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  • 1
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    Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-01-28
    Description: Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma. However, colon cancer patients harbouring the same BRAF(V600E) oncogenic lesion have poor prognosis and show only a very limited response to this drug. To investigate the cause of the limited therapeutic effect of PLX4032 in BRAF(V600E) mutant colon tumours, here we performed an RNA-interference-based genetic screen in human cells to search for kinases whose knockdown synergizes with BRAF(V600E) inhibition. We report that blockade of the epidermal growth factor receptor (EGFR) shows strong synergy with BRAF(V600E) inhibition. We find in multiple BRAF(V600E) mutant colon cancers that inhibition of EGFR by the antibody drug cetuximab or the small-molecule drugs gefitinib or erlotinib is strongly synergistic with BRAF(V600E) inhibition, both in vitro and in vivo. Mechanistically, we find that BRAF(V600E) inhibition causes a rapid feedback activation of EGFR, which supports continued proliferation in the presence of BRAF(V600E) inhibition. Melanoma cells express low levels of EGFR and are therefore not subject to this feedback activation. Consistent with this, we find that ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032. Our data suggest that BRAF(V600E) mutant colon cancers (approximately 8-10% of all colon cancers), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prahallad, Anirudh -- Sun, Chong -- Huang, Sidong -- Di Nicolantonio, Federica -- Salazar, Ramon -- Zecchin, Davide -- Beijersbergen, Roderick L -- Bardelli, Alberto -- Bernards, Rene -- England -- Nature. 2012 Jan 26;483(7387):100-3. doi: 10.1038/nature10868.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Carcinogenesis, Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22281684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents/pharmacology/therapeutic use ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cetuximab ; Colorectal Neoplasms/*drug therapy/*enzymology/genetics/pathology ; Drug Resistance, Neoplasm/*drug effects ; Drug Synergism ; Enzyme Activation/drug effects ; Erlotinib Hydrochloride ; Feedback, Physiological/*drug effects ; Female ; HEK293 Cells ; Humans ; Indoles/pharmacology/therapeutic use ; Melanoma/drug therapy/metabolism ; Mice ; Protein Kinase Inhibitors/pharmacology/therapeutic use ; Proto-Oncogene Proteins B-raf/*antagonists & ; inhibitors/chemistry/*genetics/metabolism ; Quinazolines/pharmacology/therapeutic use ; RNA Interference ; Receptor, Epidermal Growth Factor/*agonists/antagonists & inhibitors/metabolism ; Sulfonamides/pharmacology/therapeutic use ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Structural insight into substrate preference for TET-mediated oxidation (2015)
    Nature Publishing Group (NPG)
    Details
    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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  • 3
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    OTUD7B controls non-canonical NF-kappaB activation through deubiquitination of TRAF3 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-01-22
    Description: The non-canonical NF-kappaB pathway forms a major arm of NF-kappaB signalling that mediates important biological functions, including lymphoid organogenesis, B-lymphocyte function, and cell growth and survival. Activation of the non-canonical NF-kappaB pathway involves degradation of an inhibitory protein, TNF receptor-associated factor 3 (TRAF3), but how this signalling event is controlled is still unknown. Here we have identified the deubiquitinase OTUD7B as a pivotal regulator of the non-canonical NF-kappaB pathway. OTUD7B deficiency in mice has no appreciable effect on canonical NF-kappaB activation but causes hyperactivation of non-canonical NF-kappaB. In response to non-canonical NF-kappaB stimuli, OTUD7B binds and deubiquitinates TRAF3, thereby inhibiting TRAF3 proteolysis and preventing aberrant non-canonical NF-kappaB activation. Consequently, the OTUD7B deficiency results in B-cell hyper-responsiveness to antigens, lymphoid follicular hyperplasia in the intestinal mucosa, and elevated host-defence ability against an intestinal bacterial pathogen, Citrobacter rodentium. These findings establish OTUD7B as a crucial regulator of signal-induced non-canonical NF-kappaB activation and indicate a mechanism of immune regulation that involves OTUD7B-mediated deubiquitination and stabilization of TRAF3.