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The surface of poly (p-phenylene benzobisoxazole) (PBO) fibers with self-healing and ultraviolet (UV)-resistance performance play the key role in prolonging their service lifespan. Although great advances have been made in the single aspect of above two properties, integration of self-healing and anti-UV performance into the surface of PBO fiber is still a challenge. In this study, the coagulation strategy mediated by metal-organic framework (MOF) is proposed to construct the multifunctional surface of PBO fibers. The spindle-like iron (III)-based MOF (MIL-88B-NH 2) nanocrystals are firstly immobilized onto the surface of PBO-COOH through hydrothermal reaction, then serving as the medium layer to further immobilize sufficient graphene oxide (GO) nanosheets. Benefitting from the favorable near-infrared (NIR, 808 nm) photothermal conversion performance of GO nanolayers, the monofilament composite-PBO@Fe-MIL-88B-NH 2 -GO-TPU (thermoplastic polyurethane) exhibited a stable and high self-healing efficiency (approximately 80%) within five cycle times. Meanwhile, the cooperative adsorption and shielding weaken effects of MOF-GO nanolayers enabled PBO fibers with excellent anti-UV properties that are superior to much reported literatures after 96 h aging time and eventually increased by 75% compared with untreated PBO fiber. In view of the varieties and multifunctionalities of MOFs and carbon nanomaterials, MOF-mediated coagulation strategy would provide guidance for preparing multifunctional composite materials. [ABSTRACT FROM AUTHOR]

The channel-forming membrane glycoprotein pannexin 1 (Panx1) is best characterized as an ATP release channel. To investigate the trafficking and sorting of Panx1, we used polarized MDCK cells and non-polarized BICR-M1R k cells to track the fate of GFP-tagged Panx1. In non-polarized cells, Panx1 was found throughout the plasma membrane, including the lamellipodia of the tumor cells and the cell surface-targeting domain was mapped to residues 307–379. Panx1 was preferentially enriched at the apical membrane domain of polarized MDCK cells grown as monolayer sheets or as spheroids. Residual Panx1 localized within basolateral membranes of polarized MDCK cells was independent of a putative dileucine sorting motif LL365/6 found within the C-terminal of Panx1. Unexpectedly, stable expression of a Panx1 mutant, where a putative tyrosine-based basolateral sorting motif (YxxØ) was mutated (Y308F), or a truncated Δ379 Panx1 mutant, caused MDCK cells to lose cell-cell contacts and their ability to polarize as they underwent a switch to a more fibroblast-like phenotype. We conclude that Panx1 is preferentially delivered to the apical domain of polarized epithelial cells, and Panx1 mutants drive phenotypic changes to MDCK cells preventing their polarization. Synopsis: Panx1 is best known as an ATP-release channel. In the current study we found Panx1 to be preferentially trafficked to the apical domain of MDCK cells independent of encoding two putative basolateral targeting motifs. While the 307–379 polypeptide domain of Panx1 was required for cell surface delivery of Panx1, reduced transport of Panx1 to the cell surface was accompanied by phenotypic changes that prevented MDCK cell polarization. [ABSTRACT FROM AUTHOR]

Rice, the most consumed in Asian and constitute important source of amino acids. The present study evaluated the suitability of near-infrared reflectance spectroscopy to predict amino acid contents (AACs) using 1210 rice samples representing a wide range of grain qualities and genetic background. Calibration models established by combining different spectral derivatives, scatter and baseline correction methods, and regression algorithm were compared using full cross validation. A modified partial least square model (MPLS) with the spectral derivative treatment "2, 3, 3, 1" (2nd order derivative computed based on 3 data points, and 3 and 1 data points in the 1st and 2nd smoothing, respectively) and weighted multiplicative scattering correction (WMSC) method was identified as the best model for simultaneously measurement of 14 AACs in brown rice flour. The high model quality is reflected by RSQ of 0.914∼0.969, standard error of calibration (SEC) of 0.0187%∼0.0553%, 1-VR of 0.901∼0.955, SECV of 0.0214%∼0.0579%, and residual prediction deviation (RPD) of 2.58∼3.85. These results indicated that NIRS coupled with an appropriate pre-processing, multivariate regression could be a rapid and reliable method for quantification of AACs in rice breeding programs and quality control in the food industry. Factors that would influence model quality were investigated and discussed. • NIRS is capable of accurately quantifying 14 amino acids contents in diverse rice samples. • MPLS was the most robust regression method. • MSC and 2nd derivation were suitable pre-processing methods. • NIRS is applicable for high-throughput screening. [ABSTRACT FROM AUTHOR]

