Mechanistic study of transcription factor Sox18 during heart development.

Heart development is a delicate and complex process regulated by coordination of various signaling pathways. In this study, we investigated the role of sox18 in heart development by modulating Wnt/ß-Catenin signaling pathways. Our spatiotemporal expression analysis revealed that sox18 is mainly expressed in the heart, branchial arch, pharyngeal arch, spinal cord, and intersegmental vessels at the tailbud stage of Xenopus tropicalis embryo. Overexpression of sox18 in the X. tropicalis embryos causes heart edema, while loss-of-function of sox18 can change the signal of developmental heart marker gata4 at different stages, suggesting that sox18 plays an essential role in the development of the heart. Knockdown of SOX18 in human umbilical vein endothelial cells suggests a link between Sox18 and ß-CATENIN, a key regulator of the Wnt signaling pathway. Sox18 negatively regulates islet1 and tbx3, the downstream factors of Wnt/ß-Catenin signaling, during the linear heart tube formation and the heart looping stage. Taken together, our findings highlight the crucial role of Sox18 in the development of the heart via inhibiting Wnt/ß-Catenin signaling.

ZSWIM4 regulates embryonic patterning and BMP signaling by promoting nuclear Smad1 degradation.

The dorsoventral gradient of BMP signaling plays an essential role in embryonic patterning. Zinc Finger SWIM-Type Containing 4 (zswim4) is expressed in the Spemann-Mangold organizer at the onset of Xenopus gastrulation and is then enriched in the developing neuroectoderm at the mid-gastrula stages. Knockdown or knockout of zswim4 causes ventralization. Overexpression of zswim4 decreases, whereas knockdown of zswim4 increases the expression levels of ventrolateral mesoderm marker genes. Mechanistically, ZSWIM4 attenuates the BMP signal by reducing the protein stability of SMAD1 in the nucleus. Stable isotope labeling by amino acids in cell culture (SILAC) identifies Elongin B (ELOB) and Elongin C (ELOC) as the interaction partners of ZSWIM4. Accordingly, ZSWIM4 forms a complex with the Cul2-RING ubiquitin ligase and ELOB and ELOC, promoting the ubiquitination and degradation of SMAD1 in the nucleus. Our study identifies a novel mechanism that restricts BMP signaling in the nucleus.

Waste milk humification product can be used as a slow release nano-fertilizer.

The demand for milk has increased globally, accompanied by an increase in waste milk. Here, we provide an artificial humification technology to recycle waste milk into an agricultural nano-fertilizer. We use KOH-activated persulfate to convert waste milk into fulvic-like acid and humic-like acid. We mix the product with attapulgite to obtain a slow-release nano fulvic-like acid fertilizer. We apply this nano-fertilizer to chickweeds growing in pots, resulting in improved yield and root elongation. These results indicate that waste milk could be recycled for agricultural purposes, however, this nano-fertilizer needs to be tested further in field experiments.

Developmental expression of peroxiredoxin gene family in early embryonic development of Xenopus tropicalis.

Peroxidase genes (Prdx) encode a family of antioxidant proteins, which can protect cells from oxidative damage by reducing various cellular peroxides. This study investigated the spatiotemporal expression patterns of gene members in this family during the early development of Xenopus tropicalis. Real-time quantitative PCR showed that all members of this gene family have a distinct temporal expression pattern during the early development of X. tropicalis embryos. Additionally, whole mount in situ hybridization revealed that individual prdx genes display differential expression patterns, with overlapping expression in lymphatic vessels, pronephros, proximal tubule, and branchial arches. This study provides a basis for further study of the function of the prdx gene family.

Loss of circIGF1R Suppresses Cardiomyocytes Proliferation by Sponging miR-362-5p.

