This study describes the synthesis of Chitosan - corn protein (CSZ-TG) composites using TG enzyme (TG) as a cross-linking agent and the preparation of chitosan-based composite membrane material (CSZEO-TG) by blending citrus essential oil (EO) with the synthesized CSZ-TG. The prepared composite membrane material was used for fresh strawberry preservation and characterized by scanning electron microscopy, Fourier transform infrared spectroscopy, X-spectral diffraction, tensile properties, and water vapor and CO2 permeability. Scanning electron microscopy results showed a smooth surface of the composite membrane material after the addition of TG enzyme, while Fourier transforms infrared spectroscopy results showed a structural change of the composite membrane material after the addition of corn protein (Z). The tensile results showed an increase in the tensile strength of the composite membrane material after the addition of TG enzyme, while the flexibility of the composite membrane material was enhanced after the addition of EO. Compared with the pure chitosan membrane (CS), the water vapor and CO2 barrier properties of the composite membrane material after the addition of Z, TG, and EO did not change much, and they all showed better water vapor barrier properties. The results of the antioxidant analysis of the solution of the CSZEO-TG composite membrane material showed that the composite membrane material had efficient antioxidant properties. The effects of the composite film material on the storage period and quality of strawberries were evaluated by the indicators of weight loss, hardness, decay rate, soluble solids, titratable acid content, MDA content, and the content of four enzymes, SOD, POD, PPO and CAT. Comprehensive freshness data analysis showed that CSZEO-TG had the best freshness preservation performance and effectively extended the shelf life of strawberries.

As a decay product of uranium series, 210Pb spreads widely in the nature and imposes strong radiological and chemical toxicity. It is vital to establish reliable and efficient radioanalytical methods for 210Pb determination to support environment and food radioactivity monitoring programs. This article critically reviews analytical methods developed for determining 210Pb in environmental and biological samples, especially new development in recent years. Techniques applied throughout different analytical steps including sample pretreatment, separation, purification, and detection are summarized and their pros and cons are discussed to provide a holistic overview for 210Pb environmental and biological assay.

Global population aging poses a tremendous burden on the health care system worldwide. Frailty is associated with decreased physical reserve and is considered an important indicator of adverse events in the older population. Therefore, there is growing interest in the early diagnosis and intervention of frailty, but the cellular mechanisms responsible for frailty are still not completely understood. Chronic inflammation is related to decreased physical function and increased disease risk. Additionally, multiple human and animal studies suggest that inflammation probably plays the largest role in contributing to frailty. Some inflammatory markers have been proposed to predict physical frailty. However, there are still large gaps in knowledge related to the clinical application of these markers in frail patients. Therefore, understanding the biological processes and identifying recognized and reliable markers are urgent and pivotal tasks for geriatricians. In the present review, we broadly summarize the inflammatory markers that may have potential diagnostic and therapeutic use, thereby translating them into health care for older people with frailty in the near future.

The role of PPAR signaling and its associated genes in the pathogenesis and progression of chronic heart failure (CHF) remains elusive.
We accessed the gene expression profile and relevant baseline information of CHF samples from the Gene Expression Omnibus (GEO) database, specifically from the GSE57338 project.
From GSE57338 project, we derived the expression value of 126 PPAR-related genes. A protein-protein interaction network was then established to illustrate potential protein interactions. ClueGO analysis results revealed that these genes predominantly participate in functions such as export across plasma membrane, regulation of lipid metabolic process, fatty acid metabolism, circulatory system vascular processes, alcohol metabolism, triglyceride metabolism and regulation of lipid localization and response to nutrient. Using the cytohubba plug-in in Cytoscape, we pinpointed ACADM, PPARG and CPT2 as potential central molecules in HF pathogenesis and progression. Subsequent Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis delved into the potential biological role of these three genes in CHF. Immune infiltration analysis suggested that the infiltration level of neutrophils and M2 macrophages might be notably influenced by these genes, thereby playing a role in the CHF mechanism.
Our research provides a comprehensive insight into the significance of PPAR associated genes in CHF development. Notably, the genes ACADM, PPARG and CPT2 emerged as potential targets for clinical interventions.

