Search Results (20,251)

Background/Objectives: Post-cardiac arrest syndrome (PCAS) induces systemic ischemia–reperfusion injury accompanied by sepsis-like coagulopathy. This coagulopathy presents heterogeneously, yet distinct coagulation phenotypes and their impact on hypoxic–ischemic brain injury (HIBI) remain poorly defined. We aimed to identify coagulation phenotypes using latent class analysis (LCA) and assess their association with 6-month neurological outcomes. Methods: We retrospectively analyzed adult out-of-hospital cardiac arrest (OHCA) patients treated with targeted temperature management (TTM) between 2011 and 2019 from a prospective registry at a tertiary academic center. LCA was performed using coagulation biomarkers measured at admission and 24 h post-return of spontaneous circulation: D-dimer, fibrinogen, antithrombin III (ATIII), platelet count, and PT-INR. The primary outcome was poor neurological outcome (Cerebral Performance Category 3–5) at 6 months. Secondary outcomes included in-hospital mortality and cerebral edema severity assessed by gray-to-white matter ratio (GWR) on brain CT. Results: Among 325 patients, LCA identified three phenotypes: Class 1 (Preserved Coagulation, 36.9%), Class 2 (Hypercoagulable State, 41.5%) characterized by elevated D-dimer with preserved fibrinogen and ATIII, and Class 3 (Consumptive Coagulopathy, 21.5%) marked by profound D-dimer elevation with fibrinogen <150 mg/dL and ATIII <60%. Class 3 exhibited the lowest GWR and highest neuron-specific enolase levels. In multivariable analysis adjusting for age, low-flow time, initial rhythm, and lactate, Class 3 independently predicted poor neurological outcome (adjusted OR 4.52; 95% CI 2.15–9.48), whereas Class 2 did not. Conclusions: PCAS-related coagulopathy is heterogeneous. A consumptive coagulopathy phenotype identifies a high-risk subgroup associated with severe brain injury and poor long-term neurological outcomes. Early identification of this phenotype may enable targeted prognostication and guide future phenotype-specific interventional strategies.: Full article

PCIF1 is primarily recognized as an RNA methyltransferase that mediates N⁶-methylation of cap-proximal adenosine (m⁶Am) and plays diverse roles in gene expression. In this study, we uncover a novel role for PCIF1 as a crucial negative regulator of type I interferon (IFN) induction, a pathway critical for antiviral immunity whose dysregulation leads to inflammatory and autoimmune diseases. We demonstrate that PCIF1 deficiency robustly enhances the poly(I:C)-induced type I IFN response, accompanied by augmented STAT1 activation and interferon-stimulated gene (ISG) expression. Mechanistically, PCIF1 suppresses IFNB1 transcription by attenuating IRF3 phosphorylation and nuclear translocation, as shown by increased nascent IFNB1 mRNA synthesis and promoter activity in PCIF1-deficient cells, without affecting the mRNA stability. Crucially, this suppressive function was independent of PCIF1’s canonical RNA methyltransferase activity, as both wild-type PCIF1 and a methyltransferase-inactive mutant effectively attenuated type I IFN induction. Collectively, our findings establish PCIF1 as a novel methyltransferase-independent suppressor of type I IFN responses, revealing its previously unrecognized non-catalytic function. This discovery offers critical insights into the multifaceted regulation of innate immunity and highlights PCIF1’s non-catalytic function as a promising therapeutic target for modulating antiviral responses and inflammatory diseases. Full article

