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A self-powered system based on energy harvesting technology can be a potential candidate for solving the problem of supplying power to electronic devices. In this review, we focus on portable and wearable self-powered systems, starting with typical energy harvesting technology, and introduce portable and wearable self-powered systems with sensing functions. In addition, we demonstrate the potential of self-powered systems in actuation functions and the development of self-powered systems toward intelligent functions under the support of information processing and artificial intelligence technologies.

Acute myeloid leukemia (AML) is a major leukemia with high mortality. Ferroptosis is an important regulator of cancers. However, the role of ferroptosis and its regulatory mechanisms in AML remain largely unknown. In this study, we reported elevated brain and muscle ARNT‐Like protein‐1 (Bmal1) expression in AML patients and cell lines, and its upregulation indicated the poor survival of patients. The correlation analysis showed that Bmal1 expression was closely correlated with cytogenetics and the French–American–British subtypes, but was not correlated with age, gender and white blood cells. RSL3 reduced Bmal1 expression in HL‐60 and NB4 cells. Malondialdehyde, total iron, Fe2+, glutathione and lipid peroxidation were examined to evaluate ferroptosis. Overexpression of Bmal1 repressed RSL3‐induced ferroptosis in AML cells. Bmal1 recruited Enhancer of zeste homolog 2 (EZH2) to the Early B cell factor 3 (EBF3) promoter and enhanced its methylation, thus suppressing EBF3 expression. Moreover, the knockdown of Bmal1 sensitized AML cells to RSL3‐induced ferroptosis, and it was counteracted by EBF3 knockdown. Furthermore, EBF3 bound to the Arachidonate 15‐pipoxygenase (ALOX15) promoter to enhance its expression, and overexpression of EBF3 enhanced RSL3‐induced ferroptosis dependent on ALOX5. We established a subcutaneous AML xenograft tumor model and reported that knockdown of Bmal1 and overexpression of EBF3 restrained AML growth by promoting ALOX15‐mediated ferroptosis in vivo. Collectively, Bmal1 inhibits RSL3‐induced ferroptosis by promoting EZH2‐mediated EBF3 methylation and suppressing the expression of EBF3 and ALOX15, thus accelerating AML. Bmal1 inhibits RSL3‐induced ferroptosis by promoting EZH2‐mediated EBF3 methylation and suppressing the expression of EBF3 and ALOX15, thus accelerating AML.

Tumor cells possess complex immune evasion mechanisms to evade immune system attacks, primarily through metabolic reprogramming, which significantly alters the tumor microenvironment (TME) to modulate immune cell functions. When a tumor is sufficiently immunogenic, it can activate cytotoxic T-cells to target and destroy it. However, tumors adapt by manipulating their metabolic pathways, particularly glucose, amino acid, and lipid metabolism, to create an immunosuppressive TME that promotes immune escape. These metabolic alterations impact the function and differentiation of non-tumor cells within the TME, such as inhibiting effector T-cell activity while expanding regulatory T-cells and myeloid-derived suppressor cells. Additionally, these changes lead to an imbalance in cytokine and chemokine secretion, further enhancing the immunosuppressive landscape. Emerging research is increasingly focusing on the regulatory roles of non-tumor cells within the TME, evaluating how their reprogrammed glucose, amino acid, and lipid metabolism influence their functional changes and ultimately aid in tumor immune evasion. Despite our incomplete understanding of the intricate metabolic interactions between tumor and non-tumor cells, the connection between these elements presents significant challenges for cancer immunotherapy. This review highlights the impact of altered glucose, amino acid, and lipid metabolism in the TME on the metabolism and function of non-tumor cells, providing new insights that could facilitate the development of novel cancer immunotherapies.

The CCL2-CCR2 axis is one of the major chemokine signaling pathways that has received special attention because of its function in the development and progression of cardiovascular disease. Numerous investigations have been performed over the past decades to explore the function of the CCL2-CCR2 signaling axis in cardiovascular disease. Laboratory data on the CCL2-CCR2 axis for cardiovascular disease have shown satisfactory outcomes, yet its clinical translation remains challenging. In this article, we describe the mechanisms of action of the CCL2-CCR2 axis in the development and evolution of cardiovascular diseases including heart failure, atherosclerosis and coronary atherosclerotic heart disease, hypertension and myocardial disease. Laboratory and clinical data on the use of the CCL2-CCR2 pathway as a targeted therapy for cardiovascular diseases are summarized. The potential of the CCL2-CCR2 axis in the treatment of cardiovascular diseases is explored.

As a common disease in the elderly, the diagnosis of Alzheimer's disease (AD) is of great significance to the treatment and prognosis of the patients. Studies have found that magnetic resonance imaging plays an important role in the early diagnosis of Alzheimer's disease. This article tries to review the application of magnetic resonance imaging in the diagnosis and differential diagnosis of Alzheimer's disease.