BACKGROUND: Liver cancer, a common malignancy within the digestive system, presents with a particularly grim prognosis. Within the immune microenvironment, the role of natural killer (NK) cells in liver cancer remains unclear.
METHODS: We sourced data on clinical parameters and gene expressions for liver cancer patients from The Cancer Genome Atlas Program database and carried out all analyses using R software and its relevant codes.
RESULTS: In our research, we delved into the genes intertwined with NK cells in hepatocellular carcinoma (HCC). Leveraging the QUANTISEQ and MCPCOUNTER algorithms to quantify NK cells, we spotlighted genes vital to the recruitment of NK cells. Among these genes, GDE1, WDFY3, DNAJB14, PKD2, DGAT2, SGMS2 and MKNK2 showed a strong correlation with patient outcomes. We also mapped out the single-cell expression trajectories of these genes within the HCC milieu. From our findings, SGMS2 emerged as a key gene warranting further scrutiny. Our in-depth analysis of SGMS2 shed light on its influence over specific biological pathways, its contribution to the immune landscape and its role in genomic instability within HCC. Drawing from this, we formulated a predictive model rooted in SGMS2-associated genes. This model showcased remarkable precision across both training and validation cohorts.
CONCLUSIONS: Overall, our investigation underscored the profound implications of SGMS2, a gene pivotal to NK cell infiltration, in the landscape of HCC, thereby positioning it as a potential linchpin in oncological strategies.

Heparin is a negatively charged polysaccharide with various chain lengths and a hydrophilic backbone. Due to its fascinating chemical and physical properties, nontoxicity, biocompatibility, and biodegradability, heparin has been extensively used in different fields of medicine, such as cardiovascular and hematology. This review highlights recent and future advancements in designing materials based on heparin for various biomedical applications. The physicochemical and mechanical properties, biocompatibility, toxicity, and biodegradability of heparin are discussed. In addition, the applications of heparin-based materials in various biomedical fields, such as drug/gene delivery, tissue engineering, cancer therapy, and biosensors, are reviewed. Finally, challenges, opportunities, and future perspectives in preparing heparin-based materials are summarized.

Aryl hydrocarbon receptor (AHR) is a ligand-dependent receptor that belongs to the superfamily of basic helix-loop-helix (bHLH) transcription factors. The activation of the canonical AHR signaling pathway is known to induce the expression of cytochrome P450 enzymes, facilitating the detoxification metabolism in the human body. Additionally, AHR could interact with various signaling pathways such as epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3), hypoxia-inducible factor-1α (HIF-1α), nuclear factor ekappa B (NF-κβ), estrogen receptor (ER), and androgen receptor (AR) signaling pathways. Over the past 30 years, several studies have reported that various chemical, physical, or biological agents, such as tobacco, hydrocarbon compounds, industrial and agricultural chemical wastes, drugs, UV, viruses, and other toxins, could affect AHR expression or activity, promoting cancer development. Thus, it is valuable to overview how these factors regulate AHR-mediated carcinogenesis. Current findings have reported that many compounds could act as AHR ligands to drive the expressions of AHR-target genes, such as CYP1A1, CYP1B1, MMPs, and AXL, and other targets that exert a pro-proliferation or anti-apoptotic effect, like XIAP. Furthermore, some other physical and chemical agents, such as UV and 3-methylcholanthrene, could promote AHR signaling activities, increasing the signaling activities of a few oncogenic pathways, such as the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways. Understanding how various factors regulate AHR-mediated carcinogenesis processes helps clinicians and scientists plan personalized therapeutic strategies to improve anti-cancer treatment efficacy. As many studies that have reported the roles of AHR in regulating carcinogenesis are preclinical or observational clinical studies that did not explore the detailed mechanisms of how different chemical, physical, or biological agents promote AHR-mediated carcinogenesis processes, future studies should focus on conducting large-scale and functional studies to unravel the underlying mechanism of how AHR interacts with different factors in regulating carcinogenesis processes.

Organic optoelectronic devices have received appreciable attention due to their low cost, mechanical flexibility, band-gap engineering, lightness, and solution processability over a broad area. Specifically, realizing sustainability in organic optoelectronics, especially in solar cells and light-emitting devices, is a crucial milestone in the evolution of green electronics. Recently, the utilization of biological materials has appeared as an efficient means to alter the interfacial properties, and hence improve the performance, lifetime and stability of organic light-emitting diodes (OLEDs). Biological materials can be known as essential renewable bio-resources obtained from plants, animals and microorganisms. The application of biological interfacial materials (BIMs) in OLEDs is still in its early phase compared to the conventional synthetic interfacial materials; however, their fascinating features (such as their eco-friendly nature, biodegradability, easy modification, sustainability, biocompatibility, versatile structures, proton conductivity and rich functional groups) are compelling researchers around the world to construct innovative devices with enhanced efficiency. In this regard, we provide an extensive review of BIMs and their significance in the evolution of next-generation OLED devices. We highlight the electrical and physical properties of different BIMs, and address how such characteristics have been recently exploited to make efficient OLED devices. Biological materials such as ampicillin, deoxyribonucleic acid (DNA), nucleobases (NBs) and lignin derivatives have demonstrated significant potential as hole/electron transport layers as well as hole/electron blocking layers for OLED devices. Biological materials capable of generating a strong interfacial dipole can be considered as a promising prospect for alternative interlayer materials for OLED applications.

Due to their widespread occurrence and detrimental effects on human health and the environment, endocrine-disrupting hazardous chemicals (EDHCs) have become a significant concern. Therefore, numerous physicochemical and biological remediation techniques have been developed to eliminate EDHCs from various environmental matrices. This review paper aims to provide a comprehensive overview of the state-of-the-art remediation techniques for eliminating EDHCs. The physicochemical methods include adsorption, membrane filtration, photocatalysis, and advanced oxidation processes. The biological methods include biodegradation, phytoremediation, and microbial fuel cells. Each technique\'s effectiveness, advantages, limitations, and factors affecting their performance are discussed. The review also highlights recent developments and future perspectives in EDHCs remediation. This review provides valuable insights into selecting and optimizing remediation techniques for EDHCs in different environmental matrices.

Although sleep quality is known to be associated with mortality, how poor sleep quality contributes to an increased risk of mortality is still unknown. We aimed to examine whether lifestyle, psychosocial and biological factors mediate the association.
205,654 participants from UK Biobank were used for the analysis. The outcome was all-cause, cardiovascular disease (CVD) and cancer mortality by February 2022. Exposure was assessed by a sleep score consisting of five sleep behaviors at baseline. Lifestyle, psychosocial, and biological factors are regarded as potential mediators. Mediation analysis based on Cox proportional hazards models was performed.
Poor sleep quality was associated with a higher risk of all-cause (Hazard Ratio [HR] = 1.098; 95% CI: 1.058-1.140), CVD (HR = 1.139; 95% CI: 1.045-1.243) and cancer mortality (HR = 1.095; 95% CI: 1.040-1.152). Lifestyle mediators (smoking, physical activity, sedentary, BMI and diet) could explain between 2.6% and 34.0% of the increased risk of all-cause mortality in individuals with poor sleep quality. Self-reported health, frailty, depression, and loneliness were significant psychosocial mediators of this association pathway. About one-fifth of the association can be explained by the biological role of CRP. Similar mediating patterns were observed for CVD and cancer mortality.
Both exposure and mediators were measured at baseline, so the possibility of reverse causality cannot be ruled out.
Poor sleep quality is associated with an increased risk of death through a combination of lifestyle, psychosocial and biological pathways. Adopting healthy lifestyles and staying psychosocial well-being are cost-effective interventions to lower the risk of death.