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  • 1
    Publication Date: 2011-09-17
    Description: Inhomogeneity-induced magnetoresistance (IMR) reported in some non-magnetic semiconductors, particularly silicon, has generated considerable interest owing to the large magnitude of the effect and its linear field dependence (albeit at high magnetic fields). Various theories implicate spatial variation of the carrier mobility as being responsible for IMR. Here we show that IMR in lightly doped silicon can be significantly enhanced through hole injection, and then tuned by an applied current to arise at low magnetic fields. In our devices, the 'inhomogeneity' is provided by the p-n boundary formed between regions where conduction is dominated by the minority and majority charge carriers (holes and electrons) respectively; application of a magnetic field distorts the current in the boundary region, resulting in large magnetoresistance. Because this is an intrinsically spatial effect, the geometry of the device can be used to enhance IMR further: we designed an IMR device whose room-temperature field sensitivity at low fields was greatly improved, with magnetoresistance reaching 10% at 0.07 T and 100% at 0.2 T, approaching the performance of commercial giant-magnetoresistance devices. The combination of high sensitivity to low magnetic fields and large high-field response should make this device concept attractive to the magnetic-field sensing industry. Moreover, because our device is based on a conventional silicon platform, it should be possible to integrate it with existing silicon devices and so aid the development of silicon-based magnetoelectronics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, Caihua -- Zhang, Xiaozhong -- Gao, Xili -- Wang, Jimin -- Tan, Xinyu -- England -- Nature. 2011 Sep 14;477(7364):304-7. doi: 10.1038/nature10375.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Advanced Materials, Department of Materials Science and Engineering, Tsinghua University, Beijing 100084, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921912" 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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  • 2
    Publication Date: 2011-10-29
    Description: The neocortex contains excitatory neurons and inhibitory interneurons. Clones of neocortical excitatory neurons originating from the same progenitor cell are spatially organized and contribute to the formation of functional microcircuits. In contrast, relatively little is known about the production and organization of neocortical inhibitory interneurons. We found that neocortical inhibitory interneurons were produced as spatially organized clonal units in the developing ventral telencephalon. Furthermore, clonally related interneurons did not randomly disperse but formed spatially isolated clusters in the neocortex. Individual clonal clusters consisting of interneurons expressing the same or distinct neurochemical markers exhibited clear vertical or horizontal organization. These results suggest that the lineage relationship plays a pivotal role in the organization of inhibitory interneurons in the neocortex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3304494/" 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/PMC3304494/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Keith N -- Chen, She -- Han, Zhi -- Lu, Chun-Hui -- Tan, Xin -- Zhang, Xin-Jun -- Ding, Liya -- Lopez-Cruz, Alejandro -- Saur, Dieter -- Anderson, Stewart A -- Huang, Kun -- Shi, Song-Hai -- K02MH070031/MH/NIMH NIH HHS/ -- R01 DA024681/DA/NIDA NIH HHS/ -- R01 DA024681-01A1/DA/NIDA NIH HHS/ -- R01 DA024681-02/DA/NIDA NIH HHS/ -- R01 DA024681-03/DA/NIDA NIH HHS/ -- R01 DA024681-04/DA/NIDA NIH HHS/ -- R01 DA024681-05/DA/NIDA NIH HHS/ -- R01DA024681/DA/NIDA NIH HHS/ -- R01MH066912/MH/NIMH NIH HHS/ -- R21 MH083624/MH/NIMH NIH HHS/ -- R21 MH083624-01/MH/NIMH NIH HHS/ -- R21 MH083624-02/MH/NIMH NIH HHS/ -- R21 NS072483/NS/NINDS NIH HHS/ -- R21 NS072483-01/NS/NINDS NIH HHS/ -- R21 NS072483-02/NS/NINDS NIH HHS/ -- R21MH083624/MH/NIMH NIH HHS/ -- R21NS072483/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):480-6. doi: 10.1126/science.1208884.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22034427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Movement ; Clone Cells/cytology/physiology ; Gene Knock-In Techniques ; Interneurons/*cytology/*physiology ; Mice ; Mitosis ; Neocortex/*cytology/embryology ; *Neural Inhibition ; Neural Stem Cells/*cytology/physiology ; *Neurogenesis ; Neuroglia/cytology/physiology ; Preoptic Area/cytology/embryology ; Telencephalon/*cytology/embryology
    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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  • 3
    Publication Date: 2018-10-05
    Description: Biodiversity experiments have shown that species loss reduces ecosystem functioning in grassland. To test whether this result can be extrapolated to forests, the main contributors to terrestrial primary productivity, requires large-scale experiments. We manipulated tree species richness by planting more than 150,000 trees in plots with 1 to 16 species. Simulating multiple extinction scenarios, we found that richness strongly increased stand-level productivity. After 8 years, 16-species mixtures had accumulated over twice the amount of carbon found in average monocultures and similar amounts as those of two commercial monocultures. Species richness effects were strongly associated with functional and phylogenetic diversity. A shrub addition treatment reduced tree productivity, but this reduction was smaller at high shrub species richness. Our results encourage multispecies afforestation strategies to restore biodiversity and mitigate climate change.
