Antigen-specific immune therapy (CNP-106) for treatment of generalised myasthenia gravis: rationale and design of first-in-human randomised controlled trial.

Introduction: Myasthenia gravis (MG) is a T cell-dependent B cell-mediated autoimmune disease with pathogenic antibodies directed against components of the acetylcholine receptor (AChR). Current therapies do not address the root cause of the disease (autoimmune recognition of AChR) and are associated with possible serious side effects. Therefore, new therapeutic options targeting antigen-specific autoimmunity are needed.

Embracing native diversity to enhance the maximum quantum efficiency of photosystem II in maize.

The sustainability of maize cultivation would benefit tremendously from early sowing, but is hampered by low temperatures during early development in temperate climates. We show that allelic variation within the gene encoding subunit M of the NADH-dehydrogenase-like (NDH) complex (ndhm1) in a European maize landrace affects several quantitative traits that are relevant during early development in cold climates through NDH-mediated cyclic electron transport (CET) around photosystem I, a process crucial for photosynthesis and photoprotection. Beginning with a genome-wide association study for maximum potential quantum yield of photosystem II in dark-adapted leaves (Fv/Fm), we capitalized on the large phenotypic effects of a hAT transposon insertion in ndhm1 on multiple quantitative traits (early plant height, Fv/Fm, chlorophyll content, and cold tolerance) caused by the reduced protein levels of NDHM and associated NDH components.

Bridging Gaps in Cervical Cancer Care: A Web-Based Intervention to Improve Knowledge and Follow-up.

Objectives: Contributors to disparities and worse cervical cancer outcomes include limited education and loss to follow-up after an abnormal Pap smear. Effective interventions are necessary to engage diverse populations. The authors piloted an intervention to assess acceptability, knowledge uptake, and follow-up.

Wnt/β-catenin maintains epithelial IL-33 in the colonic stem and progenitor cell niche and drives its induction in colitis.

Interleukin (IL)-33 is a key responder to intestinal injury and inflammation. In the colon, it is expressed by several cell populations, with the specific cellular source likely determining its role. The colonic epithelium expresses IL-33; however, the factors controlling its production and the specific epithelial lineage(s) expressing IL-33 are poorly understood.