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Abstract The cobalt nanoparticles (10 nm) were homogeneously embedded in the porous carbon dodecahedra (about 1 μm in size) through thermal pyrolysis of the ZIF-67 (zeolitic imidazolate framework-67) dodecahedra under an inert atmosphere. The pore sizes of the carbon dodecahedra were found to disperse in three ranges of micropores, small, and large mesopores. Cyclic voltammetry measurements indicated that the porous carbon-cobalt electrode with small particle size (SPC-Co) exhibited better electrocatalytic performance than that with large particle size (LPC-Co), primarily owing to its larger electrocatalytic surface for boosting the redox reaction between iodide and triiodide ions. Dye-sensitized solar cell (DSSC) using the SPC-Co counter electrode (CE) showed a superior photovoltaic conversion efficiency of 10.6%, which was better than those achieved by means of Pt (9.8%) and LPC-Co (9.0%) CEs. The improved photovoltaic behavior of DSSC employing the SPC-Co CE could be attributed to its lower internal resistance than the other CEs. The porous carbon rhombic dodecahedra with embedded cobalt nanoparticles could achieve fast kinetics and high electroactivity in catalyzing the iodide/triiodide redox couple. Graphical abstract Image 1 Highlights • Cobalt nanoparticles are well-distributed in the porous carbon rhombic dodecahedra. • The carbon dodecahedra with different pore sizes provide high electroactivity. • Caron dodecahedron catalyst boosts redox reaction between iodide and triiodide ions. • Dye-sensitized solar cell shows a high photovoltaic conversion efficiency of 10.6%. [ABSTRACT FROM AUTHOR]

Abstract Biliproteins have extended the spectral range of fluorescent proteins into the near-infrared region (NIR, 700–770 nm) of maximal transmission of most tissues and are also favorable for multiplex labeling. Their application, however, presents considerable challenges to increase their stability under physiological conditions and, in particular, to increase their brightness while maintaining the emission in near-infrared regions: their fluorescence yield generally decreases with increasing wavelengths, and their effective brightness depends strongly on the environmental conditions. We report a fluorescent biliprotein triad, termed BDFP1.1:3.1:1.1, that combines a large red-shift (722 nm) with high brightness in mammalian cells and high stability under changing environmental conditions. It is fused from derivatives of the phycobilisome core subunits, ApcE2 and ApcF2. These two subunits are induced by far-red light (FR, 650–700 nm) in FR acclimated cyanobacteria. Two BDFP1.1 domains engineered from ApcF2 covalently bind biliverdin that is accessible in most cells. The soluble BDFP3 domain, engineered from ApcE2, binds phytochromobilin non-covalently, generating BDFP3.1. This phytochromobilin chromophore was added externally; it is readily generated by an improved synthesis in E. coli and subsequent extraction. Excitation energy absorbed in the FR by covalently bound biliverdins in the two BDFP1.1 domains is transferred via fluorescence resonance energy transfer to the non-covalently bound phytochromobilin in the BDFP3.1 domain fluorescing in the NIR around 720 nm. Labeling of a variety of proteins by fusion to the biliprotein triad is demonstrated in prokaryotic and mammalian cells, including human cell lines. Highlights • A near-infrared fluorescent biliprotein triad (BDFP1.1:3.1:1.1, λ Fmax ~ 722 nm) is reported. • The triad is 2.7-fold brighter than the known brightest near-infrared fluorescent biliprotein, iRFP720. • Labeling using the triad is demonstrated in prokaryotic and mammalian cells. • A method for conveniently isolating phytochromobilin for the labeling is established. [ABSTRACT FROM AUTHOR]

Abstract Far-red and near-infrared emitting chromophores extend applications of fluorescent proteins to regions of maximal transmission of most tissues, but present considerable engineering challenges. Far-red adapting cyanobacteria generate a novel set of biliproteins. One of them, ApcF2, from a thermophilic cyanobacterium was subjected to structure-guided, site-directed random and specific mutagenesis, and was screened for bright far-red emission. We report the generation of chromoproteins, termed BDFPs, that are small, bind auto-catalytically the ubiquitous biliverdin as chromophore, express well, and retain their fluorescence in mammalian cells and in the nematode, C. elegans. They are, moreover, photostable and tolerate high temperature, low pH and chemical denaturation. Homo-bichromophoric tandems of these proteins improve labeling, while hetero-bichromophoric systems with large Stokes shifts are suitable for applications like FRET, multi-channel or super-resolution microscopy. The BDFPs compare favorably to other biliproteins and provide a novel, extremely versatile labeling tool-box. Graphical abstract Unlabelled Image Highlights • Three far-red fluorescent phycobiliproteins (λ Fmax ~670 nm), BDFPs, are reported. • Effective brightness of BDFPs is greatly improved by molecular design. • BDFPs of large Stokes shifts between far-red and near-infrared regions are generated. • Far-red BDFPs and near-infrared BDFPs can be applied in dual-color bioimaging. [ABSTRACT FROM AUTHOR]

