Deregulation and The 2007-2008 Housing/Debt Crisis Analysis of the Housing/Debt Crisis of 2007-2008 and its impact on the Financial Strength and Vulnerability of the United States and Global Economy

One looming question has persisted in the minds of economists the world over in the aftermath of the 2007-2008 American Housing and Debt Crisis: How did it begin and who is responsible for making this happen? Another two-part question is: What measures were implemented to help end the crisis and what changes are being implemented to ensure that it will never happen again? Many speculate that the major contributing factor was the repeal of the Glass-Steagall Act in 1999 that prompted a virtual feeding frenzy among the banking community when new calls from Capitol Hill encouraged home ownership in America as well as the secondary mortgage market which skyrocketed thereafter. The Glass-Steagall Act will be among many of the topics explored in this paper along with the events leading up to the 2007-2008 housing/debt crisis as well as the aftermath.

During the initiation of fermentation overexpression of hexokinase PII in yeast transiently causes a similar deregulation of glycolysis as deletion of Tps1

In the yeast Saccharomyces cerevisiae a novel control exerted by TPS1 (=GGS1=FDP1=BYP1=CIF1=GLC6=TSS1)-encoded trehalose-6-phosphate synthase, is essential for restriction of glucose influx into glycolysis apparently by inhibiting hexokinase activity in vivo. We show that up to 50-fold overexpression of hexokinase does not noticeably affect growth on glucose or fructose in wild-type cells. However, it causes higher levels of glucose-6-phosphate, fructose-6-phosphate and also faster accumulation of fructose-1,6-bisphosphate during the initiation of fermentation. The levels of ATP and Pi correlated inversely with the higher sugar phosphate levels. In the first minutes after glucose addition, the metabolite pattern observed was intermediate between those of the tps1Δ mutant and tile wild-type strain. Apparently, during the start-up of fermentation hexokinase is more rate-limiting in the first section of glycolysis than phosphofructokinase. We have developed a method to measure the free intracellular glucose level which is based on the simultaneous addition of D-glucose and an equal concentration of radiolabelled L-glucose. Since the latter is not transported, the free intracellular glucose level can be calculated as the difference between the total B-glucose measured (intracellular + periplasmic/extracellular) and the total L-glucose measured (periplasmic/extracellular). The intracellular glucose level rose in 5 min after addition of 100 mM-glucose to 0.5-2 mM in the wild-type strain, ± 10 mm in a hxk1Δ hxk2Δ glk1Δ and 2-3 mM in a tps1Δ strain. In the strains overexpressing hexokinase PII the level of free intracellular glucose was not reduced. Overexpression of hexokinase PII never produced a strong effect on the rate of ethanol production and glucose consumption. Our results show that overexpression of hexokinase does not cause the same phenotype as deletion of Tps1. However, it mimics it transiently during the initiation of fermentation. Afterwards, the Tps1-dependent control system is apparently able to restrict Properly up to 50-fold higher hexokinase activity.

Divestiture and deregulation of public enterprises: the Mexican case

Includes bibliography

Institutional change and technology: impacts of deregulation on the national innovation system

Includes bibliography

Deregulation of Annexin-A1 and Galectin-1 Expression in Precancerous Gastric Lesions: Intestinal Metaplasia and Gastric Ulcer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Deregulation of apoptosis-related genes is associated with PRV1 overexpression and JAK2 V617F allele burden in Essential Thrombocythemia and Myelofibrosis

Background: Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF) are Chronic Myeloproliferative Neoplasms (MPN) characterized by clonal myeloproliferation/myeloaccumulation without cell maturation impairment. The JAK2 V617F mutation and PRV1 gene overexpression may contribute to MPN physiopathology. We hypothesized that deregulation of the apoptotic machinery may also play a role in the pathogenesis of ET and PMF. In this study we evaluated the apoptosis-related gene and protein expression of BCL2 family members in bone marrow CD34(+) hematopoietic stem cells (HSC) and peripheral blood leukocytes from ET and PMF patients. We also tested whether the gene expression results were correlated with JAK2 V617F allele burden percentage, PRV1 overexpression, and clinical and laboratory parameters. Results: By real time PCR assay, we observed that A1, MCL1, BIK and BID, as well as A1, BCLW and BAK gene expression were increased in ET and PMF CD34(+) cells respectively, while pro-apoptotic BAX and anti-apoptotic BCL2 mRNA levels were found to be lower in ET and PMF CD34(+) cells respectively, in relation to controls. In patients' leukocytes, we detected an upregulation of anti-apoptotic genes A1, BCL2, BCL-XL and BCLW. In contrast, pro-apoptotic BID and BIMEL expression were downregulated in ET leukocytes. Increased BCL-XL protein expression in PMF leukocytes and decreased BID protein expression in ET leukocytes were observed by Western Blot. In ET leukocytes, we found a correlation between JAK2 V617F allele burden and BAX, BIK and BAD gene expression and between A1, BAX and BIK and PRV1 gene expression. A negative correlation between PRV1 gene expression and platelet count was observed, as well as a positive correlation between PRV1 gene expression and splenomegaly. Conclusions: Our results suggest the participation of intrinsic apoptosis pathway in the MPN physiopathology. In addition, PRV1 and JAK2 V617F allele burden were linked to deregulation of the apoptotic machinery.

