Weakened Mn-O bond in Mn-Ce catalysts through K doping induced oxygen activation for boosting benzene oxidation at low temperatures.

K-doped Mn-Ce solid solution catalysts were synthesized using a combination of coprecipitation and hydrothermal methods, demonstrating excellent performance in benzene oxidation. The catalyst K1Ce5Mn5 exhibited comparable activity to noble metal catalysts, achieving a 90 % benzene conversion at approximately 194 ℃. Durable tests under dry and moist conditions revealed that the catalyst could maintain its activity for 50 h at 218 ℃ and 236 ℃, respectively. Characterization results indicated that the catalyst's enhanced activity resulted from the weakened Mn-O bonding caused by the introduction of K+, facilitating the activation of oxygen and its involvement in the reaction. CeOx, the main crystalline phase of Mn-Ce solid solutions, provided abundant oxygen vacancies for capturing and activating oxygen molecules for the weakened Mn-O structures. This conclusion was further supported by partial density of state analysis from density functional theory computations, revealing that the introduction of K+ weakened the orbital hybridization of Mn3d and O2p. Finally, in situ diffuse reflectance infrared Fourier-transform spectroscopy (in situ DRIFTS) studies on Ce5Mn5 and K1Ce5Mn5 catalysts suggested that the introduction of K+ promoted the conversion of adsorbed benzene. Furthermore, intermediate products were transformed more rapidly for K1Ce5Mn5 compared to Ce5Mn5.

AURKA Enhances the Glycolysis and Development of Ovarian Endometriosis Through ERß.

Ovarian endometriosis (EMs) is a benign, estrogen-dependent gynecological disorder. Estrogen receptor beta (ERß), a nuclear receptor for estradiol, plays an important role in the development of ovarian EMs. Here, we investigated the biological significance of aurora kinase A (AURKA) in ovarian EMs and the mechanism by which it regulates ERß. We used immunohistochemical assays to verify that AURKA and ERß were highly expressed in ectopic endometrial tissues. Cell proliferation and colony formation assays were used to demonstrate that AURKA promoted the proliferation of EMs cells. Wound-healing assay, Transwell migration assay, and Matrigel invasion assay further showed that AURKA enhanced the ability of EMs cells to migrate and invade. In addition, AURKA was shown to stimulate glycolysis in EMs cells by measuring the concentration of glucose and lactate in the cell supernatants. Moreover, the AURKA inhibitor alisertib was found to inhibit the progression of ovarian EMs and glycolysis in a mouse model of EMs by measuring ectopic tissues as well as by testing the peritoneal fluid of mice. Furthermore, coimmunoprecipitation assay showed that AURKA interacted with ERß. The rescue experiments confirmed that AURKA regulated the development and glycolysis of ovarian EMs in an ERß-dependent manner. AURKA contributed to the development of ovarian EMs by upregulating of ERß. AURKA may represent a new target for the treatment of ovarian EMs.

Natural compounds as potential therapeutic candidates for multiple sclerosis: Emerging preclinical evidence.

BACKGROUND: Multiple sclerosis is a chronic neurodegenerative disease, with main characteristics of pathological inflammation, neural damage and axonal demyelination. Current mainstream treatments demonstrate more or less side effects, which limit their extensive use. PURPOSE: Increasing studies indicate that natural compounds benefit multiple sclerosis without remarkable side effects. Given the needs to explore the potential effects of natural compounds of plant origin on multiple sclerosis and their mechanisms, we review publications involving the role of natural compounds in animal models of multiple sclerosis, excluding controlled trials. STUDY DESIGN AND METHODS: Articles were conducted on PubMed and Web of Science databases using the keywords ``multiple sclerosis'' and ``natural compounds'' published from January 1, 2008, to September 1, 2023. RESULTS: This review summarized the effects of natural ingredients (flavonoids, terpenoids, polyphenols, alkaloids, glycosides, and others) from three aspects: immune regulation, oxidative stress suppression, and myelin protection and regeneration in multiple sclerosis. CONCLUSION: Overall, we concluded 80 studies to show the preclinical evidence that natural compounds may attenuate multiple sclerosis progression via suppressing immune attacks and/or promoting myelin protection or endogenous repair processes. It would pave the roads for the future development of effective therapeutic regiments of multiple sclerosis.

Development of lung tissue models and their applications.