Circular RNAs (circRNAs) are generally formed by the back-splicing of precursor mRNA. Increasing evidence implicates the important role of circRNAs in cardiovascular diseases. However, the role of circ-insulin-like growth factor 1 receptor (circIGF1R) in cardiomyocyte (CM) proliferation remains unclear. Here, we investigated the potential role of the circIGF1R in the proliferation of CMs. We found that circIGF1R expression in heart tissues and primary CMs from adult mice was significantly lower than that in neonatal mice at postnatal 1 day (p1). Increased circIGF1R expression was detected in the injured neonatal heart at 0.5 and 1 days post-resection. circIGF1R knockdown significantly decreased the proliferation of primary CMs. Combined prediction software, luciferase reporter gene analysis, and quantitative real time-PCR (qPCR) revealed that circIGF1R interacted with miR-362-5p. A significant increase in miR-362-5p expression was detected in the adult heart compared with that in the neonatal heart. Further, heart injury significantly decreased the expression of miR-362-5p in neonatal mice. Treatment with miR-362-5p mimics significantly suppressed the proliferation of primary CMs, whereas knockdown of miR-362-5p promoted the CMs proliferation. Meanwhile, miR-362-5p silencing can rescue the proliferation inhibition of CMs induced by circIGF1R knockdown. Target prediction and qPCR validation revealed that miR-362-5p significantly inhibited the expression of Phf3 in primary CMs. In addition, decreased Phf3 expression was detected in adult hearts compared with neonatal hearts. Consistently, increased Phf3 expression was detected in injured neonatal hearts compared with that in sham hearts. Knockdown of Phf3 markedly repressed CMs proliferation. Taken together, these findings suggest that circIGF1R might contribute to cardiomyocyte proliferation by promoting Pfh3 expression by sponging miR-362-5p and provide an important experimental basis for the regulation of heart regeneration.

Genome-wide identification and spatiotemporal expression profiling of zinc finger SWIM domain-containing protein family genes.

The biological function of the novel zinc-finger SWIM domain-containing protein family (ZSWIM) during embryonic development remains elusive. Here, we conducted a genome-wide analysis to explore the evolutionary processes of the ZSWIM gene family members in mice, Xenopus tropicalis, zebrafish, and humans. We identified nine putative ZSWIM genes in the human and mouse genome, eight in the Xenopus genome, and five in the zebrafish genome. Based on multiple sequence alignment, three members, ZSWIM5, ZSWIM6, and ZSWIM8, demonstrated the highest homology across all four species. Using available RNA sequencing (RNA-seq) data, ZSWIM genes were found to be widely expressed across different tissues, with distinct tissue-specific properties. To identify the functions of the ZSWIM protein family during embryogenesis, we examined temporal and spatial expression patterns of zswim family genes in Xenopus embryos. Quantitative real-time polymerase chain reaction (qRT-PCR) revealed that each member had a distinct expression profile. Whole-mount in situ hybridization showed that both zswim1 and zswim3 were maternally expressed genes; zswim5 and zswim6 were expressed throughout embryogenesis and displayed dynamic expression in the brain, eyes, somite, and bronchial arch at the late tailbud stages; zswim7 was detected in the eye area; zswim8 showed a dynamic expression pattern during the tailbud stages, with expression detected in the brain, eyes, and somite; zswim9 was faintly expressed throughout embryonic development. This study provides a foundation for future research to delineate the functions of ZSWIM gene members.

Echocardiographic assessment of Xenopus tropicalis heart regeneration.

BACKGROUND: Recently, it was reported that the adult X. tropicalis heart can regenerate in a nearly scar-free manner after injury via apical resection. Thus, a cardiac regeneration model in adult X. tropicalis provides a powerful tool for recapitulating a perfect regeneration phenomenon, elucidating the underlying molecular mechanisms of cardiac regeneration in an adult heart, and developing an interventional strategy for the improvement in the regeneration of an adult heart, which may be more applicable in mammals than in species with a lower degree of evolution. However, a noninvasive and rapid real-time method that can observe and measure the long-term dynamic change in the regenerated heart in living organisms to monitor and assess the regeneration and repair status in this model has not yet been established. RESULTS: In the present study, the methodology of echocardiographic assessment to characterize the morphology, anatomic structure and cardiac function of injured X. tropicalis hearts established by apex resection was established. The findings of this study demonstrated for the first time that small animal echocardiographic analysis can be used to assess the regeneration of X. tropicalis damaged heart in a scar-free perfect regeneration or nonperfect regeneration with adhesion manner via recovery of morphology and cardiac function. CONCLUSIONS: Small animal echocardiography is a reliable, noninvasive and rapid real-time method for observing and assessing the long-term dynamic changes in the regeneration of injured X. tropicalis hearts.

