Formation Capacity Research Articles

The effect of concentrated growth factor on the biological performance of human dental pulp stem cells under oxidative stress status

Objective: To investigate the effect of concentrated growth factor (CGF) on the biological performance of human dental pulp stem cells (hDPSCs) under oxidative stress status induced by hydrogen peroxide (H2O2). Methods: The hDPSCs were isolated by using tissue block separation method from healthy permanent teeth extracted for orthodontic reason. hDPSCs surface markers CD34, CD45, CD90 and CD105 were detected by flow cytometry. Alkaline phosphatase (ALP), alizarin red S (ARS), oil red O staining and colony formation assay were used to identify hDPSCs. After the cell counting kit-8 (CCK-8) detection, the optimal H2O2 concentration was used to construct the hDPSCs oxidative stress model. CGF conditioned medium was prepared by repeated freeze-thaw methods. After CCK-8 detection, the optimum CGF concentration was chosen for the subsequent experiments. The hDPSCs were divided into control group, H2O2 (only H2O2 processing), H2O2+CGF group (H2O2 processing in combination with the CGF) and CGF group (only CGF processing). Subsequent experiments were performed according to these groups. The oxidative stress model was verified by reactive oxygen species, β-galactosidase staining and Western blotting. The effects of CGF on the proliferation and migration of hDPSCs under oxidative stress status were detected by CCK-8 and cell scratch assay, respectively. ALP activity and ARS staining were used to detect the effect of CGF on the osteogenic differentiation of hDPSCs under oxidative stress status. The mRNA expression levels of odontogenesis related genes were detected by real-time fluorescence quantitative PCR (RT-qPCR), and the expression levels of odontogenesis and osteogenesis related proteins were detected by Western blotting. Results: Isolated hDPSCs showed positive expression of mesenchymal stem cells surface markers of CD90, CD105, and negative expression of hematopoietic stem cells surface markers CD34, CD45. The hDPSCs were proved to have the capacity of osteogenic, adipogenic differentiation and clone formation. The optimal concentration to construct the oxidative stress model was 200 μmol/L H2O2. Twenty percent CGF was the optimal concentration for subsequent experiments. Compared with the control group, the expression of aging protein p53 was significantly up-regulated from (0.82±0.12) to (1.19±0.14) in H2O2 group (P<0.05), with deepened β-galactosidase staining and increased fluorescence intensity of reactive oxygen species. The proliferative capacity of cells in H2O2+CGF group on day 1, 3, 5 and 7 (0.23±0.01, 0.50±0.02, 1.60±0.07, 1.80±0.21) were all higher than in H2O2 group (0.15±0.01, 0.14±0.02, 0.50±0.03, 0.90±0.09) (P<0.01). Cell healing capacity of cells in H2O2+CGF group at 12 h and 24 h (0.47±0.07, 0.58±0.44) also increased compared with the H2O2 group (0.36±0.02, 0.44±0.02) (P<0.05), and similar results in the activity of ALP and the formation of mineralized nodules. On day 28, the mRNA expressions of dentin sialophosphoprotein (0.52±0.16) and dental matrix protein 1(DMP-1) (0.39±0.13) in H2O2 group were all significantly lower than those in H2O2+CGF group (0.96±0.24, 0.83±0.30, respectively) and CGF group (1.12±0.18, 1.23±0.19, respectively) (P<0.05). On day 28, the expressions of odontogenesis related protein DMP-1 (0.27±0.04) and osteogenesis related protein Runt-related transcription factor-2 (0.42±0.15) in H2O2 group were all significantly lower than those in H2O2+CGF group (0.66±0.18, 0.68±0.04) and CGF group (1.15±0.13, 1.06±0.19, respectively) (P<0.05). Conclusions: H2O2 can induce oxidative stress in hDPSCs, while CGF can promote proliferation, migration, odontogenic and osteogenic differentiation of hDPSCs under oxidative stress status.

