Business Judgment Dismissal of Shareholder Derivative Suits by Board Litigation Committees: An Expanded Role for the Courts

This Recent Development examines the legal background of the shareholder derivative suit and the business judgment rule and then traces the evolution of the offensive use of the business judgment rule in board of director terminations of stockholder derivative actions. After examining other derivative suit dismissal decisions, the Recent Development analyzes whether Zapata adequately balances the competing interests of the shareholder and the corporate board. Finally, the Recent Development discusses the potential effect of Zapata on future litigation

Molecular Mechanisms of Stem Cells Pluripotency and Cell Fate Specification

International audienc

Orbital Dimer Model for Spin-Glass State in Y2_2Mo2_2O7_7

The formation of a spin glass usually requires both structural disorder and frustrated magnetic interactions. Consequently, the origin of spin-glass behaviour in Y$_2$Mo$_2$O$_7$ $-$ in which magnetic Mo$^{4+}$ ions occupy a frustrated pyrochlore lattice with minimal compositional disorder $-$ has been a longstanding question. Here, we use neutron and X-ray pair-distribution function (PDF) analysis to develop a disorder model that resolves apparent incompatibilities between previously-reported PDF, EXAFS and NMR studies and provides a new and physical mechanism for spin-glass formation. We show that Mo$^{4+}$ ions displace according to a local "2-in/2-out" rule on each Mo$_4$ tetrahedron, driven by orbital dimerisation of Jahn-Teller active Mo$^{4+}$ ions. Long-range orbital order is prevented by the macroscopic degeneracy of dimer coverings permitted by the pyrochlore lattice. Cooperative O$^{2-}$ displacements yield a distribution of Mo$-$O$-$Mo angles, which in turn introduces disorder into magnetic interactions. Our study demonstrates experimentally how frustration of atomic displacements can assume the role of compositional disorder in driving a spin-glass transition.Comment: 6 pages, 3 figure

LNCS

Shape analysis is a promising technique to prove program properties about recursive data structures. The challenge is to automatically determine the data-structure type, and to supply the shape analysis with the necessary information about the data structure. We present a stepwise approach to the selection of instrumentation predicates for a TVLA-based shape analysis, which takes us a step closer towards the fully automatic verification of data structures. The approach uses two techniques to guide the refinement of shape abstractions: (1) during program exploration, an explicit heap analysis collects sample instances of the heap structures, which are used to identify the data structures that are manipulated by the program; and (2) during abstraction refinement along an infeasible error path, we consider different possible heap abstractions and choose the coarsest one that eliminates the infeasible path. We have implemented this combined approach for automatic shape refinement as an extension of the software model checker BLAST. Example programs from a data-structure library that manipulate doubly-linked lists and trees were successfully verified by our tool

Reconstruction of 3D Whole-Body PET Data Using Blurred Anatomical Labels

The diagnostic utility of whole-body PET is often limited by the high level of statistical noise in the images. An improvement in image quality can be obtained by incorporating correlated anatomical information during the reconstruction of the PET data. The combined PET/CT (SMART) scanner allows the acquisition of accurately aligned PET and CT whole-body data. The authors present results of incorporating aligned anatomical information from the CT during the reconstruction of 3D whole-body PET data. They use the FORE+PWLS method for the reconstruction and a label model to incorporate anatomical information via penalty weights. Since in practice mismatches between anatomical and functional data are unavoidable, the labels are “blurred” to reflect the uncertainty associated with the anatomical information. Results show the potential advantage of incorporating anatomical information by using a blurred labels with the penalty weights.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/85864/1/Fessler153.pd

