Kv3.1 Interaction with UBR5 Is Required for Chronic Inflammatory Pain.

Chronic inflammatory pain caused by neuronal hyperactivity is a common and refractory disease. Kv3.1, a member of the Kv3 family of voltage-dependent K+ channels, is a major determinant of the ability of neurons to generate high-frequency action potentials. However, little is known about its role in chronic inflammatory pain. Here, we show that although Kv3.1 mRNA expression was unchanged, Kv3.1 protein expression was decreased in the dorsal spinal horn of mice after plantar injection of complete Freund's adjuvant (CFA), a mouse model of inflammatory pain. Upregulating Kv3.1 expression alleviated CFA-induced mechanical allodynia and heat hyperalgesia, whereas downregulating Kv3.1 induced nociception-like behaviors. Additionally, we found that ubiquitin protein ligase E3 component n-recognin 5 (UBR5), a key factor in the initiation of chronic pain, binds directly to Kv3.1 to drive its ubiquitin degradation. Intrathecal injection of the peptide TP-CH-401, a Kv3.1 ubiquitination motif sequence, rescued the decrease in Kv3.1 expression and Kv currents through competitive binding to UBR5, and consequently attenuated mechanical and thermal hypersensitivity. These findings demonstrate a previously unrecognized pathway of Kv3.1 abrogation by UBR5 and indicate that Kv3.1 is critically involved in the regulation of nociceptive behavior. Kv3.1 is thus a promising new target for treating inflammatory pain.

MzmL, a novel marine derived N-acyl homoserine lactonase from Mesoflavibacter zeaxanthinifaciens that attenuates Pectobacterium carotovorum subsp. carotovorum virulence.

Quorum sensing (QS) is a conserved cell-cell communication mechanism widely distributed in bacteria, and is oftentimes tightly correlated with pathogen virulence. Quorum quenching enzymes, which interfere with QS through degrading the QS signaling molecules, could attenuate virulence instead of killing the pathogens, and thus are less likely to induce drug resistance. Many Gram-negative bacteria produce N-acyl homoserine lactones (AHLs) for interspecies communication. In this study, we isolated and identified a bacterial strain, Mesoflavibacter zeaxanthinifaciens XY-85, from an Onchidium sp. collected from the intertidal zone of Dapeng Reserve in Shenzhen, China, and found it had strong AHL degradative activity. Whole genome sequencing and blast analysis revealed that XY-85 harbors an AHL lactonase (designated MzmL), which is predicted to have an N-terminal signal peptide and share the "HXHXDH" motif with known AHL lactonases belonging to the Metallo-ß-lactamase superfamily. Phylogenetic studies showed MzmL was closest to marine lactonase cluster members, MomL and Aii20J, instead of the AiiA type lactonases. Ultra performance liquid chromatography-mass spectrometry analysis confirmed that MzmL functions as an AHL lactonase catalyzing AHL degradation through lactone hydrolysis. MzmL could degrade both short- and long-chain AHLs with or without a substitution of oxo-group at the C-3 position, and retained full bioactivity under a wide range of temperatures (28-100°C) and pHs (4-11). Furthermore, MzmL significantly reduced Pectobacterium carotovorum subsp. carotovorum virulence factor production in vitro, such as biofilm formation and plant cell wall degrading enzyme production, and inhibited soft rot development on potato slices. These results demonstrated that MzmL may be a novel type of AHL lactonase with good environmental stability, and has great potential to be developed into a novel biological control agent for bacterial disease management.

In Vitro and Ex Vivo Antifungal Activities of Metconazole against the Rice Blast Fungus Pyricularia oryzae.