    Keywords: Ecology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2018-05-24
    Description: The co-silencing of multiple tumor suppressor genes can lead to escalated malignancy in cancer cells. Given the limited efficacy of anticancer therapies targeting single tumor suppressor genes, we developed small circular single-stranded DNA (CSSD) that can up-regulate the expression of co-silenced tumor suppressor genes by sequestering microRNAs (miRNAs) that negatively regulate these genes. We found that cancer patients with low tumor expression of the tumor suppressor genes KLF17 , CDH1 , and LASS2 had shortened survival times. The up-regulation of these genes upon transfection of artificial CSSD-9 inhibited tumor proliferation and metastasis and promoted apoptosis in vitro as well as in ex vivo and patient-derived xenograft models. In addition, CSSD is more stable and effective than current miRNA inhibitors, and transfecting CSSDs via nanoparticles substantially improved delivery efficiency. The use of a single CSSD can promote the inhibition of multiple tumor suppressor genes. This study provides evidence for the possibility of using CSSDs as therapeutic miRNA inhibitors to target the co-silencing of multiple tumor suppressor genes.
    Print ISSN: 1946-6234
    Electronic ISSN: 1946-6242
    Topics: Medicine
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  • 5
    Publication Date: 2015-03-25
    Description: B cells are selected for an intermediate level of B-cell antigen receptor (BCR) signalling strength: attenuation below minimum (for example, non-functional BCR) or hyperactivation above maximum (for example, self-reactive BCR) thresholds of signalling strength causes negative selection. In approximately 25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitutively active pre-BCR signalling. Current therapeutic approaches are largely focused on the development of more potent tyrosine kinase inhibitors to suppress oncogenic signalling below a minimum threshold for survival. We tested the hypothesis that targeted hyperactivation--above a maximum threshold--will engage a deletional checkpoint for removal of self-reactive B cells and selectively kill ALL cells. Here we find, by testing various components of proximal pre-BCR signalling in mouse BCR-ABL1 cells, that an incremental increase of Syk tyrosine kinase activity was required and sufficient to induce cell death. Hyperactive Syk was functionally equivalent to acute activation of a self-reactive BCR on ALL cells. Despite oncogenic transformation, this basic mechanism of negative selection was still functional in ALL cells. Unlike normal pre-B cells, patient-derived ALL cells express the inhibitory receptors PECAM1, CD300A and LAIR1 at high levels. Genetic studies revealed that Pecam1, Cd300a and Lair1 are critical to calibrate oncogenic signalling strength through recruitment of the inhibitory phosphatases Ptpn6 (ref. 7) and Inpp5d (ref. 8). Using a novel small-molecule inhibitor of INPP5D (also known as SHIP1), we demonstrated that pharmacological hyperactivation of SYK and engagement of negative B-cell selection represents a promising new strategy to overcome drug resistance in human ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441554/" 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/PMC4441554/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhengshan -- Shojaee, Seyedmehdi -- Buchner, Maike -- Geng, Huimin -- Lee, Jae Woong -- Klemm, Lars -- Titz, Bjorn -- Graeber, Thomas G -- Park, Eugene -- Tan, Ying Xim -- Satterthwaite, Anne -- Paietta, Elisabeth -- Hunger, Stephen P -- Willman, Cheryl L -- Melnick, Ari -- Loh, Mignon L -- Jung, Jae U -- Coligan, John E -- Bolland, Silvia -- Mak, Tak W -- Limnander, Andre -- Jumaa, Hassan -- Reth, Michael -- Weiss, Arthur -- Lowell, Clifford A -- Muschen, Markus -- 101880/Wellcome Trust/United Kingdom -- CA180794/CA/NCI NIH HHS/ -- CA180820/CA/NCI NIH HHS/ -- R01 AI068150/AI/NIAID NIH HHS/ -- R01 AI113272/AI/NIAID NIH HHS/ -- R01 CA137060/CA/NCI NIH