Browsing by Author "Mikesell, Carter"

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    Bibliometric Analysis of Gender Authorship Trends and Collaboration Dynamics over 30 Years of Spine 1985 to 2015
    (Wolters Kluwer, 2018-02) Brinker, Alexander R.; Liao, Jane L.; Kraus, Kent R.; Young, Jocelyn; Sandelski, Morgan; Mikesell, Carter; Robinson, Daniel; Adjei, Michael; Lunsford, Shatoria D.; Fischer, James; Kacena, Melissa A.; Whipple, Elizabeth C.; Loder, Randall T.; Orthopaedic Surgery, School of Medicine
    Study Design. A bibliometric analysis. Objective. The aim of this article was to study bibliometric changes over the last 30 years of Spine. These trends are important regarding academic publication productivity. Summary of Background Data. Inflation in authorship number and other bibliometric variables has been described in the scientific literature. The issue of author gender is taking on increasing importance, as efforts are being made to close the gender gap. Methods. From 1985 to 2015, 10-year incremental data for several bibliometric variables were collected, including author gender. Standard bivariate statistical analyses were performed. Trends over time were assessed by the Cochran linear trend. A P < 0.05 was considered statistically significant. Results. Inclusion criteria were met for 1566 manuscripts. The majority of the manuscripts were from North America (51.2%), Europe (25.2%), and Asia (20.8%). The number of manuscripts, authors, countries, pages, and references all increased from 1985 to 2015. There was a slight increase in female first authors over time (17.5% to 18.4%, P = 0.048). There was no gender change over time for corresponding authors (14.3% to 14.0%, P = 0.29). There was an 88% increase in the percentage of female first authors having male corresponding authors (P = 0.00004), and a 123% increase in male first authors having female corresponding authors (P = 0.0002). The 14% to 18% of female authors in Spine is higher than the ∼5% female membership of the Scoliosis Research Society and North American Spine Society. Conclusion. Manuscripts in Spine over the past 30 years have shown a significant increase in the number of authors, collaborating institutions and countries, printed pages, references, and number of times each manuscript was cited. There has been a mild increase in female first authorship, but none in corresponding authorship. Increases in female authorship will likely require recruitment of more females into the discipline rather than providing females in the discipline with authorship opportunities. Level of Evidence: N/A
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    Osteolytic Breast Cancer Causes Skeletal Muscle Weakness in an Immunocompetent Syngeneic Mouse Model
    (Frontiers Media, 2017-12-19) Regan, Jenna N.; Mikesell, Carter; Reiken, Steven; Xu, Haifang; Marks, Andrew R.; Mohammad, Khalid S.; Guise, Theresa A.; Waning, David L.; Medicine, School of Medicine
    Muscle weakness and cachexia are significant paraneoplastic syndromes of many advanced cancers. Osteolytic bone metastases are common in advanced breast cancer and are a major contributor to decreased survival, performance, and quality of life for patients. Pathologic fracture caused by osteolytic cancer in bone (OCIB) leads to a significant (32%) increased risk of death compared to patients without fracture. Since muscle weakness is linked to risk of falls which are a major cause of fracture, we have investigated skeletal muscle response to OCIB. Here, we show that a syngeneic mouse model of OCIB (4T1 mammary tumor cells) leads to cachexia and skeletal muscle weakness associated with oxidation of the ryanodine receptor and calcium (Ca2+) release channel (RyR1). Muscle atrophy follows known pathways via both myostatin signaling and expression of muscle-specific ubiquitin ligases, atrogin-1 and MuRF1. We have identified a mechanism for skeletal muscle weakness due to increased oxidative stress on RyR1 via NAPDH oxidases [NADPH oxidase 2 (Nox2) and NADPH oxidase 4 (Nox4)]. In addition, SMAD3 phosphorylation is higher in muscle from tumor-bearing mice, a critical step in the intracellular signaling pathway that transmits TGFβ signaling to the nucleus. This is the first time that skeletal muscle weakness has been described in a syngeneic model of OCIB and represents a unique model system in which to study cachexia and changes in skeletal muscle.