Creating the HAPS Physiology Learning Outcomes: terminology, eponyms, inclusive language, core concepts, and skills.

Learning outcomes are an essential element in curriculum development because they describe what students should be able to do by the end of a course or program and they provide a roadmap for designing assessments. This article describes the development of competency-based learning outcomes for a one-semester undergraduate introductory human physiology course. Key elements in the development process included decisions about terminology, eponyms, use of the word "normal," and similar considerations for inclusivity. The outcomes are keyed to related physiology core concepts and to process skills that can be taught along with the content. The learning outcomes have been published under a Creative Commons license by the Human Anatomy and Physiology Society (HAPS) and are available free of charge on the HAPS website.NEW & NOTEWORTHY This article describes the development of competency-based learning outcomes for introductory undergraduate human physiology courses that were published and made available free of charge by the Human Anatomy and Physiology Society (HAPS). These learning outcomes can be edited and are keyed to physiology core concepts and to process skills that can be taught along with the content.

Maternal decidual macrophages inhibit NK cell killing of invasive cytotrophoblasts during human pregnancy.

Human pregnancy is an immunological paradox. Semiallogeneic (fetal) placental cells (extravillous cytotrophoblasts [CTBs]) invade the uterine lining (decidua), which contains a unique decidual natural killer (dNK) cell population, identified by the cell surface phenotype CD56(bright) CD16(-) CD3(-) and CD14(+) CD206(+) macrophages (dMac). Previous reports suggested that human dNK cells are not a threat to the fetoplacental unit because they are anergic. In contrast, here we showed that purified and exogenously stimulated dNK cells are capable killers of cellular targets, including semiallogeneic CTBs. However, dMacs in the decidual leukocyte (DL) population restrained dNK killing through a transforming growth factor beta1 (TGF-beta1)-dependent mechanism. Our findings support a new model whereby dNK cells, capable of killing CTBs, are prevented from doing so by neighboring macrophages, thus protecting the fetal cells from NK cell attack. We speculate that this mechanism would inhibit dNK cell-mediated killing, even under conditions where high levels of cytokines may stimulate dNK cells, which could pose a threat to the developing placenta.