Neutrophil extracellular traps (NETs) are increased in rheumatoid arthritis-associated interstitial lung disease

BackgroundNeutrophil extracellular trap (NET) formation has been implicated as a pathogenic mechanism in both rheumatoid arthritis (RA) and interstitial lung disease (ILD). However, the role of NETs in RA-associated ILD (RA-ILD) and the mechanisms driving NET formation remain unclear. This study aimed to assess the involvement of NETs in RA-ILD and elucidate the underlying mechanisms.MethodsSingle-cell sequencing was used to identify changes in the quantity and function of neutrophils in the lung tissue of a zymosan A (ZYM)-induced interstitial pneumonia arthritis model. Additionally, nuclear receptor 4A3 (NR4A3) interference was performed in HL-60 cells to assess its impact on NET formation and the transformation of MRC-5 cells into myofibroblasts. The clinical relevance of plasma myeloperoxidase-DNA (MPO-DNA), citrullinated histone 3 (Cit-H3), and cell-free DNA was evaluated in RA-ILD patients with different imaging types via a commercial enzyme-linked immunosorbent assay (ELISA).ResultsIn the ZYM-treated SKG mouse model, which recapitulates key features of RA-ILD, an increased population of neutrophils in the lung tissue was primarily responsible for NET formation. Mechanistically, we found that interference with NR4A3 expression enhanced NET formation in HL-60 cells, which in turn promoted the differentiation of MRC-5 cells into myofibroblasts. Clinically, plasma MPO-DNA levels are elevated in patients with RA-nonspecific interstitial pneumonia (RA-NSIP), whereas Cit-H3 levels are elevated in RA-usual interstitial pneumonia (RA-UIP) patients compared with healthy subjects. ROC curve analysis further revealed that the combination of plasma MPO-DNA, rheumatoid factor (RF), and anti-citrullinated protein (anti-CCP) and the combination of Cit-H3, RF, and anti-CCP were superior diagnostic panels for NSIP and UIP in RA-ILD patients, respectively. Moreover, compared with those from healthy controls, neutrophils from patients with RA-UIP and RA-NSIP demonstrated a significantly increased ability to form NETs and induce the differentiation of MRC-5 cells into myofibroblasts. Specifically, RA-UIP patients exhibited a greater capacity for NET formation and the differentiation of MRC-5 cells into myofibroblasts than did RA-NSIP patients.ConclusionsThese findings suggest that targeting NETs may be a novel therapeutic approach for treating ILD in RA patients.

Effects of Shenmai Injection on proliferation, migration, invasion and angiogenesis of colorectal carcinoma vascular endothelial cells.

Colorectal cancer, being 1 of the most significant malignant tumors globally, poses a substantial risk to human health. Unfortunately, its 5-year survival rate stands at a mere 65%. There remains an urgent need for the development of novel treatments to combat this detrimental malignancy effectively. The Shenmai Injection (SMI) is a Chinese medicine that has been proven to have significant clinical efficacy in the treatment of cardiovascular diseases. This study aimed to examine the impact of SMI on the proliferation, migration, invasion, and angiogenesis of tumor-derived endothelial cells (Td-EC). Human umbilical vein endothelial cells (HUVEC) induced Td-EC, and HUVEC were treated with conditioned media from the human colorectal carcinoma cells (HCT116). The effects of HCT116 on the proliferation, migration, and invasion of hepatocellular carcinoma cells after treatment of SMI were observed by MTS assay and Transwell techniques. Additionally, an angiogenesis experiment was used to investigate Td-EC tube formation capacity. SMI had a significant inhibiting effect on the proliferation, migration, and invasion of HCT116. SMI was also able to inhibit the angiogenesis of Td-EC. Notably, SMI did not have any effect on the normal endothelium. SMI has obvious antiproliferation, migration, infiltration, and neogenesis effects on HCT116.

COL1A1, COL1A2, CHN1, and FN1 Promote Tumorogenesis and Act as Markers of Diagnosis and Survival in Gastric Cancer Patients.

