Search Results (537)

Obesity is a significant risk factor for metabolic diseases and atherosclerotic cardiovascular disease (ASCVD). Exercise exerts beneficial effects partly through myokines secreted by skeletal muscle. This narrative review summarizes current evidence on exercise-induced myokines in obesity. We searched PubMed, Scopus, and Google Scholar up to Jan 2026 using keywords “myokines”, “obesity”, “resistance training”, “aerobic exercise”, and “HIIT”. We focused on six myokines (IL-6, irisin, FGF21, myostatin, apelin, and Metrnl) that are consistently linked to metabolic and cardiovascular health. Key findings are as follows: resistance training effectively increases irisin and decreases myostatin, promoting muscle mass and fat browning; high-intensity interval training (HIIT) induces rapid IL-6 peaks and elevates Metrnl, enhancing anti-inflammatory responses and cardiac function; aerobic exercise improves FGF21 sensitivity and supports long-term metabolic homeostasis. For clinicians and exercise practitioners, a preliminary exercise framework can be suggested based on available human evidence. In obese patients, ≥3 sessions per week of resistance training (60–80% of one-repetition maximum, 8–12 repetitions, 3–4 sets) may be considered to optimize irisin/myostatin balance, combined with ≥150 min per week of moderate-intensity aerobic exercise (50–70% of maximum heart rate) or 75 min per week of HIIT (85–95% of peak heart rate, 4 × 4 min intervals) to improve FGF21 sensitivity and Metrnl levels. These suggestions should be interpreted as hypothesis-generating rather than definitive clinical guidance, given the heterogeneity of included studies and the absence of quantitative synthesis. Nevertheless, they offer a molecular basis for hypothesis-driven precision exercise prescription that requires validation in future prospective studies and randomized controlled trials. Full article

The security of Module Learning With Errors (MLWE) relies on the assumption that the public matrix is sampled uniformly and forms a full-rank operator. In this work, we examine the structural consequences of relaxing this assumption by considering public matrices that demonstrate slot-wise rank deficiency under the Number Theoretic Transform (NTT). Focusing on the case where each NTT slot matrix has rank 1, we show that this leads to enlarged left nullspace, which allows the elimination of the secret component $s_1$, reducing the original relation to a linear system consisting only of $s_2$. Given partial knowledge of $s_2$, this projected system admits a unique solution once a sufficient number of independent constraints is available. After recovering $s_2$, the problem of determining $s_1$ reduces to solving a bounded linear system, which can be viewed as a structured instance of the Short Integer Solution (SIS) problem. These results provide a dimension-based characterization of solvability under slot-wise rank-deficient public matrices. Using ML-DSA as a concrete instantiation, we illustrate how such structural deviations affect the behavior of the system and discuss simple safeguards, such as rank verification during key generation, to mitigate these issues. Full article

Anastomotic leakage (AL) is a significant complication associated with elevated morbidity and mortality rates following colorectal surgery. This complication primarily arises due to impaired wound healing. Anastomotic and intestinal wound healing is generally divided into three phases: inflammation, proliferation, and remodeling. The physiological transition between these phases is primarily orchestrated by macrophages, which are key regulators of inflammation and tissue repair. They undergo sequential phenotypic changes from pro-inflammatory to anti-inflammatory states and are involved in the phagocytosis of bacteria or debris, but also attract fibroblasts for collagen production and deposition. Importantly, they can promote local perfusion by secreting pro-angiogenic and growth factors. Failure of this transition from pro- to anti-inflammatory properties is associated with AL, scarring, and fibrosis. Intestinal macrophages represent the largest pool of resident myeloid cells and are promising cellular targets for therapeutic interventions. In this narrative review, we focus on intestinal and anastomotic wound healing, highlight the dichotomous role of macrophages, and discuss potential therapeutic strategies. A detailed understanding of macrophage polarization, recruitment, and targeted modulation may enhance wound healing and prevent complications such as AL. Full article