The immune system plays a central role in anticancer defense by coordinating antitumor responses that inhibit the initiation, progression, and metastasis of malignancies. Emerging evidence underscores the crucial interplay between regulated cell death (RCD) pathways and immune activation, particularly immunogenic cell death (ICD). ICD refers to a specific form of regulated cell death in which tumor cells undergo death and release damage-associated molecular patterns (DAMPs) and other signaling molecules, thereby reshaping the tumor immune microenvironment (TIME). While the canonical RCD pathways are well-established, the inducers of ICD, the spatiotemporal regulation of TIME dynamics, and the functional states of immune cells remain incompletely understood. We thoroughly evaluated contemporary therapeutic approaches that exploit the mechanisms of RCD-driven immunomodulatory effects, including strategies to potentiate ICD and amplify antitumor immune responses. The novelty of this review lies in its dual perspective: delineating how tumor-intrinsic death programs reprogram the tumor TIME and how immune-cell death directly dictates its polarization toward immunostimulatory versus immunosuppressive states, ultimately shaping therapeutic outcomes. We analyzed in depth how different forms of RCD shape antigen presentation, guide immune cell infiltration, and affect checkpoint signaling, underscoring their dual potential to support or hinder antitumor responses. Furthermore, we summarized the current landscape of ICD-inducing interventions, including chemotherapy, radiotherapy, oncolytic viruses, tumor vaccines, and nanotechnology-based platforms, underscoring their potential to convert immunologically “cold” tumors into “hot” ones and to synergize with immune checkpoint blockade. In addition, we highlighted promising combination strategies aimed at directly modulating immune cell death pathways to sustain effector cell function and overcome exhaustion, offering novel insights for the development of next-generation precision immunotherapies. By delineating the crosstalk between tumor/immune cell death pathways, this study provides a roadmap for developing precise immunotherapies that exploit RCD-TIME interactions to overcome treatment resistance.

The dissipative particle dynamics simulation method is adopted to investigate the microemulsion systems prepared with surfactant (H1T1), oil (O) and water (W), which are expressed by coarse-grained models. Two topologies of O/W and W/O microemulsions are simulated with various oil and water ratios. Inverse W/O microemulsion transform to O/W microemulsion by decreasing the ratio of oil-water from 3:1 to 1:3. The stability of O/W and W/O microemulsion is controlled by shear rate, inorganic salt and the temperature, and the corresponding results are analyzed by the translucent three-dimensional structure, the mean interfacial tension and end-to-end distance of H1T1. The results show that W/O microemulsion is more stable than O/W microemulsion to resist higher inorganic salt concentration, shear rate and temperature. This investigation provides a powerful tool to predict the structure and the stability of various microemulsion systems, which is of great importance to developing new multifunctional microemulsions for multiple applications.

Single‐atomic transition metal–nitrogen–carbon (M–N–C) structures are promising alternatives toward noble‐metal‐based catalysts for oxygen reduction reaction (ORR) catalysis involved in sustainable energy devices. The symmetrical electronic density distribution of the M─N 4 moieties, however, leads to unfavorable intermediate adsorption and sluggish kinetics. Herein, a Fe–N–C catalyst with electronic asymmetry induced by one nearest carbon vacancy adjacent to Fe─N 4 is conceptually produced, which induces an optimized d‐band center, lowered free energy barrier, and thus superior ORR activity with a half‐wave potential ( E 1/2 ) of 0.934 V in a challenging acidic solution and 0.901 V in an alkaline solution. When assembled as the cathode of a Zinc–air battery (ZAB), a peak power density of 218 mW cm −2 and long‐term durability up to 200 h are recorded, 1.5 times higher than the noble metal‐based Pt/C+RuO 2 catalyst. This work provides a new strategy on developing efficient M–N–C catalysts and offers an opportunity for the real‐world application of fuel cells and metal–air batteries.

Background The occurrence and progression of asthma can be influenced by the components in food. Our study aims to determine whether dietary antioxidant and inflammatory potential are associated with the risk of mortality in asthma patients. Methods Participants from the 2001–2018 National Health and Nutrition Examination Survey (NHANES) aged 20 years and older with a diagnosis of asthma were included. Mortality status was obtained according to death certificate records from the National Death Index. The antioxidant and inflammatory potential of the diet was assessed using two widely used and dependable indices, Composite Dietary Antioxidant Index (CDAI) and Dietary Inflammatory Index (DII). Restricted cubic spline (RCS) regression was used to analyze the non-linear relationship between the two indexes and mortality. Multivariable Cox proportional risk models were used to estimate hazard ratio and 95% confidence intervals for mortality. Finally, the relationship between CDAI and DII was analyzed. Results A total of 4698 NHANES participants represented 23.2 million non-institutionalized residents of the US were enrolled in our study. Patients with higher CDAI or lower DII exhibited longer survival times. RCS regression showed a linear relationship of CDAI or DII with mortality. In the Cox regression, both crude and adjusted models demonstrated that higher CDAI or lower DII was linked to a reduced risk of all-cause mortality. Similar associations were found in subgroup analysis. Finally, a negative relationship was found between CDAI and DII. Conclusion Reducing pro-inflammatory or increasing antioxidant diets could reduce all-cause mortality among adult asthma patients.

Rockfall, as a common geological hazard, exhibits extremely complex impact dynamic behaviors that are significantly influenced by factors like the impact falling height and the composition of soil layers. To this end, this paper initially establishes a three-dimensional impact model of falling rock based on the DEM-FDM, which takes into account the near-field impact effect. In this model, the near-field DEM of the soil-rock mixture considers the spatial configuration of rock blocks, while the far-field FDM is employed to analyze the mechanical response of impact. On this basis, numerical analyses are conducted on the impact dynamic response of falling rock and the failure mechanism of soil-rock mixture at different falling heights, followed by series of parametric sensitivity analyses. The results indicate that the impact dynamic response of falling rock and the failure degree of soil-rock mixture increase significantly with the falling height, yet the failure mode remains consistent. The increase in particle stiffness reduces the dynamic amplification factor, exacerbating the failure degree of the model along with the energy dissipation through friction and damping. The increase in particle strength elevates the dynamic amplification factor and mitigates the degree of failure of the model as well as energy dissipation through friction and damping. Moreover, there is a threshold effect for the influence of the proportion of rock block on the dynamic behavior of the soil-rock mixture, but the variation of all three parameters exerts no effect on the failure mode resulting from rockfall impact against the soil-rock mixture. These findings contribute to a better understanding and prediction of the impact-collision of rockfall on soil-rock mixture.