Rice blast, caused by the filamentous fungus Pyricularia oryzae, has long been one of the major threats to almost all rice-growing areas worldwide. Metconazole, 5-(4-chlorobenzyl)-2, 2-dimethyl-1-(1H-1, 2, 4-triazol-1-ylmethyl) cyclopentanol, is a lipophilic, highly active triazole fungicide that has been applied in the control of various fungal pathogens of crops (cereals, barley, wheat), such as the Fusarium and Alternaria species. However, the antifungal activity of metconazole against P. oryzae is unknown. In this study, metconazole exhibited broad spectrum antifungal activities against seven P. oryzae strains collected from rice paddy fields and the wild type strain P131. Scanning electron microscopic analysis and fluorescein diacetate staining assays revealed that metconazole treatment damaged the cell wall integrity, cell membrane permeability and even cell viability of P. oryzae, resulting in deformed and shrunken hyphae. The supplementation of metconazole in vitro increased fungal sensitivity to different stresses, such as sodium dodecyl sulfate, congo red, sodium chloride, sorbitol and oxidative stress (H2O2). Metconazole could inhibit key virulence processes of P. oryzae, including conidial germination, germ tube elongation and appressorium formation. Furthermore, this chemical prevented P. oryzae from infecting barley epidermal cells by disturbing appressorium penetration and subsequent invasive hyphae development. Pathogenicity assays indicated a reduction of over 75% in the length of blast lesions in both barley and rice leaves when 10 µg/mL of metconazole was applied. This study provides evidence to understand the antifungal effects of metconazole against P. oryzae and demonstrates its potential in rice blast management.

DExH-box helicase 9 modulates hippocampal synapses and regulates neuropathic pain.

Experimental studies have shown that neuropathic pain impairs hippocampal synaptic plasticity. Here, we sought to determine the underlying mechanisms responsible for synaptic changes in neuropathic painful mouse hippocampal neurons. Beyond demonstrating proof-of-concept for the location of DExH-box helicase 9 (DHX9) in the nucleus, we found that it did exist in the cytoplasm and DHX9 depletion resulted in structural and functional changes at synapses in the hippocampus. A decrease of DHX9 was observed in the hippocampus after peripheral nerve injury; overexpression of DHX9 in the hippocampus significantly alleviated the nociceptive responses and improved anxiety behaviors. Mimicking DHX9 decrease evoked spontaneous pain behavioral symptoms and anxiety emotion in naïve mice. Mechanistically, we found that DHX9 bound to dendrin (Ddn) mRNA, which may have altered the level of synaptic- and dendritic-associated proteins. The data suggest that DHX9 contributes to synapses in hippocampal neurons and may modulate neuropathic pain and its comorbidity aversive emotion.

DNA N6-methyladenine methylase N6AMT1 controls neuropathic pain through epigenetically modifying Kcnj16 in dorsal horn neurons.

ABSTRACT: Nerve injury-induced aberrant changes in gene expression in spinal dorsal horn neurons are critical for the genesis of neuropathic pain. N6-methyladenine (m 6 A) modification of DNA represents an additional layer of gene regulation. Here, we report that peripheral nerve injury significantly decreased the level of m 6 A-specific DNA methyltransferase 1 ( N6amt1 ) in dorsal horn neurons. This decrease was attributed, at least partly, to a reduction in transcription factor Nr2f6 . Rescuing the decrease in N6amt1 reversed the loss of m 6 A at the promoter for inwardly rectifying potassium channel subfamily J member 16 ( Kcnj16 ), mitigating the nerve injury-induced upregulation of Kcnj16 expression in the dorsal horn and alleviating neuropathic pain hypersensitivities. Conversely, mimicking the downregulation of N6amt1 in naive mice erased DNA m 6 A at the Kcnj16 promoter, elevated Kcnj16 expression, and led to neuropathic pain-like behaviors. Therefore, decreased N6amt1 caused by NR2F6 is required for neuropathic pain, likely through its regulation of m 6 A-controlled KCNJ16 in dorsal horn neurons, suggesting that DNA m 6 A modification may be a potential new target for analgesic and treatment strategies.

Thermal process of a silicon wafer under a CW laser and 100-10000 Hz pulsed laser irradiation.

The thermal process of a (001) silicon wafer subjected to a continuous-wave (CW) laser and 100-10000 Hz pulsed laser irradiation is investigated experimentally and numerically. The temperature evolution of the spot center is measured using an infrared radiation pyrometer. The waveforms of the temperature evolution curves provide valuable information about melting, solidification, vaporization, and fracture. To gain a better understanding of the thermal process, a three-dimensional finite element model is established, and numerical simulations are conducted to analyze the temperature, stress, and dislocation field. The results show that the 10 kHz laser exhibits the highest heating efficiency before vaporization, but the lowest ablation efficiency after vaporization due to the shielding effect of vapor. The diffusion time of vapor is found to be more than 50 µs. Fracture occurs during 1 kHz laser irradiation. The motion of liquid may play a significant role, but it cannot be evidenced by a simulation due to complex dependence of material parameters on dislocation. This issue should be addressed as a priority in future studies.

