Mixed-Dimensional Partial Dealloyed PtCuBi/C as High-Performance Electrocatalysts for Methanol Oxidation with Enhanced CO Tolerance.

Developing efficient electrocatalysts for methanol oxidation reaction (MOR) is crucial in advancing the commercialization of direct methanol fuel cells (DMFCs). Herein, carbon-supported 0D/2D PtCuBi/C (0D/2D PtCuBi/C) catalysts are fabricated through a solvothermal method, followed by a partial electrochemical dealloying process to form a novel mixed-dimensional electrochemically dealloyed PtCuBi/C (0D/2D D-PtCuBi/C) catalysts. Benefiting from distinctive mixed-dimensional structure and composition, the as-obtained 0D/2D D-PtCuBi/C catalysts possess abundant accessible active sites. The introduction of Cu as a water-activating element weakens the COads , and oxophilic metal Bi facilitates the OHads , thereby enhancing its tolerance to CO poisoning and promoting MOR activity. The X-ray photoelectron spectroscopy (XPS) and X-ray absorption fine structure spectroscopy (XAFS) collectively reveal the electron transfer from Cu and Bi to Pt, the electron-enrichment effect induced by dealloying, and the strong interactions among Pt-M (Cu, Pt, and Bi) multi-active sites, which improve the tuning of the electronic structure and enhancement of electron transfer ability. Impressively, the optimized 0D/2D D-PtCuBi/C catalysts exhibit the superior mass activity (MA) of 17.68 A mgPt -1 for MOR, which is 14.86 times higher than that of commercial Pt/C. This study offers a proposed strategy for Pt-based alloy catalysts, enabling their use as efficient anodic materials in fuel cell applications.

In situ grown high-valence Mo-doped NiCo Prussian blue analogue for enhanced urea electrooxidation.

Mo-doped NiCo Prussian blue analogue (PBA) electrocatalysts self-supported on Ni foam are elaborately designed, which exhibit a low potential of 1.358 V (vs. RHE) to reach 100 mA cm-2 for catalyzing the urea oxidation reaction (UOR). The incorporation of high-valence Mo (+6) modifies the electronic structure and improves the electron transfer ability. Using X-ray photoelectron spectroscopy (XPS) and X-ray absorption spectroscopy (XAS) techniques, we confirm the effect of Mo doping on the NiCo PBA electronic structure.

Bismuth Incorporation in Palladium Hydride for the Electrocatalytic Ethanol Oxidation with Enhanced CO Tolerance.

Introducing nonmetal and oxophilic metal into palladium (Pd)-based catalysts is beneficial for boosting electrocatalysis, especially regarding the improvement of mass activity (MA) and CO tolerance. Herein, the stable bismuth-doped palladium hydride (Bi/PdH) networks have been successfully fabricated through a simple one-step method. The intercalation of interstitial H atoms expands the lattice of Pd, and the doping of oxophilic metal Bi restrains the adsorption of poisonous intermediates on the surface of Pd, thereby improving the activity and durability of the as-prepared catalysts in the ethanol oxidation reaction (EOR). The obtained Bi/PdH networks manifest a remarkable MA of 8.51 A·mgPd-1, which is 11.18 times higher than that of commercial Pd/C (0.76 A·mgPd-1). The CO-stripping analysis results indicate that Bi doping can significantly prohibit CO adsorption on the surface of the Bi/PdH networks. The density functional theory (DFT) calculations also reveal that Bi doping enhances the OH* adsorption on the catalyst surface and mitigates the interaction between Pd and CO* intermediates, providing deeper insights into the origin of the enhanced EOR activity and CO tolerance. This work describes an impactful path for producing high-performance and durable PdH-based nanocatalysts.

TLR2 mediates autophagy through ERK signaling pathway in Chlamydia psittaci CPSIT_p7 protein-stimulated RAW264.7 cells.