This study aimed to comprehensively investigate the molecular landscape of gastric cancer (GC) by integrating various bioinformatics tools and experimental validations. GSE79973 dataset, limma package, STRING, UALCAN, GEPIA, OncoDB, cBioPortal, DAVID, TISIDB, Gene Set Cancer Analysis (GSCA), tissue samples, RT-qPCR, and cell proliferation assay were employed in this study. Analysis of the GSE79973 dataset identified 300 differentially expressed genes (DEGs), from which COL1A1, COL1A2, CHN1, and FN1 emerged as pivotal hub genes using protein-protein interaction network analysis. Subsequent validation across The Cancer Genome Atlas (TCGA) datasets confirmed their up-regulation in GC tissues compared to normal controls. Promoter methylation analysis revealed decreased methylation levels of these hubs in GC tissues, suggesting their potential role in tumorigenesis. Mutational analysis using cBioPortal showcased frequent mutations in these genes, particularly FN1, further highlighting their significance in GC pathogenesis. Survival analysis indicated their correlation with reduced overall survival rates among GC patients, supported by the development of a robust prognostic model. Prediction of hub-associated miRNAs and gene enrichment analysis provided insights into their regulatory mechanisms and downstream pathways, implicating their involvement in extracellular matrix remodeling and cell migration. Drug sensitivity analysis revealed correlations between hub gene expression and drug response, while RT-qPCR validation confirmed their upregulation in clinical GC samples. Finally, functional assays demonstrated the impact of FN1 knockdown on cellular proliferation, colony formation, and wound healing capacities. Overall, this study elucidates the crucial role of COL1A1, COL1A2, CHN1, and FN1 in GC pathogenesis and underscores their potential as diagnostic markers and therapeutic targets.

A Four-Year Study of Antibiotic Resistance, Prevalence and Biofilm-Forming Ability of Uropathogens Isolated from Community- and Hospital-Acquired Urinary Tract Infections in Southern Italy.

The aim of this study was to investigate the differences between nosocomial and community microorganisms isolated from patients with UTI by determining their bacterial profile, antibiotic resistance and ability to produce biofilms. A retrospective study, based on bacterial isolates from consecutive urine samples collected between January 2019 and December 2023, was conducted at a university hospital. The main pathogens isolated from both community and hospital samples were the same, but their frequency of isolation differed. Compared with community-associated cases, hospital-associated infections have more isolates of Acinetobacter baumanii complex. In contrast, Proteus mirabilis isolates were more prevalent in community than in hospital infections. In both hospital and community isolates, gram-positive bacteria showed a lower overall antimicrobial resistance (22%) compared to gram-negative bacteria (30%). The data demonstrated that individual strains exhibited disparate degrees of capacity for biofilm formation. Additionally, the data indicate an inverse correlation between biofilm production and antibiotic resistance. Isolates from community patients exhibited lower capacities for biofilm production in comparison to the capacities demonstrated by microorganisms isolated from nosocomial patients (29% and 35%, respectively). Area-specific surveillance studies can provide valuable information on UTI pathogens and antimicrobial resistance patterns, which can be useful in guiding empirical treatment.

A Novel Cell-Penetrating Peptide-Vascular Endothelial Growth Factor Small Interfering Ribonucleic Acid Complex That Mediates the Inhibition of Angiogenesis by Human Umbilical Vein Endothelial Cells and in an ExVivo Mouse Aorta Ring Model.