Comparative analysis of mesenchymal stem/stromal cells derived from human induced pluripotent stem cells and the cognate umbilical cord mesenchymal stem/stromal cells.

Mesenchymal stem/stromal cells (MSCs) show tremendous potential for regenerative medicine due to their self-renewal, multi-differentiation and immunomodulatory capabilities. Largely studies had indicated conventional tissue-derived MSCs have considerable limited expandability and donor variability which hinders further application. Induced pluripotent stem cell (iPSCs)-derived MSCs (iMSCs) have created exciting source for standardized cellular therapy. However, the cellular and molecular differences between iMSCs and the cognate tissue-derived MSCs remains poorly explored. In this study, we first successfully reprogrammed human umbilical cords-derived mesenchymal stem/stromal cells (UMSCs) into iPSCs by using the cocktails of mRNA. Subsequently, iPSCs were further differentiated into iMSCs in xeno-free induction medium. Then, iMSCs were compared with the donor matched UMSCs by assessing proliferative state, differentiation capability, immunomodulatory potential through immunohistochemical analysis, flow cytometric analysis, transcriptome sequencing analysis, and combine with coculture with immune cell population. The results showed that iMSCs exhibited high expression of MSCs positive-makers CD73, CD90, CD105 and lack expression of negative-maker cocktails CD34, CD45, CD11b, CD19, HLA-DR; also successfully differentiated into osteocytes, chondrocytes and adipocytes. Further, the iMSCs were similar with their parental UMSCs in cell proliferative state detected by the CCK-8 assay, and in cell rejuvenation state assessed by ß-Galactosidase staining and telomerase activity related mRNA and protein analysis. However, iMSCs exhibited similarity to resident MSCs in Homeobox (Hox) genes expression profile and presented better neural differentiation potential by activation of NESTIN related pathway. Moreover, iMSCs owned enhanced immunosuppression capacity through downregulation pools of pro-inflammatory factors, including IL6, IL1B etc. and upregulation anti-inflammatory factors NOS1, TGFB etc. signals. In summary, our study provides an attractive cell source for basic research and offers fundamental biological insight of iMSCs-based therapy.

Honeycomb-like MnO2/Biochar Catalyst Fabricated by High-Energy Electron Beam Irradiation for Degradation of Antibiotics in Swine Urine.

The modification of biochar is essential for the development of multifunctional biochar materials with enhanced remediation effects on contaminated water. In this work, a biochar-based microcatalyst with sunlight sensitivity was synthesized by a creative modification method that involved the rapid fabrication of MnO2 microspheres by high-energy electron beam (HEEB) irradiation, and loading them into corn straw-derived honeycomb-like KOH-modified biochar (MBC) to obtain a sunlight-sensitive microcatalyst (SSM). The honeycomb-like structure of MBC facilitated the improvement in MnO2 dispersion and photocatalytic property through confinement effect. The effects of photocatalyst dosage, initial chlortetracycline (CTC) concentration, solution pH, temperature and coexisting ions on the photocatalytic performance of SSM were systemically investigated. The results indicated that SSM could efficiently degrade CTC in water and swine urine under sunlight, and exhibited high stability against coexistence of urea, Cl- and SO42-. Moreover, SSM showed good reusability in regeneration studies. This work provides a novel method for degrading CTC with potential application prospect.

Recognition and quantitative analysis for six phthalate esters (PAEs) through functionalized ZIF-67@Ag nanowires as surface-enhanced Raman scattering substrate.

A novel surface enhanced Raman scattering (SERS) method was developed based on Ag nanowires embedded into functionalized metal-organic framework ZIF-67 (ZIF-67@Ag NWs) composite as substrate, which was applied for rapid recognition and sensitive detection of six PAEs. The Raman signals for PAEs detection were gained at ZIF-67@Ag NWs substrate mainly due to the "sharp tip effect" of rough Ag nanowires and excellent absorptive capacity of ZIF-67 to capture targeted molecules into the electromagnetic field. Different structural PAEs, including carbon chain lengths, isomers, and substituents, were evaluated for SERS performance and characteristic peaks under the optimal conditions. The SERS spectra proved that different PAEs exhibited some typically characteristic peaks in favor of recognizing and distinguishing them. The ZIF-67@Ag NWs as SERS substrate was successfully applied to detect six PAEs and exhibited wide linear ranges, low detection limit (LOD), excellent repeatability and stability (such as dibutyl phthalate DBP: linear range of 10-2 âˆ¼ 10-12 mol/L, LOD 3 × 10-13 mol/L). The ZIF-67@Ag NWs substrate by SERS was implemented to determine trace DBP in plastics with satisfactory recoveries of 82.5 % ∼ 108.3 %. The proposed ZIF-67@Ag NWs substrate may provide an effective and promising SERS platform for recognition and quantitative determination of different structural PAEs in environment.

