Monetary and Fiscal Policies: Ordinary Recessions and Financial Crises

This paper uses two different samples to study the effects of monetary and fiscal policies on the profiles of recessions and recoveries. Several results emerge from the econometric analysis presented. First, monetary policy during ordinary recessions and banking crises is a powerful tool with lasting effects that extend to recovery growth rates. However, the effect of monetary policy during financial crises is strongly diminished in the case of forbearance – banks left to function despite being technically insolvent. Second, the effectiveness of fiscal policy is reversed – it is a powerful tool during banking crises, but it does not seem to significantly affect recovery growth rates during ordinary recessions. Finally, the policy response during past financial crisis does not seem to be particularly expansionary – on the contrary, fiscal policy is markedly procylcical, while monetary policy is neutral. This is proposed as an alternative explanation to the one usually given for the sluggishness of financial crises

The Strength of the Veblenian Critique of Neoclassical Economics

More than one hundred years ago, Thorstein Veblen wrote a powerful critique of neoclassical economics that castigated the discipline for turning the individual into a “lightning calculator of pleasures and pains, who oscillates like a homogeneous globule”, or equivalently, for the individual’s static maximization of utility based on exogenous preferences. His critique is relevant even today, since there are economists who still continue to criticize the assumptions of homo economicus and exogenous preferences, and insist on introducing more realism to economic theory. Furthermore, recent developments in game theory and experimental economics, which stand at the cutting-edge of economics today, are far more accommodating to the ideas of institutions that were central to Veblen’s theory than neoclassical economics. The goal of this paper is to examine the strengths of the Veblenian critique of neoclassical economics. In particular, it investigates whether or not Veblen’s rejection of the axiomatic approaches to economics is merely an attack on neoclassical economics which fails to provide an alternative positive theory. Starting with their conception of the individual, going through their theoretical frameworks, and ending with an investigation of how they approach a concrete issue, this paper offers a comparative exposition of the Veblenian and neoclassical approaches to economic theory. [excerpt

The "Thirty-seven Percent Rule" and the Secretary Problem with Relative Ranks

We revisit the problem of selecting an item from $n$ choices that appear before us in random sequential order so as to minimize the expected rank of the item selected. In particular, we examine the stopping rule where we reject the first $k$ items and then select the first subsequent item that ranks lower than the $l$-th lowest-ranked item among the first $k$. We prove that the optimal rule has $k \sim n/{\mathrm e}$, as in the classical secretary problem where our sole objective is to select the item of lowest rank; however, with the optimally chosen $l$, here we can get the expected rank of the item selected to be less than any positive power of $n$ (as $n$ approaches infinity). We also introduce a common generalization where our goal is to minimize the expected rank of the item selected, but this rank must be within the lowest $d$

Common ownership, firm financial policy and product market strategy

This dissertation consists of three essays which examine the importance of common institutional ownership of industry rivals for firm financial policy and product market interactions. In the first chapter, I use data on all public firms in the U.S. and their owners to construct a "modified Herfindahl-Hirschman index" (MHHID) of market concentration that is firm-specific and based on the network of institutional ownership between rival firms. I find that increases in MHHID lead to lower firm cash holdings. My findings are consistent with theories which predict that firms facing a lower competitive threat can afford to maintain lower cash buffers. To address potential endogeneity concerns, I exploit a shock to common ownership stemming from outflows associated with a large mutual fund scandal in 2003. In the second chapter, I provide evidence showing that firm pairwise common ownership leads to an increase in rival coordination. I find that pairs of commonly held firms move closer together in product space. These findings are supportive of collaboration theories of common ownership and inconsistent with anti-competitive theories. I further show that when MMHID increases, firms differentiate their products from their rivals. This result is consistent with theories according to which lower competition relaxes constraints and reduces uncertainty and enables firms to choose a more unique product market strategy. The result is inconsistent with escape-the-competition theories of product differentiation. To address potential endogeneity concerns, I exploit exogenous outflows resulting from the 2003 mutual fund scandal. In the third chapter, I propose a new identification strategy, which can be used to study the effects of MHHID. My strategy has substantially better time-series and cross-sectional coverage relative to previously used instruments. Specifically, I first identify mutual funds that are exposed to under-performing industries and are likely to face outflows. Then, I calculate the proportion of the MHHID such exposed funds are responsible for in unaffected industries. I show that this ratio strongly predicts future changes in MHHID, cash holdings and product market differentiation. Building on the same strategy, I also find that commonly held firms move closer together in product space