Angiogenesis is mediated by vascular endothelial growth factor (VEGF), a protein that plays a key role in wound healing, inflammatory diseases, cardiovascular processes, ocular diseases, and tumor growth. Indeed, modulation of angiogenesis represents a potential approach to treating cancer and, as such, therapeutic approaches targeting VEGF and its receptors have been widely investigated as part of the broader search for curative interventions. Equally, RNA interference is a powerful tool for treating diseases, but its application as a disease treatment has been limited in part because of a lack of efficient small interfering RNA (siRNA) delivery systems. The purpose of this study was to characterize an amphipathic cell-penetrating peptide, Ara27, and its potential as an effective delivery vehicle as a conjugate with VEGF siRNA (siVEGF). In our study, we demonstrate that exposure of human umbilical vein endothelial cells (HUVECs) with Ara27-siVEGF complexes did not lead to cytotoxicity and can lead to down-regulation of cellular levels of both VEGF mRNA and protein. Moreover, treatment with the Ara27-siVEGF complex attenuates the phosphorylation of VEGFR2, Akt, and ERK in HUVECs and inhibits their capacity for wound healing and tube formation, both of which characteristics reflective of angiogenesis. In addition, we performed an exvivo study to find that treatment with the Ara27-siVEGF complex inhibits aorta ring sprouting. Furthermore, the complex did not induce immunotoxicity in THP-1 and RAW264.7 cells. Taken together, our studies demonstrate that an Ara27-siVEGF conjugate is efficient for knockdown of VEGF in HUVECs to inhibit angiogenesis, without marked cytotoxic and immunotoxic effects.

Effect of black highland barley polysaccharides and low frequency-static magnetic field on casein-based coacervates: Formation, characterization, and probiotic encapsulation capacity.

To evaluate the combination effects of highland barley polysaccharides (HBP) and low-frequency static magnetic field (LF-SMF) treatment on the structure and properties of acid-induced casein (CS) coacervates, this study conducted a comprehensive investigation at various stages- before, during, and after coacervation-for the first time. Compared with native CS, adding HBP caused CS to denature owing to hydrophobic and electrostatic interactions, and LF-SMF treatment further promoted these changes. During the acidification (pH7.0-2.0) and coacervation processes, the integration of LF-SMF treatment with the addition of HBP enhanced the rate and extent of casein (CS) aggregation and crosslinking, attributable to alterations in the ζ-potential of CS. Among the formed coacervates, the yield and particle size of CS/HBP complex coacervates after being treated with LF-SMF (M-CS/HBP) increased from 67.9% to 78.4% and from 803.12nm to 1253.43nm, respectively. Additionally, M-CS/HBP demonstrated improved viscoelasticity and a more uniform, compact microstructure with denser packing. The alterations observed in CS-based coacervates were due to non-covalent interactions between CS and HBP, further promoted by LF-SMF treatment, leading to the unfolding and disordering of protein secondary structure. Consequently, M-CS/HBP complex coacervates demonstrated superior encapsulation efficiency for L. plantarum and provided enhanced protection for probiotics under adverse environments.

AZD1390, an Ataxia telangiectasia mutated inhibitor, enhances cisplatin mediated apoptosis in breast cancer cells.

Genomic instability is often caused by deficiencies in DNA damage repair pathways, making therapeutic targeting of DDR beneficial for cancer patients with specific DDR functions. ATM kinase plays a critical role in various cellular processes and its deficiency increases sensitivity to DDR-targeted agents in different cancers. Recent studies highlight ATM inhibition as a potential clinical target, with AZD1390 being a notable ATM inhibitor due to its potent and selective inhibition, ability to accumulate at DNA breaks. The study aimed to evaluate the potential anti-cancer effects of AZD1390, a key component of the DNA damage response, in breast cancer cells. The impact of the combination of AZD1390 and cisplatin on various parameters such as cell viability, proliferation, colony formation capacity, DNA damage, reactive oxygen species (ROS) levels, mitochondrial membrane potential, cell cycle progression, and cell death in breast cancer cells was evaluated using several methodologies, including WST-1 assays, real-time cell analysis, colony formation assays, comet assays, DCF-DA, MMP/JC-1 staining assays, flow cytometry along with Western blot analysis. We found that AZD1390 and cisplatin displayed synergistic antitumor effects in breast cancer cells at low doses. Addinationaly exhibited significant anti-proliferative effects in colony formation and real-time cell proliferation experiments, increasing intracellular ROS levels and mitochondrial membrane potential.The combined treatment also arrested the cell cycle at the G2-M point. Furthermore, combination of AZD1390 with cisplatin enhances its apoptotic effects in MCF-7 and MDA-MB-231cells. These findings could aid in developing new treatments for breast cancer that exploit the genomic instability of cancer cells.