Chlamydia psittaci is a zoonotic pathogen found in birds and humans. Macrophages, major components of the innate immune system, can resist chlamydial infections and trigger adaptive immune responses. However, the molecular mechanisms underlying the action of macrophages against C. psittaci infection are not well understood. This study investigated the roles and mechanisms of plasmid-encoded protein CPSIT_p7 of C. psittaci in regulating autophagy in RAW264.7 cells. The results demonstrated that stimulation of RAW264.7 with C. psittaci plasmid protein CPSIT_p7 induced the expressions of the autophagy signaling primary regulators LC3 and Beclin1, which could also significantly induce the phosphorylation levels of ERK, JNK, p38, and Akt. Next, siRNA knockdown of TLR2 resulted in significant downregulation of CPSIT_p7-triggered autophagy in RAW264.7 cells. Moreover, the extracellular regulated protein kinase (ERK) inhibitor PD98059 markedly reduced autophagy in CPSIT_p7-stimulated macrophages. In summary, these results indicated that TLR2 plays an essential role in the induction of autophagy through the ERK signaling pathway in CPSIT_p7-stimulated RAW264.7 cells.

Urea impregnation into fungus pretreated corn stover to perform pyrolysis for production of nitrogen-containing bio-oil and nitrogen-doped biochar.

Urea was introduced into the fungal pretreated corn stover and then the urea soaked materials were subjected to pyrolysis for the production of nitrogen-containing bio-oil and nitrogen-doped biochar. The urea soaking effectively realized the enrichment of nitrogen-containing compounds in the bio-oil and the maximal content of the nitrogen-containing compounds in bio-oils reached up to 66.32% under 4 wt% urea concentration. Among the nitrogen-containing compounds, amines were the most dominant component with the maximal content of 41.17%. The higher urea concentration is beneficial to make more nitrogen be fixed in the biochar. The nitrogen content of the biochar reached up to 12.86 wt% under 8 wt% urea concentration. Nitrogen on the biochar surface existed in the form of pyrrolic-N, pyridinic-N and graphite-N. In conclusion, urea simple soak on fungus pretreated biomass to perform pyrolysis is a promising approach to obtain high value-added nitrogen-containing chemicals and nitrogen-doped biochar with high nitrogen content.

Chlamydia psittaci hypothetical inclusion membrane protein CPSIT_0842 evokes a pro-inflammatory response in monocytes via TLR2/TLR4 signaling pathways.

Chlamydia psittaci (C. psittaci) is an obligate intracellular pathogen that resides within a membrane-bound compartment known as the inclusion. Upon entering the host cell, Chlamydiae secrete numerous proteins to modify the inclusion membrane. Inclusion membrane (Inc) proteins are important pathogenic factors in Chlamydia and play crucial roles in the growth and development of Chlamydia. In the present study, the C. psittaci protein, CPSIT_0842, was identified and shown to localize to the inclusion membrane. Temporal analysis revealed that CPSIT_0842 is an early expression protein of Chlamydia. Moreover, this protein was shown to induce the expression of pro-inflammatory cytokines IL-6 and IL-8 in human monocytes (THP-1 cells) via the TLR2/TLR4 signaling pathway. CPSIT_0842 increases the expression of TLR2, TLR4, and adaptor MyD88. Suppression of TLR2, TLR4, and MyD88 markedly attenuated CPSIT_0842-induced production of IL-6 and IL-8. MAP kinases and NF-κB, important downstream molecules of TLR receptors in inflammatory signaling pathways, were also confirmed to be activated by CPSIT_0842. CPSIT_0842-induced production of IL-6 was reliant on activation of the ERK, p38, and NF-κB signaling pathways while IL-8 expression was regulated by the ERK, JNK, and NF-κB signaling pathways. Specific inhibitors of these signaling pathways significantly decreased CPSIT_0842-mediated expression of IL-6 and IL-8. Together these findings demonstrate that CPSIT_0842 upregulates the expression of IL-6 and IL-8 via TLR-2/TLR4-mediated MAPK and NF-κB signaling pathways in THP-1 cells. Exploring these molecular mechanisms enhances our understanding of C. psittaci pathogenesis.

