Search Results (20,015)

Soybean production commonly faces challenges including severe pod abscission, incomplete seed filling, and uncoordinated source–sink relationships that limit yield potential. Plant growth regulator application may influence source–sink relationships and thereby affect soybean (Glycine max (L.) Merr.) yield formation. This three-year field study (2023–2025) evaluated the effects of four spray programs on soybean yield, quality, total above-ground biomass partitioning, and endogenous hormone dynamics under Xinjiang’s irrigated production conditions. The four treatments were an untreated control (CK), naphthaleneacetic acid alone (NAA; 300 g ha⁻¹), naphthaleneacetic acid plus prohexadione-calcium (NPC; 300 + 450 g ha⁻¹), and naphthaleneacetic acid plus prohexadione-calcium and iron chlorin e6 (NCE; 300 + 450 + 45 g ha⁻¹). The spray programs were applied at the fourth-trifoliolate and full-pod stages. Results showed that NCE treatment consistently produced the greatest yield increases (13.1–14.4%) compared with the control. This response was associated with greater middle-node pod retention, increased 100-seed weight (3.6–6.4%), and improved reproductive organ biomass allocation (44.7–53.3% at maturity vs. 40.9–45.7% in controls). NCE significantly elevated leaf trans-zeatin content (37.1–91.9%) within 24 h after application and improved seed protein concentration by up to 11.2%, while seed residues of all applied compounds remained well below safety thresholds (<0.05 mg kg⁻¹). Correlation analysis revealed strong positive relationships between trans-zeatin levels and both reproductive biomass allocation (r = 0.74–0.90, p < 0.01) and grain yield (r = 0.86–0.96, p < 0.01). These findings indicate that NCE was the best-performing of the four tested spray programs under Xinjiang’s irrigated production conditions, although the individual contributions and possible interactions of the three compounds require further factorial evaluation. Full article

Photorespiration and drought-induced stomatal closure are two important physiological constraints that reduce carbon assimilation and productivity in C₃ forest trees under Mediterranean climatic conditions. Türkiye’s two dominant commercial pine species, Pinus brutia Ten. (Calabrian pine) and Pinus nigra J.F. Arnold subsp. pallasiana (Anatolian black pine), together cover approximately 8.15 million hectares. This study integrated published gas-exchange measurements, radiation-use efficiency estimates from MODIS, official forest inventory data, and dendrochronological growth records into a counterfactual accounting framework and propagated parameter uncertainty by Monte Carlo simulation (N = 40,000 draws). The two constraints jointly reduced weighted-mean net primary productivity (NPP) from a radiation-limited potential of 5.61 to an actual 3.46 Mg C ha⁻¹ yr⁻¹, a reduction of 37.9% (95% CI 32.2–43.4%). Decomposition shows that 47.7% of this loss is the obligate metabolic cost of C₃ carboxylation, which no silvicultural intervention can address, while 52.3%—20.1 of the 37.9 percentage points—is drought-attributable. Nationally, the deficit corresponds to 64.3 Mt CO₂ yr⁻¹ of forgone sequestration (47.8–81.2) and 34.4 Mm³ yr⁻¹ of forgone stemwood-volume equivalent (24.9–44.5), of which approximately 20.6 Mm³ would be merchantable, giving an annual economic deficit of USD 3.37 billion (2.40–6.48). Filtering the drought-attributable component for eligible area, recovery efficiency, additionality, leakage, and permanence yields approximately 1.0 Mt CO₂ yr⁻¹ of potentially issuable credits, fewer than two per cent of the headline figure. Eco-physiological suppression of this magnitude is currently invisible in national forest carbon accounting, and its recognition bears directly on dynamic baseline design and on the credibility of offsets generated from Mediterranean conifer forests. Full article