A MXene@AgAu@PDA nanoplatform loaded with AgAu nanocages for enhancing catalytic activity and antibacterial performance.

With the rapid development of social industrialization, environmental problems seriously threaten people's health, especially water pollution. Therefore, there is an urgent need to construct a multifunctional nanoplatform for different scenarios. Two-dimensional MXene@AgAu@PDA nanosheets loaded with AgAu bimetallic nanocages have been prepared by a one-step method. First, the in situ generated MXene@Ag is used as an auxiliary template, and then HAuCl4 and dopamine are added for in situ redox-oxidizing polymerization reactions to obtain AgAu catalytic nanocages and the protective polydopamine (PDA) layer which can improve the stability and biocompatibility. MXene and PDA have excellent photothermal conversion ability while hollow AgAu nanocages have strong absorption in the near-infrared region and a local surface plasmonic resonance effect. In comparison to the catalytic reaction rates under dark and room temperature conditions, the catalytic kinetic rate of MXene@AgAu@PDA nanosheets under near-infrared irradiation increases from 0.13 to 0.69 min-1 mg-1. Density functional theory (DFT) is used to study the electron transfer behavior between AgAu nanocages and MXene nanosheets, and the mechanism of the enhanced catalytic reaction rate is analyzed. Besides, due to its Ag ions and photothermal coupling antibacterial properties, 40 µg mL-1 MXene@AgAu@PDA nanosheets inactivates nearly all E. coli and S. aureus after irradiation with near-infrared light for 6 min.

Pacificoceanicola onchidii gen. nov., sp. nov., isolated from a marine invertebrate from the South China Sea.

A Gram-stain-negative, facultative anaerobic, non-flagellated and oval-shaped (0.77-0.98 µm wide and 0.74-1.21 µm long) bacterial strain, designated XY-301T, was isolated from a marine invertebrate collected from the South China Sea. Strain XY-301T grew at 15-37 °C (optimum, 30-35 °C) and at pH 7.0-8.5 (optimum, pH 8.0). The strain was slightly halophilic and it only grew in the presence of 0.5-6.5 % (w/v) NaCl (optimum, 2.5-3.5 %). Its predominant fatty acid (>10 %) was C18 : 1 ω7c. The predominant polar lipids of XY-301T were diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, six unidentified aminolipids, three unidentified phospholipids and two unknown polar lipids. The respiratory quinone was Q-10. The genome of XY-301T was 4 979 779 bp in size, with a DNA G+C content of 61.3 mol%. The average nucleotide identity, digital DNA-DNA hybridization and average amino acid identity values between XY-301T and Pseudoprimorskyibacter insulae SSK3-2T were 73.3, 14.5 and 53.5 %, respectively. Based on the results of phylogenetic, phenotypic, chemotaxonomic and genomic analyses, strain XY-301T is considered to represent a novel species and a new genus of the family Roseobacteraceae, for which the name Pacificoceanicola onchidii gen. nov., sp. nov. is proposed. The type strain is XY-301T (=KCTC 72212T=MCCC 1K03614T).

Spinal-Specific Super Enhancer in Neuropathic Pain.