ZnT3 mRNA levels are reduced in Alzheimer's disease post-mortem brain

<p>Abstract</p> <p>Background</p> <p>ZnT3 is a membrane Zn²⁺transporter that is responsible for concentrating Zn²⁺into neuronal presynaptic vesicles. Zn²⁺homeostasis in the brain is relevant to Alzheimer's disease (AD) because Zn²⁺released during neurotransmission may bind to Aβ peptides, accelerating the assembly of Aβ into oligomers which have been shown to impair synaptic function.</p> <p>Results</p> <p>We quantified ZnT3 mRNA levels in Braak-staged human post mortem (pm) brain tissue from medial temporal gyrus, superior occipital gyrus, superior parietal gyrus, superior frontal gyrus and cerebellum from individuals with AD (n = 28), and matched controls (n = 5) using quantitative real-time PCR. ZnT3 mRNA levels were significantly decreased in all four cortical regions examined in the AD patients, to 45-60% of control levels. This reduction was already apparent at Braak stage 4 in most cortical regions examined. Quantification of neuronal and glial-specific markers in the same samples (neuron-specific enolase, NSE; and glial fibrillary acidic protein, GFAP) indicated that loss of cortical ZnT3 expression was more pronounced, and occurred prior to, significant loss of NSE expression in the tissue. Significant increases in cortical GFAP expression were apparent as the disease progressed. No gene expression changes were observed in the cerebellum, which is relatively spared of AD neuropathology.</p> <p>Conclusions</p> <p>This first study to quantify ZnT3 mRNA levels in human pm brain tissue from individuals with AD and controls has revealed a significant loss of ZnT3 expression in cortical regions, suggesting that neuronal cells in particular show reduced expression of ZnT3 mRNA in the disease. This suggests that altered neuronal Zn²⁺handling may be an early event in AD pathogenesis.</p

The quantitative verification benchmark set

We present an extensive collection of quantitative models to facilitate the development, comparison, and benchmarking of new verification algorithms and tools. All models have a formal semantics in terms of extensions of Markov chains, are provided in the Jani format, and are documented by a comprehensive set of metadata. The collection is highly diverse: it includes established probabilistic verification and planning benchmarks, industrial case studies, models of biological systems, dynamic fault trees, and Petri net examples, all originally specified in a variety of modelling languages. It archives detailed tool performance data for each model, enabling immediate comparisons between tools and among tool versions over time. The collection is easy to access via a client-side web application at qcomp.org with powerful search and visualisation features. It can be extended via a Git-based submission process, and is openly accessible according to the terms of the CC-BY license

Hearing dysfunction in heterozygous M itf Mi‐wh /+ mice, a model for W aardenburg syndrome type 2 and T ietz syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95364/1/pcmr12030.pd

Toxicity of Pb‐Contaminated Soil to Japanese Quail (\u3ci\u3eCoturnix japonica\u3c/i\u3e) and the Use of the Blood–dietary Pb Slope in Risk Assessment

This study relates tissue concentrations and toxic effects of Pb in Japanese quail (Coturnix japonica) to the dietary exposure of soil‐borne Pb associated with mining and smelting. From 0% to 12% contaminated soil, by weight, was added to 5 experimental diets (0.12 to 382mg Pb/kg, dry wt) and fed to the quail for 6 weeks. Benchmark doses associated with a 50% reduction in delta‐aminolevulinic acid dehydratase activity were 0.62mg Pb/kg in the blood, dry wt, and 27mg Pb/kg in the diet. Benchmark doses associated with a 20% increase in the concentration of erythrocyte protoporphyrin were 2.7mg Pb/kg in the blood and 152mg Pb/kg in the diet. The quail showed no other signs of toxicity (histopathological lesions, alterations in plasma–testosterone concentration, and body and organ weights). The relation of the blood Pb concentration to the soil Pb concentration was linear, with a slope of 0.013mg Pb/kg of blood (dry wt) divided by mg Pb/kg of diet. We suggest that this slope is potentially useful in ecological risk assessments on birds in the same way that the intake slope factor is an important parameter in risk assessments of children exposed to Pb. The slope may also be used in a tissue‐residue approach as an additional line of evidence in ecological risk assessment, supplementary to an estimate of hazard based on dietary toxicity reference values