Unveiling the formation capacity and characterization of pentacyclic triterpene-structured oleogels: Role of the molecular configuration and oil profile

Unveiling the formation capacity and characterization of pentacyclic triterpene-structured oleogels: Role of the molecular configuration and oil profile

Investigation of virulence factor genes and biofilm formation of antibiotic resistant clinical E.coli isolates.

The aim of this study is to investigate the antibiotic sensitivity, presence of virulence genes and biofilm formation capacity of 90 clinical E. coli isolates. The presence of virulence genes in E.coli isolates were investigated by PCR. Ninety clinical isolates of E.coli were subjected to biofilm quantitative analysis using the semi-quantitative crystal violet staining method. it was observed that the isolates were resistant to quinolone, cephalosporin, aminoglycoside, carbapenem and penicillin group antibiotics. The presence of virulence factor genes were observed in a total of 86/90E. coli. The highest rate of fim (92.2%) virulence factor gene was detected in the strains. Afa, pap, cnf, sfa, hly were detected in 30%, 13%, 13%, 3.3%, 2.2% respectively. Also, 13 different virulence factor gene patterns were determined in 90E. coli isolates. Of the 90E. coli isolates whose biofilm-forming capacities were evaluated, 42 were found to have biofilm-forming capacity. Of these 26 (28.8%) the weak, 12 (13.3%) moderate and 4 (4.4%) strong biofilm-forming. Also, statistical analysis was performed to investigate the relationship between virulence factor genes and biofilm formation, and none of the 7 genes analyzed showed a significant relationship with biofilm formation. since pathogenic E. coli is an important public health problem, investigating antibiotic resistance, virulence factor genes and biofilm formation in bacterial pathogens is important for better treatment options.

In Vivo Evaluation of Genotoxicity and Antioxidant Capacity of Ajuga Orientalis L. (Lamiaceae) Leaf Extracts

Ajuga orientalis L. (Lamiaceae) is a fragrant herb native to the Eastern Mediterranean region, widely used in traditional healing practices in Jordan and neighboring countries. Despite its extensive use, there is a lack of toxicological studies on its leaf extracts. This study aims to address this gap by evaluating the genotoxic potential of ethanolic and aqueous leaf extracts using a micronucleus (MN) assay on mice DNA, alongside assessing their antioxidant status. The median lethal dose 50% (LD50) was tested in ten groups of sixty male Balb/c mice to determine the acute toxicity of A. orientalis leaf extracts. Four groups of male Balb/c mice (n=6) were used to evaluate micronucleus (MN) formation and total antioxidant capacity for each extract. Each group received daily intraperitoneal injections of one of the following concentrations: 4000, 2000, 1000, and 500 mg/kg over 28 days. Additionally, three control groups were included for comparison purposes. Peripheral blood samples were screened for MN formation, and liver samples were assessed for total antioxidant capacity. Results revealed an LD50 of 4000 mg/kg for both extracts, alongside a significant dose-dependent increase in MN formation and lower antioxidant capacity compared to controls. The findings indicate the genotoxicity of A. orientalis leaf extracts in Balb/c mice, urging caution in human consumption. Further research is warranted to comprehensively assess their safety and toxicity, especially considering their traditional medicinal use.

IGF-1 c.258 A > G synonymous mutation ameliorates senile osteoporosis

Senile osteoporosis (SOP) is a multifactorial, age-related progressive phenomenon with a considerable morbidity and mortality. IGF-1 is an important regulator of bone reconstruction and metabolism throughout life. Nevertheless, our previous study unexpectedly found there is no change in the peak bone mass with a altered IGF-1 gene expression leaded by IGF-1 c.258 A > G synonymous mutation. Considering its involvement in the cellular senescence, we suspected c.258 A > G may participate in SOP. Therefore, the effect of IGF-1 c.258 A > G on SOP was firstly detected, the changes of bone formation and bone resorption index in SOP mice with two genotypes indicated it improved SOP. Then, the in vitro study confirmed the mutation ameliorates SOP by promoting the growth and development of senescent osteoblasts. At last, co-culture of osteoblast and osteoclast further verified the mutation prevents SOP by increasing the bone formation capacity of senescent osteoblasts. Collectively, this study illuminated the role of IGF-1 c.258 A > G in ameliorating SOP.

Interactions of the emerging fungus Candida auris with Acanthamoeba castellanii reveal phenotypic changes with direct implications on the response to stress and virulence.

Candida auris has emerged as a critical public health concern due to its resistance to multiple antifungal drugs and ability to survive on surfaces under harsh conditions, mainly due to biofilm formation. The precise origin of this emerging pathogen still awaits elucidation, but interactions with environmental protozoa may have helped C. auris to develop such virulence and resistance traits. In this work, we precisely characterize the interactions of C. auris with the free-living amoeba Acanthamoeba castellanii and how these protozoa may alter the fungal behavior in terms of virulence, thermotolerance, biofilm formation capacity, and drug resistance. It may be essential to understand the various interactions C. auris could perform in the environment, directly impacting the outcome of human infections under the One Health approach.

Regulation of AUF1 alternative splicing by hnRNPA1 and SRSF2 modulate the sensitivity of ovarian cancer cells to cisplatin.

Clarification of cisplatin resistance may provide new targets for therapy in cisplatin resistant ovarian cancer. The current study aims to explore involvement of isoforms of AU-rich element RNA-binding protein 1 (AUF1) in cisplatin resistance in ovarian cancer. The cancer stem cell-like features were analyzed using colony formation assay, tumor sphere formation assay and nude mouse xenograft experiments. AUF1 isoforms expression was analyzed using immunoblotting, qRT-PCR, and immunohistochemistry. RIP and Biotin pulldown was used to analyze the interaction of SRSF2 and hnRNPA1 with AUF1 transcript. Transcriptome regulated by AUF1 isoforms was analyzed by RNA-seq. The current study demonstrated differential expression of AUF1 isoforms in cisplatin sensitive and resistant ovarian cancer tissues and cells. P37 isoform promoted proliferation, while p45 isoform enhanced responsiveness of ovarian cancer cells to cisplatin. the clonal formation capacity of the cells, and the restoration of p45 expression reduced the capacity with cisplatin treatment. The competitive binding of phosphorylated hnRNPA1 and O-GlcNAc-modified SRSF2 on AUF1 exon 2 and exon 7 regulated the alternative splicing of AUF1. The competitive binding of phosphorylated hnRNPA1 and O-GlcNAc modified SRSF2 on exon 2 and exon 7 regulated the alternative splicing of AUF1 and subsequent isoform expression. P37 isoform played a "cancer promoter" role, p42 and p45, especially p45 played a "cancer suppressor" role in ovarian cancer. This study provides a new target for exploring the drug resistance mechanism of ovarian cancer.

Pelophen B is a non-taxoid binding microtubule-stabilizing agent with promising preclinical anticancer properties

Taxanes, such as paclitaxel (PTX), stabilize microtubules and are used as a first-line therapy in multiple cancer types. Disruption of microtubule equilibrium, which plays an essential role in mitosis and cell homeostasis, ultimately results in cell death. Even though PTX is a very potent chemotherapy, its use is associated with major side effects and therapy resistance. Pelophen B (PPH), a synthetic analog of peloruside A, stabilizes microtubules through interaction with a non-taxoid binding site of β-tubulin. We evaluated the anticancer effect of PPH in a variety of tumor types by using established cell lines, early-passage cultures and ex vivo tumor-derived cultures that preserve the 3D architecture of the tumor microenvironment. PPH significantly blocks colony formation capacity, reduces viability and exerts additivity with PTX. Interestingly, PPH overcomes resistance to PTX. Mechanistically, PPH induces a G2/M cell cycle arrest and increases the presence of tubulin polymerization promoting protein (TPPP), inducing lysine 40 acetylation of α-tubulin. Although, results induced by paclitaxel or PPH are concordant, PPH’s unique microtubule binding mechanism enables PTX additivity and ensures overcoming PTX-induced resistance. In conclusion, PPH results in remarkable anti-cancer activity in a range of preclinical models supporting further clinical investigation of PPH as a therapeutic anticancer agent.