Background: Pyrotinib, an irreversible pan-HER tyrosine kinase inhibitor, has demonstrated substantial clinical efficacy in patients with HER2-positive breast cancer (BC). However, intrinsic and acquired resistance remain important challenges limiting therapeutic benefit, and reliable biomarkers for predicting pyrotinib response are currently unavailable. This study aimed to identify molecular determinants associated with pyrotinib resistance and uncover their underlying mechanisms. Methods: Pre-treatment tumour samples from an exploratory discovery cohort of 12 patients with HER2-positive BC receiving pyrotinib-containing neoadjuvant therapy were analysed by proteomic profiling. Differentially expressed proteins (DEPs) between the pathological complete response (pCR) and non-pCR groups were integrated with weighted gene co-expression network analysis and protein–protein interaction network analysis to identify candidate proteins. The prognostic relevance of the candidate genes was subsequently evaluated using 127 machine-learning strategies across three independent BC cohorts. Models were ranked according to the mean area under the receiver operating characteristic curve (AUC) across two evaluation cohorts, and SHapley Additive exPlanations (SHAP) analysis was performed separately in both cohorts to prioritise a candidate for subsequent investigation. In vitro and in vivo experiments were then conducted to evaluate the biological role of the prioritised candidate and its association with pyrotinib sensitivity. Finally, the association between pre-treatment SLC27A2 expression and pCR was evaluated in an independent, non-overlapping retrospective cohort of 103 patients receiving pyrotinib-containing neoadjuvant therapy. Results: Exploratory proteomic profiling of 12 pre-treatment tumour samples identified 617 DEPs between the pCR and non-pCR groups. Among 127 machine-learning strategies used to evaluate the prognostic relevance of the candidate genes, the glmBoost–random forest model achieved the highest mean AUC across the two evaluation cohorts (mean AUC = 0.678). SHAP analysis showed that SLC27A2 ranked second in GSE16446 and first in GSE48390 according to mean absolute SHAP values, supporting its prioritisation for subsequent investigation. Functional experiments showed that SLC27A2 promoted proliferation, migration, invasion, and epithelial–mesenchymal transition in HER2-positive BC cells. SLC27A2 knockdown enhanced pyrotinib sensitivity in vitro. In the xenograft experiment using female BALB/c nude mice, both SLC27A2 knockdown and pyrotinib treatment reduced tumour growth, and a significant interaction between the two factors was observed for endpoint tumour weight (p for interaction = 0.041). Mechanistically, SLC27A2 knockdown reduced lipid accumulation and PPARα expression, whereas pharmacological activation of PPARα partially attenuated the increase in pyrotinib sensitivity induced by SLC27A2 knockdown. Clinical validation further showed that high-pre-treatment SLC27A2 expression was independently associated with a lower likelihood of achieving pCR after pyrotinib-containing neoadjuvant therapy (OR = 0.10, 95% CI: 0.03–0.31, p < 0.001). Conclusions: SLC27A2 is a candidate factor associated with BC prognosis and reduced pyrotinib sensitivity in HER2-positive BC. Preclinical findings suggested that PPARα-related fatty acid metabolism may contribute to the association between SLC27A2 and pyrotinib response, while clinical validation showed that high-pre-treatment SLC27A2 expression was independently associated with a lower likelihood of achieving pCR following pyrotinib-containing neoadjuvant therapy. These findings support SLC27A2 as a candidate response-associated biomarker and potential therapeutic target, although further mechanistic investigation and external clinical validation are required. Full article