HHS/ -- R01 CA139032/CA/NCI NIH HHS/ -- R01 CA157644/CA/NCI NIH HHS/ -- R01 CA169458/CA/NCI NIH HHS/ -- R01 CA172558/CA/NCI NIH HHS/ -- R01CA137060/CA/NCI NIH HHS/ -- R01CA139032/CA/NCI NIH HHS/ -- R01CA157644/CA/NCI NIH HHS/ -- R01CA169458/CA/NCI NIH HHS/ -- R01CA172558/CA/NCI NIH HHS/ -- U01 CA157937/CA/NCI NIH HHS/ -- U10 CA180794/CA/NCI NIH HHS/ -- U10 CA180820/CA/NCI NIH HHS/ -- U10 CA180827/CA/NCI NIH HHS/ -- U10 CA180886/CA/NCI NIH HHS/ -- U24 CA114737/CA/NCI NIH HHS/ -- U24 CA196172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 May 21;521(7552):357-61. doi: 10.1038/nature14231. Epub 2015 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, University of California, San Francisco, California 94143, USA. ; Crump Institute for Molecular Imaging, Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California 90095, USA. ; Rosalind Russell-Ephraim P. Engleman Medical Research Center for Arthritis, Division of Rheumatology, Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco, California 94143, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10466, USA. ; Division of Pediatric Oncology and Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, Philadelphia 19104, USA. ; University of New Mexico Cancer Center, Albuquerque, New Mexico 87102, USA. ; Departments of Medicine and Pharmacology, Weill Cornell Medical College, New York, New York 10065, USA. ; Pediatric Hematology-Oncology, University of California, San Francisco, California 94143, USA. ; Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California 90033, USA. ; Receptor Cell Biology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA. ; Autoimmunity and Functional Genomics Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA. ; The Campbell Family Institute for Breast Cancer Research, University Health Network, 620 University Avenue, Toronto, Ontario M5G 2M9, Canada. ; Department of Anatomy, University of California, San Francisco, California 94143, USA. ; Institute of Immunology, University Clinics Ulm, 89081 Ulm, Germany. ; BIOSS Centre for Biological Signalling Studies and Faculty of Biology, Albert-Ludwigs-Universitat Freiburg, and MPI of Immunbiologie and Epigenetics, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25799995" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs/genetics ; Animals ; Antigens, CD/metabolism ; Antigens, CD31/metabolism ; B-Lymphocytes/drug effects/*metabolism/*pathology ; Cell Death/drug effects ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Disease Models, Animal ; Drug Resistance, Neoplasm/drug effects ; Enzyme Activation/drug effects ; Female ; Fusion Proteins, bcr-abl/genetics ; Gene Deletion ; Humans ; Intracellular Signaling Peptides and Proteins/agonists/metabolism ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Phosphoric Monoester Hydrolases/antagonists & inhibitors/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/*metabolism/*pathology ; Precursor Cells, B-Lymphoid/drug effects/metabolism/pathology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/deficiency/genetics/metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, B-Cell/deficiency/genetics/metabolism ; Receptors, Immunologic/genetics/metabolism ; *Signal Transduction/drug effects ; Tyrosine/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2015-11-03
    Description: DNA methylation is an important epigenetic modification. Ten-eleven translocation (TET) proteins are involved in DNA demethylation through iteratively oxidizing 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). Here we show that human TET1 and TET2 are more active on 5mC-DNA than 5hmC/5fC-DNA substrates. We determine the crystal structures of TET2-5hmC-DNA and TET2-5fC-DNA complexes at 1.80 A and 1.97 A resolution, respectively. The cytosine portion of 5hmC/5fC is specifically recognized by TET2 in a manner similar to that of 5mC in the TET2-5mC-DNA structure, and the pyrimidine base of 5mC/5hmC/5fC adopts an almost identical conformation within the catalytic cavity. However, the hydroxyl group of 