The Dynamics of Abell 2125

We present 371 galaxy velocities in the field of the very rich cluster Abell 2125 (z~0.25). These were determined using optical spectroscopy collected over several years from both the WIYN 3.5m telescope and NOAO Mayall 4m telescope. Prior studies at a variety of wavelengths (radio, optical, and X-ray) have indicated that A2125 is a likely cluster-cluster merger, a scenario which we are able to test using our large velocity database. We identified 224 cluster galaxies, which were subjected to a broad range of statistical tests using both positional and velocity information to evaluate the cluster dynamics and substructure. The tests confirmed the presence of substructures within the Abell 2125 system at high significance, demonstrating that A2125 is a complex dynamical system. Comparison of the test results with existing simulations strengthens the merger hypothesis, and provides clues about the merger geometry and stage. The merger model for the system can reconcile A2125's low X-ray temperature and luminosity with its apparently high richness, and might also explain A2125's high fraction of active galaxies identified in prior radio and optical studies.Comment: 34 pages, including tables and 3 color figures; to appear in Ap

Constraints on UV Absorption in the Intracluster Medium of Abell 1030

We present results from an extensive HST spectroscopic search for UV absorption lines in the spectrum of the quasar B2~1028+313, which is associated with the central dominant galaxy in the cluster Abell~1030 ($z=0.178$). This is one of the brightest known UV continuum sources located in a cluster, and therefore provides an ideal opportunity to obtain stringent constraints on the column densities of any cool absorbing gas that may be associated with the intracluster medium (ICM). Our HST spectra were obtained with the FOS and GHRS, and provide continuous coverage at rest-frame wavelengths from $\sim 975$ to 4060~\AA, thereby allowing the investigation of many different elements and ionization levels. We utilize a new technique that involves simultaneous fitting of large numbers of different transitions for each species, thereby yielding more robust constraints on column densities than can be obtained from a single transition. This method yields upper limits of $\lesssim 10^{11} - 10^{13}$ cm$^{-2}$ on the column densities of a wide range of molecular, atomic and ionized species that may be associated with the ICM. We also discuss a possible \Lya and C IV absorption system associated with the quasar. We discuss the implications of the upper limits on cool intracluster gas in the context of the physical properties of the ICM and its relationship to the quasar.Comment: Astrophysical Journal, in press, 19 pages, includes 5 PostScript figures. Latex format, uses aas2pp4.sty and epsfig.sty file

On the Dalitz Plot Approach in Non-leptonic Charm Meson Decays

We claim that the non-resonant contribution to non-leptonic charm meson decays may not be constant in the phase space of the reaction. We argue that this can be relevant for any weak reaction. We discuss in detail the decay $D^+ \to K^- \pi^+ \pi^+$.Comment: Version accepted for publication in Physical Review Letters. 9 pages, Latex, including 2 figure

Identification of multiple rare variants associated with a disease

Identifying rare variants that are responsible for complex disease has been promoted by advances in sequencing technologies. However, statistical methods that can handle the vast amount of data generated and that can interpret the complicated relationship between disease and these variants have lagged. We apply a zero-inflated Poisson regression model to take into account the excess of zeros caused by the extremely low frequency of the 24,487 exonic variants in the Genetic Analysis Workshop 17 data. We grouped the 697 subjects in the data set as Europeans, Asians, and Africans based on principal components analysis and found the total number of rare variants per gene for each individual. We then analyzed these collapsed variants based on the assumption that rare variants are enriched in a group of people affected by a disease compared to a group of unaffected people. We also tested the hypothesis with quantitative traits Q1, Q2, and Q4. Analyses performed on the combined 697 individuals and on each ethnic group yielded different results. For the combined population analysis, we found that UGT1A1, which was not part of the simulation model, was associated with disease liability and that FLT1, which was a causal locus in the simulation model, was associated with Q1. Of the causal loci in the simulation models, FLT1 and KDR were associated with Q1 and VNN1 was correlated with Q2. No significant genes were associated with Q4. These results show the feasibility and capability of our new statistical model to detect multiple rare variants influencing disease risk

Immunological responses in human papillomavirus 16 E6/E7-transgenic mice to E7 protein correlate with the presence of skin disease