Atrial fibrillation (AF) is closely linked to atrial remodeling, while its underlying immune mechanisms remain elusive. This study sought to investigate the role of SPP1⁺ macrophages in the development and progression of AF and further elucidate the underlying mechanisms. Single-nucleus RNA sequencing was performed on right atrial tissues from 3 patients with persistent AF and 3 with sinus rhythm (all with rheumatic valvular heart disease). The results revealed significant immune cell infiltration in AF atrial tissues, with a marked increase in the proportion of SPP1⁺ macrophages, which exhibited the strongest intercellular communication with cardiomyocytes. Phenotypic scoring indicated that apoptosis was the dominant mode of cardiomyocyte death in AF. Immunohistochemical and Western blot analyses confirmed elevated levels of pro-apoptotic proteins (Bax, Cleaved-Caspase3) and reduced levels of the anti-apoptotic protein Bcl2 in AF tissues. In a mouse model with macrophage-specific SPP1 overexpression, increased AF inducibility and duration were observed, accompanied by enhanced cardiomyocyte apoptosis. In vitro co-culture experiments using SPP1-overexpressing RAW264.7 macrophages and HL-1 cardiomyocytes confirmed that SPP1⁺ macrophages could induce cardiomyocyte apoptosis. Mechanistically, KEGG and GSEA analyses identified downregulation of the PI3K/AKT pathway in AF. Treatment with the PI3K/AKT activator Recilisib reversed apoptosis and restored p-PI3K/p-AKT levels in HL-1 cells co-cultured with SPP1-overexpressing RAW264.7 macrophages. These findings demonstrate that SPP1⁺ macrophages accumulate in atrial tissues of AF patients and induce cardiomyocyte apoptosis by downregulating the PI3K/AKT pathway, thereby increasing AF susceptibility. Full article

The pathogenesis of primary osteoarthritis (OA) is complex and multifactorial. Nuclear factor erythroid 2-related factor-2 (Nrf2) is a transcription factor that regulates hundreds of genes involved with cytoprotection. The role of Nrf2 in OA remains undefined. We utilized the Hartley guinea pig model of primary OA to investigate the role of a purported Nrf2 activator, PB125, in delaying the onset of knee OA. We hypothesized that three months of daily PB125 supplementation would modify structural, molecular, and in vivo functional outcomes characteristic of disease. Fifty-six 2-month-old animals (equal sexes) were treated orally with PB125 or vehicle control for 3 months; animals were sacrificed at 5 months, which represents mild OA and early disease. Outcome measures included knee histopathology, mRNA expression, immunohistochemistry, and in vivo mobility. Notably, PB125 treatment had differing effects in males and females. Female PB125-treated animals had significantly decreased distal femur OA scores, accompanied by differential gene and protein expression patterns in articular cartilage for markers related to redox homeostasis; decreases in one compulsory mobility metric were also seen. In contrast, males demonstrated a statistical difference in voluntary mobility patterns. In summary, PB125 may modify the molecular mechanisms involved in the initiation of early OA in a potential sex-dependent fashion. Full article

Mechanical recycling of polyethylene terephthalate (PET) is a key strategy for circular packaging applications; however, repeated thermo-mechanical processing leads to progressive polymer degradation. In this study, the effect of controlled repeated extrusion on the degradation behavior of bottle-grade PET was systematically investigated under laboratory conditions. Mechanical recycling was simulated using a co-rotating twin-screw extruder, where PET was subjected to up to four consecutive processing cycles corresponding to a cumulative residence time of 8 min. Progressive processing resulted in chain scission, reflected by a decrease in intrinsic viscosity from approximately 0.80 to 0.65 dL·g⁻¹ and a corresponding reduction in molecular weight. Melt flow rate increased accordingly, indicating a gradual loss of melt strength. Differential scanning calorimetry revealed that the glass transition and melting temperatures remained nearly unchanged, while the degree of crystallinity increased from approximately 23.0% to 29.5%, accompanied by changes in crystallization behavior. These structural changes led to reduced ductility, with elongation at break decreasing from about 84% to 60%. Optical analysis showed systematic material darkening, and a strong linear correlation between lightness (L*) and intrinsic viscosity was observed. By isolating intrinsic thermo-mechanical degradation effects under controlled processing conditions, this study enables a clearer definition of realistic reuse limits for mechanically recycled bottle-grade PET. The results indicate that bottle-grade PET retains properties compatible with demanding applications only after a limited number of thermo-mechanical processing cycles, whereas further processing restricts its usability to less demanding applications such as fibers, films, and non-food packaging. Full article