Chlorophyll-a concentration is a key indicator reflecting the growth status of phytoplankton, and its accurate prediction is of great significance for assessing the degree of water eutrophication. Although existing approaches have achieved good performance, they generally pay insufficient attention to multi-scale spatial information and show limitations in characterizing the continuous spatiotemporal dynamics. To address these issues, this paper proposes a multi-scale spatiotemporal graph ODE network (MGODE) for ocean chlorophyll-a prediction. The MGODE adopts a dual-layer structure, simultaneously processing chlorophyll-a concentration data at both the region level and node level to capture multi-scale spatial features, and it enables effective interaction of cross-scale features through dynamic transmission coefficients and a gated fusion mechanism. Meanwhile, the MGODE employs a dual-ODE architecture at both the node and region levels, utilizing spatiotemporal ODE blocks to continuously and deeply capture features, thereby simulating the continuous spatiotemporal dynamic evolution of chlorophyll-a. Experiments on real-world datasets from the Bohai Sea and South China Sea show that the proposed MGODE model achieves higher prediction accuracy than several current state-of-the-art models. Compared with the best baseline, the MGODE achieves reductions of 2.78% in MAE and 1.07% in RMSE on the Bohai Sea dataset and reductions of 1.19% in MAE and 1.38% in RMSE on the South China Sea dataset. These results demonstrate the potential of the MGODE to support marine chlorophyll-a forecasting and marine ecological monitoring. Full article

Oxidative stress is a major constraint limiting animal health and productive performance by disrupting redox homeostasis, mitochondrial function, intestinal integrity, and mineral metabolism. Agronomic biofortification of forage with essential trace minerals represents a promising nutritional strategy; however, its physiological and molecular mechanisms remain poorly understood. This study evaluated the effects of dietary zinc–iron (Zn–Fe) biofortified alfalfa on oxidative stress, antioxidant defense, mineral transport, mitochondrial bioenergetics, intestinal barrier integrity, inflammatory responses, tissue mineral deposition, and growth performance in guinea pigs. Forty-eight male guinea pigs were allocated to six experimental groups according to dietary treatment (control, Zn-biofortified alfalfa, or Zn–Fe biofortified alfalfa) and oxidative stress status. Oxidative biomarkers, antioxidant enzyme activities, inflammatory mediators, mineral concentrations, targeted RT–qPCR, mitochondrial function, intestinal histomorphology, and multivariate physiological analyses were performed. Zn–Fe biofortified alfalfa markedly reduced reactive oxygen species, malondialdehyde, protein carbonyls, 8-hydroxy-2′-deoxyguanosine, advanced oxidation protein products, and the oxidative stress index while significantly increasing superoxide dismutase, catalase, glutathione peroxidase, total antioxidant capacity, and the glutathione redox ratio. Targeted gene-expression analysis demonstrated coordinated upregulation of intestinal mineral transporters (ZIP4, DMT1, and MT1), activation of the Nrf2 antioxidant pathway, increased expression of mitochondrial regulatory genes, and suppression of inflammatory mediators. These molecular responses were accompanied by improved ATP production, mitochondrial membrane potential, respiratory-chain activity, preservation of intestinal villus architecture, enhanced expression of tight-junction proteins, increased tissue Zn and Fe deposition, superior feed efficiency, and greater body weight gain. Integrated physiological analyses consistently identified the Zn–Fe biofortified treatment as the highest-performing physiological phenotype, indicating coordinated adaptation across multiple biological systems. These findings demonstrate that Zn–Fe biofortified alfalfa enhances oxidative stress resilience through simultaneous regulation of mineral transport, antioxidant defense, mitochondrial bioenergetics, intestinal barrier integrity, and systemic physiological performance. Agronomic biofortification of forage therefore represents a promising nutritional strategy for improving animal health, mineral utilization, and productive efficiency under oxidative stress. Full article

The proliferation of inverter-based resources (IBRs) and energy storage systems in power grids has led to a decline in the short-circuit ratio (SCR) and reduced fault current magnitudes, compromising the reliability of conventional overcurrent relays (OCRs) and creating protection blind zones. To resolve these vulnerabilities, this paper proposes an electromagnetic repulsion-based Superconducting Fault Current-Limiting Circuit Breaker (SFCL-CB) utilizing a flux-lock type mechanism. Unlike protection schemes that rely on secondary accessories such as current and potential transformers which introduce computational delays, the proposed SFCL-CB utilizes a driving force that scales with the square of the current gradient ((di/dt)²). This characteristic allows the device to distinguish low-magnitude fault currents from transient load growths. Through duality-based modeling and parametric simulations in PSCAD/EMTDC, the structural and electrical design configurations—including the coil turns (N₁, N₂) and the superconducting quench resistance (R_SC)—were optimized. The simulation results verify that the proposed SFCL-CB substantially reduces the OCR blind zone, securing fault clearance within a maximum of 0.131 s in the regions cleared under low SCR and high-fault-resistance conditions, while achieving mechanical separation in 0.0048 s under robust power system. This SFCL-CB offers an alternative to enhance the protection reliability and operational stability of distribution power system. Full article

Background: Fetal programming, conceptualized within the Developmental Origins of Health and Disease framework, describes how intrauterine exposures may shape long-term offspring physiology and disease susceptibility. Metformin is increasingly used during pregnancy for gestational diabetes mellitus, type 2 diabetes mellitus, and selected cases of polycystic ovary syndrome. Its developmental interpretation is complex because the drug improves the maternal metabolic environment but also crosses the placenta and directly exposes the fetus. Methods: This focused narrative review used iterative, targeted searches of PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify pharmacological, placental, mechanistic, clinical, guideline-based, and offspring follow-up evidence. The literature search covered publications available through 31 May 2026. The manuscript was subsequently revised during the editorial submission and peer-review process, and the evidence synthesis was re-evaluated against this final literature cut-off date. Earlier landmark studies were retained where necessary for historical, pharmacological, or methodological context. Results: Metformin reduces hepatic glucose production and maternal insulin resistance and may limit gestational weight gain, insulin requirements, neonatal hypoglycemia, and excessive fetal growth in selected pregnancies. Placental transfer creates biological plausibility for direct effects on AMPK, mitochondrial, mTOR, nutrient-sensing, and epigenetic pathways. Long-term studies are broadly reassuring regarding neurodevelopment and major metabolic disease, but findings on growth trajectory, adiposity, and small-for-gestational-age risk remain heterogeneous and indication-dependent. Conclusions: Metformin should be interpreted neither as uniformly beneficial nor as developmentally neutral. Its use should be individualized according to maternal phenotype, indication, glycemic benefit, placental function, fetal growth, dose, timing, and the limitations of long-term offspring evidence. Full article

Background: Fetal cardiac rhabdomyomas are strongly associated with tuberous sclerosis complex (TSC). Although many remain asymptomatic and regress spontaneously, large tumors may cause ventricular inflow or outflow obstruction, arrhythmia, impaired ventricular function, pericardial effusion, hydrops fetalis and fetal demise. Transplacental mammalian target of rapamycin (mTOR) inhibition has emerged as a potential rescue therapy. Methods: We performed a narrative review of published reports on prenatal sirolimus or everolimus therapy for fetal cardiac rhabdomyomas in suspected or confirmed TSC. Data was extracted on treatment indication, gestational age at initiation, treatment duration, fetal echocardiographic response, maternal adverse effects, delivery and postnatal outcome. Results: Available evidence consists predominantly of case reports, small case series and retrospective cohorts; no prospective controlled trials were identified. Treatment was generally initiated for progressive or hemodynamically significant disease, particularly ventricular inflow or outflow obstruction, worsening valve regurgitation, arrhythmia, pericardial effusion, ventricular dysfunction or hydrops. Therapy was usually started in the late second or third trimester and continued until hemodynamic stabilization, delivery or planned transition to neonatal treatment. Most reports described tumor regression within 1–3 weeks, accompanied by improved cardiac function and high perinatal survival. However, rebound growth after treatment withdrawal, persistent arrhythmic risk and limited long-term safety data remain important concerns. Conclusions: Prenatal mTOR-inhibitor therapy should be considered an individualized rescue or stabilization strategy for fetuses with life-threatening or progressive cardiac compromise, rather than routine treatment for all fetal rhabdomyomas. Management should be multidisciplinary and guided by fetal hemodynamics, treatment response, maternal tolerance and gestational age. Full article

