Neonicotinoid insecticide pollution in soil and water poses serious environmental risks. Microbial biodegradation is an important neonicotinoid insecticide degradation pathway in the environment. In ...this study, 70.0% of the acetamiprid in a 200 mg/L solution was degraded by actinomycetes Streptomyces canus CGMCC 13662 (isolated from soil) in 48 h, and the acetamiprid degradation half-life was 27.7 h. Acetamiprid was degraded to IM-1-2 ((E)-1-(1-(((6-chloropyridin-3-yl)methyl)(methyl) amino)ethylidene)urea) through hydrolysis of the cyanoimine moiety. Gene cloning and overexpression indicated that a novel nitrile hydratase with three unusual subunits (AnhD, AnhE, and AnhA) without accessory protein mediated IM-1-2 formation. The purified nitrile hydratase responsible for degrading acetamiprid had a K m of 5.85 mmol/L and a V max of 15.99 U/mg. A homology model suggested that AnhD-Glu56 and AnhE-His21 play important roles in the catalytic efficiency of the nitrile hydratase. S. canus CGMCC 13662 could be used to remediate environments contaminated with acetamiprid.
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IJS, KILJ, NUK, PNG, UL, UM, UPUK
The stability of engineering structure are threatened in the permafrost regions by the global warming. Therefore, it is necessary to further the study on the temperature field of the pile foundation ...in the frozen soil area. In the paper, six different forms (pile arrangement within two, three, four; pile arrangement outside two, three, four) were studied for temperature effect in the next 50 years. Date from these numerical simulation indicates that the thermal pile has a active cooling effect in the bridge and the stability of bridge pile foundation were promoted. The same number arrangement of the the thermal pile is better outside the pile foundation than that inside the pile foundation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Alzheimer's disease (AD) is a neurodegenerative disorder with limited available drugs for treatment. Enhancing autophagy attenuates AD pathology in various AD model mice. Thus, development of ...potential drugs which enhance autophagy may bring beneficial effects in AD therapy. In the present study, we show clemastine, a first-generation histamine H1R antagonist and being originally marketed for the treatment of allergic rhinitis, ameliorates AD pathogenesis in APP/PS1 transgenic mice. Chronic treatment with clemastine orally reduced amyloid-β (Aβ) load, neuroinflammation and cognitive deficits of APP/PS1 transgenic mice. Clemastine decreases Aβ generation via reducing the levels of BACE1, CTFs of APP. Mechanistically, clemastine enhances autophagy concomitant with a suppression of mTOR signaling. Therefore, we propose that clemastine attenuates AD pathology via enhancing mTOR-mediated autophagy.
•Clemastine decreases Aβ and neuroinflammation, and attenuates cognitive deficits.•Clemastine decreases Aβ production by reducing the levels of BACE1.•clemastine attenuates AD pathology via enhancing mTOR-mediated autophagy.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Sulfoxaflor (SUL,
N
-methyloxido1-6-(trifluoromethyl)-3-pyridinyl ethyl-
λ
4
-sulfanylidene cyanamide) is a widely used systemic insecticide, and its residue has frequently been detected in the ...environment, posing a potential threat to the environment. In this study,
Pseudaminobacter salicylatoxidans
CGMCC 1.17248 rapidly converted SUL into X11719474 via a hydration pathway mediated by two nitrile hydratases (AnhA and AnhB). Extensive (96.4%) degradation of 0.83 mmol/L SUL was achieved by
P. salicylatoxidans
CGMCC 1.17248 resting cells within 30 min (half-life of SUL 6.4 min). Cell immobilization by entrapment into calcium alginate remediated 82.8% of the SUL in 90 min, and almost no SUL was observed in surface water after incubation for 3 h.
P. salicylatoxidans
NHases AnhA and AnhB both hydrolyzed SUL to X11719474, although AnhA exhibited much better catalytic performance. The genome sequence of
P. salicylatoxidans
CGMCC 1.17248 revealed that this strain could efficiently eliminate nitrile-containing insecticides and adapt to harsh environments. We firstly found that UV irradiation transforms SUL to the derivatives X11719474 and X11721061, and the potential reaction pathways were proposed. These results further deepen our understanding of the mechanisms of SUL degradation as well as the environmental fate of SUL.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Flonicamid (N-cyanomethyl-4-trifluoromethylnicotinamide, FLO), a novel selective systemic pyridinecarboxamide insecticide, effectively controls hemipterous pests. However, microbial degradation of ...flonicamid, along with the enzymatic mechanism, has not been studied. Here, bacterial isolate PG13, which converts flonicamid into 4-(trifluoromethyl)nicotinol glycine (TFNG) and N-(4-trifluoromethylnicotinoyl)glycinamide (TFNG-AM), was isolated and identified as Alcaligenes faecalis CGMCC 17553. The genome of CGMCC 17553 contained five nitrilases but no nitrile hydratase, and recombinant Escherichia coli strains harboring CGMCC 17553 nitrilase gene nitA or nitD acquired the ability to degrade flonicamid. Purified NitA catalyzed flonicamid into both TFNG and TFNG-AM, indicating dual functionality, while NitD could only produce TFNG-AM. Three-dimensional homology modeling revealed that aromatic amino acid residues in the catalytic pocket affected nitrilase activity. These findings further our understanding of the enzymatic mechanism of flonicamid metabolism in the environment and may help develop a potential bioremediation agent for the elimination of flonicamid contamination.
