Investor Information, Long-Run Risk, and the Term Structure of Equity

We study the role of information in asset pricing models with long-run cash flow risk. When investors can distinguish short- from long-run consumption risks (full information), the model generates a sizable equity risk premium only if the equity term structure slopes up, contrary to the data. In general, the short- and long-run components are unidentified. We propose a sparsity-based bounded rationality model of long-run risk that is both parsimonious and fully identified from historical data. In contrast to full information, the model generates a sizable market risk premium simultaneously with a downward sloping equity term structure, as in the data.

An easy and convenient method for maintenance of embryogenic cultures of Vitis vinifera

Research Note

MicroRNAs in human cancer: from research to therapy

Numerous miRNAs are deregulated in human cancers, and experimental evidence indicates that they can play roles as oncogenes or tumor suppressor genes. Similarly to cancer genes that encode proteins, deregulation of miRNA-encoding genes is associated with genetic or epigenetic alterations, such as deletions, amplifications, point mutations and aberrant DNA methylation. The discovery that miRNAs interact with known oncogenes has established further links with molecular pathways implicated in malignant transformation. Finally, miRNAs can be used as diagnostic markers, and their potential as therapeutic molecules has moved miRNAs from the area of basic research to the field of cancer biotechnology

Investor Information, Long-Run Risk, and the Duration of Risky Cash Flows

We study the role of information in asset pricing models with long-run cash ow risk. To illustrate the importance of the information structure, we show how the implications of the long run risk paradigm for the cross-sectional properties of stock returns and cash flow duration are affected by information. When investors can fully distinguish short and long-run consumption risk components of dividend growth innovations (full information), only exposure to long-run consumption risk generates significant risk premia, implying that high return value stocks are long-duration assets, contrary to the historical data. By contrast,when investors observe the change in consumption and dividends each period but not the individual components of that change (limited information), exposure to short-run risk can generate large risk premia, so that high-return value stocks are short-duration assets while low-return growth stocks are long-duration assets, as in the data. We also show that, in order to explain empirical finding that long-horizon equity is less risky than short-horizon equity, the properties of the cash ow model and the values of primitive preference parameters must be quite different from those emphasized in the existing long-run risk literature

Surface roughness effect on ultracold neutron interaction with a wall and implications for computer simulations

We review the diffuse scattering and the loss coefficient in ultracold neutron reflection from slightly rough surfaces, report a surprising reduction in loss coefficient due to roughness, and discuss the possibility of transition from quantum treatment to ray optics. The results are used in a computer simulation of neutron storage in a recent neutron lifetime experiment that re-ported a large discrepancy of neutron lifetime with the current particle data value. Our partial re-analysis suggests the possibility of systematic effects that were not included in this publication.Comment: 39 pages, 9 figures; additional calculations include

Transcribed ultraconserved noncoding RNAs (T-UCR) are involved in Barrett's esophagus carcinogenesis.

Barretts esophagus (BE) involves a metaplastic replacement of native esophageal squamous epithelium (Sq) by columnar-intestinalized mucosa, and it is the main risk factor for Barrett-related adenocarcinoma (BAc). Ultra-conserved regions (UCRs) are a class non-coding sequences that are conserved in humans, mice and rats. More than 90% of UCRs are transcribed (T-UCRs) in normal tissues, and are altered at transcriptional level in tumorigenesis. To identify the T-UCR profiles that are dysregulated in Barretts mucosa transformation, microarray analysis was performed on a discovery set of 51 macro-dissected samples obtained from 14 long-segment BE patients. Results were validated in an independent series of esophageal biopsy/surgery specimens and in two murine models of Barretts esophagus (i.e. esophagogastric-duodenal anastomosis). Progression from normal to BE to adenocarcinoma was each associated with specific and mutually exclusive T-UCR signatures that included up-regulation of uc.58-, uc.202-, uc.207-, and uc.223- and down-regulation of uc.214+. A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-). Analogous BE-specific T-UCR profiles were shared by human and murine lesions. This study is the first demonstration of a role for T-UCRs in the transformation of Barretts mucosa