The lungs are important organs that play a critical role in the development of specific diseases, as well as responding to the effects of drugs, chemicals, and environmental pollutants. Due to the ethical concerns around animal testing, alternative methods have been sought which are more time-effective, do not pose ethical issues for animals, do not involve species differences, and provide easy investigation of the pathobiology of lung diseases. Several national and international organizations are working to accelerate the development and implementation of structurally and functionally complex tissue models as alternatives to animal testing, particularly for the lung. Unfortunately, to date, there is no lung tissue model that has been accepted by regulatory agencies for use in inhalation toxicology. This review discusses the challenges involved in developing a relevant lung tissue model derived from human cells such as cell lines, primary cells, and pluripotent stem cells. It also introduces examples of two-dimensional (2D) air-liquid interface and monocultured and co-cultured three-dimensional (3D) culture techniques, particularly organoid culture and 3D bioprinting. Furthermore, it reviews development of the lung-on-a-chip model to mimic the microenvironment and physiological performance. The applications of lung tissue models in various studies, especially disease modeling, viral respiratory infection, and environmental toxicology will be also introduced. The development of a relevant lung tissue model is extremely important for standardizing and validation the in vitro models for inhalation toxicity and other studies in the future.

Temporal and spatial patterns of recurrence in oral squamous cell carcinoma, a single-center retrospective cohort study in China.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is an invasive cancer with a high recurrence rate. Most clinical studies have focused on the prognosis of patients with OSCC, few have investigated the causes and interventions that affect the recurrence. Our study is to explore the temporal and spatial patterns of recurrence in OSCC. METHODS: 234 OSCC patients with recurrence in our hospital and 64 OSCC patients with recurrence in TCGA database were included in the study. Log-rank test and Multivariate Cox Regression Analysis were used to determine whether there was a significant difference between each selected demographic or clinical factors and recurrence. The Kaplan-Meier method was used to plot survival curves for each recurrence interval. RESULTS: The proportion of OSCC patients in clinical and TCGA with early recurrence was 93.6% and 84.4%, respectively. Age, chewing betel nut, previous radiotherapy, histopathological grading of the primary tumor (poorly differentiated), lymph node metastasis and postoperative infection were found to be associated with the timing of recurrence. It was found that tongue cancer has more regional recurrences, while buccal cancer is mostly local and loco-regional recurrences. The earlier the recurrence, the greater the possibility of local-regional recurrence and the worse the prognosis. CONCLUSION: Most of recurrent OSCC patients present early recurrence (< 18 months) with poor prognosis, and early recurrence is more prone to local recurrence. Moreover, recurrence site is related with primary site of OSCC.

IGJ suppresses breast cancer growth and metastasis by inhibiting EMT via the NF­κB signaling pathway.

Breast cancer metastasis is the primary cause of mortality of patients with breast cancer. The present study aimed to explore the role and underlying mechanisms of IGJ in the invasion and metastasis of breast cancer. The Cancer Genome Atlas database was utilized to analyze the differential gene expression profiles in patients with breast cancer with or without metastasis; the target gene, joining chain of multimeric IgA and IgM (JCHAIN, also known as IGJ, as referred to herein), with significant expression and with prognostic value was screened. The expression levels of IGJ in human breast cancer paired tissues and cell lines were detected using reverse transcription­quantitative PCR and western blot analysis. IGJ differential expression was detected in paired human breast cancer tissues using immunohistochemistry. The role of IGJ in breast cancer was verified using CCK­8, invasion and migration assays, and scratch tests in vivo and in vitro. Further exploration of the role and mechanism of IGJ in breast cancer was conducted through Gene Set Enrichment Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, western blot analysis and immunofluorescence experiments. Through the analysis of gene expression profiles, it was found that IGJ was poorly expressed in patients with breast cancer with metastasis compared to patients with non­metastatic breast cancer. The overexpression of IGJ was associated with an improved distant metastasis­free survival and overall survival (OS). COX multivariate regression analysis demonstrated that IGJ was an independent prognostic factor for the OS and relapse­free survival of patients with breast cancer. In comparison to healthy breast cancer adjacent tissues and cell lines, IGJ was poorly expressed in breast cancer tissues and cell lines (P<0.05). Further analyses indicated that the overexpression of IGJ suppressed the proliferation, invasion and metastasis of breast cancer cells in vivo and in vitro by inhibiting the occurrence of epithelial­to­mesenchymal transition (EMT) and suppressing the nuclear translocation of p65. Finally, rescue experiments indicated that IGJ restricted the proliferation and metastasis of breast cancer cells by regulating the NF­κB signaling pathway. On the whole, the present study demonstrates that IGJ suppresses the invasion and metastasis of breast cancer by inhibiting both the occurrence of EMT and the NF­κB signaling pathway. These findings may provide novel biomarkers and potential therapeutic targets for the treatment of metastatic breast cancer.