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578967/" 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/PMC3578967/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Hongbo -- Brittain, George C -- Chang, Jae-Hoon -- Puebla-Osorio, Nahum -- Jin, Jin -- Zal, Anna -- Xiao, Yichuan -- Cheng, Xuhong -- Chang, Mikyoung -- Fu, Yang-Xin -- Zal, Tomasz -- Zhu, Chengming -- Sun, Shao-Cong -- AI057555/AI/NIAID NIH HHS/ -- AI064639/AI/NIAID NIH HHS/ -- CA137059/CA/NCI NIH HHS/ -- GM84459/GM/NIGMS NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA137059/CA/NCI NIH HHS/ -- R01 GM084459/GM/NIGMS NIH HHS/ -- T32 CA009598/CA/NCI NIH HHS/ -- T32CA009598/CA/NCI NIH HHS/ -- England -- Nature. 2013 Feb 21;494(7437):371-4. doi: 10.1038/nature11831. Epub 2013 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/metabolism ; Bacteria/immunology ; Cells, Cultured ; Endopeptidases/deficiency/genetics/*metabolism ; Female ; Fibroblasts ; HEK293 Cells ; Homeostasis ; Humans ; Intestines/immunology ; Male ; Mice ; NF-kappa B/*metabolism ; Proteolysis ; Receptors, Cell Surface/metabolism ; TNF Receptor-Associated Factor 3/*metabolism ; *Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably. In contrast, colon cancers that harbour the same BRAF(V600E) mutation are intrinsically resistant to BRAF inhibitors, due to feedback activation of the epidermal growth factor receptor (EGFR). Here we show that 6 out of 16 melanoma tumours analysed acquired EGFR expression after the development of resistance to BRAF or MEK inhibitors. Using a chromatin-regulator-focused short hairpin RNA (shRNA) library, we find that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes activation of TGF-beta signalling, thus leading to upregulation of EGFR and platelet-derived growth factor receptor-beta (PDGFRB), which confer resistance to BRAF and MEK inhibitors. Expression of EGFR in melanoma or treatment with TGF-beta results in a slow-growth phenotype with cells displaying hallmarks of oncogene-induced senescence. However, EGFR expression or exposure to TGF-beta becomes beneficial for proliferation in the presence of BRAF or MEK inhibitors. In a heterogeneous population of melanoma cells having varying levels of SOX10 suppression, cells with low SOX10 and consequently high EGFR expression are rapidly enriched in the presence of drug, but this is reversed when the drug treatment is discontinued. We find evidence for SOX10 loss and/or activation of TGF-beta signalling in 4 of the 6 EGFR-positive drug-resistant melanoma patient samples. Our findings provide a rationale for why some BRAF or MEK inhibitor-resistant melanoma patients may regain sensitivity to these drugs after a 'drug holiday' and identify patients with EGFR-positive melanoma as a group that may benefit from re-treatment after a drug holiday.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Chong -- Wang, Liqin -- Huang, Sidong -- Heynen, Guus J J E -- Prahallad, Anirudh -- Robert, Caroline -- Haanen, John -- Blank, Christian -- Wesseling, Jelle -- Willems, Stefan M -- Zecchin, Davide -- Hobor, Sebastijan -- Bajpe, Prashanth K -- Lieftink, Cor -- Mateus, Christina -- Vagner, Stephan -- Grernrum, Wipawadee -- Hofland, Ingrid -- Schlicker, Andreas -- Wessels, Lodewyk F A -- Beijersbergen, Roderick L -- Bardelli, Alberto -- Di Nicolantonio, Federica -- Eggermont, Alexander M M -- Bernards, Rene -- MOP-130540/Canadian Institutes of Health Research/Canada -- England -- Nature. 2014 Apr 3;508(7494):118-22. doi: 10.1038/nature13121. Epub 2014 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Molecular Carcinogenesis, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands [2]. ; 1] Division of Molecular Carcinogenesis, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands [2] Department of Biochemistry, The Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, Quebec H3G 1Y6, Canada [3]. ; Division of Molecular Carcinogenesis, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. ; Institut Gustave Roussy, 114 Rue Edouard Vaillant, 94800 Villejuif, France. ; Division of Medical Oncology, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. ; Division of Pathology, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. ; 1] Division of Molecular Carcinogenesis, Cancer Systems Biology Centre and Cancer Genomics Centre Netherlands, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands [2] Department of Pathology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands. ; 1] University of Torino, Department of Oncology, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy [2] Candiolo Cancer Institute - FPO, IRCCS, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy. ; Candiolo Cancer Institute - FPO, IRCCS, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy. ; 1] University of Torino, Department of Oncology, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy [2] Candiolo Cancer Institute - FPO, IRCCS, Str prov 142 