Match-fixing and Money-laundering

his essay is premised on the following: a conspiracy to fix or otherwise manipulate the outcome of a sporting event for profitable purpose. That conspiracy is in turn predicated on the conspirators’ capacity to: (a) ensure that the fix takes place as pre-determined; (b) manipulate the betting markets that surround the sporting event in question; and (c) collect their winnings undetected by either the betting industry’s security systems or the attention of any national regulatory body or law enforcement agency.

Unlike many essays on this topic, this contribution does not focus on the “fix”– part (a) of the above equation. It does not seek to explain how or why a participant or sports official might facilitate a betting scam through either on-field behaviour that manipulates the outcome of a game or by presenting others with privileged inside information in advance of a game. Neither does this contribution seek to give any real insight into the second part of the above equation: how such conspirators manipulate a sports betting market by playing or laying the handicap or in-play or other offered betting odds. In fact, this contribution is not really about the mechanics of sports betting or match fixing at all; rather it is about the sometimes under explained reason why match fixing has reportedly become increasingly attractive as of late to international crime syndicates. That reason relates to the fact that given the traditional liquidity of gambling markets, sports betting can, and has long been, an attractively accessible conduit for criminal syndicates to launder the proceeds of crime. Accordingly, the term “winnings”, noted in part (c) of the above equation, takes on an altogether more nefarious meaning.

This essay’s attempt to review the possible links between match fixing in sport, gambling-related “winnings” and money laundering is presented in four parts.

First, some context will be given to what is meant by money laundering, how it is currently policed internationally and, most importantly, how the growth of online gambling presents a unique set of vulnerabilities and opportunities to launder the proceeds of crime. The globalisation of organised crime, sports betting and transnational financial services now means that money laundering opportunities have moved well beyond a flutter on the horses at your local racetrack or at the roulette table of your nearest casino. The growth of online gambling platforms means that at a click it is possible for the proceeds of crime in one jurisdiction to be placed on a betting market in another jurisdiction with the winnings drawn down and laundered in a third jurisdiction and thus the internationalisation of gambling-related money laundering threatens the integrity of sport globally.

Second, and referring back to the infamous hearings of the US Senate Special Committee to Investigate Organised Crime in Interstate Commerce of the early 1950s, (“the Kefauver Committee”), this article will begin by illustrating the long standing interest of organised crime gangs – in this instance, various Mafia families in the United States – in money laundering via sports gambling-related means.

Third, and using the seminal 2009 report “Money Laundering through the Football Sector” by the Financial Action Task Force (FATF, an inter-governmental body established in 1989 to promote effective implementation of legal, regulatory and operational measures for combating money laundering, terrorist financing and other related threats to the integrity of the international financial system), this essay seeks to assess the vulnerabilities of international sport to match fixing, as motivated in part by the associated secondary criminality of tax evasion and transnational economic crime.

The fourth and concluding parts of the essay spin from problems to possible solutions. The underlying premise here is that heretofore there has been an insularity to the way that sports organisations have both conceptualised and sought to address the match fixing threat e.g., if we (in sport) initiate player education programmes; establish integrity units; enforce codes of conduct and sanctions strictly; then our integrity or brand should be protected. This essay argues that, although these initiatives are important, the source and process of match fixing is beyond sport’s current capacity, as are the possible solutions.

E-Commerce Innovations in the Personal Tax System of the United Kingdom

This study finds evidence that attempts to reduce costs and error rates in the Inland Revenue through the use of e-commerce technology are flawed. While it is technically possible to write software that will record tax data, and then transmit it to the Inland Revenue, there is little demand for this service. The key finding is that the tax system is so complex that many people are unable to complete their own tax returns. This complexity cannot be overcome by well-designed software. The recommendation is to encourage the use of agents to assist taxpayers or simplify the tax system. The Inland Revenue is interested in saving administrative costs and errors by encouraging electronic submission of tax returns. To achieve these objectives, given the raw data it would seem clear that the focus should be on facilitating the work of agents.

Chemotherapy-Induced CXC-Chemokine/CXC-Chemokine Receptor Signaling in Metastatic Prostate Cancer Cells Confers Resistance to Oxaliplatin through Potentiation of Nuclear Factor-κB Transcription and Evasion of Apoptosis