[Display omitted] • Denitrification is significantly inhibited as CLP concentrations increased. • Zero-order kinetic and noncompetitive inhibition model are applicable for NO 3 − reduction. • Short-term exposure to CLP can inhibit microbial metabolism and ETS by inducing ROS. • ETS activity and NAR are the major factors in predicting nitrate reduction rate (DNR). • The nitrite accumulation (NIA) can be mainly predicted by the changes in NADH and NIR. The mass production and extensive application of clopyralid (CLP) have attracted much attention regarding its environmental effect in recent decades. However, studies on the acute responses and the underlying inhibition mechanisms of denitrifiers to CLP exposure are scarce. Herein, the crucial factors in denitrification were quantified through kinetics, metabolic activity analysis, and structural equation modeling (SEM). The acute response mechanisms of denitrifiers under short-term CLP exposure were further proposed according to the quantitative correlation of denitrification performance with C and N metabolism, ETS activity, and oxidative stress. The modified non-competitive inhibition model fitted well to describe the inhibitory characteristics of CLP on the nitrate reduction (R2 = 0.99), which was significantly inhibited with increasing CLP exposure concentrations. Short-term exposure to CLP could inhibit C and N metabolism and electron transport by inducing oxidative stress during denitrification. Quantitative PCR (qPCR) analysis demonstrated that CLP restrained the abundance of nar G and nir S, suggesting that down-regulation of denitrification enzyme expression was highly related to the reduction in nitrogen conversion. Moreover, SEM indicated that ETS activity and NAR were the major factors in predicting NO 3 − reduction rate (DNR) and were mainly influenced by NADH and reactive oxygen species (ROS). Consistently, NADH and NIR were closely correlated with total nitrite accumulation (NIA). Short-term CLP exposure could affect denitrification performance by directly affecting microbial physicochemical properties or indirectly interfering with the abundance of denitrifying functional genes and metabolic activity through oxidative stress. This study provided new insights into acute responses of denitrifiers to short-term CLP exposure. [ABSTRACT FROM AUTHOR]

NT157, a small-molecule tyrosine kinase inhibitor, exhibits broad-spectrum anti-tumor activity. However, NT157-mediated inhibition against glioma has not been explored yet. Herein, the anticancer effects and underlying mechanism of NT157 against human giloma growth were evaluated. The results showed that NT157 alone significantly inhibited glioma cells growth in vitro by lunching cell cycle arrest through up-regulating p21 and p27, and down-regulating cell cycle-related factors. NT157 alone also induced significant glioma cells apoptosis, followed by PARP cleavage and caspase-3 activation. Our findings further revealed that NT157 triggered significant DNA damage and dysfunction of PI3K/AKT, MAPKs and EGFR-STAT3 signaling pathways. Addition of several kinases inhibitors effectively abrogated NT157-induced DR5 up-regulation, which further confirmed the significant role of DR5 pathway. Moreover, combined treatment of NT157 and TRAIL showed enhanced apoptosis against U251 and U87 cells. However, Knockdown of DR5 expression significantly attenuated combined treatment-induced PARP cleavage and caspase-3 activation. Importantly, combined administration of NT157 and TRAIL in vivo effectively inhibited glioma xenograft growth of nude mice by inhibiting cell proliferation and angiogenesis, and inducing DNA damage and apoptosis. Taken together, our findings validated the rational design that combined strategy of NT157 and TRAIL to trigger DNA damage and apoptosis by up-regulating DR5 could be a high efficient way to combat human glioma. [Display omitted] • NT157 induced glioma cell cycle arrest and apoptosis. • NT157 enhanced TRAIL's anticancer effect by activating ROS and DR5 expression. [ABSTRACT FROM AUTHOR]

Corrigendum to "CCT128930 induces G1-phase arrest and apoptosis and synergistically enhances the anticancer efficiency of VS5584 in human osteosarcoma cells" [Biomed. Caspase-3 expression was repeated, and the correct caspase-3 expression appears below. 3B appears below: Graph The correct caspase-3 expression in Fig. [Extracted from the article]