Type II topoisomerases modify DNA supercoiling, and crystal structures suggest that they sharply bend DNA in the process. Bacterial gyrases are a class of type II topoisomerases that can introduce negative supercoiling by creating a wrap of DNA before strand passage. Isoforms of these essential enzymes were compared to reveal whether they can bend or wrap artificially stiffened DNA. Escherichia coli gyrase and human topoisomerase IIα were challenged with normal DNA or stiffer DNA produced by polymerase chain reaction reactions in which diaminopurine (DAP) replaced adenine deoxyribonucleotide triphosphates. On single DNA molecules twisted with magnetic tweezers to create plectonemes, the rates or pauses during relaxation of positive supercoils in DAP-substituted versus normal DNA were distinct for both enzymes. Gyrase struggled to bend or perhaps open a gap in DAP-substituted DNA, and segments of wider DAP DNA may have fit poorly into the N-gate of the human topoisomerase IIα. Pauses during processive activity on both types of DNA exhibited ATP dependence consistent with two pathways leading to the strand-passage-competent state with a bent gate segment and a transfer segment trapped by an ATP-loaded and latched N-gate. However, E . coli DNA gyrase essentially failed to negatively supercoil 35% stiffer DAP DNA. [ABSTRACT FROM AUTHOR]

An anionic bio-MOF-1 with 1D square channels is applied as container for the adsorption of organic dyes owing to the porous structure and charge properties. Through ion exchange, cationic acriflavine (Acf) dye with the minimum size is selected as a fluorescent dye molecule to introduce into the pores of anionic bio-MOF-1 to obtain a self-calibrating dual-emitting fluorescent composite of Acf@bio-MOF-1, which exhibits two characteristic emission peaks at 385 and 582 ​nm. The composite acts as fluorescence sensing probe for the selective and sensitive detection of Fe3+, Al3+ and Cr 2 O 7 2− among metal cations and anions and has a "turn-off" response to Fe3+ and Cr 2 O 7 2− as well as a "turn-on" response to Al3+ at the same time. Particularly, Acf@bio-MOF-1 shows higher fluorescence quenching effects of 95% for Cr 2 O 7 2− and 90% for Fe3+ and low detection limits of 0.25 ​μM for Cr 2 O 7 2− and 1.33 ​μM for Fe3+, respectively. Such a special encapsulation strategy to form a dual-emission platform can be adopted to the detection of inorganic ions sensitively. A fluorescent dye acriflavine (Acf) was encapsulated into anionic bio-MOF-1 to form a dual-emission fluorescence sensing probe for the detection of Fe3+, Al3+ and Cr 2 O 7 2− among metal ions and anions selectively and sensitively. Image 1 • A new self-calibrating dual-emitting fluorescent composite Acf@bio-MOF-1 was prepared. • Acf@bio-MOF-1 shows high fluorescence quenching effects for Fe3+ and Cr 2 O 7 2−, respectively. • Acf@bio-MOF-1 shows a unique "turn-on" response to Al3+ in all selected metal ions. [ABSTRACT FROM AUTHOR]

Abstract: Poxviruses currently are known to disrupt Jak-STAT signal transduction induced by interferon (IFN) through two distinct mechanisms: (1) secreted poxviral IFN decoy receptors that prevent the initiation of IFN signaling from type I or II receptors at the cell surface; and (2) poxviral phosphatase that dephosphorylates STAT1 intracellularly. Here, we report a novel mechanism by which poxviruses can inhibit Jak-STAT signaling in response to type I IFN. Myxoma virus (MV) is a highly species-restricted member of the poxvirus family that infects only rabbits under the natural setting. Interestingly, primary human fibroblasts support a permissive MV infection that is only partially sensitive to the antiviral state induced by type I IFN. In this study we show that when type I IFN is added to primary human fibroblasts following MV infection, the tyrosine phosphorylation of the Janus kinase Tyk2 is specifically blocked, thereby preventing the subsequent activation of downstream STAT1 and STAT2. In stark contrast, type II IFN-induced activation of Jak1, Jak2 and STAT1 remains largely unaffected in MV-infected human fibroblasts. Unlike the de-activation of STAT1 by the poxvirus phosphatase, which is delivered into the cell by the input virions, the Tyk2 inhibition by MV infection requires new viral gene expression. Thus, our study documents a previously unrecognized immune evasion mechanism exploited by a poxvirus to selectively disrupt the type I IFN-Jak-STAT signaling cascade. [Copyright &y& Elsevier]

