William Howard Taft, the Origin of the Rule of Reason, and the Actavis Challenge

The origin of the Rule of Reason can be traced to the notable decision of United States v. Addyston Pipe & Steel Co. (1898), which was written by William Howard Taft during his tenure on the Sixth Circuit Court of Appeals. There, Judge Taft distinguished between restraints that were mainly or entirely designed to restrain trade and those that are ancillary to a procompetitive main purpose. That fundamental distinction, drawn at the dawn of Sherman Act jurisprudence, forms the basis of the Rule of Reason that currently informs antitrust case law. This Article describes the context in which the Rule of Reason was debated and defended both in public discourse by President and Professor Taft and in the landmark Supreme Court decisions of Standard Oil Co. of New Jersey v. United States (1911) and United States v. American Tobacco Co.(1911). This Article then follows the development of the Rule of Reason through Board of Trade of City of Chicago v. United States (1918) to the modern era of antitrust jurisprudence. Finally, this Article describes the application of the Rule of Reason to reverse-payment settlements in the pharmaceutical sector, one of the most challenging contemporary antitrust issues. It does so through a discussion of the Supreme Court case FTC v. Actavis (2013) and the Third Circuit’s application of Actavis in In re Wellbutrin Xl Antitrust Litig. Indirect Purchaser Class (2017). This Article provided the foundation for, and introduction to, the remarks of Professor Michael A. Carrier and Mr. Saul Morgenstern that were delivered at the New York State Bar Association Antitrust Law Section’s William Howard Taft Lecture on September 28, 2017. Those remarks are reprinted in article form in this volume of the Columbia Business Law Review

Amex in Context: Tracing the Application of the Rule of Reason to Vertical Restraints

In his 1911 State of the Union address, President William Howard Taft, the former and future jurist, discussed the development of antitrust law since the Sherman Act’s passage: “Slowly the mills of the courts ground, and only gradually did the majesty of the law assert itself.” While Taft allowed for the possibility that some changes to the law may be beneficial, he also argued that the “object” of the Act was “near achievement,” and spoke against those calling to “abandon this work of twenty years and try another experiment[.]” Ultimately, the experiment was not abandoned, and the Sherman Act remains at the center of antitrust law in the United States. Meanwhile, the “mills of the courts” have continued to grind away. Various judges, justices—including the eventual Chief Justice Taft himself—and scholars have shaped the contours of antitrust law. One area of ongoing development is the organic rule of reason, which Taft played no small role in originating. The rule of reason was first articulated in United States v. Addyston Pipe & Steel Co.5 in 1898 and played an important role, not long after, in the titanic cases of Standard Oil of New Jersey v. United States6 and United States v. American Tobacco Co. During Taft’s presidency, however, the Supreme Court held that vertically imposed price restraints were per se illegal, and, over the decades that followed, the rule of reason began to wither and was gradually replaced, in significant part, by a series of per se rules

Assessing Qualitative Justifications Under Taft's Rule of Reason

In his landmark opinion in United States v. Addyston Pipe & Steel Co.,1 then-Judge William Howard Taft focused on the question of whether the restraint of trade there at issue was the primary motivation for the agreement or “merely ancillary to the main purpose of a lawful contract.”2 The doctrine of naked and ancillary restraints that Taft developed in Addyston Pipe marked the origins of the per se rule and rule of reason, which together form the fundamental framework that governs the Sherman Act today. In Taft’s presentation, restraints of trade must be understood in the context of their relationship to the purpose of the primary agreement. Where that purpose is legitimate and the relationship of the restraint is ancillary, courts should be hesitant to invalidate the restraint

Time for a New Sherman Act? The Debate on Antitrust Reform in Historical Perspective

The Sherman Antitrust Act (“Sherman Act” or “Act”), the Federal Trade Commission Act of 1914, and the Clayton Antitrust Act represent the core antitrust statutes. While these core statutes have remained largely the same, antitrust law has undergone sea changes since the late nineteenth and early twentieth centuries. To place the contemporary debate in historical context, this Introduction traces the trajectory of the Sherman Act and its diverging interpretations from the Act’s inception to date. This Introduction discusses the state of antitrust law during the early years of the twentieth-century, which featured the judicial development of the rule of reason. It also address the Progressive Era amendments to the antitrust laws, which reflected that era’s increased confidence in the efficacy of governmental and regulatory intervention as reflected in the amendments to the Clayton and FTC Acts. The Introduction then focuses on the state of antitrust law during the middle years of the twentieth century, sometimes characterized as operating according to a “big is bad” principle. It then turns to the modern era and discusses the last great revolution in antitrust thought: the arrival of the consumer welfare standard, which directs courts and practitioners to view antitrust law through the prism of how a given practice affects the consumer. This standard often, though not exclusively, focuses on a practice’s impact on prices and output. The Introduction discusses what may be the next revolution in antitrust thought, which some characterize as “the New Brandeis Movement.” It largely addresses the impact of increased concentration on economic as well as social and political issues. Finally, the Introduction concludes by discussing the various legislative proposals, from both Democrats and Republicans, to reform antitrust law, either through modest alterations or thorough overhauls

