The effect of a budget deficit on inflation: The case of Tanzania

The Tanzanian economy has remained one of the limited numbers of countries that has experienced a relatively high inflation rate, accompanied by high fiscal deficits for a prolonged period in the absence of any hyperinflation. This paper examines the deficit-inflation relationship in the Tanzanian economy and establishes the causal link that runs from the budget deficit to the inflation rate usingcointegration analysis over the period 1967-2001. Some dynamic simulations are done to gauge the effect of a change in the budget deficit and gross domestic product on inflation over time. Due to monetisation of the budget deficit, significant inflationary effects are found for increases in the budget deficit

SUPPORTING AN INFLATION TARGETING POLICY WITH THE MEASUREMENT OF INFLATION CREDIBILITY

Inflation targeting anchors inflation expectations, which are not within the sphere of control of the authorities, but can only be influenced over time by consistent policy. As public distrust of inflation figures will feed through to inflation expectations, this paper highlights pilot studies measuring the credibility of inflation in terms of an inflation credibility barometer. Despite initial discouraging results, the conclusion is that knowledge and information improve the credibility of inflation, but only one inflation rate (ideally the one used for inflation targeting purposes) should be communicated. Moreover, the rate used for targeting purposes should be specified with ease of communication in mind. Copyright 2005 Economic Society of South Africa.

ATP-sensitive potassium channels in health and disease

The ATP-sensitive potassium (KATP) channel plays a crucial role in insulin secretion and thus glucose homeostasis. KATP channel activity in the pancreatic β-cell is finely balanced; increased activity prevents insulin secretion, whereas reduced activity stimulates insulin release. β-cell metabolism tightly regulates KATP channel gating, and if this coupling is perturbed, two distinct disease states can result. Diabetes occurs when the KATP channel fails to close in response to increased metabolism, whereas congenital hyperinsulinism results when KATP channels remain closed even at very low blood glucose levels. In general there is a good correlation between the magnitude of KATP current and disease severity. Mutations that cause a complete loss of KATP channels in the β-cell plasma membrane produce a severe form of congenital hyperinsulinism, whereas mutations that partially impair channel function produce a milder phenotype. Similarly mutations that greatly reduce the ATP sensitivity of the KATP channel lead to a severe form of neonatal diabetes with associated neurological complications, while mutations that cause smaller shifts in ATP sensitivity cause neonatal diabetes alone. This chapter reviews our current understanding of the pancreatic β-cell KATP channel and highlights recent structural, functional, and clinical advances