When a 520 million-year-old Chengjiang fossil meets a modern micro-CT - a case study

The 520 million-year-old Chengjiang biota of China (UNESCO World Heritage) presents the earliest known evidence of the so-called Cambrian Explosion. Studies, however, have mainly been limited to the information exposed on the surface of the slabs. Thus far, structures preserved inside the slabs were accessed by careful removal of the matrix, in many cases with the unfortunate sacrifice of some "less important" structures, which destroys elements of exceptionally preserved specimens. Here, we show for the first time that microtomography (micro-CT) can reveal structures situated inside a Chengjiang fossil slab without causing any damage. In the present study a trilobitomorph arthropod (Xandarella spectaculum) can be reliably identified only with the application of micro-CT. We propose that this technique is an important tool for studying three-dimensionally preserved Chengjiang fossils and, most likely, also those from other biota with a comparable type of preservation, specifically similar iron concentrations

A novel COMP mutation in a pseudoachondroplasia family of Chinese origin

<p>Abstract</p> <p>Background</p> <p>Pseudoachondroplasia (PSACH) is caused exclusively by mutations in the gene for cartilage oligomeric matrix protein (<it>COMP</it>). Only a small number of studies have documented the clinical phenotype and genetic basis in Chinese PSACH patients.</p> <p>Case presentation</p> <p>We investigated a four-generation PSACH pedigree of Chinese Han origin. Two patients and two unaffected individuals were recruited for clinical evaluation and molecular genetic analysis. The genomic DNA was extracted from peripheral blood leukocytes. Polymerase chain reaction (PCR) was adopted to amplify the 8-19 exons of <it>COMP </it>gene. Then the products were sequenced bi-directionally for screening mutation. Clinical evaluation revealed that PSACH patients in this pedigree had a severe disproportionate short stature (-10SD). A heterozygous TGTCCCTGG insertion in exon 13, between nucleotide 1352T and 1353G, were identified in the patients except the unaffected individuals, which resulted in a three-amino-acid insertion (451V_452P ins VPG) in the sixth calmodulin-like repeat of the <it>COMP </it>protein.</p> <p>Conclusion</p> <p>This c. 1352_1353ins TGTCCCTGG is a novel mutation responsible for severe familial PSACH.</p

An improved observable for the forward-backward asymmetry in B -> K* l+ l- and Bs -> phi l+ l-

We study the decay B -> K* l+ l- in the QCD factorization approach and propose a new integrated observable whose dependence on the form factors is almost negligible, consequently the non--perturbative error is significantly reduced and indeed its overall theoretical error is dominated by perturbative scale uncertainties. The new observable we propose is the ratio between the integrated forward--backward asymmetry in the [4,6] GeV^2 and [1,4] GeV^2 dilepton invariant mass bins. This new observable is particularly interesting because, when compared to the location of the zero of the FBA spectrum, it is experimentally easier to measure and its theoretical uncertainties are almost as small; moreover it displays a very strong dependence on the phase of the Wilson coefficient C_10 that is otherwise only accessible through complicated CP violating asymmetries. We illustrate the new physics sensitivity of this observable within the context of few extensions of the Standard Model, namely the SM with four generations, an MSSM with non--vanishing source of flavor changing neutral currents in the down squark sector and a Z' model with tree level flavor changing couplings.Comment: 19 pages, 7 figure

New Physics in Bs -> J/psi phi: a General Analysis

Recently, the CDF and D0 collaborations measured indirect CP violation in Bs -> J/psi phi and found a hint of a signal. If taken at face value, this can be interpreted as a nonzero phase of Bs-Bsbar mixing (beta_s), in disagreement with the standard model, which predicts that beta_s ~= 0. In this paper, we argue that this analysis may be incomplete. In particular, there can be new physics (NP) in the bbar -> sbar c cbar decay. If so, the value of beta_s is different than for the case in which NP is assumed to be present only in the mixing. We have examined several models of NP and found that, indeed, there can be significant contributions to the decay. These effects are consistent with measurements in B -> J/psi K* and Bd -> J/psi Ks. Due to the NP in the decay, polarization-dependent indirect CP asymmetries and triple-product asymmetries are predicted in Bs -> J/psi phi.Comment: 28 pages, JHEP, no figures. Considerable changes made. Abstract and main text of paper modified to alter presentation. Appendix added. References added. Conclusions unchanged

Forward-backward Asymmetry and Branching Ratio of B \rar K_1 \ell^+ \ell^- Transition in Supersymmetric Models

The mass eigen states $K_1(1270)$ and $K_1(1400)$ are mixture of the strange members of two axial-vector SU(3) octet, $^3P_1(K_1^A)$ and $^1P_1(K_1^B)$. Taking into account this mixture, the forward-backward asymmetry and branching ratio of B \rar K_1(1270,1400) \ell^+ \ell^- transitions are studied in the framework of different supersymmetric models. It is found that the results have considerable deviation from the standard model predictions. Any measurement of these physical observables and their comparison with the results obtained in this paper can give useful information about the nature of interactions beyond the standard model.Comment: 14 pages, 4 figure

SH3 Domain-Peptide Binding Energy Calculations Based on Structural Ensemble and Multiple Peptide Templates

SH3 domains mediate signal transduction by recognizing short peptides. Understanding of the driving forces in peptide recognitions will help us to predict the binding specificity of the domain-peptide recognition and to understand the molecular interaction networks of cells. However, accurate calculation of the binding energy is a tough challenge. In this study, we propose three ideas for improving our ability to predict the binding energy between SH3 domains and peptides: (1) utilizing the structural ensembles sampled from a molecular dynamics simulation trajectory, (2) utilizing multiple peptide templates, and (3) optimizing the sequence-structure mapping. We tested these three ideas on ten previously studied SH3 domains for which SPOT analysis data were available. The results indicate that calculating binding energy using the structural ensemble was most effective, clearly increasing the prediction accuracy, while the second and third ideas tended to give better binding energy predictions. We applied our method to the five SH3 targets in DREAM4 Challenge and selected the best performing method

The functional head of the Cambrian radiodontan (stem-group Euarthropoda) Amplectobelua symbrachiata

© The Author(s). 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. The attached file is the published version of the article

CRISPR-assisted detection of RNA-protein interactions in living cells.

We have developed CRISPR-assisted RNA-protein interaction detection method (CARPID), which leverages CRISPR-CasRx-based RNA targeting and proximity labeling to identify binding proteins of specific long non-coding RNAs (lncRNAs) in the native cellular context. We applied CARPID to the nuclear lncRNA XIST, and it captured a list of known interacting proteins and multiple previously uncharacterized binding proteins. We generalized CARPID to explore binders of the lncRNAs DANCR and MALAT1, revealing the method's wide applicability in identifying RNA-binding proteins

Autoimmune and autoinflammatory mechanisms in uveitis

The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders