Pesticide application behavior in green tea cultivation and risk assessment of tea products: a case study of Rizhao green tea.

Previous research on pesticides in green tea mainly focused on detection technology but lacked insights into pesticide use during cultivation. To address this gap, a survey was conducted among Rizhao green tea farmers. The survey results showed that most tea farmers were approximately 60 years old and managed small, scattered tea gardens (< 0.067 ha). Notably, tea farmers who had received agricultural training executed more standardized pesticide application practices. Matrine and thiazinone are the most used pesticides. A total of 16 types of pesticides were detected in the tested green tea samples, with 65% of the samples containing residues of at least one pesticide. Notably, higher levels of residues were observed for bifenthrin, cyfluthrin, and acetamiprid. The presence of pesticide residues varied significantly between seasons and regions. The risk assessment results indicated that the hazard quotient (HQ) values for all 16 pesticides detected in green tea were < 1, suggesting that these residue levels do not pose a significant public health concern.

Metformin Mitigates Sepsis-Induced Acute Lung Injury and Inflammation in Young Mice by Suppressing the S100A8/A9-NLRP3-IL-1ß Signaling Pathway.

Background: Globally, the subsequent complications that accompany sepsis result in remarkable morbidity and mortality rates. The lung is among the vulnerable organs that incur the sepsis-linked inflammatory storm and frequently culminates into ARDS/ALI. The metformin-prescribed anti-diabetic drug has been revealed with anti-inflammatory effects in sepsis, but the underlying mechanisms remain unclear. This study aimed to ascertain metformin's effects and functions in a young mouse model of sepsis-induced ALI. Methods: Mice were randomly divided into 4 groups: sham, sham+ Met, CLP, and CLP+ Met. CLP was established as the sepsis-induced ALI model accompanied by intraperitoneal metformin treatment. At day 7, the survival state of mice was noted, including survival rate, weight, and M-CASS. Lung histological pathology and injury scores were determined by hematoxylin-eosin staining. The pulmonary coefficient was used to evaluate pulmonary edema. Furthermore, IL-1ß, CCL3, CXCL11, S100A8, S100A9 and NLRP3 expression in tissues collected from lungs were determined by qPCR, IL-1ß, IL-18, TNF-α by ELISA, caspase-1, ASC, NLRP3, P65, p-P65, GSDMD-F, GSDMD-N, IL-1ß and S100A8/A9 by Western blot. Results: The data affirmed that metformin enhanced the survival rate, lessened lung tissue injury, and diminished the expression of inflammatory factors in young mice with sepsis induced by CLP. In contrast to sham mice, the CLP mice were affirmed to manifest ALI-linked pathologies following CLP-induced sepsis. The expressions of pro-inflammatory factors, for instance, IL-1ß, IL-18, TNF-α, CXCL11, S100A8, and S100A9 are markedly enhanced by CLP, while metformin abolished this adverse effect. Western blot analyses indicated that metformin inhibited the sepsis-induced activation of GSDMD and the upregulation of S100A8/A9, NLRP3, and ASC. Conclusion: Metformin could improve the survival rate, lessen lung tissue injury, and minimize the expression of inflammatory factors in young mice with sepsis induced by CLP. Metformin reduced sepsis-induced ALI via inhibiting the NF-κB signaling pathway and inhibiting pyroptosis by the S100A8/A9-NLRP3-IL-1ß pathway.

Hypermethylation and low expression of FOXM1 predisposes women to unexplained recurrent miscarriage by impairing trophoblast stem cell proliferation.

Recurrent miscarriage (RM) is a distressing pregnancy complication with an unknown etiology. Increasing evidence indicates the relevance of dysregulation of human trophoblast stem cells (hTSCs), which may play a role in the development of RM. However, the potential molecular regulatory mechanism underlying the initiation and maintenance of hTSCs is yet to be fully elucidated. In this study, we performed data analysis and identified Forkhead box M1 (FOXM1) as a potential factor associated with RM. FOXM1 is a typical transcription factor known for its involvement in various pathophysiological processes, while the precise function of FOXM1 functions in hTSCs and RM remains incompletely understood. Utilizing RNA-seq, CUT&Tag, ChIP-qPCR, and sodium bisulfite conversion methods for methylation analysis, we elucidate the underlying regulatory mechanisms of FOXM1 in hTSCs and its implications in RM. Our findings demonstrate the relative high expression of FOXM1 in proliferating cytotrophoblasts (CTBs) compared to differentiated extravillous cytotrophoblasts (EVTs) and syncytiotrophoblasts (STBs). Besides, we provide evidence supporting a significant correlation between FOXM1 downregulation and the incidence of RM. Furthermore, we demonstrate the significant role of FOXM1 in regulating hTSCs proliferation and cell cycle through the transcriptional regulation of CDKN3, CCNB2, CCNA2, MAD2L1 and CDC25C. Notably, we observed a correlation between the downregulation of FOXM1 in RM and hypermethylation in its promoter region. Collectively, these results provide insights into the impact of FOXM1 on trophoblast regulation and offer a novel perspective on RM.

Successful treatment of Giant keloid on the right toes using trepanation combined with superficial radiotherapy (SRT-100): a case report with literature review.

In dermatology, a keloid is one of the most common skin morphological abnormalities caused by excessive proliferation of fibroblasts. Keloids that are large or occur near important joint sites often cause varying degrees of physiological dysfunction in patients, therefore requiring medical treatment. A boy with congenital syndactyly developed huge keloids at the surgical site after undergoing surgical correction treatment. After treatment using trepanation combined with superficial radiotherapy (SRT-100) in our hospital, most of the boy's keloids shrank and flattened. The affected foot returned to its normal appearance, and the boy could wear shoes normally. The boy did not complain of pain, numbness, or any other distinctive discomfort after completing the treatment. This suggested that the combination of trepanation and SRT-100 may be one of the options for treating hypertrophic keloids that cannot be treated by surgical excision.

Direct effects of barley yellow dwarf virus on the performance, parasitoid resistance, and feeding behavior of its vector Sitobion avenae (Hemiptera: Aphididae).

BACKGROUND: The complex interaction between plant viruses and their insect vectors is the basis for the epidemiology of plant viruses. The 'Vector Manipulation Hypothesis' (VMH) was proposed to demonstrate the evolution of strategies in plant viruses to enhance their transmission to new hosts through direct effects on insect vector behavior and/or physiology. However, the aphid vectors used in previous studies were mostly obtained by feeding on virus-infected plants and as a result, it was difficult to eliminate the confounding effects of infected host plants. Furthermore, the mechanisms of the direct effects of plant viruses on insect vectors have rarely been examined comprehensively. RESULTS: We fed Sitobion avenae on an artificial diet infused with a purified suspension of Barley yellow dwarf virus (BYDV) PAV strain to obtain viruliferous aphids. We then examined their growth and reproduction performance, resistance to the parasitoid Aphidius gifuensis Ashmead, and feeding behavior. The results indicate that (1) viruliferous aphids had a shorter life span and a lower relative growth rate at the nymphal stage; (2) A. gifuensis had a lower parasitism rate, mummification rate, and emergence rate in viruliferous aphids; (3) Viruliferous aphids spent more time on non-probing and salivation behavior and had a shorter total duration of penetration and ingestion compared with healthy conspecifics. CONCLUSION: These results suggest that plant virus infection may directly alter vector fitness and behavior that improves plant virus transmission, but not vector growth. These findings highlight the mechanisms of VMH and the ecological significance of vector manipulation by plant viruses, and have implications for plant virus disease and vector management. © 2024 Society of Chemical Industry.

A biomimetic ion channel shortens the QT interval of type 2 long QT syndrome through efficient transmembrane transport of potassium ions.

Potassium ion transport across myocardial cell membrane is essential for type 2 long QT syndrome (LQT2). However, the dysfunction of potassium ion transport due to genetic mutations limits the therapeutic effect in treating LQT2. Biomimetic ion channels that selectively and efficiently transport potassium ions across the cellular membranes are promising for the treatment of LQT2. To corroborate this, we synthesized a series of foldamer-based ion channels with different side chains, and found a biomimetic ion channel of K+ (BICK) with the highest transport activity among them. The selected BICK can restore potassium ion transport and increase transmembrane potassium ion current, thus shortening phase 3 of action potential (AP) repolarization and QT interval in LQT2. Moreover, BICK does not affect heart rate and cardiac rhythm in treating LQT2 model induced by E4031 in isolated heart as well as in guinea pigs. By restoring ion transmembrane transport tactic, biomimetic ion channels, such as BICK, will show great potential in treating diseases related to ion transport blockade. STATEMENT OF SIGNIFICANCE: Type 2 long QT syndrome (LQT2) is a disease caused by K+ transport disorder, which can cause malignant arrhythmia and even death. There is currently no radical cure, so it is critical to explore ways to improve K+ transmembrane transport. In this study, we report that a small-molecule biomimetic ion channel BICK can efficiently simulate natural K+ channel proteins on the cardiomyocyte and cure E4031-induced LQT2 in guinea pig by restoring K+ transport function for the first time. This study found that the potassium transmembrane transport by BICK significantly reduced the QT interval, which provides a conceptually new strategy for the treatment of LQT2 disease.

Prenatal exposure to fenvalerate causes depressive-like behavior in adulthood by inhibiting brain-derived 5-HT synthesis.

The developmental toxicity of fenvalerate, a representative pyrethroid insecticide, is well documented. The present study aimed to explore whether prenatal exposure to fenvalerate causes depression-like behavior in adulthood. Pregnant mice were orally administrated with either corn oil or fenvalerate (2 or 20 mg/kg) during pregnancy. Depressive-like behaviors were assessed by tail suspension test (TST), forced swim test (FST) and sucrose preference test (SPT). Immobility times in TST and FST were increased in offspring whose mothers were exposed to fenvalerate throughout pregnancy. By contrast, sugar preference index, as determined by SPT, was decreased in fenvalerate-exposed offspring. Prefrontal PSD95, a postsynaptic membrane marker, was downregulated in fenvalerate-exposed adulthood offspring. Fenvalerate-induced reduction of prefrontal PSD95 began at GD18 fetal period. Accordingly, prefrontal 5-HT, a neurotransmitter for synaptogenesis, was also reduced in fenvalerate-exposed GD18 fetuses. Tryptophan hydroxylase 2 (TPH2), a key enzyme for 5-HT synthesis, was downregulated in the midbrain of fenvalerate-exposed GD18 fetuses. Additional experiment showed that GRP78 and p-eIF2α, two endoplasmic reticulum stress-related proteins, were increased in the midbrain of fenvalerate-exposed fetal mice. The present results suggest that prenatal exposure to fenvalerate causes depressive-like behavior in adulthood, partially by inhibiting brain-derived 5-HT synthesis.

Quercetin-Loaded Bioglass Injectable Hydrogel Promotes m6A Alteration of Per1 to Alleviate Oxidative Stress for Periodontal Bone Defects.

Periodontal disease ranks third among noncommunicable illnesses, behind cancer and cardiovascular disease, and is closely related to the occurrence and progression of various systemic diseases. However, elucidating the processes of periodontal disease and promoting periodontal bone regeneration remains a challenge. Here, quercetin is demonstrated to reduce the oxidative stress state of orofacial mesenchymal stem cells (OMSCs) in vitro and to affect the osteogenic growth of OMSCs through molecular mechanisms that mediate the m6A change in Per1. Nevertheless, the limited therapeutic efficacy of systemic medication and the limitations of local medication resulting from the small, moist, and highly dynamic periodontal environment make it challenging to treat periodontal tissues with medication. Herein, a biosafe injectable hydrogel drug-controlled delivery system is constructed as a bone-enhancing factory and loaded with quercetin to treat oxidative stress injury in periodontal tissues. This drug-carrying system made up of nanoscale bioglass microspheres and a light-cured injectable hydrogel, allows effective drug particle loading and cementation in the dynamic and moist periodontal environment. Furthermore, the system demonstrates the ability to stimulate OMSCs osteogenic differentiation in a Per1-dependent manner, which ultimately promotes periodontal bone repair, suggesting that this system has potential for clinical periodontal therapy.

Photochemical Degradation of the New Nicotine Pesticide Acetamiprid in Water.

Acetamiprid is a novel nicotinic pesticide widely used in modern agriculture because of its low toxicity and specific biological target properties. The objective of this study was to understand the photolysis pattern of acetamiprid in the water column and elucidate its degradation products and mechanism. It was observed that acetamiprid exhibited different photolysis rates under different light source conditions in pure water, with ultraviolet > fluorescence > sunlight; furthermore, its photolysis half-life ranged from 17.3 to 28.6 h. In addition, alkaline conditions (pH 9.0) accelerated its photolysis rate, which increased with pH. Using gas chromatography-mass spectrometry, five direct photolysis products generated during the exposure of acetamiprid to pure water were successfully separated and identified. The molecular structure of acetamiprid was further analyzed using density functional theory, and the active photodegradation sites of acetamiprid were predicted. The mechanism of the photolytic transformation of acetamiprid in water was mainly related to hydroxyl substitution and oxidation. Based on these findings, a comprehensive transformation pathway for acetamiprid was proposed.

Insights from the neural guidance factor Netrin-1 into neurodegeneration and other diseases.

Netrin-1 was initially discovered as a neuronal growth cue for axonal guidance, and its functions have later been identified in inflammation, tumorigenesis, neurodegeneration, and other disorders. We have recently found its alterations in the brains with Alzheimer's disease, which might provide important clues to the mechanisms of some unique pathologies. To provide better understanding of this promising molecule, we here summarize research progresses in genetics, pathology, biochemistry, cell biology and other studies of Netrin-1 about its mechanistic roles and biomarker potentials with an emphasis on clinical neurodegenerative disorders in order to expand understanding of this promising molecular player in human diseases.

The biological functions and pathological mechanisms of CASK in various diseases.

Background: As a scaffold protein, calcium/calmodulin-dependent serine protein kinase (CASK) has been extensively studied in a variety of tissues throughout the body. The Cask gene is ubiquitous in several tissues, such as the neurons, islets, heart, kidneys and sperm, and is mostly localised in the cytoplasm adjacent to the basement membrane. CASK binds to a variety of proteins through its domains to exerting its biological activity. Scope of review: Here, we discuss the role of CASK in multiple tissues throughout the body. The role of different CASK domains in regulating neuronal development, neurotransmitter release and synaptic vesicle secretion was emphasised; the regulatory mechanism of CASK on the function of pancreatic islet ß cells was analysed; the role of CASK in cardiac physiology, kidney and sperm development was discussed; and the role of CASK in different tumours was compared. Finally, we clarify the importance of the Cask gene in the body, and how deletion or mutation of the Cask gene can have adverse consequences. Major conclusions: CASK is a conserved gene with similar roles in various tissues. The function of the Cask gene in the nervous system is mainly involved in the development of the nervous system and the release of neurotransmitters. In the endocrine system, an involvement of CASK has been reported in the process of insulin vesicle transport. CASK is also involved in cardiomyocyte ion channel regulation, kidney and sperm development, and tumour proliferation. CASK is an indispensable gene for the whole body, and CASK mutations can cause foetal malformations or death at birth. In this review, we summarise the biological functions and pathological mechanisms of CASK in various systems, thereby providing a basis for further in-depth studies of CASK functions.

The Combined Anti-Aging Effect of Hydrolyzed Collagen Oligopeptides and Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells on Human Skin Fibroblasts.

Stem cell-derived exosomes (SC-Exos) are used as a source of regenerative medicine, but certain limitations hinder their uses. The effect of hydrolyzed collagen oligopeptides (HCOPs), a functional ingredient of SC-Exos is not widely known to the general public. We herein evaluated the combined anti-aging effects of HCOPs and exosomes derived from human umbilical cord mesenchymal stem cells (HucMSC-Exos) using a senescence model established on human skin fibroblasts (HSFs). This study discovered that cells treated with HucMSC-Exos + HCOPs enhanced their proliferative and migratory capabilities; reduced both reactive oxygen species production and senescence-associated ß-galactosidase activity; augmented type I and type III collagen expression; attenuated the expression of matrix-degrading metalloproteinases (MMP-1, MMP-3, and MMP-9), interleukin 1 beta (IL-1ß), and tumor necrosis factor-alpha (TNF-α); and decreased the expression of p16, p21, and p53 as compared with the cells treated with HucMSC-Exos or HCOPs alone. These results suggest a possible strategy for enhancing the skin anti-aging ability of HucMSC-Exos with HCOPs.

Immune profiling analysis of double-negative T cells in patients with systemic sclerosis.

OBJECTIVE: To construct a molecular immune map of patients with systemic sclerosis (SSc) by mass flow cytometry, and compare the number and molecular expression of double-negative T (DNT) cell subsets between patients and healthy controls (HC). METHODS: Peripheral blood mononuclear cells (PBMCs) were extracted from the peripheral blood of 17 SSc patients and 9 HC. A 42-channel panel was set up to perform mass cytometry by time of flight (CyTOF) analysis for DNT subgroups. Flow cytometry was used to validate subpopulation functions. The clinical data of patients were collected for correlation analysis. RESULTS: Compared with HC, the number of total DNT cells decreased in SSc patients. Six DNT subsets were obtained from CyTOF analysis, in which the proportion of cluster1 increased, while the proportion of cluster3 decreased. Further analysis revealed that cluster1 was characterized by high expression of CD28 and CCR7, and cluster3 was characterized by high expression of CD28 and CCR5. After in vitro stimulation, cluster1 secreted more IL-4 and cluster3 secreted more IL-10 in SSc patients compared to HC. Clinical correlation analysis suggested that cluster1 may play a pathogenic role while cluster3 may play a protective role in SSc. ROC curve analysis further revealed that cluster3 may be a potential indicator for determining disease activity in SSc patients. CONCLUSION: We found a new CCR5+CD28+ DNT cell subset, which played a protective role in the pathogenesis of SSc. Key Points • The number of DNT cells decreased in SSc patients' peripheral blood. • DNT cells do not infiltrate in the skin but secrete cytokines to participate in the pathogenesis of SSc. • A CCR5+CD28+ DNT cell population may play a protective role in SSc.

LGGA-MPP: Local Geometry-Guided Graph Attention for Molecular Property Prediction.

Molecular property prediction is a fundamental task of drug discovery. With the rapid development of deep learning, computational approaches for predicting molecular properties are experiencing increasing popularity. However, these existing methods often ignore the 3D information on molecules, which is critical in molecular representation learning. In the past few years, several self-supervised learning (SSL) approaches have been proposed to exploit the geometric information by using pre-training on 3D molecular graphs and fine-tuning on 2D molecular graphs. Most of these approaches are based on the global geometry of molecules, and there is still a challenge in capturing the local structure and local interpretability. To this end, we propose local geometry-guided graph attention (LGGA), which integrates local geometry into the attention mechanism and message-passing of graph neural networks (GNNs). LGGA introduces a novel method to model molecules, enhancing the model's ability to capture intricate local structural details. Experiments on various data sets demonstrate that the integration of local geometry has a significant impact on the improved results, and our model outperforms the state-of-the-art methods for molecular property prediction, establishing its potential as a promising tool in drug discovery and related fields.

APOE from patient-derived astrocytic extracellular vesicles alleviates neuromyelitis optica spectrum disorder in a mouse model.

Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune astrocytopathy of the central nervous system, mediated by antibodies against aquaporin-4 water channel protein (AQP4-Abs), resulting in damage of astrocytes with subsequent demyelination and axonal damage. Extracellular communication through astrocyte-derived extracellular vesicles (ADEVs) has received growing interest in association with astrocytopathies. However, to what extent ADEVs contribute to NMOSD pathogenesis remains unclear. Here, through proteomic screening of patient-derived ADEVs, we observed an increase in apolipoprotein E (APOE)-rich ADEVs in patients with AQP4-Abs-positive NMOSD. Intracerebral injection of the APOE-mimetic peptide APOE130-149 attenuated microglial reactivity, neuroinflammation, and brain lesions in a mouse model of NMOSD. The protective effect of APOE in NMOSD pathogenesis was further established by the exacerbated lesion volume in APOE-deficient mice, which could be rescued by exogenous APOE administration. Genetic knockdown of the APOE receptor lipoprotein receptor-related protein 1 (LRP1) could block the restorative effects of APOE130-149 administration. The transfusion ADEVs derived from patients with NMOSD and healthy controls also alleviated astrocyte loss, reactive microgliosis, and demyelination in NMOSD mice. The slightly larger beneficial effect of patient-derived ADEVs as compared to ADEVs from healthy controls was further augmented in APOE-/- mice. These results indicate that APOE from astrocyte-derived extracellular vesicles could mediate disease-modifying astrocyte-microglia cross-talk in NMOSD.

Potential Protein Signatures for Recurrence Prediction of Ischemic Stroke.

BACKGROUND: Acute ischemic stroke is a major cause of mortality and disability worldwide, with approximately 7.4% to 7.7% recurrence within the first 3 months. This study aimed to identify potential biomarkers for predicting stroke recurrence. METHODS AND RESULTS: We conducted a nested case-control study using a hospital-based cohort from the Third China National Stroke Registry selecting 214 age- and sex-matched patients with ischemic stroke with hypertension and no history of diabetes or heart disease. Using data-independent acquisition for discovery and multiple reaction monitoring for quantitative validation, we identified 26 differentially expressed proteins in large-artery atherosclerosis (Causative Classification of Ischemic Stroke [CCS]1), 16 in small-artery occlusion (CCS3), and 25 in undetermined causes (CCS5) among patients with recurrent stroke. In the CCS1 and CCS3 subgroups, differentially expressed proteins were associated with platelet aggregation, neuronal death/cerebroprotection, and immune response, whereas differentially expressed proteins in the CCS5 subgroup were linked to altered metabolic functions. Validated recurrence predictors included proteins associated with neutrophil activity and vascular inflammation (TAGLN2 [transgelin 2], ITGAM [integrin subunit α M]/TAGLN2 ratio, ITGAM/MYL9 [myosin light chain 9] ratio, TAGLN2/RSU1 [Ras suppressor protein 1] ratio) in the CCS3 subgroup and proteins associated with endothelial plasticity and blood-brain barrier integrity (ITGAM/MYL9 ratio and COL1A2 [collagen type I α 2 chain]/MYL9 ratio) in the CCS3 and CCS5 subgroups, respectively. CONCLUSIONS: These findings provide a foundation for developing a blood-based biomarker panel, using causative classifications, which may be used in routine clinical practice to predict stroke recurrence.

Life-cycle comparisons of economic and environmental consequences for pig production with four different models in China.

China, the world's largest consumer and producer of pork in the world, is attracting increasing attention due to the environmental impacts of its pig production. Previous studies seldom comprehensively compare the environmental impacts of the pig production system with different models, resulting in different intensities of environmental impacts. We aim to comprehensively evaluate Chinese pig production with different breeding models and explore a more sustainable way for pig production. We use life cycle assessment (LCA) to evaluate and compare environmental impacts of pig production system with four main breeding models in China from 1998 to 2020: domestic breeding, small-scale breeding, medium-scale breeding, and large-scale breeding. The life cycle encompasses fertilizer production, feed production, feed processing, pig raising, waste treatment, and slaughtering. The impact categories including energy consumption (EN), global warming (GWP), acidification (AP), eutrophication (EU), water use (WD), and land occupation (LO) are expressed with "100 kg live weight of fattening pig at farm gate." The results show that driven by governmental support, growing meat demand, and cost advantage, the scale breeding especially large-scale breeding simultaneously yielded greater net economic benefit and less environmental impact compared to other breeding models especially the domestic breeding. Due to mineral fertilizer application, feed production contributed over 50% of the total environmental impacts. Notably, the composition of feeds exerted significant influence on the environmental impacts arising from fertilizer production and feed processing. Furthermore, attributable to the substantial use of electricity and heat, as well as the concomitant emissions, pig raising contributed the largest GWP, while ranking second in terms of AP and EU. Notably, waste management constituted the third-largest EU, AP, and WD. In addition to promote scale breeding, we put forth several sustainable measures encompassing feed composition, cultivation practices, fertilizer utilization, and waste management for consideration.

GP60 and SPARC as albumin receptors: key targeted sites for the delivery of antitumor drugs.

Albumin is derived from human or animal blood, and its ability to bind to a large number of endogenous or exogenous biomolecules makes it an ideal drug carrier. As a result, albumin-based drug delivery systems are increasingly being studied. With these in mind, detailed studies of the transport mechanism of albumin-based drug carriers are particularly important. As albumin receptors, glycoprotein 60 (GP60) and secreted protein acidic and rich in cysteine (SPARC) play a crucial role in the delivery of albumin-based drug carriers. GP60 is expressed on vascular endothelial cells and enables albumin to cross the vascular endothelial cell layer, and SPARC is overexpressed in many types of tumor cells, while it is minimally expressed in normal tissue cells. Thus, this review supplements existing articles by detailing the research history and specific biological functions of GP60 or SPARC and research advances in the delivery of antitumor drugs using albumin as a carrier. Meanwhile, the deficiencies and future perspectives in the study of the interaction of albumin with GP60 and SPARC are also pointed out.

A multifunctional quercetin/polycaprolactone electrospun fibrous membrane for periodontal bone regeneration.

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The anoikis-related gene signature predicts survival and correlates with immune infiltration in osteosarcoma.

Anoikis is essential for the progression of many malignant tumors. However, the understanding of anoikis' roles in osteosarcoma remains scarce. This study conducted an extensive bioinformatics analysis to identify anoikis-related genes (ARGs), developed ARGs modeles for predicting OS and RFS, and evaluated the effect of these ARGs on osteosarcoma cell migration and invasion. The GSE16088 and GSE28425 datasets provided the differentially expressed genes (DEGs). The prognostic significance and functions of these DEGs were systematically investigated using several bioinformatics techniques. Transwell assays were conducted to determine the effect of OGT on osteosarcoma cell migration and invasion. Seven genes were identified as hub genes, including FN1, CD44, HRAS, TP53, PPARG, CTNNB1, and VEGFA, while 71 ARGs were identified as DEGs. Four ARGs-BRMS, COL4A2, FGF2, and OGT-were used to develop an RFS-predicting model, whereas seven ARGs-CD24, FASN, MMP2, EIF2AK3, ID2, PPARG, and PIK3R3-were used to develop an OS-predicting model in patients with osteosarcoma. In both the training and validation cohorts, high-risk group patients had significantly shorter OS and RFS duration than low-risk group patients. Furthermore, using the aforementioned ARGs, we developed clinically applicable nomograms for OS and RFS prediction. The proportion of tumor-infiltrating immune cells was significantly linked to risk scores. In vitro experiments revealed that knocking down OGT significantly inhibited the ability of MG63 and U2OS cells to invade and migrate. ARG-based gene signatures reliably predicted RFS and OS in osteosarcoma, and OGT showed promise as a potential biomarker. These findings contribute to a better understanding of ARGs' prognostic roles in osteosarcoma.