Dysfunctional gene expression in nociceptive pathways plays a critical role in the development and maintenance of neuropathic pain. Super enhancers (SEs), composed of a large cluster of transcriptional enhancers, are emerging as new players in the regulation of gene expression. However, whether SEs participate in nociceptive responses remains unknown. Here, we report a spinal-specific SE (SS-SE) that regulates chronic constriction injury (CCI)-induced neuropathic pain by driving Ntmt1 and Prrx2 transcription in dorsal horn neurons. Peripheral nerve injury significantly enhanced the activity of SS-SE and increased the expression of NTMT1 and PRRX2 in the dorsal horn of male mice in a bromodomain-containing protein 4 (BRD4)-dependent manner. Both intrathecal administration of a pharmacological BRD4 inhibitor JQ1 and CRISPR-Cas9-mediated SE deletion abolished the increased NTMT1 and PRRX2 in CCI mice and attenuated their nociceptive hypersensitivities. Furthermore, knocking down Ntmt1 or Prrx2 with siRNA suppressed the injury-induced elevation of phosphorylated extracellular-signal-regulated kinase (p-ERK) and glial fibrillary acidic protein (GFAP) expression in the dorsal horn and alleviated neuropathic pain behaviors. Mimicking the increase in spinal Ntmt1 or Prrx2 in naive mice increased p-ERK and GFAP expression and led to the genesis of neuropathic pain-like behavior. These results redefine our understanding of the regulation of pain-related genes and demonstrate that BRD4-driven increases in SS-SE activity is responsible for the genesis of neuropathic pain through the governance of NTMT1 and PRRX2 expression in dorsal horn neurons. Our findings highlight the therapeutic potential of BRD4 inhibitors for the treatment of neuropathic pain.SIGNIFICANCE STATEMENT SEs drive gene expression by recruiting master transcription factors, cofactors, and RNA polymerase, but their role in the development of neuropathic pain remains unknown. Here, we report that the activity of an SS-SE, located upstream of the genes Ntmt1 and Prrx2, was elevated in the dorsal horn of mice with neuropathic pain. SS-SE contributes to the genesis of neuropathic pain by driving expression of Ntmt1 and Prrx2 Both inhibition of SS-SE with a pharmacological BRD4 inhibitor and genetic deletion of SS-SE attenuated pain hypersensitivities. This study suggests an effective and novel therapeutic strategy for neuropathic pain.

Developmental Mapping of Hair Follicles in the Embryonic Stages of Cashmere Goats Using Proteomic and Metabolomic Construction.

The hair follicle (HF) is the fundamental unit for fleece and cashmere production in cashmere goats and is crucial in determining cashmere yield and quality. The mechanisms regulating HF development in cashmere goats during the embryonic period remain unclear. Growing evidence suggests that HF development involves complex developmental stages and critical events, and identifying the underlying factors can improve our understanding of HF development. In this study, samples were collected from embryonic day 75 (E75) to E125, the major HF developmental stages. The embryonic HFs of cashmere goats were subjected to proteomic and metabolomic analyses, which revealed dynamic changes in the key factors and signalling pathways controlling HF development at the protein and metabolic levels. Gene ontology and the Kyoto Encyclopaedia of Genes and Genomes were used to functionally annotate 1784 significantly differentially expressed proteins and 454 significantly differentially expressed metabolites enriched in different HF developmental stages. A joint analysis revealed that the oxytocin signalling pathway plays a sustained role in embryonic HF development by activating the MAPK and Ca2+ signalling pathways, and a related regulatory network map was constructed. This study provides a global perspective on the mechanism of HF development in cashmere goats and enriches our understanding of embryonic HF development.

The impact of iron-boron electrocatalysts on the charge transport and oxygen evolution reaction of bismuth vanadate photoanodes.

BiVO4 possesses a suitable band gap for photoelectrochemical (PEC) water splitting to produce hydrogen; however, the performance of BiVO4 is limited by several adverse factors. The bulk charge recombination and the slow surface water oxidation reaction of BiVO4 are main unfavorable factors. In view of these disadvantages, an Fe-Bi electrocatalyst is loaded on BiVO4 to improve the PEC performance of BiVO4. After modification, the onset potential of BiVO4 shifts negatively by 60 mV, and the saturated photocurrent is greatly increased. Systematic studies demonstrate that the Fe-Bi electrocatalyst not only enhances the bulk charge separation, but also accelerates the surface water oxidation rate of BiVO4 and greatly reduces the resistance of the reaction interface.

Downregulation of ciRNA-Kat6b in dorsal spinal horn is required for neuropathic pain by regulating Kcnk1 in miRNA-26a-dependent manner.

