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Quantum key distribution (QKD) promises provably secure communications. In order to improve the secret key rate, combining a biased basis choice with the decoy-state method is proposed. Concomitantly, there is a basis-independent detection efficiency condition, which usually cannot be satisfied in a practical system, such as the time-phase encoding. Fortunately, this flaw has been recently removed theoretically and experimentally in the four-intensity decoy-state BB84 QKD protocol using the fact that the expected yields of single-photon states prepared in two bases stay the same for a given measurement basis. However, the security proofs do not fully consider the finite-key effects for general attacks. In this work, we provide the rigorous finite-key security bounds in the universally composable framework for the four-intensity decoy-state BB84 QKD protocol. We build a time-phase encoding system with 200 MHz clock to implement this protocol, in which the real-time secret key rate is more than 60 kbps over 50 km single-mode fiber.
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Lost circulation is a common and complicated situation in drilling engineering. Serious lost circulation may lead to pressure drop in the well, affect normal drilling operations, and even cause wellbore instability, formation fluid flooding into the wellbore, and blowout. Therefore, appropriate preventive and treatment measures need to be taken to ensure the safe and smooth operation of drilling operations. So, it is necessary to conduct in-depth research on the development and performance of the plugging materials. In this study, urea formaldehyde resin with high temperature resistance and strength was used as the main raw material, and the curing conditions were optimized and adjusted by adding a variety of additives. The curing time, compressive strength, temperature resistance, and other key performance indexes of the resin plugging agent were studied, and a resin plugging agent system with excellent plugging performance was prepared. The formula is as follows: 25% urea formaldehyde resin +1% betaine +1% silane coupling agent KH-570 + 3% ammonium chloride +1% hexamethylenetetramine +1% sodium carboxymethyl cellulose. The optimal curing temperature is between 60 and 80 °C, with a controllable curing time of 1-3 h. Experimental studies examined the rheological and curing properties of the resin plugging agent system. The results showed that the viscosity of the high-strength curable resin system before curing remained stable with increasing shear rates. Additionally, the storage modulus and loss modulus of the resin solutions increased with shear stress, with the loss modulus being greater than the storage modulus, indicating a viscous fluid. The study also investigated the effect of different salt ion concentrations on the curing effect of the resin plugging system. The results showed that formation water containing Na+ at concentrations between 500 mg/L and 10,000 mg/L increased the resin's curing strength and reduced curing time. However, excessively high concentrations at lower temperatures reduced the curing strength. Formation water containing Ca2+ increased the curing time of the resin plugging system and significantly impacted the curing strength, reducing it to some extent. Moreover, the high-strength curable resin plugging agent system can effectively stay in various fracture types (parallel, wedge-shaped) and different fracture sizes, forming a high-strength consolidation under certain temperature conditions for effective plugging. In wedge-shaped fractures with a width of 10 mm, the breakthrough pressure of the high-strength curable resin plugging agent system reached 8.1 MPa. As the fracture width decreases, the breakthrough pressure increases, reaching 9.98 MPa in wedge-shaped fractures with an outlet fracture width of 3 mm, forming a high-strength plugging layer. This research provides new ideas and methods for solving drilling fluid loss in fractured loss zones and has certain application and promotion value.
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Soil health arguably depends on biodiversity and has received wide attention in heavy-metal (HM) contaminated farmland remediation in recent years. However, long-term effects and mechanisms of soil amendment remain poorly understood with respect to soil microbal community. In this in-situ field study, four soil amendments (attapulgite-At, apatite-Ap, montmorillonite-M, lime-L) at three rates were applied once only for ten years in a cadmium (Cd)-copper (Cu) contaminated paddy soil deprecated for over five years. Results showed that after ten years and in compared with CK (no amendment), total Cd concentration and its risk in plot soils were not altered by amendments (p > 0.05), but total Cu concentration and its risk were significantly increased by both Ap and L, especially the former, rather than At and M (p < 0.05), through increased soil pH and enhanced bacterial alpha diversity as well as plant community. Soil microbial communities were more affected by amendment type (30%) than dosage (11%), microbial network characteristics were dominated by rare taxa, and soil multifunctionality was improved in Ap- and L-amended soils. A structural equation model (SEM) indicated that 57.3% of soil multifunctionality variances were accounted for by soil pH (+0.696) and microbial network robustness (-0.301). Moreover, microbial robustness could be potentially used as an indicator of soil multifunctionality, and Ap could be optimized to improve soil health in combined with biomass removal. These findings would advance the understanding of soil microbial roles, especially its network robustness, on soil multifunctionality for the remediation of metal contaminated soils and metal control management strategies in acidic soils. ENVIRONMENTAL IMPLICATION: Farmland soil contamination by heavy metals (HMs) has been becoming a serious global environmental challenge. However, most studies have been conducted over the short term, leading to a gap in the long-term remediation efficiency and ecological benefits of soil amendments. For the successful deployment of immobilization technologies, it is critical to understand the long-term stability of the immobilized HMs and soil health. Our study, to the best of our knowlege, is the first to state the long-term effects and mechanisms of soil amendments on soil health and optimize an effective and eco-friendly amendment for long-term Cd/Cu immobilization.