An Apical Resection Model in the Adult Xenopus tropicalis Heart.

It is known that in adult mammals, the heart has lost its regenerative capacity, making heart failure one of the leading causes of death worldwide. Previous research has demonstrated the regenerative ability of the heart of the adult Xenopus tropicalis, an anuran amphibian with a diploid genome and a close evolutionary relationship with mammals. Additionally, studies have shown that following ventricular apex resection, the heart can regenerate without scarring in X. tropicalis. Consequently, these previous results suggest that X. tropicalis is an appropriate alternative vertebrate model for the study of adult heart regeneration. A surgical model of cardiac regeneration in the adult X. tropicalis is presented herein. Briefly, the frogs were anesthetized and fixed; then, a small incision was made with iridectomy scissors, penetrating the skin and pericardium. Gentle pressure was applied to the ventricle, and the apex of the ventricle was then cut out with scissors. Cardiac injury and regeneration were confirmed by histology at 7-30 days post resection (dpr). This protocol established an apical resection model in adult X. tropicalis, which can be employed to elucidate the mechanisms of adult heart regeneration.

Mettl3-mediated m6A modification of Fgf16 restricts cardiomyocyte proliferation during heart regeneration.

Cardiovascular disease is the leading cause of death worldwide due to the inability of adult heart to regenerate after injury. N6-methyladenosine (m6A) methylation catalyzed by the enzyme methyltransferase-like 3 (Mettl3) plays an important role in various physiological and pathological bioprocesses. However, the role of m6A in heart regeneration remains largely unclear. To study m6A function in heart regeneration, we modulated Mettl3 expression in vitro and in vivo. Knockdown of Mettl3 significantly increased the proliferation of cardiomyocytes and accelerated heart regeneration following heart injury in neonatal and adult mice. However, Mettl3 overexpression decreased cardiomyocyte proliferation and suppressed heart regeneration in postnatal mice. Conjoint analysis of methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq identified Fgf16 as a downstream target of Mettl3-mediated m6A modification during postnatal heart regeneration. RIP-qPCR and luciferase reporter assays revealed that Mettl3 negatively regulates Fgf16 mRNA expression in an m6A-Ythdf2-dependent manner. The silencing of Fgf16 suppressed the proliferation of cardiomyocytes. However, the overexpression of ΔFgf16, in which the m6A consensus sequence was mutated, significantly increased cardiomyocyte proliferation and accelerated heart regeneration in postnatal mice compared with wild-type Fgf16. Our data demonstrate that Mettl3 post-transcriptionally reduces Fgf16 mRNA levels through an m6A-Ythdf2-dependen pathway, thereby controlling cardiomyocyte proliferation and heart regeneration.

Cardiovascular diseases are one of the world's biggest killers. Even for patients who survive a heart attack, recovery can be difficult. This is because ­ unlike some amphibians and fish ­ humans lack the ability to produce enough new heart muscle cells to replace damaged tissue after a heart injury. In other words, the human heart cannot repair itself. Molecules known as messenger RNA (mRNA) carry the 'instructions' from the DNA inside the cell nucleus to its protein-making machinery in the cytoplasm of the cell. These messenger molecules can also be altered by different enzymes that attach or remove chemical groups. These modifications can change the stability of the mRNA, or even 'silence' it altogether by stopping it from interacting with the protein-making machinery, thus halting production of the protein it encodes. For example, a protein called Mettl3 can attach a methyl group to a specific part of the mRNA, causing a reversible mRNA modification known as m⁶A. This type of alteration has been shown to play a role in many conditions, including heart disease, but it has been unclear whether m⁶A could also be important for the regeneration of heart tissue. To find out more, Jiang, Liu, Chen et al. studied heart injury in mice of various ages. Newborn mice can regenerate their heart muscle for a short time, but adult mice lack this ability, which makes them a useful model to study heart disease. Analyses of the proteins and mRNAs in mouse heart cells confirmed that both Mettl3 and m⁶A-modified mRNAs were present. The amount of each also increased with age. Next, experiments in genetically manipulated mice revealed that removing Mettl3 greatly improved tissue repair after heart injury in both newborn and adult mice. In contrast, mouse hearts that produced abnormally high quantities of Mettl3 were unable to regenerate ­ even if the mice were young. Moreover, a detailed analysis of gene activity revealed that Mettl3 was suppressing heart regeneration by decreasing the production of a growth-promoting protein called FGF16. These results reveal a key biological mechanism controlling the heart's ability to repair itself after injury. In the future, Jiang et al. hope that Mettl3 can be harnessed for new, effective therapies to promote heart regeneration in patients suffering from heart disease.

