Does lower use of academic affiliation by university faculty in top U.S. newspapers contribute to misinformation about abortion?

BACKGROUND: University faculty are considered trusted sources of information to disseminate accurate information to the public that abortion is a common, safe and necessary medical health care service. However, misinformation persists about abortion's alleged dangers, commonality, and medical necessity. METHODS: Systematic review of popular media articles related to abortion, gun control (an equally controversial topic), and cigarette use (a more neutral topic) published in top U.S. newspapers between January 2015 and July 2020 using bivariate analysis and logistic regression to compare disclosure of university affiliation among experts in each topic area. RESULTS: We included 41 abortion, 102 gun control, and 130 smoking articles, which consisted of 304 distinct media mentions of university-affiliated faculty. Articles with smoking and gun control faculty experts had statistically more affiliations mentioned (90%, n = 195 and 88%, n = 159, respectively) than abortion faculty experts (77%, n = 54) (p = 0.02). The probability of faculty disclosing university affiliation was similar between smoking and gun control (p = 0.73), but between smoking and abortion was significantly less (Ave Marginal Effects - 0.13, p = 0.02). CONCLUSIONS: Fewer faculty members disclose their university affiliation in top U.S. newspapers when discussing abortion. Lack of academic disclosure may paradoxically make these faculty appear less 'legitimate.' This leads to misinformation, branding abortion as a 'choice,' suggesting it is an unessential medical service. With the recent U.S. Supreme Court landmark decision, Dobbs v. Jackson Women's Health Organization, and subsequent banning of abortion in many U.S. states, faculty will probably be even less likely to disclose their university affiliation in the media than in the past.

Phleboliths mistaken for intraperitoneal copper-containing intrauterine device in the presence of missing strings.

Although rare, pelvic phleboliths may confound the diagnosis of an intraperitoneal or malpositioned intrauterine device (IUD). Pelvic phleboliths are focal calcifications in pelvic veins, often in multiples near the ureters, occurring in about 40% of adult patients. We treated a 35-year-old woman requesting removal of her copper-containing IUD (TCu380A IUD). She had missing IUD strings on clinical examination. A clinic-based transvaginal ultrasound and anteroposterior abdominal radiograph that followed suggested prior TCu380A IUD expulsion. A radiologist later interpreted several ambiguous radiodensities in the abdominal radiograph as a possible intraperitoneal or malpositioned IUD. In collaboration with radiologists and family planning specialists, it was suggested that the patient further undergo a three-dimensional ultrasonography and a CT of the pelvis. The radiodensities first noted on the radiograph were revealed to be phleboliths, a diagnostic possibility not initially considered by any of the primary clinical care team, radiologists or family planning specialists.

12/15-lipoxygenase is an interleukin-13 and interferon-γ counterregulated-mediator of allergic airway inflammation.

Interleukin-13 and interferon-γ are important effectors of T-helper cells. Interleukin-13 increases expression of the arachidonic acid-metabolizing enzyme, 15-lipoxygenase-1, in a variety of cell types. 15-lipoxygenase-1 is dramatically elevated in the airways of subjects with asthma. Studies in animals indicate that 15-lipoxygenase-1 contributes to the development of allergic airway inflammation but is protective in some other forms of inflammation. We tested the hypothesis that the ability of interleukin-13 and interferon-γ to counterregulate allergic airway inflammation was potentially mediated by counterregulation of 12/15-lipoxygenase, the mouse ortholog of 15-lipoxygenase-1. The airways of mice were treated with interleukin-13 or interferon-γ one day prior to each of the four allergen exposures. Interleukin-13 augmented and interferon-γ inhibited allergic airway inflammation independently of systemic IgE and mucosal IgA responses but in association with counterregulation of 12/15-lipoxygenase. Interleukin-13 and interferon-γ counterregulate 12/15-lipoxygenase potentially contributing to the effects of these cytokines on allergic airway inflammation.

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels.

BACKGROUND: Induction of 15-lipoxygenase-1 (15-LO-1) has been observed in the airways of subjects with asthma, although its physiologic role in the airways has remained largely undefined. OBJECTIVES: We sought to test the hypothesis that the mouse 15-LO-1 ortholog 12/15-LO contributes to the development of allergic airways inflammation. METHODS: Two models were used to evaluate wild-type and 12/15-LO-deficient mice. The systemic model involved intraperitoneal injections of allergen, and the mucosal model involved allergen exposures occurring exclusively in the airways. The systemic and mucosal-specific contributions of 12/15-LO to allergic sensitization and airways inflammation were determined by comparing the results obtained in the 2 models. RESULTS: In the mucosal model 12/15-LO knockout mice were protected from the development of allergic sensitization and airways inflammation, as evidenced by circulating levels of allergen-specific IgE, IgG1, and IgG2a; the profile of inflammatory cells in bronchoalveolar lavage fluid; and the expression of cytokines and mediators in lung tissue. In the systemic model 12/15-LO knockout mice were not protected. This suggested the presence of a lung-restricted protective role for 12/15-LO deficiency that was potentially accounted for by increased activation of mucosal B cells and increased production of the known mucosal-specific protective mediator secretory IgA. CONCLUSIONS: Induction of 15-LO-1 in asthma might contribute to allergic sensitization and airways inflammation, potentially by causing suppression of secretory IgA.