Spinning samaras provide a promising biological basis for small wind turbine rotors, but the engineering translation of their three-dimensional morphology and the mechanisms governing performance losses below and above the low-tip-speed-ratio optimum remain insufficiently understood. In this study, a small horizontal-axis wind turbine rotor was developed from a µCT-informed engineering reconstruction of an Acer buergerianum samara. Its aerodynamic performance was evaluated using transient URANS simulations with the SST k-ω model and a sliding mesh, supported by grid and time-step sensitivity studies and validation against NREL Phase VI torque measurements. At U = 5 m/s and λ = 3, increasing the blade number from two to five raised C_p from 0.2445 to 0.3767, whereas a sixth blade provided only a further 1.01% increase. Among the sampled pitch angles, β = 20° produced the highest C_p of approximately 0.388. For N_b = 5 and β = 20°, a refined sweep identified a near-flat peak over λ ≈ 3.0-3.25 and a high-efficiency interval defined by C_p/C_p,max ≥ 0.90 of λ ≈ 2.28-3.70. For the same configuration, C_p at λ = 3 increased from 0.3698 to 0.4021 as Re_0.75R increased from 1.23 × 10^5 to 3.69 × 10^5. Mechanistic analysis showed that the peak is sustained by a continuous positive power-contribution band over the mid-to-outer span. At low TSR, suction-side separation, near-wake recirculation, and axial-velocity deficit restrict the effective work-producing region; at high TSR, viscous resisting torque largely cancels the pressure-driven torque. Together, these findings explain the low-TSR peak and provide mechanism-based guidance for blade-number selection and TSR control of the present samara-derived rotor.

Foot-and-mouth disease (FMD) represents a significant global economic burden and remains the primary constraint on Ethiopia's livestock economy and international trade. This desk review synthesized 60 years of data (1957-2025) using a structured, multidatabase search across four domains: disease, genotype/lineage, geographic spread, and temporal context. Data were stratified into three periods: Period I (1957-1980), Period II (1981-2000), and Period III (2001-2025). Results indicate that Period I saw the identification of serotypes O, A, and C, though serotype C has not been detected after 1983. Period II was marked by the continued circulation of serotypes O and A, and the first emergence of Serotype SAT 2 near the Kenya-Ethiopia border, which temporarily disappeared until its major re-emergence in 2007. Period III is characterized by a significant intensification and modernization of FMD virus (FMDV) outbreak investigation that provided more granular data on viral activity in the country. The period saw four major endemic serotypes O, A, SAT 2, and SAT 1, SAT one being confirmed for the first time during this period, circulate simultaneously and covering the entire country. Molecular analyses revealed a heterogeneous landscape: serotype O is dominated the serotype distribution in the country by its O/EA-3 and O/EA-4 topotypes, while serotype A involving complex lineages (Africa G-I, G-IV, and G-VII) follows in serotype O and precedes serotype SAT 2 in distribution. Notably, serotype SAT 2 has historically comprised four topotypes (IV, VII, XIII, and XIV), with the recent dominance of the re-emergent SAT 2/XIV topotype. The global biosecurity threat posed by FMDV SAT 2 topotype XIV stems from its unprecedented transcontinental dissemination into immunologically naive regions, rather than inherent lethality. This expansion highlights the complex evolutionary dynamics of the virus and the vulnerability of current surveillance system. The global dissemination of emerging lineages, such as SAT 2 topotype XIV, underscores the complex evolutionary dynamics and environmental plasticity inherent across all FMDV serotypes. The rapid shift of these viruses into nonendemic territories highlights critical vulnerabilities in existing biosecurity. Ultimately, these dynamics necessitate a shift toward adaptive, multiserotype surveillance and integrated control frameworks to address the continuous antigenic evolution and geographical expansion of the virus. Advancing Ethiopia along the progressive control pathway (PCP-FMD) is critically contingent upon evaluating the protective efficacy of current trivalent vaccines against rapidly evolving field strains. Immediate intervention is required to address diverged genotypes that jeopardize both national herd health and international market access.

Foot-and-mouth disease (FMD) causes significant losses for livestock farmers in affected countries and regions, including Southeast Asia, where several countries are progressing through different stages of the Progressive Control Pathway (PCP) under diverse resource settings. The PCP, developed by the World Organization for Animal Health and the Food and Agriculture Organization of the United Nations, is an outcome-oriented strategy designed to support progress toward the elimination of FMD. In this review paper, we propose an evidence-based framework linking epidemiological tools to each PCP stage requirements based on studies conducted in eight Southeast Asian countries through peer-reviewed research and gray literature. The findings indicate that Stage 1 progression is supported through risk-factor analyses, seroprevalence studies, and participatory epidemiology, while Stage 2 relies on spatial analyses and evaluations of control strategies. Progression to Stage 3 requires evidence of active surveillance systems for rapid detection of new viral incursions, whereas later stages depend on risk assessment, sustained surveillance, and restricting transboundary animal movement. Regional challenges include underreporting, surveillance-system deficiencies, and inconsistent vaccination monitoring. The framework proposed herein provides a practical approach for aligning the generation of evidence with PCP requirements. Ultimately, strengthened regional collaboration that coordinates transboundary risk management is crucial for progress toward sustainable FMD control in Southeast Asia.

