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  • Rats  (284)
  • American Association for the Advancement of Science (AAAS)  (284)
  • 1995-1999  (89)
  • 1980-1984  (195)
  • 1940-1944
Collection
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  • American Association for the Advancement of Science (AAAS)  (284)
  • Springer  (2)
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  • 1
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    A physical map of 30,000 human genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: A map of 30,181 human gene-based markers was assembled and integrated with the current genetic map by radiation hybrid mapping. The new gene map contains nearly twice as many genes as the previous release, includes most genes that encode proteins of known function, and is twofold to threefold more accurate than the previous version. A redesigned, more informative and functional World Wide Web site (www.ncbi.nlm.nih.gov/genemap) provides the mapping information and associated data and annotations. This resource constitutes an important infrastructure and tool for the study of complex genetic traits, the positional cloning of disease genes, the cross-referencing of mammalian genomes, and validated human transcribed sequences for large-scale studies of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deloukas, P -- Schuler, G D -- Gyapay, G -- Beasley, E M -- Soderlund, C -- Rodriguez-Tome, P -- Hui, L -- Matise, T C -- McKusick, K B -- Beckmann, J S -- Bentolila, S -- Bihoreau, M -- Birren, B B -- Browne, J -- Butler, A -- Castle, A B -- Chiannilkulchai, N -- Clee, C -- Day, P J -- Dehejia, A -- Dibling, T -- Drouot, N -- Duprat, S -- Fizames, C -- Fox, S -- Gelling, S -- Green, L -- Harrison, P -- Hocking, R -- Holloway, E -- Hunt, S -- Keil, S -- Lijnzaad, P -- Louis-Dit-Sully, C -- Ma, J -- Mendis, A -- Miller, J -- Morissette, J -- Muselet, D -- Nusbaum, H C -- Peck, A -- Rozen, S -- Simon, D -- Slonim, D K -- Staples, R -- Stein, L D -- Stewart, E A -- Suchard, M A -- Thangarajah, T -- Vega-Czarny, N -- Webber, C -- Wu, X -- Hudson, J -- Auffray, C -- Nomura, N -- Sikela, J M -- Polymeropoulos, M H -- James, M R -- Lander, E S -- Hudson, T J -- Myers, R M -- Cox, D R -- Weissenbach, J -- Boguski, M S -- Bentley, D R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanger Centre, Hinxton Hall, Hinxton, Cambridge CB10 1SA UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human/*genetics ; Expressed Sequence Tags ; Gene Expression ; Genetic Markers ; *Genome, Human ; Human Genome Project ; Humans ; Internet ; *Physical Chromosome Mapping ; Rats ; Sequence Tagged Sites
    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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    A receptor in pituitary and hypothalamus that functions in growth hormone release (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Small synthetic molecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to stimulate and amplify pulsatile growth hormone (GH) release. A heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPC-R) of the pituitary and arcuate ventro-medial and infundibular hypothalamus of swine and humans was cloned and was shown to be the target of the GHSs. On the basis of its pharmacological and molecular characterization, this GPC-R defines a neuroendocrine pathway for the control of pulsatile GH release and supports the notion that the GHSs mimic an undiscovered hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howard, A D -- Feighner, S D -- Cully, D F -- Arena, J P -- Liberator, P A -- Rosenblum, C I -- Hamelin, M -- Hreniuk, D L -- Palyha, O C -- Anderson, J -- Paress, P S -- Diaz, C -- Chou, M -- Liu, K K -- McKee, K K -- Pong, S S -- Chaung, L Y -- Elbrecht, A -- Dashkevicz, M -- Heavens, R -- Rigby, M -- Sirinathsinghji, D J -- Dean, D C -- Melillo, D G -- Patchett, A A -- Nargund, R -- Griffin, P R -- DeMartino, J A -- Gupta, S K -- Schaeffer, J M -- Smith, R G -- Van der Ploeg, L H -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688086" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; DNA, Complementary/genetics ; GTP-Binding Proteins/metabolism ; Growth Hormone/*secretion ; Hormones/*metabolism ; Humans ; Hypothalamus, Middle/chemistry ; Indoles/*metabolism/pharmacology ; Macaca mulatta ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Pituitary Gland/chemistry ; RNA, Complementary/genetics ; Rats ; Receptors, Cell Surface/analysis/chemistry/genetics/*metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Ghrelin ; Spiro Compounds/*metabolism/pharmacology ; Swine
    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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    Embryonic stem cell-derived glial precursors: a source of myelinating transplants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Self-renewing, totipotent embryonic stem (ES) cells may provide a virtually unlimited donor source for transplantation. A protocol that permits the in vitro generation of precursors for oligodendrocytes and astrocytes from ES cells was devised. Transplantation in a rat model of a human myelin disease shows that these ES cell-derived precursors interact with host neurons and efficiently myelinate axons in brain and spinal cord. Thus, ES cells can serve as a valuable source of cell type-specific somatic precursors for neural transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brustle, O -- Jones, K N -- Learish, R D -- Karram, K -- Choudhary, K -- Wiestler, O D -- Duncan, I D -- McKay, R D -- NS33710/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):754-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropathology, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. brustle@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Brain/embryology/metabolism ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebral Ventricles/embryology/surgery ; Diffuse Cerebral Sclerosis of Schilder/genetics/*therapy ; Embryo, Mammalian/cytology ; Growth Substances/pharmacology ; Humans ; Male ; Mice ; Myelin Basic Protein/biosynthesis ; Myelin Proteolipid Protein/biosynthesis/genetics ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/metabolism/*transplantation/ultrastructure ; Rats ; Spinal Cord ; Stem Cell Transplantation ; Stem Cells/*cytology
