Labeling Fruits and Vegetables for Sale in Ohio

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Statutory Interdependence in Severability Analysis

According to conventional wisdom, when a court rules a statutory provision unconstitutional, it must sever that provision or strike down the entire statute. This understanding is incomplete. In practice, courts may engage in compound severance: invalidating additional, otherwise constitutional provisions of the statute without striking down the entire statute. They reason that the degree of interrelation between those provisions is so significant that severance of one compels severance of the other. As a result, a subset of the statute remains law. The power to craft such subsets raises constitutional concerns, and yet the jurisprudence concerning statutory interdependence is inconsistent and unclear. Courts analyze provisions for interdependence in three distinct ways: by divining congressional purpose, speculating the terms of the legislative bargain, and searching for textual evidence of congressional intent. Greater predictability in this area would alleviate constitutional concerns and better ensure democratic accountability. This Note argues for adoption of a qualified clear statement rule in which courts only find related provisions interdependent either when Congress has provided a clear statement to that effect or when allowing a related provision to have effect would result in an objectively irrational law. It then applies this rule to resolve a circuit split concerning severability of the Food and Drug Modernization Act. The qualified clear statement rule not only is consistent with the Court\u27s severability test but also would provide better guidance to courts evaluating provisions for statutory interdependence as well as limit instances of judicial overreach

Is there Really a When-Issued Premium?

We use a unique set of equities in the when-issued market to provide new tests of the law of one price in financial markets. We compare the prices of when-issued and regular-way shares of publicly-traded subsidiaries and their parents around the time the subsidiaries are fully divested. In contrast to prior analyses of when-issued trading in equity markets, we find that the when-issued shares of the subsidiary trade at a discount. Some of the pricing differences stem from measurement factors such as exchange location and bid-ask clustering that bias the observed when-issued pricing differential away from zero. The remaining difference between the when-issued and regular-way prices is due to asymmetric movements in bid and ask quotes in the two markets. We also find evidence of temporary price pressures on the date of execution of the spinoff of the subsidiary firms that bear resemblance to the pricing in the when-issued market. We interpret the evidence as consistent with the law of one price in the presence of transaction costs.Law of One Price; Market Efficiency; Market Microstructure

Activity of the Bacillus anthracis 20 kDa protective antigen component

<p>Abstract</p> <p>Background</p> <p>Anthrax is caused by <it>Bacillus anthracis </it>that produce two exotoxins, lethal toxin and edema toxin. The lethal toxin is composed of the lethal factor (LF) complexed with the cell binding protective antigen (PA₈₃, 83 kDa). Likewise, the edema factor (EF) binds to the PA₈₃to form the edema toxin. Once PA83 is bound to the host cell surface, a furin-like protease cleaves the full-length, inactive protein into 63 kDa and 20 kDa antigens (PA₆₃and PA₂₀). PA₆₃forms a heptamer and is internalized via receptor mediated endocytosis forming a protease-stable pore, which allows EF and LF to enter the cell and exert their toxic effects.</p> <p>Both proteolytically cleaved protective antigens (PA₆₃and PA₂₀fragments) are found in the blood of infected animals. The 63 kDa protective antigen PA₆₃fragment has been thoroughly studied while little is known about the PA₂₀.</p> <p>Methods</p> <p>In this study we examined the role of PA₂₀using high throughput gene expression analysis of human peripheral blood mononuclear cells (PBMC) exposed to the PA₂₀. We constructed a PA mutant in which a Factor Xa proteolytic recognition site was genetically engineered into the protective antigen PA₈₃to obtain PA₂₀using limited digestion of this recombinant PA₈₃with trypsin.</p> <p>Results</p> <p>Global gene expression response studies indicated modulation of various immune functions and showed gene patterns indicative of apoptosis via the Fas pathway in a subset of the lymphoid cells. This finding was extended to include observations of increased Caspase-3 enzymatic activity and the identification of increases in the population of apoptotic, but not necrotic cells, based on differential staining methods. We identified a list of ~40 inflammatory mediators and heat-shock proteins that were altered similarly upon exposure of PBMC to either rPA₂₀or <it>B. anthracis </it>spores/vegetative cells.</p> <p>Conclusion</p> <p>This study shows that the PA₂₀has an effect on human peripheral blood leukocytes and can induce apoptosis in the absence of other PA components.</p

Dynamical simulation via quantum machine learning with provable generalization

Much attention has been paid to dynamical simulation and quantum machine learning (QML) independently as applications for quantum advantage, while the possibility of using QML to enhance dynamical simulations has not been thoroughly investigated. Here we develop a framework for using QML methods to simulate quantum dynamics on near-term quantum hardware. We use generalization bounds, which bound the error a machine learning model makes on unseen data, to rigorously analyze the training data requirements of an algorithm within this framework. This provides a guarantee that our algorithm is resource-efficient, both in terms of qubit and data requirements. Our numerics exhibit efficient scaling with problem size, and we simulate 20 times longer than Trotterization on IBMQ-Bogota.Comment: Main text: 5 pages & 3 Figures. Supplementary Information: 12 pages & 2 Figure