Asunto(s)
Restauración y Remediación Ambiental , Metales Pesados , Contaminantes del Suelo , Cadmio/análisis , Suelo , Contaminantes del Suelo/análisis , Metales Pesados/análisis , Concentración de Iones de HidrógenoRESUMEN
Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial protection, promoting RGC survival. Soluble adenylyl cyclase (sAC) is one of the key regulators of the cAMP/PKA signaling pathway. However, the precise molecular mechanisms underlying the sAC-mediated signaling pathway and mitochondrial protection in RGCs that counter oxidative stress are not well characterized. Here, we demonstrate that sAC plays a critical role in protecting RGC mitochondria from oxidative stress. Using mouse models of oxidative stress, we found that activating sAC protected RGCs, blocked AMP-activated protein kinase activation, inhibited glial activation, and improved visual function. Moreover, we found that this is the result of preserving mitochondrial dynamics (fusion and fission), promoting mitochondrial bioenergetics and biogenesis, and preventing metabolic stress and apoptotic cell death in a paraquat oxidative stress model. Notably, sAC activation ameliorated mitochondrial dysfunction in RGCs by enhancing mitochondrial biogenesis, preserving mitochondrial structure, and increasing ATP production in oxidatively stressed RGCs. These findings suggest that activating sAC enhances the mitochondrial structure and function in RGCs to counter oxidative stress, consequently promoting RGC protection. We propose that modulation of the sAC-mediated signaling pathway has therapeutic potential acting on RGC mitochondria for treating glaucoma and other retinal diseases.
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Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial protection, promoting RGC survival. Soluble adenylyl cyclase (sAC) is a key regulator of the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway, which is known to protect mitochondria and promote RGC survival. However, the precise molecular mechanisms connecting the sAC-mediated signaling pathway with mitochondrial protection in RGCs against oxidative stress are not well characterized. Here, we demonstrate that sAC plays a critical role in protecting RGC mitochondria from oxidative stress. Using mouse models of oxidative stress induced by ischemic injury and paraquat administration, we found that administration of bicarbonate, as an activator of sAC, protected RGCs, blocked AMP-activated protein kinase activation, inhibited glial activation, and improved visual function. Moreover, we found that this is the result of preserving mitochondrial dynamics (fusion and fission), promoting mitochondrial bioenergetics and biogenesis, and preventing metabolic stress and apoptotic cell death. Notably, the administration of bicarbonate ameliorated mitochondrial dysfunction in RGCs by enhancing mitochondrial biogenesis, preserving mitochondrial structure, and increasing ATP production in oxidatively stressed RGCs. These findings suggest that activating sAC enhances the mitochondrial structure and function in RGCs to counter oxidative stress, consequently promoting RGC protection. We propose that modulation of the sAC-mediated signaling pathway has therapeutic potential acting on RGC mitochondria for treating glaucoma and other retinal diseases.
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Alien invasive aquatic-plant (AIA) species are severely threatening the aquatic ecosystems worldwide, especially biodiversity. Although plankton have been used to monitor and address biodiversity, some gaps remain in understanding of the relationships between plankton communities and AIA species. Here, the effects of two typical AIA species (Pistia stratiotes and Eichhornia crassipes) on plankton communities in freshwater with a native plant Vallisneria natans were investigated using a 50-d microcosm experiment. Results showed that AIA species significantly decreased water pH and dissolved oxygen while increased oxidation-reduction potential (p < 0.05). AIA species, especially P. stratiotes, significantly inhibited dry biomass accumulation in V. natans by an average rate of 39.0 %, decreased water pH by up to 14.62 %, and increased aboveground lengths and chlorophyll contents of V. natans by up to 36.2 % and 63.7 % (p < 0.05), respectively. These species further modified the growth strategy of V. natans from dry biomass accumulation to aboveground elongation. Although the AIA species did not alter plankton diversity (p > 0.05), but they changed their dominant species, functional communities (e.g., Groups D and TB), and co-occurrence networks. P. stratiotes decreased the average degree of the networks by 12.37-19.02 % and the graph density by 10.53-14.47 %, while E. crassipes decreased the modularity of the networks by 10.24 % compared with the control (without AIA species), respectively. Overall, AIA species inhibited the growth of V. natans and decreased the stability of plankton communities and their resistance to environmental disturbances. These findings enhance our understanding of how AIA species affect the growth of native plants and variations in plankton communities, thereby providing a theoretical basis for improving the ecological function and safety of freshwater.
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A-Kinase anchoring protein 1 (AKAP1) is a multifunctional mitochondrial scaffold protein that regulates mitochondrial dynamics, bioenergetics, and calcium homeostasis by anchoring several proteins, including protein kinase A, to the outer mitochondrial membrane. Glaucoma is a complex, multifactorial disease characterized by a slow and progressive degeneration of the optic nerve and retinal ganglion cells (RGCs), ultimately resulting in vision loss. Impairment of the mitochondrial network and function is linked to glaucomatous neurodegeneration. Loss of AKAP1 induces dynamin-related protein 1 dephosphorylation-mediated mitochondrial fragmentation and loss of RGCs. Elevated intraocular pressure triggers a significant reduction in AKAP1 protein expression in the glaucomatous retina. Amplification of AKAP1 expression protects RGCs from oxidative stress. Hence, modulation of AKAP1 could be considered a potential therapeutic target for neuroprotective intervention in glaucoma and other mitochondria-associated optic neuropathies. This review covers the current research on the role of AKAP1 in the maintenance of mitochondrial dynamics, bioenergetics, and mitophagy in RGCs and provides a scientific basis to identify and develop new therapeutic strategies that could protect RGCs and their axons in glaucoma.