Inhibition of miR-141-3p attenuates apoptosis of neural stem cells via targeting PBX1 to regulate PROK2 transcription in MCAO mice.

MicroRNA-141-3p (miR-141-3p) has been found to be altered in the brain following a stroke. Herein, we investigate the impact of miR-141-3p on the apoptosis of neural stem cells (NSCs) in mice with middle cerebral artery occlusion (MCAO) and the potential mechanisms involved. Eight-week-old mice were injected intracerebroventricularly with miR-141-3p, antagomir-141-3p, or agomir negative control 2 h before MCAO, and animal behavior tests and infraction volume measurements were performed 24 h later. MCAO-mediated brain injury and NSCs apoptosis were observed by H&E, TTC, and TUNEL staining. The expression of cleaved caspase-3 and Ki67 was detected by western blotting. The luciferase reporter assay proved that miR-141-3p in combination with its target gene PBX homeobox 1 (PBX1). Exogenous miR-141-3p (agomir-141-3p) treatment increased infraction volume and brain edema and damaged neurological functions compared to control mice. Agomir-141-3p increased miR-141-3p expression in brain tissue of mice with MCAO and suppressed PBX1 expression. The effects of the agomir-141-3p-induced apoptosis in NSCs treated with oxygen-glucose deprivation (OGD)/reoxygenation (R) were abolished by PBX1 overexpression. The results from UCSC and JASPAR database showed that prokineticin 2 (PROK2) was a transcription factor of PBX1. The expression of PROK2 was transcriptionally regulated by PBX1 using RT-PCR and western blot assays. The effects of the apoptosis-promoting caused by PBX1 inhibition in NSCs treated with OGD/R were reversed by PROK2 inhibition. In conclusion, the miR-141-3p/PBX1/PROK2 axis might be a novel therapeutic target for the apoptosis of NSCs in MCAO.

Ternary PdCoP nanoparticles with nanopore structures: synergic boosting of electrocatalytic activity for ethanol oxidation.

PdCoP nanoparticles (PdCoP NPs) with nanopore structures were synthesized by a facile one-pot solvothermal approach. Due to their unique geometric structures and the electronic and synergistic effects among multiple components, the optimized PdCoP NPs (PdCoP-NPs-1) show superior mass activity (5.97 A mgPd-1) for the ethanol oxidation reaction under alkaline conditions.

Effect of pretreatment with Phanerochaete chrysosporium on physicochemical properties and pyrolysis behaviors of corn stover.

Fungal pretreatment can selectively degrade partial biomass components, which undoubtedly exerts a significant influence on biomass pyrolysis behavior. The corn stover was pretreated with Phanerochaete chrysosporium, and its influence on the physicochemical properties and pyrolysis behaviors of biomass together with the product characteristics were investigated. The Phanerochaete chrysosporium was more active to degrade hemicellulose and lignin. The hemicellulose and lignin contents in corn stover were decreased by 35.14 % and 31.80 %, respectively, after five weeks pretreatment, compared to the untreated sample. The reaction activation energy decreased from 52.89 kJ·mol-1 for the untreated sample to 40.88 kJ·mol-1 for the sample pretreated for five weeks. The Phanerochaete chrysosporium pretreatment was beneficial to the biochar production but exerted an unfavorable effect on the texture structure. The Phanerochaete chrysosporium also had an obvious influence on the bio-oil compositions. This study can provide a scientific reference for the application of biological pretreatment for biomass pyrolysis technology.

Low Pt-Doped Crystalline/Amorphous Heterophase Pd12P3.2 Nanowires as Efficient Catalysts for Methanol Oxidation.

