Multiple Transactions Model: A Panel Data Approach to Estimate Housing Market Indices

In this paper, a multiple transactions model with a panel data approach is used to estimate housing market indices. The multiple transactions model keeps the same features of the repeat transactions index model (i.e., tracking the price appreciation of same houses). However, the multiple transactions model overcomes the shortcomings of the repeat transactions model by avoiding the correlated error terms. The indicative empirical analysis on a small sample of actual house transaction data demonstrates that the proposed multiple transactions model is superior to the repeat transactions model in terms of index variance, robustness of estimate, index revision volatility, and out-of-sample prediction of individual house prices.

Determining the squark mass at the LHC

We propose a new way to determine the squark mass based on the shape of di-jet invariant mass distribution of supersymmetry (SUSY) di-jet events at the Large Hadron Collider (LHC). Our algorithm, which is based on event kinematics, requires that the branching ratio $B(\tilde{q} \rightarrow q \tilde{z}_1)$ is substantial for at least some types of squarks, and that $m_{\tilde{z}_1}^2/m_{\tilde{q}}^2 \ll 1$. We select di-jet events with no isolated leptons, and impose cuts on the total jet transverse energy, $E_T^{tot}=E_T(j_1)+E_T(j_2)$, on $\alpha = E_T(j_2)/m_{jj}$, and on the azimuthal angle between the two jets to reduce SM backgrounds. The shape of the resulting di-jet mass distribution depends sensitively on the squark mass, especially if the integrated luminosity is sufficient to allow a hard enough cut on $E_T^{tot}$ and yet leave a large enough signal to obtain the $m_{jj}$ distribution. We simulate the signal and Standard Model (SM) backgrounds for 100 fb$^{-1}$ integrated luminosity at 14 TeV requiring $E_T^{tot}> 700$ GeV. We show that it should be possible to extract $m_{\tilde{q}}$ to within about 3% at 95% CL --- similar to the precision obtained using $m_{T2}$ --- from the di-jet mass distribution if $m_{\tilde{q}} \sim 650$ GeV, or to within $\sim 5$% if $m_{\tilde{q}}\sim 1$ TeV.Comment: 20 pages, 9 figures. Footnote added, updated reference

High-precision optical-frequency dissemination on branching optical-fiber networks

We present a technique for the simultaneous dissemination of high-precision optical-frequency signals to multiple independent remote sites on a branching optical-fiber network. The technique corrects optical-fiber length fluctuations at the output of the link, rather than at the input as is conventional. As the transmitted optical signal remains unaltered until it reaches the remote site, it can be transmitted simultaneously to multiple remote sites on an arbitrarily complex branching network. This technique maintains the same servo-loop bandwidth limit as in conventional techniques and is compatible with active telecommunication links.Sascha W. Schediwy, David Gozzard, Kenneth G. H. Baldwin, Brian J. Orr, R. Bruce Warrington, Guido Aben and Andre N. Luite

Modeling the Dust Properties of z ~ 6 Quasars with ART^2 -- All-wavelength Radiative Transfer with Adaptive Refinement Tree

The detection of large quantities of dust in z ~ 6 quasars by infrared and radio surveys presents puzzles for the formation and evolution of dust in these early systems. Previously (Li et al. 2007), we showed that luminous quasars at z > 6 can form through hierarchical mergers of gas-rich galaxies. Here, we calculate the dust properties of simulated quasars and their progenitors using a three-dimensional Monte Carlo radiative transfer code, ART^2 -- All-wavelength Radiative Transfer with Adaptive Refinement Tree. ART^2 incorporates a radiative equilibrium algorithm for dust emission, an adaptive grid for inhomogeneous density, a multiphase model for the ISM, and a supernova-origin dust model. We reproduce the SED and dust properties of SDSS J1148+5251, and find that the infrared emission are closely associated with the formation and evolution of the quasar host. The system evolves from a cold to a warm ULIRG owing to heating and feedback from stars and AGN. Furthermore, the AGN has significant implications for the interpretation of observation of the hosts. Our results suggest that vigorous star formation in merging progenitors is necessary to reproduce the observed dust properties of z~6 quasars, supporting a merger-driven origin for luminous quasars at high redshifts and the starburst-to-quasar evolutionary hypothesis. (Abridged)Comment: 26 pages, 22 figures, accepted by ApJ. Version with full resolution images is available at http://www.cfa.harvard.edu/~yxli/ARTDUST/astroph0706.3706.pd