Km 3.95, 10060 Candiolo, Torino, Italy [3] FIRC Institute of Molecular Oncology (IFOM), 20139 Milano, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*administration & dosage/*pharmacology ; Cell Aging/drug effects ; Cell Proliferation/drug effects ; Drug Resistance, Neoplasm/drug effects/genetics ; Female ; Flow Cytometry ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Library ; Humans ; Indoles/administration & dosage/pharmacology ; Melanoma/*drug therapy/enzymology/genetics/pathology ; Mice ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Protein Kinase Inhibitors/*administration & dosage/*pharmacology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors/*genetics/metabolism ; RNA, Small Interfering ; Receptor Protein-Tyrosine Kinases/biosynthesis/genetics/metabolism ; Receptor, Epidermal Growth Factor/biosynthesis/genetics/metabolism ; Receptor, Platelet-Derived Growth Factor beta/biosynthesis/genetics/metabolism ; SOXE Transcription Factors/deficiency/genetics ; Signal Transduction/drug effects ; Sulfonamides/administration & dosage/pharmacology ; Transforming Growth Factor beta/metabolism/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    NF-kappa B controls expression of inhibitor I kappa B alpha: evidence for an inducible autoregulatory pathway (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: The eukaryotic transcription factor nuclear factor-kappa B (NF-kappa B) participates in many parts of the genetic program mediating T lymphocyte activation and growth. Nuclear expression of NF-kappa B occurs after its induced dissociation from its cytoplasmic inhibitor I kappa B alpha. Phorbol ester and tumor necrosis factor-alpha induction of nuclear NF-kappa B is associated with both the degradation of performed I kappa B alpha and the activation of I kappa B alpha gene expression. Transfection studies indicate that the I kappa B alpha gene is specifically induced by the 65-kilodalton transactivating subunit of NF-kappa B. Association of the newly synthesized I kappa B alpha with p65 restores intracellular inhibition of NF-kappa B DNA binding activity and prolongs the survival of this labile inhibitor. Together, these results show that NF-kappa B controls the expression of I kappa B alpha by means of an inducible autoregulatory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, S C -- Ganchi, P A -- Ballard, D W -- Greene, W C -- 5T32CA09111/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1912-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096091" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cycloheximide/pharmacology ; Cytoplasm/metabolism ; DNA/metabolism ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Humans ; *I-kappa B Proteins ; Immunoblotting ; Kinetics ; Molecular Weight ; Mutagenesis ; NF-kappa B/*antagonists & inhibitors/genetics/*physiology ; RNA, Messenger/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators/pharmacology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Comment on "Reconstructing the origin of Andaman islanders" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: On the basis of mitochondrial DNA sequence analyses, Thangaraj et al. (Brevia, 13 May 2005, p. 996) proposed that Andaman islanders descended from the first humans to migrate out of Africa. We identified mitochondrial DNA from two northeast Indian Rajbanshi individuals that shares three specific mutations with the M31a lineage observed in the Great Andamanese, which suggests that the predecessor of haplogroup M31 originated on the Indian subcontinent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palanichamy, Malliya Gounder -- Agrawal, Suraksha -- Yao, Yong-Gang -- Kong, Qing-Peng -- Sun, Chang -- Khan, Faisal -- Chaudhuri, Tapas Kumar -- Zhang, Ya-Ping -- New York, N.Y. -- Science. 2006 Jan 27;311(5760):470; author reply 470.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Conservation and Utilization of Bio-resource, Yunnan University, Kunming 650091, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439647" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Asia ; DNA, Mitochondrial/*genetics ; Emigration and Immigration ; Ethnic Groups/*genetics ; Genetics, Population ; Geography ; *Haplotypes ; Humans ; India ; Mutation ; Phylogeny
    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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  • 7
    Electronic Resource
    Electronic Resource
    Tracer diffusion of aromatic hydrocarbons in liquid cyclohexane up to its critical temperature (1985)
    Hoboken, NJ : Wiley-Blackwell
    AIChE Journal 31 (1985), S. 1510-1515 
    Details
    ISSN: 0001-1541
