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  • 1
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    Virus attenuation by genome-scale changes in codon pair bias (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-28
    Description: As a result of the redundancy of the genetic code, adjacent pairs of amino acids can be encoded by as many as 36 different pairs of synonymous codons. A species-specific "codon pair bias" provides that some synonymous codon pairs are used more or less frequently than statistically predicted. We synthesized de novo large DNA molecules using hundreds of over-or underrepresented synonymous codon pairs to encode the poliovirus capsid protein. Underrepresented codon pairs caused decreased rates of protein translation, and polioviruses containing such amino acid-independent changes were attenuated in mice. Polioviruses thus customized were used to immunize mice and provided protective immunity after challenge. This "death by a thousand cuts" strategy could be generally applicable to attenuating many kinds of viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754401/" 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/PMC2754401/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coleman, J Robert -- Papamichail, Dimitris -- Skiena, Steven -- Futcher, Bruce -- Wimmer, Eckard -- Mueller, Steffen -- AI075219/AI/NIAID NIH HHS/ -- AI15122/AI/NIAID NIH HHS/ -- R01 AI075219/AI/NIAID NIH HHS/ -- R01 AI075219-01A1/AI/NIAID NIH HHS/ -- R37 AI015122/AI/NIAID NIH HHS/ -- R37 AI015122-34/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1784-7. doi: 10.1126/science.1155761.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18583614" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Antibodies, Viral/biosynthesis ; Capsid Proteins/*genetics ; Cloning, Molecular ; *Codon ; Cytopathogenic Effect, Viral ; *Genome, Viral ; HeLa Cells ; Hot Temperature ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Poliomyelitis/immunology/virology ; Poliovirus/*genetics/growth & development/immunology/*pathogenicity ; *Poliovirus Vaccines/genetics/immunology ; Protein Biosynthesis ; Vaccination ; Vaccines, Attenuated/genetics/immunology ; Viral Plaque Assay ; Virulence
    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
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    Circadian rhythm of redox state regulates excitability in suprachiasmatic nucleus neurons (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: Daily rhythms of mammalian physiology, metabolism, and behavior parallel the day-night cycle. They are orchestrated by a central circadian clock in the brain, the suprachiasmatic nucleus (SCN). Transcription of clock genes is sensitive to metabolic changes in reduction and oxidation (redox); however, circadian cycles in protein oxidation have been reported in anucleate cells, where no transcription occurs. We investigated whether the SCN also expresses redox cycles and how such metabolic oscillations might affect neuronal physiology. We detected self-sustained circadian rhythms of SCN redox state that required the molecular clockwork. The redox oscillation could determine the excitability of SCN neurons through nontranscriptional modulation of multiple potassium (K(+)) channels. Thus, dynamic regulation of SCN excitability appears to be closely tied to metabolism that engages the clockwork machinery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3490628/" 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/PMC3490628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Tongfei A -- Yu, Yanxun V -- Govindaiah, Gubbi -- Ye, Xiaoying -- Artinian, Liana -- Coleman, Todd P -- Sweedler, Jonathan V -- Cox, Charles L -- Gillette, Martha U -- EY014024/EY/NEI NIH HHS/ -- P30 DA018310/DA/NIDA NIH HHS/ -- P30DA018310/DA/NIDA NIH HHS/ -- R01 EY014024/EY/NEI NIH HHS/ -- R01 HL086870/HL/NHLBI NIH HHS/ -- R01 HL092571/HL/NHLBI NIH HHS/ -- R01HL086870/HL/NHLBI NIH HHS/ -- R01HL092571/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):839-42. doi: 10.1126/science.1222826. Epub 2012 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859819" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics ; Animals ; *Circadian Rhythm ; Fluorometry ; Glutathione/metabolism ; Membrane Potentials ; Mice ; Mice, Mutant Strains ; NADP/metabolism ; Neurons/metabolism/*physiology ; Oxidation-Reduction ; Potassium Channels/metabolism ; Rats ; Suprachiasmatic Nucleus/cytology/metabolism/*physiology
    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
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    dSarm/Sarm1 is required for activation of an injury-induced axon death pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-09
