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  • 1
    Publication Date: 2011-07-02
    Description: Transmission through a spinning window slightly rotates the polarization of the light, typically by a microradian. It has been predicted that the same mechanism should also rotate an image. Because this rotary photon drag has a contribution that is inversely proportional to the group velocity, the image rotation is expected to increase in a slow-light medium. Using a ruby window under conditions for coherent population oscillations, we induced an effective group index of about 1 million. The resulting rotation angle was large enough to be observed by the eye. This result shows that rotary photon drag applies to images as well as polarization. The possibility of switching between different rotation states may offer new opportunities for controlled image coding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franke-Arnold, Sonja -- Gibson, Graham -- Boyd, Robert W -- Padgett, Miles J -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):65-7. doi: 10.1126/science.1203984.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Physics and Astronomy (SUPA), University of Glasgow, Glasgow G12 8QQ, Scotland. sonja.franke-arnold@glasgow.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21719672" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Daniel G -- Venter, J Craig -- England -- Nature. 2014 May 8;509(7499):168-9. doi: 10.1038/509168a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. Craig Venter Institute, La Jolla, California 92037, USA, and at Synthetic Genomics, La Jolla.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24805340" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosomes, Fungal ; Saccharomyces cerevisiae/*genetics ; Synthetic Biology/*methods
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-02-28
    Description: Epistasis is the phenomenon whereby one polymorphism's effect on a trait depends on other polymorphisms present in the genome. The extent to which epistasis influences complex traits and contributes to their variation is a fundamental question in evolution and human genetics. Although often demonstrated in artificial gene manipulation studies in model organisms, and some examples have been reported in other species, few examples exist for epistasis among natural polymorphisms in human traits. Its absence from empirical findings may simply be due to low incidence in the genetic control of complex traits, but an alternative view is that it has previously been too technically challenging to detect owing to statistical and computational issues. Here we show, using advanced computation and a gene expression study design, that many instances of epistasis are found between common single nucleotide polymorphisms (SNPs). In a cohort of 846 individuals with 7,339 gene expression levels measured in peripheral blood, we found 501 significant pairwise interactions between common SNPs influencing the expression of 238 genes (P 〈 2.91 x 10(-16)). Replication of these interactions in two independent data sets showed both concordance of direction of epistatic effects (P = 5.56 x 10(-31)) and enrichment of interaction P values, with 30 being significant at a conservative threshold of P 〈 9.98 x 10(-5). Forty-four of the genetic interactions are located within 5 megabases of regions of known physical chromosome interactions (P = 1.8 x 10(-10)). Epistatic networks of three SNPs or more influence the expression levels of 129 genes, whereby one cis-acting SNP is modulated by several trans-acting SNPs. For example, MBNL1 is influenced by an additive effect at rs13069559, which itself is masked by trans-SNPs on 14 different chromosomes, with nearly identical genotype-phenotype maps for each cis-trans interaction. This study presents the first evidence, to our knowledge, for many instances of segregating common polymorphisms interacting to influence human traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984375/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984375/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemani, Gibran -- Shakhbazov, Konstantin -- Westra, Harm-Jan -- Esko, Tonu -- Henders, Anjali K -- McRae, Allan F -- Yang, Jian -- Gibson, Greg -- Martin, Nicholas G -- Metspalu, Andres -- Franke, Lude -- Montgomery, Grant W -- Visscher, Peter M -- Powell, Joseph E -- AA014041/AA/NIAAA NIH HHS/ -- AA07535/AA/NIAAA NIH HHS/ -- AA10248/AA/NIAAA NIH HHS/ -- AA13320/AA/NIAAA NIH HHS/ -- AA13321/AA/NIAAA NIH HHS/ -- AA13326/AA/NIAAA NIH HHS/ -- DA12854/DA/NIDA NIH HHS/ -- GM057091/GM/NIGMS NIH HHS/ -- GM099568/GM/NIGMS NIH HHS/ -- P01 GM099568/GM/NIGMS NIH HHS/ -- R01 GM075091/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Apr 10;508(7495):249-53. doi: 10.1038/nature13005. Epub 2014 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia [2] University of Queensland Diamantina Institute, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4072, Australia. ; Department of Genetics, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. ; 1] Estonian Genome Center, University of Tartu, Tartu 51010, Estonia [2] Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts 02142, USA [3] Divisions of Endocrinology, Children's Hospital, Boston, Massachusetts 02115, USA. ; Queensland Institute of Medical Research, Brisbane, Queensland 4006, Australia. ; Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia. ; School of Biology and Centre for Integrative Genomics, Georgia Institute of Technology, Atlanta, Georgia 30332, USA. ; Estonian Genome Center, University of Tartu, Tartu 51010, Estonia. ; 1] Queensland Institute of Medical Research, Brisbane, Queensland 4006, Australia [2]. ; 1] Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia [2] University of Queensland Diamantina Institute, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4072, Australia [3].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572353" target="_blank"〉PubMed〈/a〉
    Keywords: Cohort Studies ; Epistasis, Genetic/*genetics ; Europe/ethnology ; Female ; Gene Expression Profiling ; Gene Expression Regulation/*genetics ; Genetic Association Studies ; Humans ; Linkage Disequilibrium ; Male ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci ; Reproducibility of Results ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2014-10-04
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404158/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404158/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemani, Gibran -- Shakhbazov, Konstantin -- Westra, Harm-Jan -- Esko, Tonu -- Henders, Anjali K -- McRae, Allan F -- Yang, Jian -- Gibson, Greg -- Martin, Nicholas G -- Metspalu, Andres -- Franke, Lude -- Montgomery, Grant W -- Visscher, Peter M -- Powell, Joseph E -- P01 GM099568/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):E5-6. doi: 10.1038/nature13692.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia [2] University of Queensland Diamantina Institute, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4072, Australia. ; Department of Genetics, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. ; 1] Estonian Genome Center, University of Tartu, Tartu, 51010, Estonia [2] Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts 02142, USA [3] Divisions of Endocrinology, Children's Hospital, Boston, Massachusetts 02115, USA. ; Queensland Institute of Medical Research, Brisbane, Queensland 4006, Australia. ; Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia. ; School of Biology and Centre for Integrative Genomics, Georgia Institute of Technology, Atlanta, Georgia 30332, USA. ; Estonian Genome Center, University of Tartu, Tartu, 51010, Estonia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25279929" target="_blank"〉PubMed〈/a〉
    Keywords: Epistasis, Genetic/*genetics ; Female ; Gene Expression Regulation/*genetics ; Humans ; Male ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-06-08
    Description: The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicholson, Jeremy K -- Holmes, Elaine -- Kinross, James -- Burcelin, Remy -- Gibson, Glenn -- Jia, Wei -- Pettersson, Sven -- R01AA020212/AA/NIAAA NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1262-7. doi: 10.1126/science.1223813. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomolecular Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK. j.nicholson@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674330" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Bacteria/*metabolism ; Diet ; Gastrointestinal Tract/*metabolism/*microbiology ; Health ; Humans ; Immune System/physiology ; Inflammation ; Liver/metabolism ; Metabolic Diseases/metabolism/*microbiology ; *Metabolic Networks and Pathways ; *Metagenome ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2014-08-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Greg -- England -- Nature. 2014 Aug 7;512(7512):31-2. doi: 10.1038/nature13649. Epub 2014 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, Georgia 30309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079332" target="_blank"〉PubMed〈/a〉
    Keywords: Colorectal Neoplasms/*genetics ; Gene Expression Regulation, Neoplastic/*genetics ; Humans ; Regulatory Sequences, Nucleic Acid/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2016-03-26
    Description: We used whole-genome design and complete chemical synthesis to minimize the 1079-kilobase pair synthetic genome of Mycoplasma mycoides JCVI-syn1.0. An initial design, based on collective knowledge of molecular biology combined with limited transposon mutagenesis data, failed to produce a viable cell. Improved transposon mutagenesis methods revealed a class of quasi-essential genes that are needed for robust growth, explaining the failure of our initial design. Three cycles of design, synthesis, and testing, with retention of quasi-essential genes, produced JCVI-syn3.0 (531 kilobase pairs, 473 genes), which has a genome smaller than that of any autonomously replicating cell found in nature. JCVI-syn3.0 retains almost all genes involved in the synthesis and processing of macromolecules. Unexpectedly, it also contains 149 genes with unknown biological functions. JCVI-syn3.0 is a versatile platform for investigating the core functions of life and for exploring whole-genome design.