Disconnection of Network Hubs Underlying the Executive Function Deficit in Patients with Ischemic Leukoaraiosis.

BACKGROUND: Cognitive impairment is the most common clinical manifestation of ischemic leukoaraiosis (ILA), but the underlying neurobiological pathways have not been well elucidated. Recently, it was thought that ILA is a "disconnection syndrome". Disorganized brain connectome were considered the key neuropathology underlying cognitive deficits in ILA patients. OBJECTIVE: We aimed to detect the disruption of network hubs in ILA patients using a new analytical method called voxel-based eigenvector centrality (EC) mapping. METHODS: Subjects with moderate to severe white matters hyperintensities (Fazekas score ≥3) and healthy controls (HCs) (Fazekas score = 0) were included in the study. The resting-state functional magnetic resonance imaging and the EC mapping approach were performed to explore the alteration of whole-brain network connectivity in ILA patients. RESULTS: Relative to the HCs, the ILA patients exhibited poorer cognitive performance in episodic memory, information processing speed, and executive function (all ps < 0.0125). Additionally, compared with HCs, the ILA patients had lower functional connectivity (i.e., EC values) in the medial parts of default-mode network (i.e., bilateral posterior cingulate gyrus and ventral medial prefrontal cortex [vMPFC]). Intriguingly, the functional connectivity strength at the right vMPFC was positively correlated with executive function deficit in the ILA patients. CONCLUSION: The findings suggested disorganization of the hierarchy of the default-mode regions within the whole-brain network in patients with ILA and advanced our understanding of the neurobiological mechanism underlying executive function deficit in ILA.

PIM2 Promotes the Development of Ovarian Endometriosis by Enhancing Glycolysis and Fibrosis.

Endometriosis is a common gynecological disorder characterized by the presence of the endometrial glands and the stroma outside the uterine cavity. The disease affects reproductive function and quality of life in women of reproductive age. Endometriosis is similar to tumors in some characteristics, such as glycolysis. PIM2 can promote the development of tumors, but the mechanism of PIM2 in endometriosis is still unclear. Therefore, our goal is to study the mechanism of PIM2 in endometriosis. Through immunohistochemistry, we found PIM2, HK2, PKM2, SMH (smooth muscle myosin heavy chain), Desmin, and α-SMA (α-smooth muscle actin) were strongly expressed in the ovarian endometriosis. In endometriotic cells, PIM2 enhanced glycolysis and fibrosis via upregulating the expression of PKM2. Moreover, the PIM2 inhibitor SMI-4a inhibited the development of endometriosis. And we established a PIM2 knockout mouse model of endometriosis to demonstrate the role of PIM2 in vivo. In summary, our study indicates that PIM2 promotes the development of endometriosis. PIM2 may serve as a promising therapeutic target for endometriosis.

Cellular Senescence: Ageing and Androgenetic Alopecia.

Androgenetic alopecia (AGA) is the most common type of hair loss and features progressive miniaturization of hair follicles. Generally, the occurrence of AGA has long been thought to be driven by genetic and androgen predisposition. However, increasingly, data proposed ageing and AGA are intimately linked. Elevated senescent cell burden and androgen and oxidative stress-induced senescence mechanisms in ageing may be initial targets to improve AGA. This review summarizes the biological links between ageing and AGA, with special focus on cellular senescence. In addition, we discuss the potential therapeutic strategies for improving cellular senescence in AGA, such as inhibiting dermal papilla cells and hair follicle stem cells senescence driven by androgen and reactive oxygen species, removing senescent cell, and reducing senescence-associated secretory phenotype (SASP).

An improved U-Net-based in situ root system phenotype segmentation method for plants.