5hmC and carbonyl group of 5fC face towards the opposite direction because the hydroxymethyl group of 5hmC and formyl group of 5fC adopt restrained conformations through forming hydrogen bonds with the 1-carboxylate of NOG and N4 exocyclic nitrogen of cytosine, respectively. Biochemical analyses indicate that the substrate preference of TET2 results from the different efficiencies of hydrogen abstraction in TET2-mediated oxidation. The restrained conformation of 5hmC and 5fC within the catalytic cavity may prevent their abstractable hydrogen(s) adopting a favourable orientation for hydrogen abstraction and thus result in low catalytic efficiency. Our studies demonstrate that the substrate preference of TET2 results from the intrinsic value of its substrates at their 5mC derivative groups and suggest that 5hmC is relatively stable and less prone to further oxidation by TET proteins. Therefore, TET proteins are evolutionarily tuned to be less reactive towards 5hmC and facilitate the generation of 5hmC as a potentially stable mark for regulatory functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Lulu -- Lu, Junyan -- Cheng, Jingdong -- Rao, Qinhui -- Li, Ze -- Hou, Haifeng -- Lou, Zhiyong -- Zhang, Lei -- Li, Wei -- Gong, Wei -- Liu, Mengjie -- Sun, Chang -- Yin, Xiaotong -- Li, Jie -- Tan, Xiangshi -- Wang, Pengcheng -- Wang, Yinsheng -- Fang, Dong -- Cui, Qiang -- Yang, Pengyuan -- He, Chuan -- Jiang, Hualiang -- Luo, Cheng -- Xu, Yanhui -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Nov 5;527(7576):118-22. doi: 10.1038/nature15713. Epub 2015 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fudan University Shanghai Cancer Center, Institute of Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China. ; Key Laboratory of Molecular Medicine, Ministry of Education, Department of Systems Biology for Medicine, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China. ; State Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200433, China. ; Drug Discovery and Design Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China. ; Beijing Synchrotron Radiation Facility, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China. ; Laboratory of Structural Biology, Tsinghua University, Beijing 100084, China. ; MOE Laboratory of Protein Science, School of Medicine, Tsinghua University, Beijing 100084, China. ; Department of Chemistry, University of California-Riverside, Riverside, California 92521-0403, USA. ; Theoretical Chemistry Institute, Department of Chemistry, University of Wisconsin-Madison, 1101 University Avenue, Madison, Wisconsin 53706, USA. ; Department of Chemistry and Institute for Biophysical Dynamics, The University of Chicago, 929 East 57th Street, Chicago, Illinois 60637, USA. ; Howard Hughes Medical Institute, The University of Chicago, 929 East 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26524525" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Biocatalysis ; Catalytic Domain ; Crystallography, X-Ray ; Cytosine/analogs & derivatives/metabolism ; DNA/*chemistry/*metabolism ; DNA Methylation ; DNA-Binding Proteins/*chemistry/*metabolism ; Humans ; Hydrogen Bonding ; Models, Molecular ; Oxidation-Reduction ; Protein Binding ; Proto-Oncogene Proteins/*chemistry/*metabolism ; Substrate Specificity
    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: 2016-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhengshan -- Shojaee, Seyedmehdi -- Buchner, Maike -- Geng, Huimin -- Lee, Jae Woong -- Klemm, Lars -- Titz, Bjorn -- Graeber, Thomas G -- Park, Eugene -- Tan, Ying Xim -- Satterthwaite, Anne -- Paietta, Elisabeth -- Hunger, Stephen P -- Willman, Cheryl L -- Melnick, Ari -- Loh, Mignon L -- Jung, Jae U -- Coligan, John E -- Bolland, Silvia -- Mak, Tak W -- Limnander, Andre -- Jumaa, Hassan -- Reth, Michael -- Weiss, Arthur -- Lowell, Clifford A -- Muschen, Markus -- Nature. 2016 Mar 9. doi: 10.1038/nature16997.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958840" 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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  • 8
