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  • 1
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    Linkage analysis of IL4 and other chromosome 5q31.1 markers and total serum immunoglobulin E concentrations (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: Sib-pair analysis of 170 individuals from 11 Amish families revealed evidence for linkage of five markers in chromosome 5q31.1 with a gene controlling total serum immunoglobulin E (IgE) concentration. No linkage was found between these markers and specific IgE antibody concentrations. Analysis of total IgE within a subset of 128 IgE antibody-negative sib pairs confirmed evidence for linkage to 5q31.1, especially to the interleukin-4 gene (IL4). A combination of segregation and maximum likelihood analyses provided further evidence for this linkage. These analyses suggest that IL4 or a nearby gene in 5q31.1 regulates IgE production in a nonantigen-specific (noncognate) fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, D G -- Neely, J D -- Breazeale, D R -- Ghosh, B -- Freidhoff, L R -- Ehrlich-Kautzky, E -- Schou, C -- Krishnaswamy, G -- Beaty, T H -- 1 P41 RR03655/RR/NCRR NIH HHS/ -- AI20059/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1152-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Asthma and Allergy Center, School of Medicine, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178175" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Allergens/immunology ; Base Sequence ; Child ; Child, Preschool ; *Chromosomes, Human, Pair 5 ; Female ; Genes, MHC Class II ; *Genetic Linkage ; Genetic Markers ; Humans ; Hypersensitivity, Immediate/genetics ; Immunoglobulin E/*blood ; Interleukin-4/*genetics ; Likelihood Functions ; Lod Score ; Male ; Middle Aged ; Molecular Sequence Data
    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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    Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: In a search for genes that regulate circadian rhythms in mammals, the progeny of mice treated with N-ethyl-N-nitrosourea (ENU) were screened for circadian clock mutations. A semidominant mutation, Clock, that lengthens circadian period and abolishes persistence of rhythmicity was identified. Clock segregated as a single gene that mapped to the midportion of mouse chromosome 5, a region syntenic to human chromosome 4. The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" 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/PMC3839659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitaterna, M H -- King, D P -- Chang, A M -- Kornhauser, J M -- Lowrey, P L -- McDonald, J D -- Dove, W F -- Pinto, L H -- Turek, F W -- Takahashi, J S -- P30-CA07175/CA/NCI NIH HHS/ -- R01-DK40493/DK/NIDDK NIH HHS/ -- T32 NS071040/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):719-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
    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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  • 3
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    Localization of a breast cancer susceptibility gene, BRCA2, to chromosome 13q12-13 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: A small proportion of breast cancer, in particular those cases arising at a young age, is due to the inheritance of dominant susceptibility genes conferring a high risk of the disease. A genomic linkage search was performed with 15 high-risk breast cancer families that were unlinked to the BRCA1 locus on chromosome 17q21. This analysis localized a second breast cancer susceptibility locus, BRCA2, to a 6-centimorgan interval on chromosome 13q12-13. Preliminary evidence suggests that BRCA2 confers a high risk of breast cancer but, unlike BRCA1, does not confer a substantially elevated risk of ovarian cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wooster, R -- Neuhausen, S L -- Mangion, J -- Quirk, Y -- Ford, D -- Collins, N -- Nguyen, K -- Seal, S -- Tran, T -- Averill, D -- CA-48711/CA/NCI NIH HHS/ -- CN-05222/CN/NCI NIH HHS/ -- HG-00571/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2088-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Carcinogenesis, Institute of Cancer Research, Sutton, Surrey, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091231" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Female ; Genes, Retinoblastoma ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Lod Score ; Male ; Ovarian Neoplasms/genetics ; Pedigree ; Phenotype
    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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    Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: The 2;5 chromosomal translocation occurs in most anaplastic large-cell non-Hodgkin's lymphomas arising from activated T lymphocytes. This rearrangement was shown to fuse the NPM nucleolar phosphoprotein gene on chromosome 5q35 to a previously unidentified protein tyrosine kinase gene, ALK, on chromosome 2p23. In the predicted hybrid protein, the amino terminus of nucleophosmin (NPM) is linked to the catalytic domain of anaplastic lymphoma kinase (ALK). Expressed in the small intestine, testis, and brain but not in normal lymphoid cells, ALK shows greatest sequence similarity to the insulin receptor subfamily of kinases. Unscheduled expression of the truncated ALK may contribute to malignant transformation in these lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, S