A Bibliometric Analysis of Citation Classics in the Journal of Ultrasound in Medicine.

OBJECTIVES: A bibliometric analysis of articles in the Journal of Ultrasound in Medicine (JUM) identified the journals' most impactful articles. METHODS: A bibliometric analysis of citation classics that were published in the JUM from its inception in 1982 to 2019 was performed. All citation classics, defined as articles cited 100 or more times, were evaluated for the number of citations, citations per year, publication year, subspecialty, design, and country of origin. Characteristics were compared before and after 1998 by the Mann-Whitney test for unpaired data and 2-sample z tests of sample proportions. The Kruskal-Wallis test for nonparametric continuous data was used to compare the median number of citations per year by decade of publication. RESULTS: A total of 7868 articles were published in the JUM between 1982 and 2019; 54 (0.7%) were citation classics. The median citation classics year of publication was 1998 (interquartile range [IQR], 1991-2003). Most citation classics originated from the United States (36 of 54 [66.7%]), were observational (47 of 54 [87%]), and were related to obstetric and gynecologic topics (16 of 54 [29.6%]). Citation classics after 1998 received significantly more citations per year (9.3 versus 4.7; P < .001), with no other differences noted. The median number of citations per year increased for each decade, with medians of 4 citations (IQR, 3.6-4.7) in 1982 to 1991 and 11.2 citations (IQR, 9-13.9) in 2002 to 2012 (P < .001). CONCLUSIONS: This list provides insight into the most influential articles that were published in the JUM. Most citation classics were observational, were from the United States, and covered obstetric and gynecologic topics. Citation classics received more citations per year after 1998.

p66Shc longevity protein regulates the proliferation of human ovarian cancer cells.

p66Shc functions as a longevity protein in murine and exhibits oxidase activity in regulating diverse biological activities. In this study, we investigated the role of p66Shc protein in regulating ovarian cancer (OCa) cell proliferation. Among three cell lines examined, the slowest growing OVCAR-3 cells have the lowest level of p66Shc protein. Transient transfection with p66Shc cDNA expression vector in OVCAR-3 cells increases cell proliferation. Conversely, knock-down of p66Shc by shRNA in rapidly growing SKOV-3 cells results in decreased cell growth. In estrogen (E2)-treated CaOV-3 cells, elevated p66Shc protein level correlates with ROS level, ErbB-2 and ERK/MAPK activation, and cell proliferation. Further, the E2-stimulated proliferation of CaOV-3 cells was blocked by antioxidants and ErbB-2 inhibitor. Additionally, in E2-stimulated cells, the tartrate-sensitive, but not the tartrate-resistant, phosphatase activity decreases; concurrently, the tyrosine phosphorylation of ErbB-2 increases. Conversely, inhibition of phosphatase activity by L(+)-tartrate treatment increases p66Shc protein level, ErbB-2 tyrosine phosphorylation, ERK/MAPK activation, and cell growth. Further, inhibition of the ERK/MAPK pathway by PD98059 blocks E2-induced ERK/MAPK activation and cell proliferation in CaOV-3 cells. Moreover, immunohistochemical analyses showed that the p66Shc protein level was significantly higher in cancerous cells than in noncancerous cells in archival OCa tissues (n = 76; P = 0.00037). These data collectively indicate that p66Shc protein plays a critical role in up-regulating OCa progression.