    Publication Date: 2012-12-22
    Description: Polyploidy often confers emergent properties, such as the higher fibre productivity and quality of tetraploid cottons than diploid cottons bred for the same environments. Here we show that an abrupt five- to sixfold ploidy increase approximately 60 million years (Myr) ago, and allopolyploidy reuniting divergent Gossypium genomes approximately 1-2 Myr ago, conferred about 30-36-fold duplication of ancestral angiosperm (flowering plant) genes in elite cottons (Gossypium hirsutum and Gossypium barbadense), genetic complexity equalled only by Brassica among sequenced angiosperms. Nascent fibre evolution, before allopolyploidy, is elucidated by comparison of spinnable-fibred Gossypium herbaceum A and non-spinnable Gossypium longicalyx F genomes to one another and the outgroup D genome of non-spinnable Gossypium raimondii. The sequence of a G. hirsutum A(t)D(t) (in which 't' indicates tetraploid) cultivar reveals many non-reciprocal DNA exchanges between subgenomes that may have contributed to phenotypic innovation and/or other emergent properties such as ecological adaptation by polyploids. Most DNA-level novelty in G. hirsutum recombines alleles from the D-genome progenitor native to its New World habitat and the Old World A-genome progenitor in which spinnable fibre evolved. Coordinated expression changes in proximal groups of functionally distinct genes, including a nuclear mitochondrial DNA block, may account for clusters of cotton-fibre quantitative trait loci affecting diverse traits. Opportunities abound for dissecting emergent properties of other polyploids, particularly angiosperms, by comparison to diploid progenitors and outgroups.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paterson, Andrew H -- Wendel, Jonathan F -- Gundlach, Heidrun -- Guo, Hui -- Jenkins, Jerry -- Jin, Dianchuan -- Llewellyn, Danny -- Showmaker, Kurtis C -- Shu, Shengqiang -- Udall, Joshua -- Yoo, Mi-jeong -- Byers, Robert -- Chen, Wei -- Doron-Faigenboim, Adi -- Duke, Mary V -- Gong, Lei -- Grimwood, Jane -- Grover, Corrinne -- Grupp, Kara -- Hu, Guanjing -- Lee, Tae-ho -- Li, Jingping -- Lin, Lifeng -- Liu, Tao -- Marler, Barry S -- Page, Justin T -- Roberts, Alison W -- Romanel, Elisson -- Sanders, William S -- Szadkowski, Emmanuel -- Tan, Xu -- Tang, Haibao -- Xu, Chunming -- Wang, Jinpeng -- Wang, Zining -- Zhang, Dong -- Zhang, Lan -- Ashrafi, Hamid -- Bedon, Frank -- Bowers, John E -- Brubaker, Curt L -- Chee, Peng W -- Das, Sayan -- Gingle, Alan R -- Haigler, Candace H -- Harker, David -- Hoffmann, Lucia V -- Hovav, Ran -- Jones, Donald C -- Lemke, Cornelia -- Mansoor, Shahid -- ur Rahman, Mehboob -- Rainville, Lisa N -- Rambani, Aditi -- Reddy, Umesh K -- Rong, Jun-kang -- Saranga, Yehoshua -- Scheffler, Brian E -- Scheffler, Jodi A -- Stelly, David M -- Triplett, Barbara A -- Van Deynze, Allen -- Vaslin, Maite F S -- Waghmare, Vijay N -- Walford, Sally A -- Wright, Robert J -- Zaki, Essam A -- Zhang, Tianzhen -- Dennis, Elizabeth S -- Mayer, Klaus F X -- Peterson, Daniel G -- Rokhsar, Daniel S -- Wang, Xiyin -- Schmutz, Jeremy -- England -- Nature. 2012 Dec 20;492(7429):423-7. doi: 10.1038/nature11798.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Genome Mapping Laboratory, University of Georgia, Athens, Georgia 30602, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23257886" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; *Biological Evolution ; Cacao/genetics ; Chromosomes, Plant/genetics ; *Cotton Fiber ; Diploidy ; Gene Duplication/genetics ; Genes, Plant/genetics ; Genome, Plant/*genetics ; Gossypium/classification/*genetics ; Molecular Sequence Annotation ; Phylogeny ; *Polyploidy ; Vitis/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2018-06-02
