
ABSTRACT Biological, molecular, and functional states evolve across multiple timescales, limiting the utility of conventional diagnostics based on isolated measurements. This Perspective introduces on‐chip biomimetic intelligence as an integrated approach combining biomimetic molecular recognition and signal transduction with dynamic sensing, adaptive local computation, and longitudinal interpretation of molecular changes. It focuses on multiplexed molecular‐affinity measurements of selected disease‐associated protein panels, coupled with event‐driven signal processing to reduce redundant data generation. Where appropriate, sensing outputs may inform patient‐specific digital twin models and dynamically update PBPK or PK–PD models. Rather than treating intelligent biosensors, neuromorphic biosensing, edge AI, and digital twins as isolated technologies, it integrates their functions and describes architectural and functional requirements for chip‐level biomimetic intelligence. Implementation requires regenerable molecular–recognition interfaces, reliable molecular‐to‐signal transduction, and computational methods capable of estimating protein states and temporal trajectories. Causal validation and constrained closed‐loop control may support clinically relevant decision‐making when sufficient evidence is available. However, complete architecture has not yet been demonstrated as a single clinically validated system. Its realization requires advances in sensing stability, biocompatibility, antifouling performance, calibration, drift control, and clinical validation. Thus, biosensing shifts from static biomarker detection to longitudinal, adaptive, and clinically interpretable monitoring of changes in biological state.
ABSTRACT Diabetic neuropathy (DN) remains a debilitating complication of diabetes, characterized by chronic pain and progressive nerve damage. While current therapies often fall short, curcumin has emerged as a potent therapeutic candidate due to its pleiotropic pharmacological profile. This review evaluates the neuroprotective potential of curcumin, focusing on its ability to mitigate oxidative stress and systemic inflammation by modulating key signaling hubs, including Nrf2, MAPK, and NF‐κB. Preclinical evidence suggests that curcumin not only stabilizes glucose metabolism but also modulates the molecular pathways responsible for nerve degradation. However, its therapeutic translation is frequently limited by poor aqueous solubility and low bioavailability. We therefore highlight recent breakthroughs in nano‐drug delivery systems and novel formulations designed to enhance its metabolic stability. By synthesizing the latest mechanistic insights and delivery innovations, this review positions curcumin as a vital component in future integrative strategies for treating diabetic neuropathy.
ABSTRACT Discovering lead compounds from complex natural matrices traditionally requires resource‐intensive isolation steps. Integrating computational biology with untargeted metabolomics offers a more efficient alternative for rapid target prediction and screening. Here, we present a computational pipeline combining LC–MS/MS metabolomics, network pharmacology, and molecular docking to identify bioactive scaffolds. We applied this approach to the methanolic extract of the Antarctic moss Chorisodontium aciphyllum as a model matrix. Profiling the bioactive fraction (Fr.3) identified 17 secondary metabolites, primarily featuring fatty acid and steroidal scaffolds. Network pharmacology and functional annotation predicted ERBB2 and AKT1 as key protein targets for anti‐lung cancer activity. Molecular docking supported these predictions, showing that steroidal and secosteroidal compounds such as 5α‐ergosta‐7,22‐diene‐3β,5‐diol and 25‐hydroxyvitamin D2 exhibit high binding affinities to these targets. As a preliminary in vitro validation of the computationally predicted pathways, we found that Fr.3 significantly increased intracellular reactive oxygen species (ROS) levels and induced apoptosis‐mediated cell death in LLC1 murine lung cancer cells (IC 50 ≈ 45.79 µg/mL). Our findings demonstrate that combining untargeted metabolomics with computational analysis can effectively streamline the discovery of therapeutic leads from uncharacterized natural extracts.
ABSTRACT Purple sweet potato is rich in acylated anthocyanins that exhibit pH‐dependent color changes, making it a promising natural indicator for smart packaging. In this study, purple sweet potato powders were prepared by steaming and freeze‐drying, which retained the anthocyanin, phenolic, and antioxidant contents. Purple sweet potato was combined with PVA at a ratio of 75% to create a film capable of changing color due to the properties of anthocyanins. The physicochemical properties of the film included a thickness of 210 um, moisture 3.53%, solubility of 50.99%, swelling of 237.53%, water permeability of 9.77 g/s.cm, TPC of 10.94 mg/g, TFC of 4.78 mg/g, and TAC of 3 mg/g. When applied to the pork sample, the polyvinyl alcohol/purple sweet potato film at 75% signaled a color change from pink to blue, indicating increased mold bacteria and yeast concentrations. These findings highlight the feasibility of polyvinyl alcohol/purple sweet potato films as biodegradable, pH‐responsive smart packaging materials for monitoring meat quality.
ABSTRACT The increase in global life expectancy has resulted in a significant rise in the occurrence of Alzheimer's disease (AD), making it a critical public health burden. Therefore, there is an urgent need to create effective methods to prevent or slow down the progression of the disease. In this regard, fifteen previously reported hybrid molecules ( 7a–c , 10a–j , and 13a,b ), combining 4‐hydroxycoumarin and pyrazolyl indolin‐2‐one structures, were resynthesized and tested for their antioxidant and anti‐Alzheimer properties. Several of these compounds showed moderate to strong biological activity. Among these, compound 7a demonstrated excellent antioxidant capacity (TAC = 80.65 mg gallic acid/g; IRP = 68.90 µg/mL) and impressive free radical scavenging abilities (DPPH = 5.33 µg/mL; ABTS = 4.59 µg/mL; NO = 6.76 µg/mL), comparable to the standard antioxidant ascorbic acid. Additionally, compound 7a demonstrated the robust inhibition of acetylcholinesterase (AChE) with an IC 50 of 6.89 µg/mL, as well as potent inhibition of butyrylcholinesterase (BChE) (IC 50 = 5.93 µg/mL). Molecular docking analyses of compound 7a revealed favorable binding interactions and stable conformations within the enzyme's active site, supporting its strong inhibitory effect. Overall, these findings indicate that this group of hybrid molecules offers a promising framework for developing new cholinesterase‐targeting treatments for AD.