    Description: Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile alpha/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterloh, Jeannette M -- Yang, Jing -- Rooney, Timothy M -- Fox, A Nicole -- Adalbert, Robert -- Powell, Eric H -- Sheehan, Amy E -- Avery, Michelle A -- Hackett, Rachel -- Logan, Mary A -- MacDonald, Jennifer M -- Ziegenfuss, Jennifer S -- Milde, Stefan -- Hou, Ying-Ju -- Nathan, Carl -- Ding, Aihao -- Brown, Robert H Jr -- Conforti, Laura -- Coleman, Michael -- Tessier-Lavigne, Marc -- Zuchner, Stephan -- Freeman, Marc R -- 5R01-NS050557-05/NS/NINDS NIH HHS/ -- AI030165/AI/NIAID NIH HHS/ -- R01NS059991/NS/NINDS NIH HHS/ -- R01NS072248/NS/NINDS NIH HHS/ -- RC2-NS070-342/NS/NINDS NIH HHS/ -- U54NS065712/NS/NINDS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):481-4. doi: 10.1126/science.1223899. Epub 2012 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis ; Armadillo Domain Proteins/analysis/*genetics/*physiology ; Axons/*physiology/ultrastructure ; Axotomy ; Cell Survival ; Cells, Cultured ; Cytoskeletal Proteins/analysis/*genetics/*physiology ; Denervation ; Drosophila/embryology/genetics/physiology ; Drosophila Proteins/analysis/*genetics/*physiology ; Mice ; Mutation ; Neurons/*physiology ; Sciatic Nerve/injuries/physiology ; Signal Transduction ; Superior Cervical Ganglion/cytology ; Tissue Culture Techniques ; *Wallerian Degeneration
    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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  • 4
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    Derivatives of erythropoietin that are tissue protective but not erythropoietic (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Erythropoietin (EPO) is both hematopoietic and tissue protective, putatively through interaction with different receptors. We generated receptor subtype-selective ligands allowing the separation of EPO's bioactivities at the cellular level and in animals. Carbamylated EPO (CEPO) or certain EPO mutants did not bind to the classical EPO receptor (EPOR) and did not show any hematopoietic activity in human cell signaling assays or upon chronic dosing in different animal species. Nevertheless, CEPO and various nonhematopoietic mutants were cytoprotective in vitro and conferred neuroprotection against stroke, spinal cord compression, diabetic neuropathy, and experimental autoimmune encephalomyelitis at a potency and efficacy comparable to EPO.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leist, Marcel -- Ghezzi, Pietro -- Grasso, Giovanni -- Bianchi, Roberto -- Villa, Pia -- Fratelli, Maddalena -- Savino, Costanza -- Bianchi, Marina -- Nielsen, Jacob -- Gerwien, Jens -- Kallunki, Pekka -- Larsen, Anna Kirstine -- Helboe, Lone -- Christensen, Soren -- Pedersen, Lars O -- Nielsen, Mette -- Torup, Lars -- Sager, Thomas -- Sfacteria, Alessandra -- Erbayraktar, Serhat -- Erbayraktar, Zubeyde -- Gokmen, Necati -- Yilmaz, Osman -- Cerami-Hand, Carla -- Xie, Qiao-Wen -- Coleman, Thomas -- Cerami, Anthony -- Brines, Michael -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉H. Lundbeck A/S, 2500 Valby, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Binding Sites ; Cells, Cultured ; Diabetic Neuropathies/drug therapy ; Drug Design ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Erythropoiesis ; Erythropoietin/*analogs & ; derivatives/chemistry/genetics/metabolism/pharmacology/*therapeutic use ; Female ; Hematocrit ; Humans ; Ligands ; Mice ; Mice, Inbred C3H ; Mutagenesis ; Nervous System Diseases/*drug therapy ; Neurons/metabolism ; Neuroprotective Agents/chemistry/metabolism/pharmacology/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Receptors, Erythropoietin/metabolism ; Recombinant Proteins ; Signal Transduction ; Spinal Cord Compression/drug therapy ; Stroke/drug therapy ; Structure-Activity Relationship
    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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  • 5
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    Dynamic regulatory network controlling TH17 cell differentiation (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-08
    Description: Despite their importance, the molecular circuits that control the differentiation of naive T cells remain largely unknown. Recent studies that reconstructed regulatory networks in mammalian cells have focused on short-term responses and relied on perturbation-based approaches that cannot be readily applied to primary T cells. Here we combine transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based perturbation tools to systematically derive and experimentally validate a model of the dynamic regulatory network that controls the differentiation of mouse TH17 cells, a proinflammatory T-cell subset that has been implicated in the pathogenesis of multiple autoimmune diseases. The TH17 transcriptional network consists of two self-reinforcing, but mutually antagonistic, modules, with 12 novel regulators, the coupled action of which may be essential for maintaining the balance between TH17 and other CD4(+) T-cell subsets. Our study identifies and validates 39 regulatory factors, embeds them within a comprehensive temporal network and reveals its organizational principles; it also highlights novel drug targets for controlling TH17 cell differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637864/" 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/PMC3637864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yosef, Nir -- Shalek, Alex K -- Gaublomme, Jellert T -- Jin, Hulin -- Lee, Youjin -- Awasthi, Amit -- Wu, Chuan -- Karwacz, Katarzyna -- Xiao, Sheng -- Jorgolli, Marsela -- Gennert, David -- Satija, Rahul -- Shakya, Arvind -- Lu, Diana Y -- Trombetta, John J -- Pillai, Meenu R -- Ratcliffe, Peter J -- Coleman, Mathew L -- Bix, Mark -- Tantin, Dean -- Park, Hongkun -- Kuchroo, Vijay K -- Regev, Aviv -- 1P50HG006193-01/HG/NHGRI NIH HHS/ -- 5DP1OD003893-03/OD/NIH HHS/ -- AI073748/AI/NIAID NIH HHS/ -- AI45757/AI/NIAID NIH HHS/ -- DP1 OD003893/OD/NIH HHS/ -- DP1 OD003958/OD/NIH HHS/ -- DP1OD003958-01/OD/NIH HHS/ -- F32 HD075541/HD/NICHD NIH HHS/ -- K01 DK090105/DK/NIDDK NIH HHS/ -- NS 30843/NS/NINDS NIH HHS/ -- NS045937/NS/NINDS NIH HHS/ -- P01 AI045757/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P50 HG006193/HG/NHGRI NIH HHS/ -- R01 AI100873/AI/NIAID NIH HHS/ -- R01 NS030843/NS/NINDS NIH HHS/ -- R01 NS045937/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 25;496(7446):461-8. doi: 10.1038/nature11981. Epub 2013 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23467089" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; Cell Differentiation/*genetics ; Cells, Cultured ; DNA/genetics/metabolism ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; Gene Regulatory Networks/*genetics ; Genome/genetics ; Interferon-gamma/biosynthesis ; Interleukin-2/genetics ; Mice ; Mice, Inbred C57BL ; Nanowires ; Neoplasm Proteins/metabolism ; Nuclear Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Reproducibility of Results ; Silicon ; Th17 Cells/*cytology/immunology/*metabolism ; Time Factors ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic/genetics
    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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  • 6
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    Activated ClpP kills persisters and eradicates a chronic biofilm infection (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-15
    Description: Chronic infections are difficult to treat with antibiotics but are caused primarily by drug-sensitive pathogens. Dormant persister cells that are tolerant to killing by antibiotics are responsible for this apparent paradox. Persisters are phenotypic variants of normal cells and pathways leading to dormancy are redundant, making it challenging to develop anti-persister compounds. Biofilms shield persisters from the immune system, suggesting that an antibiotic for treating a chronic infection should be able to eradicate the infection on its own. We reasoned that a compound capable of corrupting a target in dormant cells will kill persisters. The acyldepsipeptide antibiotic (ADEP4) has been shown to activate the ClpP protease, resulting in death of growing cells. Here we show that ADEP4-activated ClpP becomes a fairly nonspecific protease and kills persisters by degrading over 400 proteins, forcing cells to self-digest. Null mutants of clpP arise with high probability, but combining ADEP4 with rifampicin produced complete eradication of Staphylococcus aureus biofilms in vitro and in a mouse model of a chronic infection. Our findings indicate a general principle for killing dormant cells-activation and corruption of a target, rather than conventional inhibition. Eradication of a biofilm in an animal model by activating a protease suggests a realistic path towards developing therapies to treat chronic infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031760/" 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/PMC4031760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conlon, B P -- Nakayasu, E S -- Fleck, L E -- LaFleur, M D -- Isabella, V M -- Coleman, K -- Leonard, S N -- Smith, R D -- Adkins, J N -- Lewis, K -- P41 GM103493/GM/NIGMS NIH HHS/ -- P41 GM103493-11/GM/NIGMS NIH HHS/ -- R01 AI085585/AI/NIAID NIH HHS/ -- T-R01AI085585/AI/NIAID NIH HHS/ -- Y1-AI-8401/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Nov 21;503(7476):365-70. doi: 10.1038/nature12790. Epub 2013 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Antimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24226776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*pharmacology ; Bacterial Proteins/metabolism ; Biofilms/*drug effects/*growth & development ; Depsipeptides/pharmacology ; Drug Resistance, Bacterial/drug effects ; Enzyme Activation/drug effects ; Female ; Mice ; Microbial Viability/drug effects ; Proteolysis/*drug effects ; Proteomics ; Rifampin/pharmacology ; Serine Endopeptidases/*metabolism ; Staphylococcal Infections/drug therapy/microbiology ; Staphylococcus aureus/classification/*drug effects/*enzymology/metabolism
    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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  • 7
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    Diabetic mouse incorrectly typed (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prochazka, M -- Leiter, E H -- Serreze, D V -- Coleman, D L -- Jackson, R A -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):945.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; DNA/genetics ; Diabetes Mellitus, Type 1/*genetics ; *Genes, Recessive ; Major Histocompatibility Complex ; Mice ; Recombination, Genetic
