Genshin Impact publisher Cognosphere wants to know who Ubatcha is.
That's where the infringing content was posted, according to the first, and as a result Cognosphere lawyers are asking that Discord be ordered"to disclose the identity, including the name, address, telephone number, and email address of the user Ubatcha#2719, who is responsible for posting infringing content."also notes that"the information obtained will be used only for the purposes of protecting the rights granted to Cognosphere under the Copyright Act.
Discord will almost certainly comply with the request when it's received—lawsuits like this are typically a formality to ensure that everyone involved is meeting their legal and contractual obligations—after which Ubatcha will be revealed and Cognosphere can go after them as it sees fit. At a bare minimum, it seems likely that Ubatcha's leaks will come to a halt; but a broader chilling effect on Genshin Impact leaks is another potential outcome.
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The E46K mutation modulates α-synuclein prion replication in transgenic miceAuthor summary The underlying cause of disease in a group of movement disorders called syncleinopathies is the misfolding of the protein α-synuclein into a shape that self-templates to spread disease. The type of synucleinopathy that a patient develops depends on the shape α-synuclein adopts during misfolding. For example, α-synuclein misfolds into one shape in patients with Parkinson’s disease (PD) and into another in patients with multiple system atrophy (MSA). These distinct forms are referred to as strains. Understanding α-synuclein strain biology, and the factors that impact strain formation and spread, is imperative for developing successful diagnostics and therapeutics. In this study, we investigated the effect of the E46K mutation in α-synuclein, which causes PD, on α-synuclein strain biology to determine how the patient’s genetic background can impact disease. Our results showed that this particular mutation modulates α-synuclein spread; while mice expressing E46K α-synuclein were resistant to MSA prion replication, synthetic E46K fibrils induced neurological disease in the mice. In contrast, heterotypic seeding of wild-type synthetic fibrils yielded inefficient propagation that could not induce neurological signs in the mice. These results indicate that patient genotype can greatly impact α-synuclein strain formation and, therefore, clinical presentation in synucleinopathy patients.
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