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This thesis studies the role of multi-stage production for the monetary transmission mechanism. I employ a monetary search model to show how multi-stage production influences both the long run and the short run effects of money growth. Multi-stage production provides an additional channel for money growth having effects through intermediate goods between different production stages. Extending Shi's (1998) model from a single-stage to a multi-stage production model, I show that money growth rate has an unconventional long run effect on quantities per match, and the long run response of input inventory investment is different from that of output inventory investment. Contrary to classic search models, the steady state effect of money growth on the quantity of finished goods per match is not monotonic and depends on the money growth rate. Furthermore, in steady state the quantities per match first increase with the growth rate of money, before falling for large growth rates. Input inventories arise due to search frictions. Money growth also has hump-shaped real effects on steady state input inventory investment. The intermediate goods build a bridge between the labor market and the finished goods market. Intuitively, households hire more labor with higher future revenue and produce more intermediate goods in order to match the employment level. With more labor and more intermediate goods, finished goods producers can produce more when matched. As a consequence, they are stuck with more input inventories. Moreover, my model suggests that changes in the money growth rate would be one of the reasons for the decline of the inventory-to-sales ratio since the mid-1980s. Finally, I calibrate my model to quarterly US data. Contrary to other work, my model is able to replicate the stylized facts on inventory movements over the business cycle by solely relying on monetary shocks. The theoretical impulse response functions can quantitatively reproduce the corresponding empirical ones estimated in a structure autoregressive model. Moreover, the quantitative analysis supports the argument that input inventories amplify aggregate fluctuations over business cycles. / Thesis (Ph.D, Economics) -- Queen's University, 2012-09-16 20:44:21.876

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Excess rural and urban nutrient inputs have led to downstream water quality degradation. Landowners in a small watershed in south central Manitoba, Canada have installed small dams as flood control mechanisms. Previous work has shown these dams and reservoirs are effective at decreasing total phosphorus (P) export, however questions of permanence, daily P fluctuation, and mechanisms influencing P retention still remain. Sediment nutrient dynamics can exert an important control on water quality on daily, monthly, and yearly timescales. To help better understand spatial and temporal patterns of P retention, P sorption assays were constructed (equilibrium P concentration or EPC0) and compared monthly measurements of EPC0 in small dammed reservoirs with their natural analog, stream pools. Dammed reservoirs and stream pools both showed a strong capacity to sorb P from the water column and as such, sediment processes represent a P sink across much of the catchment. In situ high frequency P sensors were deployed to assess short-term changes in P concentrations in four dammed reservoirs. Diel changes were only apparent later in the summer (August) but what drives these changes is unknown. Dam design to optimize nutrient retention should consider factors affecting P retention, including sediment geochemistry, but also residence time, and water chemistry as potential controls on P sorption. Diel sampling results suggest that water quality monitoring regimes that rely on singular grab samples should aim to sample in the mid-morning, especially later in the summer, so as to not over or underestimate P concentrations in water bodies.

Part I deals with the estimation of money demand functions. Several non-structural interpretations of the conventionally estimated functions are surveyed and discussed (Chapter 1). An application to Italian data is then presented, focusing on two such interpretations. First (Chapter 2), the role of expectations in determining money demand behaviour is assessed. Since monetary policy regimes have a direct effect on the time-series properties of interest rates, the identification of clear regime changes may provide a powerful test of forward-looking models of money demand. An expectations model is constructed, which is stable in the face of the Italian monetary policy regime change in 1970, when traditional backward-looking money demand functions show remarkable instability. Second (Chapter 3), the existence of multiple long-run relations among the variables relevant to money demand is shown to create problems for the interpretation of single-equation estimates. To obtain a satisfactory specification of the long-run relations and the short-run dynamics of the system around equilibrium, a sequential procedure is devised and applied. In Part II, the controversy between "real" and "monetary" theories of fluctuations is examined (Chapter 4). A "monetary" equilibrium model of the cycle is constructed, extending the original Lucas "island" framework to allow for a powerful role for stabilization policy. The implications of alternative monetary policy regimes are derived and tested on U.S. data, comparing two periods (1922-1940 and 1952-1968) with a different policy stance. Chapter 5 investigates the relative importance of the "money" and "credit" channels of monetary transmission for Italy in the 1982-1994 period, using a structural VAR methodology. Monetary policy is effective, though not through a "credit channel", and independent disturbances to credit supply have sizeable real effects. In Chapter 6 the focus is shifted to anticipated fiscal policy actions and their effect on consumption. A long series of pre-announced income tax changes is examined for the U.K. Consumption reacts to such fiscally-induced disposable income changes only at the implementation dates.

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How do precursor cells know when it is time to stop dividing and differentiate? The phenomenon of lineage-specific progenitor cells undergoing a limited period of proliferation prior to terminal differentiation is a common theme in multicellular development. Despite this, little is understood about how these two events are co-ordinated during the normal schedule of development. I have studied the question of how proliferation and differentiation are co-regulated in the oligodendrocyte lineage in the rodent optic nerve. Oligodendrocytes are post-mitotic cells that myelinate axons in the vertebrate central nervous system. They develop from precursor cells whose maturation is controlled by a timer, which is an intrinsic property of the cells, that limits proliferation. The timer seems not to control the number of divisions the cell can undergo but rather the length of time during which divisions can occur. Significant effort has been devoted to understanding how the intracellular timer regulates oligodendrocyte development. The timer consists of two components that are modulated by distinct kinds of extracellular signals. Mitogens drive a timing component whose value increases as precursor cells continue to divide. Once this value exceeds a critical threshold, it signals that the proliferative period has elapsed, and hydrophobic signalling molecules trigger an effector component that elicits cell-cycle arrest and differentiation. The value of the timing component is determined by several intracellular molecules whose activities change as the timer runs. One of these molecules is the cell-cycle inhibitor p27: it accumulates in oligodendrocyte precursor cells as they proliferate in culture. When p27 expression is high the precursor cells are more likely to stop dividing and differentiate than when it is low. In oligodendrocyte precursor cells derived from mice that lack p27, the timer runs aberrantly and cell-cycle arrest and terminal differentiation are delayed. It is not understood how the molecular mechanics of the timer control oligodendrocyte development. Does the timer serve to arrest the cell-cycle, with differentiation following by default, or is cell-cycle arrest subordinate to the programme of terminal differentiation? These questions remain unanswered, largely because of a persistent inability to experimentally manipulate the genome of oligodendrocyte precursor cells. The present study was an attempt to overcome these problems and had two aims - first, to devise a reliable system for transfecting oligodendrocyte precursor cells and second, to determine whether the timer primarily controls the timing of cell-cycle arrest. I developed a new retroviral vector that co-expresses p27 and green fluorescent protein (GFP) in precursor cells. The use of GFP allows the identification of living precursor cells that over-express p27, which can then be followed over many days in culture. My findings support previous work showing that p27 plays a role in governing the timing of oligodendrocyte differentiation. They show that over-expression of p27 promotes oligodendrocyte differentiation by advancing the value of the timing component, although it does not promote differentiation if the effector component is inoperative. The cell-cycle time of precursor cells that over-express p27 is dramatically extended, but not stopped. It appears that a firm cell-cycle arrest and entry into a quiescent state may be required to elicit terminal differentiation.