Out-of-distribution generalization for learning quantum dynamics

Generalization bounds are a critical tool to assess the training data requirements of Quantum Machine Learning (QML). Recent work has established guarantees for in-distribution generalization of quantum neural networks (QNNs), where training and testing data are assumed to be drawn from the same data distribution. However, there are currently no results on out-of-distribution generalization in QML, where we require a trained model to perform well even on data drawn from a distribution different from the training distribution. In this work, we prove out-of-distribution generalization for the task of learning an unknown unitary using a QNN and for a broad class of training and testing distributions. In particular, we show that one can learn the action of a unitary on entangled states using only product state training data. We numerically illustrate this by showing that the evolution of a Heisenberg spin chain can be learned using only product training states. Since product states can be prepared using only single-qubit gates, this advances the prospects of learning quantum dynamics using near term quantum computers and quantum experiments, and further opens up new methods for both the classical and quantum compilation of quantum circuits.Comment: 7 pages (main body) + 14 pages (references and appendix); 4+1 figure

IMRT commissioning: multiple institution planning and dosimetry comparisons, a report from AAPM Task Group 119.

AAPM Task Group 119 has produced quantitative confidence limits as baseline expectation values for IMRT commissioning. A set of test cases was developed to assess the overall accuracy of planning and delivery of IMRT treatments. Each test uses contours of targets and avoidance structures drawn within rectangular phantoms. These tests were planned, delivered, measured, and analyzed by nine facilities using a variety of IMRT planning and delivery systems. Each facility had passed the Radiological Physics Center credentialing tests for IMRT. The agreement between the planned and measured doses was determined using ion chamber dosimetry in high and low dose regions, film dosimetry on coronal planes in the phantom with all fields delivered, and planar dosimetry for each field measured perpendicular to the central axis. The planar dose distributions were assessed using gamma criteria of 3%/3 mm. The mean values and standard deviations were used to develop confidence limits for the test results using the concept confidence limit = /mean/ + 1.96sigma. Other facilities can use the test protocol and results as a basis for comparison to this group. Locally derived confidence limits that substantially exceed these baseline values may indicate the need for improved IMRT commissioning

cMET inhibitor crizotinib impairs angiogenesis and reduces tumor burden in the C3(1)-Tag model of basal-like breast cancer

Epidemiologic studies have associated obesity with increased risk of the aggressive basal-like breast cancer (BBC) subtype. Hepatocyte growth factor (HGF) signaling through its receptor, cMET, is elevated in obesity and is a pro-tumorigenic pathway strongly associated with BBC. We previously reported that high fat diet (HFD) elevated HGF, cMET, and phospho-cMET in normal mammary gland, with accelerated tumor development, compared to low fat diet (LFD)-fed lean controls in a murine model of BBC. We also showed that weight loss resulted in a significant reversal of HFD-induced effects on latency and elevation of HGF/cMET signaling in normal mammary and cMET in normal mammary and tumors. Here, we sought to inhibit BBC tumor progression in LFD- and HFD-fed C3(1)-Tag BBC mice using a small molecule cMET inhibitor, and began crizotinib treatment (50mg/kg body weight by oral gavage) upon identification of the first palpable tumor. We next investigated if administering crizotinib in a window prior to tumor development would inhibit or delay BBC tumorigenesis. Treatment: Crizotinib significantly reduced mean tumor burden by 27.96 and 37.29%, and mean tumor vascularity by 35.04 and 33.52%, in our LFD- and HFD-fed C3(1)-Tag BBC mice, respectively. Prevention: Crizotinib significantly accelerated primary tumor progression in both diet groups but had no effect on total tumor progression or total tumor burden. In sum, cMET inhibition by crizotinib limited tumor development and microvascular density in basal-like tumor-bearing mice but did not appear to be an effective preventive agent for BBC.Electronic supplementary materialThe online version of this article (doi:10.1186/s40064-016-1920-3) contains supplementary material, which is available to authorized users

Delayed Toxicity Associated with Soluble Anthrax Toxin Receptor Decoy-Ig Fusion Protein Treatment

Soluble receptor decoy inhibitors, including receptor-immunogloubulin (Ig) fusion proteins, have shown promise as candidate anthrax toxin therapeutics. These agents act by binding to the receptor-interaction site on the protective antigen (PA) toxin subunit, thereby blocking toxin binding to cell surface receptors. Here we have made the surprising observation that co-administration of receptor decoy-Ig fusion proteins significantly delayed, but did not protect, rats challenged with anthrax lethal toxin. The delayed toxicity was associated with the in vivo assembly of a long-lived complex comprised of anthrax lethal toxin and the receptor decoy-Ig inhibitor. Intoxication in this system presumably results from the slow dissociation of the toxin complex from the inhibitor following their prolonged circulation. We conclude that while receptor decoy-Ig proteins represent promising candidates for the early treatment of B. anthracis infection, they may not be suitable for therapeutic use at later stages when fatal levels of toxin have already accumulated in the bloodstream