Colorectal cancer (CRC) cachexia is a multifactorial, treatment-limiting syndrome characterized by progressive loss of skeletal muscle with or without loss of fat mass, accompanied by systemic inflammation, anorexia, metabolic dysregulation, and impaired treatment tolerance. Despite decades of work, cachexia remains clinically underdiagnosed and therapeutically underserved, in part because canonical models treat tumor-derived factors and host inflammatory mediators as a largely ‘host-only’ network. In parallel, CRC is strongly linked to intestinal dysbiosis, barrier disruption, and microbial translocation. Extracellular vesicles (EVs)—host small EVs, tumor-derived EVs, and bacterial extracellular vesicles (including outer membrane vesicles)—may provide a mechanistically plausible, information-dense route by which these domains could be coupled. Here, we synthesize emerging evidence suggesting that cross-kingdom EV signaling may operate as a vesicular ecosystem spanning gut lumen, mucosa, circulation, and peripheral organs. We propose the “vesicular intersection layer” as a unifying framework for how heterogeneous EV cargos converge on shared host decoding hubs (e.g., pattern-recognition receptors and stress-response pathways) to potentially contribute to muscle catabolism. We critically evaluate what is known—and what remains unproven—about EV biogenesis, trafficking, and causal mechanisms in CRC cachexia, highlight methodological constraints in microbial EV isolation and attribution, and outline minimum evidentiary standards for cross-kingdom claims. Finally, we translate the framework into actionable hypotheses for EV-informed endotyping, biomarker development (including stool EV assays), and therapeutic strategies targeting shared signaling nodes (e.g., TLR4–p38) and endocrine mediators that are predominantly soluble but may be fractionally vesicle-associated (e.g., GDF15). By reframing CRC cachexia as an emergent property of tumor–host–microbiota vesicular communication, this review provides a roadmap for mechanistic studies and clinically tractable interventions. Full article

Background: This study investigated the hypolipidemic and hepatoprotective effects of refined soybean oil supplemented with an Ocimum basilicum L. extract, characterized by HPLC and found to be rich in caftaric, caffeic, chicoric, and rosmarinic acids. Methods: After a 12-week model of diet-induced hyperlipidemia, we examined the plasma levels of TC, TG, Glucose, HDL-C, and LDL-C and the LDL-C/HDL-C ratio using enzymatic kits. The Plasma Hepatic and Biliary Marker Analysis was analysed following standardized hospital protocols with quality-controlled instrumentation. Results: The supplementation with Basil-Enriched Oil (BEO) resulted in a notable redistribution of lipids, significantly reducing the plasma total cholesterol (−75%), triglycerides (−96%), and glucose (−22%), while enhancing their hepatic sequestration. This was accompanied by a marked improvement in the LDL-C/HDL-C ratio and a reduction in hepatic oxidative stress (measured by MDA). Importantly, BEO preserved liver structure and prevented steatosis, despite inducing an increase in adaptive hepatomegaly. Conclusions: The results reveal a dual mechanism whereby the antioxidant properties of BEO collaborate with reprogrammed lipid metabolism, promoting safe hepatic storage rather than harmful circulating levels. These findings strongly advocate for the extract’s potential as a nutraceutical for addressing hyperlipidemia and related metabolic disorders by targeting both oxidative stress and lipid imbalance. Further research is required to confirm these effects in clinical settings and to confirm its long-term efficacy. Full article

Background/Objectives: Chronic kidney disease (CKD) in older adults is frequently accompanied by substantial medication burden, increasing risks of adverse drug events and poor adherence. The Planetary Health Diet Index (PHDI), emphasizing plant-based foods and sustainable dietary patterns, may improve cardiometabolic health and reduce medication requirements. This study examined the association between PHD adherence as measured by the PHDI and medication burden among older adults with CKD. Methods: We analyzed cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) 2003–2018 cycles. Older individuals aged ≥ 65 years with CKD (estimated glomerular filtration rate < 60 mL/min/1.73 m² or albumin-to-creatinine ratio > 30 mg/g) at the baseline visit were included (n = 3161). PHDI scores (0–150) were calculated from two consecutive 24 h dietary recalls. Medication burden was assessed as the total prescription medication count and frequency of individual classes. Multivariable Poisson regression models evaluated associations between PHDI score and number of prescribed medications, adjusting for sociodemographic, lifestyle, and clinical covariates; logistic regression models were used to evaluate the association between PHDI score and specific medication classes. Results: Mean (SD) age was 75.0 (5.5) years; mean PHDI score was 62.4 (18.7). Participants in the highest PHDI tertile had significantly lower medication burden compared to the lowest tertile. In fully adjusted Poisson regression models, each 10-point increase in PHDI score was associated with 3% fewer medications (RR: 0.97, 95% CI: 0.96–0.99, p = 0.011). Participants in the highest PHDI tertile had 8% fewer medications compared to the lowest tertile (RR: 0.92, 95% CI: 0.87–0.98, p = 0.013). Higher PHDI scores were significantly associated with lower odds of proton pump inhibitor use (OR: 0.86, 95% CI: 0.79–0.94 per 10-point increase) and nonsteroidal anti-inflammatory drug prescription (OR: 0.86, 95% CI: 0.76–0.97 per 10-point increase). Participants in the highest PHDI tertile had 34% lower odds of PPI use (OR: 0.66, 95% CI: 0.49–0.89) and nonsignificant lower odds of NSAID use (OR: 0.67, 95% CI: 0.40–1.11) compared to those in the lowest tertile. Conclusions: Higher PHDI adherence was independently associated with lower medication burden in older adults with CKD. These findings suggest that plant-forward, sustainable dietary patterns may reduce pharmacological complexity in this vulnerable population. Prospective studies are needed to assess causality and clinical implementation strategies. Full article

