The Definition of Voting Stock and the Computation of Voting Power Under Sections 368(c) and 1504(a): Recent Developments and Tax Lore

Although the concepts of voting stock and voting power are pervasive throughout the Code, until recently, courts, commentators and the Service have devoted minimal energy to demystifying the confusion surrounding the definition of voting stock and even less to expanding upon the methodology of computing voting power. Recent developments, however, may prompt practitioners to take a second look at these terms. While a 1995 decision by the Tax Court adds little to the existing body of authority with respect to the determination of the owner of voting stock, the Service\u27s analysis of the voting power requirement in a 1994 private letter ruling sheds new light on the method of computing voting power. This article reviews and analyzes the current state of the law concerning the voting stock and voting power requirements in two areas of the tax law: section 368(c), which defines the level of stock ownership in a corporation that a taxpayer must possess in order to qualify for many forms of tax-free reorganizations, and section 1504(a), which requires a corporation attempting to form an affiliated group with a subsidiary corporation to own an amount of voting stock in the subsidiary having a specified level of voting power. Part II of this article briefly explains the statutory requirements of both section 368(c) and section 1504(a). Part III reviews the case law and administrative precedents that have shaped the definition of voting stock and attempts to distinguish the ownership requirement of section 368(c) from the direct ownership requirement of section 1504(a). Accordingly, part III of this article also analyzes the Tax Court\u27s most recent decision regarding the meaning of the term direct ownership. Part IV examines the mechanical test developed by the courts and the Service for computing the voting power inherent in the stock of a corporation, explores ways in which taxpayers have attempted to manipulate a corporation\u27s capital structure in order to satisfy the control requirement of section 368(c), and discusses the Service\u27s latest pronouncement regarding the use of this mechanical test in measuring voting power. Finally, this article highlights the remaining ambiguities that continue to create uncertainty for taxpayers with regard to the voting stock definition and the voting power formula

The Unreasonable Case for a Reasonable Compensation Standard in the Public Company Context: Why it is Unreasonable to Insist on Reasonableness

There is no question that corporate executives are well paid. But does high executive compensation mean excessive or unreasonable compensation? And if so, what is the solution to curbing the problem of excessive executive pay? More specifically, should the Internal Revenue Code be used as a means for regulating the actions of public companies? This Article briefly explores these issues. In Part I, this Article provides a narrative of the excessive compensation debate. Without drawing a conclusion as to whether executive compensation is reasonably set or excessive in nature, Part I summarizes the history of public outrage surrounding executive pay. Part I also provides a short discussion of the arguments on each side of the debate. Part II of this Article analyzes Section 162(a)(1) of the Code, which provides for the deduction for a reasonable allowance for compensation. This Part explores the history behind Section 162(a)(1) and how the provision has been interpreted to apply only to compensation paid by private, closely held companies. Part II concludes by determining that the deduction for reasonable compensation allowed under Section 162(a)(1) is different than a deduction only for reasonable compensation and that there is no basis for judging the reasonableness of compensation in the public company context. Part III discusses prior tax legislation enacted in an attempt to control executive pay by setting forth objective standards of reasonableness in the public company context. In addition, Part III summarizes the literature that shows that each attempt to limit executive compensation not only failed to achieve its goal, but also may have led to executives of public corporations receiving larger pay packages. Part IV critiques a recent law review piece which argues that, not only should the Code be used as an instrument to regulate executive compensation, but that the Service should use the vague language of Section 162(a)(1) to achieve this goal. The Article concludes by urging Congress to refrain from using the tax laws to further regulate behavior in this area

Business Lobbying as an Informational Public Good: Can Tax Deductions for Lobbying Expenses Promote Transparency?

The view that “lobbying is essentially an informational activity” has persistently served the suggestion that lobbying provides a public good by educating legislators about policy and the consequences of legislation. In this article, we link a proposed tax reform with a substantive disclosure requirement to promote the kind of “information subsidy” that serves the public interest, while mitigating – at least to some extent – the distortion that may result from the imbalance of financial resources on the business side and other institutional contraints identified in the literature. We argue that corporate lobbying should be encouraged – by allowing business to deduct lobbying expenses – but only to the extent that the information subsidy that corporate lobbying supplies in fact educates lawmakers on complex policy issues. In other words, to the extent that lobbying supplies an informational public good, such information should actually be made generally available through full and timely publication, rather than inserted strategically into the legislative process at a time, and in such manner, that excludes others from using the information to assess the merits of proposed legislation

Environment, human reproduction, menopause, and andropause.

As the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator is an integrator of hormonal, metabolic, and neural signals, it is not surprising that the function of the hypothalamogonadal axis is subject to the influence of a large array of environmental factors. Before puberty, the central nervous system (CNS) restrains the GnRH pulse generator. Undernutrition, low socioeconomic status, stress, and emotional deprivation, all delay puberty. During reproductive life, among peripheral factors that effect the reproductive system, stress plays an important role. Stress, via the release of corticotropin-releasing factor (CRF), eventually triggered by interleukin 1, inhibits GnRH release, resulting in hypogonadism. Effects of CRF are probably mediated by the opioid system. Food restriction and underweight (anorexia nervosa), obesity, smoking, and alcohol all have negative effects on the GnRH pulse generator and gonadal function. Age and diet are important determinants of fertility in both men and women. The age-associated decrease in fertility in women has as a major determinant chromosomal abnormalities of the oocyte, with uterine factors playing a subsidiary role. Age at menopause, determined by ovarian oocyte depletion, is influenced by occupation, age at menarche, parity, age at last pregnancy, altitude, smoking, and use of oral contraceptives. Smoking, however, appears to be the major determinant. Premature menopause is most frequently attributable to mosaicism for Turner Syndrome, mumps ovaritis, and, above all, total hysterectomy, which has a prevalence of about 12-15% in women 50 years old. Premature ovarian failure with presence of immature follicles is most frequently caused by autoimmune diseases or is the consequence of irradiation or chemotherapy with alkylating cytostatics. Plasma estrogens have a physiological role in the prevention of osteoporosis. Obese women have osteoporosis less frequently than women who are not overweight. Early menopause, suppression of adrenal function (corticoids), and thyroid hormone treatment all increase the frequency of osteoporosis. Aging in men is accompanied by decreased Leydig cell and Sertoli cell function, which has a predominantly primary testicular origin, although changes also occur at the hypothalamopituitary level. Plasma testosterone levels, sperm production, and sperm quality decrease, but fertility, although declining, is preserved until senescence. Stress and disease states accelerate the decline on Leydig cell function. Many occupational noxious agents have a negative effect on fertility.(ABSTRACT TRUNCATED AT 400 WORDS

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts