Charity Oversight: An Alternative Approach

In this paper, a former director of the Internal Revenue Services Exempt Organization Division argues that the IRS is structurally ill suited for the task of providing vigorous oversight of the nations growing number of nonprofit organizations. The author proposes a new, national institution, modeled loosely on the corporate sectors National Association of Securities Dealers that would, among other features, derive sufficient funding for vigorous oversight through contributions from nonprofit organizations. The author envisions an amendment to the Internal Revenue Code that would enable the nonprofit organizations to take a credit against excise taxes, particularly the excise tax on the net investment income of private foundations, they would otherwise pay to the federal government. This publication is Hauser Center Working Paper No. 33.4. Hauser Working Paper Series Nos. 33.1-33.9 were prepared as background papers for the Nonprofit Governance and Accountability Symposium October 3-4, 2006.The author, Marcus S. Owens is with Caplin & Drysdale; Chartered

Charity Oversight: An Alternative Approach

A number of years ago, I suggested that the time might be ripe to consider a new model for charity regulation, one modeled on the combination of self-regulation and government oversight provided to U.S. security markets by the Securities Exchange Commission (“SEC”) and the National Association of Securities Dealers (“NASD”) and similar self-regulatory organizations. The intervening years have not been quiet for either the charitable community or the securities industry. On the charitable side, we have seen the passage of extensive charity reform legislation in the Pension Protection Act of 2006 (the “PPA”), which, while aimed at some well-publicized and clear abuses, is written so broadly that it creates new prohibitions, administrative burdens, and legal uncertainty for many legitimate charities. In the securities industry, the SEC has considered whether the self-regulation model needs to be revisited, and the trend is toward more consolidated and more publicly accountable mechanisms for industry self-regulation, as evidenced by the structure of the Financial Industry Regulatory Authority (“FINRA”), the result of a merger of the NASD and the regulatory functions of the New York Stock Exchange (“NYSE”). Developments in both the charitable and financial sectors continue to persuade me that restructuring the federal regulation of charities along the lines of FINRA or other hybrid public/private regulators makes sense. In addition, the federal/state structure for the investigation and prosecution of Medicaid fraud, as embodied by Medicaid Fraud Control Units, suggests a model for federal/state cooperation in charities oversight. In this paper, I expand on what a new public/private charity regulator might look like, taking into account lessons from the financial sector and Medicaid fraud investigation. While there are obviously numerous points along the spectrum between a purely public regulator like the IRS and a purely private “regulator” like a voluntary standard-setting organization, the regime I favor features a strong regulator with minority representation from the sector along with significant government representation. Its closest analogues in the securities industry are FINRA itself and the Public Companies Accounting Oversight Board (PCAOB) created by the Sarbanes-Oxley Act of 2002 to oversee public company auditors. Although there are important differences between these models, both offer several advantages over the current IRS-managed enforcement structure. They also preserve important advantages of a self-regulatory model while mitigating its potential drawbacks

Delivering a “Dose of Hope”: A Faith-Based Program to Increase Older African Americans’ Participation in Clinical Trials

Background: Underrepresentation of older-age racial and ethnic minorities in clinical research is a significant barrier to health in the United States, as it impedes medical research advancement of effective preventive and therapeutic strategies. Objective: The objective of the study was to develop and test the feasibility of a community-developed faith-based intervention and evaluate its potential to increase the number of older African Americans in clinical research. Methods: Using a cluster-randomized design, we worked with six matched churches to enroll at least 210 persons. We provided those in the intervention group churches with three educational sessions on the role of clinical trials in addressing health disparity topics, and those in the comparison group completed surveys at the same timepoints. All persons enrolled in the study received ongoing information via newsletters and direct outreach on an array of clinical studies seeking participants. We evaluated the short-, mid-, and longer-term effects of the interventional program on clinical trial-related outcomes (ie, screening and enrollment)

Tied to the worldly work of writing: parent as ethnographer

Parent narratives have contributed to ethnographic accounts of the lives of autistic children (Kelly, 2005) but there are fewer examples of parents producing their own autoethnographies. This paper explores the affordances of an online blog for enabling a parent of an autistic child to produce a written record of practice which may be considered 'autoethnographic'. Richardson’s (2005) framework for ethnography as Creative Analytic Process is applied to extracts from a blog post in order to consider its contribution; reflexivity; aesthetic merit; and impact. The paper addresses the methodological and ethical implications of reconceptualising parents as researchers and the potential contribution of new writing platforms to the development of auto/ethnography. Key words: Autism, Auto/ethnography, Blog, Disability, Mothe

International criteria for electrocardiographic interpretation in athletes: Consensus statement.

Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport. A variety of mostly hereditary, structural or electrical cardiac disorders are associated with SCD in young athletes, the majority of which can be identified or suggested by abnormalities on a resting 12-lead electrocardiogram (ECG). Whether used for diagnostic or screening purposes, physicians responsible for the cardiovascular care of athletes should be knowledgeable and competent in ECG interpretation in athletes. However, in most countries a shortage of physician expertise limits wider application of the ECG in the care of the athlete. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from distinctly abnormal findings suggestive of underlying pathology. Since the original 2010 European Society of Cardiology recommendations for ECG interpretation in athletes, ECG standards have evolved quickly, advanced by a growing body of scientific data and investigations that both examine proposed criteria sets and establish new evidence to guide refinements. On 26-27 February 2015, an international group of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle, Washington (USA), to update contemporary standards for ECG interpretation in athletes. The objective of the meeting was to define and revise ECG interpretation standards based on new and emerging research and to develop a clear guide to the proper evaluation of ECG abnormalities in athletes. This statement represents an international consensus for ECG interpretation in athletes and provides expert opinion-based recommendations linking specific ECG abnormalities and the secondary evaluation for conditions associated with SCD

