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Reef predators play a critical role in maintaining the balance of marine ecosystems and are an important component of Hawaii’s recreational and commercial fisheries. In response to the increasing anthropogenic demands on these populations across the main Hawaiian Islands, the study of predator movements in marine protected areas has become a research priority. To this aim, we used passive acoustic telemetry to investigate the spatial and temporal movement patterns of five reef predator species: bluefin trevally ( Caranx melampygus ), giant trevally ( Caranx ignobilis ), green jobfish ( Aprion virescens ), whitetip reef sharks ( Triaenodon obesus ) and gray reef sharks ( Carcharhinus amblyrhynchos ) at the 31 ha Molokini Marine Life Conservation District (MLCD) off Maui, Hawaii (Lat: 20°37′56.70″N, Lon: 156°29′44.52″W) from November 13, 2013 to August 28, 2015. Our results indicate that the predator assemblage in the MLCD was dominated by teleost fishes during the day and sharks at night. Residency was variable across species, with bluefin trevally exhibiting the highest residency in the MLCD, green jobfish the lowest, and long-distance movements between the Molokini MLCD and the other islands of the Maui Nui Complex were common for gray reef sharks and giant trevally. These results indicate that despite its small size, the Molokini MLCD provides a high level of protection to resident species such as bluefin trevally. However, this MLCD is less effective at protecting more mobile predators such as green jobfish, gray reef sharks and giant trevally.

Review(s) of: Connecting kids to history with museum exhibitions, by McRainey, D.L. and Russick, J. (editors) 2010, Walnut Creek: Left Coast Press, 333 pp. ISBN 978-1-59874-383-8 (paperback). Price 24.67 pounds.

The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is commonly used to model Parkinson’s disease (PD) as it specifically damages the nigrostriatal dopaminergic pathway. Recent studies in mice have, however, provided evidence that MPTP also compromises the integrity of the brain’s vasculature. Photobiomodulation (PBM), the irradiation of tissue with low-intensity red light, mitigates MPTP-induced loss of dopaminergic neurons in the midbrain, but whether PBM also mitigates MPTP-induced damage to the cerebrovasculature has not been investigated. This study aimed to characterize the time course of cerebrovascular disruption following MPTP exposure and to determine whether PBM can mitigate this disruption. Young adult male C57BL/6 mice were injected with 80 mg/kg MPTP or isotonic saline and perfused with fluorescein isothiocyanate FITC-labelled albumin at various time points post-injection. By 7 days post-injection, there was substantial and significant leakage of FITC-labelled albumin into both the substantia nigra pars compacta (SNc; p < 0.0001) and the caudate-putamen complex (CPu; p ≤ 0.0003); this leakage partly subsided by 14 days post-injection. Mice that were injected with MPTP and treated with daily transcranial PBM (670 nm, 50 mW/cm2, 3 min/day), commencing 24 h after MPTP injection, showed significantly less leakage of FITC-labelled albumin in both the SNc (p < 0.0001) and CPu (p = 0.0003) than sham-treated MPTP mice, with levels of leakage that were not significantly different from saline-injected controls. In summary, this study confirms that MPTP damages the brain’s vasculature, delineates the time course of leakage induced by MPTP out to 14 days post-injection, and provides the first direct evidence that PBM can mitigate this leakage. These findings provide new understanding of the use of the MPTP mouse model as an experimental tool and highlight the potential of PBM as a therapeutic tool for reducing vascular dysfunction in neurological conditions.

RIPK1 is a key regulator of innate immune signalling pathways. To ensure an optimal inflammatory response, RIPK1 is regulated post-translationally by well-characterized ubiquitylation and phosphorylation events, as well as by caspase-8-mediated cleavage 1 – 7 . The physiological relevance of this cleavage event remains unclear, although it is thought to inhibit activation of RIPK3 and necroptosis 8 . Here we show that the heterozygous missense mutations D324N, D324H and D324Y prevent caspase cleavage of RIPK1 in humans and result in an early-onset periodic fever syndrome and severe intermittent lymphadenopathy—a condition we term ‘cleavage-resistant RIPK1-induced autoinflammatory syndrome’. To define the mechanism for this disease, we generated a cleavage-resistant Ripk1 D325A mutant mouse strain. Whereas Ripk1 −/− mice died postnatally from systemic inflammation, Ripk1 D325A/D325A mice died during embryogenesis. Embryonic lethality was completely prevented by the combined loss of Casp8 and Ripk3 , but not by loss of Ripk3 or Mlkl alone. Loss of RIPK1 kinase activity also prevented Ripk1 D325A/D325A embryonic lethality, although the mice died before weaning from multi-organ inflammation in a RIPK3-dependent manner. Consistently, Ripk1 D325A/D325A and Ripk1 D325A /+ cells were hypersensitive to RIPK3-dependent TNF-induced apoptosis and necroptosis. Heterozygous Ripk1 D325A /+ mice were viable and grossly normal, but were hyper-responsive to inflammatory stimuli in vivo. Our results demonstrate the importance of caspase-mediated RIPK1 cleavage during embryonic development and show that caspase cleavage of RIPK1 not only inhibits necroptosis but also maintains inflammatory homeostasis throughout life. Heterozygous mutateons in the caspase-8 cleavage site of RIPK1 cause a range of autoinflammatory symptoms in humans, and caspase-8 cleavage of RIPK1 in a mouse model limits TNF-induced cell death and inflammation.

Effective communication with patients and between members of the health care team are important strategies to enhance health care outcomes. Despite the prevalence of low health literacy and associated risks in the population, health professionals are often not trained adequately in health literacy communication practices. The purpose of this pilot program is to determine if offering learners an opportunity to practice health literacy communication techniques in a simulated patient care team can increase skills, attitudes, and confidence in this important area of patient care. We implemented a novel, team-based interprofessional Objective Structured Clinical Examination (iOSCE) focused on health literacy. Evaluation took place on three levels: student self-assessment of health literacy communication skills and beliefs about interprofessional teamwork, standardized patient assessment of skills during the clinical encounter, and observer assessment of interprofessional teamwork. Statistically significant gains were seen in students' health literacy communication confidence, as well as beliefs, attitudes and understanding of interprofessional teamwork. The aim of this article is to describe our pilot health literacy iOSCE findings. This pilot shows that an OSCE is an effective assessment tool for a mix of health professional learners at different levels to demonstrate health literacy practices in an interprofessional teamwork environment. [HLRP: Health Literacy Research and Practice. 2023;7(3):e139–e143.]

Background: The purpose of the present study was to clarify the relationship between the recognition of emotion and physiological response to emotion (i.e. arousal) in alexithymia. Methods: This study investigated differences in physiological arousal state, as measured by continuous heart rate, electrodermal activity (EDA) and self-reported emotional intensity before and after exposure to an emotionally arousing or neutral videotape among 41 high- or low-alexithymic young adult participants. Results: Across subjects, emotionally negative stimuli produced increased physiological arousal. However, high-alexithymic participants exposed to the arousing videotape did not report increased subjective emotional intensity, as did low-alexithymic participants. In addition, the baseline EDA of high-alexithymic participants was significantly higher than that of the low-alexithymic participants. Conclusions: Results support the prediction that alexithymia leads to a decoupling between subjective and physiological arousal when exposed to emotionally negative stimuli. This decoupling may increase alexithymic individuals’ risks for stress-related illness.