Practical failures of cryptographic key management rarely stem from weak algorithms: they arise from the difficulty users face in memorizing and reliably recalling high-entropy secrets. Password-based and brainwallet approaches collapse under selection bias, while machine-generated mnemonics such as BIP-39 impose a significant memory burden. This paper introduces GeoVault, a key derivation framework that uses remembered geographic locations as the cryptographic input. Keys are derived from a small set of user-selected map points, encoded deterministically using a geospatial scheme and hardened with the Argon2id memory-hard function. We develop a formal entropy model that distinguishes nominal from effective spatial entropy under attacker-prioritized geographic dictionaries and quantifies the additional reduction caused by demographic selection bias. Through information-theoretic analysis and CPU-GPU benchmarking, we show that spatial secrets carry a substantially higher effective entropy floor than human-chosen passwords, and that Argon2id creates a strong asymmetry between legitimate users and offline adversaries: at a memory cost of 1 GiB, an attacker using a high-end GPU can test approximately 66 candidate secrets per one defender key derivation. This residual throughput advantage is, however, overwhelmed by the exponential growth of the search space when multiple locations are selected. Selecting $n\ge 3$ geographic points is necessary and sufficient to achieve cryptographic-strength brute-force resistance under the global attacker prior across all evaluated Argon2id configurations. Against a demographically targeted attacker with city-level knowledge of the user, $n=3$ maintains Human-Scale Secure resistance; $n=4$ with a chaining depth of $k=6$ restores the Super Secure zone at an ≈8 s user-side wait. Single-point configurations remain insecure regardless of memory cost hardening. Full article

Degenerative disc disease is a leading cause of chronic low back pain and disability worldwide, and current treatments primarily address symptoms rather than the underlying biological degeneration of the intervertebral disc. Mesenchymal stem cells (MSCs) have emerged as a promising regenerative approach due to their capacity for differentiation, immunomodulation, and secretion of bioactive factors that promote tissue repair. This review summarises findings from experimental and clinical studies investigating the therapeutic potential of MSC-based therapies for intervertebral disc regeneration, with particular focus on translational challenges that limit their clinical application. Preclinical studies generally show that MSC implantation can enhance extracellular matrix production, improve disc hydration, and modulate inflammatory processes within degenerated discs. Early clinical trials report improvements in pain and functional outcomes; however, consistent structural regeneration has not been reliably demonstrated. The limited clinical translation of MSC therapy is associated with several key challenges, including poor cell survival in the harsh disc microenvironment, variability in cell sources and manufacturing protocols, inadequate cell retention following intradiscal injection, and a lack of standardised outcome measures. In addition, regulatory and manufacturing barriers further complicate the development of reproducible and scalable MSC-based therapies. Although MSC-based therapies represent a promising strategy for the biological treatment of intervertebral disc degeneration, further research is required to improve cell survival, optimise delivery systems, standardise manufacturing procedures, and conduct large-scale controlled clinical trials to establish long-term safety and efficacy. Addressing these translational barriers will be essential for the successful integration of MSC-based therapies into clinical practice. Full article

Dengue infection remains a major global health concern, with a subset of patients progressing from self-limited dengue fever to severe disease characterised by plasma leakage, shock, and organ dysfunction. The dengue non-structural protein 1 (NS1), a multifunctional glycoprotein expressed on infected cells and secreted into circulation, has emerged as a key mediator linking viral infection to immune-driven vascular pathology. This review synthesises experimental, animal, and human clinical evidence on NS1-driven immunopathogenesis, focusing on mechanisms leading to endothelial dysfunction and increased vascular permeability. NS1 modulates the complement system in a context-dependent manner, contributing to immune evasion by inhibiting terminal complement complex formation, while also promoting antibody-dependent complement activation associated with severe disease. Additionally, NS1 directly disrupts endothelial barrier integrity through disruption of adherens and tight junction architecture, Ang-2/Tie2 imbalance, activation of RhoA/ROCK (RhoA/Rho-associated coiled-coil-containing protein kinase) signalling, and enzymatic degradation of the endothelial glycocalyx, with further amplification through inflammatory mediators. In addition, evidence shows that NS1 activates innate immune signalling, perturbs platelet biology and haemostasis, and forms pro-inflammatory complexes with lipoproteins. Moreover, anti-NS1 antibodies may be both protective and pathogenic. Collectively, these data position NS1-linked pathways as rational targets for adjunctive therapies and next-generation vaccines aimed at preventing vascular leakage and severe dengue infection. Full article

