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A polyanion cluster H Na Cs [Co (μ -OH) (H O) (HPO ) (B-α-PW O ) ]Cl·40H O ( ) was made with the guidance of the lacunary directing strategy under hydrothermal conditions. Compound was characterized by single-crystal X-ray diffraction, powder X-ray diffraction, and thermogravimetric analysis, respectively. Single-crystal X-ray diffraction analyses showed that consists of three anions [B-α-PW O ] and a cyclic cationic [Co (μ -OH) (H O) ] and two anions HPO . Variable-magnetic properties indicate antiferromagnetic interactions in . Visible-light-driven hydrogen evolution tests demonstrated that was an efficient water reduction catalyst with an H evolution rate of 1217.6 μmol h g .

Viruses have evolved sophisticated mechanisms to manipulate host cell organelles to serve as niches for persistence and proliferation. In the present study, we aimed to investigate the role of cellular organelles in the replication of porcine reproductive and respiratory syndrome virus (PRRSV). We found that the morphology of mitochondria and the endoplasmic reticulum (ER) were both altered, and the contact between these two organelles was enhanced during PRRSV infection. By the overexpression of PRRSV-encoded open reading frames, we identified that only glycoprotein 5 (GP5) was essential for ER-mitochondria contact. Further investigation revealed that GP5 interacted with the ER inositol 1,4,5-triphosphate receptor (IP3R) and the mitochondrial voltage-dependent anion channel (VDAC1) to promote the Ca 2+ efflux from ER into mitochondria. Excessive mitochondrial Ca 2+ uptake resulted in mitochondrial dysfunction and substantial mitochondrial reactive oxygen species (mROS) production. Elevated mROS activated autophagy through the AMPK/mROR/ULK1 axis to facilitate PRRSV replication. GP5-induced mROS also triggered the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome. Inhibition of autophagy augmented NLRP3 inflammasome activation and exhibited an anti-PRRSV effect, suggesting autophagy counteracted the NLRP3-mediated innate immune response. Overall, our findings highlighted the importance of cellular organelles in virus-host interactions and provided new insights into the complex interplay between virus replication and innate immune responses. Porcine reproductive and respiratory syndrome virus (PRRSV) presents a significant economic concern for the global swine industry due to its connection to serious production losses and increased mortality rates. There is currently no specific treatment for PRRSV. Previously, we had uncovered that PRRSV-activated lipophagy to facilitate viral replication. However, the precise mechanism that PRRSV used to trigger autophagy remained unclear. Here, we found that PRRSV GP5 enhanced mitochondrial Ca 2+ uptake from ER by promoting ER-mitochondria contact, resulting in mROS release. Elevated mROS induced autophagy, which alleviated NLRP3 inflammasome activation for optimal viral replication. Our study shed light on a novel mechanism revealing how PRRSV exploits mROS to facilitate viral replication.

The urgent demands for high-energy-density rechargeable batteries promote a flourishing development of Li metal anode. However, the uncontrollable dendrites growth and serious side reactions severely limit its commercial application. Herein, an artificial LiF-rich solid electrolyte interphase (SEI) is constructed at molecular-level using one-step photopolymerization of hexafluorobutyl acrylate based solution, where the LiF is in situ generated during photopolymerization process (denoted as PHALF). The LiF-rich layer comprised flexible polymer matrix and inorganic LiF filler not only ensures intimate contact with Li anode and adapts volume fluctuations during cycling but also regulates Li deposition behavior, enabling it to suppress the dendrite growth and block side reactions between the electrolyte and Li metal. Accordingly, the PHALF-Li anode presents superior stable cycling performance over 500 h at 1 mA·cm −2 for 1 mA·h·cm −2 without dendrites growth in carbonate electrolyte. The work provides a novel approach to design and build in situ artificial SEI layer for high-safety and stable Li metal anodes.