Chronic liver injury is accompanied by coordinated disturbances in lipid trafficking and inflammatory–fibrogenic signaling. Transforming growth factor beta 1 (TGF-β1) signaling has been implicated in hepatic fibrogenesis and tumor-associated remodeling and may co-vary with disturbances in lipid trafficking. Lisosan G (LG), a fermented wheat-derived nutraceutical, has reported antioxidant and anti-inflammatory activity and may influence these interconnected pathways. This study evaluated whether dietary LG alters the lipid composition of plasma lipoprotein fractions and hepatic TGF-β1 levels across distinct liver contexts. Seventy-two female Wistar rats were randomized into nine groups (n = 8/group) defined by liver condition, consisting of healthy control (Control), non-neoplastic liver (PH), and neoplastic liver injury (HCC; PH followed by diethylnitrosamine, DEN), and diet (standard diet, SD + 2.5% LG, or SD + 5% LG). Plasma lipoproteins (VLDL, LDL, HDL₁, HDL₂) were isolated by stepwise KBr density-gradient ultracentrifugation, and cholesterol (TC), phospholipids (PL), and triacylglycerols (TG) were quantified in each fraction. Hepatic TGF-β1 was measured by ELISA and normalized to total protein. LG effects depended strongly on baseline liver status, with significant Condition × Diet interactions for most lipid endpoints and for hepatic TGF-β1. In healthy rats, LG produced fraction-selective remodeling rather than uniform lipid lowering, including increased VLDL-TG at both doses and non-linear changes in cholesterol distribution across LDL and HDL subfractions. After PH, LG broadened lipid remodeling, including reduced VLDL-PL, increased VLDL-TG (both doses), and an increase in LDL-TC at 5% LG, accompanied by marked changes in HDL₁/HDL₂ cholesterol partitioning. In HCC, LG induced pronounced, often dose-dependent increases in LDL-associated lipids (LDL-PL, LDL-TG, LDL-TC) and increased HDL₁-TC while decreasing HDL₂-TC. Hepatic TGF-β1 was elevated in PH and further increased in HCC versus controls; LG reduced hepatic TGF-β1 in a condition-dependent manner, with the strongest reduction at 5% LG in HCC. Dietary Lisosan G remodels circulating lipoprotein lipid composition in a liver-status-dependent manner and is associated with reduced hepatic TGF-β1 abundance in injured liver, most prominently in neoplastic injury. These findings are consistent with the notion that nutraceutical interventions may show stronger phenotypic effects under perturbed metabolic–fibrogenic states than under stable physiology, while highlighting the need for mechanistic work to distinguish altered lipoprotein secretion from changes in peripheral clearance and to assess pathway-level TGF-β signaling. Full article