The increasing trend in the transmission of image-based data across various ecosystems like telemedicine, multimedia communication, Internet of Things (IoT), and cloud storage demands a strong security system that can withstand both classical and emerging computational threats. Classical cryptographic solutions require complex processing, and hence, meeting the real-time processing requirements is challenging. In contrast, visual cryptography (VC) provides a lightweight security solution. This study proposes a new XOR-based Dynamic Multiple Secret Sharing Visual Cryptography Scheme (XDMSSVCS) designed to share multiple binary image secrets with resistance to emerging computational threats. This work introduces a novel base share creation algorithm designed to generate statistically independent shares while maintaining the symmetric reconstruction property inherent in XOR-based visual cryptography. Also, a lightweight chaotic scrambling mechanism is integrated to address the information leakage problem during transmission. The experimental results indicate pixel-perfect reconstruction (MSE = 0, PSNR = ∞, SSIM = 1), near-ideal entropy, near-zero correlation between shares, high key sensitivity (10⁻¹⁴ variation leading to decorrelated outputs), and a large key space exceeding 2¹²⁸, ensuring resistance against brute-force attacks. The framework also exhibits low computational overhead (XOR: ~0.90 ms, scrambling: ~383.72 ms, memory: ~15.58 MB), and strong resistance to attacks, establishing the XDMSSVCS as a secure and scalable framework for dynamic multi-secret sharing. Full article

We introduce a quantum multiplexer (GHZ MUX) architecture that enables deterministic routing of an unknown qubit from a single sender to one of $2^n$ receivers using only local tripartite Greenberger–Horne–Zeilinger (GHZ) states arranged in a binary tree. At each level of the hierarchy, a Bell-basis measurement and classical feed-forward propagate the encoded quantum information along a selected branch while maintaining the appropriate Pauli correction frame. Unlike quantum routing architectures that rely on globally entangled multipartite states, the proposed design composes small GHZ clusters into a modular teleportation hierarchy that requires only local entanglement generation and coherence. This structure achieves full input–output connectivity while preserving deterministic routing control and experimental feasibility for near-term small-scale quantum networks. Beyond routing functionality, we show that the same GHZ-tree structure naturally supports hidden-destination communication. We formalize this extension as the Hidden-Secret GHZ-Tree Routing (HS-GTR) protocol, in which the final receiver remains unknown to external observers and the transmitted quantum state may optionally be protected by a quantum one-time pad. This construction demonstrates that hierarchical GHZ routing can serve not only as a quantum switching architecture but also as a building block for privacy-preserving communication and multi-receiver key establishment in distributed quantum networks. Full article

Quantum Key Distribution (QKD) enables two parties to securely share encryption keys by leveraging the principles of quantum mechanics, offering protection against eavesdropping. In practical implementations, QKD systems often rely on a layered architecture where a key manager stores secret key material in a buffer and delivers it to higher communication layers as needed. However, this buffer can be depleted under high demand, requiring efficient replenishment strategies that minimize resource waste. Given the importance of optimizing time and resources in quantum cryptography protocols, we introduce a variable-length adaptation of the BB84 protocol designed to meet user-defined output key length constraints in non-ideal scenarios. We present a method for dynamically configuring the protocol’s initial parameters to generate secret keys of a desired length. To validate our approach, we developed simulation tools to model general QKD networks and discrete-variable protocols. These tools were used to implement and evaluate our strategies, which were developed within the BB84 framework but can be extended to other QKD protocols under reasonable assumptions. The results highlight their usefulness in optimizing quantum resource usage and supporting key management, contributing to the long-term goal of scaling and strengthening secure quantum networks. Full article

