Search Results (171)

This study conducts a detailed and systematic Life Cycle Assessment (LCA) of demineralized (DEMI) water production at the Al-Hilla Second Gas Power Plant in Iraq, employing the Open LCA-ReCiPe 8 Midpoint (H) method to evaluate potential environmental impacts across 18 midpoint categories. The analysis focuses on the production of 1 cubic meter of high-purity water, offering a comprehensive evaluation of the environmental burdens associated with chemical usage, energy consumption, and resource depletion. The results indicate that terrestrial ecotoxicity is the most dominant impact category (20.383 kg 1,4-DCB-eq), largely driven by the extensive use of treatment chemicals such as coagulants, disinfectants, and antiscalants. Climate change follows as the second highest impact category (3.496 kg CO₂-eq), primarily due to significant electricity consumption during energy-intensive stages, particularly reverse osmosis (RO) and electro-deionization (EDI). These stages also contribute notably to fossil resource depletion (1.097 kg oil-eq) and particulate matter formation, reflecting the heavy reliance on fossil fuel-based energy in the region. Additional environmental concerns identified include human toxicity (both carcinogenic and non-carcinogenic), freshwater and marine ecotoxicity, and metal/mineral resource depletion, all of which underscore the need for improved chemical and material management throughout the treatment process. While impacts from categories such as ozone layer depletion, ionizing radiation, and eutrophication are relatively low, their cumulative effect over time remains a concern for long-term sustainability. The energy assessment reveals that the RO and EDI units alone account for over 70% of the total energy consumption, estimated at 3.143 kWh/m³. This research provides insights into minimizing environmental burdens in water treatment systems, especially in regions facing energy and water stress. Full article

The health impacts of atmospheric fine particulate matter (PM_2.5) in plateau regions have attracted concerns, along with local population growth and rapid urbanization. This study collected PM_2.5 samples at summer and winter in Xining, a city located in the northeastern Tibetan Plateau. The chemical composition of PM_2.5 and its cytotoxicity on human lung epithelial cells (A549) are characterized, and composition–cytotoxicity correlation is discussed. The toxic mechanisms of PM_2.5 in different seasons were further investigated through metabolomic analysis using high-resolution mass spectrometry. The average PM_2.5 mass concentration in Xining during winter was 2.10 times higher than that during summer. The carbonaceous components in PM_2.5 were dominated by OC, while the main water-soluble ions were SO₄²⁻, NO₃⁻, and NH₄⁺, with Mg, Al, Fe, and Ca also present in high concentrations in metal elements. LDH and ROS emerged as the most PM_2.5-affected toxicity indices in summer (34.59 ± 4.86 ng/L, 1.19× control) and winter (8.62 ± 1.25 ng/mL, 1.77× control), respectively. OC, Cl⁻, F⁻, Sn, Cr, SO₄²⁻, Pb, Zn, Mg, NO₃⁻, and NH₄⁺ may synergistically exacerbate oxidative stress and inflammatory responses on A549 cells in Xining. Furthermore, glutathione metabolism, amino acid metabolism, and sphingolipid metabolism were identified as key pathways influencing cellular oxidation and inflammation. Thimonacic, 9-(2,3-dihydroxypropoxy)-9-oxononanoic acid, and hypoxanthine were common metabolites in both seasons. Our findings greatly enhance the understanding of health risks associated with PM_2.5 in the plateau city. Full article