W -- Kirstein, M N -- Valentine, M B -- Dittmer, K G -- Shapiro, D N -- Saltman, D L -- Look, A T -- CA 21765/CA/NCI NIH HHS/ -- KO8 CA 01702/CA/NCI NIH HHS/ -- P01 CA 20180/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain/enzymology ; Cell Transformation, Neoplastic ; Chromosome Walking ; Chromosomes, Human, Pair 2 ; Chromosomes, Human, Pair 5 ; Cloning, Molecular ; Gene Expression Regulation, Neoplastic ; Humans ; Intestine, Small/enzymology ; Lymphoma, Large-Cell, Anaplastic/chemistry/enzymology/*genetics ; Male ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*genetics ; Phosphoproteins/chemistry/*genetics ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases/chemistry/*genetics ; RNA, Messenger/genetics/metabolism ; Receptor Protein-Tyrosine Kinases ; Sequence Alignment ; Signal Transduction ; Testis/enzymology ; *Translocation, Genetic ; Tumor Cells, Cultured
    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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    Implications of FRA16A structure for the mechanism of chromosomal fragile site genesis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: Fragile sites are chemically induced nonstaining gaps in chromosomes. Different fragile sites vary in frequency in the population and in the chemistry of their induction. DNA sequences encompassing and including the rare, autosomal, folate-sensitive fragile site, FRA16A, were isolated by positional cloning. The molecular basis of FRA16A was found to be expansion of a normally polymorphic p(CCG)n repeat. This repeat was adjacent to a CpG island that was methylated in fragile site-expressing individuals. The FRA16A locus in individuals who do not express the fragile site is not a site of DNA methylation (imprinting), which suggests that the methylation associated with fragile sites may be a consequence and not a cause of their genesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nancarrow, J K -- Kremer, E -- Holman, K -- Eyre, H -- Doggett, N A -- Le Paslier, D -- Callen, D F -- Sutherland, G R -- Richards, R I -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1938-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cytogenetics and Molecular Genetics, Women's and Children's Hospital, North Adelaide, South Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009225" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Fragile Sites ; *Chromosome Fragility ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 16 ; Dinucleoside Phosphates/metabolism ; Female ; Fragile X Syndrome/genetics ; Humans ; Male ; Methylation ; Molecular Sequence Data ; Pedigree ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
    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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    Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: A gene involved in psoriasis susceptibility was localized to the distal region of human chromosome 17q as a result of a genome-wide linkage analysis with polymorphic microsatellites and eight multiply affected psoriasis kindreds. In the family which showed the strongest evidence for linkage, the recombination fraction between a psoriasis susceptibility locus and D17S784 was 0.04 with a maximum two-point lod score of 5.33. There was also evidence for genetic heterogeneity and although none of the linked families showed any association with HLA-Cw6, two unlinked families showed weak levels of association. This study demonstrates that in some families, psoriasis susceptibility is due to variation at a single major genetic locus other than the human lymphocyte antigen locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomfohrde, J -- Silverman, A -- Barnes, R -- Fernandez-Vina, M A -- Young, M -- Lory, D -- Morris, L -- Wuepper, K D -- Stastny, P -- Menter, A -- P01-AI2327/AI/NIAID NIH HHS/ -- R01 HL47145/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1141-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235-8591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178173" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; DNA Primers ; DNA, Satellite/genetics ; Disease Susceptibility ; Female ; Genetic Linkage ; Genetic Markers ; HLA-C Antigens/genetics ; Haplotypes ; Humans ; Lod Score ; Male ; Molecular Sequence Data ; Pedigree ; Polymorphism, Genetic ; Psoriasis/*genetics ; Software
    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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    Mutation of a mutL homolog in hereditary colon cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Some cases of hereditary nonpolyposis colorectal cancer (HNPCC) are due to alterations in a mutS-related mismatch repair gene. A search of a large database of expressed sequence tags derived from random complementary DNA clones revealed three additional human mismatch repair genes, all related to the bacterial mutL gene. One of these genes (hMLH1) resides on chromosome 3p21, within 1 centimorgan of markers previously linked to cancer susceptibility in HNPCC kindreds. Mutations of hMLH1 that would disrupt the gene product were identified in such kindreds, demonstrating that this gene is responsible for the disease. These results suggest that defects in any of several mismatch repair genes can cause HNPCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papadopoulos, N -- Nicolaides, N C -- Wei, Y F -- Ruben, S M -- Carter, K C -- Rosen, C A -- Haseltine, W A -- Fleischmann, R D -- Fraser, C M -- Adams, M D -- CA35494/CA/NCI NIH HHS/ -- CA47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128251" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; *Adenosine Triphosphatases ; Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Carrier Proteins ; Chromosome Mapping ; *Chromosomes, Human, Pair 3 ; Codon ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; *DNA Repair ; *DNA-Binding Proteins ; *Escherichia coli Proteins ; Female ; Frameshift Mutation ; *Genes ; Genetic Markers ; Humans ; Male ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; Nuclear Proteins ; Open Reading Frames ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/genetics ; Sequence Deletion ; Tumor Cells, Cultured
