Mangrove ecosystems function as important carbon sinks; however, accurately quantifying their carbon dynamics remains challenging because of the complex interplay of tidal fluctuations, sediment-water interface interactions, and biogeochemical cycling. Many existing models lack the temporal resolution and mechanistic precision necessary to adequately capture these dynamic processes, particularly in intertidal environments. To address this issue, we developed a mangrove ecosystem model [EMAGIN-B.C_MG] by incorporating mangrove physiology and tidal hydrodynamics into the EMAGIN-B.C. model, which represents benthic-pelagic coupled ecosystems, including phytoplankton, benthic algae, zooplankton, benthic fauna, detritus, and nutrients, through biological, chemical, and physical processes. Model validation was conducted by comparing the results with time series observations of dissolved inorganic carbon (DIC), total alkalinity (TA), and dissolved oxygen, as well as annual carbon flux measurements. Simulation results showed that carbon absorption and fixation increased during spring and summer because of enhanced photosynthetic activity, whereas carbon storage remained relatively stable throughout the year. Residual ponding during ebb tide significantly influenced DIC and TA concentrations via benthic mineralization and calcium carbonate (CaCO3) dissolution. Comparative analysis revealed that the presence of mangroves increased carbon absorption, fixation, and storage by factors of 9, 3, and 6, respectively. These findings demonstrate that high-temporal resolution ecosystem models can effectively reproduce key material cycling functions of mangrove ecosystems and contribute to more accurate assessments of Blue Carbon dynamics in intertidal wetlands. EMAGIN-B.C_MG provides a novel framework for evaluating the carbon mitigation potential of mangroves in the context of climate change.
As one of the problems in his list [20], T. Ohtsuki proposed to study relations between quandle cocycle invariants and quantum invariants. The aim of this paper is to answer one of those questions. We prove that the coefficient of the finite perturbative expansion of the quandle shadow cocycle invariant defined by ( /p)-Laurent polynomial quandle is Vassiliev invariant for any braids.
The GRAPES-3 large area muon telescope with its sixteen independent modules records the high energy (>1 GeV) muons continuously over 2.3 sr of the sky. However, the recorded muon rates are contaminated by instrumental effects and instabilities spanning both short- and long-timescales, such as variations in the efficiency of the detector. We present an automated, algorithmic method, which employs Bayesian blocks to discretize the data stream into periods and exploits the correlations among the sixteen independent modules of the muon telescope to separate the impact of these instrumental problems from those originating in physical effects of interest, allowing the Savitzky-Golay filter to be employed to mitigate the former. Compared to legacy methods, this method is less dependent on subjective input from experimental operators and provides a data stream in which known instrumental effects are substantially mitigated over long timescales. The muon rate obtained with the new method shows a modestly better correlation with neutron monitor data than that obtained with the legacy method.
We study crossed Andreev reflection occurring in quantum dots connected to one superconducting lead and two normal leads at low temperatures T. Specifically, we derive an exact formula for the conductance up to order T2 in the large-superconducting-gap limit, which is expressed in terms of the transmission probabilities of Cooper pairs and interacting Bogoliubov quasiparticles. Our formulation is based on the latest version of Fermi-liquid theory for the Anderson impurity model, which has clarified that the quasiparticle energy shifts of order omega 2 and T2-namely, corrections of the same order as those arising from the finite lifetime of quasiparticles-can be expressed exactly in terms of three-body correlations of impurity electrons. We also demonstrate how the three-body contributions evolve and affect the Cooper-pair tunneling as the Andreev level moves away from the Fermi level, using the numerical renormalization group approach. The results show that the Cooper-pair contribution to the T2 terms of the local and nonlocal conductances becomes comparable to the Bogoliubovquasiparticle contribution in the parameter region in which superconducting proximity effects dominate over the Kondo effect.
BACKGROUND:Autoantibodies in the blistering skin disease pemphigus primarily target desmosomal cadherins and cause loss of keratinocyte adhesion and epidermal blistering via signalling events. Pemphigus vulgaris (PV) is associated with autoantibodies (PV IgG) against desmoglein (Dsg)1 and Dsg3 and pemphigus foliaceus (PF) with antibodies against Dsg1 only. In previous studies, protein kinase C (PKC) inhibition was protective in murine but not in human epidermis. OBJECTIVES:To investigate the roles of PKC subtypes in in PV IgG-induced epidermal blistering in human skin. METHODS:We applied an ex vivo human skin organ culture model, dispase-based dissociation assays, Western blot analysis and confocal and simulated emission depletion (STED) microscopy, to study the underlying mechanisms of pemphigus pathogenesis in vitro. RESULTS:The inhibitor of atypical PKC (aPKC) isoforms CRT0066854 (CRT) completely abolished acantholysis, whereas the conventional PKC (cPKC) inhibitor Gö6976 (Gö) did not. In cultured keratinocytes, both CRT and Gö effectively inhibited the loss of cell adhesion, keratin filament retraction and Dsg3 depletion in response to PV IgG, as well the pathogenic Dsg3-specific IgGs AK23 and 2G4. In contrast, reduced cell adhesion and keratin filament retraction in response to PKC activation by phorbol-12-myristate-13-acetate and PF IgG was blocked by the inhibition of cPKC but not of aPKC. Mechanistically, cPKC and aPKC were both required for PV IgG-induced translocation of PKC towards peripheral keratin filaments and conformational changes in desmoplakin. CONCLUSIONS:These findings show that aPKC is critical for the blistering seen in human epidermis in PV and is dependent on the autoantibody profile.