Aluminum (Al) toxicity in acidic soils severely limits the productivity of Chinese fir (Cunninghamia lanceolata) plantations. Despite being a crucial timber species in southern China, the regulatory mechanisms underlying phenolic accumulation and Al tolerance pathways under Al stress in Chinese fir remain unidentified. In this study, 5-month-old Chinese fir seedlings were treated with an exogenous phenolic synthesis inhibitor (AIP) and precursor (MJ) to establish the following groups: CK, AIP, MJ, Al, Al+AIP, and Al+MJ. Physiological and biochemical indicator analyses, transcriptome analysis, and protein interaction network predictions were conducted. The findings revealed that phenolic compounds enhance Al tolerance in Chinese fir through two mechanisms: (1) regulation of active oxygen homeostasis (elevating SOD and POD activities, promoting AsA and GSH accumulation, and augmenting total antioxidant capacity); and (2) modulation of cell wall characteristics (increasing pectin content and pectinase activity, and facilitating Al sequestration in the cell wall). Moreover, MJ was found to synergistically enhance these processes, while AIP impeded them. Genes associated with antioxidant enzymes, secondary metabolite synthesis, and cell wall modification were implicated in the regulatory mechanisms. This study provides a theoretical foundation for elucidating the adaptation of Chinese fir to Al toxicity in acidic soil environments, offers insights for enhancing Chinese fir productivity in acidic soils, and presents a novel target for breeding trees with stress resistance. Full article

Hypoxic stress is increasingly recognized as a convergent pathological factor in various age-related neurodegenerative diseases (NDDs), encompassing both acute events such as stroke and traumatic brain injury (TBI), and chronic disorders including Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS). Recent studies have revealed that hemoglobin (Hb), beyond its classical oxygen-transport function, exhibits unexpected expression and functional relevance within the central nervous system. Notably, both cerebral and circulating Hb appear to be dysregulated under hypoxic and aging conditions, potentially influencing disease onset and progression of these diseases. However, Hb’s impact on neurodegeneration appears to be context-dependent: in acute NDDs, it may exert neuroprotective effects by stabilizing mitochondrial and iron homeostasis, whereas in chronic NDDs, aberrant Hb accumulation may contribute to toxic protein aggregation and neuronal dysfunction. This review provides an integrative overview of the emerging roles of Hb in hypoxia-related NDDs, highlighting both shared and distinct mechanisms across acute and chronic conditions. We further discuss potential therapeutic implications of targeting Hb-related pathways in NDDs and identify key gaps for future investigation. Full article

Amyotrophic lateral sclerosis (ALS) is still a heterogeneous neurodegenerative disorder that can be identified clinically and biologically, without a strong set of biomarkers that can adequately measure its fast rate of progression and molecular heterogeneity. In this review, we intend to consolidate the most relevant and timely advances in ALS biomarker discovery, in order to begin to bring molecular, imaging, genetic, and digital areas together for potential integration into a precision medicine approach to ALS. Our goal is to begin to display how several biomarkers in development (e.g., neurofilament light chain (NfL), phosphorylated neurofilament heavy chain (pNfH), TDP-43 aggregates, mitochondrial stress markers, inflammatory markers, etc.) are changing our understanding of ALS and ALS dynamics. We will attempt to provide a framework for thinking about biomarkers in a systematic way where our candidates are not signals alone but part of a tethered pathophysiological cascade. We are particularly interested in the fast progressor phenotype, a devastating and under-characterized subset of ALS due to a rapid axonal degeneration, early respiratory failure, and very short life span. We will try to highlight the salient molecular features of this ALS subtype, including SOD1 A5V toxicity, C9orf72 repeats, FUS variants, mitochondrial collapse, and impaired autophagy mechanisms, and relate these features to measurable blood and CSF (biomarkers) and imaging platforms. We will elaborate on several interesting tools, for example, single-cell transcriptomics, CSF exosomal cargo analysis, MRI techniques, and wearable sensor outputs that are developing into high-resolution windows of disease progression and onset. Instead of providing a static catalog, we plan on providing a conceptual roadmap to integrate biomarker panels that will allow for earlier diagnosis, real-time disease monitoring, and adaptive therapeutic trial design. We hope this synthesis will make a meaningful contribution to the shift from observational neurology to proactive biologically informed clinical care in ALS. Although there are still considerable obstacles to overcome, the intersection of a precise molecular or genetic association approach, digital phenotyping, and systems-level understandings may ultimately redefine how we monitor, care for, and treat this challenging neurodegenerative disease. Full article