A 2-year pure biochar addition enhances soil carbon sequestration and reduces aggregate stability in understory conditions

The enhancement of soil aggregate size and stability is crucial for mitigating climate change and improving carbon sequestration in forest ecosystems. Biochar, derived from rice husks, has been suggested as an effective mean to increase soil carbon storage. However, isolating biochar’s specific effects on soil aggregate formation and carbon sink capacity can be complex due to the overlapping influences of fertilization and understory vegetation cultivation. Our study circumvented these variables by incorporating different amounts of biochar into plantation soil without any additional cultivation or fertilization, conducting a detailed two–year field experiment. The findings revealed that biochar significantly increased the organic carbon content and density in the uncultivated under–forest Ferralsols, thus enhancing its carbon sink function. Intriguingly, while biochar raised the proportion of small soil aggregates (< 0.25 mm) and their organic carbon levels, it decreased the fraction of larger aggregates (> 0.25 mm), adversely affecting soil aggregate stability. These results suggest that biochar may compromise soil aggregate structure and stability in the absence of plant growth. The positive impact of biochar on soil carbon storage was found to depend more on its inherent inert carbon content than on soil type. Moreover, biochar alone was insufficient to increase the quantity of soil macroaggregates without the binding action of plant root exudates. Biochar’s key function appears to be in enhancing the soil aggregate–forming processes facilitated by plant roots and microorganisms. Therefore, for optimal carbon sequestration in forest soils, integrating biochar application with appropriate agricultural practices is advisable.

Establishment and characterization of the novel myxofibrosarcoma cell line, SMU-MFS.

Myxofibrosarcoma (MFS) is one of the most common soft-tissue sarcomas in elderly patients. Owing to the limited efficacy of chemotherapy and radiotherapy, complete resection is the only available curative treatment. Therefore, developing novel therapies for MFS is important to improve clinical outcomes. Herein, a novel MFS cell line, namely SMU-MFS, was established to better understand the biologic characteristics of MFS and develop new therapies. A tissue sample from the surgically resected tumor tissue of a 56-year-old patient with a tumor was subjected to primary culture. The cell line was established and authenticated by assessing the short tandem repeats of DNA microsatellites. The monolayer cultures of SMU-MFS cells exhibited constant growth, spheroid formation, and invasive capacity. Furthermore, the cells exhibited low chemosensitivity to doxorubicin, eribulin, and pazopanib, which are used to inhibit metastatic progression. In addition, of the four mice inoculated with SMU-MFS cells, tumors developed in two mice after 8weeks. Altogether, the findings of this study suggest that the SMU-MFS cell line can be a useful tool for investigating MFS development and evaluating novel therapeutic agents.

Structural, Magnetic, and Mössbauer Study on Nb and Heat Treatment of Fe-Si-B-P-Cu-Nb Ribbons

This study aims to enhance the amorphous formation ability and magnetic properties that are crucial for the production of high-quality nanocrystalline alloys. The structural, thermal, and magnetic characteristics of the alloy ribbons were analyzed through a systematic adjustment of Nb content, and, including Nb, significantly improved the amorphous formation ability and thermal stability of the alloy, which is vital for nanocrystalline production. By varying the Nb content within Fe85-xSi2B8P4Cu1Nbx (x = 0.0, 0.5, 1.0, and 1.5), we explored finer adjustments to achieve homogeneous amorphousness during the melt spinning process. Careful control over the Nb content facilitated the production of amorphous ribbons with consistent homogeneity, which was critical for the subsequent fabrication of nanocrystalline structures through heat treatment. As a result, the amorphous ribbon of Fe85.5Si2B8P4Cu1Nb0.5 showed a low coercivity of 7 A/m. The heat treatment showed a remarkably high saturation magnetic flux density of 1.94 T. Additionally, the grain size (D) decreased as the Nb content increased, with D values ranging from 25.09 nm to 24.29 nm, as calculated by the Scherrer formula. Mössbauer spectroscopy confirmed the formation of nanocrystalline and residual amorphous phases. The hyperfine magnetic field values (Beff) decreased from 25.7 T to 24.7 T in the amorphous samples and reached 33.0 T in the nanocrystalline phases. This study highlights Nb’s positive impact on thermal stability and amorphous formation capacity in Fe-Si-B-P-Cu alloys, culminating in the successful fabrication of nanocrystalline ribbons with superior structural and magnetic properties.

The biocontrol strain Bacillus mojavensis KRS009 confers resistance to cotton Verticillium wilt and improves tolerance to salt stress

AbstractBiological control has gained increasing attention as a strategy to address biotic and abiotic stresses in crops. In this study, we identified the strain KRS009 as Bacillus mojavensis through morphological identification and multilocus sequence analysis. KRS009 exhibited broad‐spectrum antifungal activity against various phytopathogenic fungi by secreting soluble and volatile compounds. Additionally, the physio‐biochemical traits of strain KRS009 were characterized, including its growth‐promoting capabilities and active enzymes. Notably, KRS009 demonstrated the capacity for biofilm formation and exhibited tolerance to saline‐alkali conditions. The biological security evaluation confirmed the safety of KRS009 for both humans and plants. Furthermore, strain KRS009 was found to trigger plant immunity by inducing systemic resistance through salicylic acid‐ and jasmonic acid‐dependent signaling pathways. Greenhouse experiments conducted on cotton plants proved that the treatment with strain KRS009 effectively protected cotton against Verticillium wilt caused by Verticillium dahliae and promoted the growth of cotton under salt stress. These findings highlight the potential of B. mojavensis KRS009 as a promising biocontrol and biofertilizer agent for promoting plant growth, combating fungal diseases and mitigating salt stress in plants.

Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is characterized by high vascularity and notable abnormality of blood vessels, where angiogenesis is a key process in tumorigenesis and metastasis. The main functions of Nei Like DNA Glycosylase 3 (NEIL3) include DNA alcoholization repair, immune response regulation, nervous system development and function, and DNA damage signal transduction. However, the underlying mechanism of high expression NEIL3 in the development and progression of HCC and whether the absence or silencing of NEIL3 inhibits the development of cancer remain unclear. Therefore, a deeper understanding of the mechanisms by which increased NEIL3 expression promotes cancer development is needed. Expression of NEIL3 and its upstream transcription factor MAZ in HCC tumor tissues was analyzed in bioinformatics efforts, while validation was done by qRT-PCR and western blot in HCC cell lines. The migration and tube formation capacity of HUVEC cells were analyzed by Transwell and tube formation assays. Glycolytic capacity was analyzed by extracellular acidification rate, glucose uptake, and lactate production levels. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assays were utilized to investigate specific interactions between MAZ and NEIL3. NEIL3 and MAZ were substantially upregulated in HCC tissues and cells. NEIL3 was involved in modulating the glycolysis pathway, suppression of which reversed the stimulative impact of NEIL3 overexpression on migration and angiogenesis in HUVEC cells. MAZ bound to the promoter of NEIL3 to facilitate NEIL3 transcription. Silencing MAZ reduced NEIL3 expression and suppressed the glycolysis pathway, HUVEC cell migration, and angiogenesis. MAZ potentiated the upregulated NEIL3-mediated glycolysis pathway and HCC angiogenesis. This study provided a rationale for the MAZ/NEIL3/glycolysis pathway as a possible option for anti-angiogenesis therapy in HCC.