(1) Background: Attention-deficit/hyperactivity disorder (ADHD) is characterized by persistent difficulties related to inattention, hyperactivity, and impulsivity, which significantly impair daily functioning. The primary objective of this study is to examine the utility of intra-individual metrics as indicators of dynamic cognitive regulation during the intervention with a serious video game (The Secret Trail of Moon, MOON). (2) Methods: Performance data were collected from participants with ADHD enrolled in a randomized clinical trial. Within the MOON group, intra-individual metrics were derived from repeated gameplay sessions of a continuous performance task. For each participant, simple linear regression models were used to estimate the slope of performance across repeated exposures to the task. Slopes were interpreted as indicators of intra-individual change over time. The within-subject standard deviation was also calculated to observe how much a person’s performance fluctuates between sessions. (3) Results: A total of 76 patients with ADHD participated in the clinical trial and were randomized in a 1:1 ratio (MOON: n = 38, 50% and control: n = 38, 50%). The mean performance index of the MOON group (M = 0.88, SD = 0.09) indicates a generally high level of response accuracy, with moderate inter-individual variability across participants. Notably, moderate intra-individual variability (e.g., RT variability, lapse-related indices) was observed, suggesting fluctuations in attentional control despite stable average performance. The absence of linear improvement should not be interpreted as a lack of intervention effect, but rather as evidence of rapid task familiarization and ceiling effects. (4) Conclusions: Intra-individual variability may be a key metric for understanding attentional control in ecological, game-based environments. In this context, performance variability and attentional stability emerge as more sensitive indicators of cognitive regulation than mean-level changes. Full article

Lymphocyte activation gene-3 (LAG-3) is a pivotal immune checkpoint receptor that exerts a negative regulatory effect on T-cell function. Although LAG-3-blocking antibodies have shown promising clinical potential, the inherent limitations of conventional monoclonal antibodies necessitate the development of novel antibody formats with enhanced biological and pharmacological properties. In this study, a panel of single-domain antibodies (sdAbs) targeting human LAG-3 was generated via phage display technology. Among these candidates, 2H-G7 was identified as a high-affinity sdAb that binds to LAG-3 with an equilibrium dissociation constant (K_D) in the nanomolar range. Notably, 2H-G7 potently blocks the interactions of LAG-3 with both of its key ligands, fibrinogen-like protein 1 (FGL1) and major histocompatibility complex class II (MHC-II). Its capacity to restore impaired T-cell function was validated by quantifying interleukin-2 (IL-2) secretion and CD69 expression in stimulated primary human peripheral blood mononuclear cells (PBMCs). Epitope mapping studies localized the binding site of 2H-G7 to the D1D2 extracellular domains of LAG-3, distinct from relatlimab, a clinically approved LAG-3-blocking antibody serving as the benchmark. In a xenogeneic mouse model of non-small-cell lung cancer (NSCLC), 2H-G7-Fc exhibited superior tumor growth inhibition efficacy compared with relatlimab. These findings demonstrate that 2H-G7 is a promising lead candidate for the development of next-generation LAG-3-targeted tumor immunotherapies. Full article

Within the complex regulatory network of the gastrointestinal tract, enteroendocrine cells play a fundamental role in coordinating digestive processes and maintaining metabolic balance. These cells produce a wide range of hormones that influence secretion, motility, and nutrient utilization, constituting an essential component of gastrointestinal physiology in ruminants. Despite the growing interest in the role of endocrine regulation in digestive system function, comprehensive studies evaluating enteroendocrine cell populations across different segments of the gastrointestinal tract in cattle remain limited. In particular, the organization of these cell populations in key digestive segments such as the abomasum and small intestine requires further investigation to better understand their functional significance. The aim of the present study was to provide a comparative characterization of selected enteroendocrine cell populations in the abomasum and small intestine of young and adult Holstein–Friesian bulls. Tissue samples collected from the abomasum, duodenum, jejunum, and ileum were subjected to histological and immunohistochemical analyses. Chromogranin A (CgA) was used as a general marker of enteroendocrine cells, and the number of cells immunoreactive to CgA as well as to gastrin, secretin, somatostatin (SOM), glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1) was quantified in the examined segments of the gastrointestinal tract. All types of immunoreactive cells were counted using a standardized quantitative method based on the assessment of positively stained cells in randomly selected microscopic fields of histological sections. The results revealed clear differences in the number of enteroendocrine cells between the analyzed segments of the gastrointestinal tract as well as between the studied age groups. These findings indicate regional and age-related variation in enteroendocrine cell populations within the gastrointestinal tract and highlight their association with the functional organization of individual segments of the digestive system. Full article