    Description: Clostridium acetobutylicum is a strict anaerobic, endospore-forming bacterium, which is used for the production of the high energy biofuel butanol in metabolic engineering. The life cycle of C. acetobutylicum can be divided into two phases, with acetic and butyric acids being produced in the exponential phase (acidogenesis) and butanol formed in the stationary phase (solventogenesis). During the transitional phase from acidogenesis to solventogenesis and latter stationary phase, concentration peaks of the metabolic intermediates butyryl phosphate and acetyl phosphate are observed. As an acyl group donor, acyl-phosphate chemically acylates protein substrates. However, the regulatory mechanism of lysine acetylation and butyrylation involved in the phenotype and solventogenesis of C. acetobutylicum remains unknown. In our study, we conducted quantitative analysis of protein acetylome and butyrylome to explore the dynamic change of lysine acetylation and butyrylation in the exponential phase, transitional phase, and stationary phase of C. acetobutylicum . Total 458 lysine acetylation sites and 1078 lysine butyrylation sites were identified in 254 and 373 substrates, respectively. Bioinformatics analysis uncovered the similarities and differences between the two acylation modifications in C. acetobutylicum . Mutation analysis of butyrate kinase and the central transcriptional factor Spo0A was performed to characterize the unique role of lysine butyrylation in the metabolic pathway and sporulation process of C. acetobutylicum . Moreover, quantitative proteomic assays were performed to reveal the relationship between protein features ( e.g. gene expression level and lysine acylation level) and metabolites in the three growth stages. This study expanded our knowledge of lysine acetylation and butyrylation in Clostridia and constituted a resource for functional studies on lysine acylation in bacteria.
    Print ISSN: 1535-9476
    Electronic ISSN: 1535-9484
    Topics: Biology , Medicine
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  • 10
    Publication Date: 2018-03-17
    Description: Objective General practitioners (GPs) are highly underutilised in China with many patients going directly to hospitals when seeking routine care. Multiple countries around the world have successfully used GPs in routine care, and as such, China may benefit from the use of GPs. This study examines the status of, and factors associated with, knowledge related to GPs among outpatient populations from China’s tertiary hospitals. Design This is a cross-sectional survey study. Study setting and participants The questionnaires were completed by 565 outpatients from four tertiary hospitals in China during 2016. Convenience sampling on different floors and throughout the outpatient building was carried out. Primary outcome measures We used the logistic regression models to identify GP-related knowledge among different populations. Results Overall, 50.27% of respondents said they had never heard of GPs. This was also true among females (adjusted OR (AOR)=1.57, 95% CI 1.43 to 2.71), older adults (AOR 46–65 =1.61, 95% CI 1.39 to 2.98; AOR 〉65 =2.01, 95% CI 1.62 to 3.59), those with lower education level (AOR Bachelor’s degree =0.61, 95% CI 0.20 to 0.81; AOR ≥Master’s degree =0.49, 95% CI 0.23 to 0.76), rural residents (AOR=1.51, 95% CI 1.35 to 2.82) and those with chronic disease (AOR without chronic disease =0.61, 95% CI 0.22 to 0.71). What is more, less than one-in-ten (9.03%) outpatients were able to accurately describe what a GP was, with less than 30% accurately describing a GP among those receiving GPs’ services. Conclusions Outpatients who could have received less costly health services from GPs in primary medical institutions were more likely to choose costlier specialist physicians in tertiary hospitals, which is likely linked to limited knowledge about GPs. Policy makers should invest in outreach efforts to improve public awareness of GPs, while at the same time conducting continued surveillance of these efforts to evaluate progress towards this goal.
    Keywords: Open access, Health policy
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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