Comparing motivational, self-regulatory and habitual processes in a computer-tailored physical activity intervention in hospital employees - Protocol for the PATHS randomised controlled trial

Background: Most people do not engage in sufficient physical activity to confer health benefits and to reduce risk of chronic disease. Healthcare professionals frequently provide guidance on physical activity, but often do not meet guideline levels of physical activity themselves. The main objective of this study is to develop and test the efficacy of a tailored intervention to increase healthcare professionals' physical activity participation and quality of life, and to reduce work-related stress and absenteeism. This is the first study to compare the additive effects of three forms of a tailored intervention using different techniques from behavioural theory, which differ according to their focus on motivational, self-regulatory and/or habitual processes. Methods/Design: Healthcare professionals (N = 192) will be recruited from four hospitals in Perth, Western Australia, via email lists, leaflets, and posters to participate in the four group randomised controlled trial. Participants will be randomised to one of four conditions: (1) education only (non-tailored information only), (2) education plus intervention components to enhance motivation, (3) education plus components to enhance motivation and self-regulation, and (4) education plus components to enhance motivation, self-regulation and habit formation. All intervention groups will receive a computer-tailored intervention administered via a web-based platform and will receive supporting text-messages containing tailored information, prompts and feedback relevant to each condition. All outcomes will be assessed at baseline, and at 3-month follow-up. The primary outcome assessed in this study is physical activity measured using activity monitors. Secondary outcomes include: quality of life, stress, anxiety, sleep, and absenteeism. Website engagement, retention, preferences and intervention fidelity will also be evaluated as well as potential mediators and moderators of intervention effect. Discussion: This is the first study to examine a tailored, technology-supported intervention aiming to increase physical activity in healthcare professionals. The study will evaluate whether including additional theory-based behaviour change techniques aimed at promoting motivation, self-regulation and habit will lead to increased physical activity participation relative to information alone. The online platform developed in this study has potential to deliver efficient, scalable and personally-relevant intervention that can be translated to other occupational settings. Trial registration: Australian New-Zealand Clinical Trial Registry: ACTRN12616000462482, submitted 29/03/2016, prospectively registered 8/04/2016

Inhibition of STAT3 signaling prevents vascular smooth muscle cell proliferation and neointima formation

Dedifferentiation, migration, and proliferation of resident vascular smooth muscle cells (SMCs) are key components of neointima formation after vascular injury. Activation of signal transducer and activator of transcription-3 (STAT3) is suggested to be critically involved in this process, but the complex regulation of STAT3-dependent genes and the functional significance of inhibiting this pathway during the development of vascular proliferative diseases remain elusive. In this study, we demonstrate that STAT3 was activated in neointimal lesions following wire-induced injury in mice. Phosphorylation of STAT3 induced trans-activation of cyclin D1 and survivin in SMCs in vitro and in neointimal cells in vivo, thus promoting proliferation and migration of SMCs as well as reducing apoptotic cell death. WP1066, a highly potent inhibitor of STAT3 signaling, abrogated phosphorylation of STAT3 and dose-dependently inhibited the functional effects of activated STAT3 in stimulated SMCs. The local application of WP1066 via a thermosensitive pluronic F-127 gel around the dilated arteries significantly inhibited proliferation of neointimal cells and decreased the neointimal lesion size at 3 weeks after injury. Even though WP1066 application attenuated the injury-induced up-regulation of the chemokine RANTES at 6 h after injury, there was no significant effect on the accumulation of circulating cells at 1 week after injury. In conclusion, these data identify STAT3 as a key molecule for the proliferative response of SMC and neointima formation. Moreover, inhibition of STAT3 by the potent and specific compound WP1066 might represent a novel and attractive approach for the local treatment of vascular proliferative diseases

Hsp90 inhibition differentially destabilises MAP kinase and TGF-beta signalling components in cancer cells revealed by kinase-targeted chemoproteomics

<p>Abstract</p> <p>Background</p> <p>The heat shock protein 90 (Hsp90) is required for the stability of many signalling kinases. As a target for cancer therapy it allows the simultaneous inhibition of several signalling pathways. However, its inhibition in healthy cells could also lead to severe side effects. This is the first comprehensive analysis of the response to Hsp90 inhibition at the kinome level.</p> <p>Methods</p> <p>We quantitatively profiled the effects of Hsp90 inhibition by geldanamycin on the kinome of one primary (Hs68) and three tumour cell lines (SW480, U2OS, A549) by affinity proteomics based on immobilized broad spectrum kinase inhibitors ("kinobeads"). To identify affected pathways we used the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway classification. We combined Hsp90 and proteasome inhibition to identify Hsp90 substrates in Hs68 and SW480 cells. The mutational status of kinases from the used cell lines was determined using next-generation sequencing. A mutation of Hsp90 candidate client RIPK2 was mapped onto its structure.</p> <p>Results</p> <p>We measured relative abundances of > 140 protein kinases from the four cell lines in response to geldanamycin treatment and identified many new potential Hsp90 substrates. These kinases represent diverse families and cellular functions, with a strong representation of pathways involved in tumour progression like the BMP, MAPK and TGF-beta signalling cascades. Co-treatment with the proteasome inhibitor MG132 enabled us to classify 64 kinases as true Hsp90 clients. Finally, mutations in 7 kinases correlate with an altered response to Hsp90 inhibition. Structural modelling of the candidate client RIPK2 suggests an impact of the mutation on a proposed Hsp90 binding domain.</p> <p>Conclusions</p> <p>We propose a high confidence list of Hsp90 kinase clients, which provides new opportunities for targeted and combinatorial cancer treatment and diagnostic applications.</p