Overview of International Arbitration in the Intellectual Property Context

Resolving intellectual property rights (“IPR”) issues through alternative dispute resolution (“ADR”) proceedings was a technique long-developing in many major countries. Despite the earlier presence of the Arbitration Act in United States law, the subject of use of arbitration in IPR situations, especially regarding U.S. patents, remained an open and contested issue, until the original addition of 35 U.S.C. § 294 to the U.S. Patent Act in 1982. U.S. law is now resolved in the availability of IPR arbitration as an ADR tool, either through a “pre-problem” contract, such as a license, or as a “post-problem” mechanism elected and/or established by agreement. There are basics that underlie use of arbitration generally, which are also primary in IPR situations

The Curse of Copying , 7 J. Marshall Rev. Intell. Prop. L. 296 (2008)

The concept of “copying” has long been involved with various aspects of intellectual property law, particularly in regard to patents and trademarks. In the absence of legally determined exclusive rights, “copying” is permitted, and is in fact, encouraged. However, because the term “copying” carries an undercurrent of disapproval and unfavorable practices, it is a favorite of patentees looking to portray an accused infringer in the most negative light, especially before a jury. Hence, the curse of “copying.” This article will review the current state of “copying” by addressing the substantive precedent in areas where “copying” has traditionally had a substantive effect—willfulness of any accused infringing conduct and obviousness of the patented invention. With respect to “copying” and willful infringement, this article outlines two important considerations that the precedent is weak upon—“‘copying’ what?” and “‘copying’ when?” Lifting the curse requires care and some courage at trial, in view of a precedential framework that is less than favorable to the accused infringer and the pejorative impact the term “copying” will likely have on the jury and the court. These issues will be discussed and suggestions are advanced throughout as to how one might lift the curse once it is pronounced

Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization.

The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP