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  • 1
    Keywords: Life sciences ; Plant breeding ; Plant physiology ; Life sciences ; Plant Breeding/Biotechnology ; Plant Genetics & Genomics ; Plant physiology ; Springer eBooks
    Description / Table of Contents: Expression analysis and genome annotations with RNA sequencing -- The application of Next Generation Sequencing techniques to Plant Epigenomics -- Whole genome sequencing to identify genes and QTL in rice -- Variant calling using NGS data in European aspen (Populus tremula) -- Leafy Spurge Genomics: A Model Perennial Weed To Investigate Development, Stress Responses, And Invasiveness -- Utilization of NGS and proteomic-based approaches to gain insights on cellular responses to singlet oxygen and improve energy yields for bacterial stress adaptation -- Experimental evolution and next generation sequencing illuminate the evolutionary trajectories of microbes -- Plant carbohydrate active enzyme (CAZyme) repertoires: a comparative Study -- Metagenomics of Plant- Microbe Interactions -- Genes and trans-factors underlying embryogenic transition in plant soma-cells -- Bioinformatics tools to analyze the proteome and genome data -- High through-put transcriptome analysis of plant stress responses -- CNV and structural variation in plants: prospects of NGS Approaches
    Abstract: This work is a compiled catalogue of such findings, where several NGS technologies ranging from the genomics, transcriptomics, metagenomics, single cell genomics, QTL, patho-genomics and patho-transcriptomics have been applied to delineate the mystery of the associated mutations, biological pathway transitions, transcriptional fluxes and patterns of host associated or adaptations to certain climatic conditions. The aims and scope of this book focuses more on the biological underpinning to initiate the cross-talks across the traits acquired or lost during the course of evolution. The structured framework of the present volume provides the applicative point of view of the NGS technologies and demonstrates the conceptual way of linking the experimentation to the NGS technologies, to aid in researchers to place their biological hypothesis in a larger context
    Pages: XII, 241 p. 40 illus., 31 illus. in color. : online resource.
    ISBN: 9783319171579
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  • 2
    Publication Date: 2018-07-19
    Description: The structure of crystalline [60]fullerene with a lithium cation inside (Li + @C 60 ) was determined by synchrotron radiation X-ray diffraction measurements to understand the electrostatic and thermal properties of the encapsulated Li + cation. Although the C 60 cages show severe orientation disorder in [Li + @C 60 ](TFPB – )·C 4 H 10 O and [Li + @C 60 ](TFSI – )·CH 2 Cl 2 , the Li + cations are rather ordered at specific positions by electrostatic interactions with coordinated anions outside the C 60 cage. The Li + @C 60 molecules in [Li + @C 60 ](ClO 4 – ) with a rock-salt-type cubic structure are fully disordered with almost uniform spherical shell charge densities even at 100 K by octahedral coordination of ClO 4 – tetrahedra and show no orientation ordering, unlike [Li + @C 60 ](PF 6 – ) and pristine C 60 . Single-bonded (Li + @C 60 – ) 2 dimers in [Li + @C 60 – ](NiOEP)⋅CH 2 Cl 2 are thermally stable even at 400 K and form Li + –C bonds which are shorter than Li + –C bonds in [Li + @C 60 ](PF 6 – ) and suppress the rotational motion of the Li + cations.
    Keywords: materials science
    Electronic ISSN: 2054-5703
    Topics: Natural Sciences in General
    Published by Royal Society
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  • 3
    Publication Date: 2018-07-31
    Description: Background/Aim: The present study investigated the impact of the lymph node ratio (LNR) on survival and recurrence in patients with pancreatic cancer after curative surgery followed by adjuvant chemotherapy. Patients and Methods: This study included 189 patients who underwent curative surgery followed by adjuvant chemotherapy for pancreatic cancer between 2005 and 2014. The risk factors for overall survival (OS) and recurrence-free survival (RFS) were identified. Results: A lymph node ratio of 0.1 was considered to be the optimal cut-off point for classification based on the 3-year and 5-year survival rates. The OS rates at three and five years after surgery were 34.4% and 28.2% in the LNR 〈0.1 group, respectively, and 23.1% and 5.8% in the LNR ≥0.1 group, which amounted to a statistically significant difference (p=0.003). The RFS rates at one and three years after surgery were 26.6% and 20.5% in the LNR 〈0.1 group, respectively, and 8.0% and 0% in the LNR ≥0.1 group, which was a significant difference (p=0.001). A multivariate analysis demonstrated that the LNR was a significant independent risk factor for both the OS and RFS. Conclusion: The LNR was a risk factor for overall survival in patients who underwent curative surgery followed by adjuvant chemotherapy for pancreatic cancer. It is necessary to develop strategies to effectively utilize the lymph node metastasis status.
    Print ISSN: 0250-7005
    Electronic ISSN: 1791-7530
    Topics: Medicine
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  • 4
    Publication Date: 2018-05-31
    Description: Background/Aim: High mobility group box-1 (HMGB1) induces the release of proinflammatory cytokines and chemokines as a late-acting mediator of inflammation. Hepatocellular carcinoma (HCC) is a typical inflammation-related cancer. However, little is known about the relationship between HCC and HMGB1 and its receptor RAGE (receptor for advanced glycation end products). This study analyzes the clinicopathological relevance of HMGB1 expression level and the effect of HMGB1 expression on the characteristics of HCC. Materials and Methods: Samples from 75 HCC patients including 13 with positive hepatitis B surface antigen and 36 with hepatitis C antibody were studied. The expression of HMGB1 in paired cancer and non-cancerous tissues from patients with HCC was assessed using reverse-transcription polymerase chain reaction (RT-PCR) and western blotting. Quantitative RT-PCR data were analyzed in association with the clinicopathological factors of patients with HCC. Results: The expression of HMGB1 mRNA in HCC was high in well-differentiated tumors, but declined as tumors dedifferentiated to moderately and poorly differentiated HCC. The levels of HMGB1 mRNA showed a negative correlation with the presence of portal invasion (p=0.005) and the rise of serum PIVKA-II (p=0.034). There was no clear correlation between HMGB1 expression and proliferation activity of HCC using Ki-67 staining. Conclusion: In HCC, HMGB1 expression level correlated inversely with tumor differentiation. The RAGE-HMGB1 interaction may play a greater role in the early stages of HCC tumorigenesis than during cancer development.
    Print ISSN: 0250-7005
    Electronic ISSN: 1791-7530
    Topics: Medicine
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  • 5
    Publication Date: 2018-11-21
    Description: Eicosapentaenoic acid in combination with EPHA2 inhibition shows efficacy in preclinical models of triple-negative breast cancer by disrupting cellular cholesterol efflux Eicosapentaenoic acid in combination with EPHA2 inhibition shows efficacy in preclinical models of triple-negative breast cancer by disrupting cellular cholesterol efflux, Published online: 20 November 2018; doi:10.1038/s41388-018-0569-5 Eicosapentaenoic acid in combination with EPHA2 inhibition shows efficacy in preclinical models of triple-negative breast cancer by disrupting cellular cholesterol efflux
    Print ISSN: 0950-9232
    Topics: Medicine
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  • 6
    Publication Date: 2016-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Feng -- Lin, Qibing -- Zhu, Lihong -- Ren, Yulong -- Zhou, Kunneng -- Shabek, Nitzan -- Wu, Fuqing -- Mao, Haibin -- Dong, Wei -- Gan, Lu -- Ma, Weiwei -- Gao, He -- Chen, Jun -- Yang, Chao -- Wang, Dan -- Tan, Junjie -- Zhang, Xin -- Guo, Xiuping -- Wang, Jiulin -- Jiang, Ling -- Liu, Xi -- Chen, Weiqi -- Chu, Jinfang -- Yan, Cunyu -- Ueno, Kotomi -- Ito, Shinsaku -- Asami, Tadao -- Cheng, Zhijun -- Wang, Jie -- Lei, Cailin -- Zhai, Huqu -- Wu, Chuanyin -- Wang, Haiyang -- Zheng, Ning -- Wan, Jianmin -- England -- Nature. 2016 Apr 21;532(7599):402. doi: 10.1038/nature16537. Epub 2016 Jan 13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26760207" target="_blank"〉PubMed〈/a〉
    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: 2018-09-13
    Description: Molecular pathogenesis of disease progression in MLL -rearranged AML Molecular pathogenesis of disease progression in 〈i〉MLL〈/i〉-rearranged AML, Published online: 12 September 2018; doi:10.1038/s41375-018-0253-3 Molecular pathogenesis of disease progression in MLL -rearranged AML
    Print ISSN: 0887-6924
    Electronic ISSN: 1476-5551
    Topics: Medicine
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  • 8
    Publication Date: 2018-07-17
    Description: Krebs-cycle-deficient hereditary cancer syndromes are defined by defects in homologous-recombination DNA repair Krebs-cycle-deficient hereditary cancer syndromes are defined by defects in homologous-recombination DNA repair, Published online: 16 July 2018; doi:10.1038/s41588-018-0170-4 High levels of fumarate or succinate suppress the homologous-recombination DNA-repair pathway in cancer cells that are deficient for FH or SDH, respectively. These tumor cells are vulnerable to PARP inhibitors.
    Print ISSN: 1061-4036
    Electronic ISSN: 1546-1718
    Topics: Biology , Medicine
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  • 9
    Publication Date: 2018-07-31
    Description: Enhanced water splitting under modal strong coupling conditions Enhanced water splitting under modal strong coupling conditions, Published online: 30 July 2018; doi:10.1038/s41565-018-0208-x Strong coupling between a Fabry–Pérot cavity mode and plasmonic modes enhances the internal quantum efficiency of a water splitting device.
    Print ISSN: 1748-3387
    Electronic ISSN: 1748-3395
    Topics: Physics
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  • 10
    Publication Date: 2016-05-03
    Description: We analysed whole-genome sequences of 560 breast cancers to advance understanding of the driver mutations conferring clonal advantage and the mutational processes generating somatic mutations. We found that 93 protein-coding cancer genes carried probable driver mutations. Some non-coding regions exhibited high mutation frequencies, but most have distinctive structural features probably causing elevated mutation rates and do not contain driver mutations. Mutational signature analysis was extended to genome rearrangements and revealed twelve base substitution and six rearrangement signatures. Three rearrangement signatures, characterized by tandem duplications or deletions, appear associated with defective homologous-recombination-based DNA repair: one with deficient BRCA1 function, another with deficient BRCA1 or BRCA2 function, the cause of the third is unknown. This analysis of all classes of somatic mutation across exons, introns and intergenic regions highlights the repertoire of cancer genes and mutational processes operating, and progresses towards a comprehensive account of the somatic genetic basis of breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nik-Zainal, Serena -- Davies, Helen -- Staaf, Johan -- Ramakrishna, Manasa -- Glodzik, Dominik -- Zou, Xueqing -- Martincorena, Inigo -- Alexandrov, Ludmil B -- Martin, Sancha -- Wedge, David C -- Van Loo, Peter -- Ju, Young Seok -- Smid, Marcel -- Brinkman, Arie B -- Morganella, Sandro -- Aure, Miriam R -- Lingjaerde, Ole Christian -- Langerod, Anita -- Ringner, Markus -- Ahn, Sung-Min -- Boyault, Sandrine -- Brock, Jane E -- Broeks, Annegien -- Butler, Adam -- Desmedt, Christine -- Dirix, Luc -- Dronov, Serge -- Fatima, Aquila -- Foekens, John A -- Gerstung, Moritz -- Hooijer, Gerrit K J -- Jang, Se Jin -- Jones, David R -- Kim, Hyung-Yong -- King, Tari A -- Krishnamurthy, Savitri -- Lee, Hee Jin -- Lee, Jeong-Yeon -- Li, Yilong -- McLaren, Stuart -- Menzies, Andrew -- Mustonen, Ville -- O'Meara, Sarah -- Pauporte, Iris -- Pivot, Xavier -- Purdie, Colin A -- Raine, Keiran -- Ramakrishnan, Kamna -- Rodriguez-Gonzalez, F German -- Romieu, Gilles -- Sieuwerts, Anieta M -- Simpson, Peter T -- Shepherd, Rebecca -- Stebbings, Lucy -- Stefansson, Olafur A -- Teague, Jon -- Tommasi, Stefania -- Treilleux, Isabelle -- Van den Eynden, Gert G -- Vermeulen, Peter -- Vincent-Salomon, Anne -- Yates, Lucy -- Caldas, Carlos -- Veer, Laura Van't -- Tutt, Andrew -- Knappskog, Stian -- Tan, Benita Kiat Tee -- Jonkers, Jos -- Borg, Ake -- Ueno, Naoto T -- Sotiriou, Christos -- Viari, Alain -- Futreal, P Andrew -- Campbell, Peter J -- Span, Paul N -- Van Laere, Steven -- Lakhani, Sunil R -- Eyfjord, Jorunn E -- Thompson, Alastair M -- Birney, Ewan -- Stunnenberg, Hendrik G -- van de Vijver, Marc J -- Martens, John W M -- Borresen-Dale, Anne-Lise -- Richardson, Andrea L -- Kong, Gu -- Thomas, Gilles -- Stratton, Michael R -- Nature. 2016 May 2. doi: 10.1038/nature17676.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; East Anglian Medical Genetics Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge CB2 9NB, UK. ; Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund SE-223 81, Sweden. ; Theoretical Biology and Biophysics (T-6), Los Alamos National Laboratory, Los Alamos, NM 87545, New Mexico, USA. ; Center for Nonlinear Studies, Los Alamos National Laboratory, Los Alamos, New Mexico 87545, USA. ; Department of Human Genetics, University of Leuven, B-3000 Leuven, Belgium. ; Department of Medical Oncology, Erasmus MC Cancer Institute and Cancer Genomics Netherlands, Erasmus University Medical Center, Rotterdam 3015CN, The Netherlands. ; Radboud University, Department of Molecular Biology, Faculty of Science, 6525GA Nijmegen, The Netherlands. ; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo 0310, Norway. ; K. G. Jebsen Centre for Breast Cancer Research, Institute for Clinical Medicine, University of Oslo, Oslo 0310, Norway. ; Department of Computer Science, University of Oslo, Oslo, Norway. ; Gachon Institute of Genome Medicine and Science, Gachon University Gil Medical Center, Incheon, South Korea. ; Translational Research Lab, Centre Leon Berard, 28, rue Laennec, 69373 Lyon Cedex 08, France. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. ; The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands. ; Breast Cancer Translational Research Laboratory, Universite Libre de Bruxelles, Institut Jules Bordet, Bd de Waterloo 121, B-1000 Brussels, Belgium. ; Translational Cancer Research Unit, Center for Oncological Research, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. ; Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. ; Department of Pathology, Asan Medical Center, College of Medicine, Ulsan University, Ulsan, South Korea. ; Department of Pathology, College of Medicine, Hanyang University, Seoul 133-791, South Korea. ; Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA. ; Morgan Welch Inflammatory Breast Cancer Research Program and Clinic, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard., Houston, Texas 77030, USA. ; Institute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University, Seoul, South Korea. ; Institut National du Cancer, Research Division, Clinical Research Department, 52 avenue Morizet, 92513 Boulogne-Billancourt, France. ; University Hospital of Minjoz, INSERM UMR 1098, Bd Fleming, Besancon 25000, France. ; Pathology Department, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. ; Oncologie Senologie, ICM Institut Regional du Cancer, Montpellier, France. ; The University of Queensland, UQ Centre for Clinical Research and School of Medicine, Brisbane, Queensland 4029, Australia. ; Cancer Research Laboratory, Faculty of Medicine, University of Iceland, 101 Reykjavik, Iceland. ; IRCCS Istituto Tumori "Giovanni Paolo II", Bari, Italy. ; Department of Pathology, Centre Leon Berard, 28 rue Laennec, 69373 Lyon Cedex 08, France. ; Department of Pathology, GZA Hospitals Sint-Augustinus, Antwerp, Belgium. ; Institut Curie, Paris Sciences Lettres University, Department of Pathology and INSERM U934, 26 rue d'Ulm, 75248 Paris Cedex 05, France. ; Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK. ; Breast Cancer Now Research Unit, King's College London, London SE1 9RT, UK. ; Breast Cancer Now Toby Robins Research Centre, Institute of Cancer Research, London SW3 6JB, UK. ; Department of Clinical Science, University of Bergen, 5020 Bergen, Norway. ; Department of Oncology, Haukeland University Hospital, 5021 Bergen, Norway. ; National Cancer Centre Singapore, 11 Hospital Drive, 169610, Singapore. ; Singapore General Hospital, Outram Road, 169608, Singapore. ; Equipe Erable, INRIA Grenoble-Rhone-Alpes, 655, Avenue de l'Europe, 38330 Montbonnot-Saint Martin, France. ; Synergie Lyon Cancer, Centre Leon Berard, 28 rue Laennec, Lyon Cedex 08, France. ; Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, Texas 77230, USA. ; Department of Radiation Oncology, Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen 6525GA, The Netherlands. ; Pathology Queensland, The Royal Brisbane and Women's Hospital, Brisbane, Queensland 4029, Australia. ; Department of Breast Surgical Oncology, University of Texas MD Anderson Cancer Center, 1400 Pressler Street, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27135926" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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