Ablation of cardiomyocyte-derived BDNF during development causes myocardial degeneration and heart failure in the adult mouse heart.

Objective: Brain-derived neurotrophic factor (BDNF) and its receptor TrkB-T1 were recently found to be expressed in cardiomyocytes. However, the functional role of cardiomyocyte-derived BDNF in heart pathophysiology is not yet fully known. Recent studies revealed that BDNF-TrkB pathway plays a critical role to maintain integrity of cardiac structure and function, cardiac pathology and regeneration of myocardial infarction (MI). Therefore, the BDNF-TrkB pathway may be a novel target for myocardial pathophysiology in the adult heart. Approach and results: In the present study, we established a cardiomyocyte-derived BDNF conditional knockout mouse in which BDNF expression in developing cardiomyocytes is ablated under the control of the Myosin heavy chain 6 (MYH6) promoter. The results of the present study show that ablation of cardiomyocyte-derived BDNF during development does not impair survival, growth or reproduction; however, in the young adult heart, it causes cardiomyocyte death, degeneration of the myocardium, cardiomyocyte hypertrophy, left atrial appendage thrombosis, decreased cardiac function, increased cardiac inflammation and ROS activity, and metabolic disorders, leading to heart failure (HF) in the adult heart and eventually resulting in a decrease in the one-year survival rate. In addition, ablation of cardiomyocyte-derived BDNF during the developmental stage leads to exacerbation of cardiac dysfunction and poor regeneration after MI in adult hearts. Conclusion: Cardiomyocyte-derived BDNF is irreplaceable for maintaining the integrity of cardiac structure and function in the adult heart and regeneration after MI. Therefore, the BDNF-TrkB pathway will be a novel target for myocardial pathophysiology in the adult heart.

Fabrication of a waste cotton fabrics-based nanosystem for simultaneous removal of Cu(II) and Pb(II).

Herein, a waste cotton fabrics-based nanosystem was fabricated to simultaneously remove copper (Cu(II)) and lead ions (Pb(II)) from water and soil. Therein, carboxyl-functionalized zinc oxide microsphere (ZnO-COOH) with peanut shape was carried by cotton fabric (CF) to get CF/ZnO-COOH nanosystem. CF/ZnO-COOH with a good foldable property possessed a high removal capacity for Cu(II) and Pb(II) via electrostatic attraction and chelation. The result indicated that their removal efficiencies of CF/ZnO-COOH could reach over 95% after 2 h. The adsorption process was consistent with Langmuir (R2 = 0.9905 of Cu(II) and R2 = 0.9846 of Pb(II)) and pseudo-second-order kinetic models (R2 = 0.9999 of Cu(II) and R2 = 0.9999 of Pb(II)). The thermodynamic data showed that the adsorption process was spontaneous and exothermic. Additionally, CF/ZnO-COOH also possessed a high fixation ability for Cu(II) and Pb(II) in sand-soil column, especially for Pb(II) (15 cm, 0.4 µg kg-1). Therefore, this wok provides an environmentally friendly and efficient way to remove Cu(II) and Pb(II) from water and soil concurrently.

miR-486 improves fibrotic activity in myocardial infarction by targeting SRSF3/p21-Mediated cardiac myofibroblast senescence.