Prebiotics are predominantly indigestible carbohydrate-based substrates selectively-utilized by beneficial gut-microbes to support host-health. We previously developed protein-containing prebiotics that co-deliver carbohydrate and protein substrates to the colon, where gut-microbes compete for the limited nitrogen availability, thereby enhancing microbial growth, metabolic activity, and host health compared with conventional carbohydrate prebiotics. Resveratrol is a grape-derived polyphenol with antioxidant, anti-inflammatory, and emerging prebiotic activity. Here, we developed a multifunctional protein-containing prebiotic system based on Maillard conjugates of 2′-fucosyllactose–potato protein hydrolysate (2′-FL-PPH) micelles encapsulating resveratrol, followed by genipin crosslinking. This crosslinked 2′-FL-PPH-resveratrol system is designed to limit premature protein and resveratrol absorption, enhancing their colonic co-delivery. We characterized the encapsulation efficacy, physicochemical properties, digestibility and colonic delivery. The conjugates (10 mg/mL 2′-FL-PPH) effectively entrapped resveratrol (600 µM), exhibiting an average particle size of ~28 nm and an encapsulation efficiency of 79.5 ± 4.9%. Binding studies demonstrated predominantly hydrophobic interactions between resveratrol and 2′-FL-PPH. The conjugates prevented resveratrol crystallization in aqueous media, while genipin crosslinking enhanced resistance to simulated gastrointestinal digestion and inhibited premature resveratrol release, increasing the fraction expected to reach the colon. Collectively, this system enables colonic co-delivery of carbohydrate, peptides, and resveratrol, providing a novel strategy for promoting beneficial-microbiota and gut-health. Full article

Nanomaterials are increasingly used in manufacturing, medicine, consumer products, and environmental technologies due to their unique physicochemical properties. Although these materials offer substantial technological and societal benefits, their widespread use has raised concerns about potential health risks. Of particular importance is exposure during pregnancy, as certain nanoparticles can cross the placental barrier and reach the developing embryo. Fetal tissues are highly sensitive to environmental insults, so maternal exposure to nanoparticles may disrupt normal development and increase the risk of abnormal pregnancy outcomes. This review examines the current understanding of nanoparticle-induced developmental toxicity, with a focus on the vulnerability of the maternal–fetal unit. We discuss the structure and function of the placental barrier and the mechanisms that enable nanoparticle transfer from mother to fetus. Particular attention is given to how nanoparticle characteristics, including size, shape, composition, and surface chemistry, influence biodistribution, placental transport, tissue accumulation, and toxicity. We summarize the major molecular and cellular mechanisms implicated in fetotoxicity, highlighting oxidative stress, apoptosis, autophagy, and DNA damage as recurring pathways identified across experimental studies. These interconnected processes contribute to placental dysfunction, impaired fetal growth, developmental abnormalities, and adverse pregnancy outcomes. We also compare findings across different classes of nanoparticles, including metal, metal oxide, carbon-based, and polymeric nanomaterials, identifying both shared toxicological mechanisms and material-specific effects. Evidence from animal models demonstrates that susceptibility varies according to nanoparticle properties, exposure conditions, and species, underscoring the complexity of nanoparticle–biological interactions and the limitations of extrapolating experimental findings directly to humans. Overall, the available evidence indicates that nanoparticle exposure during pregnancy represents a potential risk to fetal health, although important knowledge gaps remain regarding human exposure and long-term developmental outcomes. A better understanding of the mechanisms underlying nanoparticle-induced fetotoxicity is essential for improving human health risk assessment, refining experimental models, informing regulatory policies, and supporting the safe-by-design development of nanomaterials. Such knowledge will help ensure the responsible application of nanotechnology while minimizing potential risks during pregnancy. Finally, this review is distinguished by its integrated analysis of how the chemical characteristics of nanoparticles govern placental transfer and the mechanistic pathways of fetotoxicity across multiple nanomaterial classes, providing a unified framework that connects material properties with their potential for abnormal fetal development and adverse pregnancy outcomes. Full article

