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Heavy metal pollution has become more and more serious with industrial development and resource exploitation. Because heavy metal ions are difficult to be biodegraded, they accumulate in the human body and cause serious threat to human health. However, the conventional methods to detect heavy metal ions are more strictly to the requirements by detection equipment, sample pretreatment, experimental environment, etc. Aptasensor has the advantages of strong specificity, high sensitivity and simple preparation to detect small molecules, which provides a new direction platform in the detection of heavy metal ions. This paper reviews the selection of aptamers as target for heavy metal ions since the 21th century and aptasensors application for detection of heavy metal ions that were reported in the past five years. Firstly, the selection methods for aptamers with high specificity and high affinity are introduced. Construction methods and research progress on sensor based aptamers as recognition element are also introduced systematically. Finally, the challenges and future opportunities of aptasensors in detecting heavy metal ions are discussed.

While hydrogel-based flexible sensors find extensive applications in fields such as medicine and robotics, their performance can be hindered by the rapid evaporation of water, leading to diminished sensitivity and mechanical durability. Despite the exploration of some effective solutions, such as introducing organic solvents, electrolytes, and elastomer composites, these approaches still suffer from problems including diminished conductivity, interface misalignment, and insufficient protection under dynamic conditions. Inspired by cell membrane structures, we developed an adaptive lipid-integrated bilayer coating (ALIBC) to enhance water retention in hydrogel-based sensors. Lipid layers and long-chain amphiphilic molecules are used as compact coating and anchoring agents on the hydrogel surface, mimicking the roles of lipids and membrane proteins in cell membranes, while spare lipids from aggregates within hydrogels can migrate to the surface to combat dehydration under deformation. This lipid-integrated bilayer coating prevents the water evaporation of hydrogels at both static and dynamic states without affecting the inherent flexibility, conductivity, and no cytotoxicity. Hydrogel-based sensors with ALIBC exhibited significantly enhanced performance in conditions of body temperature, extensive deformation, and long-term dynamic sensing. This work presents a general approach for precisely controlling the water-retaining capacity of hydrogels and hydrogel-based sensors without compromising their intrinsic physical properties. Hydrogel-based flexible sensors have potential in a number of fields, but mechanical properties can be compromised as a result of water evaporation. Here, the authors report a method for limiting of water loss by addition of a lipid-based coating to the surface of the hydrogel.

Background Exosomes from cancer cells or immune cells, carrying bio-macromolecules or microRNAs (miRNAs), participate in tumor pathogenesis and progression by modulating microenvironment. Our study aims to investigate the role of these microRNA-501-3p (miR-501-3p) containing exosomes derived from tumor-associated macrophage (TAM) in the progression of pancreatic ductal adenocarcinoma (PDAC). Methods Firstly, the function of TAM recruitment in PDAC tissues was assessed, followed by identification of the effects of M2 macrophage-derived exosomes on PDAC cell activities and tumor formation and metastasis in mice. In silico analysis was conducted to predict differentially expressed genes and regulatory miRNAs related to PDAC treated with macrophages, which determined miR-501-3p and TGFBR3 for subsequent experiments. Next, gain- and loss-of-function experiments were performed to examine their role in PDAC progression with the involvement of the TGF-β signaling pathway. Results TAM recruitment in PDAC tissues was associated with metastasis. Highly expressed miR-501-3p was observed in PDAC tissues and TAM-derived exosomes. Both M2 macrophage-derived exosomes and miR-501-3p promoted PDAC cell migration and invasion, as well as tumor formation and metastasis in nude mice. MiR-501-3p was verified to target TGFBR3. PDAC cells presented with down-regulated TGFBR3, which was further decreased in response to M2 macrophage treatment. TGF-β signaling pathway activation was implicated in the promotion of miR-501-3p in PDAC development. The suppression of macrophage-derived exosomal miR-501-3p resulted in the inhibition of tumor formation and metastasis in vivo. Conclusion M2 macrophage-derived exosomal miR-501-3p inhibits tumor suppressor TGFBR3 gene and facilitates the development of PDAC by activating the TGF-β signaling pathway, which provides novel targets for the molecular treatment of PDAC.

