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  • Articles  (48)
  • Male  (48)
  • 2000-2004  (48)
  • 1990-1994
  • 2003  (48)
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  • Articles  (48)
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  • 2000-2004  (48)
  • 1990-1994
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  • 1
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    Inferring nonneutral evolution from human-chimp-mouse orthologous gene trios (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
    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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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    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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    Does rejection hurt? An FMRI study of social exclusion (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-11
    Description: A neuroimaging study examined the neural correlates of social exclusion and tested the hypothesis that the brain bases of social pain are similar to those of physical pain. Participants were scanned while playing a virtual ball-tossing game in which they were ultimately excluded. Paralleling results from physical pain studies, the anterior cingulate cortex (ACC) was more active during exclusion than during inclusion and correlated positively with self-reported distress. Right ventral prefrontal cortex (RVPFC) was active during exclusion and correlated negatively with self-reported distress. ACC changes mediated the RVPFC-distress correlation, suggesting that RVPFC regulates the distress of social exclusion by disrupting ACC activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenberger, Naomi I -- Lieberman, Matthew D -- Williams, Kipling D -- R21MH66709-01/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):290-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Franz Hall, University of California, Los Angeles, Los Angeles, CA 90095-1563, USA. neisenbe@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14551436" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Mapping ; *Emotions ; Female ; Gyrus Cinguli/*physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; Prefrontal Cortex/*physiology ; *Rejection (Psychology) ; *Social Isolation
    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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    Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulation of vascular tone. Activation of L-type Ca2+ channels initiates muscle contraction; however, the role of T-type Ca2+ channels (T-channels) is not clear. We show that mice deficient in the alpha1H T-type Ca2+ channel (alpha(1)3.2-null) have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from alpha(1)3.2-null arteries showed normal contractile responses, but reduced relaxation in response to acetylcholine and nitroprusside. Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chien-Chang -- Lamping, Kathryn G -- Nuno, Daniel W -- Barresi, Rita -- Prouty, Sally J -- Lavoie, Julie L -- Cribbs, Leanne L -- England, Sarah K -- Sigmund, Curt D -- Weiss, Robert M -- Williamson, Roger A -- Hill, Joseph A -- Campbell, Kevin P -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631046" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Arteries/drug effects/*physiology ; Calcium/*metabolism ; Calcium Channels, T-Type/genetics/*physiology ; Coronary Vessels/drug effects/pathology/*physiology ; Echocardiography ; Electrocardiography ; Endothelium, Vascular/drug effects/physiology ; Female ; Fibrosis ; Ganglia, Spinal/cytology ; Gene Targeting ; Heart/physiology ; Heart Rate ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/physiology ; Myocardium/pathology ; Neurons/metabolism ; Nickel/pharmacology ; Nitric Oxide/physiology ; Nitric Oxide Donors/pharmacology ; Nitroprusside/pharmacology ; Patch-Clamp Techniques ; Vasoconstriction/drug effects ; *Vasodilation/drug effects
    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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    Thalamic control of visceral nociception mediated by T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G T-type Ca2+ channels show hyperalgesia to visceral pain. Thalamic infusion of a T-type blocker induced similar hyperalgesia in wild-type mice. In response to visceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes, which then slowly decayed as T type-dependent burst spikes gradually increased. In alpha1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca2+ channels underlie an antinociceptive mechanism operating in the thalamus andsupport the idea that burst firing plays a critical role in sensory gating in the thalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Daesoo -- Park, Donghyun -- Choi, Soonwook -- Lee, Sukchan -- Sun, Minjeong -- Kim, Chanki -- Shin, Hee-Sup -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):117-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526084" target="_blank"〉PubMed〈/a〉
    Keywords: Abdominal Pain/physiopathology ; Acetic Acid/pharmacology ; Action Potentials ; Analysis of Variance ; Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/genetics/*physiology ; Female ; Magnesium Sulfate/pharmacology ; Male ; Mibefradil/pharmacology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neurons/physiology ; Pain/*physiopathology ; Pain Measurement ; Ventral Thalamic Nuclei/*physiology ; Viscera
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Loss of IGF2 imprinting: a potential marker of colorectal cancer risk (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: Loss of imprinting (LOI), an epigenetic alteration affecting the insulin-like growth factor II gene (IGF2), is found in normal colonic mucosa of about 30% of colorectal cancer (CRC) patients, but it is found in only 10% of healthy individuals. In a pilot study to investigate the utility of LOI as a marker of CRC risk, we evaluated 172 patients at a colonoscopy clinic. The adjusted odds ratio for LOI in lymphocytes was 5.15 for patients with a positive family history [95% confidence interval (95% CI), 1.70 to 16.96; probability P = 0.002], 3.46 for patients with adenomas (95% CI, 1.14 to 11.37; P = 0.026), and 21.7 for patients with CRC (95% CI, 3.48 to 153.6; P = 0.0005). LOI can be assayed with a DNA-based blood test, and it may be a valuable predictive marker of an individual's risk for CRC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, Hengmi -- Cruz-Correa, Marcia -- Giardiello, Francis M -- Hutcheon, David F -- Kafonek, David R -- Brandenburg, Sheri -- Wu, Yiqian -- He, Xiaobing -- Powe, Neil R -- Feinberg, Andrew P -- K07 CA092445/CA/NCI NIH HHS/ -- R01 CA65145/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1753-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, 1064 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637750" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Aging ; *Biomarkers, Tumor/analysis ; Child ; Colon/*metabolism/pathology ; Colorectal Neoplasms/*diagnosis/*genetics/pathology ; Cross-Sectional Studies ; Disease Progression ; Family Health ; Female ; Genetic Predisposition to Disease ; Genetic Testing ; *Genomic Imprinting ; Humans ; Insulin-Like Growth Factor II/*genetics ; Intestinal Mucosa/metabolism/pathology ; Lymphocytes ; Male ; Odds Ratio ; Pilot Projects