This study presents a multiscale numerical simulation of the behavior of crack growth in the heat-affected zone (HAZ) of AH36 marine steel welded joints under fatigue loading from the micro-scale to the macro-scale. The MD-FEM method and the multiscale coupling-optimized XFEM method were used to simulate fatigue crack propagation from micro-scale to meso-scale and from meso-scale to macro-scale. A total of 10,900,788 tension–tension fatigue cycles was realized. Information across different scales was transferred via boundary displacement transfer, crack morphology equivalence, and tip tracking. Building upon our previous investigation into fatigue crack growth behavior at the micro-scale, in which crack extension was limited to 469 Å, the present study encompasses the complete process of fatigue cracking from micro-scale initiation to macro-scale instability. Furthermore, the crack tip morphology and propagation pathways obtained from micro-scale molecular dynamics simulations are employed to optimize and calibrate the corresponding XFEM simulations at both the meso- and macro-scales. Results demonstrate that the phenomenon of interconnection between voids and the main crack near the crack tip has a significant influence on the crack propagation rate and path. During cycling, the propagation rate of the main crack increases significantly during its interconnection with voids, whereas crack propagation is significantly hindered when the interconnection is completed or when voids undergo self-closure. Furthermore, both theoretical simulations and experiments revealed the occurrence of crack propagation instability at the meso-scale. The present examination of the entire fatigue crack propagation process indicates that the MD-FEM method and the multiscale coupling optimized XFEM method in this study are fundamentally accurate in representing both the crack propagation process and the crack tip morphology. The results obtained in this paper can serve as a reasonable prediction of fatigue damage mechanisms in the HAZ of AH36 marine steel welded joints. Full article

Sphingolipids, a class of lipids, are widely present in the cell membranes of all eukaryotic and some prokaryotic organisms. These lipids play crucial roles in the formation of the lipid bilayer and are categorised into several groups, including sphingomyelins, ceramides, sphingosine-1-phosphate, and glycosphingolipids. In addition to their structural significance, sphingolipids also show bioactivity, regulating various signalling pathways involved in cell growth, differentiation, ageing, and apoptosis, and are closely associated with several chronic diseases, including obesity and type 2 diabetes mellitus. Notably, dysregulated sphingolipid metabolism contributes to obesity-related metabolic dysfunction through altered lipid accumulation, insulin signalling, organelle stress, and inflammation. This review summarises the various mechanisms and recent research advances related to sphingolipids and their association with obesity. It further examines how the metabolic effects of ceramides vary according to their acyl-chain length, enzyme of origin, tissue distribution, and metabolic context, as well as how adipose depot, sex, age, and metabolic phenotype influence the sphingolipid response to obesity. It further considers plant-derived sphingolipids as a compositionally distinct exogenous input to host sphingolipid pools, comparing their structural and enzymatic features with those of mammalian sphingolipids. Pharmacological, dietary, and lifestyle approaches that modify sphingolipid metabolism are also considered. Accordingly, the review summarises our current knowledge regarding the dietary occurrence, intestinal handling, and metabolic effects of sphingolipids and identifies the evidence gaps that currently limit conclusions regarding their relevance to obesity. Full article