Pulmonary hypertension (PH) is characterized by progressive pulmonary vascular remodeling and a paucity of effective therapeutic interventions. Although dysregulated mitochondrial dynamics are implicated in this remodeling process, the key regulatory molecules and downstream mechanisms remain incompletely defined. This study aimed to systematically characterize molecular alterations associated with mitochondrial dynamics in PH and to explore the functional relevance and potential mechanisms of prioritized candidate genes. We integrated transcriptomic datasets from PH models with MitoCarta annotations to identify mitochondria-related differentially expressed genes. Candidate genes were prioritized using WGCNA and three machine-learning algorithms (LASSO, SVM-RFE, and random forest). These candidates were then experimentally evaluated in a hypoxia-induced PH mouse model and hypoxia-stimulated mouse pulmonary artery smooth muscle cells (mPASMCs) using qRT–PCR, Western blotting, immunohistochemistry, and transmission electron microscopy. Functional assays and assessments of mitochondrial injury were performed to investigate pathogenic relevance. Our analysis identified four key genes, with FIS1 showing high ROC/AUC-based discriminatory performance in both the training dataset and the independent replication dataset. Hypoxia was associated with increased FIS1 expression, mitochondrial fragmentation, loss of mitochondrial membrane potential, and ROS accumulation. We further observed that FIS1 knockdown suppressed mPASMC proliferation and migration, alleviated mitochondrial injury, and attenuated ferroptosis-associated alterations, accompanied by reduced lipid peroxidation, decreased Fe²⁺ accumulation, and partial normalization of ferroptosis-related marker proteins. Taken together, these findings suggest that FIS1 may contribute to PH pathogenesis through mitochondrial fission and ferroptosis-associated stress, potentially promoting aberrant PASMC phenotypes and pulmonary vascular remodeling. This work provides a mechanistic rationale and molecular leads that may inform molecular stratification and mechanistically informed therapeutic exploration targeting mitochondrial pathways in PH. Full article

Peroxiredoxin 6 (Prdx6) is a bifunctional antioxidant enzyme with glutathione peroxidase and phospholipase A₂ activities that plays an essential role in cellular redox regulation. However, the modulation of Prdx6 activity by endogenous small metabolites remains poorly understood. In this study, we investigated the effect of β alanine on Prdx6 structure and function using biochemical, biophysical, computational, and cellular approaches. Enzymatic assays revealed that β alanine enhances the peroxidase activity of Prdx6 in a dose-dependent manner. Spectroscopic analyses demonstrated β alanine-induced conformational stabilization of Prdx6, which was further supported by increased thermal stability. Molecular docking and molecular dynamics simulations identified a stable interaction of β alanine at a distinct allosteric site on Prdx6, accompanied by reduced local flexibility. In a proof-of-concept cellular system, β alanine treatment resulted in a significant reduction in intracellular reactive oxygen species, consistent with enhanced Prdx6-associated antioxidant activity. Collectively, these findings identify β alanine as a biochemical modulator of Prdx6 activity. The study is limited to mechanistic and cellular redox regulation and does not address tissue- or disease-specific physiology. Full article

Shoreline variations in closed-basin lakes are closely linked to hydrological fluctuations and long-term changes in water balance, making them important indicators of environmental change. This study analyzes historical shoreline dynamics in Lake Van (Türkiye), the world’s largest soda lake, and provides scenario-based shoreline projections for 2032 and 2042 to support hydrological assessment and water-related management. Multi-temporal Landsat satellite images from 1982, 1992, 2002, 2012, and 2022 were processed using the Digital Shoreline Analysis System (DSAS 5.0) to quantify shoreline retreat and accretion, while future shoreline positions were estimated using the Kalman filter model. The results show pronounced spatial variability, with the most significant shoreline retreat observed in the Çelebibağ and Karahan regions, where sediment supplied by major inflowing streams contributes to shoreline instability through reworking and redistribution rather than stable accretion. Net shoreline movement values reached −2580.1 m for erosion and up to 1700 m for accretion. Model projections indicate an increasing trend of shoreline retreat by 2032 and 2042, accompanied by localized accretion zones. These hydrological-driven shoreline changes have potential implications for littoral habitats, water–land interactions, and human use of the shoreline, including fisheries infrastructure. The study demonstrates the value of integrating remote sensing and statistical forecasting for monitoring shoreline dynamics in closed-basin lake systems. Full article