AIMS: Nerve injury-induced maladaptive changes in gene expression in the spinal neurons are essential for neuropathic pain genesis. Circular RNAs (ciRNA) are emerging as key regulators of gene expression. Here, we identified a nervous-system-tissues-specific ciRNA-Kat6 with conservation in humans and mice. We aimed to investigate whether and how spinal dorsal horn ciRNA-Kat6b participates in neuropathic pain. METHODS: Unilateral sciatic nerve chronic constrictive injury (CCI) surgery was used to prepare the neuropathic pain model. The differentially expressed ciRNAs were obtained by RNA-Sequencing. The identification of nervous-system-tissues specificity of ciRNA-Kat6b and the measurement of ciRNA-Kat6b and microRNA-26a (miRNA-26a) expression level were carried out by quantitative RT-PCR. The ciRNA-Kat6b that targets miRNA-26a and miRNA-26a that targets Kcnk1 were predicted by bioinformatics analysis and verified by in vitro luciferase reports test and in vivo experiments including Western-blot, immunofluorescence, and RNA-RNA immunoprecipitation. The correlation between neuropathic pain and ciRNA-Kat6b, miRNA-26a, or Kcnk1 was examined by the hypersensitivity response to heat and mechanical stimulus. RESULTS: Peripheral nerve injury downregulated ciRNA-Kat6b in the dorsal spinal horn of male mice. Rescuing this downregulation blocked nerve injury-induced increase of miRNA-26a, reversed the miRNA-26a-triggered decrease of potassium channel Kcnk1, a key neuropathic pain player, in the dorsal horn, and alleviates CCI-induced pain hypersensitivities. On the contrary, mimicking this downregulation increased the miRNA-26a level and decreased Kcnk1 in the spinal cord, resulting in neuropathic pain-like syndrome in naïve mice. Mechanistically, the downregulation of ciRNA-Kat6b reduced the accounts of miRNA-26a binding to ciRNA-Kat6b, and elevated the binding accounts of miRNA-26a to the 3' untranslated region of Kcnk1 mRNA and degeneration of Kcnk1 mRNA, triggering in the reduction of KCNK1 protein in the dorsal horn of neuropathic pain mice. CONCLUSION: The ciRNA-Kat6b/miRNA-26a/Kcnk1 pathway in dorsal horn neurons regulates the development and maintenance of neuropathic pain, ciRNA-Kat6b may be a potential new target for analgesic and treatment strategies.

Deciphering photocatalytic degradation of methylene blue by surface-tailored nitrogen-doped carbon quantum dots derived from Kraft lignin.

Lignin in black liquor can be used to manufacture carbon nanomaterials on a large scale. However, the effect of nitrogen doping on the physicochemical properties and photocatalytic performance of carbon quantum dots (NCQDs) remains to be explored. In this study, NCQDs with different properties were prepared hydrothermally by using kraft lignin as the raw material and EDA as a nitrogen dopant. The amount of EDA added affects the carbonization reaction and surface state of NCQDs. Raman spectroscopy showed that the surface defects increased from 0.74 to 0.84. Photoluminescence spectroscopy (PL) showed that NCQDs had different intensities of fluorescence emission at 300-420 nm and 600-900 nm. Meanwhile, NCQDs can photo-catalytically degrade 96 % of MB under simulated sunlight irradiation within 300 min. After three months of storage, the fluorescence intensity of NCQDs remained above 94 %, showing remarkable fluorescence stability. After four times of recycling, the photo-degradation rate of NCQDs was maintained above 90 %, confirming its outstanding stability. As a result, a clear understanding of the design of carbon-based photo-catalyst fabricated from the waste of the paper-making industry has been gained.

DHX9/DNA-tandem repeat-dependent downregulation of ciRNA-Fmn1 in the dorsal horn is required for neuropathic pain.

Circular RNAs (ciRNAs) are emerging as new players in the regulation of gene expression. However, how ciRNAs are involved in neuropathic pain is poorly understood. Here, we identify the nervous-tissue-specific ciRNA-Fmn1 and report that changes in ciRNA-Fmn1 expression in spinal cord dorsal horn neurons play a key role in neuropathic pain after nerve injury. ciRNA-Fmn1 was significantly downregulated in ipsilateral dorsal horn neurons after peripheral nerve injury, at least in part because of a decrease in DNA helicase 9 (DHX9), which regulates production of ciRNA-Fmn1 by binding to DNA-tandem repeats. Blocking ciRNA-Fmn1 downregulation reversed nerve-injury-induced reductions in both the binding of ciRNA-Fmn1 to the ubiquitin ligase UBR5 and the level of ubiquitination of albumin (ALB), thereby abrogating the nerve-injury-induced increase of ALB expression in the dorsal horn and attenuating the associated pain hypersensitivities. Conversely, mimicking downregulation of ciRNA-Fmn1 in naïve mice reduced the UBR5-controlled ubiquitination of ALB, leading to increased expression of ALB in the dorsal horn and induction of neuropathic-pain-like behaviors in naïve mice. Thus, ciRNA-Fmn1 downregulation caused by changes in binding of DHX9 to DNA-tandem repeats contributes to the genesis of neuropathic pain by negatively modulating UBR5-controlled ALB expression in the dorsal horn.