International Graduate Students and U.S. Innovation

This paper attempts to empirically evaluate the contribution of international graduate students to U.S. innovation. The main framework used is a simplified version of the ―national ideas production function‖. Two econometric specification are estimated – one in which a time trend is incorporated to observe the short-term relationship between the variables and one in which no time trend is included with the goal of capturing the variables‘ long term equilibrium relationship. The results suggest that in the long-term the number of international graduate students significantly (at the 10% level) affects innovative activity. However, when the short-term relationship of the variables is analyzed it is found that the effect of the foreign students is negative and insignificant. This is attributed to the fixed size of graduate programs in the short run and their tendency to expand in the long-run

Distribution analysis of the putative cancer marker S100A4 across invasive squamous cell carcinoma penile tissue

MS-based proteomic methods were utilised for the first time in the discovery of novel penile cancer biomarkers. MALDI MS imaging was used to obtain the in situ biomolecular MS profile of squamous cell carcinoma of the penis which was then compared to benign epithelial MS profiles. Spectra from cancerous and benign tissue areas were examined to identify MS peaks that best distinguished normal epithelial cells from invasive squamous epithelial cells, providing crucial evidence to suggest S100A4 to be differentially expressed. Verification by immunohistochemistry resulted in positive staining for S100A4 in a sub-population of invasive but not benign epithelial cells

Annexin II/Annexin II receptor axis regulates adhesion, migration, homing, and growth of prostate cancer

One of the most life-threatening complications of prostate cancer is skeletal metastasis. In order to develop treatment for metastasis, it is important to understand its molecular mechanisms. Our work in this field has drawn parallels between hematopoietic stem cell and prostate cancer homing to the marrow. Our recent work demonstrated that annexin II expressed by osteoblasts and endothelial cells plays a critical role in niche selection. In this study, we demonstrate that annexin II and its receptor play a crucial role in establishing metastasis of prostate cancer. Prostate cancer cell lines migrate toward annexin II and the adhesion of prostate cancer to osteoblasts and endothelial cells was inhibited by annexin II. By blocking annexin II or its receptor in animal models, short-term and long-term localization of prostate cancers are limited. Annexin II may also facilitate the growth of prostate cancer in vitro and in vivo by the MAPK pathway. These data strongly suggest that annexin II and its receptor axis plays a central role in prostate cancer metastasis, and that prostate cancer utilize the hematopoietic stem cell homing mechanisms to gain access to the niche. J. Cell. Biochem. 105: 370–380, 2008. © 2008 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/60982/1/21835_ftp.pd

Activation of tissue plasminogen activator by metastasis-inducing S100P protein

S100P protein in human breast cancer cells is associated with reduced patient survival and, in a model system of metastasis, it confers a metastatic phenotype upon benign mammary tumour cells. S100P protein possesses a C-terminal lysine residue. Using a multiwell in vitro assay, S100P is now shown for the first time to exhibit a strong, C-terminal lysine-dependent activation of tissue plasminogen activator (tPA), but not of urokinase-catalysed plasminogen activation. The presence of 10 μM calcium ions stimulates tPA activation of plasminogen 2-fold in an S100P-dependent manner. S100P physically interacts with both plasminogen and tPA in vitro, but not with urokinase. Cells constitutively expressing S100P exhibit detectable S100P protein on the cell surface, and S100P-containing cells show enhanced activation of plasminogen compared with S100P-negative control cells. S100P shows C-terminal lysine-dependent enhancement of cell invasion. An S100P antibody, when added to the culture medium, reduced the rate of invasion of wild-type S100P-expressing cells, but not of cells expressing mutant S100P proteins lacking the C-terminal lysine, suggesting that S100P functions outside the cell. The protease inhibitors, aprotinin or α-2-antiplasmin, reduced the invasion of S100P-expressing cells, but not of S100P-negative control cells, nor cells expressing S100P protein lacking the C-terminal lysine. It is proposed that activation of tPA via the C-terminal lysine of S100P contributes to the enhancement of cell invasion by S100P and thus potentially to its metastasis-promoting activity