    Keywords: Chemistry ; Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Tracer diffusion coefficients in liquid cyclohexane of benzene, toluene, p-xylene, mesitylene, naphthalene, and phenanthrene have been determined from 298.2 to 523.2 K (TR = 0.54 ∼ 0.95) using the Taylor dispersion method. Positive deviations from the Arrhenius relationship are observed as the critical temperature is approached, but a rough-hard-sphere theory is found to be adequate for describing the data across the entire temperature range. On the basis of the computer simulation results for hard-sphere fluids, correlations involving solute and solvent critical volumes and their molecular weights have also been developed for practical applications. Tracer diffusivities in supercritical carbon dioxide are also adequately represented by the proposed correlation, as the fluid density is not far removed from that of liquid carbon dioxide.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aic.690310914
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  • 8
    Electronic Resource
    Electronic Resource
    Diffusion of benzene, toluene, naphthalene, and phenanthrene in supercritical dense 2,3-dimethylbutane (1985)
    Hoboken, NJ : Wiley-Blackwell
    AIChE Journal 31 (1985), S. 1904-1910 
    Details
    ISSN: 0001-1541
    Keywords: Chemistry ; Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: The conditions under which the Taylor-Aris dispersion phenomenon can be employed to generate accurate tracer diffusion data in supercritical dense fluids are established. The technique is used to determine the diffusivities of benzene, toluene, naphthalene, and phenanthrene in supercritical dense 2,3-dimethylbutane as a function of temperature and pressure. A molecular theory incorporating the Sung-Stell formulation of molecular dynamic correlations in smooth-hardsphere fluids and the Baleiko-Davis molecular roughness for polyatomics with the Enskog-Thorne dense gas diffusivity relationship is found to represent our experimental data to within ±4%. The values of the effective hard-sphere diameters involved in the present theory can be predicted fairly accurately from the critical volumes of the solutes and solvent considered here.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aic.690311115
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  • 9
    Electronic Resource
    Electronic Resource
    Tracer diffusion in dense ethanol: A generalized correlation for nonpolar and hydrogen-bonded solvents (1986)
    Hoboken, NJ : Wiley-Blackwell
    AIChE Journal 32 (1986), S. 1367-1371 
    Details
    ISSN: 0001-1541
    Keywords: Chemistry ; Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Tracer diffusion coefficients were measured for benzene, toluene, mesitylene, naphthalene, and phenanthrene in dense ethanol at 0.56 ≤ TR ≤ 1.07 and ρR ≥ 1.44. The results were used to examine the temperature dependence of the degree of association between ethanol molecules across the entire range of temperature. The hard-sphere tracer diffusion equation and the Stokes-Einstein equation were used to develop two engineering correlations. The former approach was found to be adequate for solvents of relatively compact molecules, and the latter to be more general in its applications. The absolute deviation of prediction from observed values of tracer diffusivities is 4%, with a maximum error of 13%.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aic.690320814
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  • 10
    Electronic Resource
    Electronic Resource
    Mechanical characterization of sheet molding compound composites (1983)
    Brookfield, Conn. : Wiley-Blackwell
    Polymer Composites 4 (1983), S. 167-171 
    Details
    ISSN: 0272-8397
    Keywords: Chemistry ; Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: The present work was aimed at providing basic mechanical property characterization of five different sheet molding compound (SMC) materials with glass content varying from 30 to 65 percent by weight. In particular, the objectives were to find variation in their tensile, flexural, and shear properties along with some information on fabrication-induced anisotropy that may be present in these materials. The flexural properties were measured using three-point bend tests, and double-rail shear tests were conducted for in-plane shear properties. A significant scatter was observed in all the properties, and no conclusive evidence about the fabrication-induced anisotropy was found, Flexural strength of each material was found to be significantly greater than the tensile strength. Finally, some interesting features associated with their tensile and flexural failure modes have also been discussed.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/pc.750040306
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