Changing the reaction pathway in TiO2 photocatalytic dehalogenation of halogenated aromatic pollutants by surface hydroxyl regulation.

Understanding the photocatalytic reductive dehalogenation mechanism of halogenated aromatic pollutants is of great research value. However, the proton source in the photocatalytic dehalogenation process of representative halogenated aromatic pollutants by TiO2 is not clear. In this study, the TiO2 surface was modified by hydrochloric acid, sodium hydroxide, and sodium fluoride to obtain TiO2 samples with different hydroxyl groups. It was found that the hydroxyl groups on the surface of TiO2 affects the sequence of proton and electron transfer in dehalogenation. The abundance of hydroxyl groups on the surface of TiO2 can accelerate the reductive dehalogenation process of representative halogenated aromatic pollutants. The kinetic solvent isotope effect was used to study the proton-coupled electron transfer process in the reaction. It shows that the enriching of protons on TiO2 bridging oxygen (bridging hydroxyl groups) is conducive to the rapid step of protonation of the reactant, and subsequent proton and electron transfer. On the contrary, the bridging hydroxyl groups can be removed by reacting with strongly basic sodium hydroxide and sodium ions can occupy the bridging oxygen. The substitution of bridging oxygen by fluorine ions can also lead to the destruction of bridge hydroxyl groups. Significantly, the absence of bridging hydroxyl groups on titanium dioxide will lead to the dehalogenation of representative halogenated aromatic pollutants initiated by electron transfer. This study is helpful to understand dehalogenation reaction paths catalyzed by TiO2.

W18O49@EP nanoparticles improve the anti-tumor effect of radiotherapy and photodynamic therapy by avoiding the limitation of hypoxia.

Insufficient oxygen supply at the tumor site and hypoxia caused during tumor treatment lead to a poor therapeutic effect and poor prognosis. Therefore, effectively overcoming the problem of hypoxia in tumors and avoiding hypoxia that compromises the efficacy of the treatment could improve the anti-tumor therapeutic effect. Thus, this study reports the ability of W18O49@EP nanoparticles to release reactive oxygen species (ROS) during the combined tumor radiotherapy (RT) and photodynamic therapy (PDT). The release of ROS by the nanoparticles during near infrared light (NIR) irradiation was demonstrated by in vitro and in vivo experiments, realizing an effective PDT without inducing hypoxia. Indeed, the ROS did not derive from the oxygen in the tumor microenvironment but they were released by the nanoparticles. Thus, ROS could improve the therapeutic effect of RT avoiding the problem of hypoxia after RT. Hence, W18O49@EP nanoparticles greatly improved the anti-tumor effect due to their effectiveness despite the insufficient oxygen supply and hypoxia caused by traditional RT and PDT.

Effects of Crotonylation on Reprogramming of Cashmere Goat Somatic Cells with Different Differentiation Degrees.

Failure in the epigenetic reprogramming of somatic cells is considered the main reason for lower cloned embryo development efficiency. Lysine crotonylation (Kcr) occupies an important position in epigenetic modification, while its effects on somatic cell reprogramming have not been reported. In this study, we detected the influence of sodium crotonate (NaCr) on the Kcr levels in three types of somatic cells (muscle-derived satellite cells, MDSCs; fetal fibroblast cells, FFCs; and ear tip fibroblast cells, EFCs). The three types of somatic cells were treated with NaCr for cloned embryo construction, and the cleavage rates and Kcr, H3K9cr, and H3K18cr levels in the cloned embryos were analyzed. The results showed that the abnormal levels of Kcr, H3K9cr, and H3K18cr were corrected in the treatment groups. Although there was no significant difference in the cloned embryo cleavage rate in the FFC treatment group, the cleavage rates of the cloned embryos in the MDSCs and EFCs treatment groups were increased. These findings demonstrated that the Kcr level was increased with NaCr treatment in somatic cells from Cashmere goat, which contributed to proper reprogramming. The reprogramming of somatic cells can be promoted and cloned embryo development can be improved through the treatment of somatic cells with NaCr.