• Microfluidic BBB chips composed of brain microvascular endothelial cells, pericytes, astrocytes and multifarious neurons can simulate the complex and dynamic 3D structure of human brain. • In vitro microfluidic BBB chips reproduce the mesh of the human brain anatomical structure and physiological function. • Brain on a chip has a great potential in exploring the mechanisms of CNS diseases and drug development. • Microfluidized BBB-related target organ chip platform can in vitro comprehensively investigate the dynamic process of brain-related multi-organ diseases. The human blood-brain barrier (BBB) is a complex multi-dimensional reticular barrier system composed of cerebral microvascular endothelial cells, pericytes, astrocytes and a variety of neurons. The conventional in vitro cell culture model fails to truly present the dynamic hemodynamics of BBB and the interaction between neurons. And it is even more impossible to explore brain-related multi-organ diseases, which brings huge obstacles to explore diseases of the central nervous system and the interaction between brain-related multi-organs, and evaluate drug efficacy. Miniaturized microfluidics based BBB chips are being commonly used to co-culture a variety of cells on a small-sized chip to construct a three-dimensional (3D) BBB or BBB-related organ disease models. By combining with other electrophysiological, biochemical sensors or equipment and imaging systems, it can in real time and quickly screen disease-related markers and evaluate drug efficacy. This review systematically summarized the research progress of in vitro BBB and BBB-related organ chips, and analyzed the obstacles of BBB models in depth. Parallelly combined with the current research trends and hot spots, we give the further improvement measures of microfluidic BBB chips. [ABSTRACT FROM AUTHOR]

Osteosarcoma is a highly invasive primary malignant bone tumor. PI3K/mTOR pathway plays a key role in tumor progression, and inhibition of PI3K/mTOR pathway represents a novel strategy in therapy of osteosarcoma. CCT128930 and VS5584 are both inhibitors of PI3K/mTOR, but the anticancer mechanism of CCT128930 or/and VS5584 against human osteosarcoma cells remains unclear. Herein, U2OS and MG63 human osteosarcoma cells were cultured, and the anticancer effects of CCT128930 alone and the combined effect of CCT128930 and VS5584 against human osteosarcoma cells were explored. The results showed that CCT128930 as PI3K/mTOR inhibitor effectively inhibited p-p70 and p-AKT expression and dose-dependently inhibited U2OS cells and MG63 human osteosarcoma cells growth. Further studies found that CCT128930 triggered significant G-1 phase arrest and apoptosis, as convinced by the dysfunction of p27, Cyclin B1, Cyclin D1 and Cdc2, and PARP cleavage and caspase-3 activation. Moreover, CCT128930 treatment obviously enhanced VS5584-induced growth inhibition and apoptosis in human osteosarcoma cells, followed by enhanced PARP cleavage and caspase-3 activation. Taken together, CCT128930 alone or combined treatment with CCT128930 and VS5584 both effectively inhibited human osteosarcoma cells growth by induction of G1-phase arrest and apoptosis through regulating PI3K/mTOR and MAPKs pathways. [ABSTRACT FROM AUTHOR]

The stable phase equilibrium data of Mg2+, NH 4 +//Cl−, SO 4 2−−H 2 O quaternary interaction system and its four ternary subsystems at 363.15 K were determined by isothermal dissolution equilibrium method, and the corresponding stable phase diagrams of the above systems were plotted. According to the phase diagram, there are seven solid phase crystalline regions, which correspond to MgSO 4 ·(NH 4) 2 SO 4 ·6H 2 O, MgSO 4 ·6H 2 O, MgSO 4 ·4H 2 O, MgCl 2 ·6H 2 O, (NH 4) 2 SO 4 , MgCl 2 ·NH 4 Cl·6H 2 O and NH 4 Cl, respectively. MgSO 4 ·(NH 4) 2 SO 4 ·6H 2 O has the largest crystalline region among these crystalline regions, which indicates that the double salt MgSO 4 ·(NH 4) 2 SO 4 ·6H 2 O is the easiest to crystallize out. Based on the extended Pitzer model, the solubility data of the ternary subsystems and the quaternary system were calculated. The results showed that the calculated values were close to the experimental values. According to the comparison between the stable phase diagram of the quaternary system at 298.15 K and 363.15 K, a new process of preparing N–Mg compound fertilizer (MgSO 4 ·(NH 4) 2 SO 4 ·6H 2 O) at 298.15 K and crystallizing NH 4 Cl at 363.15 K by using ammonium sulfate and magnesium chloride as raw materials was designed in this paper and the process route was verified by experiment. [ABSTRACT FROM AUTHOR]