The condition of plant root systems plays an important role in plant growth and development. The Minirhizotron method is an important tool to detect the dynamic growth and development of plant root systems. Currently, most researchers use manual methods or software to segment the root system for analysis and study. This method is time-consuming and requires a high level of operation. The complex background and variable environment in soils make traditional automated root system segmentation methods difficult to implement. Inspired by deep learning in medical imaging, which is used to segment pathological regions to help determine diseases, we propose a deep learning method for the root segmentation task. U-Net is chosen as the basis, and the encoder layer is replaced by the ResNet Block, which can reduce the training volume of the model and improve the feature utilization capability; the PSA module is added to the up-sampling part of U-Net to improve the segmentation accuracy of the object through multi-scale features and attention fusion; a new loss function is used to avoid the extreme imbalance and data imbalance problems of backgrounds such as root system and soil. After experimental comparison and analysis, the improved network demonstrates better performance. In the test set of the peanut root segmentation task, a pixel accuracy of 0.9917 and Intersection Over Union of 0.9548 were achieved, with an F1-score of 95.10. Finally, we used the Transfer Learning approach to conduct segmentation experiments on the corn in situ root system dataset. The experiments show that the improved network has a good learning effect and transferability.

Terpenoids from the Sponge Sarcotragus sp. Collected in the South China Sea.

Sarcotragusolides A-D (1-4), four new butenolide sesterterpenes featuring a rare methyl-transferred 6/6/6-tricyclic fused ring system with a butyrolactone moiety, and echinohalimane B (8), an unprecedented monocyclic diterpenoid featuring a 2,7-ring-opened halimane-type skeleton, were isolated from the sponge Sarcotragus sp. A γ-hydroxybutenolide sesterterpene derivative (5), a new scalarane sesterterpene (7), a new subersin-type diterpenoid (10), and two known terpenoids were also isolated and identified. The discovery of sarcotragusolides C and D (3 and 4) with an unprecedented inversion of configuration implied a distinct biosynthetic pathway. The structures of these compounds were elucidated based on their spectroscopic data, single-crystal X-ray diffraction, chemical derivatization, and quantum chemical calculations. Compounds 1a, 1b, and 2 presented modest cytotoxic activities against several human cancer cell lines.

Poly(arylene ether)s-Based Polymeric Membranes Applied for Water Purification in Harsh Environment Conditions: A Mini-Review.

Confronting the pressing challenge of freshwater scarcity, polymeric membrane-based water treatment technology has emerged as an essential and effective approach. Poly(arylene ether)s (PAEs) polymers, a class of high-performance engineering thermoplastics, have garnered attention in recent decades as promising membrane materials for advanced water treatment approaches. The PAE-Based membranes are employed to resist the shortages of most common polymeric membranes, such as chemical instability, structural damage, membrane fouling, and shortened lifespan when deployed in harsh environments, owing to their excellent comprehensive performance. This article presents the advancements in the research of several typical PAEs, including poly(ether ether ketone) (PEEK), polyethersulfone (PES), and poly(arylene ether nitrile) (PEN). Techniques for membrane formation, modification strategies, and applications in water treatment have been reviewed. The applications encompass processes for oil/water separation, desalination, and wastewater treatment, which involve the removal of heavy metal ions, dyes, oils, and other organic pollutants. The commendable performance of these membranes has been summarized in terms of corrosion resistance, high-temperature resistance, anti-fouling properties, and durability in challenging environments. In addition, several recommendations for further research aimed at developing efficient and robust PAE-based membranes are proposed.

Fabrication of High-Performance Colorimetric Membrane by Incorporation of Polydiacetylene into Polyarylene Ether Nitriles Electrospinning Nanofibrous Membranes.