The Pre-1980 Roots of Neoliberal Financial Deregulation

U.S. financial deregulation is often popularly presented as a fundamental attack on financial regulation that began with neoliberalism's Big Bang in 1980. This paper argues this position is wrong in two ways. First, it is a process that stretches back decades before 1980. Textbook mentions of 1970s precursor "financial innovations" fall far short of presenting the breadth and duration of the pre-1980 attack on the system of regulation. Second, it has not been an across-the-board attack on financial regulation in the name of market efficiency as required by its ideology and claimed by its advocates, but rather a focused attack on only one of the five pillars of the system of regulation. This paper develops both of these assertions through a presentation of the five central pillars of the pre-1980 system of financial regulation, and the four major attacks on the three different aspects of the restrictions on financial competition.

Investigation of the deregulation of interleukin-6 in two non-Hodgkin's lymphoma cell lines

Increased serum interleukin-6 (IL-6) is a poor prognostic factor for patients with lymphoma. This may be related to the fact that IL-6 has been shown to be an autocrine and paracrine growth factor for lymphoma cells. We have investigated the regulation of IL-6 in two lymphoma cell lines which produce IL-6 as an autocrine growth factor. The cell lines, LY3 and LY12, were established from two patients with non-Hodgkin's lymphoma. One patient had diffuse large cell lymphoma (LY3), whereas the other had small noncleaved cell lymphoma (LY12). There was no rearrangement or amplification of the IL-6 gene, but we detected IL-1 alpha and TNF production in addition to IL-6. We investigated the effect of inhibitors of IL-1 and TNF on IL-6 production in LY3 and LY12. Our results show that IL-6 production is mainly secondary to endogenous IL-1 production in LY3 cells, however LY12 cells produce IL-6 via a different mechanism since neither anti-IL-1 nor anti-TNF significantly inhibited IL-6 production.^ Transfection of LY12 cells with wildtype and mutant IL-6 promoter-chloramphenicol acetyl transferase constructs, showed increased activity of a trans-acting factor that binds to the NF-kB motif. Therefore, we determined whether there were abnormalities in members of the NF-kB family of transcription factors, such as p65, p50, p52/lyt-10 or rel, which bind to kB motifs. We found increased expression of the p52/lyt-10 transcription factor and activation of the NF-kB pathway in LY12. However, expression of p50, p65 and rel was not increased in LY12 cells. Future investigations could be aimed at determining the effect of inhibitors of NF-kB on IL-6 production. ^

Deregulation strategies and its regulating effects: The case of the termination of Social Assistance for rejected asylum seekers in Switzerland

Deregulation strategies and their regulating effects: The case of the termination of Social Assistance for rejected asylum seekers in Switzerland. In Switzerland, rejected asylum seekers no longer have any residence rights. In 2003 the Swiss state decided to terminate the so far granted social assistance for people with a non-entry decision on their asylum request. In 2008 the termination of social assistance was expanded to all rejected asylum seekers. Nevertheless, facing the impossibility of deporting them, the Swiss state entitled this group of people to emergency assistance. It is a basic, which is stated in the Swiss Federal constitution. In this context, new structures were established specially for rejected asylum seekers. These structures had to be set up, financed, controlled, managed and legitimized. For example, collective centres were set up exclusively for rejected asylum seekers. In this speech, I want to analyze the political and bureaucratic process of terminating social assistance for rejected asylum seekers. The exclusion of rejected asylum seekers from social aid was embedded in a wider austerity program of the Federal State. The Federal Migration Office had been requested to save money. The main official goal was to reduce the support of these illegalized people, reduce any structures that would prolong their stay on Swiss ground and to set incentives so that they would leave the country on their own. But during the implementation, new regulating effects emerged. Drawing on ethnographic material, I will highlight these “messy procedures” (Sciortino 2004). First, I will analyze the means and goals developed by the Federal authorities while conceptualising the termination of social assistance. Second, I will focus on the new built structures and elaborate the practices and legitimating strategies of the authorities. As a conclusion, I will analyze the ambivalences of these processes which, at the end, established specific structures for the “unwanted”.

