Search Results (1,776)

The rapidly urbanizing peripheries of the Global South face significant demographic pressures, leading to governance deficits that often neglect the long-term structural safety of new buildings. While regulatory frameworks predominantly emphasize initial construction quality, they frequently overlook the critical “post-occupancy” phase, during which distinct structural risks accumulate. This study introduces a reproducible, open-data risk identification framework designed to trace theoretical “windows of vulnerability” in Çekmeköy, a peripheral district of Istanbul. By triangulating temporal, spatial, and demographic municipal administrative records from 2018 to 2024, we illustrated how low-cost data can serve as proxies for prioritizing structural risk assessments. The findings demonstrate that a 103% population increase between 2008 and 2023, coupled with a 21% reduction in the average household size, has generated urgent housing demand that outpaces supply. We hypothesize that these conditions create high-probability zones for “informality creep,” where demographic pressures induce informal practices, such as unauthorized structural modifications within ostensibly formal high-rise settings. The primary contribution is a transferable algorithmic tool, the Weighted Post-Occupancy Vulnerability Index (POVI). Rather than serving as a deterministic building-level diagnostic, this framework operates much like an epidemiological screening process; it acts as a macroscopic prioritization heuristic that allows resource-constrained municipalities to proactively direct their inspection efforts. By mathematically quantifying the conditions under which post-occupancy risks develop, this framework provides an essential resource for enhancing urban resilience during reactive urbanism planning. Full article

Post-translational modification (PTM) neoantigens have emerged as key drivers of autoimmune inflammation. However, standardized protocols for MHC Class II tetramer preparation for the detection of such antigen-specific T cells remain limited, hindering the broader application of this important discovery. This study systematically engineered an HLA-DR4 (HLA-DRB1*04:02 and HLA-DRA*01:01) tetramer platform based on carboxyethyl-modified neoantigen ITGA2B peptide (ITG-CE), a PTM associated with autoimmune diseases (AUIDs) such as Ankylosing Spondylitis (AS). The platform provides a major histocompatibility complex (MHC) Class II tetramer associated with the PTM neoantigen and integrates modular protein construct, a controllable PTM peptide exchange strategy, and a specific T cell receptor (TCR) validation model. It can be employed to investigate PTM neoantigen presentation and CD4⁺ T cell auto-reactivity, providing extensive application value for future research into the mechanisms of PTM-induced AUIDs and immune monitoring. Full article

The second most prevalent neurodegenerative illness in the world, Parkinson’s disease (PD), currently has no viable treatments. Although it is yet unknown if mitochondrial dysfunction is an initial event or evolves as a result of neurodegeneration, it is thought to be a crucial component of Parkinson’s disease etiology. From the perspective of mitochondrial quality control (MQC), which includes PINK1/Parkin-mediated mitophagy, mitochondrial dynamics, and mitochondrial proteostasis, this article examines mitochondrial dysfunction. Together, these processes preserve mitochondrial homeostasis and prevent the buildup of damaged mitochondria. Dysfunctional mitochondria gradually build up and cause oxidative stress and aberrant cellular signaling when mitochondrial quality control is compromised. According to available data, mitochondrial reactive oxygen species (mtROS) primarily worsen pre-existing mitochondrial damage by encouraging α-synuclein aggregation, cardiolipin remodeling, and dopamine oxidation. In addition, innate immune pathways like cGAS–STING and TLR9 signaling can be triggered by mitochondrial damage-associated molecular patterns (mtDAMPs), especially mitochondrial DNA, which can lead to long-term neuroinflammatory reactions in PD. While new research suggests that m⁶A RNA modification may be involved in the regulation of mitochondrial stress, the PINK1/Parkin pathway is crucial for maintaining mitochondrial homeostasis. Therapeutic approaches that target mitophagy augmentation, neuroinflammatory signaling, and mitochondrial protection have garnered increasing attention. In an attempt to improve mitochondrial function and lessen persistent neuroinflammatory activation, future research will probably need to concentrate on combination treatment techniques. Full article

Natural compounds are increasingly explored as complementary strategies to enhance the effectiveness of chemotherapy and reduce toxicity. Among these are isothiocyanates (ITCs), bioactive metabolites derived from glucosinolates in cruciferous vegetables, which have gained substantial attention for their chemopreventive and antileukemic potential. ITCs exert diverse biological effects driven by the high reactivity of the –NCS group, enabling covalent modification of key cellular proteins and modulation of signaling pathways. Well-studied representatives, including sulforaphane (SFN), allyl isothiocyanate (AITC), 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC), benzyl isothiocyanate (BITC), and phenethyl isothiocyanate (PEITC), exhibit diverse antileukemic activities, including cytotoxic, pro-apoptotic, differentiation-inducing, and cell-cycle-modulating effects. Although individual compounds differ in their relative potency and predominant biological responses, their activities are generally mediated through multiple interconnected mechanisms including oxidative stress modulation, mitochondrial dysfunction, regulation of apoptosis-related proteins, and interference with key signaling pathways. In addition to apoptosis, several ITCs have also been reported to induce autophagy, ferroptosis, or cellular differentiation in leukemic cells. Taken together, the existing evidence highlights ITCs as promising candidates for leukemia chemoprevention or therapy, acting through multi-targeted mechanisms that may complement conventional treatment strategies. Further studies are needed to clarify their selectivity, mechanistic diversity, and translational potential. Full article

Single-crystal diamond (SCD) is an ideal substrate material for semiconductor devices due to its extremely wide bandgap and exceptionally high thermal conductivity. However, diamond’s extreme hardness and chemical inertness pose challenges for the fabrication of ultra-smooth surfaces. Traditional polishing processes are not only inefficient but also prone to introducing subsurface defects, which severely degrade device performance. To address the above issues, this study proposes a hybrid polishing process combining reactive ion etching (RIE) surface modification with chemical mechanical polishing (CMP), which enables low-loss atomic-level processing of SCD. The study found that RIE treatment induces lattice disorder on the diamond surface, forming a sp²-hybridized amorphous carbon-modified layer. Compared to the sp³ structure of native diamond, this modified layer has lower hardness and is easier to remove. We conducted the verification of the optimized process using high-quality single-crystalline diamond (SCD) samples with an initial surface roughness Ra of 0.68 nm. Under the optimized RIE parameters (substrate bias power: 200 W, etching time: 600 s, gas flow ratio of Ar:O₂:CF₄ = 40:50:10), the surface roughness Ra was reduced to as low as 0.35 nm after 2 h of CMP treatment. Furthermore, systematic characterization of the SCD’s as-received surface, RIE-modified surface, and CMP-treated surface was performed using Raman spectroscopy and X-ray photoelectron spectroscopy (XPS), elucidating the “etching modification–mechanical removal” polishing mechanism. Full article

Abiotic stresses, including drought, salinity, alkalinity, temperature extremes, flooding, heavy metals, and emerging pollutants, challenge plant growth and productivity by disturbing water relations, ion balance, redox homeostasis, membrane stability, energy metabolism, and developmental progression. Although substantial progress has been made in the identification of stress-responsive hormones, second messengers, kinases, transcription factors, transporters, and metabolic regulators, plant stress adaptation cannot be fully explained by linear signaling cascades or single tolerance genes. A major unresolved question is how early molecular events are reorganized into coordinated physiological and developmental outputs that support survival, recovery, and productivity. In this review, we propose an intermolecular interaction-driven adaptive remodeling framework for plant abiotic stress responses. This framework emphasizes that stress tolerance emerges from dynamic changes in receptor–ligand recognition, protein–protein interactions, calcium decoding, redox-sensitive modification, phosphorylation networks, transcriptional regulation, chromatin-associated control, and metabolite-mediated feedback. We further emphasize ROS as integrative redox switches that connect stress sensing, defense activation, senescence-related transitions, and recovery, and chromatin-associated mechanisms as regulators that may stabilize primed or memory-like adaptive states. We discuss how these interaction networks converge on core signaling hubs, including abscisic acid, reactive oxygen species, Ca²⁺, and kinase/phosphatase systems, and how they remodel stomatal behavior, root architecture, ion and pH homeostasis, redox buffering, metabolism, development, and reproductive resilience. We further highlight how natural variation, multi-omics, genome editing, high-throughput phenotyping, and field validation can translate interaction-centered stress biology into crop resilience. This perspective provides a conceptual bridge between molecular stress perception, network behavior, physiological adaptation, and climate-resilient agriculture. Full article

