Faculty Bibliography

OBJECTIVE:Our objective was to characterize the most frequently cited articles published in obstetrics and gynecology journals during the last 50 years. STUDY DESIGN/METHODS:We utilized the 2008 edition of Journal Citation Reports and Social Sciences Citation Index database to determine the most frequently cited articles published after 1956. Articles were evaluated for several characteristics, and an unadjusted categorical analysis was performed to compare pre- and post-1980 articles. RESULTS:The 100 most frequently cited articles were published in 11 journals between 1957 and 2004. Most articles were published by US-based authors. Forty-four articles were related to obstetrics and 56 were related to gynecology. The most common study design was observational. There were only 7 randomized controlled trials, and randomized controlled trials were not more common after 1980 (6.3% vs 8.1%; P = .71). CONCLUSION/CONCLUSIONS:Most "citation classics" in obstetrics and gynecology are observational studies published in high-impact journals by US-based authors after 1980.

BACKGROUND:Multiple studies have demonstrated a link between periodontal infections and vascular disease. Porphyromonas gingivalis, a major periodontal pathogen, has been shown to adhere to and invade endothelial cells. OBJECTIVE:In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis. METHODS:Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants. RESULTS:Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms. CONCLUSIONS:Taken together these data demonstrate for the first time that infection with a periodontal pathogen induces procoagulant responses in HAEC.

OBJECTIVE:To study bone marrow (BM) stromal damage in a mouse model of infusion-induced BM failure. MATERIALS AND METHODS/METHODS:Sublethally irradiated CByB6F1 mice were infused with 5 x 10(6) C57BL/6 (B6) lymph node (LN) cells. Recipient BM cells were taken at 3, 7, 10, and 14 days following LN infusion and were cultured in vitro in alpha-modified Eagle media for 2-3 weeks. Peripheral blood and was analyzed by complete blood counts while BM lymphocyte infiltration/expansion was analyzed by flow cytometry. Marrow cells from affected and control mice were mixed and cultured in vitro to test nonspecific stromal damage. RESULTS:Donor lymphocytes infiltrated host BM within 3-7 days and expanded significantly between 7 and 10 days, concurrent with the development of leukopenia, thrombocytopenia, and marrow hypoplasia. BM cells from mice at 7, 10, and 14 days after B6-LN cell infusion were progressively defective in forming stromal feeder layers. A 1:1 mixture of BM cells from affected CByB6F1 mice and normal B6 mice failed to form an effective stromal feeder layer that could support cobblestone colony formation, indicating that lymphocytes in the BM of affected CByB6F1 mice were able to damage stromal cells in the normal B6 BM. CONCLUSION/CONCLUSIONS:Activated lymphocytes destroy both hematopoietic and stromal cells as innocent bystanders in the infusion-induced BM failure model.