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hutchison, Clyde A 3rd -- Chuang, Ray-Yuan -- Noskov, Vladimir N -- Assad-Garcia, Nacyra -- Deerinck, Thomas J -- Ellisman, Mark H -- Gill, John -- Kannan, Krishna -- Karas, Bogumil J -- Ma, Li -- Pelletier, James F -- Qi, Zhi-Qing -- Richter, R Alexander -- Strychalski, Elizabeth A -- Sun, Lijie -- Suzuki, Yo -- Tsvetanova, Billyana -- Wise, Kim S -- Smith, Hamilton O -- Glass, John I -- Merryman, Chuck -- Gibson, Daniel G -- Venter, J Craig -- P41GM103412/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):aad6253. doi: 10.1126/science.aad6253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. Craig Venter Institute, La Jolla, CA 92037, USA. ; National Center for Microscopy and Imaging Research, University of California-San Diego, La Jolla, CA 92037, USA. ; Synthetic Genomics, La Jolla, CA 92037, USA. ; National Institute of Standards and Technology, Gaithersburg, MD 20899, USA. ; J. Craig Venter Institute, La Jolla, CA 92037, USA. Synthetic Genomics, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013737" target="_blank"〉PubMed〈/a〉
    Keywords: Artificial Cells ; Codon/genetics ; DNA Transposable Elements ; DNA, Bacterial/*chemical synthesis/genetics ; Genes, Essential ; Genes, Synthetic/genetics/*physiology ; *Genome, Bacterial ; Mutagenesis ; Mycoplasma mycoides/*genetics ; Proteins/genetics ; RNA/genetics ; Synthetic Biology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Greg -- New York, N.Y. -- Science. 2015 May 8;348(6235):640-1. doi: 10.1126/science.aab3002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, GA 30332, USA. greg.gibson@biology.gatech.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25953996" target="_blank"〉PubMed〈/a〉
    Keywords: Disease/*genetics ; Female ; *Gene Expression Regulation ; *Genetic Variation ; Genome, Human/*genetics ; Humans ; Male ; Proteins/*genetics ; *Quantitative Trait Loci ; *Transcriptome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Keywords: PEPTIDE ; CANCER ; CELLS ; tumor ; carcinoma ; CELL ; COMBINATION ; human ; MODEL ; MODELS ; GENERATION ; NEW-YORK ; PROTEIN ; cell line ; TUMORS ; MICE ; PATIENT ; RESPONSES ; MECHANISM ; DENDRITIC CELLS ; mechanisms ; T cell ; T cells ; T-CELL ; T-CELLS ; TOLERANCE ; TARGET ; virus ; MALIGNANCIES ; HUMANS ; NUMBER ; CELL-LINE ; LINE ; p53 ; LENGTH ; KNOCK-IN MICE ; VACCINE ; CANCER-PATIENTS ; CD8(+) ; IMMUNITY ; IMMUNOTHERAPY ; CANCER-IMMUNOTHERAPY ; REJECTION ; CANCER PATIENTS ; ANTITUMOR IMMUNITY ; WILD-TYPE P53 ; CYTOTOXIC T-LYMPHOCYTES ; targeting ; IMMUNIZATION ; CANCER VACCINES ; MALIGNANCY ; ONCOLOGY ; CAPACITY ; LIBRARIES ; TRANSLATION ; MURINE MODEL ; LIBRARY ; USA ; function ; E ; immunology ; mammary ; CELL RESPONSE ; systemic ; in combination ; FULL-LENGTH ; VACCINIA-VIRUS ; animal models of cancer ; CELL RESPONSES ; immune response to cancer ; mammary carcinoma ; MURINE TUMORS ; TARGETING P53 ; TUMOR-ERADICATION ; VIRUS ANKARA
    Abstract: Background The cellular regulatory protein p53 is overexpressed by almost 50% of all malignancies making it an attractive target for a vaccine approach to cancer. A number of immunotherapy approaches targeting p53 have been evaluated successfully in murine models, but translation of these preclinical findings to the clinic has been unsuccessful. Prior studies in our laboratory employing murine models demonstrated that a modified vaccinia virus Ankara (MVA) vaccine expressing murine p53 could stimulate p53 specific immunity. Systemic administration of the MVA vaccine was able to effect the rejection of established tumors. To better understand the immunologic mechanisms that underlie the vaccine function of human p53, we utilized a murine model in which the murine germ line copy of p53 was replaced with a modified human one. These mice, referred to as Hupki, were evaluated as a tolerant model to explore the capacity of MVA expressing human p53 to overcome tolerance and reject human p53-expressing tumors. Results MVAp53 immunization of Hupki mice resulted in the generation of p53-specific CD8(+) T cells and the rejection of a highly aggressive murine mammary carcinoma cell line 4T1(H-2d) transfected with human p53 (4T1p53). An immunologic correlate of tumor protection was evaluated utilizing an overlapping peptide library spanning the full length of human p53. This reagent was also used in combination with MVAp53 to stimulate p53-specific CD8(+) T cell responses in cancer patients. Conclusion These studies demonstrate the potential of MVAp53 to overcome tolerance to p53 for cancer immunotherapy
    Type of Publication: Journal article published
    PubMed ID: 17219151
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  • 10
    ISSN: 0168-583X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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