    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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    Obesity genes: beneficial effects in heterozygous mice (1979)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1979-02-16
    Description: The mouse mutant genes obese (ob) and diabetes (db) cause similar obesity-diabetes states in homozygotes. These obesity syndromes are characterized by a more efficient conversion of food to lipid and, once stored, a slower rate of catabolism on fasting. Heterozygous mice, either ob/+ or db/+, survived a prolonged fast significantly longer than normal homozygotes (+/+); this suggests that the heterozygotes exhibited increased metabolic efficiency, a feature normally associated with both homozygous mutants. The existence of this thriftiness trait, if manifested by heterozygous carriers in wild populations, would lend credence to the thrifty gene concept of diabetes. Beneficial effects of normally deleterious genes may have played a role in the development of diabetes-susceptible human populations, as well as having provided the survival advantage that has allowed both the development and successful establishment of species in desert and other less affluent regions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coleman, D L -- New York, N.Y. -- Science. 1979 Feb 16;203(4381):663-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/760211" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Temperature Regulation ; Diabetes Mellitus, Experimental/*genetics/metabolism ; Fasting ; Glucose/metabolism ; Heterozygote ; Insulin/blood ; Mice ; Mice, Obese/*genetics
    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
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    Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: A polygenic basis for susceptibility to insulin-dependent diabetes in nonobese diabetic (NOD) mice has been established by outcross to a related inbred strain, nonobese normal (NON). Analysis of first and second backcross progeny has shown that at least three recessive genes are required for development of overt diabetes. One, Idd-1s, is tightly linked to the H-2K locus on chromosome 17; another, Idd-2s, is localized proximal to the Thy-1/Alp-1 cluster on chromosome 9. Segregation of a third, Idd-3s, could be shown in a second backcross. Neither Idd-1s nor Idd-2s could individually be identified as the locus controlling insulitis; leukocytic infiltrates in pancreas were common in most asymptomatic BC1 mice. Both F1 and BC1 mice exhibited the unusually high percentage of splenic T lymphocytes characteristic of NOD, suggesting dominant inheritance of this trait. The polygenic control of diabetogenesis in NOD mice, in which a recessive gene linked to the major histocompatibility complex is but one of several controlling loci, suggests that similar polygenic interactions underlie this type of diabetes in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prochazka, M -- Leiter, E H -- Serreze, D V -- Coleman, D L -- AM 14461/AM/NIADDK NIH HHS/ -- AM 27722/AM/NIADDK NIH HHS/ -- AM 36175/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Diabetes Mellitus, Type 1/*genetics/immunology ; *Genes, Recessive ; Islets of Langerhans/immunology ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; T-Lymphocytes/physiology
    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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  • 10
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    Radioimmunotherapy with alpha-particle-emitting immunoconjugates (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-05-20
    Description: Alpha particles are energetic short-range ions whose higher linear energy transfer produces extreme cytotoxicity. An alpha-particle-emitting radioimmunoconjugate consisting of a bismuth-212-labeled monoclonal immunoglobulin M specific for the murine T cell/neuroectodermal surface antigen Thy 1.2 was prepared. Analysis in vitro showed that the radioimmunoconjugate was selectively cytotoxic to a Thy 1.2+ EL-4 murine tumor cell line. Approximately three bismuth-212-labeled immunoconjugates per target cell reduced the uptake of [3H]thymidine by the EL-4 target cells to background levels. Mice inoculated intraperitoneally with EL-4 cells were cured of their ascites after intraperitoneal injection of 150 microcuries of the antigen-specific radioimmunoconjugate, suggesting a possible role for such conjugates in intracavitary cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macklis, R M -- Kinsey, B M -- Kassis, A I -- Ferrara, J L -- Atcher, R W -- Hines, J J -- Coleman, C N -- Adelstein, S J -- Burakoff, S J -- 5 PO1-CA39542-03/CA/NCI NIH HHS/ -- 5T32 CA 09536-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 May 20;240(4855):1024-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Center for Radiation Therapy, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897133" target="_blank"〉PubMed〈/a〉
    Keywords: *Alpha Particles ; Animals ; *Antigens, Surface ; Antigens, Thy-1 ; Bismuth/therapeutic use ; *Immunoglobulin M ; Immunotherapy ; Lymphoma/*radiotherapy ; Mice ; Mice, Inbred C57BL ; Radioisotopes/therapeutic use
    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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