Streptococcus cristatus (S. cristatus) belongs to the viridans group of streptococci and is a commensal of the human upper respiratory tract. With the non-phosphorylating glyceraldehyde-3-phosphate dehydrogenase, GapN, and the oxidative part of the pentose phosphate pathway (oxPPP), S. cristatus can use two different metabolic pathways to provide reduced nicotinamide adenine dinucleotide phosphate (NADPH), an essential cofactor of anabolic reactions such as fatty acid and amino acid biosynthesis. Regarding their NADP-reducing capacity, streptococci can be categorized into three groups: those that have only GapN, those that use only the oxPPP, and those that use both pathways. Here, we report on the experimental and computational characterization of the catalytic properties of the three NADP-reducing enzymes: GapN, glucose-6-phosphate dehydrogenase (G6PDH), and 6-phosphogluconate dehydrogenase (6PGDH) of S. cristatus. Kinetic analyses showed moderate substrate and cofactor affinities, with GapN displaying the tightest substrate binding, followed by 6PGDH and G6PDH, in agreement with structural and computational predictions. All three enzymes preferentially utilized NADP⁺, with only G6PDH exhibiting limited NAD⁺ promiscuity. Growth-phase-dependent activity patterns suggest dynamic adjustment of NADPH-generating pathways, with reduced GapN contribution and sustained oxPPP activity in the stationary phase. Regulatory screening indicated limited allosteric control, though feedback inhibition by NADPH and the ATP sensitivity of G6PDH point to conserved redox regulatory mechanisms. Comparative analysis across streptococci supports the concept that the coexistence of GapN and the oxidative pentose phosphate pathway in S. cristatus may provide metabolic flexibility by offering alternative routes for NADPH generation. Full article

Persister cells pose severe threats and serve as the primary drivers of chronic and recurrent infections. Nevertheless, clinical laboratories rarely quantify persister fractions of pathogenic bacteria due to the limited number of detection approaches and scarce available detection biomarkers. In our prior study, we identified a transposon insertion mutant of the essential gene pth. The growth curve, lag time and persister fraction measurements indicated that the pth-Tn strain exhibited slow growth with a markedly elevated persister cell proportion. Transcriptomic and metabolomic analyses revealed that the pth-Tn strain exhibited typical persister phenotypic characteristics, including reduced energy metabolism, membrane biogenesis, substrate transport and translational activity, among others. The pth mutations in host-transmitted E. coli could serve as indicators of persister levels, as also demonstrated in vitro. Thus, we identified seven point mutations in pth among clinical isolates. Compared with clinical isolates harboring the wild-type pth gene, the G109S mutants displayed higher persister fractions. Multiple linear regression models revealed that the G109S mutation was independently associated with elevated persister levels. Collectively, these findings reveal an association between the pth G109S mutation and elevated persister levels in clinical isolates. Full article

Hydraulic perturbations are among the earliest plant-wide consequences of drought, salinity and wounding, yet they are often treated as passive outcomes rather than as biologically interpreted inputs. This review distinguishes hydraulic state, hydraulic perturbation and hydraulic signal, and evaluates how organ-scale pressure and water-potential changes are converted into local membrane tension, wall strain, turgor and water-flux cues. We propose, as a testable model rather than an established mechanism, a distributed architecture comprising OSCA/TMEM63 and other mechanosensitive channels, cell-wall integrity pathways, aquaporin-mediated conductance control and vacuolar buffering. Evidence for the individual components is substantial, but evidence that they act together within a single physiological event is still limited. These layers are reciprocally coupled to Ca²⁺, ROS, electrical, hormonal and peptide networks. Hydraulic cues are fast, and they differ in amplitude, direction, rise time, duration, recovery and anatomical route, so they are not informationally inert. Specificity nevertheless appears to emerge from the integration of the hydraulic waveform with tissue state and coincident ionic, electrical and biochemical inputs rather than from any single variable. We compare drought, salinity and wounding; clarify the roles of roots, vasculature, bundle sheath, mesophyll and guard cells; and outline experiments that combine calibrated physical perturbations with live reporters, tissue-specific genetics and hydromechanical modeling. The key frontier is no longer to document that pressure changes occur. It is to identify the variables directly sensed, to separate instructive from permissive roles, and to test whether dynamic decoding traits improve crop resilience at acceptable carbon and growth cost. Full article