Plasmin Plays an Essential Role in Amplification of Psoriasiform Skin Inflammation in Mice

BACKGROUND: Although increased levels of plasminogen activators have been found in psoriatic lesions, the role of plasmin converted from plasminogen by plasminogen activators in pathogenesis of psoriasis has not been investigated. METHODOLOGY/PRINCIPAL FINDINGS: Here we examined the contribution of plasmin to amplification of inflammation in patients with psoriasis. We found that plasminogen was diminished, but that the amount and activity of its converted product plasmin were markedly increased in psoriasis. Moreover, annexin II, a receptor for plasmin was dramatically increased in both dermis and epidermis in psoriasis. Plasmin at sites of inflammation was pro-inflammatory, eliciting production of inflammatory factors, including CC chemokine ligand 20 (CCL20) and interleukin-23 (IL-23), that was mediated by the nuclear factor-kappaB (NF-κB) signaling pathway and that had an essential role in the recruitment and activation of pathogenic C-C chemokine receptor type 6 (CCR6)+ T cells. Moreover, intradermal injection of plasmin or plasmin together with recombinant monocyte/macrophage chemotactic protein-1 (MCP-1) resulted in induction of psoriasiform skin inflammation around the injection sites with several aspects of human psoriasis in mice. CONCLUSIONS/SIGNIFICANCE: Plasmin converted from plasminogen by plasminogen activators plays an essential role in amplification of psoriasiform skin inflammation in mice, and targeting plasmin receptor--annexin II--may harbor therapeutic potential for the treatment of human psoriasis

Large-scale proteomic identification of S100 proteins in breast cancer tissues

<p>Abstract</p> <p>Background</p> <p>Attempts to reduce morbidity and mortality in breast cancer is based on efforts to identify novel biomarkers to support prognosis and therapeutic choices. The present study has focussed on S100 proteins as a potentially promising group of markers in cancer development and progression. One reason of interest in this family of proteins is because the majority of the S100 genes are clustered on a region of human chromosome 1q21 that is prone to genomic rearrangements. Moreover, there is increasing evidence that S100 proteins are often up-regulated in many cancers, including breast, and this is frequently associated with tumour progression.</p> <p>Methods</p> <p>Samples of breast cancer tissues were obtained during surgical intervention, according to the bioethical recommendations, and cryo-preserved until used. Tissue extracts were submitted to proteomic preparations for 2D-IPG. Protein identification was performed by N-terminal sequencing and/or peptide mass finger printing.</p> <p>Results</p> <p>The majority of the detected S100 proteins were absent, or present at very low levels, in the non-tumoral tissues adjacent to the primary tumor. This finding strengthens the role of S100 proteins as putative biomarkers. The proteomic screening of 100 cryo-preserved breast cancer tissues showed that some proteins were ubiquitously expressed in almost all patients while others appeared more sporadic. Most, if not all, of the detected S100 members appeared reciprocally correlated. Finally, from the perspective of biomarkers establishment, a promising finding was the observation that patients which developed distant metastases after a three year follow-up showed a general tendency of higher S100 protein expression, compared to the disease-free group.</p> <p>Conclusions</p> <p>This article reports for the first time the comparative proteomic screening of several S100 protein members among a large group of breast cancer patients. The results obtained strongly support the hypothesis that a significant deregulation of multiple S100 protein members is associated with breast cancer progression, and suggest that these proteins might act as potential prognostic factors for patient stratification. We propose that this may offer a significant contribution to the knowledge and clinical applications of the S100 protein family to breast cancer.</p