The regulation of fibrotic activities is key to improving pathological remodelling post-myocardial infarction (MI). Currently, in the clinic, safe and curative therapies for cardiac fibrosis and improvement of the pathological fibrotic environment, scar formation and pathological remodelling post-MI are lacking. Previous studies have shown that miR-486 is involved in the regulation of fibrosis. However, it is still unclear how miR-486 functions in post-MI regeneration. Here, we first demonstrated that miR-486 targeting SRSF3/p21 mediates the senescence of cardiac myofibroblasts to improve their fibrotic activity, which benefits the regeneration of MI by limiting scar size and post-MI remodelling. miR-486-targeted silencing has high potential as a novel target to improve fibrotic activity, cardiac fibrosis and pathological remodelling.

A high-performance electrochemical sensor for sensitive detection of tetracycline based on a Zr-UiO-66/MWCNTs/AuNPs composite electrode.

Herein, a high-performance electrochemical sensor was constructed based on a metal-organic framework (Zr-UiO-66)/multi-carbon nanotubes/gold nanoparticles (Zr-UiO-66/MWCNTs/AuNPs) composite modified glassy carbon electrode for sensitive determination of tetracycline. The morphology, structure, and performance of Zr-UiO-66/MWCNTs/AuNPs were characterized by scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), energy dispersive spectroscopy (EDS), Fourier transform infrared spectroscopy (FT-IR), and electrochemical techniques. The Zr-UiO-66/MWCNTs/AuNPs nanohybrids exhibited excellent electrocatalytic activity towards the oxidation of tetracycline, mainly because of the synergistic effect of the MOFs, MWCNTs, and gold nanoparticles. The electrochemical kinetics and catalytical mechanism of tetracycline were demonstrated, proving that tetracycline's electrocatalytic oxidation reaction was an absorption-controlled two-step process involving the transfer of two protons and two electrons, respectively. Furthermore, a simple and facile method was used to achieve the regeneration of the absorbed saturated electrode. A low concentration of tetracycline was detected by amperometry with the linear ranges of 5 × 10-7 to 2.25 × 10-4 mol L-1 (R2 = 0.9941), the sensitivity was 45.4 mA L mol-1, and the limit of detection was as low as 1.67 × 10-7 mol L-1 (S/N = 3). In addition, the composite electrode demonstrated high selectivity (interference deviation of ± 5%), satisfactory reproductivity (RSD of 5.31%), and long-term stability (easy regeneration) and was successfully applied in the analysis of tetracycline antibiotics in actual samples. Thus, the proposed electrode provides a promising and prospective MOFs-based sensing platform for the detection of tetracyclines in the environment.

Carbon Nanotubes-Based Fuel Cell for Cr(VI) Removal and Electricity Generation.

A fuel cell, an energy transducer, can convert chemical energy into electrical energy. In this work, graphite felt (GF) loaded with polypyrrole (PPy) and carboxylic carbon nanotubes (CNTs-COOH) was used as a cathode (GF/PPy/CNTs-COOH) in a double-chamber nonbiofuel cell (D-nBFC) to remove Cr(VI) efficiently. Therein, Na2S2O3 in an alkaline solution and Cr(VI) in a strongly acidic solution were employed as anode and cathode solutions, respectively. An agar salt bridge, consisting of saturated KCl solution, was used to transport ions between the anode and cathode. This system suggested that the removal efficiency of Cr(VI) could reach 99.6%. The maximum current, power, and power density could achieve 136.8 µA, 18.7 µW, and 20.8 mW/m2 at 90 min, respectively. Additionally, GF/PPy/CNTs-COOH also had good electrocatalytic stability and reusability after four cycles, which played an important role in the development of the D-nBFC system. Therefore, this study provides an environmentally friendly and efficient method to remove Cr(VI) and generate electricity simultaneously.

Tobacco Waste Liquid-Based Organic Fertilizer Particle for Controlled-Release Fulvic Acid and Immobilization of Heavy Metals in Soil.