In this study, we developed a pro-endothelial-functionalization surface by immobilizing a natural factors-loaded nanoparticle, exosome, onto the poly-dopamine (PDA) coated materials via electrostatic binding. • A novel PDA/Exosome coating was successfully prepared onto the cardiovascular biomaterial. • The PDA/Exosome coating could enhance the endothelial cell growth, CD31 expression and NO release. • The PDA/Exosome coating could regulate SMC into contractile phenotype and macrophage into M2 phenotype. • The PDA/Exosome coating could reduce hyperplasia of the implant. • The PDA/Exosome coating regulated the endothelial cell behavior by entering into cells. Stent intervention as available method in clinic has been widely applied for cardiovascular disease treatment for decades. However, the restenosis caused by late thrombosis and hyperplasia still limits the stents long-term application, and the essential cause is usually recognized as endothelial functionalization insufficiency of the stent material surface. Here, we address this limitation by developing a pro-endothelial-functionalization surface that immobilized a natural factors-loaded nanoparticle, exosome, onto the poly-dopamine (PDA) coated materials via electrostatic binding. This PDA/Exosome surface not only increased the endothelial cells number on the materials, but also improved their endothelial function, including platelet endothelial cell adhesion molecule-1 (CD31) expression, cell migration and nitric oxide release. The pro-inflammation macrophage (M1 phenotype) attachment and synthetic smooth muscle cell proliferation as the interference factors for the endothelialization were not only inhibited by the PDA/Exosome coating, while the cells were also regulated to anti-inflammation macrophage (M2 phenotype) and contractile smooth muscle cell, which may contribute to endothelialization. Thus, it can be summarized this method has potential application on surface modification of cardiovascular biomaterials. [ABSTRACT FROM AUTHOR]

The mechanical properties of a stem cell culture substrate significantly impact cell adhesion, survival, migration, proliferation, and differentiation in vitro. A major challenge in engineering artificial stem cell substrate is to properly identify the relevant physical features of native stem cell niches, which are likely different for each stem cell type. The behavior of tendon stem cells has potentially significant implications for tendon repair. Here, microfiber scaffolds with various modulus of elasticity are fabricated by near-field electrospinning, and their regulating effects on the in vitro behavior of tendon stem cells (TSCs) are discussed in this study. The number of pseudopodia shows a biphasic relationship with the modulus of scaffold. The proliferation, polarization ratio and alignment degree along the fibers of the TSCs increase with the increase of fiber modulus. TSCs cultured on the scaffold with moderate modulus (1429 MPa) show the upregulation of tendon-specific genes (Col-I, Tnmd, SCX and TNCF). These microfiber scaffolds provide great opportunities to modulate TSCs behavior at the micrometer scales. In conclusion, this study provides an instructive mechanical microenvironment for TSCs behaviors and may lead to the development of desirable engineered artificial stem cell substrate for tendon healing. [Display omitted] • The cross PA56 fiber scaffolds with various modulus were fabricated by NEFS. • The proliferation, number and cell polarization ratio of TSCs increased with the modulus. • The number of pseudopodia of TSCs showed a biphasic response to the modulus. • The arrangement of actin cytoskelenton tended to align toward the fiber with the increase of fiber modulus. • Microfiber scaffolds with moderate modulus (1429 MPa) demonstrated the potential to upregulate the tendon-specific genes. [ABSTRACT FROM AUTHOR]

Biliproteins have extended the spectral range of fluorescent proteins into the region of maximal transmission of most tissues and are favorable for multiplexing, but their application presents considerable challenges. Their fluorescence derives from open-chain tetrapyrrole chromophores which often require the introduction of dedicated reductases and lyases. In addition, their fluorescence yield generally decreases with increasing wavelengths and depends strongly on the state of the binding protein. We report fluorescent biliproteins, termed BDFPs, that are derived from the phycobilisome core subunit, ApcF2: this subunit is induced in the thermophilic cyanobacterium, Chroococcidiopsis thermalis, by far-red light and binds phycocyanobilin non-covalently. The BDFPs obtained by molecular evolution of ApcF2 bind the more readily accessible biliverdin covalently while retaining the red-shifted fluorescence in the near-infrared spectral region (~ 710 nm). They are small monomers (~ 15 kDa) and not only show excellent photostability, but are also thermostable up to 80 °C, tolerate acid down to pH 2 and high concentrations of denaturants. The result indicates far-red adapting cyanobacteria as a useful source for designing extremely red-shifted fluorescent markers. In vivo performance of BDFPs as biomarkers in conventional and super-resolution microscopy, alone or fused to target proteins, is exemplified in several mammalian cells, including, human cell lines, in the nematode, Caenorhabditis elegans and, at low pH, in Lactobacillus lactis . [ABSTRACT FROM AUTHOR]