Polyarylene ether nitrile (PEN) is a novel high-performance engineering plastic with various applications, particularly in thermoresistance-required fields. In this study, a well-known stimuli-response polydiacetylene monomer, 10, 12-pentacosadiynoic acid (PCDA), was encapsulated within electrospun PEN nanofibers to fabricate a colorimetric membrane with satisfactory thermal and corrosion resistance. To optimize the compatibility with PCDA, two PENswith distinct molecular chains were utilized: PEN−PPL and PEN−BPA. The chemical structure and elemental mapping analysis revealed that the PCDA component was successfully incorporated into the PEN fibrous. The PCDA bound significantly better to the PEN−PPL than to the PEN−BPA; due to the carboxyl groups present on the side chains of PEN−PPL, the surface was smooth and the color changed uniformly as the temperature rose. However, owing to its poor compatibility with PEN−BPA, the PCDA formed agglomerations on the fibers. The thermal analysis demonstrated that the membranes obtained after PCDA compounding maintained their excellent heat resistance. The 5% weight loss temperatures of composite nanofibrous membranes manufactured by PEN−PPL and PEN−BPA were 402 °C and 506 °C, respectively, and their glass transition temperatures were 219 °C and 169 °C, respectively, indicating that the blended membranes can withstand high temperatures. The evaluation of application performance revealed that the composite membranes exhibited good dimensional stability upon high thermal and corrosive situations. Specifically, the PEN−P−PCDA did not shrink at 170 °C. Both composite membranes were dimensionally stable when exposed to the alkali aqueous solution. However, PEN−P−PCDA is more sensitive to OH−, exhibiting color transition at pH > 8, whereas PEN−B−PCDA exhibited color transition at high OH− concentrations (pH ≥ 13), with enhanced alkali resistance stability owing to its nanofibrous architecture. This exploratory study reveals the feasibility of PEN nanofibers functionalized using PCDA as a desirable stimulus-response sensor even in high-temperature and corrosive harsh environments.

Curcumin alleviates experimental colitis via a potential mechanism involving memory B cells and Bcl-6-Syk-BLNK signaling.

BACKGROUND: Immune dysfunction is the crucial cause in the pathogenesis of inflammatory bowel disease (IBD), which is mainly related to lymphocytes (T or B cells, incl-uding memory B cells), mast cells, activated neutrophils, and macrophages. As the precursor of B cells, the activation of memory B cells can trigger and differentiate B cells to produce a giant variety of inducible B cells and tolerant B cells, whose dysfunction can easily lead to autoimmune diseases, including IBD. AIM: To investigate whether or not curcumin (Cur) can alleviate experimental colitis by regulating memory B cells and Bcl-6-Syk-BLNK signaling. METHODS: Colitis was induced in mice with a dextran sulphate sodium (DSS) solution in drinking water. Colitis mice were given Cur (100 mg/kg/d) orally for 14 con-secutive days. The colonic weight, colonic length, intestinal weight index, occult blood scores, and histological scores of mice were examined to evaluate the curative effect. The levels of memory B cells in peripheral blood of mice were measured by flow cytometry, and IL-1ß, IL-6, IL-10, IL-7A, and TNF-α expression in colonic tissue homogenates were analyzed by enzyme-linked immunosorbent assay. Western blot was used to measure the expression of Bcl-6, BLNK, Syk, and other signaling pathway related proteins. RESULTS: After Cur treatment for 14 d, the body weight, colonic weight, colonic length, colonic weight index, and colonic pathological injury of mice with colitis were ameliorated. The secretion of IL-1ß, IL-6, TNF-α, and IL-7A was statistically decreased, while the IL-35 and IL-10 levels were considerably increased. Activation of memory B cell subsets in colitis mice was confirmed by a remarkable reduction in the expression of IgM, IgG, IgA, FCRL5, CD103, FasL, PD-1, CD38, and CXCR3 on the surface of CD19+ CD27+ B cells, while the number of CD19+ CD27+ IL-10+ and CD19+ CD27+ Tim-3+ B cells increased significantly. In addition, Cur significantly inhibited the protein levels of Syk, p-Syk, Bcl-6, and CIN85, and increased BLNK and p-BLNK expression in colitis mice. CONCLUSION: Cur could effectively alleviate DSS-induced colitis in mice by regulating memory B cells and the Bcl-6-Syk-BLNK signaling pathway.

Development of genomic instability-associated long non-coding RNA signature: A prognostic risk model of clear cell renal cell carcinoma.