We present a fully controlled thermodynamic study of the two-dimensional dipolar Q-state clock model on small square lattices with free boundaries, combining exhaustive state enumeration with noise-free evaluation of canonical observables. We resolve the complete energy spectra and degeneracies $\{E_n,c_n\}$ for the Ising case ($Q=2$) on lattices of size $L=3,4,5$, and for clock symmetries $Q=4,6,8$ on a $3\times 3$ lattice, tracking how the competition between exchange and long-range dipolar interactions reorganizes the low-energy manifold as the ratio $\alpha =D/J$ is varied. Beyond a finite-size characterization, we identify several qualitatively new thermodynamic signatures induced solely by dipolar anisotropy. First, we demonstrate that ground-state level crossings generated by long-range interactions appear as exact zeros of the specific heat in the limit $C(T\to 0,\alpha )$, establishing an unambiguous correspondence between microscopic spectral rearrangements and macroscopic caloric response. Second, we show that the shape of the associated Schottky-like anomalies encodes detailed information about the degeneracy structure of the competing low-energy states: odd lattices ($L=3,5$) display strongly asymmetric peaks due to unbalanced multiplicities, whereas the even lattice ($L=4$) exhibits three critical values of $\alpha$ accompanied by nearly symmetric anomalies, reflecting paired degeneracies and revealing lattice parity as a key organizing principle. Third, we uncover a symmetry-driven crossover with increasing Q: while the $Q=2$ and $Q=4$ models retain sharp dipolar-induced critical points and pronounced low-temperature structure, for $Q\ge 6$, the energy landscape becomes sufficiently smooth to suppress ground-state crossings altogether, yielding purely thermal specific-heat maxima. Altogether, our results provide a unified, size- and symmetry-resolved picture of how long-range anisotropy, lattice parity, and discrete rotational symmetry shape the thermodynamics of mesoscopic magnetic systems. We show that dipolar interactions alone are sufficient to generate nontrivial critical-like caloric behavior in clusters as small as $3\times 3$, establishing exact finite-size benchmarks directly relevant for van der Waals nanomagnets, artificial spin-ice arrays, and dipolar-coupled nanomagnetic structures. Full article

C. spectabilis (Crotalaria spectabilis), a large leguminous herb species, is widely distributed in tropical and subtropical regions, and it has important ecological and economic values. However, the ecological adaptation of the major leaf functional traits of the species across different habitats and canopy positions remains poorly understood. To address this gap, we sampled leaves from the upper, middle, and lower canopy positions in two common habitats—forest understory and exposed land—and quantified key leaf traits as well as trait–trait relationships to assess differences. The results showed that irradiance and air temperature were significantly lower in the understory than in exposed land, whereas soil moisture and relative humidity were higher, indicating that habitat exerted a stronger influence on leaf traits than canopy position. Canopy position also significantly affected most traits and showed significant interactions with habitat. In exposed land, middle plants exhibited higher individual leaf dry mass (180.049 ± 68.480 mg), larger vein diameter (1.692 ± 0.288 mm), and longer petioles (5.406 ± 0.940 mm). These traits were accompanied by a higher morphology-based leaf dry matter accumulation rate and greater stability of the leaf-trait network, reflecting an adaptive strategy characterized by increased structural investment. In contrast, understory middle leaves were generally longer (13.361 ± 2.714 cm) and wider (7.005 ± 1.464 cm), along with lower photosynthate accumulation rates and weaker trait-network stability, indicating a strategy that enhances light-use efficiency under low-light conditions. In both habitats, leaves from the middle canopy position generally exhibited the highest values for most measured traits. Overall, leaf traits of C. spectabilis and their interrelationships showed considerable plasticity in response to external environmental pressures, primarily differences in light availability. However, from a practical production perspective, minimizing shading is recommended to maximize its ecological benefits. Full article

Faster lower-limb motion is closely related to soccer performance, but the contribution of lumbopelvic motion to achieving it remains unclear. This cross-sectional study aimed to examine whether faster lower-limb motion in soccer players was accompanied by greater lumbopelvic motion. Fifty-one male high school soccer players performed a thigh-raising (hip flexion) task from a standing position at low (approximately 100°/s) and high (approximately 400°/s) speeds. Lumbopelvic motion was measured at the lumbar spinous process (L3). Rotation (LBrot, transverse plane) and flexion–extension (LBf/e, sagittal plane) were derived from the angular velocity. Motions were compared between speeds using the Wilcoxon tests. In the dominant leg, both LBrot (10.2° vs. 8.1°, r = 0.62) and LBf/e (6.4° vs. 5.0°, r = 0.57) were greater at high speed. In the non-dominant leg, both LBrot (11.2° vs. 8.6°, r = 0.49) and LBf/e (6.9° vs. 5.3°, r = 0.62) were also greater at high speed. High-speed trials exhibited consistent movement patterns, whereas low-speed trials did not. These findings suggest that minimizing lumbopelvic motion may not always be optimal for achieving faster lower-limb motion, which may inform coaching and clinical practice regarding the appropriate degree of lumbopelvic motion during lower-limb tasks across movement speeds. Full article