Long noncoding RNAs (lncRNAs) play crucial roles in tumor progression and are aberrantly expressed in various cancers. However, the functional roles of lncRNAs in breast cancer remain largely unknown. Based on public databases and integrating bioinformatics analyses, the overexpression of lncRNA BCRT1 in breast cancer tissues was detected and further validated in a cohort of breast cancer tissues. The effects of lncRNA BCRT1 on proliferation, migration, invasion and macrophage polarization were determined by in vitro and in vivo experiments. Luciferase reporter assay and RNA immunoprecipitation (RIP) were carried out to reveal the interaction between lncRNA BCRT1, miR-1303, and PTBP3. Chromatin immunoprecipitation (ChIP) and RT-PCR were used to evaluate the regulatory effect of hypoxia-inducible factor-1α (HIF-1α) on lncRNA BCRT1. LncRNA BCRT1 was significantly upregulated in breast cancer tissues, which was correlated with poor prognosis in breast cancer patients. LncRNA BCRT1 knockdown remarkably suppressed tumor growth and metastasis in vitro and in vivo. Mechanistically, lncRNA BCRT1 could competitively bind with miR-1303 to prevent the degradation of its target gene PTBP3, which acts as a tumor-promoter in breast cancer. LncRNA BCRT1 overexpression could promote M2 polarization of macrophages, mediated by exosomes, which further accelerated breast cancer progression. Furthermore, lncRNA BCRT1 was upregulated in response to hypoxia, which was attributed to the binding of HIF-1α to HREs in the lncRNA BCRT1 promoter. Collectively, these results reveal a novel HIF-1α/lncRNA BCRT1/miR-1303/PTBP3 pathway for breast cancer progression and suggest that lncRNA BCRT1 might be a potential biomarker and therapeutic target for breast cancer.

Evidence has indicated that M2 macrophages promote the progression of cancers, but few focus on the ability of M2 macrophage‐derived exosomes in pancreatic cancer (PC). This study aims to explore how M2 macrophages affect malignant phenotypes of PC through regulating long non‐coding RNA SET‐binding factor 2 antisense RNA 1 (lncRNA SBF2‐AS1)/microRNA‐122‐5p (miR‐122‐5p)/X‐linked inhibitor of apoptosis protein (XIAP) axis. THP‐1 cells were transformed into M1 macrophages by lipopolysaccharide and interferon‐γ treatment, and into M2 macrophages after interleukin‐4 treatment. The PANC‐1 PC cell line with the largest lncRNA SBF2‐AS1 expression was selected, and M2 macrophage‐derived exosomes were isolated and identified. A number of assays were applied for the examination of lncRNA SBF2‐AS1 expression, PC cell biological functions and subcellular localization of lncRNA SBF2‐AS1. XIAP expression was detected, along with the interaction among lncRNA SBF2‐AS1, miR‐122‐5p and XIAP. M2 macrophage exosomal lncRNA SBF2‐AS1 expression's effects on the tumorigenic ability of PANC‐1 cells in nude mice were also investigated. M2 macrophage‐derived exosomes promoted progression of PC cells. Overexpressed lncRNA SBF2‐AS1 promoted progression of PC cells. LncRNA SBF2‐AS1 was found to act as a competing endogenous RNA to repress miR‐122‐5p and up‐regulate XIAP. Constrained lncRNA SBF2‐AS1 in M2 macrophage‐derived exosomes contributed to restraining tumorigenic ability of PC cells. Collectively, our study reveals that constrained lncRNA SBF2‐AS1 in M2 macrophage‐derived exosomes increases miR‐122‐5p expression to restrain XIAP expression, which further inhibits PC progression.

Cancer remains one of the leading causes of mortality, posing a significant threat to human health and consistently serving as a focal point for scientific research. In recent years, immunotherapy has garnered increasing attention as a promising approach to cancer treatment, leading to substantial improvements in patient outcomes. Among the various immunotherapeutic strategies, tumor vaccines have emerged as a particularly innovative field. Research on tumor vaccines has focused on improving their immunogenicity and safety, aiming to elicit stronger and more durable antitumor immune responses. Probiotics, as bacteria that are “foreign” to the body, can induce a variety of beneficial responses and stimulate numerous positive biological effects, holding significant promise in the field of immunotherapy. Research on probiotic-based tumor vaccines has illustrated the unique advantages of in situ vaccines, neoantigenic vaccines, and oral vaccines with specific routes of administration, each of which has its own advantages. Owing to advancements in biosynthetic technologies and the inherent plasticity of probiotics, probiotics can be used as carriers or components that offer safety benefits and a range of health-promoting effects. Moreover, accumulating evidence suggests that probiotic-based tumor vaccines may be even more effective when combined with other therapeutic modalities, such as radiation therapy. Graphical Abstract

Chemoresistance is one of the major causes of therapeutic failure and poor prognosis for breast cancer patients, especially for triple-negative breast cancer patients. However, the underlying mechanism remains elusive. Here, we identified novel functional roles of heat shock protein beta-1 (HSPB1), regulating chemoresistance and ferroptotic cell death in breast cancer. Based on TCGA and GEO databases, HSPB1 expression was upregulated in breast cancer tissues and associated with poor prognosis of breast cancer patients, which was considered an independent prognostic factor for breast cancer. Functional assays revealed that HSPB1 could promote cancer growth and metastasis in vitro and in vivo. Furthermore, HSPB1 facilitated doxorubicin (DOX) resistance through protecting breast cancer cells from drug-induced ferroptosis. Mechanistically, HSPB1 could bind with Ikβ-α and promote its ubiquitination-mediated degradation, leading to increased nuclear translocation and activation of NF-κB signaling. In addition, HSPB1 overexpression led to enhanced secretion of IL6, which further facilitated breast cancer progression. These findings revealed that HSPB1 upregulation might be a key driver to progression and chemoresistance through regulating ferroptosis in breast cancer while targeting HSPB1 could be an effective strategy against breast cancer.

Biotic and abiotic stress factors are pivotal considerations in agriculture due to their potential to cause crop losses, food insecurity, and economic repercussions. Zinc oxide nanoparticles (ZnO nanoparticles) have gained substantial attention from researchers worldwide for their capacity to alleviate the detrimental impacts of both biotic and abiotic stress on plants, concurrently reducing dependence on environmentally harmful chemicals. This article provides an overview of methods for synthesizing ZnO nanoparticles, encompassing physical vapor deposition, ball milling, hydrothermal methods, solvothermal methods, precipitation methods, microwave methods, microbial synthesis, and plant-mediated synthesis. Additionally, it delves into the absorption, translocation, and biotransformation pathways of ZnO nanoparticles within plants. The emphasis lies in elucidating the potential of ZnO nanoparticles to safeguard plants against biotic and abiotic stress, enhance plant performance, and modulate various plant processes. The article also offers a preliminary exploration of the mechanisms underlying plant stress tolerance mediated by ZnO nanoparticles. In conclusion, ZnO nanoparticles present an environmentally friendly and cost-effective strategy for plant stress management, paving the way for the integration of nanotechnology in sustainable agriculture. This opens new possibilities for leveraging nanotechnology to bolster plant resilience against stress in the ever-changing climate conditions, ensuring global food security.

Highly efficient removal of bilirubin from blood by hemoperfusion for liver failure therapy remains a challenge in the clinical field due to the low adsorption capacity and slow adsorption kinetics of currently used bilirubin adsorbents (e.g., activated carbon and ion‐exchange resin). Recently, porous aromatic frameworks (PAFs) with high surface areas, tunable structures, and remarkable stability provide numerous possibilities to obtain satisfying adsorbents. Here, a cationic PAF with more mesopores, named iPAF‐6, is successfully constructed via a de novo synthetic strategy for bilirubin removal. The prepared iPAF‐6 exhibits a record‐high adsorption capacity of 1249 mg g−1 and can adsorb bilirubin from 150 mg L−1 to normal concentration in just 5 min. Moreover, iPAF‐6 shows a removal efficiency of 96% toward bilirubin in the presence of 50 g L−1 bovine serum albumin. It is demonstrated that positively charged aromatic frameworks and large pore size make a significant contribution to its excellent adsorption ability. More notably, iPAF‐6/polyethersulfone composite fibers or beads are fabricated for practical hemoperfusion adsorption, which also show better removal performance than commercial adsorbents. This work can offer a new possibility for designing PAF‐based bilirubin adsorbents with an appealing application prospect. Cationic porous aromatic framework with more mesopores (iPAF‐6) is synthesized through the targeted design for highly efficient removal of bilirubin. The iPAF‐6 exhibits fast and high bilirubin uptake with a record‐high adsorption capacity of 1249 mg g−1. In addition, iPAF‐6/polyethersulfone composite fibers or beads show promising potential in practical hemoperfusion applications.

Glioblastoma-derived exosomes (GDEs), containing nucleic acids, proteins, fatty acids and other substances, perform multiple important functions in glioblastoma microenvironment. Tumor-derived exosomes serve as carriers of fatty acids and induce a shift in metabolism towards oxidative phosphorylation, thus driving immune dysfunction of dendritic cells (DCs). Lipid peroxidation is an important characteristic of ferroptosis. Nevertheless, it remains unclear whether GDEs can induce lipid accumulation and lipid oxidation to trigger ferroptosis in DCs. In our study, we investigate the impact of GDEs on lipid accumulation and oxidation in DCs by inhibiting GDEs secretion through knocking down the expression of Rab27a using a rat orthotopic glioblastoma model. The results show that inhibiting the secretion of GDEs can reduce lipid accumulation in infiltrating DCs in the brain and decrease mature dendritic cells (mDCs) lipid peroxidation levels, thereby suppressing glioblastoma growth. Mechanistically, we employed in vitro treatments of bone marrow-derived dendritic cells (BMDCs) with GDEs. The results indicate that GDEs decrease the viability of mDCs compared to immature dendritic cells (imDCs) and trigger ferroptosis in mDCs via the NRF2/GPX4 pathway. Overall, these findings provide new insights into the development of immune-suppressive glioblastoma microenvironment through the interaction of GDEs with DCs.