No New Tax Cuts? Examining the Rescue Plan\u27s New State Tax Limits

In this article, Clarke and Fox examine the American Rescue Plan Act’s restrictions on state tax cuts, arguing that the restrictions are a variation on more familiar maintenance-of-effort provisions. These provisions are common, and are designed to help ensure that federal grants supplement rather than supplant state spending by requiring the state to maintain its level of spending on a program. Clarke and Fox conclude that the Rescue Plan’s requirements create similar incentives, and argue that the similarity makes it more likely that the act’s tax provisions are consonant with the Constitution’s spending clause

Economic Crises and the Integration of Law and Finance: The Impact of Volatility Spikes

The 2008 financial crisis raised puzzles important for understanding how the capital market prices common stocks and in turn, for the intersection between law and finance. During the crisis, there was a dramatic five-fold spike, across all industries, in “idio­syncratic risk”—the volatility of individual-firm share prices after adjustment for movements in the market as a whole. This phenomenon is not limited to the most recent financial crisis. This Article uses an empirical review to show that a dramatic spike in idiosyncratic risk has occurred with every major downturn from the 1920s through the recent financial crisis. It canvasses three possible explanations for this phenomenon. Thereafter, this Article explores the implications of these crisis-induced volatility spikes for certain legal issues that depend analytically on valuation methodology and hence are affected by volatility: using event studies to determine materiality and loss causation in fraud-on-the-market securities litigation, determining materiality in cases involving claims of both insider trading and misstatements or omissions in registered public offerings, and deter­mining the extent of deference given to a corporate board that rejects an acquisition offer at a premium above the pre-offer market price. This analysis shows that the conventional use of event studies during periods of economic-crisis-induced volatility spikes results in understating the number of occasions when a corporate misstatement can be shown to have had a meaningful impact on a firm’s stock price. Relatedly, the analysis suggests that during crisis times, insiders have substantially more opportunities to profit from trading on the nonpublic information that they possess and issuers conducting offerings have more opportunities to sell securities at an inflated price. Analysis shows that trying to cure this problem by lowering the standard of what is considered statistically significant is as likely to be socially harmful as socially beneficial. These conclusions counsel that the best response to the reduced effectiveness of private litigation as a deterrent to securities law violations during crisis times is to provide additional resources to SEC enforcement. Lastly, with respect to Delaware courts’ recognition of “substantive coercion” as a justification for target-corporation deploy­ment of takeover defenses—arguably a dubious justification in normal times—crisis-induced idiosyncratic-risk spikes provide an unusually plausible claim that target shareholders may indeed make a mistake in tendering into a hostile offer. Analysis of the timing of the spikes in recent cases, however, shows that the claim is tenuous even in these circumstances

Idiosyncratic Risk During Economic Downturns: Implications for the Use of Event Studies in Securities Litigation

We reported in a recent paper that during the 2008-09 financial crisis, for the average firm, idiosyncratic risk, as measured by variance, increased by five-fold. This finding is important for securities litigation because idiosyncratic risk plays a central role in event study methodology. Event studies are commonly used in securities litigation to determine materiality and loss causation. Many bits of news affect an issuer’s share price at the time of a corporate disclosure that is the subject of litigation. Because of this, even if an issuer’s market–adjusted price changes at the time of the disclosure, one cannot determine with certainty whether the disclosure itself had any effect on price. An event study is used to make a probabilistic assessment of whether in fact it did. Use of event studies generates a certain rate of Type I errors (disclosures that had no actual effect on price being identified as having had an effect) and a certain rate of Type II errors (disclosures that had an actual effect not being identified as such). This paper sets out a simple model of the tradeoff between these Type I and Type II errors. The model is used to establish three fundamental points. First, an economic crisis can radically worsen this tradeoff by making it much more difficult to catch a disclosure of a certain size without introducing more Type I errors. Second, during crisis periods a relaxation of this standard (and hence an increase in the acceptable rate of Type I errors) may actually decrease Type II errors by less than it would in normal times. We prove that whether the decrease is greater or smaller in crisis times depends on whether the disclosure’s actual impact on price is more or less negative than a definable crossover point. Third, whether relaxation of the standard in troubled times would increase or decrease social welfare is ambiguous. It depends on distribution of potentially actionable disclosures in terms of their actual impact on price and the social costs and social benefits of imposing liability for disclosures of each given level of actual negative impact on price

Draft Genome Sequences of Listeria monocytogenes Serotype 4b Strains 944 and 2993 and Serotype 1/2c Strains 198 and 2932

Listeria monocytogenes is a foodborne pathogen and the causative agent of listeriosis among humans and animals. The draft genome sequences of L. monocytogenes serotype 4b strains 944 and 2993 and serotype 1/2c strains 198 and 2932 are reported here

The Passing of Print

This paper argues that ephemera is a key instrument of cultural memory, marking the things intended to be forgotten. This important role means that when ephemera survives, whether accidentally or deliberately, it does so despite itself. These survivals, because they evoke all those other objects that have necessarily been forgotten, can be described as uncanny. The paper is divided into three main sections. The first situates ephemera within an uncanny economy of memory and forgetting. The second focuses on ephemera at a particular historical moment, the industrialization of print in the nineteenth century. This section considers the liminal place of newspapers and periodicals in this period, positioned as both provisional media for information as well as objects of record. The third section introduces a new configuration of technologies – scanners, computers, hard disks, monitors, the various connections between them – and considers the conditions under which born-digital ephemera can linger and return. Through this analysis, the paper concludes by considering digital technologies as an apparatus of memory, setting out what is required if we are not to be doubly haunted by the printed ephemera within the digital archive