Every year, a large amount of tobacco waste liquid (TWL) is discharged into the environment, resulting in serious pollution for the environment. In this work, a TWL-based particle (OACT) was fabricated by CaO, attapulgite (ATP), and TWL, and, then, OACT was coated by amino silicon oil (ASO) to form OACT@ASO. Therein, OACT@ASO had high controlled-release ability for fulvic acid (FA), because of the nanonetworks structure for ATP and the high content of FA in TWL. The release ratio (RR) of FA from OACT@ASO reached 94% at 75 h in deionized water, and 23% at 32 d in silica sand. Furthermore, the release mechanism of FA from OACT@ASO was consistent with the First-order law. Additionally, OACT@ASO also possessed high immobilization capacity for Cu(II), Cd(II), and Pb(II) (CCP) in soil. Notably, a pot experiment indicated that OACT@ASO could facilitate the growth of pakchoi seedlings and decrease the absorption of CCP by pakchoi seedlings. Thus, this study provides a new kind of organic fertilizer which could not only release FA, but also immobilize CCP in soil.

FoxO3 restricts liver regeneration by suppressing the proliferation of hepatocytes.

Upon injury, the liver is capable of substantial regeneration from the original tissue until an appropriate functional size. The underlying mechanisms controlling the liver regeneration processes are not well elucidated. Previous studies have proposed that the transcription factor FoxO3 is involved in various liver diseases, but its exact role in the regulation of liver regeneration remains largely unclear. To directly test the detailed role of FoxO3 in liver regeneration, both a constitutive Albumin-Cre driver line and adeno-associated virus serotype 8 (AAV8)-Tbg-Cre (AAV-Cre)-injected adult FoxO3fl/fl mice were subjected to 70% partial hepatectomy (PH). Our data demonstrate that FoxO3 deletion accelerates liver regeneration primarily by limiting polyploidization and promoting the proliferation of hepatocytes during liver regeneration. RNA-seq analysis indicates that FoxO3 deficiency greatly alters the expression of gene sets associated with cell proliferation and apoptosis during liver regeneration. Chromatin immunoprecipitation-PCR (ChIP-PCR) and luciferase reporter assays reveal that FoxO3 promotes the expression of Nox4 but suppresses the expression of Nr4a1 in hepatocytes. AAV8 virus-mediated overexpression of Nox4 and knockdown of Nr4a1 significantly suppressed hepatocyte proliferation and liver regeneration in FoxO3-deficient mice. We demonstrate that FoxO3 negatively controls hepatocyte proliferation through Nox4 upregulation and Nr4a1 downregulation, thereby ensuring appropriate functional regeneration of the liver. Our findings provide novel mechanistic insight into the therapeutic mechanisms of FoxO3 in liver damage and repair.

Highly Efficient and Simultaneous Removal of Cr(VI) and Imidacloprid through a Ferrocene-Modified MIL-100(Fe) Composite from an Aqueous Solution.

A novel nanocomposite [Fc-MIL-100(Fe)] was constructed by combining ferrocene (Fc) with the porous structural metal-organic framework [MIL-100(Fe)]. The proposed composite material could simultaneously and efficiently remove hexavalent chromium [Cr(VI)] and imidacloprid and reduced strongly noxious Cr(VI) to weakly noxious trivalent chromium [Cr(III)]. The removal efficiencies of the composite material for Cr(VI) and imidacloprid could reach 95% after 15 h. The adsorption process was determined by kinetics, isotherms, and thermodynamics. The results demonstrated that the adsorption kinetics of Cr(VI) followed the pseudo-second-order model mainly by chemisorption; meanwhile, the adsorption of imidacloprid by the material conformed to the pseudo-first-order kinetics, which indicated that physical adsorption was the main process. Additionally, the intraparticle diffusion model revealed that the uptake of imidacloprid and Cr(VI) occurred via intraparticle diffusion at the composite material. The adsorption procedure for Cr(VI) was fitted to the Langmuir model (R2 = 0.995) via monolayer adsorption, and that for imidacloprid was fitted to the Freundlich model (R2 = 0.995) due to multilayer or heterogeneous adsorption. The thermodynamic research confirmed that the adsorption procedure was exothermic and spontaneous. Infrared spectroscopy, X-ray photoelectron spectra, and the pH effect implied that intermolecular hydrogen bonding and electrostatic interaction played a crucial role during the removal process. Fc-MIL-100(Fe) also exhibited long-term stability and satisfactory regeneration and reusability. Therefore, this method may enhance an environmentally friendly and prospective approach for concurrently removing imidacloprid and Cr(VI) from wastewater.