Negligence at the Breach: Information Fiduciaries and the Duty to Care for Data

Personal data is a cost of admission for much of modern life. Employers, tech companies, advertisers, information brokers, and others collect huge quantities of data about us all. Yet outside of a few highly-regulated industries, American companies face few legal restrictions on how they manage and use that data. Until now, individuals have had very limited remedies when their data is stolen from data collectors. But change is afoot. In a significant recent decision, the Pennsylvania Supreme Court took a consequential step holding that entities collecting personal data owe a duty of reasonable care to protect data subjects against harm. This tort decision left a critical question unresolved. What is “harm” in the context of privacy? What is it exactly that data collectors must protect data subjects against? This Article takes one state’s doctrinal move as a jumping-off point to consider a question of immense national importance—how to apply common law negligence principles in cases involving the disclosure and misuse of personal data, and specifically, what a “duty to care” means in the unsettled realm of privacy law. Building off Jack Balkin’s work, this Article proposes that fiduciary law offers an appealing framework for conceptualizing privacy harms and the corresponding responsibilities of the entities who are collecting our data. In doing so, it begins the conversation of how tort law can take a central place in protecting individuals when data holders betray their trust

Weak ferromagnetism of quasi-one-dimensional S=1/2 antiferromagnet BaCu2_2Ge2_2O7_7

Weak ferromagnetism of quasi-one-dimensional S = 1/2 antiferromagnet BaCu$_2$Ge$_2$O$_7$ is studied by the magnetization measurement. The spontaneous magnetization appears along the b axis. The local symmetry between the in-chain nearest neighbor spins allows the presence of Dzyaloshinskii-Moriya interaction, and the only possible spatial configuration of the weak ferromagnetic moment per spin determines the sign of the inter-chain interaction. A weak $a$-axis magnetic field can change the direction of the magnetization to the $a$-axis direction, which shows that the spin chain forms a weakly coupled weak-ferromagnetic chain system.Comment: 10 pages, 4 figure

Chiral Heterocyclic Ligands. XI. Self-assembly and X-Ray Crystal Structures of Chiral Silver Coordination Polymers of (S)-(-)-Nicotine

Three chiral coordination polymers have been prepared by reaction of (S)-(-)-nicotine with silver(I) salts. X-Ray crystal structure determinations revealed that these all contain polymer chains in which the nicotine molecule acts as a bridging ligand between four-coordinate silver atoms. In one case additional bridging by nitrate anions leads to a three-dimensional network structure

Integrated Expression Profiling and ChIP-seq Analyses of the Growth Inhibition Response Program of the Androgen Receptor

Background: The androgen receptor (AR) plays important roles in the development of male phenotype and in different human diseases including prostate cancers. The AR can act either as a promoter or a tumor suppressor depending on cell types. The AR proliferative response program has been well studied, but its prohibitive response program has not yet been thoroughly studied. Methodology/Principal Findings: Previous studies found that PC3 cells expressing the wild-type AR inhibit growth and suppress invasion. We applied expression profiling to identify the response program of PC3 cells expressing the AR (PC3-AR) under different growth conditions (i.e. with or without androgens and at different concentration of androgens) and then applied the newly developed ChIP-seq technology to identify the AR binding regions in the PC3 cancer genome. A surprising finding was that the comparison of MOCK-transfected PC3 cells with AR-transfected cells identified 3,452 differentially expressed genes (two fold cutoff) even without the addition of androgens (i.e. in ethanol control), suggesting that a ligand independent activation or extremely low-level androgen activation of the AR. ChIP-Seq analysis revealed 6,629 AR binding regions in the cancer genome of PC3 cells with an FDR (false discovery rate) cut off of 0.05. About 22.4 % (638 o