Commentary: Where Is the Economic Analysis of Payment Law?

Modem payment law began precisely a quarter of a millennium ago, when Lord Mansfield decided Miller v. Race. After 250 years, we know little more than Mansfield, even with the analytic power of modern neoclassical microeconomics. Many of the simplest questions have no easy answer: What is a payment? (The U.C.C. has no definition.) What is payment finality, and why is it important? (There is no consensus, especially because payment finality was law long before bankers discovered its connection to systemic risk.) What is the normative rationale of the clearing and settlement rules in the U.C.C.? (Again, no consensus, and not even much commentary.) What is the proper scope of payment law? (Explain why U.C.C. Article 5 is in most payment casebooks, and the law of suretyship is not.) Neoclassical microeconomics has been a general success in business law: a facile framework for difficult legal problems. But it has not worked in payment law, with a few exceptions such as the allocation of risk for fraud and mistake. Is there a reason for this? Read this commentary to find out

Commentary: Where Is the Economic Analysis of Payment Law?

Modem payment law began precisely a quarter of a millennium ago, when Lord Mansfield decided Miller v. Race. After 250 years, we know little more than Mansfield, even with the analytic power of modern neoclassical microeconomics. Many of the simplest questions have no easy answer: What is a payment? (The U.C.C. has no definition.) What is payment finality, and why is it important? (There is no consensus, especially because payment finality was law long before bankers discovered its connection to systemic risk.) What is the normative rationale of the clearing and settlement rules in the U.C.C.? (Again, no consensus, and not even much commentary.) What is the proper scope of payment law? (Explain why U.C.C. Article 5 is in most payment casebooks, and the law of suretyship is not.) Neoclassical microeconomics has been a general success in business law: a facile framework for difficult legal problems. But it has not worked in payment law, with a few exceptions such as the allocation of risk for fraud and mistake. Is there a reason for this? Read this commentary to find out

Beam Element Structural Dynamics Modification Using Experimental Modal Rotational Data

Structural dynamic modification (SDM) of a fixed-free (cantilever) beam to convert it into a fixed-fixed beam with experimental modal data is presented. The SDM focuses on incorporating experimental rotational degrees-of-freedom (DOF) measured with a novel laser measurement technique. A cantilever beam is tested to develop the experimental modal database including rotational degrees of freedom. A modal database from a finite-element model also is developed for comparison. A structural dynamic modification, with both databases, is performed using a Bernoulli-Euler beam to ground the free end of the cantilever beam. The hardware is then modified and a second experimental modal analysis of the resulting fixed-fixed beam performed. A finite-element model of the fixed-fixed beam also was created. Comparison of results from these four tests are used to assess the effectiveness of SDM using experimental modal rotational data. The evaluation shows that provided high quality experimental rotational modal data can be acquired, SDM work with beam elements can be effective in yielding accurate results

Anomalous Workfunction Anisotropy in Ternary Acetylides

Anomalous anisotropy of workfunction values in ternary alkali metal transition metal acetylides is reported. Workfunction values of some characteristic surfaces in these emerging semiconducting materials may differ by more than $\approx$ 2 eV as predicted by Density Functional Theory calculations. This large anisotropy is a consequence of the relative orientation of rod-like [MC$_{2}$]$_{\infty}$ negatively charged polymeric subunits and the surfaces, with M being a transition metal or metalloid element and C$_{2}$ refers to the acetylide ion C$_{2}^{2-}$, with the rods embedded into an alkali cation matrix. It is shown that the conversion of the seasoned Cs$_{2}$Te photo-emissive material to ternary acetylide Cs$_{2}$TeC$_{2}$ results in substantial reduction of its $\approx$ 3 eV workfunction down to 1.71-2.44 eV on the Cs$_{2}$TeC$_{2}$(010) surface while its high quantum yield is preserved. Similar low workfunction values are predicted for other ternary acetylides as well, allowing for a broad range of applications from improved electron- and light-sources to solar cells, field emission displays, detectors and scanners.Comment: Accepted for publication in Phys. Rev.

