Brief of Amici Curiae Law and Economics Scholars in Support of Appellee and Affirmance

In reliance on Qualcomm’s FRAND promises, key SSOs incorporated its technologies into wireless standards. Qualcomm takes the position that its patented technologies are essential to those standards and, therefore, that any firm making or selling a standard-compliant product infringes its patents. As a result, the SSOs’ incorporation of Qualcomm’s patented technologies into wireless standards created a huge market for licenses to Qualcomm’s SEPs.The district court held that Qualcomm used its chipset monopolies, not only to extract the high chip-set prices to which it was entitled, but also to perpetuate those monopolies by disadvantaging rival chip-makers and raising entry barriers. As a matter of law and economics, that holding is sound. At its core, this is yet another in a long line of cases dating back to the Supreme Court’s decision in Standard Oil of New Jersey v. United States and United States v. American Telephone & Telegraph Co. in which a monopolist violates the antitrust laws by using its market power to exclude rivals and entrench its monopoly.We address Qualcomm’s exclusionary conduct in two Parts. Part I explains why Qualcomm’s no license, no chips policy is unlawful under well-established antitrust principles. Part II discusses Qualcomm’s refusal to license chip-set rivals, which reinforces the no license, no chips policy and violates the antitrust laws

Response to Wang and Luo

This article is a response to Wang and Luo

Burden of Production in Merger Cases Litigating Divestiture Fixes: Amicus Brief

In this amicus brief to the D.C. District Court judge, Amy Berman Jackson, in the U.S. v Assa Abloy, we explain the legal and policy rationales for courts to place the burden of on the merging parties to produce sufficient evidence that the divestiture will preserve competition to rebut the anticompetitive structural presumption based on the market shares of the unremedied merger that was reported to the agencies in the Hart-Scott-Rodino filing

Arctic air pollution: Challenges and opportunities for the next decade

The Arctic is a sentinel of global change. This region is influenced by multiple physical and socio-economic drivers and feedbacks, impacting both the natural and human environment. Air pollution is one such driver that impacts Arctic climate change, ecosystems and health but significant uncertainties still surround quantification of these effects. Arctic air pollution includes harmful trace gases (e.g. tropospheric ozone) and particles (e.g. black carbon, sulphate) and toxic substances (e.g. polycyclic aromatic hydrocarbons) that can be transported to the Arctic from emission sources located far outside the region, or emitted within the Arctic from activities including shipping, power production, and other industrial activities. This paper qualitatively summarizes the complex science issues motivating the creation of a new international initiative, PACES (air Pollution in the Arctic: Climate, Environment and Societies). Approaches for coordinated, international and interdisciplinary research on this topic are described with the goal to improve predictive capability via new understanding about sources, processes, feedbacks and impacts of Arctic air pollution. Overarching research actions are outlined, in which we describe our recommendations for 1) the development of trans-disciplinary approaches combining social and economic research with investigation of the chemical and physical aspects of Arctic air pollution; 2) increasing the quality and quantity of observations in the Arctic using long-term monitoring and intensive field studies, both at the surface and throughout the troposphere; and 3) developing improved predictive capability across a range of spatial and temporal scales

Gender Dimorphism of the Cardiac Dysfunction in Murine Sepsis: Signalling Mechanisms and Age-Dependency

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.JC is supported by a jointly funded PhD-studentship of the China Scholarship Council (grant number 201206240146) and Queen Mary University of London (QMUL). SMC is supported by a Research Fellowship of the German Research Foundation (Deutsche Forschungsgemeinschaft; DFG CO 912/1-1). NSAP is, in part, supported by the Bart’s and The London Charity (753/1722). This work is supported, in part, by the William Harvey Research Foundation and by a grant from the University of Turin (Ricerca Locale ex-60% 2013). This work forms part of the research themes contributing to the translational research portfolio of Barts and the London Cardiovascular Biomedical Research Unit, which is supported and funded by the National Institute of Health Research. This work also contributes to the Organ Protection research theme of the Barts Centre for Trauma Sciences, supported by the Barts and The London Charity (Award 753/1722)

Part I. SARS-CoV-2 triggered \u27PANIC\u27 attack in severe COVID-19

The coronavirus disease 2019 (COVID-19) pandemic has produced a world-wide collapse of social and economic infrastructure, as well as constrained our freedom of movement. This respiratory tract infection is nefarious in how it targets the most distal and highly vulnerable aspect of the human bronchopulmonary tree, specifically, the delicate yet irreplaceable alveoli that are responsible for the loading of oxygen upon red cell hemoglobin for use by all of the body\u27s tissues. In most symptomatic individuals, the disease is a mild immune-mediated syndrome, with limited damage to the lung tissues. About 20% of those affected experience a disease course characterized by a cataclysmic set of immune activation responses that can culminate in the diffuse and irreversible obliteration of the distal alveoli, leading to a virtual collapse of the gas-exchange apparatus. Here, in Part I of a duology on the characterization and potential treatment for COVID-19, we define severe COVID-19 as a consequence of the ability of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to trigger what we now designate for the first time as a ‘Prolific Activation of a Network-Immune-Inflammatory Crisis’, or ‘PANIC’ Attack, in the alveolar tree. In Part II we describe an immunotherapeutic hypothesis worthy of the organization of a randomized clinical trial in order to ascertain whether a repurposed, generic, inexpensive, and widely available agent is capable of abolishing ‘PANIC’; thereby preventing or mitigating severe COVID-19, with monumental ramifications for world health, and the global pandemic that continues to threaten it