    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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    Transmission of chronic nociception by spinal neurons expressing the substance P receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Substance P receptor (SPR)-expressing spinal neurons were ablated with the selective cytotoxin substance P-saporin. Loss of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated with persistent neuropathic and inflammatory pain states. This loss appeared to be permanent. Responses to mildly painful stimuli and morphine analgesia were unaffected by this treatment. These results identify a target for treating persistent pain and suggest that the small population of SPR-expressing neurons in the dorsal horn of the spinal cord plays a pivotal role in the generation and maintenance of chronic neuropathic and inflammatory pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nichols, M L -- Allen, B J -- Rogers, S D -- Ghilardi, J R -- Honore, P -- Luger, N M -- Finke, M P -- Li, J -- Lappi, D A -- Simone, D A -- Mantyh, P W -- 23970/PHS HHS/ -- 31223/PHS HHS/ -- DEO 7288/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preventive Sciences, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Ganglia, Spinal/drug effects/physiology ; *Immunotoxins ; Inflammation/physiopathology ; Ligation ; *N-Glycosyl Hydrolases ; Neuralgia/drug therapy/physiopathology ; Pain/*drug therapy/*physiopathology ; Plant Proteins/administration & dosage/*pharmacology ; Posterior Horn Cells/drug effects/*physiology ; Rats ; Receptors, Neurokinin-1/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Spinal Nerves ; Substance P/administration & dosage/*pharmacology ; Time Factors
    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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    Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holash, J -- Maisonpierre, P C -- Compton, D -- Boland, P -- Alexander, C R -- Zagzag, D -- Yancopoulos, G D -- Wiegand, S J -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1994-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/blood supply/pathology ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/pathology ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/pathology/physiology ; Glioblastoma/blood supply/pathology ; Glioma/blood supply/pathology ; In Situ Hybridization ; Lymphokines/genetics/*physiology ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/pathology/physiology ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*pathology ; *Neovascularization, Pathologic ; Proteins/genetics/*physiology ; Rats ; Rats, Sprague-Dawley ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
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  • 6
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    An MTP inhibitor that normalizes atherogenic lipoprotein levels in WHHL rabbits (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Patients with abetalipoproteinemia, a disease caused by defects in the microsomal triglyceride transfer protein (MTP), do not produce apolipoprotein B-containing lipoproteins. It was hypothesized that small molecule inhibitors of MTP would prevent the assembly and secretion of these atherogenic lipoproteins. To test this hypothesis, two compounds identified in a high-throughput screen for MTP inhibitors were used to direct the synthesis of a highly potent MTP inhibitor. This molecule (compound 9) inhibited the production of lipoprotein particles in rodent models and normalized plasma lipoprotein levels in Watanabe-heritable hyperlipidemic (WHHL) rabbits, which are a model for human homozygous familial hypercholesterolemia. These results suggest that compound 9, or derivatives thereof, has potential applications for the therapeutic lowering of atherogenic lipoprotein levels in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wetterau, J R -- Gregg, R E -- Harrity, T W -- Arbeeny, C -- Cap, M -- Connolly, F -- Chu, C H -- George, R J -- Gordon, D A -- Jamil, H -- Jolibois, K G -- Kunselman, L K -- Lan, S J -- Maccagnan, T J -- Ricci, B -- Yan, M -- Young, D -- Chen, Y -- Fryszman, O M -- Logan, J V -- Musial, C L -- Poss, M A -- Robl, J A -- Simpkins, L M -- Slusarchyk, W A -- Sulsky, R -- Taunk, P -- Magnin, D R -- Tino, J A -- Lawrence, R M -- Dickson, J K Jr -- Biller, S A -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):751-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543-4000, USA. Wetterau_John_R@msmail.bms.