A short-term performance test of blended biodiesel (FAME), green diesel (HVO), and diesel was experimentally assessed in a 100 kW Cummins 6BTAA5.9-G12 diesel engine under multiple load conditions. The objective was to determine the technical feasibility, operational trade-offs, and optimal blend formulations for renewable energy deployment in diesel power plants. All tested blends operated stably without engine modification, confirming the “drop-in capability” of FAME–HVO mixtures for existing diesel engines. Specific fuel consumption (SFC) increased notably at high loads, with penalties up to 15.15% for B30D20 and B35D15 relative to neat diesel, although overall efficiency improved with load. Among the ternary fuels, B30D10 and B30D20 provided the most balanced compromise between combustion reactivity and flow properties. Exhaust gas temperatures rose with load for all fuels, with FAME-rich blends exhibiting higher temperatures than neat diesel, while coolant-side analysis showed D100 and D50 as thermally favorable and B50–B100 imposing the highest cooling demand. The results emphasize the need for injection system recalibration on an energy basis for HVO-rich fuels, and for strengthened filtration and maintenance practices for FAME-rich blends to avoid filter clogging and injection instability. Considering performance, operability, and system stability up to 100 kW, B30D10 and B35D15 are identified as optimal compromise blends. The study highlights the necessity of future work on long-term durability, fuel system compatibility, supply chain robustness, and techno-economic viability to safely scale green diesel use in Indonesian stationary power generation. Full article

Reparative macrophage polarization and macrophage-derived reactive oxygen species (ROS) are required for ischemia-induced revascularization in peripheral artery disease (PAD). Our previous study showed that mitochondrial fission protein dynamin-related protein 1 (DRP1) promotes reparative polarization and metabolic reprogramming in macrophages and post-ischemic neovascularization. However, the redox-dependent mechanism governing DRP1 activation in this context remains elusive. Here, using a mouse hindlimb ischemia (HLI) model of PAD, we identify cysteine sulfenylation (CysOH) of DRP1 as a critical redox modification induced in ischemic bone marrow (BM)-derived cells. BM chimeric mice reconstituted with CRISPR/Cas9-generated “redox-dead” DRP1-C631A knock-in mutant (Drp1^C/A) BM exhibited markedly reduced limb perfusion recovery and CD31⁺ capillary density in ischemic muscles following HLI. These defects were associated with enhanced Ly6G⁺ neutrophil accumulation, pro-inflammatory F4/80⁺CD80⁺ M1-like macrophages and reduced anti-inflammatory F4/80⁺CD206⁺ M2-like macrophages in ischemic muscle. Mechanistically, using an in vitro PAD model, hypoxia serum starvation (HSS) rapidly induced NADPH oxidase 2-dependent cytosolic ROS production and DRP1-CysOH formation in wild-type macrophages. In contrast, Drp1^C/A macrophages failed to undergo DRP1-CysOH-dependent mitochondrial fission under HSS, resulting in aberrant metabolic reprogramming characterized by enhanced glycolysis and mitochondrial ROS, pro-inflammatory p-NF-κB and M1-genes, and suppressed anti-inflammatory p-AMPK, efferocytosis and M2-genes. Thus, our findings establish DRP1 sulfenylation as a previously unrecognized redox-sensing mechanism that links ischemia-induced ROS to reparative macrophage reprogramming and revascularization, identifying a novel therapeutic target for PAD. Full article