The human papillomavirus (HPV) oncogenes, E6 and E7, are believed to contribute to the development of cervical cancers in women infected with certain HPV genotypes, most notably HPV-16 and HPV-18. Given their expression in tumor tissue, E6 and E7 have been implicated as potential tumor-specific antigens. We have examined an HPV-16 E6- and E7-transgenic mouse lineage for immune responses to these viral oncoproteins. Mice in this lineage express the HPV-16 E6 and E7 genes in their skin and eyes, and on aging, these mice frequently develop squamous cell carcinomas and lenticular tumors. Young transgenic mice, which had measurable E7 protein in the eye but not in the skin, were immunologically naive to E7 protein. They mounted an immune response to E7 on immunization comparable to that of nontransgenic controls, suggesting a lack of immune tolerance to this protein. Older line 19 mice, which are susceptible to skin disease associated with transcription of the E6 and E7 open reading frames, had measurable E7 protein in their skin. These older transgenic mice spontaneously developed antibody responses to endogenous E7 protein, particularly in association with skin disease. Also detected in older mice were delayed-type hypersensitivity responses to E7. These finding parallel the humoral immune response to E7 protein in patients with HPV-associated cervical cancer and suggest that line 19 mice may provide a model for studying the immunobiology of HPV-associated cancers

How U.S. Ocean Policy and Market Power Can Reform the Coral Reef Wildlife Trade

As the world’s largest importer of marine ornamental species for the aquaria, curio, home décor, and jewelry industries, the United States has an opportunity to leverage its considerable market power to promote more sustainable trade and reduce the effects of ornamental trade stress on coral reefs worldwide. Evidence indicates that collection of some coral reef animals for these trades has caused virtual elimination of local populations, major changes in age structure, and promotion of collection practices that destroy reef habitats. Management and enforcement of collection activities in major source countries such as Indonesia and the Philippines remain weak. Strengthening US trade laws and enforcement capabilities combined with increasing consumer and industry demand for responsible conservation can create strong incentives for improving management in source countries. This is particularly important in light of the March 2010 failure of the parties to the Convention on International Trade in Endangered Species (CITES) to take action on key groups of corals

An RNA editing fingerprint of cancer stem cell reprogramming

BackgroundDeregulation of RNA editing by adenosine deaminases acting on dsRNA (ADARs) has been implicated in the progression of diverse human cancers including hematopoietic malignancies such as chronic myeloid leukemia (CML). Inflammation-associated activation of ADAR1 occurs in leukemia stem cells specifically in the advanced, often drug-resistant stage of CML known as blast crisis. However, detection of cancer stem cell-associated RNA editing by RNA sequencing in these rare cell populations can be technically challenging, costly and requires PCR validation. The objectives of this study were to validate RNA editing of a subset of cancer stem cell-associated transcripts, and to develop a quantitative RNA editing fingerprint assay for rapid detection of aberrant RNA editing in human malignancies.MethodsTo facilitate quantification of cancer stem cell-associated RNA editing in exons and intronic or 3'UTR primate-specific Alu sequences using a sensitive, cost-effective method, we established an in vitro RNA editing model and developed a sensitive RNA editing fingerprint assay that employs a site-specific quantitative PCR (RESSq-PCR) strategy. This assay was validated in a stably-transduced human leukemia cell line, lentiviral-ADAR1 transduced primary hematopoietic stem and progenitor cells, and in primary human chronic myeloid leukemia stem cells.ResultsIn lentiviral ADAR1-expressing cells, increased RNA editing of MDM2, APOBEC3D, GLI1 and AZIN1 transcripts was detected by RESSq-PCR with improved sensitivity over sequencing chromatogram analysis. This method accurately detected cancer stem cell-associated RNA editing in primary chronic myeloid leukemia samples, establishing a cancer stem cell-specific RNA editing fingerprint of leukemic transformation that will support clinical development of novel diagnostic tools to predict and prevent cancer progression.ConclusionsRNA editing quantification enables rapid detection of malignant progenitors signifying cancer progression and therapeutic resistance, and will aid future RNA editing inhibitor development efforts