Single phase multiferroics are rare in nature, because ferroelectric and ferromagnetic orderings require empty d -orbits and filled d -orbits, respectively. Here we demonstrate that ferroelectricity can be induced by ion-pair doping in ferromagnetic oxide such as ferrites with filled d -orbits. Our study shows that a new kind of room temperature multiferroic can be achieved in single phase thin films of CoFe 2 O 4 with Li + -Al 3+ pair substitution of Co 2+ along 〈110〉 direction. A ferroelectric domain mechanism related to ion-pairs in co-doped thin films was revealed. Importantly, a new way for fabricating single phase multiferroic materials is provided in the present study. [ABSTRACT FROM AUTHOR]

Considering the limited efficacy of current therapies in lung, colorectal, and pancreatic cancers, innovative combination treatments with diverse mechanisms of action are needed to improve patients' outcomes. Chitinase-3 like-1 protein (CHI3L1) emerges as a versatile factor with significant implications in various diseases, particularly cancers, fostering an immunosuppressive tumor microenvironment for cancer progression. Therefore, pre-clinical validation is imperative to fully realize its potential in cancer treatment. We developed phage display-derived fully human monoclonal CHI3L1 neutralizing antibodies (nAbs) and verified the nAbs-antigen binding affinity and specificity in lung, pancreatic and colorectal cancer cell lines. Tumor growth signals, proliferation and migration ability were all reduced by CHI3L1 nAbs in vitro. Orthotopic or subcutaneous tumor mice model and humanized mouse model were established for characterizing the anti-tumor properties of two CHI3L1 nAb leads. Importantly, CHI3L1 nAbs not only inhibited tumor growth but also mitigated fibrosis, angiogenesis, and restored immunostimulatory functions of immune cells in pancreatic, lung, and colorectal tumor mice models. Mechanistically, CHI3L1 nAbs directly suppressed the activation of pancreatic stellate cells and the transformation of macrophages into myofibroblasts, thereby attenuating fibrosis. These findings strongly support the therapeutic potential of CHI3L1 nAbs in overcoming clinical challenges, including the failure of gemcitabine in pancreatic cancer. [Display omitted] • CHI3L1 nAb restricts tumor growth and restores immune functions in various cancers. • CHI3L1 nAb ameliorates tumor fibrosis & angiogenesis in preclinical mouse models. • CHI3L1 nAb inhibits fibroblast activation & macrophage to myofibroblast transition. [ABSTRACT FROM AUTHOR]

Cantleyoside (CA) is a kind of iridoid glycosides in Pterocephalus hookeri (C. B. Clarke) Höeck. The purpose of this study was to investigate the effects of CA on human rheumatoid arthritis fibroblast synovial cells (HFLS-RA). Cell proliferation of HFLS-RA was assessed by CCK-8. ELISA was used to detect cytokines NO, TNF-α, IL-1β/6, MCP-1, MMP-1/3/9 and metabolism-related ATPase activities and ATP levels. JC-1, DCFH-DA, Fluo-3 AM and Calcein AM probes were used to detect mitochondrial membrane potential (MMP), reactive oxygen species (ROS), Ca2+ and mitochondrial permeability conversion pore (MPTP), respectively. Isolated mitochondria assay was used to detect mitochondrial swelling. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR) and real-time ATP production were measured using a Seahorse analyzer. Apoptosis was detected by TUNEL and Hoechst staining. Western blot was used to detect the expressions of AMPK/p-AMPK, Sirt 1, IκBα, NF-κB p65/p-NF-κB p65, Bcl-2 and Bax. Cytoplasmic nuclear isolation was also performed to detect the translocation of NF-κB. CA significantly suppressed cell proliferation and the levels of NO, TNF-α, IL-1β/6, MCP-1 and MMP-1/3/9 in HFLS-RA. In addition, CA promoted the apoptosis of HFLS-RA by increasing TUNEL and Hoechst positive cells and the ratio of Bax/Bcl-2. Inhibition of energy metabolism in HFLS-RA by CA reduced OCR, ECAR and real-time ATP generation rate. Importantly, CA promoted p-AMPK and Sirt 1 expression, inhibited IκBα degradation to reduce p-NF-κB and translocation. The results suggest that CA activates the AMPK/Sirt 1/NF-κB pathway by promoting mitochondrial dysfunction, thereby exerting anti-inflammatory and pro-apoptotic effects. [Display omitted] • CA could inhibit inflammatory responses by weakening the expression of inflammatory cytokines, chemokines and MMPs. • CA could induce mitochondrial dysfunction by overloading intracellular ROS and Ca2+ in HFLS-RA. • CA could reduce mitochondrial energy metabolism by restraining OCR, ECAR and real-time ATP production rates in HFLS-RA. • CA could promote apoptosis of HFLS-RA by the activation of AMPK/Sirt 1/NF-κB pathway. [ABSTRACT FROM AUTHOR]

