Constitutional Analogies in the International Legal System

This Article explores issues at the frontier of international law and constitutional law. It considers five key structural and systemic challenges that the international legal system now faces: (1) decentralization and disaggregation; (2) normative and institutional hierarchies; (3) compliance and enforcement; (4) exit and escape; and (5) democracy and legitimacy. Each of these issues raises questions of governance, institutional design, and allocation of authority paralleling the questions that domestic legal systems have answered in constitutional terms. For each of these issues, I survey the international legal landscape and consider the salience of potential analogies to domestic constitutions, drawing upon and extending the writings of international legal scholars and international relations theorists. I also offer some preliminary thoughts about why some treaties and institutions, but not others, more readily lend themselves to analysis in constitutional terms. And I distinguish those legal and political issues that may generate useful insights for scholars studying the growing intersections of international and constitutional law from other areas that may be more resistant to constitutional analogies

Wrong Turn in Cyberspace: Using ICANN to Route Around the APA and the Constitution

The Internet relies on an underlying centralized hierarchy built into the domain name system (DNS) to control the routing for the vast majority of Internet traffic. At its heart is a single data file, known as the root. Control of the root provides singular power in cyberspace. This Article first describes how the United States government found itself in control of the root. It then describes how, in an attempt to meet concerns that the United States could so dominate an Internet chokepoint, the U. S. Department of Commerce (DoC) summoned into being the Internet Corporation for Assigned Names and Numbers (ICANN), a formally private nonprofit California corporation. DoC then signed contracts with ICANN in order to clothe it with most of the U. S. government\u27s power over the DNS, and convinced other parties to recognize ICANN\u27s authority. ICANN then took regulatory actions that the U. S. Department of Commerce was unable or unwilling to make itself, including the imposition on all registrants of Internet addresses of an idiosyncratic set of arbitration rules and procedures that benefit third-party trademark holders. Professor Froomkin then argues that the use of ICANN to regulate in the stead of an executive agency violates fundamental values and policies designed to ensure democratic control over the use of government power, and sets a precedent that risks being expanded into other regulatory activities. He argues that DoC\u27s use of ICANN to make rules either violates the APA\u27s requirement for notice and comment in rulemaking and judicial review, or it violates the Constitution\u27s nondelegation doctrine. Professor Froomkin reviews possible alternatives to ICANN, and ultimately proposes a decentralized structure in which the namespace of the DNS is spread out over a transnational group of policy partners with DoC

The sdB pulsating star V391 Peg and its putative giant planet revisited after 13 years of time-series photometric data

V391 Peg (alias HS 2201+2610) is a subdwarf B (sdB) pulsating star that shows both p- and g-modes. By studying the arrival times of the p-mode maxima and minima through the O-C method, in a previous article the presence of a planet was inferred with an orbital period of 3.2 years and a minimum mass of 3.2 MJup. Here we present an updated O-C analysis using a larger data set of 1066 h of photometric time series ( 2.5× larger in terms of the number of data points), which covers the period between 1999 and 2012 (compared with 1999-2006 of the previous analysis). Up to the end of 2008, the new O-C diagram of the main pulsation frequency (f1) is compatible with (and improves) the previous two-component solution representing the long-term variation of the pulsation period (parabolic component) and the giant planet (sine wave component). Since 2009, the O-C trend of f1 changes, and the time derivative of the pulsation period (p.) passes from positive to negative; the reason of this change of regime is not clear and could be related to nonlinear interactions between different pulsation modes. With the new data, the O-C diagram of the secondary pulsation frequency (f2) continues to show two components (parabola and sine wave), like in the previous analysis. Various solutions are proposed to fit the O-C diagrams of f1 and f2, but in all of them, the sinusoidal components of f1 and f2 differ or at least agree less well than before. The nice agreement found previously was a coincidence due to various small effects that are carefully analyzed. Now, with a larger dataset, the presence of a planet is more uncertain and would require confirmation with an independent method. The new data allow us to improve the measurement of p. for f1 and f2: using only the data up to the end of 2008, we obtain p.1 = (1.34 ± 0.04) × 10-12 and p.2 = (1.62 ± 0.22) × 10-12. The long-term variation of the two main pulsation periods (and the change of sign of p.1) is visible also in direct measurements made over several years. The absence of peaks near f1 in the Fourier transform and the secondary peak close to f2 confirm a previous identification as l = 0 and l = 1, respectively, and suggest a stellar rotation period of about 40 days. The new data allow constraining the main g-mode pulsation periods of the star

Towards Customary Legal Empowerment

Rule of Law and Development: Formation, Implementation and Improvement of Law and Governance in Developing Countrie

Writing in Britain and Ireland, c. 400 to c. 800

No abstract available

Neurocalcin Delta Suppression Protects against Spinal Muscular Atrophy in Humans and across Species by Restoring Impaired Endocytosis

This document is the Accepted Manuscript version of the following article: Riessland et al., 'Neurocalcin Delta Suppression Protects against Spinal Muscular Atrophy in Humans and across Species by Restoring Impaired Endocytosis', The American Journal of Human Genetics, Vol. 100 (2): 297-315, first published online 26 January 2017. The final, published version is available online at doi: http://dx.doi.org/10.1016/j.ajhg.2017.01.005 © 2017 American Society of Human Genetics.Homozygous SMN1 loss causes spinal muscular atrophy (SMA), the most common lethal genetic childhood motor neuron disease. SMN1 encodes SMN, a ubiquitous housekeeping protein, which makes the primarily motor neuron-specific phenotype rather unexpected. SMA-affected individuals harbor low SMN expression from one to six SMN2 copies, which is insufficient to functionally compensate for SMN1 loss. However, rarely individuals with homozygous absence of SMN1 and only three to four SMN2 copies are fully asymptomatic, suggesting protection through genetic modifier(s). Previously, we identified plastin 3 (PLS3) overexpression as an SMA protective modifier in humans and showed that SMN deficit impairs endocytosis, which is rescued by elevated PLS3 levels. Here, we identify reduction of the neuronal calcium sensor Neurocalcin delta (NCALD) as a protective SMA modifier in five asymptomatic SMN1-deleted individuals carrying only four SMN2 copies. We demonstrate that NCALD is a Ca(2+)-dependent negative regulator of endocytosis, as NCALD knockdown improves endocytosis in SMA models and ameliorates pharmacologically induced endocytosis defects in zebrafish. Importantly, NCALD knockdown effectively ameliorates SMA-associated pathological defects across species, including worm, zebrafish, and mouse. In conclusion, our study identifies a previously unknown protective SMA modifier in humans, demonstrates modifier impact in three different SMA animal models, and suggests a potential combinatorial therapeutic strategy to efficiently treat SMA. Since both protective modifiers restore endocytosis, our results confirm that endocytosis is a major cellular mechanism perturbed in SMA and emphasize the power of protective modifiers for understanding disease mechanism and developing therapies.Peer reviewedFinal Accepted Versio