The Neuronal EGF-Related Gene Nell2 Interacts with Macf1 and Supports Survival of Retinal Ganglion Cells after Optic Nerve Injury

Nell2 is a neuron-specific protein containing six epidermal growth factor-like domains. We have identified Nell2 as a retinal ganglion cell (RGC)-expressed gene by comparing mRNA profiles of control and RGC-deficient rat retinas. The aim of this study was to analyze Nell2 expression in wild-type and optic nerve axotomized retinas and evaluate its potential role in RGCs. Nell2-positive in situ and immunohistochemical signals were localized to irregularly shaped cells in the ganglion cell layer (GCL) and colocalized with retrogradely-labeled RGCs. No Nell2-positive cells were detected in 2 weeks optic nerve transected (ONT) retinas characterized with approximately 90% RGC loss. RT-PCR analysis showed a dramatic decrease in the Nell2 mRNA level after ONT compared to the controls. Immunoblot analysis of the Nell2 expression in the retina revealed the presence of two proteins with approximate MW of 140 and 90 kDa representing glycosylated and non-glycosylated Nell2, respectively. Both products were almost undetectable in retinal protein extracts two weeks after ONT. Proteome analysis of Nell2-interacting proteins carried out with MALDI-TOF MS (MS) identified microtubule-actin crosslinking factor 1 (Macf1), known to be critical in CNS development. Strong Macf1 expression was observed in the inner plexiform layer and GCL where it was colocalizied with Thy-1 staining. Since Nell2 has been reported to increase neuronal survival of the hippocampus and cerebral cortex, we evaluated the effect of Nell2 overexpression on RGC survival. RGCs in the nasal retina were consistently more efficiently transfected than in other areas (49% vs. 13%; n = 5, p<0.05). In non-transfected or pEGFP-transfected ONT retinas, the loss of RGCs was approximately 90% compared to the untreated control. In the nasal region, Nell2 transfection led to the preservation of approximately 58% more cells damaged by axotomy compared to non-transfected (n = 5, p<0.01) or pEGFP-transfected controls (n = 5, p<0.01)

Recurrent Chromosomal Copy Number Alterations in Sporadic Chordomas

The molecular events in chordoma pathogenesis have not been fully delineated, particularly with respect to copy number changes. Understanding copy number alterations in chordoma may reveal critical disease mechanisms that could be exploited for tumor classification and therapy. We report the copy number analysis of 21 sporadic chordomas using array comparative genomic hybridization (CGH). Recurrent copy changes were further evaluated with immunohistochemistry, methylation specific PCR, and quantitative real-time PCR. Similar to previous findings, large copy number losses, involving chromosomes 1p, 3, 4, 9, 10, 13, 14, and 18, were more common than copy number gains. Loss of CDKN2A with or without loss of CDKN2B on 9p21.3 was observed in 16/20 (80%) unique cases of which six (30%) showed homozygous deletions ranging from 76 kilobases to 4.7 megabases. One copy loss of the 10q23.31 region which encodes PTEN was found in 16/20 (80%) cases. Loss of CDKN2A and PTEN expression in the majority of cases was not attributed to promoter methylation. Our sporadic chordoma cases did not show hotspot point mutations in some common cancer gene targets. Moreover, most of these sporadic tumors are not associated with T (brachyury) duplication or amplification. Deficiency of CDKN2A and PTEN expression, although shared across many other different types of tumors, likely represents a key aspect of chordoma pathogenesis. Sporadic chordomas may rely on mechanisms other than copy number gain if they indeed exploit T/ brachyury for proliferation

The Relationship of DNA Methylation with Age, Gender and Genotype in Twins and Healthy Controls

Cytosine-5 methylation within CpG dinucleotides is a potentially important mechanism of epigenetic influence on human traits and disease. In addition to influences of age and gender, genetic control of DNA methylation levels has recently been described. We used whole blood genomic DNA in a twin set (23 MZ twin-pairs and 23 DZ twin-pairs, N = 92) as well as healthy controls (N = 96) to investigate heritability and relationship with age and gender of selected DNA methylation profiles using readily commercially available GoldenGate bead array technology. Despite the inability to detect meaningful methylation differences in the majority of CpG loci due to tissue type and locus selection issues, we found replicable significant associations of DNA methylation with age and gender. We identified associations of genetically heritable single nucleotide polymorphisms with large differences in DNA methylation levels near the polymorphism (cis effects) as well as associations with much smaller differences in DNA methylation levels elsewhere in the human genome (trans effects). Our results demonstrate the feasibility of array-based approaches in studies of DNA methylation and highlight the vast differences between individual loci. The identification of CpG loci of which DNA methylation levels are under genetic control or are related to age or gender will facilitate further studies into the role of DNA methylation and disease