Cluster-based functional materials have made remarkable progress owing to their wonderful structures and distinctive physicochemical performances, one of on-going advancements of which is basically driven by synthetic chemistry of exploring and constructing novel nanosized gigantic polyoxometalate (POM) aggregates. In this article, an unprecedented nanoscale hexameric arsenotungstate aggregate Na 9 K 16 H 4 [Er 0.5 K 0.5 (H 2 O) 7 ][Er 5 W 10 O 26 (H 2 O) 14 ][B- α -AsW 9 O 33 ] 6 ·102H 2 O ( 1 ) has been synthesized by the combined synthetic strategy of simultaneously using the arsenotungstate precursor and simple tungstate material in a highly acidic aqueous solution. The {[Er 5 W 10 O 26 (H 2 O) 14 ][B-α-AsW 9 O 33 ] 6 } 31− polyanion in 1 consists of an intriguing dumbbell-shaped pentadeca-nuclear W-Er heterometal {Er 5 W 10 O 26 (H 2 O) 14 } 23+ cluster connecting six trilacunary [B-α-AsW 9 O 33 ] 9− moieties, which has never been seen previously. Furthermore, through electropolymerization of 1 and pyrrole on the conductive substrate, a thickness-controllable and robust 1 -PPY (PPY = polypyrrole) hybrid film was successfully prepared, which represents the first POM-PPY film assembled from high-nuclear lanthanide (Ln) encapsulated POM and PPY hitherto. The 1 -PPY film-based electrochemical biosensor exhibits a favorable recognition performance for ochratoxin A in multiple media. This work not only provides a feasible combined synthetic strategy of the POM precursor and simple tungstate material for constructing complicated multi-Ln-inserted POM aggregates, but also offers a promising electrochemical platform constructed from POM-based conductive films for identifying trace biomolecules in complex environments.

Viral infection is a significant risk factor for fertility issues. Here, we demonstrated that infection by neurotropic alphaherpesviruses, such as pseudorabies virus (PRV), could impair female fertility by disrupting the hypothalamus-pituitary-ovary axis (HPOA), reducing progesterone (P4) levels, and consequently lowering pregnancy rates. Our study revealed that PRV exploited the transient receptor potential mucolipin 1 (TRPML1) and its lipid activator, phosphatidylinositol 3,5-bisphosphate (PI(3,5)P 2 ), to facilitate viral entry through lysosomal cholesterol and Ca 2+ . P4 antagonized this process by inducing lysosomal storage disorders and promoting the proteasomal degradation of TRPML1 via murine double minute 2 (MDM2)-mediated polyubiquitination. Overall, the study identifies a novel mechanism by which PRV hijacks the lysosomal pathway to evade P4-mediated antiviral defense and impair female fertility. This mechanism may be common among alphaherpesviruses and could contribute significantly to their impact on female reproductive health, providing new insights for the development of antiviral therapies.

Two new nonaborates, Na2Ba0.5[B9O15]·H2O (1) and Na4Ca1.5[B9O16(OH)2] (2), have been solvothermally made with mixed alkali and alkaline-earth metal cationic templates. 1 and 2 are constructed by two different types of nonaborate clusters. In 1, the [B9O19]11− cluster is composed of three corner-sharing [B3O7]5− clusters, of which two of them interconnect to the 1D B3O7-based chains and are further bridged to the 3D framework with 7 types of 10-MR channels by another [B3O7]5− bridging cluster. The [B9O18(OH)2]11− cluster in 2 is made of four BO4-sharing [B3O8]7− clusters. As a 4-connected node, the interconnections of [B9O18(OH)2]11− construct the unpreceded 2D layer with large 14-MR windows, which are further joined by H-bonds to the 3D supramolecular framework. UV–Vis absorption spectra reveal that both 1 and 2 have short cutoff edges below 190 nm, exhibiting bandgaps of 6.31 and 6.39 eV, respectively, indicating their potential applications in deep UV (DUV) regions.

Three new hexa-Ni-substituted Keggin-type polyoxometalates (POMs), [Ni6(OH)3- (DACH)3(H2O)6(PW9O34)]·31H2O (1), [Ni(DACH)2][Ni6(OH)3(DACH)3(HMIP)2(H2O)2(PW9O34)]·56 H2O (2), and [Ni(DACH)2][Ni6(OH)3(DACH)2(AP)(H2O)5(PW9O34)]·2H2O (3) (DACH = 1,2-Diami- nocyclohexane, MIP = 5-Methylisophthalate, AP = Adipate) were successfully made in the presence of DACH under hydrothermal conditions. 1 is an isolated hexa-Ni-substituted Keggin unit decorated by DACH. In order to further construct POM cluster-organic frameworks (POMCOFs) on the basis of 1, by analyzing the steric hindrances and orientations of the POM units, the rigid HMIP and flexible AP ligands were successively incorporated, and another anionic monomeric POM 2 and the new 1D POM cluster organic chain (POMCOC) 3 were obtained. HMIP ligand still acts as a decorating group on the Ni6 core of 2 but results in the different spatial arrangement of the {Ni6PW9} units. AP ligands in 3 successfully bridge adjacent isolated POM cluster units to 1D POMCOC with left-hand helices. The AP in 3 is the longest aliphatic carboxylic acid ligand in POMs, and the 1D POM cluster-AP helical chain represents the first 1D POMCOC with a helical feature.