Has Deregulation Affected Births, Deaths, and Marriages 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 culminating with the Interstate Banking and Branching Efficiency Act of 1994. Banking analysts anticipated dramatic consolidation with large numbers of mergers and acquisitions. Less well documented, but equally important, was the continuing entry of new banks, tempering the decline in the overall number of banking institutions. This paper examines whether deregulation affected bank new-charter (birth), failure (death), and merger (marriage) rates during the 1980s and 1990s after controlling for bank performance and state economic activity. We find evidence that intrastate deregulation stimulated births and marriages, but not deaths. Moreover, we find little evidence that interstate deregulation affected births, deaths, or marriages, except that the marriage rate rose after the implementation of the Interstate Banking and Branching Efficiency Act. Finally, pair-wise temporal causality tests among births, deaths, and marriages show that mergers temporally lead new charters and that failures lead mergers (a demonstration effect).

Has Deregulation Affected Births, Deaths, and Marriages 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 culminating with the Interstate Banking and Branching Efficiency Act of 1994. Banking analysts anticipated dramatic consolidation with large numbers of mergers and acquisitions. Less well documented, but equally important, was the continuing entry of new banks, tempering the decline in the overall number of banking institutions. This paper examines whether deregulation affected bank new-charter, failure, and merger rates during the 1980s and 1990s after controlling for bank performance and state economic activity. We find evidence that intrastate deregulation stimulated new charters and mergers, but not failures. Moreover, we find little evidence that interstate deregulation affected new charters, failures, or mergers.

Geographic Deregulation and Commercial Bank Performance in US State Banking Markets

This paper examines the effects of geographical deregulation on commercial bank performance across states. We reach some general conclusions. First, the process of deregulation on an intrastate and interstate basis generally improves bank profitability and performance. Second, the macroeconomic variables -- the unemployment rate and real personal income per capita -- and the average interest rate affect bank performance as much, or more, than the process of deregulation. Finally, while deregulation toward full interstate banking and branching may produce more efficient banks and a healthier banking system, we find mixed results on this issue.

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.

The low molecular weight (LMW) isoforms of cyclin E provide a novel mechanism of cell cycle deregulation

Cyclin E, in complex with cyclin dependent kinase 2 (CDK2), is a positive regulator of G1 to S phase progression of the cell cycle. Deregulation of G1/S phase transition occurs in the majority of tumors. Cyclin E is overexpressed and post-translationally generates low molecular weight (LMW) isoforms in breast cancer, but not normal cells. Such alteration of cyclin E is linked to poor prognosis. Therefore, we hypothesized that the LMW isoforms of cyclin E provide a novel mechanism of cell cycle de-regulation in cancer cells. Insect cell expression system was used to explore the biochemical properties of the cyclin E isoforms. Non-tumorigenic (76NE6) and tumorigenic (T47D) mammary epithelial cells transfected with the cyclin E isoforms and breast tumor tissue endogenously expressing the LMW isoforms were used to study the biologic consequences of the LMW isoforms of cyclin E. All model systems studied show that the LMW forms (compared to full-length cyclin E) have increased kinase activity when partnered with CDK2. Increases in the percentage of cells in S phase and colony formation were also observed after overexpression of LMW compared to full-length cyclin E. The LMW isoforms of cyclin E utilize several mechanisms to attain their hyper-activity. They bind CDK2 more efficiently, and are resistant to inhibition by cyclin dependent kinase inhibitors (CKIs) as compared to full-length cyclin E. In addition, the LMW isoforms sequester the CKIs from full-length cyclin E abrogating the overall negative regulation of cyclin E. Despite their correlation with adverse biological consequences, the direct role of the LMW isoforms of cyclin E in mediating tumorigenesis remained unanswered. Subsequent to LMW cyclin E expression in 76NE6 cells, they lose their ability to enter quiescence and exhibit genomic instability, both characteristic of a tumor cell phenotype. Furthermore, injection of 76NE6 cells overexpressing each of the cyclin E isoforms into the mammary fat pad of nude mice revealed that the LMW isoforms of cyclin E yield tumors, whereas the full-length cyclin E does not. In conclusion, the LMW isoforms of cyclin E utilize several mechanisms to acquire a hyperactive phenotype that results in deregulation of the cell cycle and initiates the tumorigenic process in otherwise non-transformed mammary epithelial cells. ^