Credit Card Fraud: A New Perspective On Tackling An Intransigent Problem

This article offers a new perspective on battling credit card fraud. It departs from a focus on post factum liability, which characterizes most legal scholarship and federal legislation on credit card fraud and applies corrective mechanisms only after the damage is done. Instead, this article focuses on preempting credit card fraud by tackling the root causes of the problem: the built-in incentives that keep the credit card industry from fighting fraud on a system-wide basis. This article examines how credit card companies and banks have created a self-interested infrastructure that insulates them from the liabilities and costs of credit card fraud. Contrary to widespread belief, retailers, not card companies or banks, absorb much of the loss caused by thieves who shop with stolen credit cards. Also, credit card companies and banks earn fees from every credit card transaction, including those that are fraudulent. In addressing these problems, this article advocates broad reforms, including legislation that would mandate data security standards for the industry, empower multiple stakeholders to create the new standards, and offer companies incentives to comply by capping bank fees for those that are compliant, while deregulating fees for those that are not compliant

The Incremental Information Content of Tone Change in Management Discussion and Analysis

This study explores whether the Management Discussion and Analysis (MD&A) section of Form 10-Q and 10-K has incremental information content beyond financial measures such as earnings surprises, accruals and operating cash flows (OCF). It uses a well-established classification scheme of words into positive and negative categories to measure the tone change in a specific MD&A section as compared to those of the prior four filings. Our results indicate that short window market reactions around the SEC filing are significantly associated with the tone of the MD&A section, even after controlling for accruals, OCF and earnings surprises. We also show that the tone of the MD&A section adds significantly to portfolio drift returns in the window of two days after the SEC filing date through one day after the subsequent quarter’s preliminary earnings announcement, beyond financial information conveyed by accruals, OCF and earnings surprises. The incremental information of tone change is larger the weaker is the firm’s information environment

Adverse childhood experiences, non-response and loss to follow-up: Findings from a prospective birth cohort and recommendations for addressing missing data

Adverse childhood experiences have wide-ranging impacts on population health but are inherently difficult to study. Retrospective self-report is commonly used to identify exposure but adult population samples may be biased by non-response and loss to follow-up. We explored the implications of missing data for research on child abuse and neglect, domestic violence, parental mental illness and parental substance use. Using 15 waves of data collected over 28 years in a population-based birth cohort, the Australian Temperament Project, we examined the relationship between retrospective self-reports of adverse childhood experiences and parent- and cohort-responsiveness at other time points. We then compared prevalence estimates under complete case analysis, inverse probability-weighting using baseline auxiliary variables, multiple imputation using baseline auxiliary variables, multiple imputation using auxiliary variables from all waves, and multiple imputation using additional measures of participant responsiveness. Retrospective self-reports of adverse childhood experiences were strongly associated with non-response by both parents and cohort members at all observable time points. Biases in complete case estimates appeared large and inverse probability-weighting did not reduce them. Multiple imputation increased the estimated prevalence of any adverse childhood experiences from 30.0% to 36.9% with only baseline auxiliary variables, 39.7% with a larger set of auxiliary variables and 44.0% when measures of responsiveness were added. Close attention must be paid to missing data and non-response in research on adverse childhood experiences as data are unlikely to be missing at random. Common approaches may greatly underestimate their prevalence and compromise analysis of their causes and consequences. Sophisticated techniques using a wide range of auxiliary variables are critical in this field of research, including, where possible, measures of participant responsiveness.Funding for this analysis was supported by a PhD scholarship from the University of South Australia, and the South Australian Health Economics Collaborative (funded by the South Australian Department of Health)

IL‐12‐polarized Th1 cells produce GM‐CSF and induce EAE independent of IL‐23

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/115966/1/eji3410.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/115966/2/eji3410-sup-0002-PRC.pd

The Th17–ELR+ CXC chemokine pathway is essential for the development of central nervous system autoimmune disease

The ELR+ CXC chemokines CXCL1 and CXCL2 are up-regulated in the central nervous system (CNS) during multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, their functional significance and the pathways regulating their expression are largely unknown. We show that transfer of encephalitogenic CD4+ Th17 cells is sufficient to induce CXCL1 and CXCL2 transcription in the spinal cords of naive, syngeneic recipients. Blockade or genetic silencing of CXCR2, a major receptor for these chemokines in mice, abrogates blood–brain barrier (BBB) breakdown, CNS infiltration by leukocytes, and the development of clinical deficits during the presentation as well as relapses of EAE. Depletion of circulating polymorphonuclear leukocytes (PMN) had a similar therapeutic effect. Furthermore, injection of CXCR2+ PMN into CXCR2−/− mice was sufficient to restore susceptibility to EAE. Our findings reveal that a Th17–ELR+ CXC chemokine pathway is critical for granulocyte mobilization, BBB compromise, and the clinical manifestation of autoimmune demyelination in myelin peptide–sensitized mice, and suggest new therapeutic targets for diseases such as MS

Stage-Specific Immune Dysregulation in Multiple Sclerosis

A large body of data indicates that multiple sclerosis (MS) is an autoimmune disease which is initiated by CD4+ T-helper 1 (Th1) and Th17 cells that are reactive against proteins in the myelin sheath. MS typically begins with a relapsing-remitting course, punctuated by clinical exacerbations associated with the development of focal inflammatory lesions in central nervous system white matter, followed by a secondary progressive (SP) phase, characterized by a gradual accumulation of neurological disability associated with widespread microglial activation and axonal loss. The molecular and cellular basis for this transition is unclear, and the role of inflammation during the SP stage is a subject of active debate. As of now, no immunological biomarkers have been identified in MS that are predictive of the clinical course or therapeutic responsiveness to disease-modifying agents, or that correlate with new lesion development, cumulative lesion load, or degree of disability. The discovery of such biomarkers would greatly facilitate clinical management and provide power for smaller and shorter clinical trials. In this article, we discuss the literature on immunological biomarkers in MS with a focus on stage-specific differences and similarities.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140109/1/jir.2014.0025.pd