RAB GTPases (RABs) control intracellular membrane trafficking with high precision. In the present study, we carried out a short hairpin RNA (shRNA) screen focused on a library of 62 RABs during infection with porcine reproductive and respiratory syndrome virus 2 (PRRSV-2), a member of the family Arteriviridae . We found that 13 RABs negatively affect the yield of PRRSV-2 progeny virus, whereas 29 RABs have a positive impact on the yield of PRRSV-2 progeny virus. Further analysis revealed that PRRSV-2 infection transcriptionally regulated RAB18 through RIG-I/MAVS-mediated canonical NF-κB activation. Disrupting RAB18 expression led to the accumulation of lipid droplets (LDs), impaired LDs catabolism, and flawed viral replication and assembly. We also discovered that PRRSV-2 co-opts chaperone-mediated autophagy (CMA) for lipolysis via RAB18, as indicated by the enhanced associations between RAB18 and perlipin 2 (PLIN2), CMA-specific lysosomal associated membrane protein 2A (LAMP2A), and heat shock protein family A (Hsp70) member 8 (HSPA8/HSC70) during PRRSV-2 infection. Knockdown of HSPA8 and LAMP2A impacted on the yield of PRRSV-2 progeny virus, implying that the virus utilizes RAB18 to promote CMA-mediated lipolysis. Importantly, we determined that the C-terminal domain (CTD) of HSPA8 could bind to the switch II domain of RAB18, and the CTD of PLIN2 was capable of associating with HSPA8, suggesting that HSPA8 facilitates the interaction between RAB18 and PLIN2 in the CMA process. In summary, our findings elucidate how PRRSV-2 hijacks CMA-mediated lipid metabolism through innate immune activation to enhance the yield of progeny virus, offering novel insights for the development of anti-PRRSV-2 treatments.

Chromatin dynamics regulated by epigenetic modification is crucial in genome stability and gene expression. Various epigenetic mechanisms have been identified in the pathogenesis of human diseases. Here, we examined the effects of ten epigenetic agents on pseudorabies virus (PRV) infection by using GFP-reporter assays. Inhibitors of bromodomain protein 4 (BRD4), which receives much more attention in cancer than viral infection, was found to exhibit substantial anti-viral activity against PRV as well as a range of DNA and RNA viruses. We further demonstrated that BRD4 inhibition boosted a robust innate immune response. BRD4 inhibition also de-compacted chromatin structure and induced the DNA damage response, thereby triggering the activation of cGAS-mediated innate immunity and increasing host resistance to viral infection both in vitro and in vivo. Mechanistically, the inhibitory effect of BRD4 inhibition on viral infection was mainly attributed to the attenuation of viral attachment. Our findings reveal a unique mechanism through which BRD4 inhibition restrains viral infection and points to its potent therapeutic value for viral infectious diseases.

Interleukin 10 (IL‐10)‐producing B cells (B10 cells) are a canonical cell fraction for regulating other activities of immune cells. Posttranscriptional modification of IL‐10 in B10 cells is not yet fully understood. Short‐chain fatty acids play an important role to regulate the functions of immune cells. This study aims to clarify the role of propionic acid (PA), a short‐chain fatty acid, in regulating the expression of IL‐10 in B10 cells. Blood samples were collected from patients with food allergy (FA) and healthy subjects. Serum and cellular components were prepared with the samples, and analysed by enzyme‐linked immunosorbent assay and flow cytometry, respectively. The results showed that serum PA levels were lower in FA patients. PA concentrations were negatively correlated with serum cytokine Th2 concentrations, specific IgE concentrations in serum and skin prick test results. The peripheral frequency of B10 cells and the production of IL‐10 in B cells were also associated with serum PA concentrations. Activation of B cells by CpG induced the production of IL‐10 and tristetretrprolin (TTP), in which TTP caused the spontaneous decay of IL‐10 mRNA. PA was necessary to stabilize the IL‐10 mRNA in B cells by inducing the production of granzyme B, which resulted in the degradation of the IL‐10 mRNA. Administration of PA attenuated FA response in mice by maintaining homeostasis of B10 cells. In conclusion, PA is needed to stabilize the expression of IL‐10 in B10 cells. PA administration can mitigate experimental FA by maintaining B10 cell functions.