Pd-based catalysts are attractive anodic electrocatalysts for direct methanol fuel cells owing to their low cost and natural abundance. However, they suffer from sluggish reaction kinetic and insufficient electroactivity in methanol oxidation reaction (MOR). In this work, we developed a facile one-pot approach to fabricate low Pt-doped Pd12P3.2 nanowires with crystalline/amorphous heterophase (termed Pt-Pd12P3.2 NWs) for MOR. The unique crystalline/amorphous heterophase structures promote the catalytic activity by the plentiful active sites at the phase boundaries and/or interfaces and the synergistic effect between different phases. Moreover, the incorporation of trace Pt into Pd lattices modifies the electronic structure and improves the electron transfer ability. Therefore, the obtained Pt-Pd12P3.2 NWs display significantly enhanced electrocatalytic performance toward MOR with the mass activity of 2.35 A mgPd+Pt-1, which is 9.0, 2.9, and 2.0 times higher than those of the commercial Pd/C (0.26 A mgPd-1), Pd12P3.2 NWs (0.82 A mgPd-1), and commercial Pt/C (1.19 A mgPt-1). The high mass activity enables the Pt-Pd12P3.2 NWs to be the promising Pd-based catalysts for MOR.

The increase of α-synuclein and alterations of dynein in A53T transgenic and aging mouse.

The dynein protein plays a key role in the degradation pathway by attaching to targeted molecules and transporting the autophagosome to the centrosome. Aging plays an important role in the pathogenesis of Parkinson's disease (PD), but its effect on dynein is not clear. In this study we analyzed behavioral characteristics using the rod endurance test and climbing rod time test in different aged mice (3 months, 12 months, 20 months), and measured protein expression of dynein, α-synuclein, Tctex-1, and LC3 in the substantianigra of the mice by Western blot. The mRNA levels of dynein, α-synuclein, LC3 and Tctex-1 were measured by quantitative real time reverse transcription PCR, and detecting expression of dynein and α-synuclein by immunofluorescence. We found the motor functions of A53T mutant mice, in 12 months and 20 months, decreased more significantly compared with normal mice (p < 0.05). In addition, the expression of dynein, LC3-Ⅱ and Tctex-1 proteins in the substantia nigra of the two groups decreased with age. However, α-synuclein protein increased gradually with age, with significantly higher levels in the PD groups compared with age matched controls (p < 0.05). These results were confirmed by immunofluorescence. Our data demonstrates that dynein and other autophagy proteins change with age, and this is associated with increased α-synuclein. Therefore, therapeutics that prevent dynein dysfunction may offer novel treatments for PD and other autophagy related diseases.

The role of an enzymatically inactive CPAF mutant vaccination in Chlamydia muridarum genital tract infection.

Chlamydia trachomatis urogenital tract infection causes pelvic inflammatory disease and infertility, increases the risk of co-infection with HPV and HIV. Chlamydial vaccination is considered the most promising approach to prevent and control its infection. Among various chlamydial vaccine candidates, chlamydial protease-like activity factor (CPAF) have been reported to provide robust protective immunity against genital chlamydial infection in mice with reduced vaginal shedding and oviduct pathology. However, CPAF is a serine protease which has enzymatical activity to degrade a large number of substrates. In order to increase the safety of CPAF vaccine, in this study, we used a mutant CPAF that is deficient in enzymatical activity to determine whether proteolytic activity of CPAF affect its vaccine efficacy. The wild type or mutant CPAF immunization causes a significant lower chlamydial shedding from the vaginal and resolve the infection as early as day 20, compared to day 28 in adjuvant control mice. More important, reduced upper reproductive tract pathology were also observed in these two groups. The mutant or wild type CPAF immunization induced not only robust splenic IFN-γ and serum IgG2a but also sIgA secretion in the vaginal fluids. Furthermore, neutralization of chlamydia with immune sera did not provide protection against oviduct pathology. However, adoptive transfer of CD4+ splenocytes isolated from the mutant or wild type CPAF immunized mice resulted in a significant and comparable reduced oviduct pathology. Our results indicate mutant CPAF vaccination is as same efficacy as wild type, and the protection relies on CD4+ T cells, which will further promote the development of CPAF as clinical chlamydial vaccine.