Purpose: Renal clear cell carcinoma (ccRCC) is the most lethal of all pathological subtypes of renal cell carcinoma (RCC). Genomic instability was recently reported to be related to the occurrence and development of kidney cancer. The biological roles of long non-coding RNAs (lncRNAs) in tumorigenesis have been increasingly valued, and various lncRNAs were found to be oncogenes or cancer suppressors. Herein, we identified a novel genomic instability-associated lncRNA (GILncs) model for ccRCC patients to predict the overall survival (OS). Methods: The Cancer Genome Atlas (TCGA) database was utilized to obtain full transcriptome data, somatic mutation profiles, and clinical characteristics. The differentially expressed lncRNAs between the genome-unstable-like group (GU) and the genome-stable-like group (GS) were defined as GILncs, with |logFC| > 1 and an adjusted p-value< 0.05 for a false discovery rate. All samples were allocated into GU-like or GS-like types based on the expression of GILncs observed using hierarchical cluster analyses. A genomic instability-associated lncRNA signature (GILncSig) was constructed using parameters of the included lncRNAs. Quantitative real-time PCR analysis was used to detect the in vitro expression of the included lncRNAs. Validation of the risk model was performed by the log-rank test, time-dependent receiver operating characteristic (ROC) curves analysis, and multivariate Cox regression analysis. Results: Forty-six lncRNAs were identified as GILncs. LINC00460, AL139351.1, and AC156455.1 were employed for GILncSig calculation based on the results of Cox analysis. GILncSig was confirmed as an independent predictor for OS of ccRCC patients. Additionally, it presented a higher efficiency and accuracy than other RCC prognostic models reported before. Conclusion: GILncSig score was qualified as a critical indicator, independent of other clinical factors, for prognostic prediction of ccRCC patients.

Role of inflammatory factors in the etiology and treatment of recurrent implantation failure.

Recurrent implantation failure (RIF) is characterized by the absence of implantation after high-grade embryos are transferred to the endometrium by at least three in vitro fertilization cycles. It is one of the most important factors contributing to reproductive failure. After numerous barriers have been overcome to obtain good-quality embryos, RIF causes extreme distress and frustration in women and couples. In recent years, significant progress has been made in understanding how inflammatory factors, which include pro-inflammatory factors, anti-inflammatory factors, chemokines, and other molecules, contribute to RIF. Immunological abnormalities, hypercoagulability, and reproductive diseases are considered potential causes of RIF. In alloimmune disorders, inflammatory factors can affect the success rate of embryo implantation by altering T helper (Th)1/Th2 and Th17/regulatory T cell ratios and causing imbalances of uterine natural killer cells and macrophages. Autoimmune disorders can also lead to RIF. Inflammatory factors also play key roles in RIF-related disorders such as hypercoagulability, chronic endometritis, adenomyosis, hydrosalpinx, and endometriosis. This review focuses on the roles of inflammatory factors in RIF, including immune factors, blood hypercoagulable states, and reproductive diseases such as chronic endometritis, adenomyosis, hydrosalpinx, and endometriosis. It also summarizes the different treatments according to the causes of RIF and discusses the efficacy of sirolimus, peripheral blood mononuclear cells, low-dose aspirin combined with low-molecular-weight heparin, blocking interleukin-22, and gonadotropin-releasing hormone agonists in the treatment of RIF.

New Insights on Ferroptosis and Gynecological Malignancies.

Ferroptosis is a new type of cell death different from apoptosis and necrosis, which can regulate the accumulation of lipid peroxidation through different pathways, ultimately leading to cell death. An increasing number of studies have revealed that the relationship between ferroptosis and cancer is extremely complex, which holds promise as a new treatment. In gynecological malignancies, ferroptosis has been found to have excellent antitumor activity, which can regulate the proliferation, metastasis and radiochemotherapy resistance. With the continuous progress of research, nanodrugs, gene therapy and other new therapeutic techniques for inducing ferroptosis have been proposed. However, the study of ferroptosis in gynecological malignancies is still in its infancy, and further research is needed to design safe and effective cancer therapies based on ferroptosis. This article reviews the mechanism of ferroptosis and the latest research progress and prospects in gynecological malignancies.

Immunostimulatory activity of soybean hull polysaccharide on macrophages.