The Assembly Factor Pet117 Couples Heme a Synthase Activity to Cytochrome Oxidase Assembly

Heme a is an essential metalloporphyrin cofactor of the mitochondrial respiratory enzyme cytochrome c oxidase (CcO). Its synthesis from heme b requires several enzymes, including the evolutionarily conserved heme a synthase (Cox15). Oligomerization of Cox15 appears to be important for the process of heme a biosynthesis and transfer to maturing CcO. However, the details of this process remain elusive, and the roles of any additional CcO assembly factors that may be involved remain unclear. Here we report the systematic analysis of one such uncharacterized assembly factor, Pet117, and demonstrate in Saccharomyces cerevisiae that this evolutionarily conserved protein is necessary for Cox15 oligomerization and function. Pet117 is shown to reside in the mitochondrial matrix, where it is associated with the inner membrane. Pet117 functions at the later maturation stages of the core CcO subunit Cox1 that precede Cox1 hemylation. Pet117 also physically interacts with Cox15 and specifically mediates the stability of Cox15 oligomeric complexes. This Cox15-Pet117 interaction observed by co-immunoprecipitation persists in the absence of heme a synthase activity, is dependent upon Cox1 synthesis and early maturation steps, and is further dependent upon the presence of the matrix-exposed, unstructured linker region of Cox15 needed for Cox15 oligomerization, suggesting that this region mediates the interaction or that the interaction is lost when Cox15 is unable to oligomerize. Based on these findings, it was concluded that Pet117 mediates coupling of heme a synthesis to the CcO assembly process in eukaryotes

Mutational spectra of aflatoxin B

Aflatoxin B₁ (AFB₁) and/or hepatitis B and C viruses are risk factors for human hepatocellular carcinoma (HCC). Available evidence supports the interpretation that formation of AFB₁-DNA adducts in hepatocytes seeds a population of mutations, mainly G:C→T:A, and viral processes synergize to accelerate tumorigenesis, perhaps via inflammation. Responding to a need for early-onset evidence predicting disease development, highly accurate duplex sequencing was used to monitor acquisition of high-resolution mutational spectra (HRMS) during the process of hepatocarcinogenesis. Four-day-old male mice were treated with AFB₁ using a regimen that induced HCC within 72 wk. For analysis, livers were separated into tumor and adjacent cellular fractions. HRMS of cells surrounding the tumors revealed predominantly G:C→T:A mutations characteristic of AFB₁ exposure. Importantly, 25% of all mutations were G→T in one trinucleotide context (CGC; the underlined G is the position of the mutation), which is also a hotspot mutation in human liver tumors whose incidence correlates with AFB₁ exposure. The technology proved sufficiently sensitive that the same distinctive spectrum was detected as early as 10 wk after dosing, well before evidence of neoplasia. Additionally, analysis of tumor tissue revealed a more complex pattern than observed in surrounding hepatocytes; tumor HRMS were a composite of the 10-wk spectrum and a more heterogeneous set of mutations that emerged during tumor outgrowth. We propose that the 10-wk HRMS reflects a short-term mutational response to AFB₁, and, as such, is an early detection metric for AFB₁-induced liver cancer in this mouse model that will be a useful tool to reconstruct the molecular etiology of human hepatocarcinogenesis.National Institutes of Health (U.S.) (Grant R01-ES016313)National Institutes of Health (U.S.) (Grant P30-ES002109)National Institutes of Health (U.S.) (Grant T32-ES007020)National Institutes of Health (U.S.) (Grant R01-CA080024

Human arachnoid granulations Part I: a technique for quantifying area and distribution on the superior surface of the cerebral cortex

<p>Abstract</p> <p>Background</p> <p>The arachnoid granulations (AGs) are herniations of the arachnoid membrane into the dural venous sinuses on the surface of the brain. Previous morphological studies of AGs have been limited in scope and only one has mentioned surface area measurements. The purpose of this study was to investigate the topographic distribution of AGs on the superior surface of the cerebral cortex.</p> <p>Methods</p> <p><it>En face </it>images were taken of the superior surface of 35 formalin-fixed human brains. AGs were manually identified using Adobe Photoshop, with a pixel location containing an AG defined as 'positive'. A set of 25 standard fiducial points was marked on each hemisphere for a total of 50 points on each image. The points were connected on each hemisphere to create a segmented image. A standard template was created for each hemisphere by calculating the average position of the 25 fiducial points from all brains. Each segmented image was mapped to the standard template using a linear transformation. A topographic distribution map was produced by calculating the proportion of AG positive images at each pixel in the standard template. The AG surface area was calculated for each hemisphere and for the total brain superior surface. To adjust for different brain sizes, the proportional involvement of AGs was calculated by dividing the AG area by the total area.</p> <p>Results</p> <p>The total brain average surface area of AGs was 78.53 ± 13.13 mm²(n = 35) and average AG proportional involvement was 57.71 × 10^-4± 7.65 × 10^-4. Regression analysis confirmed the reproducibility of AG identification between independent researchers with r²= 0.97. The surface AGs were localized in the parasagittal planes that coincide with the region of the lateral lacunae.</p> <p>Conclusion</p> <p>The data obtained on the spatial distribution and <it>en face </it>surface area of AGs will be used in an <it>in vitro </it>model of CSF outflow. With an increase in the number of samples, this analysis technique can be used to study the relationship between AG surface area and variables such as age, race and gender.</p