• We summarized and analyzed the prescriptions, herbs and identified compounds of TCM on the treatment of DR from the aspects of anti-inflammation, anti-oxidative stress, anti-angiogenesis and anti-apoptosis. • The detailed mechanisms and involved network pathways of herbs-compounds-targets of TCM in treating DR were reviewed and visualized by Cytoscape software. • We discussed the limitations or deficiencies of TCM on the treatment of DR, and gave the further suggestions. As a common ocular complication and microangiopathy of type 2 diabetic mellitus, diabetic retinopathy (DR) can lead to vision loss or even blindness in diabetic patients. At present, the treatment methods of DR mainly include laser and anti-VEGF therapies. Nevertheless, the higher cost and obvious side effects seriously disturb the normal life of DR patients. Promisingly, traditional Chinese medicine (TCM) has been demonstrated to be effective in treating DR by tonifying Qi and nourishing Yin, as well clearing heat and breeding body fluids, thus activating blood and removing blood stasis. Therefore, we screened the literatures on TCM treatment of DR through the web of science, ScienceDirect, PubMed, Google scholar and CNKI online databases. The representative prescriptions, herbs and extracts, and identified compounds for treatment of DR were further summarized and analyzed. Moreover, the detailed mechanisms and involved network pathways of herbs-compounds-targets were visualized by Cytoscape software. Meanwhile, we discussed the existing limitations and deficiencies of TCM on treatment of DR and gave corresponding measures. In conclusion, TCM could significantly ameliorate DR via anti-inflammation, anti-oxidative stress, anti-angiogenesis and anti-apoptosis. [ABSTRACT FROM AUTHOR]

Due to the low absorbance in the far-red (FR) and near-infrared (NIR) "optical window", NIR fluorescent proteins (FPs) are powerful tools for deep imaging. Here, we report three new, highly bright NIR FPs termed BDFP1.8, BDFP1.8:1.8 (tandem BDFP1.8) and BDFP1.9, which evolved from a previously reported FR FP, BDFP1.6: a derivative of ApcF2 from Chroococcidiopsis thermalis sp. PCC7203. ApcF2 binds phycocyanobilin (PCB) non-covalently, while BDFPs, the derivatives of ApcF2, can bind biliverdin (BV) covalently. We identified that dimeric BDFP1.8 and monomeric BDFP1.8:1.8 have a 2.4-and 4.4-fold higher effective brightness, respectively, than iRFP720, which has the highest effective brightness among the reported NIR FPs. Monomeric DBFP1.9 (17 kDa) has one of the smallest masses among highly bright FPs in the FR and NIR regions. Enhancing the affinity between the apo-proteins and the BV chromophore is an effective method to improve the effective brightness of biliprotein FPs. Moreover, BDFP1.8 and 1.9 exhibit higher stability to temperature, pH and light than iRFP720. Finally, the highly bright NIR BDFP1.8 together with FR BDFP1.6 could effectively biolabel cells in dual colors. Unlabelled Image • Enhancing the affinity between the apo-proteins and BV improves the brightness of biliprotein FPs in mammalian cells. • BDFP1.8:1.8 is the brightest FP in NIR regions. • DBFP1.9 (17 kDa) has one of the smallest masses among highly bright FPs in the FR and NIR regions. • BDFP1.8 and 1.9 exhibit high stability to temperature, pH and light. [ABSTRACT FROM AUTHOR]