Deploying post-quantum cryptography on highly constrained devices remains challenging due to the large key sizes and substantial storage and memory-traffic demands of leading lattice-based schemes. Although constructions such as Kyber, Dilithium, and NTRU offer strong resistance against quantum adversaries, their multi-kilobyte public keys and intensive memory access patterns limit practical adoption in microcontrollers, smart cards, and low-power edge environments. This work proposes a hybrid key-encapsulation mechanism that integrates a compact, seed-generated Module-LWE structure with a quantum-secure hash-based authentication layer. The design employs a small public seed to instantiate lattice matrices on demand via a lightweight pseudorandom generator and incorporates a Merkle-tree commitment to represent compressed auxiliary error information. Additional design considerations—including sparsity-aware secret keys, SIMD-friendly polynomial operations, and cache-efficient decryption paths—are intended to reduce runtime memory usage and computational overhead. The security of the proposed construction is analysed under both Module-LWE and hash-based one-way assumptions, with further consideration of constant-time execution and cache-line alignment to mitigate side-channel risks. This hybrid approach outlines a design pathway toward post-quantum key-encapsulation mechanisms suitable for deployment on memory-limited and energy-constrained platforms. Full article

Skin aging is driven by both intrinsic and extrinsic factors, including ultraviolet (UV) radiation and environmental stressors. Tumor necrosis factor-alpha (TNF-α) is a key pro-aging cytokine that promotes reactive oxygen species (ROS) production, leading to collagen degradation and inflammatory responses in skin cells. In this study, we investigated the protective effects of Prunus persica flower extract and its major constituents (1–4) against TNF-α–induced oxidative and inflammatory responses in human dermal fibroblasts (HDFs) and human epidermal keratinocytes (HEKs). In HDFs, the extract and isolated compounds significantly suppressed TNF-α–induced ROS generation and matrix metalloproteinase-1 (MMP-1) secretion while enhancing collagen synthesis. Notably, mandelamide (4) markedly reduced MMP-1 secretion (from 7.53 ± 0.28 to 2.97 ± 0.12, p < 0.001) and restored collagen levels (from 3.3 ± 0.03 to 19.1 ± 0.58, p < 0.001). In HEKs, mandelamide attenuated the production of inflammatory mediators under TNF-α stimulation and further suppressed MMP expression while restoring the mRNA expression of hyaluronan synthase genes under TNF-α/ interferon-γ (IFN-γ) co-stimulation. Importantly, mandelamide exhibited selective activity under inflammatory conditions without affecting basal cellular states. Collectively, these findings demonstrate that mandelamide is a key bioactive constituent of Prunus persica (P. persica) flowers and exerts protective effects against inflammation-associated skin aging through the modulation of oxidative stress and extracellular matrix homeostasis. Full article

In response to the plastic pollution crisis, bioplastics emerged as a sustainable alternative. However, low degradation rate and abiotic decomposition generate micro- and nanoplastics. These particles enter the food chain, establishing oral intake as a key route of human exposure. This review gathered studies on the biotransformation of bioplastics in the gastrointestinal tract and on their toxicity in human cells and murine models. Most studies focused on polylactic acid particles due to widespread use in food packaging. Under simulated gastrointestinal conditions in vitro, particles were modulated, resulting in cavity and pore formation, fragmentation, lipase competition, protein corona formation, and alterations in the gut microbiota (including Selenomonadaceae, Bifidobacterium, and Prevotellaceae). Also, particle breakdown increases surface area, enhancing interactions with biomolecules and causing higher in vitro and in vivo toxicity. Indeed, pro-inflammatory cytokine secretion, oxidative stress induction, and redox imbalance were found in both models. In mice, alterations in gut microbiota involving Bacillales indirectly mediated hepatotoxicity, leading to uric acid and triglyceride accumulation. Furthermore, microbiota adaptation over time was suggested with an increase in microorganisms and the potential conversion of L-lactic into harmful D-lactic acid. Despite limited studies, this review highlighted that ingested bioplastic-derived micro- and nanoplastics can lead to toxic effects. Full article