Rapid ecosystem-scale consequences of acute deoxygenation on a Caribbean coral reef

Loss of oxygen in the global ocean is accelerating due to climate change and eutrophication, but how acute deoxygenation events affect tropical marine ecosystems remains poorly understood. Here we integrate analyses of coral reef benthic communities with microbial community sequencing to show how a deoxygenation event rapidly altered benthic community composition and microbial assemblages in a shallow tropical reef ecosystem. Conditions associated with the event precipitated coral bleaching and mass mortality, causing a 50% loss of live coral and a shift in the benthic community that persisted a year later. Conversely, the unique taxonomic and functional profile of hypoxia-associated microbes rapidly reverted to a normoxic assemblage one month after the event. The decoupling of ecological trajectories among these major functional groups following an acute event emphasizes the need to incorporate deoxygenation as an emerging stressor into coral reef research and management plans to combat escalating threats to reef persistence

Rapid ecosystem-scale consequences of acute deoxygenation on a Caribbean coral reef

© The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Johnson, M. D., Scott, J. J., Leray, M., Lucey, N., Bravo, L. M. R., Wied, W. L., & Altieri, A. H. Rapid ecosystem-scale consequences of acute deoxygenation on a Caribbean coral reef. Nature Communications, 12(1), (2021): 4522, https://doi.org/10.1038/s41467-021-24777-3.Loss of oxygen in the global ocean is accelerating due to climate change and eutrophication, but how acute deoxygenation events affect tropical marine ecosystems remains poorly understood. Here we integrate analyses of coral reef benthic communities with microbial community sequencing to show how a deoxygenation event rapidly altered benthic community composition and microbial assemblages in a shallow tropical reef ecosystem. Conditions associated with the event precipitated coral bleaching and mass mortality, causing a 50% loss of live coral and a shift in the benthic community that persisted a year later. Conversely, the unique taxonomic and functional profile of hypoxia-associated microbes rapidly reverted to a normoxic assemblage one month after the event. The decoupling of ecological trajectories among these major functional groups following an acute event emphasizes the need to incorporate deoxygenation as an emerging stressor into coral reef research and management plans to combat escalating threats to reef persistence.M.D.J. was funded by postdoctoral fellow awards from the Smithsonian Institution’s Marine Global Earth Observatory (MarineGEO) and the Smithsonian Tropical Research Institute (STRI); M.L. and N.L. were funded by postdoctoral support from the STRI Office of Fellowships. J.J.S. was funded by a grant from the Gordon and Betty Moore Foundation awarded to STRI and UC Davis (doi:10.37807/GBMF5603). L.M.R.B., W.L.W., and A.H.A. were supported by MarineGEO, a private funder, and STRI funds to A.H.A. Many of the computations were conducted on the Smithsonian High-Performance Cluster (SI/HPC), Smithsonian Institution (doi:10.25572/SIHPC). We thank Rachel Collin for facilities support at the Bocas del Toro Research Station, Plinio Gondola and the research station staff for logistical support, Roman Barco for insight into the functional analyses, Sherly Castro for informative feedback, and Mike Fox for assistance with community analyses. Research permits were provided by the Autoridad Nacional del Ambiente de Panamá. This paper is the result of research funded by the National Oceanic and Atmospheric Administration’s National Centers for Coastal Ocean Science Competitive Research Program under award NA18NOS4780170 to A.H.A. and M.D.J. through the University of Florida. This is contribution 257 from the Coastal Hypoxia Research Program and 86 from the Smithsonian’s MarineGEO and Tennenbaum Marine Observatories Network

Computational psychiatry approach to stigma subtyping in patients with mental disorders: explicit and implicit internalized stigma

BACKGROUND: Psychiatric stigma has potentially controversial effects on patients health-related behaviors. It appears that both stigmatization and motivation in psychiatric patients are heterogeneous and multi-dimensional, and that the relationship between stigma and treatment motivation may be more complex than previously believed. AIM: To determine psychiatric stigma subtypes as they relate to treatment motivation among inpatients with various mental disorders. METHODS: Sixy-three psychiatric inpatients were examined by the Treatment Motivation Assessment Questionnaire (TMAQ) and the Russian version of Internalized Stigma of Mental Illness scale (ISMI). K-Means cluster and dispersion analysis were conducted. RESULTS: Cluster 3 (25 subjects) was the least stigmatized. Cluster 1 (18 subjects) showed an explicit stigma. Cluster 2 (20 subjects) showed an implicit stigma that took the form of the lowest treatment motivation compared to other clusters. Implicitly stigmatized patients, in contrast to explicitly stigmatized individuals, showed a decline in 3 out of 4 TMAQ factors (Mean dif.=1.051.67). CONCLUSION: Cooperation with doctors, together with reliance on ones own knowledge and skills to cope with the disorder, might be the way to overcome an internalized stigma for patients with mental disorders