Aluminium (Al) is a widespread environmental contaminant known to induce oxidative stress and genotoxic effects in aquatic organisms. While its neurotoxic properties are well documented, the molecular impact of Al on the visual system remains poorly understood. In this study, adult zebrafish (Danio rerio) were exposed to 11 mg/L Al for 10, 15, and 20 days to investigate the oxidative and genotoxic responses in ocular tissue. Activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were measured in eye supernatants to detect oxidative stress. Additionally, the activities of poly (ADP-ribose) polymerase (PARP) and poly (ADP-ribose) glycohydrolase (PARG) were assessed in tissue homogenates to evaluate oxidative DNA damage and repair processes. The results indicate that these enzymes respond to counteract the increased reactive oxygen species (ROS) induced by aluminium exposure. However, their activity may not sufficiently reduce ROS levels to fully prevent oxidative DNA damage, as evidenced by a significant rise in PARP activity during short exposure times. Over longer exposures, PARP activity returned to baseline, suggesting ocular cells may adapt to aluminium toxicity. We propose that this reduction in PARP activity is a cellular survival mechanism, as sustained activation can deplete energy reserves and trigger cell death. Finally, thin-layer chromatography confirmed that PARG facilitates the breakdown of poly (ADP-ribose) (PAR) into ADP-ribose, demonstrating the dynamic regulation of the PAR cycle, which is crucial to preventing parthanatos. Full article

Total ankle arthroplasty (TAA) has evolved significantly through advances in alloy selection and manufacturing technologies. This narrative review examines the metallurgical foundations of contemporary TAA implants, analyzing primary alloy systems and their mechanical properties. Cobalt-chromium alloys provide superior mechanical strength and durability but present metal ion release concerns, while titanium alloys (Ti6Al4V) optimize biocompatibility with elastic modulus values (101–113 GPa) closer to bone, despite tribological limitations. Novel β-titanium formulations (Ti-35Nb-7Zr-5Ta, Ti10Mo6Zr4Sn3Nb) eliminate toxic aluminum and vanadium components while achieving lower elastic modulus values (50–85 GPa) that better match cortical bone properties. Manufacturing has transitioned from traditional methods (investment casting, forging, CNC machining) toward additive manufacturing technologies. Selective laser melting and electron beam melting enable patient-specific geometries, controlled porosity, and optimized microstructures, though challenges remain with residual stresses, surface finish requirements, and post-processing needs. Emerging biodegradable materials, composite structures, and hybrid implant designs represent promising future directions for addressing current material limitations. This review provides evidence-based insights for alloy selection and manufacturing approaches, emphasizing the critical role of materials engineering in TAA implant performance and clinical outcomes. Full article

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that affects motor neurons of people, leading to death. This pathology can be caused by mutations in different genes, including superoxide dismutase 1 (SOD1). Previous studies have pointed out the presence of two transcripts of SOD1, a short one and a long one. The aim of this study was the investigation of these two transcripts both in the SH-SY5Y cell line and in patients’ peripheral blood mononuclear cells. We found that the shortest SOD1 transcript is upregulated under stress conditions in both the cellular model and the patients’ cells. Moreover, we found a potential correlation between the short SOD1 transcript and the severity of the pathology, which also correlates with the age of patients. No correlation was found between SOD1 transcripts and the progression of the disease. These data suggest a toxic effect of short SOD1 transcripts in ALS patients, by affecting the severity of the pathology making it a possible biomarker for this disease. Interestingly, our data suggest that a short SOD1 transcript does not influence and drive disease progression. The finding of a biomarker will have suitable implications as indicators of disease severity and from the perspective of drug development. Full article

