The use of waste-based biomaterials for energy harvesting is a new frontier in triboelectric nanogenerator (TENG) research and self-powered sensing systems. In this study, we demonstrate a triboelectric interface based on jamun seed powder embedded in an ethylene-vinyl acetate (EVA) polymer matrix for handwriting recognition. Jamun seed waste contains cellulose, lignin, polyphenols, and oxygenated functional groups, which contribute to the accumulation of surface charge during contact electrification. The optimal peak-to-peak output voltage and current of the EVA-JB composite at 15 wt% filler (EVA-JB15 abbreviated) loading was 260 V and 1500 nA, respectively. XRD- and FTIR-based structural evaluation showed that the filler was successfully incorporated into the EVA matrix without disturbing the basic semicrystalline polymer structure. The composite has an increased dielectric constant (∼4.55 at 10 kHz), suggesting higher charge storage capacity and interfacial polarisation than the pure EVA. The produced TENG exhibited a maximum power of 78.125 μW at the 200 MΩ external load resistance. A convolutional neural network (CNN) model was trained using TENG-derived handwriting signals from five individuals and obtained an overall classification accuracy of 99.18%. This study opens a possible path towards triboelectric interfaces for advanced self-powered sensing.
Epigenetic deregulation is a defining feature of cancer, and histone modification remodeling plays a central role in reshaping malignant transcriptional programs. Histone marks collectively organize chromatin states that govern enhancer activity, promoter competence, and stability of repressive domains. Across diverse tumor types, redistribution of active and repressive histone modifications reconfigures regulatory landscapes that sustain oncogenic amplification, lineage plasticity, and adaptive resistance. In this review, we examine histone mark remodeling in cancer through an enhancer-centered perspective. We discuss how the gain of H3K27ac-marked enhancers, super-enhancer formation, the erosion of lineage-restrictive regulatory elements, and the redistribution of repressive marks cooperate to reorganize transcriptional circuitry. We further outline the convergent mechanisms driving these alterations, including mutations in chromatin regulators, signal-dependent modulation of epigenetic enzymes, metabolic influences on chromatin state, and changes in three-dimensional genome architecture. The functional consequences of histone mark reprogramming, ranging from cell state transitions and tumor heterogeneity to transcriptional dependency and therapy-associated chromatin adaptation, are considered in the context of tumor evolution. Finally, we highlight emerging single-cell, spatial, and integrative multi-omics approaches that enable systems-level interpretation of chromatin landscapes and identification of context-specific vulnerabilities. By framing histone modification dynamics in terms of enhancer reconfiguration, this review provides a mechanistic and translational perspective on how chromatin remodeling sustains malignant identity and offers opportunities for therapeutic intervention.
Black phosphorus (BP) exhibits net opposite pseudospin polarizations for the electron and hole states. The pseudospin structure of BP causes a selectivity in the optical excitation engaging the symmetry between the optical pump polarization and the pseudospin state, which is confirmed in a simulation of the time-resolved angle-resolved photoemission spectroscopy (tr-ARPES). Further, the pseudospin selectivity is found to drive a unique polarimetric singularity in the high-harmonic generation (HHG). Given the nth-order high-harmonic signal, we reveal that the singularity arises predominantly through the multiphoton interband pathway and thereby becomes markedly substantial at n omega pump >= Eg. omega pump is the pump photon energy and Eg the energy gap of BP. This permits a coherent understanding of the pseudospin selectivity from tr-ARPES to HHG. In particular, the pseudospin-selective polarimetric singularity suggests a potential for the pseudospintronics to be integrated into the intrinsic dynamics due to the light-matter interaction in two-dimensional materials.
The excessive dependence on synthetic materials in our daily lives is increasing continuously, which has resulted in marine debris. The dependency on these materials has raised a serious concern for aquatic ecosystems. This study focuses on addressing the serious issue of the remediation of synthetic debris in marine environments by exploring the ability of algae to decompose polymers. Microalgae have the ability to break down plastic by producing special chemicals (toxins) and enzymes. These enzymes aid in the breakdown of the synthetic polymers into smaller pieces, and the carbon from these materials is eaten by the algae as a food source to support their growth. The main objective of this study is to identify low-impact algae species that are capable of reducing marine debris with minimal disruption to marine life through an integrated hybrid fuzzy multi-criteria decision making (F-MCDM) framework. A case study is shown to illustrate the most effective marine-friendly algae for handling synthetic debris. The proposed study develops methods to deal with uncertain and ambiguous information using the q-rung Fuzzy Set and the Linear Diophantine Fuzzy Set (LDFS). Chlorella vulgaris was ranked top according to the selection parameters out of the criteria and alternatives that were evaluated. The feasibility, reliability, and system’s stability are validated through comparative and sensitivity assessments, emphasizing the applicability of this multi-criteria decision making approach to similar challenges in various circumstances. This study paves the way for environmental researchers, policymakers, and marine conservationists to implement algae-based bioremediation strategies on a broader scale.
BACKGROUND:Mutations in isocitrate dehydrogenase 1 (IDH1) are hallmark features of diffuse gliomas and drive extensive metabolic and epigenetic reprogramming through accumulation of the oncometabolite 2-hydroxyglutarate (2-HG). However, the downstream transcriptional programs and chromatin-based mechanisms linking mutant IDH1 to oncogenic signaling remain incompletely understood. OBJECTIVE:This study aimed to define transcriptional changes associated with the IDH1 R132H mutation and to determine how epigenetic mechanisms influence KRAS-associated gene expression. METHODS:We analyzed transcriptomic data from the TCGA-LGG cohort and public RNA-seq datasets to identify differentially expressed genes and enriched pathways. Key findings were validated using qRT-PCR in cellular models expressing IDH1 R132H. To assess epigenetic regulation, we performed knockdown experiments targeting the H3K36 methyltransferases SETD2 and SMYD5. RESULTS:Integrated transcriptomic analyses revealed consistent enrichment of KRAS signaling-related gene signatures in IDH1 R132H tumors and cell models. qRT-PCR validation confirmed altered expression of key KRAS-associated genes involved in immune response, extracellular matrix remodeling, and tumor-related processes. Notably, the knockdown of SETD2 or SMYD5 significantly reduced the expression of these genes, indicating that H3K36 methylation-associated chromatin regulation contributes to their transcriptional activation. CONCLUSION:These findings demonstrate that mutant IDH1 promotes KRAS-associated transcriptional programs, at least in part, through epigenetic mechanisms involving H3K36 methylation-dependent chromatin regulation in glioma.