Dimensional Gradient Structure of CoSe2@CNTs-MXene Anode Assisted by Ether for High-Capacity, Stable Sodium Storage.

Recently, abundant resources, low-cost sodium-ion batteries are deemed to the new-generation battery in the field of large-scale energy storage. Nevertheless, poor active reaction dynamics, dissolution of intermediates and electrolyte matching problems are significant challenges that need to be solved. Herein, dimensional gradient structure of sheet-tube-dots is constructed with CoSe2@CNTs-MXene. Gradient structure is conducive to fast migration of electrons and ions with the association of ether electrolyte. For half-cell, CoSe2@CNTs-MXene exhibits high initial coulomb efficiency (81.7%) and excellent cycling performance (400 mAh g-1 cycling for 200 times in 2 A g-1). Phase transformation pathway from crystalline CoSe2-Na2Se with Co and then amorphous CoSe2 in the discharge/charge process is also explored by in situ X-ray diffraction. Density functional theory study discloses the CoSe2@CNTs-MXene in ether electrolyte system which contributes to stable sodium storage performance owing to the strong adsorption force from hierarchical structure and weak interaction between electrolyte and electrode interface. For full cell, CoSe2@CNTs-MXene//Na3V2 (PO4)3/C full battery can also afford a competitively reversible capacity of 280 mAh g-1 over 50 cycles. Concisely, profiting from dimensional gradient structure and matched electrolyte of CoSe2@CNTs-MXene hold great application potential for stable sodium storage.

Interface Engineering of a Sandwich Flexible Electrode PAn@CoHCF Rooted in Carbon Cloth for Enhanced Sodium-Ion Storage.

With the growth of demand for flexible devices, the development of flexible electrodes used in energy storage devices has attracted much attention of researchers. In this work, a thin flexible cathode of Prussian blue analogue@polyaniline rooted in carbon cloth has been fabricated. The Prussian blue analogue (PBA) is an electrochemically active material grafted on flexible carbon cloth substrates, which had been precoated with polyaniline. Polyaniline as an intermediate layer can not only improve the overall electronic conductivity of the electrode but also enhance the adhesion and load of the PBAs. The electrochemical properties of the flexible cathode with a "sandwich" structure were determined in half-cells, with a superior capacity of 151 mA h·g-1 and a striking cyclability with 96% capacity retention over 100 cycles at 100 mA h·g-1. This work proposes a novel perspective for the structural construction and material synthesis of flexible positive electrodes and gives new options for the practical application of flexible batteries.

Chlamydia trachomatis glycogen synthase promotes MAPK-mediated proinflammatory cytokine production via TLR2/TLR4 in THP-1 cells.

AIMS: To investigate the roles and mechanisms of C. trachomatis glycogen synthase (GlgA) in regulating the inflammatory response in THP-1 cells. MAIN METHODS: In this work, after THP-1 cells were stimulated with GlgA, transcript and protein expression levels were measured by qRT-PCR and ELISA, respectively. Western blotting and immunofluorescence were used to determine the signaling pathway involved in the inflammatory mechanism. KEY FINDINGS: GlgA elicited the expression of interleukin-8 (IL-8), interleukin-1beta (IL-1ß) and tumor necrosis factor alpha (TNF-α) in THP-1 cells, and the blockade of TLR2 and TLR4 signaling abrogated the induction of IL-8, TNF-α and IL-1ß expression. Similarly, IL-8, IL-1ß and TNF-α secretion was reduced by transfection with a dominant negative plasmid (pDeNyhMyD88). Moreover, Western blotting and immunofluorescence experiments further validated that MAPKs and NF-кB signaling are involved in the transcription and translation of these cytokines. Treatment of the cells with ERK and JNK inhibitors dramatically attenuated the induction of IL-8, IL-1ß and TNF-α. SIGNIFICANCE: These results suggest that GlgA contributes to inflammation during C. trachomatis infection via the TLR2, TLR4 and MAPK/NF-кB pathways, which may enhance our understanding of the pathogenesis of C. trachomatis.