The increasing release of nanoparticles into aquatic environments, particularly via wastewater, raises concerns about their biological effects on microbial communities. This study investigated the molecular response of Pseudomonas putida to aluminum oxide nanoparticles (Al₂O₃NPs) under controlled conditions and in synthetic wastewater, both before and after biological treatment. Acute toxicity was evaluated using growth inhibition assays, while the expression of katE, ahpC, and ctaD—genes associated with oxidative stress and energy metabolism—was quantified via RT-qPCR. Exposure to pristine Al₂O₃NPs induced a strong, time-dependent upregulation of all tested genes (e.g., katE and ahpC up to 4.5-fold). In untreated wastewater, this effect persisted but at a lower intensity; bulk Al₂O₃ caused only moderate changes. Treated wastewater samples showed markedly reduced gene expression, indicating partial detoxification. Nanoparticles elicited stronger biological responses than their bulk counterparts, confirming the material form-specific effects. Comparative analysis with Daphnia magna revealed similar patterns of oxidative stress gene activation. These findings highlight the influence of nanoparticle form and environmental matrix on microbial responses and support the use of gene expression analysis as a sensitive biomarker for nanoparticle-induced stress in environmental risk assessment. Full article

Background: Aluminum (Al) toxicity severely limits Medicago sativa (alfalfa) production on acidic soils, resulting in major yield losses worldwide. The highly conserved miRNA156 (miR156) functions by downregulating at least 11 SQUAMOSA promoter-binding protein-like (SPL) transcription factors in alfalfa, including SPL13, but its role in Al stress remains unclear. This study aimed to investigate the miR156/SPL regulatory network’s function in alfalfa under Al stress. Methods: Gene expression analyses, histochemical staining, nutrient profiling, phenotypic assays, transcriptome profiling, and ChIP-seq were conducted on alfalfa plants with altered miR156 and SPL13 expression to assess their roles in the Al stress response. Results: Al stress induced SPL13 expression while repressing miR156 in the roots. Elevated miR156 intensified Al accumulation, lipid peroxidation, and plasma membrane damage, accompanied by reduced leaf nitrogen, magnesium, sulfur, and phosphorus content. Phenotypically, increased SPL13 enhanced the root length and Al tolerance, whereas SPL13 silencing reduced tolerance. Transcriptome profiling of SPL13-silenced plants identified differentially expressed genes involved in the Al response, including aluminum-activated malate transporters and various transcription factors (GRAS, Myb-related, bHLH041, NAC, WRKY53, bZIP, and MADS-box). ChIP-seq revealed that SPL13 directly regulates genes encoding a protein kinase, cytochrome P450, and fasciclin-like arabinogalactan proteins. Conclusions: The MsmiR156/MsSPL13 network plays a crucial regulatory role in alfalfa’s response to Al toxicity. These findings provide novel genetic targets and foundational knowledge to advance molecular breeding for enhanced Al tolerance in alfalfa. Full article

The cell wall, acting as the first line of defense against aluminum (Al) toxicity, is the primary cellular structure that encounters and perceives Al³⁺. Xyloglucan endotransglucosylase/hydrolase (XTH) plays a pivotal role in mediating cell wall remodeling, a critical mechanism for Al toxicity tolerance. In our previous studies, the candidate gene BnaXTH22 was identified through GWAS and RNA-seq analyses. Under Al toxicity stress, overexpression lines (OEs) exhibited a significant increase in the relative elongation of taproots (9.44–13.32%) and total root length (8.15–12.89%) compared to the wild type (WT). Following Al treatment, OEs displayed reduced MDA content and lower relative electrical conductivity, alongside a significantly higher root activity than WT. Transcriptomic analysis revealed that differentially expressed genes in OE under Al toxicity were predominantly enriched in stress-related biological processes, including phenylpropanoid metabolism, fatty acid biosynthesis, and lignin biosynthesis. These results suggest that BnaXTH22 overexpression could enhance Al toxicity tolerance in rapeseed, potentially by modulating cell wall synthesis to bolster plant resistance. Full article