Identification of chemokine receptors as potential modulators of endocrine resistance in oestrogen receptor–positive breast cancers

Introduction Endocrine therapies target oestrogenic stimulation of breast cancer (BC) growth, but resistance remains problematic. Our aims in this study were (1) to identify genes most strongly associated with resistance to endocrine therapy by intersecting global gene transcription data from patients treated presurgically with the aromatase inhibitor anastrazole with those from MCF7 cells adapted to long-term oestrogen deprivation (LTED) (2) to assess the clinical value of selected genes in public clinical data sets and (3) to determine the impact of targeting these genes with novel agents. Methods Gene expression and Ki67 data were available from 69 postmenopausal women with oestrogen receptor–positive (ER+) early BC, at baseline and 2 weeks after anastrazole treatment, and from cell lines adapted to LTED. The functional consequences of target genes on proliferation, ER-mediated transcription and downstream cell signalling were assessed. Results By intersecting genes predictive of a poor change in Ki67 with those upregulated in LTED cells, we identified 32 genes strongly correlated with poor antiproliferative response that were associated with inflammation and/or immunity. In a panel of LTED cell lines, C-X-C chemokine receptor type 7 (CXCR7) and CXCR4 were upregulated compared to their wild types (wt), and CXCR7, but not CXCR4, was associated with reduced relapse-free survival in patients with ER+ BC. The CXCR4 small interfering RNA variant (siCXCR4) had no specific effect on the proliferation of wt-SUM44, wt-MCF7 and their LTED derivatives. In contrast, siCXCR7, as well as CCX733, a CXCR7 antagonist, specifically suppressed the proliferation of MCF7-LTED cells. siCXCR7 suppressed proteins associated with G1/S transition and inhibited ER transactivation in MCF7-LTED, but not wt-MCF7, by impeding association between ER and proline-, glutamic acid– and leucine-rich protein 1, an ER coactivator. Conclusions These data highlight CXCR7 as a potential therapeutic target warranting clinical investigation in endocrine-resistant BC

Heterotic Model Building: 16 Special Manifolds

We study heterotic model building on 16 specific Calabi-Yau manifolds constructed as hypersurfaces in toric four-folds. These 16 manifolds are the only ones among the more than half a billion manifolds in the Kreuzer-Skarke list with a non-trivial first fundamental group. We classify the line bundle models on these manifolds, both for SU(5) and SO(10) GUTs, which lead to consistent supersymmetric string vacua and have three chiral families. A total of about 29000 models is found, most of them corresponding to SO(10) GUTs. These models constitute a starting point for detailed heterotic model building on Calabi-Yau manifolds in the Kreuzer-Skarke list

Genome-wide association and HLA fine-mapping studies identify risk loci and genetic pathways underlying allergic rhinitis

Allergic rhinitis is the most common clinical presentation of allergy, affecting 400 million people worldwide, with increasing incidence in westernized countries1,2. To elucidate the genetic architecture and understand the underlying disease mechanisms, we carried out a meta-analysis of allergic rhinitis in 59,762 cases and 152,358 controls of European ancestry and identified a total of 41 risk loci for allergic rhinitis, including 20 loci not previously associated with allergic rhinitis, which were confirmed in a replication phase of 60,720 cases and 618,527 controls. Functional annotation implicated genes involved in various immune pathways, and fine mapping of the HLA region suggested amino acid variants important for antigen binding. We further performed genome-wide association study (GWAS) analyses of allergic sensitization against inhalant allergens and nonallergic rhinitis, which suggested shared genetic mechanisms across rhinitis-related traits. Future studies of the identified loci and genes might identify novel targets for treatment and prevention of allergic rhinitis

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN