The value of a remote orthodontic assessment for children having permanent teeth extracted under general anaesthesia.

Introduction The number of children undergoing dental extractions under general anaesthetic (GA) remains high. The newly published Royal College of Surgeons guidelines in 2023 take a less prescriptive approach on balancing and compensating extractions for first permanent molars. In an effort to maintain an effective and efficient patient care pathway, an orthodontic remote assessment triage model was developed in West Dorset for the special care dentistry and community dental service.

Spatiotemporal proteomic profiling of cellular responses to NLRP3 agonists.

Nucleotide-binding domain and leucine-rich repeat pyrin-domain containing protein 3 (NLRP3) is an innate immune sensor that forms an inflammasome in response to various cellular stressors. Gain-of-function mutations in NLRP3 cause autoinflammatory diseases and NLRP3 signalling itself exacerbates the pathogenesis of many other human diseases. Despite considerable therapeutic interest, the primary drivers of NLRP3 activation remain controversial due to the diverse array of signals that are integrated through NLRP3.

NINJ1 mediates plasma membrane rupture by cutting and releasing membrane disks.

The membrane protein NINJ1 mediates plasma membrane rupture in pyroptosis and other lytic cell death pathways. Here, we report the cryo-EM structure of a NINJ1 oligomer segmented from NINJ1 rings. Each NINJ1 subunit comprises amphipathic (⍺1, ⍺2) and transmembrane (TM) helices (⍺3, ⍺4) and forms a chain of subunits, mainly by the TM helices and ⍺1.

Host E3 ubiquitin ligase ITCH mediates effector GRA35-triggered NLRP1 inflammasome activation and cell-autonomous immunity.

is an intracellular parasite that can activate the NLRP1 inflammasome leading to macrophage pyroptosis in Lewis rats, but the underlying mechanism is not well understood. In this study, we performed a genome-wide CRISPR screen and identified the dense granule proteins GRA35, GRA42, and GRA43 as the effectors mediating cell death in Lewis rat macrophages. GRA35 localizes on the parasitophorous vacuole membrane, where it interacts with the host E3 ubiquitin ligase ITCH.

Host E3 ubiquitin ligase ITCH mediates effector GRA35-triggered NLRP1 inflammasome activation and cell-autonomous immunity.

is an intracellular parasite that can activate the NLRP1 inflammasome leading to macrophage pyroptosis in Lewis rats, but the underlying mechanism is not well understood. In this study, we performed a genome-wide CRISPR screen and identified the dense granule proteins GRA35, GRA42, and GRA43 as the effectors mediating cell death in Lewis rat macrophages. GRA35 localizes on the parasitophorous vacuole membrane, where it interacts with the host E3 ubiquitin ligase ITCH.