Smad，a member of the TGF-β superfamily，controls cell proliferation，growth and guiding cell differentiation, thus playing a crucial role in diseases. However, the presence as well as specific function of Smad in crabs is still unknown. In this study, two Smads (Smad1 and Smad2/3) were identified for the first time from the mud crab Scylla paramamosain. The complete open reading frames of SpSmad1 and SpSmad2/3 were 1,497bp and 1,338bp, encoding deduced proteins of 498 and 445 amino acids respectively. Moreover, under the administration of Vibrio alginolyticus and WSSV, the relative expression levels of SpSmad1 and SpSmad2/3 were significantly increased, indicating their involvement in the innate immune response of mud crabs. Knockdown of SpSmad1 and SpSmad2/3 in vivo not only led to the increasement of the expressions of NF-κB signaling genes and antimicrobial peptides genes, but also significantly affected the bacterial clearance process of mud crabs. Additionally, overexpression of SpSmad1 and SpSmad2/3 in HEK293T cells could markedly activate NF-κB signaling. These results indicated that Smad1 and Smad2/3 participated in the innate immunity of Scylla paramamosain , and might provide a better understanding of the presence and immune regulatory functions of Smad1 and Smad2/3 in crabs and even invertebrates. • Two Smad genes were firstly identified from the crab species. • The role of Smads in bacterial clearance in vivo was first studied in arthropods. • SpSmad1 and SpSmad2/3 functioned in innate immune response by Toll and IMD signaling. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is generally considered to be characterized by progressive articular cartilage destruction. Increasing evidence demonstrates that CDK9, which is a member of cyclin-dependent kinase family, plays a significant role in the regulation of acute and chronic inflammatory diseases. IL-1β, a major proinflammatory cytokine, was used to establish a model of OA in vitro after stimulating chondrocytes. We found that CDK9 was highly expressed in in vitro and in vivo models of inflammation. The role of LDC000067 (abbreviated as LDC067), a specific inhibitor of CDK9, in protecting articular cartilage from immune response has not been fully clarified. Intriguingly, in this study, we demonstrated that LDC067 prevented IL-1β-induced production of metalloproteinases (MMPs) and inflammatory cytokines, including MMP3, MMP9, MMP13, IL-6, IL-8 and TNF-ɑ. Furthermore, we revealed that LDC067 inhibited IL-1β-induced NF-κB signaling pathway activation in chondrocytes. The inhibition of CDK9 could also delay cartilage degeneration in an anterior cruciate ligament transection (ACLT) mouse model in vivo. Taken together, these results highlighted the significance of this CDK9 inhibitor in preventing cartilage destruction and indicated that LDC067 might serve as a potential therapeutic agent for OA. • CDK9 is upregulated in osteoarthritis cartilage and is correlated with the severity of OA. • The specific inhibitor of CDK9, LDC067 attenuates the catabolism and hypertrophic changes of chondrocytes in vitro. • LDC067 suppresses the activation of the NF-κB signaling pathway. • LDC067 ameliorates OA cartilage destruction in vivo and may be a novel therapeutic agent. [ABSTRACT FROM AUTHOR]

After the severe initial insults of acute kidney injury, progressive kidney tubulointerstitial fibrosis may occur, the peritubular capillary (PTC) rarefaction plays a key role in the disease progression. However, the mechanisms of PTC damage were not fully understood and potential therapeutic interventions were not explored. Previous studies of our research team and others in this field suggested that bone marrow-derived mesenchymal stem cells (BMSCs) transplanted into the AKI rat model may preserve the kidney function and pathological changes. In the current study, with the ischemia/reperfusion AKI rat model, we revealed that BMSCs transplantation attenuated the renal function decrease in the AKI model through preserving the peritubular capillaries (PTCs) function. The density of PTCs is maintained by BMSCs transplantation in the AKI model, detachment and relocation of pericytes in the PTCs diminished. Then we established that BMSCs transplantation may attenuate the renal fibrosis and preserve the kidney function after AKI by repairing the PTCs. Improving the vitality of pericytes, suppressing the detachment and trans -differentiation of pericytes, directly differentiation of BMSCs into pericytes by BMSCs transplantation all participate in the PTC repair. Through these processes, BMSCs rescued the microvascular damage and improved the density of PTCs. As a result, a preliminary conclusion can be reached that BMSCs transplantation can be an effective therapy for delaying renal fibrosis after AKI. [ABSTRACT FROM AUTHOR]

Highlights: [•] CagA stimulated cell proliferation and the production of IgA1 in DAKIKI cells. [•] CagA promoted the underglycosylation of IgA1 in DAKIKI cells. [•] CagA decreased the expression of C1GALT1 and its chaperone Cosmc in DAKIKI cells. [•] Helicobacter pylori infection may participate in the pathogenesis of IgAN via CagA. [ABSTRACT FROM AUTHOR]