Creating ethics guidelines for artificial intelligence and big data analytics customers: The case of the consumer European insurance market.

The European Union (EU) has a strong reputation and track record for the development of guidelines for the ethical use of artificial intelligence (AI) generally. In this paper, we discuss the development of an AI and ethical framework by the European Insurance and Occupational Pensions Authority (EIOPA), for the European insurance market. EIOPA's earlier report on big data analytics (EIOPA, 2019) provided a foundation to analyze the complex range of issues associated with AI being deployed in insurance, such as behavioral insurance, parametric products, novel pricing and risk assessment algorithms, e-service, and claims management. The paper presents an overview of AI in insurance applications throughout the insurance value chain. A general discussion of ethics, AI, and insurance is provided, and a new hierarchical model is presented that describes insurance as a complex system that can be analyzed by taking a layered, multi-level approach that maps ethical issues directly to specific level(s).

USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors.

Nucleotide excision repair (NER) is a pathway involved in the repair of a variety of potentially mutagenic lesions that distort the DNA double helix. The ubiquitin E3-ligase complex UV-DDB is required for the recognition and repair of UV-induced cyclobutane pyrimidine dimers (CPDs) lesions through NER. DDB2 directly binds CPDs and subsequently undergoes ubiquitination and proteasomal degradation. DDB2 must remain on damaged chromatin, however, for sufficient time to recruit and hand-off lesions to XPC, a factor essential in the assembly of downstream repair components. Here we show that the tumor suppressor USP44 directly deubiquitinates DDB2 to prevent its premature degradation and is selectively required for CPD repair. Cells lacking USP44 have impaired DDB2 accumulation on DNA lesions with subsequent defects in XPC retention. The physiological importance of this mechanism is evident in that mice lacking Usp44 are prone to tumors induced by NER lesions introduced by DMBA or UV light. These data reveal the requirement for highly regulated ubiquitin addition and removal in the recognition and repair of helix-distorting DNA damage and identify another mechanism by which USP44 protects genomic integrity and prevents tumors.