The daily-scale entrance dynamics of intermittently open/closed estuaries

Intermittently open/closed estuaries (IOCE) are a dynamic form of estuary characterised by periodic entrance closure to the ocean. Entrance closure is a function of the relative balance between on and offshore sediment transport with closures occurring during periods of low fluvial discharge whereby the estuary ebb-tidal prism is reduced. Although the broad scale processes of entrance closure are becoming better understood, there remains limited knowledge on channel morphodynamics during an individual closure event. In this study, the entrance dynamics of three IOCE on the coast of Victoria, Australia, were monitored over a daily timescale following both artificial and natural openings. The influence of changing marine and fluvial conditions on the relative sedimentation rate within the entrance channel was examined. IOCE in Victoria showed two distinct modes of entrance closure: (a) lateral accretion, whereby the estuary gradually closes by longshore drift-driven spit growth during low river flows; and (b) vertical accretion, where the channel rapidly aggrades under high (> 2 m), near-normal waves. During storms, when fluvial discharge and wave heights simultaneously increase, large swells will not always close the mouth due to an increase in the ebb-tidal prism. The estuary water depth and the maximum channel dimensions following opening were not proportional to the opening duration, with this being a function of the wave and fluvial conditions occurring following lagoon drainage. Based on the findings of this work, implementing a successful artificial entrance opening is dependent on reduced onshore sedimentation rates which occur when wave energy is low (< 2 m Hs) relative to river flow. Copyrigh

DNA sensor associated type I Interferon signalling is increased in ulcerative colitis and induces JAK-dependent inflammatory cell death in colonic organoids

DNA sensor pathways can initiate inflammasome, cell death and type I interferon (IFN) signalling in immune-mediated inflammatory diseases (IMIDs); including type I interferonopathies. We investigated the involvement of these pathways in the pathogenesis of ulcerative colitis (UC); by analysing expression of DNA sensor, inflammasome, and type I IFN biomarker genes in colonic mucosal biopsy tissue from control (n=31), inactive UC (n=31), active UC (n=33) and a UC single cell RNA-Seq dataset. The effects of type I IFN (IFN-β), IFN-γ and TNF-α on gene expression, cytokine production and cell death were investigated in human colonic organoids. In organoids treated with cytokines alone, or in combination with NLRP3, caspase or JAK inhibitors, cell death was measured, and supernatants were assayed for IL-1β/IL-18/CXCL10. The expression of DNA sensor pathway genes - PYHIN family members (AIM2, IFI16, MNDA, PYHIN1), as well as ZBP1, cGAS and DDX41 were increased in active UC and expressed in a cell type restricted pattern. Inflammasome genes (CASP1, IL1B, IL18), type I IFN inducers (STING, TBK1, IRF3), IFNB1 and type I IFN biomarker genes (OAS2, IFIT2, MX2) were also increased in active UC. Co-treatment of organoids with IFN-β or IFN-γ and TNFα increased expression of IFI16, ZBP1, CASP1, cGAS and STING, induced cell death and IL-1β/IL-18 secretion. This inflammatory cell death was blocked by the JAK inhibitor tofacitinib but not by inflammasome or caspase inhibitors. Increased type I IFN activity may drive elevated expression of DNA sensor genes and JAK-dependent but inflammasome-independent inflammatory cell death of colonic epithelial cells in UC

The neurophysiological brain-fingerprint of Parkinson’s diseaseResearch in context

