Molecular Discovery of Filarial Nematode DNA in an Endangered Wild Pinniped (Galapagos Sea Lion, ).

Rapidly changing environments are contributing to the spread of non-native species and their associated pathogens into new and vulnerable ecosystems, such as the Galapagos archipelago. These pathogens represent a significant threat to emblematic species. The Galapagos sea lion () (GSL) is an endangered and endemic pinniped that is increasingly at risk of acquiring infectious diseases due to interactions with introduced companion animals.

Optimizing parenting and child outcomes following parent-child interaction therapy - toddler: a randomized controlled trial.

Background: Parent-Child Interaction Therapy-Toddler (PCIT-T) is an attachment-informed intervention model designed to meet the specific developmental needs of toddlers aged 12-24 months presenting with challenging behaviors.

Methods: This study used a randomized controlled design to evaluate outcomes of PCIT-T for children aged 14-24 months with disruptive behaviors. Ninety toddlers with parent-reported disruptive behavior were randomly allocated to PCIT-T (intervention), an active control condition (Circle of Security- Parenting™; COS-P), or a non-treatment control condition (wait-list; WL).

MLKL deficiency elevates testosterone production in male mice independently of necroptotic functions.

Mixed lineage kinase domain-like (MLKL) is a pseudokinase, best known for its role as the terminal effector of the necroptotic cell death pathway. MLKL-mediated necroptosis has long been linked to various age-related pathologies including neurodegeneration, atherosclerosis and male reproductive decline, however many of these attributions remain controversial. Here, we investigated the role of MLKL and necroptosis in the adult mouse testis: an organ divided into sperm-producing seminiferous tubules and the surrounding testosterone-producing interstitium.

Divergent roles of RIPK3 and MLKL in high-fat diet-induced obesity and MAFLD in mice.

Cell death frequently occurs in the pathogenesis of obesity and metabolic dysfunction-associated fatty liver disease (MAFLD). However, the exact contribution of core cell death machinery to disease manifestations remains ill-defined. Here, we show via the direct comparison of mice genetically deficient in the essential necroptotic regulators, receptor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL), as well as mice lacking apoptotic caspase-8 in myeloid cells combined with RIPK3 loss, that RIPK3/caspase-8 signaling regulates macrophage inflammatory responses and drives adipose tissue inflammation and MAFLD upon high-fat diet feeding.