Water-soluble polysaccharide isolated from soybean hull and fractionated using ion-exchange chromatography were investigated to determine their molecular characteristics and immunostimulating activity. In the present study, soybean hull polysaccharide (SHP) was separated and purified to obtain three main fractions (F1, F2 and F3), and their chemical and monosaccharide compositions were analyzed. SHP was mainly composed of carbohydrates (64.3%), proteins (16.2%) and sulfates (12.5%), with minor levels of uronic acid (3.2%), and predominantly contained glucose and mannose as monosaccharides. Moreover, when compared with cells treated with RPMI medium, SHP was revealed to promote the proliferation and pinocytosis of RAW264.7 cells, and to enhance the production of nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6. Furthermore, flow cytometry demonstrated that CD11b and CD40 were involved in the immune regulation of RAW264.7 cells by SHP. Moreover, western blotting and other experiments revealed that SHP, a type of pathogen-associated molecular pattern, was specifically recognized by the Toll-like receptor 2, which, in turn, upregulated the expression levels of proteins downstream of the mitogen-activated protein kinase and nuclear factor κB pathways. Notably, the immune activity of the F2 fraction was markedly higher than that of the crude polysaccharides. In summary, the purified F2 fraction of SHP may be an effective nutritional supplement for human disorders associated with low immunity.

Ginsenoside Rg1 ameliorated experimental colitis by regulating the balance of M1/M2 macrophage polarization and the homeostasis of intestinal flora.

Aberrant M1/M2 macrophage polarization and dysbiosis are involved in the pathogenesis of ulcerative colitis (UC). Ginsenoside Rg1 exhibits optimal immunomodulatory and anti-inflammatory effects in treating UC of humans and animals, but the action mechanism through the regulation of M1/M2 macrophage polarization and intestinal flora composition remain unclear. Here, experimental colitis was induced in BALB/c mice using dextran sulfate sodium, and Rock1 inhibitor Y27632 was used to explore the action mechanism of ginsenoside Rg1. Following treatment with ginsenoside Rg1 (200 mg/kg/day) and Y27632 (10 mg/kg/day) for 14 consecutive days, the rate of change in mouse body weight, mouse final weight, colonic weight, colonic length, colonic weight index and pathological damage scores of colitis mice were effectively improved, accompanied by less ulcer formation and inflammatory cell infiltration, lower levels of interleukin (IL)-6, IL-33, chemokine (C-C motif) ligand 2 (CCL-2), tumor necrosis factor alpha (TNF-α), and higher IL-4 and IL-10. Importantly, ginsenoside Rg1 and Y27632 significantly down-regulated CD11b+F4/80+, CD11b+F4/80+Tim-1+ and CD11b+F4/80+TLR4+ macrophages, and CD11b+F4/80+iNOS+ M1 macrophages, and significantly up-regulated CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ M2 macrophages in colitis mice; concomitantly, ginsenoside Rg1 improved the diversity of colonic microbiota and regulated Lachnospiraceae, Staphylococcus, Bacteroide and Ruminococcaceae_UCG_014 at genus level in colitis mice, but the flora regulated by Y27632 was not identical to it. Moreover, ginsenoside Rg1 and Y27632 down-regulated the protein levels of Rock1, RhoA and Nogo-B in colitis mice. These results suggested that ginsenoside Rg1 and Y27632 ameliorated colitis by regulating M1/M2 macrophage polarization and microbiota composition, associated with inhibition of the Nogo-B/RhoA signaling pathway.

Construction of durable superhydrophilic activated carbon fibers based material for highly-efficient oil/water separation and aqueous contaminants degradation.

Developing filtering materials with high permeation flux and contaminant removal rate is of great importance for oily wastewater remediation. Herein, a robust three-dimensional (3D) activated carbon fibers (ACFs) based composite with uniformly grown layered double hydroxide (LDH) on the surface was successfully constructed through a feasible hydrothermal strategy. The LDH with a high surface energy and vertically aligned structure could provide superhydrophilicity to ACFs. Systematic investigation confirmed that the 3D material could overcome the size mismatch between the ACFs macropores and tiny emulsified droplets through the combination of size-sieving filtration on the surface and oil droplet coalescence in the fiber network. This process efficiently separated the intractable surfactant-stabilized oil-in-water emulsions with high permeation flux (up to 4.16 × 106 L m-2 h-1 bar-1). Notably, the LDH also had well-dispersed catalytic active sites, which could initiate advanced oxidation processes (AOPs) to efficiently eliminate various types of water-soluble organic pollutants (e.g., pharmaceuticals, phenolic compounds and organic dyes). The resulting modified ACFs exhibited exceptional removal rates for both oil and organic pollutants in the complex sewage during the continuous filtration process. These versatile abilities integrated with the facile preparation method reported herein provide outstanding prospects for the large-scale treatment of oily wastewater.