Book Reviews

Teaching/Communication/Extension/Profession,

AN OPTIMAL-CONTROL APPROACH TO STABILISING AUSTRALIAN WOOL PRICES

In this paper, some aspects of the application of optimal-control techniques to wool industry price stabilisation are considered. It is not intended to provide a blueprint for the immediate adoption of optimal-control techniques in the management of wool price stablisation. Rather, the contribution is to the developmental and evaluative process involved in considering these techniques. A new econometric model of wool price and supply is also presented, since none of the existing models satisfied the requirements of the study

AN OPTIMAL-CONTROL APPROACH TO STABILISING AUSTRALIAN WOOL PRICES

In this paper, some aspects of the application of optimal-control techniques to wool industry price stabilisation are considered. It is not intended to provide a blueprint for the immediate adoption of optimal-control techniques in the management of wool price stablisation. Rather, the contribution is to the developmental and evaluative process involved in considering these techniques. A new econometric model of wool price and supply is also presented, since none of the existing models satisfied the requirements of the study.Demand and Price Analysis,

Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.

Mitochondrial glutathione (GSH) and thioredoxin (Trx) systems function independently of the rest of the cell. While maintenance of mitochondrial thiol redox state is thought vital for cell survival, this was not testable due to the difficulty of manipulating the organelle's thiol systems independently of those in other cell compartments. To overcome this constraint we modified the glutathione S-transferase substrate and Trx reductase (TrxR) inhibitor, 1-chloro-2,4-dinitrobenzene (CDNB) by conjugation to the mitochondria-targeting triphenylphosphonium cation. The result, MitoCDNB, is taken up by mitochondria where it selectively depletes the mitochondrial GSH pool, catalyzed by glutathione S-transferases, and directly inhibits mitochondrial TrxR2 and peroxiredoxin 3, a peroxidase. Importantly, MitoCDNB inactivates mitochondrial thiol redox homeostasis in isolated cells and in vivo, without affecting that of the cytosol. Consequently, MitoCDNB enables assessment of the biomedical importance of mitochondrial thiol homeostasis in reactive oxygen species production, organelle dynamics, redox signaling, and cell death in cells and in vivo.We acknowledge the Biotechnology and Biological Sciences Research Council (BB/I012826/1), the Wellcome Trust (WT110158/Z/15/Z, 110159/Z/15/Z and RG88195), the University of Glasgow (JMG Studentship), and the Medical Research Council (MC_U105663142 and MC_ UU_00015/7)