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784135" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/blood ; Animals ; Apolipoproteins B/*blood ; Aspartate Aminotransferases/blood ; Carrier Proteins/*antagonists & inhibitors ; Cholesterol/*blood ; Cricetinae ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Design ; Drug Evaluation, Preclinical ; Fluorenes/chemistry/pharmacokinetics/*pharmacology ; Humans ; Hyperlipidemias/blood/drug therapy ; Hyperlipoproteinemia Type II/*blood/drug therapy ; Lipids/blood ; Lipoproteins/blood ; Liver/metabolism ; Mice ; Piperidines/chemistry/pharmacokinetics/*pharmacology ; Rabbits ; Rats ; Triglycerides/*blood/metabolism ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-pituitary-adrenal responses to stress (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Variations in maternal care affect the development of individual differences in neuroendocrine responses to stress in rats. As adults, the offspring of mothers that exhibited more licking and grooming of pups during the first 10 days of life showed reduced plasma adrenocorticotropic hormone and corticosterone responses to acute stress, increased hippocampal glucocorticoid receptor messenger RNA expression, enhanced glucocorticoid feedback sensitivity, and decreased levels of hypothalamic corticotropin-releasing hormone messenger RNA. Each measure was significantly correlated with the frequency of maternal licking and grooming (all r's 〉 -0.6). These findings suggest that maternal behavior serves to "program" hypothalamic-pituitary-adrenal responses to stress in the offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, D -- Diorio, J -- Tannenbaum, B -- Caldji, C -- Francis, D -- Freedman, A -- Sharma, S -- Pearson, D -- Plotsky, P M -- Meaney, M J -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neuroendocrinology Laboratory, Douglas Hospital Research Center, McGill University, Montreal, Canada H4H 1R3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287218" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood ; Animals ; Animals, Newborn ; Corticosterone/blood/pharmacology ; Corticotropin-Releasing Hormone/genetics ; Feedback ; Female ; Gene Expression Regulation ; Grooming ; Handling (Psychology) ; Hippocampus/*physiology ; Hypothalamo-Hypophyseal System/*physiology ; *Maternal Behavior ; Pituitary-Adrenal System/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Glucocorticoid/genetics/*metabolism ; Stress, Physiological/*physiopathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Inhibition of hyperalgesia by ablation of lamina I spinal neurons expressing the substance P receptor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear. When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- Rogers, S D -- Honore, P -- Allen, B J -- Ghilardi, J R -- Li, J -- Daughters, R S -- Lappi, D A -- Wiley, R G -- Simone, D A -- MH56368/MH/NIMH NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- NS31223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417, USA. manty001@maroon.tc.umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin ; Cell Membrane/metabolism ; Cells, Cultured ; Fluorescent Antibody Technique ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Injections, Spinal ; *N-Glycosyl Hydrolases ; Neurons/cytology/*metabolism ; Pain/physiopathology ; *Pain Management ; Pain Measurement ; Plant Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/biosynthesis/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord/*cytology/metabolism ; Substance P/*metabolism/pharmacology
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  • 9
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    Epidermal growth factor immunoreactive material in the central nervous system: location and development (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-08
    Description: Epidermal growth factor (EGF) is a potent mitogen with hormonal activity in the gastrointestinal tract. Material cross-reacting with EGF was detected in the central nervous system of the developing and adult albino rat by the indirect immunofluorescence technique. High concentrations of EGF-cross-reacting material were identified in forebrain and midbrain structures of pallidal areas of the brain. These include the globus pallidus, ventral pallidum, entopeduncular nucleus, substantia nigra pars reticulata, and the islands of Calleja . Thus, EGF may represent another gut-brain peptide with potential neurotransmitter-neuromodulator functions in pallidal structures of the extrapyramidal motor systems of the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fallon, J H -- Seroogy, K B -- Loughlin, S E -- Morrison, R S -- Bradshaw, R A -- Knaver, D J -- Cunningham, D D -- GM31609/GM/NIGMS NIH HHS/ -- NS16017/NS/NINDS NIH HHS/ -- NS19964/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1107-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6144184" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/growth & development/*physiology ; Epidermal Growth Factor/*physiology ; Fluorescent Antibody Technique ; Globus Pallidus/physiology ; Mitogens/physiology ; Neurotransmitter Agents/physiology ; Rats
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  • 10
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    Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B J -- Robin, E D -- Tapper, D P -- Wong, R J -- Clayton, D A -- 5 R01 HL23701-14/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):707-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320368" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Anaerobiosis ; Animals ; Anoxia/physiopathology ; Citrate (si)-Synthase/genetics/*metabolism ; DNA, Mitochondrial/*genetics ; Electron Transport Complex IV/genetics/*metabolism ; Macrophages/*enzymology ; Mice ; Mitochondria/*enzymology ; Mitochondria, Muscle/*enzymology ; Oxidoreductases/genetics/*metabolism ; Oxo-Acid-Lyases/*metabolism ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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