Charge-Convertible and Reduction-Sensitive Cholesterol-Containing Amphiphilic Copolymers for Improved Doxorubicin Delivery.

For achieving successful chemotherapy against cancer, designing biocompatible drug delivery systems (DDSs) with long circulation times, high cellular endocytosis efficiency, and targeted drug release is of upmost importance. Herein, a well-defined PEG-b-P(MASSChol-co-MANBoc) block copolymer bearing redox-sensitive cholesteryl-side group was prepared via reversible addition-fragmentation chain transfer (RAFT) polymerization (with non-redox PEG-b-P(MACCChol-co-MAN-DCA) as the reference), and 1,2-dicarboxylic-cyclohexene acid (DCA) was then grafted onto the hydrophobic block to endow it with charge-convertible characteristics under a tumor microenvironment. The amphiphilic copolymer could be assembled into polymeric spherical micelles (SSMCs) with polyethylene glycol (PEG) as the corona/shell, and anti-cancer drug doxorubicin (DOX) was successfully encapsulated into the micellar core via strong hydrophobic and electrostatic interactions. This nanocarrier showed high stability in the physiological environment and demonstrated "smart" surface charge conversion from negative to positive in the slightly acidic environment of tumor tissues (pH 6.5~6.8), as determined by dynamic light scattering (DLS). Moreover, the cleavage of a disulfide bond linking the cholesterol grafts under an intracellular redox environment (10 mM GSH) resulted in micellar dissociation and accelerated drug release, with the non-redox-responsive micelles (CCMCs) as the control. Additionally, a cellular endocytosis and tumor proliferation inhibition study against MCF-7 tumor cells demonstrated the enhanced endocytosis and tumor cell inhibitory efficiency of dual-responsive SSMCs/DOX nanomedicines, revealing potentials as multifunctional nanoplatforms for effective oncology treatment.

Heterogeneous Cu2O-Au nanocatalyst anchored on wood and its insight for synergistic photodegradation of organic pollutants.

In this study, a Cu2O-Au nanoparticles (NPs) heterojunction catalyst anchored on wood was developed by in situ reduction and hydrothermal treatment, and the properties of the catalyst were systematically characterized. The catalyst exhibited prominent photocatalysis of methyl orange (MO, 0.169 min- 1), and tetracycline (TC, 0.122 min-1) which were degraded completely within 20 min. Even after four recyclings, the efficiency of MO degradation by the catalyst remained at 80%. The natural wood with three-dimensional porous structures acted as a reducing agent and a stabilizer for Au NPs and Cu2O, which helped to maintain high performance and reusability. The presence of Au NPs mediated the light-induced electron transfer and enhanced the absorption of visible light for promoting photocatalytic activity. The intermediates of contaminants within the degradation process were characterized by liquid chromatography-mass spectrometry. Additionally, the photogenerated superoxide radicals and holes were identified by electron spin resonance. Thus, the potential degradation mechanism catalyzed by the Cu2O-Au NPs-wood was proposed. This findings of this study valorizes biomass as a photocatalyst for wastewater remediation.

Recent Advances in Zinc Hydroxystannate-Based Flame Retardant Polymer Blends.

During the combustion of polymeric materials, plenty of heat, smoke, and toxic gases are produced that may cause serious harm to human health. Although the flame retardants such as halogen- and phosphorus-containing compounds can inhibit combustion, they cannot effectively reduce the release of toxic fumes. Zinc hydroxystannate (ZHS, ZnSn(OH)6) is an environmentally friendly flame retardant that has attracted extensive interest because of its high efficiency, safety, and smoke suppression properties. However, using ZHS itself may not contribute to the optimal flame retardant effect, which is commonly combined with other flame retardants to achieve more significant efficiency. Few articles systematically review the recent development of ZHS in the fire safety field. This review aims to deliver an insight towards further direction and advancement of ZHS in flame retardant and smoke suppression for multiple polymer blends. In addition, the fire retarded and smoke suppression mechanism of ZHS will be demonstrated and discussed in depth.