The Rule of Liability for Loss of Use When Property is Totally Destroyed: Some Economic Considerations

In this article Professor De Alessi applies economic analysis to a California case which held that a tortfeasor who negligently destroys property which he rented is liable to the lessor for loss of use during the time in which a replacement is being procured. In arriving at the conclusion that the court may have made the correct decision despite the lack of economic considerations, a framework for economic analysis is suggested which may well be extendable to other factual situations

The Rule of Liability for Loss of Use When Property is Totally Destroyed: Some Economic Considerations

In this article Professor De Alessi applies economic analysis to a California case which held that a tortfeasor who negligently destroys property which he rented is liable to the lessor for loss of use during the time in which a replacement is being procured. In arriving at the conclusion that the court may have made the correct decision despite the lack of economic considerations, a framework for economic analysis is suggested which may well be extendable to other factual situations

Structural and biochemical characterization of the KLHL3-WNK kinase interaction important in blood pressure regulation

WNK1 [with no lysine (K)] and WNK4 regulate blood pressure by controlling the activity of ion co-transporters in the kidney. Groundbreaking work has revealed that the ubiquitylation and hence levels of WNK isoforms are controlled by a Cullin-RING E3 ubiquitin ligase complex (CRL3KLHL3) that utilizes CUL3 (Cullin3) and its substrate adaptor, KLHL3 (Kelch-like protein 3). Loss-of-function mutations in either CUL3 or KLHL3 cause the hereditary high blood pressure disease Gordon's syndrome by stabilizing WNK isoforms. KLHL3 binds to a highly conserved degron motif located within the C-terminal non-catalytic domain of WNK isoforms. This interaction is essential for ubiquitylation by CRL3KLHL3 and disease-causing mutations in WNK4 and KLHL3 exert their effects on blood pressure by disrupting this interaction. In the present study, we report on the crystal structure of the KLHL3 Kelch domain in complex with the WNK4 degron motif. This reveals an intricate web of interactions between conserved residues on the surface of the Kelch domain β-propeller and the WNK4 degron motif. Importantly, many of the disease-causing mutations inhibit binding by disrupting critical interface contacts. We also present the structure of the WNK4 degron motif in complex with KLHL2 that has also been reported to bind WNK4. This confirms that KLHL2 interacts with WNK kinases in a similar manner to KLHL3, but strikingly different to how another KLHL protein, KEAP1 (Kelch-like enoyl-CoA hydratase-associated protein 1), binds to its substrate NRF2 (nuclear factor-erythroid 2-related factor 2). The present study provides further insights into how Kelch-like adaptor proteins recognize their substrates and provides a structural basis for how mutations in WNK4 and KLHL3 lead to hypertension

Private Ownership and Limits to Retroactive Regulation of Utility Rates

The author critically evaluates the effect of retroactive ratemaking on regulated public utilities, particularly the costs and disincentives inherent in the process. If the trend is not corrected, the author suggests that public utilities will ultimately become much like nationalized industries, with consumers bearing the risk and regulators managing the firm