Summary: Background: Research in healthy young adults shows that characteristic patterns of brain activity define individual “brain-fingerprints” that are unique to each person. However, variability in these brain-fingerprints increases in individuals with neurological conditions, challenging the clinical relevance and potential impact of the approach. Our study shows that brain-fingerprints derived from neurophysiological brain activity are associated with pathophysiological and clinical traits of individual patients with Parkinson’s disease (PD). Methods: We created brain-fingerprints from task-free brain activity recorded through magnetoencephalography in 79 PD patients and compared them with those from two independent samples of age-matched healthy controls (N = 424 total). We decomposed brain activity into arrhythmic and rhythmic components, defining distinct brain-fingerprints for each type from recording durations of up to 4 min and as short as 30 s. Findings: The arrhythmic spectral components of cortical activity in patients with Parkinson’s disease are more variable over short periods, challenging the definition of a reliable brain-fingerprint. However, by isolating the rhythmic components of cortical activity, we derived brain-fingerprints that distinguished between patients and healthy controls with about 90% accuracy. The most prominent cortical features of the resulting Parkinson’s brain-fingerprint are mapped to polyrhythmic activity in unimodal sensorimotor regions. Leveraging these features, we also demonstrate that Parkinson’s symptom laterality can be decoded directly from cortical neurophysiological activity. Furthermore, our study reveals that the cortical topography of the Parkinson’s brain-fingerprint aligns with that of neurotransmitter systems affected by the disease’s pathophysiology. Interpretation: The increased moment-to-moment variability of arrhythmic brain-fingerprints challenges patient differentiation and explains previously published results. We outline patient-specific rhythmic brain signaling features that provide insights into both the neurophysiological signature and symptom laterality of Parkinson’s disease. Thus, the proposed definition of a rhythmic brain-fingerprint of Parkinson’s disease may contribute to novel, refined approaches to patient stratification. Symmetrically, we discuss how rhythmic brain-fingerprints may contribute to the improved identification and testing of therapeutic neurostimulation targets. Funding: Data collection and sharing for this project was provided by the Quebec Parkinson Network (QPN), the Pre-symptomatic Evaluation of Novel or Experimental Treatments for Alzheimer’s Disease (PREVENT-AD; release 6.0) program, the Cambridge Centre for Aging Neuroscience (Cam-CAN), and the Open MEG Archives (OMEGA). The QPN is funded by a grant from Fonds de Recherche du Québec - Santé (FRQS). PREVENT-AD was launched in 2011 as a $13.5 million, 7-year public-private partnership using funds provided by McGill University, the FRQS, an unrestricted research grant from Pfizer Canada, the Levesque Foundation, the Douglas Hospital Research Centre and Foundation, the Government of Canada, and the Canada Fund for Innovation. The Brainstorm project is supported by funding to SB from the NIH (R01-EB026299-05). Further funding to SB for this study included a Discovery grant from the Natural Sciences and Engineering Research Council of Canada of Canada (436355-13), and the CIHR Canada research Chair in Neural Dynamics of Brain Systems (CRC-2017-00311)

Indicative Distribution Maps for Ecological Functional Groups - Level 3 of IUCN Global Ecosystem Typology

This dataset includes the original version of the indicative distribution maps and profiles for Ecological Functional Groups - Level 3 of IUCN Global Ecosystem Typology (v2.0). Please refer to Keith et al. (2020). The descriptive profiles provide brief summaries of key ecological traits and processes for each functional group of ecosystems to enable any ecosystem type to be assigned to a group. Maps are indicative of global distribution patterns are not intended to represent fine-scale patterns. The maps show areas of the world containing major (value of 1, coloured red) or minor occurrences (value of 2, coloured yellow) of each ecosystem functional group. Minor occurrences are areas where an ecosystem functional group is scattered in patches within matrices of other ecosystem functional groups or where they occur in substantial areas, but only within a segment of a larger region. Most maps were prepared using a coarse-scale template (e.g. ecoregions), but some were compiled from higher resolution spatial data where available (see details in profiles). Higher resolution mapping is planned in future publications. We emphasise that spatial representation of Ecosystem Functional Groups does not follow higher-order groupings described in respective ecoregion classifications. Consequently, when Ecosystem Functional Groups are aggregated into functional biomes (Level 2 of the Global Ecosystem Typology), spatial patterns may differ from those of biogeographic biomes. Differences reflect the distinctions between functional and biogeographic interpretations of the term, biome