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    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    In vivo studies of increased incidence of sister chromatid exchanges in target cells of replication-component Friend murine leukemia virus

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    The sister chromatid exchange (SCE) incidence in hemopoietic organs of mice infected with polycythemic or anemic strains of Friend leukemia virus was increased early after infection only in spleen and bone marrow cells of susceptible DBA/2 mice, but not in the same types of cells of genetically resistant BALB/c and C57BL/6 mice or in lymphoid cells of DBA/2 mice. Because a comparable increase of SCE incidence was observed in DBA/2 mice given either virus strain, the effect is seemingly due to the replication-competent leukemogenic component of the two strains of Friend leukemia virus (polycythemic or anemic, either identical of intimately cross-related) rather than to the defective spleen focus-forming virus that is not biologically active in the anemic strain used in this study. The increase of SCE was dependent upon virus dosage and viability, was short lasting, and was not detectable in mice with overt leukemia. The increased SCE values were accompanied by the detection of a small (10 to 15%) fraction of cells scoring “high” (5 to 20) for SCE. Statistical evaluation shows that this fraction contributes heavily to the significance of SCE increase. It is suggested that these cells may represent the target for the Friend murine leukemia virus component of the Friend leukemia virus complex. © 1982, American Association for Cancer Research. All rights reserved

    The novel human gene Aprataxin is directly involved in the DNA Single Strand Break Repair Complex

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    The cells of an ataxia-oculomotor apraxia type 1 (AOA1) patient, homozygous for a new aprataxin mutation (T739C), were treated with camptothecin, an inhibitor of DNA topoisomerase I which induces DNA single-strand breaks. DNA damage was evaluated by cytogenetic analysis of chromosomal aberrations. The results obtained showed marked and dose-related increases in induced chromosomal aberrations in the patient and her heterozygous mother compared to the intrafamilial wild-type control. The alkaline comet assay confirmed this pattern. Moreover, the AOA1 cells did not show hypersensitivity to ionizing radiation, i.e. X-rays. These findings clearly indicate the direct involvement of aprataxin in the DNA single-strand-break repair machinery
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