Patterns and implications of spatial covariation in herbivore functions on resilience of coral reefs.

Persistent shifts to undesired ecological states, such as shifts from coral to macroalgae, are becoming more common. This highlights the need to understand processes that can help restore affected ecosystems. Herbivory on coral reefs is widely recognized as a key interaction that can keep macroalgae from outcompeting coral.

Changing disturbance regimes, material legacies, and stabilizing feedbacks: Dead coral skeletons impair key recovery processes following coral bleaching.

Ecosystem responses to disturbance depend on the nature of the perturbation and the ecological legacies left behind, making it critical to understand how climate-driven changes in disturbance regimes modify resilience properties of ecosystems. For coral reefs, recent increases in severe marine heat waves now co-occur with powerful storms, the historic agent of disturbance. While storms kill coral and remove their skeletons, heat waves bleach and kill corals but leave their skeletons intact.

Multiphase optimization strategy to establish optimal delivery of nutrition-related services in healthcare settings: A step towards clinical trial.

Background: Minorities living in the Southern US generally have greater incidence and prevalence of cardiometabolic diseases compared to other groups. Cardiometabolic disease prevalence and risk can be reduced by focusing on diet and lifestyle modifications. There is need for holistic and integrated care models for community-based healthcare organizations who are already working with minorities.

Poly-alanine-tailing is a modifier of neurodegeneration caused by Listerin mutation.

The surveillance of translation is critical for the fitness of organisms from bacteria to humans. Ribosome-associated Quality Control (RQC) is a surveillance mechanism that promotes the elimination of truncated polypeptides, byproducts of ribosome stalling during translation. In canonical mammalian RQC, NEMF binds to the large ribosomal subunit and recruits the E3 ubiquitin ligase Listerin, which marks the nascent-chains for proteasomal degradation.

Clinically relevant mouse models of severe spinal muscular atrophy with respiratory distress type 1.

Spinal Muscular Atrophy with Respiratory Distress (SMARD1) is a lethal infantile disease, characterized by the loss of motor neurons leading to muscular atrophy, diaphragmatic paralysis, and weakness in the trunk and limbs. Mutations in IGHMBP2, a ubiquitously expressed DNA/RNA helicase, have been shown to cause a wide spectrum of motor neuron disease. Though mutations in IGHMBP2 are mostly associated with SMARD1, milder alleles cause the axonal neuropathy, Charcot-Marie-Tooth disease type 2S (CMT2S), and some null alleles are potentially a risk factor for sudden infant death syndrome (SIDS).