Aluminum (Al) is one of the most abundant metals on Earth and is well known as an environmental neurotoxic agent in the pathogenesis of Alzheimer’s disease. Aluminum toxicity is associated with oxidative stress, reduction of antioxidant enzymes, and disruption of the balance of cellular metals, such as iron (Fe), calcium (Ca), and copper (Cu), which causes structural and functional changes in the nervous tissue of the brain or peripheral nervous system. The intake of functional foods, rich in antioxidants, such as quercetin, may be beneficial in combating oxidative stress and neurodegenerative changes in the brain. The aim of this study was to provide deeper insight into the cellular and molecular neuroprotective effects of quercetin in regulating amyloid-beta (Aβ) accumulation, tau pathology, and neuroinflammation in the Al/D-galactose-induced rat model (Al/D-gal) of AD. The results showed that quercetin successfully modulated the impaired homeostatic and neuropathological consequences of aluminum chloride and D-galactose administration over 28 days: it directly protected neurons by regulating the level of oxidative stress and antioxidants, reduced Aβ aggregation by inhibiting the activity of acetylcholinesterase (AChE), increased the survival, growth, and differentiation of nerve cells by maintaining the level of brain-derived neurotrophic factor (BDNF), and regulated microglial immunoreactivity and neuroinflammation by reducing the level of proinflammatory cytokines. The multiple effects confirm that quercetin can be applied as an alternative non-pharmaceutical approach in reducing Al-induced neurotoxicity and maintaining adaptive homeostasis, which consequently affects the functioning of the central nervous system and the whole organism. Full article

Aluminum toxicity severely inhibits root elongation and nutrient uptake, causing global agricultural yield losses. Dissolved Al³⁺ are accumulating in plants and subsequently entering food chains via crops and forage plants. Chronic dietary exposure to Al³⁺ poses a risk to human health. In this study, Pseudomonas sp. strain ADAl3–4, isolated from plant rhizosphere soil, significantly enhanced plant development and biomass. Phenotypic validation using Arabidopsis mutants showed that strain ADAl3–4 regulates plant growth and development under aluminum stress by reprogramming the cell cycle, regulating auxin and ion homeostasis, and enhancing the root absorption of Al³⁺ from the soil. Transcriptomic and biochemical analyses showed that strain ADAl3–4 promotes plant growth via regulating signal transduction, phytohormone biosynthesis, flavonoid biosynthesis, and antioxidant capacity, etc., under aluminum stress. Our findings indicate that Pseudomonas sp. strain ADAl3–4 enhances plant development and stress resilience under Al³⁺ toxicity through a coordinated multi-dimensional regulatory network. Furthermore, strain ADAl3–4 promoted the root absorption of aluminum rather than the transportation of Al to the aerial part, endowing it with application prospects. Full article

Amyotrophic lateral sclerosis (ALS) is a fatal adult neurodegenerative disorder. Since no cure has been found, finding effective therapeutic targets for ALS remains a major challenge. Gene C9orf72 mutations with the formation of hexanucleotide repeat (GGGGCC) expansion (HRE) have been considered the most common genetic pathogenesis of ALS. The literature review indicates that the C9orf72 HRE causes both the gain-of-function toxicity and loss of function of C9ORF72. The formation of RNA foci and dipeptide repeats (DPRs) resulting from HRE is responsible for toxic function gain. The RNA foci can interfere with RNA processing, while DPRs directly bind to and sequester associated proteins to disrupt processes of rRNA synthesis, mRNA translation, autophagy, and nucleocytoplasmic transport. The mutations of C9orf72 and HRE result in the loss of functional C9ORF72. Under physiological conditions, C9ORF72 binds to Smith–Magenis chromosome region 8 and WD repeat-containing protein and forms a protein complex. Loss of C9ORF72 leads to autophagic impairment, increased oxidative stress, nucleocytoplasmic transport impairment, and inflammatory response. The attempted treatments for ALS have been tried by targeting C9orf72 HRE; however, the outcomes are far from satisfactory yet. More studies should be performed on pharmacological and molecular modulators against C9orf72 HRE to evaluate their efficacy by targeting HRE. Full article