    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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    Dependence on REM sleep of overnight improvement of a perceptual skill (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: Several paradigms of perceptual learning suggest that practice can trigger long-term, experience-dependent changes in the adult visual system of humans. As shown here, performance of a basic visual discrimination task improved after a normal night's sleep. Selective disruption of rapid eye movement (REM) sleep resulted in no performance gain during a comparable sleep interval, although non-REM slow-wave sleep disruption did not affect improvement. On the other hand, deprivation of REM sleep had no detrimental effects on the performance of a similar, but previously learned, task. These results indicate that a process of human memory consolidation, active during sleep, is strongly dependent on REM sleep.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karni, A -- Tanne, D -- Rubenstein, B S -- Askenasy, J J -- Sagi, D -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036518" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Electrodiagnosis ; Female ; Form Perception/*physiology ; Humans ; Learning/*physiology ; Male ; Sleep Deprivation/physiology ; Sleep Stages/physiology ; Sleep, REM/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    Quantitative trait locus for reading disability on chromosome 6 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Interval mapping of data from two independent samples of sib pairs, at least one member of whom was reading disabled, revealed evidence for a quantitative trait locus (QTL) on chromosome 6. Results obtained from analyses of reading performance from 114 sib pairs genotyped for DNA markers localized the QTL to 6p21.3. Analyses of corresponding data from an independent sample of 50 dizygotic twin pairs provided evidence for linkage to the same region. In combination, the replicate samples yielded a chi 2 value of 16.73 (P = 0.0002). Examination of twin and kindred siblings with more extreme deficits in reading performance yielded even stronger evidence for a QTL (chi 2 = 27.35, P 〈 0.00001). The position of the QTL was narrowly defined with a 100:1 confidence interval to a 2-centimorgan region within the human leukocyte antigen complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardon, L R -- Smith, S D -- Fulker, D W -- Kimberling, W J -- Pennington, B F -- DeFries, J C -- HD-11681/HD/NICHD NIH HHS/ -- HD-27802/HD/NICHD NIH HHS/ -- HG-00085/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Health Sciences Program, SRI International, Menlo Park, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939663" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Child ; Chromosome Mapping ; *Chromosomes, Human, Pair 6 ; Diseases in Twins/*genetics ; Dyslexia/*genetics ; Female ; Genetic Linkage ; Genetic Markers ; HLA Antigens/genetics ; Humans ; Major Histocompatibility Complex ; Male ; Nuclear Family ; Regression Analysis ; Twins, Dizygotic
    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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  • 10
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    Variable gearing during locomotion in the human musculoskeletal system (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: Human feet and toes provide a mechanism for changing the gear ratio of the ankle extensor muscles during a running step. A variable gear ratio could enhance muscle performance during constant-speed running by applying a more effective prestretch during landing, while maintaining the muscles near the high-efficiency or high-power portion of the force-velocity curve during takeoff. Furthermore, during acceleration, variable gearing may allow muscle contractile properties to remain optimized despite rapid changes in running speed. Forceplate and kinematic analyses of running steps show low gear ratios at touchdown that increase throughout the contact phase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carrier, D R -- Heglund, N C -- Earls, K D -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):651-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036513" target="_blank"〉PubMed〈/a〉
    Keywords: Acceleration ; Achilles Tendon/physiology ; Ankle Joint/physiology ; Biomechanical Phenomena ; Female ; Foot/physiology ; Humans ; Leg/*physiology ; Locomotion/*physiology ; Male ; Multivariate Analysis ; Muscles/*physiology ; Running/physiology ; Toes/physiology
    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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