The latest Batman movie, released in May, took more than $770m at the box office; Warner has two sequels planned. Yet from 2035, anyone will have the right to make one
Save time by listening to our audio articles as you multitaskA.A. Milne, who created Pooh in 1926, might not have approved of “Winnie-the-Pooh: Blood and Honey”, a low-budget slasher film due out in February. But no approval from his estate was needed. In January 2022 the copyright on “Winnie-the-Pooh” expired in America and the work entered the public domain.
In January “The Jazz Singer”, one of the first successful “talkies”, will go out of copyright. Warner Bros, which released the film in 1927, is unlikely to worry much about losing the rights to what is today a historical curiosity. But a year later “Steamboat Willie”, the first film featuring Mickey Mouse, who sits at the centre of Disney’s merchandise business which brings in more than $5bn a year, will be there for the taking.
The internet also changed the balance of lobbying power. Publishers, record labels and film studios had always pushed for lengthy copyright terms; no commercial interest had reason to push hard against them. That is, until the arrival of companies such as Google and YouTube, which make their money by sharing other people’s content. Google won legal battles over its use of copyrighted pictures in its image search.
As the copyright deadline approaches, Hollywood is preparing another defence. Lawyers for studios such as Disney are getting ready to make the case that characters like Mickey Mouse are not just literary works, but logos. Brands and emblems fall under trademark law, which exists to help consumers identify products as originating from a certain company. And while copyright expires, trademarks can last for ever.
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Peripheral Auditory Nerve Impairment in a Mouse Model of Syndromic AutismDysfunction of the peripheral auditory nerve (AN) contributes to dynamic changes throughout the central auditory system, resulting in abnormal auditory processing, including hypersensitivity. Altered sound sensitivity is frequently observed in autism spectrum disorder (ASD), suggesting that AN deficits and changes in auditory information processing may contribute to ASD-associated symptoms, including social communication deficits and hyperacusis. The MEF2C transcription factor is associated with risk for several neurodevelopmental disorders, and mutations or deletions of MEF2C produce a haploinsufficiency syndrome characterized by ASD, language, and cognitive deficits. A mouse model of this syndromic ASD ( Mef2c -Het) recapitulates many of the MEF2C haploinsufficiency syndrome-linked behaviors, including communication deficits. We show here that Mef2c -Het mice of both sexes exhibit functional impairment of the peripheral AN and a modest reduction in hearing sensitivity. We find that MEF2C is expressed during development in multiple AN and cochlear cell types; and in Mef2c -Het mice, we observe multiple cellular and molecular alterations associated with the AN, including abnormal myelination, neuronal degeneration, neuronal mitochondria dysfunction, and increased macrophage activation and cochlear inflammation. These results reveal the importance of MEF2C function in inner ear development and function and the engagement of immune cells and other non-neuronal cells, which suggests that microglia/macrophages and other non-neuronal cells might contribute, directly or indirectly, to AN dysfunction and ASD-related phenotypes. Finally, our study establishes a comprehensive approach for characterizing AN function at the physiological, cellular, and molecular levels in mice, which can be applied to animal models with a wide range of human auditory processing impairments. SIGNIFICANCE STATEMENT This is the first report of peripheral auditory nerve (AN) impairment in a mouse
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