Motor Vehicle Accident Fatalities for the Week Ending, December 28, 2007

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, December 14, 2007

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, January 11, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, January 18, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, January 25, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, February 1, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, February 8, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, February 15, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, February 22, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, February 29, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, March 7, 2008

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Motor Vehicle Accident Fatalities for the Week Ending, May 2, 2006

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Contractual allocation of decision rights and incentives: The case of automobile distribution

We analyze empirically the allocation of rights and monetary incentives in automobile franchise contracts. These contracts substantially restrict the decision rights of dealers and grant manufacturers extensive contractual completion and enforcement powers, converting the manufacturers, de facto, in a sort of quasi-judiciary instance. Variation in the allocation of decision rights andincentive intensity is explained by the incidence of moral hazard in the relation. In particular, when the cost of dealer moral hazard is higher and the risk of manufactureropportunism is lower, manufacturers enjoy more discretion in determining the performance required from their dealers and in using mechanisms such as monitoring, termination and monetary incentives to ensure such performance is provided. We also explore the existence of interdependencies between the different elements of the system. and find some complementarities between completion and termination rights, and between monitoring rights and the intensity of incentives.

NOTCH1 can initiate NF-κB activation via cytosolic interactions with components of the T cell Signalosome.

T cell stimulation requires the input and integration of external signals. Signaling through the T cell receptor (TCR) is known to induce formation of the membrane-tethered CBM complex, comprising CARMA1, BCL10, and MALT1, which is required for TCR-mediated NF-κB activation. TCR signaling has been shown to activate NOTCH proteins, transmembrane receptors also implicated in NF-κB activation. However, the link between TCR-mediated NOTCH signaling and early events leading to induction of NF-κB activity remains unclear. In this report, we demonstrate a novel cytosolic function for NOTCH1 and show that it is essential to CBM complex formation. Using a model of skin allograft rejection, we show in vivo that NOTCH1 acts in the same functional pathway as PKCθ, a T cell-specific kinase important for CBM assembly and classical NF-κB activation. We further demonstrate in vitro NOTCH1 associates physically with PKCθ and CARMA1 in the cytosol. Unexpectedly, when NOTCH1 expression was abrogated using RNAi approaches, interactions between CARMA1, BCL10, and MALT1 were lost. This failure in CBM assembly reduced inhibitor of kappa B alpha phosphorylation and diminished NF-κB-DNA binding. Finally, using a luciferase gene reporter assay, we show the intracellular domain of NOTCH1 can initiate robust NF-κB activity in stimulated T cells, even when NOTCH1 is excluded from the nucleus through modifications that restrict it to the cytoplasm or hold it tethered to the membrane. Collectively, these observations provide evidence that NOTCH1 may facilitate early events during T cell activation by nucleating the CBM complex and initiating NF-κB signaling.