Insulin resistance (IR) is traditionally viewed within the context of type 2 diabetes. However, it increasingly appears to represent a broader systemic metabolic risk state with potential relevance for carcinogenesis. Chronic hyperinsulinemia can activate insulin-like growth factor-1-dependent pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin and mitogen-activated protein kinase signaling, promoting cellular proliferation while limiting apoptosis. At the same time, IR is closely linked to oxidative stress, chronic low-grade inflammation, and epigenetic alterations, together shaping a tumor-promoting microenvironment. Epidemiological studies report consistent associations between IR and increased cancer risk, particularly for endometrial, liver, and colorectal cancers. Yet causality remains uncertain and likely varies by tumor type. Notably, metabolic dysfunction may also occur in individuals with normal body mass index (BMI), underscoring the limitations of BMI-based risk assessment. Unlike previous reviews that primarily focused on individual mechanisms or epidemiological associations, this review examines IR as a systemic metabolic risk state by integrating molecular, epidemiological, biomarker-based, and prevention-oriented perspectives. Particular emphasis is placed on strategies for earlier risk identification using integrated biomarker approaches, including fasting glucose, homeostatic model assessment of insulin resistance, triglyceride-to-high-density lipoprotein ratio, high-sensitivity C-reactive protein, and insulin-like growth factor-1. Emerging tools such as continuous glucose monitoring and hepatokine profiling may further refine risk detection. Sustained lifestyle modification—diet, physical activity, sleep, and stress regulation—remains central to prevention. Pharmacological therapies, including glucagon-like peptide-1 receptor agonists and dual incretin agents, offer additional metabolic benefits, although their long-term impact on cancer risk is still unclear. Therefore, IR is best understood not as an isolated risk factor, but as a systemic metabolic risk state that may influence cancer development, with implications for prevention and early risk stratification. Full article

This study investigated the production of spodumene concentrate and lithium carbonate from a low-grade pegmatite ore containing approximately 0.26 wt.% Li₂O. The ore consisted predominantly of a quartz–feldspar aluminosilicate matrix with dispersed spodumene mineralization, which complicates conventional processing approaches. Preliminary lithium concentration was performed by dense media separation (DMS) using an industrially applicable ferrosilicon-based suspension. The highest separation efficiency was achieved for the −4.0/+2.8 mm fraction, producing a DMS concentrate containing 5.77 wt.% Li₂O with 98% lithium recovery. The obtained spodumene concentrate was subjected to decrepitation at 1000–1100 °C to convert α-spodumene into the more reactive β-modification, followed by sulfation roasting with concentrated sulfuric acid at 250–270 °C. The productive leach solution obtained after water leaching contained up to 12.1 g/L Li₂O. After purification from iron-bearing impurities and precipitation with sodium carbonate, a lithium carbonate product containing at least 98.8 wt.% Li₂CO₃ was obtained. Approximately 53% of the lithium contained in the original ore was recovered into the DMS feed fraction, whereas the overall lithium recovery into lithium carbonate reached about 45% relative to the ore and approximately 70% relative to the concentrate. Full article