NB synergistically enhanced DOX-induced ROS generation and dysfunction of MAPKs and PI3 K/AKT pathways. ROS overproduction subsequently activated DNA damage, initiated a G2/M-phase arrest, and eventually inhibited human glioma growth. Doxorubicin (DOX) as a first-line chemotherapeutic drug has been widely used for therapy of human cancers. However, side effects and chemo-resistance severely blocked its clinic application. Herein, natural borneol (NB) as a novel monoterpenoid chemosensitizer was found to have the potential to increase the blood brain barrier (BBB) permeability and intracellular uptake of DOX in vitro , and synergistically enhanced DOX-induced cytotoxicity in human glioma cells. NB treatment significantly potentiated DOX-induced G2/M cell cycle arrest by triggering reactive oxygen species (ROS)-mediated DNA damage. NB also enhanced DOX-induced dysfunction of MAPKs and PI3 K/AKT pathways. Furthermore, U251 human glioma xenograft growth in vivo was also effectively inhibited by combined treatment of DOX with NB through induction of G2/M-phase arrest and antiangiogenesis. Taken together, our finding validated that NB could act as novel chemosensitizer to enhance DOX-induced anticancer efficacy, and strategy of using NB and DOX could be a high efficient way in therapy of human cancers. [ABSTRACT FROM AUTHOR]

Osteoporosis is a bone-related disease characterized by decreased bone density and mass, leading to brittle fractures. Osteoporosis assessment from radiographs using a deep learning algorithm has proven a low-cost alternative to the golden standard DXA. Due to the considerable noise and low contrast, automated diagnosis of osteoporosis in X-ray images still poses a significant challenge for traditional diagnostic methods. In this paper, an end-to-end transformer-style network was proposed, termed FCoTNet, to overcome the shortcoming of insufficient fusion of texture information and local features in the traditional CoTNet. To extract complementary geometric representations at each scale of the transformer module, we integrated parallel multi-scale feature extraction architectures in each unit layer of FCoTNet to utilize convolution to aggregate features from different receptive fields. Moreover, in order to extract small-scale texture features which were more critical to the diagnosis of osteoporosis in radiographs, larger fusion weights were assigned to the feature maps with small-size receptive fields. Afterward, the multi-scale global modeling was conducted by self-attention mechanism. The proposed model was first investigated on a private lumbar spine X-ray dataset with the 5-fold cross-validation strategy, obtaining an average accuracy of 78.29 ± 0.93 %, an average sensitivity of 69.72 ± 2.35 %, and an average specificity of 88.92 ± 0.67 % for the multi-classification of normal, osteopenia, and osteoporosis categories. We then conducted a controlled trial with five orthopedic clinicians to evaluate the clinical value of the model. The average clinician's accuracy improved from 61.50 ± 10.79 % unaided to 80.00 ± 5.92 % aided (18.50 % improvement), sensitivity improved from 64.38 ± 8.07 % unaided to 83.31 ± 5.43 % aided (18.93 % improvement), and specificity improved from 80.11 ± 4.72 % unaided to 89.94 ± 3.82 % aided (9.83 % improvement). Meanwhile, the prediction consistency among clinicians significantly improved with the assistance of FCoTNet. Furthermore, the proposed model showed good robustness on an external test dataset. These investigations indicate that the proposed deep learning model achieves state-of-the-art performance for osteoporosis prediction, which substantially improves osteoporosis screening and reduced osteoporosis fractures. • Osteoporosis is a prevalent but underdiagnosed condition. • A multi-scale weighted fusion contextual transformer-style model to classify normal, osteopenia and osteoporosis. • The feasible and low-cost AI-assistant system has potential to be used in the clinical practice for osteoporosis screening. [ABSTRACT FROM AUTHOR]

Abstract Graphene oxide(GO) membrane has the potential to become the next generation of water purification membrane, which could help to ease water crisis in many counties. However, organic membrane fouling is still difficult to avoid. In this study, we used a trace of ·OH to mitigate fouling by tuning surface functional groups of GO membrane and altering fouling layer. X-ray photoelectron spectroscopy (XPS) analysis indicated that ·OH changed the epoxide-dominated GO surface to a hydroxyl-dominated surface. The adhesion force between the GO membrane and organic microspheres decreased from 0.37 ± 0.16 mN/m to 0.08 ± 0.14 mN/m after functionalization by ·OH. Quantum mechanical simulations showed that the interaction energy of the hydroxyl-dominated GO surface with a modified alginic acid monomer was 4.07 eV, which was lower than that (5.68 eV) between the epoxide-dominated GO surface and the modified alginic acid monomer. A thicker water molecule layer formed on the hydroxyl-dominated GO surface than on the epoxide-dominated GO surface through hydrogen bonding, thus repelling organic foulants. Combined with the oxidative effect of ·OH, the current method achieved the nearly complete prevention of membrane fouling. This result could provide us a new perspective for the fouling-free membrane-based water purification process. Graphical abstract fx1 Highlights • Trace ·OH were introduced to the GO membrane filtration process to control fouling. • Almost complete prevention of fouling was observed after ·OH was introduced. • AFM results showed adhesion force decreased significantly after ·OH was introduced. • XPS results proved that ·OH became temporarily stable hydroxyl groups on GO. • Simulation showed that water shield layer formed on GO surface repelled foulants. [ABSTRACT FROM AUTHOR]

