experiments showed that despite E2 co-administration stearic acid (C18:0), a fatty acid elevated in plasma from HFD-fed atERαKO mice, blocks M2-polarization, a process known to be enhanced by E2. In this study we demonstrate an unexpected phenotype in HFD-fed atERαKO involving severe uterine bacterial infections likely resulting from a previously unknown negative interference between dietary FAs and ERα- signaling during anti-microbial defence

    Human skin aging is associated with increased expression of the histone variant H2A.J in the epidermis

    Get PDF
    Cellular senescence is an irreversible growth arrest that occurs as a result of damaging stimuli, including DNA damage and/or telomere shortening. Here, we investigate histone variant H2A.J as a new biomarker to detect senescent cells during human skin aging. Skin biopsies from healthy volunteers of different ages (18–90 years) were analyzed for H2A.J expression and other parameters involved in triggering and/or maintaining cellular senescence. In the epidermis, the proportions of H2A.J-expressing keratinocytes increased from ≈20% in young to ≈60% in aged skin. Inverse correlations between Ki67- and H2A.J staining in germinative layers may reflect that H2A.J-expressing cells having lost their capacity to divide. As cellular senescence is triggered by DNA-damage signals, persistent 53BP1-foci, telomere lengths, and telomere-associated damage foci were analyzed in epidermal keratinocytes. Only slight age-related telomere attrition and few persistent nuclear 53BP1-foci, occasionally colocalizing with telomeres, suggest that unprotected telomeres are not a significant cause of senescence during skin aging. Quantification of integrin-α6+ basal cells suggests that the number and function of stem/progenitor cells decreased during aging and their altered proliferation capacities resulted in diminished tissue renewal with epidermal thinning. Collectively, our findings suggest that H2A.J is a sensitive marker of epidermal aging in human skin
    • 

    corecore