Thiopurines are efficient triplet-state photosensitisers; however, the practical application of canonical derivatives such as 6-thioguanine (6TG) and 6-thioguanosine (6TGuo) is limited by competing deactivation pathways that reduce the fraction of triplet states available for productive interaction with molecular oxygen. In this work, we investigated how structural modification of the thiopurine scaffold through introducing of an additional five-membered etheno ring affects triplet-state energetics, deactivation pathways, and singlet oxygen sensitisation. The photophysical properties of four tricyclic thiopurine analogues—9-thio-1,N²-ethenoguanine (TEGua), 9-thio-1,N²-ethenoguanosine (TEGuo), 6-methyl-9-thio-1,N²-ethenoguanine (6MeTEGua), and 6-methyl-9-thio-1,N²-ethenoguanosine (6MeTEGuo)—were investigated using steady-state spectroscopy, low-temperature phosphorescence, nanosecond transient absorption spectroscopy, and direct detection of singlet oxygen phosphorescence. All investigated compounds exhibited efficient intersystem crossing and microsecond-lived triplet states. Compared with canonical thiopurines, the tricyclic analogues displayed lower triplet-state energies and significantly enhanced singlet oxygen generation. Quantum yields of singlet oxygen sensitisation reached ~0.56 in acetonitrile, approximately twofold higher than those observed for 6TG and 6TGuo under identical conditions. Analysis of triplet-state deactivation pathways showed that the enhanced photosensitising efficiency does not result from increased triplet formation, but from more effective use of the triplet-state population for energy transfer to molecular oxygen leading to singlet oxygen formation. These findings demonstrate that structural modification of the thiopurine scaffold enables control over triplet-state reactivity and provides a strategy for designing improved thiopurine-based photosensitisers for photodynamic therapy applications (PDT). Full article

Background/Objectives: Resistant pathogenic bacteria and fungi are a growing problem worldwide; therefore, the discovery of new active ingredients is an important challenge for which the functionalization of natural terpenes with biologically active heterocycles can provide a basis. To reach this goal, a series of 1,4-disubstituted-1,2,3-triazole conjugates was designed and synthesized starting from commercially available α-santonin. Methods: The key azido derivative intermediate was prepared according to literature procedures via Michael addition between dehydrosantonin and the TMSN₃/AcOH/Et₃N system at its highly reactive α-methylene-γ-lactone motif. Subsequently, the obtained azide was applied to regioselective Huisgen 1,3-dipolar cycloaddition reaction with a wide range of terminal alkynes bearing N-, S- and O-heterocycles. These include pyridine, pyrimidine, purine, quinoline, indol, or coumarin to afford the sesquiterpene–heterocycle chimaeras. All triazole conjugates were screened for in vitro antiproliferative activity by MTT assay against HeLa, MDA-MB231, SiHa, MCF-7 and A2780 human cancer cell lines compared with fibroblast cells (NIH/3T3) to check their cytotoxicity and antimicrobial effects on two Gram-positive (B. subtilis, S. aureus) pathogenic bacteria, two Gram-negative (E. coli and P. aeruginosa) pathogenic bacteria, and two yeasts (C. krusei and C. albicans). Results: The results indicated that most of the examined compounds expressed weak activity against human cell lines, while some of them showed moderate activity against S. aureus (up to 99% inhibition at 100 µg/mL conc.), C. krusei (up to 51% inhibition at 10 µg/mL conc.) and C. albicans (up to 52% inhibition at 10 µg/mL conc.). Conclusions: Further structural modification of the best, selective antibacterial and antifungal compounds may open the possibility to the development of effective natural sesquiterpene-based selective antimicrobial agents. Full article