A bright blue emitting excited-state intramolecular proton transfer (ESIPT) molecule, 2-(4,5-bis(4-chlorophenyl)-1 H -imidazol-2-yl)-4-chlorolphenol (HPICl) has been designed and synthesized, whose solvent-dependent PLQY is up to 0.53 in EtOH, and 0.46 as solid state. Fluorescence quenching experiments manifest the selective detection of picric acid (PA) and p -nitrophenol ( p -NP) over other nitroaromatic explosive compounds, which is closely related with the presence of OH groups on these two molecules that affect the ESIPT-based luminescence character of HPICl. [ABSTRACT FROM AUTHOR]

Recently, the discharge of flue gas has become a global issue due to the rapid development in industrial and anthropogenic activities. Various dry and wet treatment approaches including conventional and hybrid hybrid wet scrubbing have been employing to combat against these toxic exhaust emissions. However, certain issues i.e., large energy consumption, generation of secondary pollutants, low regeneration of scrubbing liquid and high efficieny are hindering their practical applications on industrial level. Despite this, the hybrid wet scrubbing technique (advanced oxidation, ionic-liquids and solid engineered interface hybrid materials based techniques) is gaining great attention because of its low installation costs, simultaneous removal of multi-air pollutants and low energy requirements. However, the lack of understanding about the basic principles and fundamental requirements are great hurdles for its commercial scale application, which is aim of this review article. This review article highlights the recent developments, minimization of GHG, sustainable improvements for the regeneration of used catalyst via green and electron rich donors. It explains, various hybrid wet scrubbing techniques can perform well under mild condition with possible improvements such as development of stable, heterogeneous catalysts, fast and in-situ regeneration for large scale applications. Finally, it discussed recovery of resources i.e. , N 2 O, NH 3 and N 2 , the key challenges about several competitive side products and loss of catalytic activity over time to treat toxic gases via feasible solutions by hybrid wet scrubbing techniques. [Display omitted] • A critical and detail discussion of traditional wet scrubbing with its limitations and solutions. • Significance of hybrid wet scrubbing, recent innovations for simultaneous removal of air-pollutants. • Newly developed low-cost and stable engineered interface green catalysts are presented. • Utilization of hybrid-materials for the recovery of useful products from a waste gas. [ABSTRACT FROM AUTHOR]

Gallic acid (GA), also known as 3,4,5-trihydroxybenzoic acid, is a natural secondary metabolite and widely isolated from various fruits, plants and nuts. In recent years, GA has received increasing attention for its powerful anti-inflammatory properties. The purpose of this review is to clearly illuminate the pharmacological activities and related molecular mechanisms of GA in inflammatory diseases. After consulting a large number of literatures, we made a comprehensive exposition on the chemical characteristics, plant origins, pharmacokinetics and toxicity of GA, especially its pharmacological activities and mechanisms of action. Although the plant source of GA is very rich, its lower extraction rate limits the application of GA in development. It is worth mentioning that GA can not only be separated from many plants, but also be produced in large quantities through biological and chemical synthesis. According to pharmacokinetic studies, the absorption and elimination of GA after oral administration are fast, while the structural optimization or dosage form adjustment of GA is beneficial to increase its bioavailability. Promisingly, toxicity studies have shown that GA scarcely has obvious toxicity or side effects in a variety of animal experiments and clinical trials. The results show that the anti-inflammatory mechanisms of GA mainly involved MAPK and NF-κB signaling pathways. It thus weakens the inflammatory response by reducing the release of inflammatory cytokines, chemokines, adhesion molecule and cell infiltration. Due to its excellent pharmacological activities, GA is expected to be a potential candidate for the treatment of various inflammation-related diseases. This paper will provide theoretical basis for the clinical application of GA and guide the future research and medicinal development of GA. [ABSTRACT FROM AUTHOR]