Constitutive activation of nuclear factor (NF)-kappa B is linked with the intrinsic resistance of androgen-independent prostate cancer (AIPC) to cytotoxic chemotherapy. Interleukin-8 (CXCL8) is a transcriptional target of NF-kappa B whose expression is elevated in AIPC. This study sought to determine the significance of CXCL8 signaling in regulating the response of AIPC cells to oxaliplatin, a drug whose activity is reportedly sensitive to NF-kappa B activity. Administration of oxaliplatin to PC3 and DU145 cells increased NF-kappa B activity, promoting antiapoptotic gene transcription. In addition, oxaliplatin increased the transcription and secretion of CXCL8 and the related CXC-chemokine CXCL1 and increased the transcription and expression of CXC-chemokine receptors, especially CXC-chemokine receptor (CXCR) 2, which transduces the biological effects of CXCL8 and CXCL1. Stimulation of AIPC cells with CXCL8 potentiated NF-kappa B activation in AIPC cells, increasing the transcription and expression of NF-kappa B-regulated antiapoptotic genes of the Bcl-2 and IAP families. Coadministration of a CXCR2-selective antagonist, AZ10397767 (Bioorg Med Chem Lett 18:798-803, 2008), attenuated oxaliplatin-induced NF-kappa B activation, increased oxaliplatin cytotoxicity, and potentiated oxaliplatin-induced apoptosis in AIPC cells. Pharmacological inhibition of NF-kappa B or RNA interference-mediated suppression of Bcl-2 and survivin was also shown to sensitize AIPC cells to oxaliplatin. Our results further support NF-kappa B activity as an important determinant of cancer cell sensitivity to oxaliplatin and identify the induction of autocrine CXCR2 signaling as a novel mode of resistance to this drug.

Managing time: integration of care and paid work amongst low income families and the role of the United Kingdom’s tax credit system

Under the New Labour Governments in the UK, successive reforms of the tax and benefit system sought to improve the financial benefits of paid work. Drawing on two waves of qualitative interviews with low-income working families this article examines the role of the UK tax credit system in shaping decisions about employment and unpaid care work. The article suggests that the financial support provided for lone parent participants by the tax credit system enhanced their temporal autonomy, permitting participation in paid work to align more closely with temporally situated notions of parental responsibility for caring. For couple families however, parental perceptions of responsibility for pre-school children, along with childcare constraints and the structure of the tax credit system served to constrain the autonomy of the main carer and implicitly encourage a gendered specialisation in caring or employment.

Long-term return reversals-Value and growth or tax? UK evidence

This paper examines (i) whether value-growth characteristics have more power than past performance in predicting return reversals; and (ii) whether typical rational behaviour such as incentives to delay paying capital gain taxes can better explain long-term reversals than past performance. We find that value-growth characteristics generally provide better explanations for long-term stock returns than past performance. The evidence also shows that winners identified by capital gains dominate past performance winners in predicting reversals in the cross-sectional comparison. However, in the time-series analysis, when returns on capital gain winners are adjusted by the Fama and French (1996) risk factors, the predictive power of capital gain winners disappears. Our results show that capital gain winners are heavily featured as growth stocks. Return reversals in capital gain winners potentially reflect market price corrections for growth stocks. We conclude that investors’ incentives to delay paying capital gain taxes cannot fully rationalise long-term reversals in the UK market. Our results also imply that the long-term return pattern potentially reflects a mixture of investor rational and irrational behaviour.

Europe's New Border Tax.

Instead of abolishing internal border controls in 1993, the European Union (EU) replaced them with VAT and statistical requirements that appear to be just as onerous. For Dutch businesses, the compliance costs of the new requirements are, on average, 5 per cent of the value of their intra-EU trade. The figure is probably higher for other EU Member States. Obviously, the costs constitute a (differentiated) border tax that impedes intra-EU trade. The article analyses the determinants of the compliance costs, as well as their effect on intra-EU trade intensity. The article submits that the differential compliance costs violate the non-discrimination provisions of the EC Treaty. Suggestions are made to reduce them.

Financial Taxes and the Sand in the Wheels of Financialization:Legal Challenges for the EU Directive Implementing Enhanced Cooperation in the Area of Financial Transaction Tax

One of the many results of the Global Financial Crisis was the insight that the financial sector is under-taxed compared to other industries. In light of the huge bailouts and continued subsidies for financial institutions that are characterized as too-big-to-fail demands came on the agenda to make finance pay for the mega-crisis it caused. The most prominent examples of such taxes are a Financial Transaction Tax (FTT) and a Financial Activities Tax (FAT). Possible effects of such taxes on the economic constitution and increasingly in particular on the European Single Market have been discussed controversially over the last decades already. Especially with the decision of eleven EU member states to adapt an FTT using the enhanced cooperation procedure a number of additional legal challenges for implementing such a tax have emerged. This paper analyzes how tax measures of indirectly regulating the financial industry differ, what legal challenges they pose, and what their overall contribution would be in making the financial system more stable and resilient. It also analyzes the legal arguments against enhanced cooperation in this area and the legal issues related to the British lawsuit against the Commission’s Directive proposal in the European Court of Justice on grounds of the extra-territoriality application of tax. The paper concludes that the feasibility of an FTT is legally sound and given the FTT’s advantages over a FAT the EU Directive should be implemented as a first step for a European-wide FTT. However, significant uncertainties about its implementation remain at this stage.