    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
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    alpha-Synuclein locus triplication causes Parkinson's disease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singleton, A B -- Farrer, M -- Johnson, J -- Singleton, A -- Hague, S -- Kachergus, J -- Hulihan, M -- Peuralinna, T -- Dutra, A -- Nussbaum, R -- Lincoln, S -- Crawley, A -- Hanson, M -- Maraganore, D -- Adler, C -- Cookson, M R -- Muenter, M -- Baptista, M -- Miller, D -- Blancato, J -- Hardy, J -- Gwinn-Hardy, K -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):841.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA. singleta@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593171" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Exons ; Family ; Female ; *Gene Dosage ; Genetic Linkage ; Haplotypes ; Humans ; In Situ Hybridization, Fluorescence ; Male ; *Mutation ; Nerve Tissue Proteins/*genetics ; Parkinson Disease/*genetics ; Pedigree ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Reverse Transcriptase Polymerase Chain Reaction ; Synucleins ; alpha-Synuclein
    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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    Epigenetic dynamics of imprinted X inactivation during early mouse development (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: The initiation of X-chromosome inactivation is thought to be tightly correlated with early differentiation events during mouse development. Here, we show that although initially active, the paternal X chromosome undergoes imprinted inactivation from the cleavage stages, well before cellular differentiation. A reversal of the inactive state, with a loss of epigenetic marks such as histone modifications and polycomb proteins, subsequently occurs in cells of the inner cell mass (ICM), which give rise to the embryo-proper in which random X inactivation is known to occur. This reveals the remarkable plasticity of the X-inactivation process during preimplantation development and underlines the importance of the ICM in global reprogramming of epigenetic marks in the early embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamoto, Ikuhiro -- Otte, Arie P -- Allis, C David -- Reinberg, Danny -- Heard, Edith -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):644-9. Epub 2003 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR218, Curie Institute, 26 rue d'Ulm, Paris 75005, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671313" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Blastocyst/physiology ; Blastomeres/physiology ; Chromatin/metabolism ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; *Embryonic and Fetal Development ; *Epigenesis, Genetic ; Female ; *Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Mice ; Morula/physiology ; RNA, Long Noncoding ; RNA, Untranslated/metabolism ; Transcription, Genetic ; X Chromosome/*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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  • 9
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    Myc-induced T cell leukemia in transgenic zebrafish (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: The zebrafish is an attractive model organism for studying cancer development because of its genetic accessibility. Here we describe the induction of clonally derived T cell acute lymphoblastic leukemia in transgenic zebrafish expressing mouse c-myc under control of the zebrafish Rag2 promoter. Visualization of leukemic cells expressing a chimeric transgene encoding Myc fused to green fluorescent protein (GFP) revealed that leukemias arose in the thymus, spread locally into gill arches and retro-orbital soft tissue, and then disseminated into skeletal muscle and abdominal organs. Leukemic cells homed back to the thymus in irradiated fish transplanted with GFP-labeled leukemic lymphoblasts. This transgenic model provides a platform for drug screens and for genetic screens aimed at identifying mutations that suppress or enhance c-myc- induced carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langenau, David M -- Traver, David -- Ferrando, Adolfo A -- Kutok, Jeffery L -- Aster, Jon C -- Kanki, John P -- Lin, Shuo -- Prochownik, Ed -- Trede, Nikolaus S -- Zon, Leonard I -- Look, A Thomas -- CA-06516/CA/NCI NIH HHS/ -- CA-68484/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):887-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Lineage ; *Cell Transformation, Neoplastic ; Clone Cells ; DNA-Binding Proteins/genetics ; *Disease Models, Animal ; Female ; Fertilization in Vitro ; Gene Expression Profiling ; *Genes, myc ; Green Fluorescent Proteins ; Kidney/pathology ; *Leukemia-Lymphoma, Adult T-Cell/genetics/pathology ; Leukemic Infiltration ; Luminescent Proteins/metabolism ; Male ; Mice ; Mutation ; Neoplasm Transplantation ; Olfactory Bulb/pathology ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Spleen/pathology ; T-Lymphocytes/immunology/*pathology/physiology ; Thymus Gland/pathology ; Transgenes ; *Zebrafish/embryology/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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  • 10
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    Comment on "Little evidence for developmental plasticity of adult hematopoietic stem cells" (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Theise, Neil D -- Krause, Diane S -- Sharkis, Saul -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1317; author reply 1317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610282" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain ; *Cell Differentiation ; Cell Separation ; Female ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Male ; Mice ; Mice, Transgenic ; Parabiosis ; Phenotype ; Stem Cell Transplantation ; Stem Cells/cytology/*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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