A Ni-doping-induced phase transition and electron evolution in cobalt hexacyanoferrate as a stable cathode for sodium-ion batteries.

Prussian blue analogues are potential competitive energy storage materials due to their diverse metal combinations and wide three-dimensional ion channels. Here, we prepared a new highly crystalline monoclinic nickel-doped cobalt hexacyanoferrate via a feasible and simple one-step co-precipitation method. In the process of sodium-ion de-intercalation, three stable charge and discharge platforms, which are consistent with the cyclic voltammetry performance, are seen for the first time, showing the function of nickel ions in Prussian blue. Furthermore, the charge transfer and structural evolution caused by the transmission of sodium ions were well revealed via ex situ XRD, ex situ XPS, and in situ EIS studies. Simulation calculations are performed relating to the energy band structure and the highest-occupied bonding orbitals of the system in different charge states, revealing the charge and discharge mechanism of the nickel-doped material and the reason for the emergence of the new platform at low voltages. In addition, NaNi0.17Co0.83Fe(CN)6 also delivers a striking capacity of 146 mA h g-1 and superior cyclability, with 93% capacity retention over 100 cycles; it can be considered as a promising alternative cathode material for use in sodium-ion batteries.

Inhibition of SGLT1 protects against glycemic variability-induced cardiac damage and pyroptosis of cardiomyocytes in diabetic mice.

AIMS: Glycemic variability has been shown to be more harmful in the development of diabetic complication than sustained chronic hyperglycemia. In this present study, we tried to reveal the effects of glycemic variability on cardiac damage in diabetic mice and investigate whether sodium-glucose cotransporter 1 (SGLT1), an important cardiac glucose transporter, functions as an important mediator in the process. MATERIALS AND METHODS: Type 2 diabetes mellitus (DM) mice were induced by a high-fat diet and intraperitoneal injection of streptozotocin (STZ), and then glycemic variability in type 2 diabetes mellitus (GVDM) was induced by alternately injecting insulin and glucose to DM mice. In order to determine the roles of SGLT1 in GVDM mice, SGLT1 inhibition was performed using shRNA against SGLT1. The blood glucose level, the cardiac function and myocardial injury were assessed. And the expressions of SGLT1 and the activations of NLRP3/caspase-1 pathway and NF-κB in left ventricular tissues were measured. KEY FINDINGS: The results showed that SGLT1 was highly expressed in heart of GVDM mice compared to control and DM groups, and knockdown of SGLT1 reduced glycemic variability in GVDM mice. Moreover, glycemic variability impaired cardiac function, aggravated cardiac injury and induced NLRP3/caspase-1-mediated inflammatory response and pyroptosis. And knockdown of SGLT1 significantly attenuated the cardiac damages that induced by glycemic variability. SIGNIFICANCE: The results indicated that glycemic variability could cause cardiac damage and induce inflammatory response and pyroptosis of cardiomyocytes in diabetic mice, which could be partially blocked by SGLT1 silence.

Higher uric acid is associated with better discharge recovery and short-term outcome in stroke patients treated with thrombolysis.

BACKGROUND: Uric acid (UA) possesses antioxidant features and potential neuroprotective effects. However, conflicting results regarding the association between serum uric acid (SUA) levels and the prognosis of stroke have been obtained. We aimed to assess whether SUA is related to discharge recovery and short-term outcomes in patients who underwent thrombolysis therapy. METHODS: We recruited 393 consecutive patients who were diagnosed with acute ischaemic stroke (AIS) and treated with thrombolysis. The demographic information, including sex and age, was collected. Haematology tests, including SUA, fasting plasma glucose (FPG), and blood lipid parameters, were performed under fasting conditions the morning after admission. The modified Rankin Scale (mRS) was used to assess the functional outcome of patients at discharge and 3 months after onset. RESULTS: A negative correlation was observed between the levels of SUA and the National Institute of Health Stroke Scale (NIHSS) score at discharge (r = - 0.171, P = 0.003). Additionally, a positive correlation was observed between the levels of SUA and the difference between the baseline NIHSS and discharge NIHSS (r = 0.118, P = 0.032). The levels of SUA in the patients with good outcomes (353.76 ± 93.05) were higher than those in the patients with poor outcomes (301.99 ± 92.24; P = 0.015) at 3 months. The multivariate logistic regression analysis demonstrated that a higher SUA level (odds ratio 0.988, 95% confidence interval 0.985-0.991, P = 0.002) was an independent predictor of a good outcome at 3 months. CONCLUSION: Higher SUA levels were associated with better discharge recovery and 3-month outcomes in patients with ischaemic stroke who received thrombolysis.