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IJS, KILJ, NUK, PNG, UL, UM, UPUK
Microvirga flocculans CGMCC 1.16731 can degrade many cyano group-containing neonicotinoid insecticides. Here, its genome was sequenced, and a novel nitrile hydratase gene cluster was discovered in a ...plasmid. The NHase gene cluster (pnhF) has gene structure β-subunit 1, α-subunit, and β-subunit 2, which is different from previously reported NHase gene structures. Phylogenetic analysis of α-subunits indicated that NHases containing the three subunit (β1αβ2) structure are independent from NHases containing two subunits (αβ). pnhF was successfully expressed in Escherichia coli, and the purified PnhF could convert the nitrile-containing insecticide flonicamid to N-(4-trifluoromethylnicotinoyl)glycinamide. The enzymatic properties of PnhF were investigated using flonicamid as a substrate. Homology models revealed that amino acid residue β1-Glu56 may strongly affect the catalytic activity of PnhF. This study expands our understanding of the structures and functions of NHases and the enzymatic mechanism of the environmental fate of flonicamid.
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IJS, KILJ, NUK, PNG, UL, UM, UPUK
Thiacloprid is a widely-used neonicotinoid insecticide, but its enzymatic conversion and the toxicity of the amide metabolite are poorly understood. Here, a N2-fixing bacterium, Microvirga flocculans ...CGMCC 1.16731, was reported to metabolize thiacloprid via hydration and hydroxylation to thiacloprid amide and 4-hydroxy thiacloprid respectively. M. flocculans transformed 90.5% of 0.63 mmol/L thiacloprid in 30 h with a half-life of 9.0 h. In soil, the bacterium transformed 92.4% of 80 μmol/kg soil thiacloprid in 9 d. A cobalt-type nitrile hydratase (NHase) composed of an α-subunit (TnhA) and a β-subunit (TnhB) converted thiacloprid to thiacloprid amide. Co-expression of activator (TnhC) with NHase could improve the TnhA solubility and therefore enhanced 4-folds higher NHase activity. The NHase produced recombinantly in Escherichia coli transformed 97% of 0.76 mmol/L thiacloprid in 10 min. M. flocculans NHase had a Km value of 0.63 mmol/L and Vmax of 10.2 μmol/min/mg toward thiacloprid. Thiacloprid amide has higher toxic effect on growth of M. flocculans than thiacloprid, whereas lower toxic on the aquatic invertebrate Daphnia magna. Both thiacloprid and thiacloprid amide inhibited tnhA transcription. This increases our understanding of the enzymatic mechanism of environmental fate of thiacloprid and toxicity of its amide metabolite toward soil microbes and aquatic organisms.
•A novel N2-fixing bacterium Microvirga flocculans efficiently transformed thiacloprid.•M. flocculans transformed thiacloprid via hydrolysis and hydroxylation pathways.•A thermally stable nitrile hydratase converted thiacloprid to amide metabolite.•Co-expression of TnhC with NHase enhanced 4-folds higher NHase activity.•Thiacloprid amide inhibited the growth of M. flocculans and tnhA transcription.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The endoplasmic reticulum, a key cellular organelle, regulates a wide variety of cellular activities. Endoplasmic reticulum autophagy, one of the quality control systems of the endoplasmic reticulum, ...plays a pivotal role in maintaining endoplasmic reticulum homeostasis by controlling endoplasmic reticulum turnover, remodeling, and proteostasis. In this review, we briefly describe the endoplasmic reticulum quality control system, and subsequently focus on the role of endoplasmic reticulum autophagy, emphasizing the spatial and temporal mechanisms underlying the regulation of endoplasmic reticulum autophagy according to cellular requirements. We also summarize the evidence relating to how defective or abnormal endoplasmic reticulum autophagy contributes to the pathogenesis of neurodegenerative diseases. In summary, this review highlights the mechanisms associated with the regulation of endoplasmic reticulum autophagy and how they influence the pathophysiology of degenerative nerve disorders. This review would help researchers to understand the roles and regulatory mechanisms of endoplasmic reticulum-phagy in neurodegenerative disorders.
Isothermal sintering experiments were performed on the 316L stainless steel fiber felts with fiber diameters of 8 μm and 20 μm. Surface morphologies of the sintered specimens were investigated by ...using scanning electron microscopy (SEM) and optical microscopy. The results show that the amount of the sintering necks and the relative densities of the fiber felt increase with the increasing of both the sintering temperature and the sintering time. And the activation energies estimated present a decline at high relative densities for both 8 μm and 20 μm fiber felts. Moreover, the sintering densification of the fiber felts is dominated by volume diffusion mechanism at low temperature and relative densities. As more grain boundaries are formed at higher temperature and relative density, grain boundary diffusion will also contribute to the densification of the specimen.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Excitatory (E) and inhibitory (I) balance of neural network activity is essential for normal brain function and of particular importance to memory. Disturbance of E/I balance contributes to various ...neurological disorders. The appearance of neural hyperexcitability in Alzheimer's disease (AD) is even suggested as one of predictors of accelerated cognitive decline. In this study, we found that GAD67+, Parvalbumin+, Calretinin+, and Neuropeptide Y+ interneurons were progressively lost in the brain of APP/PS1 mice. Transplanted embryonic medial ganglionic eminence derived interneuron progenitors (IPs) survived, migrated, and differentiated into GABAergic interneuron subtypes successfully at 2 months after transplantation. Transplantation of IPs hippocampally rescued impaired synaptic plasticity and cognitive deficits of APP/PS1 transgenic mice, concomitant with a suppression of neural hyperexcitability, whereas transplantation of IPs failed to attenuate amyloid-β accumulation, neuroinflammation, and synaptic loss of APP/PS1 transgenic mice. These observations indicate that transplantation of IPs improves learning and memory of APP/PS1 transgenic mice via suppressing neural hyperexcitability. This study highlights a causal contribution of GABAergic dysfunction to AD pathogenesis and the potentiality of IP transplantation in AD therapy.
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