Overview of ectopic pregnancy diagnosis, management, and innovation.

Ectopic pregnancies are the leading cause of maternal mortality in the first trimester, with an incidence of 5%-10% of all pregnancy-related deaths. Diagnosis of ectopic pregnancies is difficult due to clinical mimics and non-specific symptoms of abdominal pain and vaginal bleeding. The current standard for ectopic pregnancy diagnosis includes ultrasound imaging and ß-human chorionic gonadotropin (ß-hCG) monitoring. In addition to ß-hCG, serum markers are being explored as a potential for diagnosis, with activin-AB and pregnancy-associated plasma protein A specifically showing promise. Other diagnostic methods include endometrial sampling, with dilation and curettage showing the highest specificity; however, frozen section reduces the diagnostic timeline which may improve outcomes. Treatment options for confirmed ectopic pregnancies include medical, surgical, and expectant management. Chosen treatment methodology is based on ß-hCG levels, hematologic stability, and risk of ectopic pregnancy rupture. Current innovations in ectopic pregnancy management aim to preserve fertility and include laparoscopic partial tubal resection with end-to-end anastomosis and uterine artery embolization with intrauterine infusion of methotrexate. Psychological interventions to improve patient mental health surrounding ectopic pregnancy diagnosis and treatment are also valuable innovations. This literature review aims to bring light to current ectopic pregnancy diagnostics, treatments, and future directions.

CD2 Regulates Pathogenesis of Asthma Induced by House Dust Mice Extract.

Characteristic of allergic asthma, CD4+Th2 lymphocytes secrete Th2 cytokines, interleukin (IL)-4, IL-13, and IL-5 that mediate the inflammatory immune response. Surface expression of CD2 and its ligand, CD58, is increased on the monocytes and eosinophils of asthma patients, which correlate with elevated serum IgE levels, suggesting that CD2 may contribute to allergic airway inflammation. Using a murine model of asthma, we observed that house dust mice extract (HDME)-exposed Balb/c mice have increased airway hyperresponsiveness (AHR), lung inflammation, goblet cell hyperplasia, and elevated levels of Th2 cytokines in the lungs, as well as increased serum IgE levels as compared to the control mice. In contrast, with the exception of serum IgE levels, all the other parameters were significantly reduced in HDME-treated Cd2-/- mice. Interestingly, Il13 but not Il4 or Il5 gene expression in the lungs was dramatically decreased in HDME-exposed Cd2-/- mice. Of note, the gene expression of IL-13 downstream targets (Muc5b and Muc5ac) and high affinity IL-13Rα2 were upregulated in the lungs of HDME-exposed Balb/c mice but were significantly reduced in HDME-exposed Cd2-/- mice. Consistently, gene expression of microRNAs regulating mucin production, inflammation, airway smooth muscle cell proliferation and IL-13 transcripts were increased in the lungs of HDME-exposed Cd2-/- mice. Given the established role of IL-13 in promoting goblet cell hyperplasia, lung inflammation and AHR in allergic asthma, our studies reveal a unique role for CD2 in the regulation of Th2-associated allergic asthma.