A new online-test for changes in correlations between assets

Abstract We apply a new test to determine whether correlations between assets are constant over time. The test statistic is a suitably standardized maximum of cumulative empirical correlation coefficients. An empirical application to various assets suggests that the test performs well in applications. We also propose a portfolio strategy based on our test which hedges against potential financial crises and show that it works in practice

Verbal, Facial and Autonomic Responses to Empathy-Eliciting Film Clips by Disruptive Male Adolescents with High Versus Low Callous-Unemotional Traits

This study examined empathy-related responding in male adolescents with disruptive behavior disorder (DBD), high or low on callous-unemotional (CU) traits. Facial electromyographic (EMG) and heart rate (HR) responses were monitored during exposure to empathy-inducing film clips portraying sadness, anger or happiness. Self-reports were assessed afterward. In agreement with expectations, DBD adolescents with high CU traits showed significantly lower levels of empathic sadness than healthy controls across all response systems. Between DBD subgroups significant differences emerged at the level of autonomic (not verbal or facial) reactions to sadness, with high CU respondents showing less HR change from baseline than low CU respondents. The study also examined basal patterns of autonomic function. Resting HR was not different between groups, but resting respiratory sinus arrhythmia (RSA) was significantly lower in DBD adolescents with high CU traits compared to controls. Results support the notion that CU traits designate a distinct subgroup of DBD individuals

A meta-analysis of GFR slope as a surrogate endpoint for kidney failure

Glomerular filtration rate (GFR) decline is causally associated with kidney failure and is a candidate surrogate endpoint for clinical trials of chronic kidney disease (CKD) progression. Analyses across a diverse spectrum of interventions and populations is required for acceptance of GFR decline as an endpoint. In an analysis of individual participant data, for each of 66 studies (total of 186,312 participants), we estimated treatment effects on the total GFR slope, computed from baseline to 3 years, and chronic slope, starting at 3 months after randomization, and on the clinical endpoint (doubling of serum creatinine, GFR < 15 ml min−1 per 1.73 m2 or kidney failure with replacement therapy). We used a Bayesian mixed-effects meta-regression model to relate treatment effects on GFR slope with those on the clinical endpoint across all studies and by disease groups (diabetes, glomerular diseases, CKD or cardiovascular diseases). Treatment effects on the clinical endpoint were strongly associated with treatment effects on total slope (median coefficient of determination (R2) = 0.97 (95% Bayesian credible interval (BCI) 0.82–1.00)) and moderately associated with those on chronic slope (R2 = 0.55 (95% BCI 0.25–0.77)). There was no evidence of heterogeneity across disease. Our results support the use of total slope as a primary endpoint for clinical trials of CKD progression

Somatostatin Receptor 1 and 5 Double Knockout Mice Mimic Neurochemical Changes of Huntington's Disease Transgenic Mice

Selective degeneration of medium spiny neurons and preservation of medium sized aspiny interneurons in striatum has been implicated in excitotoxicity and pathophysiology of Huntington's disease (HD). However, the molecular mechanism for the selective sparing of medium sized aspiny neurons and vulnerability of projection neurons is still elusive. The pathological characteristic of HD is an extensive reduction of the striatal mass, affecting caudate putamen. Somatostatin (SST) positive neurons are selectively spared in HD and Quinolinic acid/N-methyl-D-aspartic acid induced excitotoxicity, mimic the model of HD. SST plays neuroprotective role in excitotoxicity and the biological effects of SST are mediated by five somatostatin receptor subtypes (SSTR1-5). and R6/2 mice. Conversely, the expression of somatostatin receptor subtypes, enkephalin and phosphatidylinositol 3-kinases were strain specific. SSTR1/5 appears to be important in regulating NMDARs, DARPP-32 and signaling molecules in similar fashion as seen in HD transgenic mice.This is the first comprehensive description of disease related changes upon ablation of G- protein coupled receptor gene. Our results indicate that SST and SSTRs might play an important role in regulation of neurodegeneration and targeting this pathway can provide a novel insight in understanding the pathophysiology of Huntington's disease