IL-21 receptor expression in human tendinopathy

The pathogenetic mechanisms underlying tendinopathy remain unclear, with much debate as to whether inflammation or degradation has the prominent role. Increasing evidence points toward and early inflammatory infiltrate and associated inflammatory cytokine production in human and animal models of tendon disease. The IL-21/IL-21R axis is a proinflammatory cytokine complex that has been associated with chronic inflammatory diseases including rheumatoid arthritis and inflammatory bowel disease. This project aimed to investigate the role and expression of the cytokine/receptor pair IL-21/IL-21R in human tendinopathy. We found significantly elevated expression of IL-21 receptor message and protein in human tendon samples but found no convincing evidence of the presence of IL-21 at message or protein level. The level of expression of IL-21R message/protein in human tenocytes was significantly up regulated by proinflammatory cytokines (TNFα/IL-1β) in vitro. These findings demonstrate that IL-21R is present in early human tendinopathy mainly expressed by tenocytes and macrophages. Despite a lack of IL-21 expression these data again suggest that early tendinopathy has an inflammatory/cytokine phenotype, which may provide novel translational targets in the treatment of tendinopathy

Genome evolution in the genus Sorghum (Poaceae)

BACKGROUND AND AIMS: The roles of variation in DNA content in plant evolution and adaptation remain a major biological enigma. Chromosome number and 2C DNA content were determined for 21 of the 25 species of the genus Sorghum and analysed from a phylogenetic perspective. METHODS: DNA content was determined by flow cytometry. A Sorghum phylogeny was constructed based on combined nuclear ITS and chloroplast ndhF DNA sequences. KEY RESULTS: Chromosome counts (2n = 10, 20, 30, 40) were, with few exceptions, concordant with published numbers. New chromosome numbers were obtained for S. amplum (2n = 30) and S. leiocladum (2n = 10). 2C DNA content varies 8.1-fold (1.27-10.30 pg) among the 21 Sorghum species. 2C DNA content varies 3.6-fold from 1.27 pg to 4.60 pg among the 2n = 10 species and 5.8-fold (1.52-8.79 pg) among the 2n = 20 species. The x = 5 genome size varies over an 8.8-fold range from 0.26 pg to 2.30 pg. The mean 2C DNA content of perennial species (6.20 pg) is significantly greater than the mean (2.92 pg) of the annuals. Among the 21 species studied, the mean x = 5 genome size of annuals (1.15 pg) and of perennials (1.29 pg) is not significantly different. Statistical analysis of Australian species showed: (a) mean 2C DNA content of annual (2.89 pg) and perennial (7.73 pg) species is significantly different; (b) mean x = 5 genome size of perennials (1.66 pg) is significantly greater than that of the annuals (1.09 pg); (c) the mean maximum latitude at which perennial species grow (-25.4 degrees) is significantly greater than the mean maximum latitude (-17.6) at which annual species grow. CONCLUSIONS: The DNA sequence phylogeny splits Sorghum into two lineages, one comprising the 2n = 10 species with large genomes and their polyploid relatives, and the other with the 2n = 20, 40 species with relatively small genomes. An apparent phylogenetic reduction in genome size has occurred in the 2n = 10 lineage. Genome size evolution in the genus Sorghum apparently did not involve a 'one way ticket to genomic obesity' as has been proposed for the grasses

Comparison of baricitinib, upadacitinib, and tofacitinib mediated regulation of cytokine signaling in human leukocyte subpopulations

BACKGROUND: The in vitro pharmacology of baricitinib, upadacitinib, and tofacitinib was evaluated to understand differences among these JAK inhibitors (JAKis) at the cellular level. METHODS: Peripheral blood mononuclear cells from healthy donors were incubated with different JAKis, levels of phosphorylated signal transducer and activator of transcription (pSTAT) were measured following cytokine stimulation, and half maximum inhibitory concentration (IC50) values were calculated in phenotypically gated leukocyte subpopulations. Therapeutic dose relevance of the in vitro analysis was assessed using calculated mean concentration-time profiles over 24 h obtained from JAKi-treated subjects. Time above IC50 and average daily percent inhibition of pSTAT formation were calculated for each JAKi, cytokine, and cell type. RESULTS: Distinct JAKis displayed different in vitro pharmacologic profiles. For example, tofacitinib and upadacitinib were the most potent inhibitors of the JAK1/3-dependent cytokines tested (interleukin [IL]-2, IL-4, IL-15, and IL-21) with lower IC50 values and increased time above IC50 translating to a greater overall inhibition of STAT signaling during the dosing interval. All JAKis tested inhibited JAK1/2-dependent cytokines (e.g., IL-6 and interferon [IFN]-γ), the JAK1/tyrosine kinase 2 (TYK2)-dependent cytokines IL-10 and IFN-α, the JAK2/2-dependent cytokines IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), and the JAK2/TYK2-dependent cytokine granulocyte colony-stimulating factor (G-CSF), but often to significantly differing degrees. CONCLUSIONS: Different JAKis modulated distinct cytokine pathways to varying degrees, and no agent potently or continuously inhibited an individual cytokine signaling pathway throughout the dosing interval. Notably, baricitinib inhibited JAK1/3 signaling to a lesser extent than upadacitinib and tofacitinib, while upadacitinib, baricitinib, and tofacitinib inhibited the signaling of JAK2/2-dependent cytokines, including GM-CSF and IL-3, as well as the signaling of the JAK2/TYK2-dependent cytokine G-CSF