Identification of the Flagellin Glycosylation System in Burkholderia cenocepacia and the Contribution of Glycosylated Flagellin to Evasion of Human Innate Immune Responses

Burkholderia cenocepacia is an opportunistic pathogen threatening patients with cystic fibrosis. Flagella are required for biofilm formation, as well as adhesion to and invasion of epithelial cells. Recognition of flagellin via the Toll-like receptor 5 (TLR5) contributes to exacerbate B. cenocepacia-induced lung epithelial inflammatory responses. In this study, we report that B. cenocepacia flagellin is glycosylated on at least 10 different sites with a single sugar, 4,6-dideoxy-4-(3-hydroxybutanoylamino)-d-glucose. We have identified key genes that are required for flagellin glycosylation, including a predicted glycosyltransferase gene that is linked to the flagellin biosynthesis cluster and a putative acetyltransferase gene located within the O-antigen lipopolysaccharide cluster. Another O-antigen cluster gene, rmlB, which is required for flagellin glycan and O-antigen biosynthesis, was essential for bacterial viability, uncovering a novel target against Burkholderia infections. Using glycosylated and nonglycosylated purified flagellin and a cell reporter system to assess TLR5-mediated responses, we also show that the presence of glycan in flagellin significantly impairs the inflammatory response of epithelial cells. We therefore suggest that flagellin glycosylation reduces recognition of flagellin by host TLR5, providing an evasive strategy to infecting bacteria.

Epstein-Barr Virus Large Tegument Protein BPLF1 Contributes to Innate Immune Evasion through Interference with Toll-Like Receptor Signaling

Viral infection triggers an early host response through activation of pattern recognition receptors, including Toll-like receptors (TLR). TLR signaling cascades induce production of type I interferons and proinflammatory cytokines involved in establishing an anti-viral state as well as in orchestrating ensuing adaptive immunity. To allow infection, replication, and persistence, (herpes)viruses employ ingenious strategies to evade host immunity. The human gamma-herpesvirus Epstein-Barr virus (EBV) is a large, enveloped DNA virus persistently carried by more than 90% of adults worldwide. It is the causative agent of infectious mononucleosis and is associated with several malignant tumors. EBV activates TLRs, including TLR2, TLR3, and TLR9. Interestingly, both the expression of and signaling by TLRs is attenuated during productive EBV infection. Ubiquitination plays an important role in regulating TLR signaling and is controlled by ubiquitin ligases and deubiquitinases (DUBs). The EBV genome encodes three proteins reported to exert in vitro deubiquitinase activity. Using active site-directed probes, we show that one of these putative DUBs, the conserved herpesvirus large tegument protein BPLF1, acts as a functional DUB in EBV-producing B cells. The BPLF1 enzyme is expressed during the late phase of lytic EBV infection and is incorporated into viral particles. The N-terminal part of the large BPLF1 protein contains the catalytic site for DUB activity and suppresses TLR-mediated activation of NF-κB at, or downstream of, the TRAF6 signaling intermediate. A catalytically inactive mutant of this EBV protein did not reduce NF-κB activation, indicating that DUB activity is essential for attenuating TLR signal transduction. Our combined results show that EBV employs deubiquitination of signaling intermediates in the TLR cascade as a mechanism to counteract innate anti-viral immunity of infected hosts.

Chp8, a diguanylate cyclase from Pseudomonas syringae pv tomato DC3000 suppresses the PAMP flagellin, increases EPS and promotes plant immune evasion.

The bacterial plant pathogen Pseudomonas syringae causes disease in a wide range of plants. The associated decrease in crop yields results in economic losses and threatens global food security. Competition exists between the plant immune system and the pathogen, the basic principles of which can be applied to animal infection pathways. P. syringae uses a type III secretion system (T3SS) to deliver virulence factors into the plant that promote survival of the bacterium. The P. syringae T3SS is a product of the hypersensitive response and pathogenicity (hrp) and hypersensitive response and conserved (hrc) gene cluster, which is strictly controlled by the codependent enhancer-binding proteins HrpR and HrpS. Through a combination of bacterial gene regulation and phenotypic studies, plant infection assays, and plant hormone quantifications, we now report that Chp8 (i) is embedded in the Hrp regulon and expressed in response to plant signals and HrpRS, (ii) is a functional diguanylate cyclase, (iii) decreases the expression of the major pathogen-associated molecular pattern (PAMP) flagellin and increases extracellular polysaccharides (EPS), and (iv) impacts the salicylic acid/jasmonic acid hormonal immune response and disease progression. We propose that Chp8 expression dampens PAMP-triggered immunity during early plant infection.