Oceans and Human Heath: Hand in Hand

Healthy oceans and healthy humans are inseparable. This article discusses new pharmaceuticals that are coming from the sea, and also ocean problems like harmful algal blooms that impact humans.

The Role of Raf Kinase Inhibitor Protein in Cell Motility

Raf Kinase Inhibitor Protein (RKIP) has been identified as a phosphatidylethanolamine-binding protein capable of inhibiting Raf-1 kinase, an enzyme significant in cell proliferation and cancer development. When properly functioning, RKIP can mediate the expression of Raf-1 kinase and help prevent uncontrolled cell division. RKIP also has suggested, but unclear, roles in spindle fiber formation during mitosis, regulation of apoptosis, and cell motility. The Fenteany laboratory in the Chemistry Department identified a new small molecule, named Locostatin, as a cell migration inhibitor in mammalian cells, with RKIP as its primary molecular target. Dictyostelium discoideum possess two RKIP proteins, RKIP-A and RKIP-B. In order to begin to study the function of RKIP in D. discoideum and its role in cell motility, I created a mutant cell line which lacks a functional RKIP-A gene. In this paper, we show that removal of RKIP-A does not affect vegetative motility, but impairs chemotaxis and development in the presence of drug. Interestingly, RKIP-A knockout mutants appear more resistant to drug effects on vegetative motility than wild-type cells. More research is needed to reconcile these seemingly contrasting results, and to better develop a model for RKIP-A’s role in cell motility.

Analysis of the Phosphorylated Forms of Protein Kinase R

Protein Kinase R (PKR) is induced by interferon and activated by dsRNA. Subsequent autophosphorylation and phosphorylation of eIF2alpha inhibits viral replication. In the latent state PKR exists as an unphosphorylated monomer. Work in the Cole laboratory has shown two additional states, a phosphorylated monomeric state (pPKRm) and a phosphorylated dimeric state (pPKRd). RNA serves as a scaffold bringing two PKRs together allowing dimerization and autophosphorylation to occur. The contribution of each state to the function of PKR remains unclear. Western blots were performed to examine the phosphorylation states of the essential residues, T446 and T451. Activity assays have shown activation of pPKRm at a level comparable to pPKRd in its ability to phosphorylate eIF2alpha. Phosphorylation of eIF2alpha by both pPKRm and pPKRd was shown to be RNA independent. Despite reaching similar terminal levels of eIF2alpha phosphorylation, kinetic measurements revealed a faster reaction from pPKRd. Therefore, pPKRm and pPKRd may both contribute to the activity of PKR.

Economic Reforms and Pro-Poor Growth: Lessons for Africa and other Developing Regions and Economies in Transition

The paper discusses the meaning and measurement of pro-poor growth and also reviews evidence of pro-poor growth (or the lack of it) in a large cross-section of countries and time periods. The emerging story is that many episodes of growth are not pro-poor and also that although economic reforms have had positive effects in those countries that have been steadfast in implementing market reforms, the overall impact on growth has been small for many countries and in most cases not pro-poor. I present a general theory of pro-poor growth that includes ten principles that should be incorporated in all economic reforms that seek to generate pro-poor growth. These principles highlight the importance of understanding the poor, their economic activities, capabilities, constraints that impede their participation in markets and also an appreciation of linkages within sectors and regions. It is argued that pro-poor reforms cannot have the intended impact unless there are significant changes in the institutions of governance. Finally, the principles presented underscore the fact that pro-poor growth policies cannot be sustained without workable partnerships between markets and states in the ever changing and complex processes of social and economic development.

Deregulation and Structural Change in the U.S. Commercial Banking Industry

Regulatory change not seen since the Great Depression swept the U.S. banking industry beginning in the early 1980s and culminated with the Interstate Banking and Branching Efficiency Act of 1994. Banking analysts anticipated dramatic consolidation with large numbers of mergers and acquisitions. Some expressed concern about the long-term health of the smaller community banks. This paper describes and discusses the actual evolution of the U.S. banking industry over the past two decades, using the 1976 to 1998 Report of Condition and Income (Call Report) and merger data recently posted on the web site of the Federal Reserve Bank of Chicago. Among several results, more permissive interstate banking and branching regulation significantly associates with higher merger rates, with lower net entry rates, and with higher concentration within states. Interestingly, more permissive intrastate banking and branching regulation only associates with higher concentration.