Remediation of artificially contaminated soil and groundwater with copper using hydroxyapatite/calcium silicate hydrate recovered from phosphorus-rich wastewater.

Excessive copper (Cu) in contaminated soil and groundwater has attracted continuous attentions due to the bioaccumulation and durability. In this study, the feasibility of remediation of heavy metal pollution in soil and groundwater was investigated using hydroxyapatite/calcium silicate hydrate (HAP/C-S-H) recovered from phosphorus-rich wastewater in farmland. The results show that the pH has a strong effect on copper removal from Cu-contaminated groundwater but the impact of ion strength on the removal is weak. In general, high pH and low ion strength give better results in copper removal. Kinetic and isotherm data from the study fit well with Pseudo-second-order kinetic model and Langmuir isotherm model, respectively. The maximum adsorption capacity of HAP/C-S-H (138 mg/g) was higher than that of C-S-H (90.3 mg/g) when pH value, temperature, and ionic strength were 5, 308 K, and 0.01 M, respectively. Thermodynamics results indicate that Cu removal is a spontaneous and endothermic process. X-ray diffraction (XRD) results show that the mechanism of copper removal involves physical adsorption, chemical precipitation and ion exchange. For the remediation of Cu-contaminated soil, 76.3% of leachable copper was immobilized by HAP/C-S-H after 28 d. Acid soluble Cu, the main contributor to biotoxicity, decreased significantly while reducible and residual Cu increased. After immobilization, the acid neutralization capacity of the soil increased and the dissolution of copper was substantially reduced in near-neutral pH. It can be concluded that HAP/C-S-H is an effective, low-cost and eco-friendly reagent for in-situ remediation of heavy metal polluted soil and groundwater.

Chlamydia psittaci Plasmid-Encoded CPSIT_P7 Elicits Inflammatory Response in Human Monocytes via TLR4/Mal/MyD88/NF-κB Signaling Pathway.

The chlamydial plasmid, an essential virulence factor, encodes plasmid proteins that play important roles in chlamydial infection and the corresponding immune response. However, the virulence factors and the molecular mechanisms of Chlamydia psittaci are not well understood. In the present study, we investigated the roles and mechanisms of the plasmid-encoded protein CPSIT_P7 of C. psittaci in regulating the inflammatory response in THP-1 cells (human monocytic leukemia cell line). Based on cytokine arrays, CPSIT_P7 induces the expression of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) in THP-1 cells. Moreover, the expression levels of IL-6, IL-8, and MCP-1 stimulated by CPSIT_P7 declined after silencing of the Toll-like receptor 4 (TLR4) gene using small interfering RNA and transfection of a dominant negative plasmid encoding TLR4 (pZERO-hTLR4). We further demonstrated that transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) and the dominant negative plasmid encoding Mal (pDeNy-hMal) could also abrogate the expression of the corresponding proteins. Western blot and immunofluorescence assay results showed that CPSIT_P7 could activate nuclear factor κB (NF-κB) signaling pathways in THP-1 cells. Altogether, our results indicate that the CPSIT_P7 induces the TLR4/Mal/MyD88/NF-κB signaling axis and therefore contributes to the inflammatory cytokine response.