Surface modification of zinc oxide nanoparticles (ZnO NPs) with organosilane capping agents represents an effective strategy to control their physicochemical and biological properties. In this work, we report for the first time the use of halogenosilanes, namely (3-chloropropyl)trimethoxysilane (CPTMS), (3-bromopropyl)trimethoxysilane (BPTMS) and (3-iodopropyl)trimethoxysilane (IPTMS), for the surface functionalization of ZnO NPs obtained by chemical precipitation. Structural and morphological characterization (PXRD, TEM, SEM-EDX and FTIR) confirmed successful surface modification and revealed a significant particle size reduction from ~31 nm for unmodified ZnO to ~8 nm for BPTMS-modified ZnO (ZnO_b). The biological evaluation showed that halogenosilane-modified ZnO NPs exhibit enhanced cytotoxic activity against prostate cancer cell lines (PC3 and 22Rv1), with ZnO_b displaying the highest activity, likely associated with improved cellular uptake and increased reactive oxygen species (ROS) generation. In contrast, antimicrobial assays revealed only moderate bactericidal effects against Escherichia coli and Staphylococcus aureus at relatively high concentrations (≥1250 µg mL⁻¹), while no significant activity was observed against Pseudomonas aeruginosa, Burkholderia contaminans or Candida spp., within the tested range. These findings suggest that halogenosilane functionalization modulates the biological profile of ZnO nanoparticles by enhancing anticancer effects while also influencing microbiocidal activity, highlighting the role of surface chemistry in tuning biological selectivity. The present study supports the concept that rational surface engineering of ZnO-based nanoplatforms can be exploited to favor tumor-targeted activity over broad-spectrum antimicrobial effects, providing new perspectives for the design of application-oriented nanomaterials. Full article

Wildfires significantly affect wood properties and usability, yet their impact on hardwood species remains insufficiently understood. This study presents an exploratory characterization of moderately fire-affected pedunculate oak (Quercus robur L.) wood, combining physical, mechanical, chemical, and thermal analyses to evaluate depth-related changes within outer stem zones. Samples were collected from bark and from wood originating approximately 1 cm and 1–2 cm beneath the cambial region to evaluate radial variation associated with moderate surface fire exposure. The oven-dry density of fire-affected wood reached 720 kg·m⁻³, corresponding to values marginally below the literature reference ranges reported for unaffected oak wood. Bending strength decreased to 85.56 MPa, while compressive strength remained within or marginally above the literature reference (71.16 MPa), and Brinell hardness (42.75 MPa) stayed within the typical range for oak. Chemical and elemental analyses revealed degradation of polysaccharides and carbon enrichment in surface layers. FTIR and DSC analyses suggested partial hemicellulose degradation, structural modification of cellulose, and reduced thermal reactivity in outer stem regions. Despite these changes, the higher heating value (19.09–19.56 MJ·kg⁻¹) remained within the literature reference ranges reported for oak wood. The results suggest that under moderate surface fire conditions, fire-induced changes were primarily concentrated in outer stem layers, while inner wood retained properties comparable to the literature reference values for unaffected oak wood. These findings indicate that moderately fire-affected oak wood may remain suitable for selected material or energy-related applications following appropriate quality assessment and removal of thermally altered surface zones. Full article

To enhance flame retardancy of waterborne polyurethane (WPU) coatings, this paper proposes a co-modification method using modified graphene oxide (SiO₂@GO) and a phosphorus flame retardant (P-). SiO₂@GO refers to graphene oxide (GO) with an attached silicon dioxide (SiO₂) layer, while the phosphorus flame retardant (P-) in this work is THPO, a reactive flame retardant used as a chain extender. The influence of component additions on flame retardancy was systematically investigated. Modified WPU coatings (P-SiO₂@GO/WPU) were prepared using THPO and SiO₂@GO as flame-retardant chain extenders. The morphology, structure, and thermal stability of P-SiO₂@GO/WPU were characterized by scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, and thermogravimetric analysis (TGA). At 2% SiO₂@GO, coatings showed enhanced hydrophobicity (water repellency) and thermal stability. With 4% phosphorus flame retardant (P-), the limiting oxygen index (LOI, a measure of flame retardancy) reached 32.2%, and the heat release rate was 32.4% lower than before modification. A continuous, dense P/Si-containing carbonaceous ceramic-like barrier layer was formed, effectively blocking the release of combustible gases and the transfer of heat, thereby demonstrating excellent flame retardancy. This synergistic P-SiO₂@GO/WPU modification offers theoretical support and practical guidance for optimizing and enhancing the flame-retardant performance of WPU coatings. Full article