Purpose: This study aimed to evaluate the effects of active transcranial direct current stimulation (tDCS) compared with sham stimulation on circulating brain-derived neurotrophic factor (BDNF), pain-related outcomes, working memory, and inflammatory and neuroplasticity biomarkers. Methods: PubMed/MEDLINE, Embase, the Cochrane Central Register of Controlled Trials, Web of Science, and ClinicalTrials.gov were searched from inception to May 2026. Randomized and controlled clinical trials comparing active with sham tDCS in adults were included. The primary outcome was post-treatment BDNF concentration. Secondary outcomes included pain intensity, pain catastrophizing, pain-related disability and functional interference, working memory, and circulating inflammatory or neuroplasticity biomarkers. Risk of bias was assessed using the revised Cochrane risk-of-bias tool. Mean differences (MDs) with 95% confidence intervals (CIs) were pooled using random-effects models. Serum and plasma BDNF were analyzed separately. Results: Twenty-one studies were included in the systematic review, of which 15 contributed to at least one quantitative synthesis and 12 study comparisons contributed to the primary BDNF analyses. Active tDCS did not significantly affect serum BDNF (MD = -0.01 [-0.15, 0.13], p = 0.890) or plasma BDNF (MD = 0.02 [-0.25, 0.29], p = 0.870) compared with sham stimulation. In contrast, active tDCS was associated with lower pain intensity (MD = -1.79 [-2.34, -1.23], p < 0.00001). No statistically significant difference was observed in the PCS total score or in the helplessness, magnification, or rumination subscales, although the point estimates generally favored active tDCS. For pain-related disability and functional interference, active tDCS was associated with lower PCP:S total scores and lower emotional interference, whereas no significant differences were observed for interference with daily activities or pain frequency. No significant differences were observed for working memory, interleukins, tumor necrosis factor-alpha, glial cell line-derived neurotrophic factor, interleukin-18, or soluble tumor necrosis factor receptors. Substantial heterogeneity was present in several pain-related and inflammatory biomarker analyses. Conclusions: Active tDCS was not associated with consistent differences in circulating serum or plasma BDNF or in the assessed peripheral inflammatory and neuroplasticity biomarkers compared with sham stimulation; however, these null peripheral findings should not be interpreted as evidence of absent central neuroplastic effects, because circulating measures may not adequately capture localized or transient biological changes within the central nervous system. Active tDCS was associated with improvements in some pain-related outcomes; however, the limited number of studies, substantial heterogeneity, and low certainty of the available evidence preclude firm conclusions regarding its clinical effectiveness for pain management.

IntroductionScreening for lung, breast, and cervical cancer can reduce morbidity and mortality by enabling earlier detection and treatment. However, participation remains below target levels, particularly among individuals experiencing marginalization. While primary care providers (PCPs) can play a key role in improving screening uptake, few reviews have focused on interventions targeting individuals experiencing marginalization that are aimed at PCPs, delivered by PCPs, or that occurred in a primary care setting.MethodsThe aim of this scoping review was to examine the extent and types of PCP interventions implemented to increase lung, breast, and cervical cancer screening uptake among individuals experiencing marginalization and identify gaps to inform future practice and research. We searched for studies of PCP interventions aimed at increasing lung, cervical, and/or breast cancer screening among marginalized populations in Ovid MEDLINE, Ovid Embase, Scopus, EBSCO CINAHL Complete and Ovid EBM Reviews - Cochrane Central Register of Controlled Trials from 2000 to March 31, 2022. Title, abstract, and full-text articles were screened, and data extraction was performed by three independent reviewers. The charted data were summarized using narrative synthesis.ResultsForty-two studies were included: 13 for cervical cancer, 15 for breast cancer, one for lung cancer, and 13 on multiple cancer sites. Interventions included education (for both patients and PCPs), self-collected human papillomavirus (HPV) testing, patient navigation, clinic system tools, event-based, and multicomponent. Increases in screening rates were observed across various intervention types for breast and cervical cancer, with multi-site interventions evaluated based on their reported effects on breast and cervical cancer screening independently.ConclusionsEducational interventions demonstrated the greatest effectiveness for breast cancer screening, and self-collected HPV testing demonstrated the greatest effectiveness for cervical cancer screening. There is a clear gap in the literature regarding interventions aimed at increasing lung cancer screening participation, and further research is needed to evaluate the effectiveness of such interventions. Screening programs and PCPs should consider targeted strategies to support greater participation among individuals experiencing marginalization.

Adsorption-desorption and differential scanning calorimetry (DSC) experiments have been extensively used to investigate the phase behavior of pure fluids and fluid mixtures in synthetic adsorbents but their application to natural nanoporous media remains relatively unexplored. In this study, these complementary methods are extended for the first time to examine the phase behavior and criticality of propane confined in a natural nanoporous medium, Mowry Shale. Capillary evaporation conditions are obtained from both methods and agree closely, providing confidence in the measured transition behavior. In contrast to observations in synthetic nanoporous media, capillary evaporation still occurs above the bulk critical point and therefore the pore critical point (PCP) exceeds the bulk critical point. The three-line approach is applied to determine, for the first time, the PCP of propane confined in shale. Since the hysteresis end point cannot be determined in the present work, its potential impact on determining the exact location of PCP remains uncertain. These findings demonstrate both the applicability and the additional complexities of extending conventional confined phase behavior and criticality methods from well-defined synthetic nanopores to natural porous media. Using the experimentally determined PCP, the Peng-Robinson equation of state (EOS) is applied to the confined fluid system and accurately reproduces the whole capillary evaporation curve.

Anal sphincter injury is a major cause of anal incontinence (AI), and current treatments rarely restore anal sphincter muscle function. Secreted frizzled-related protein-2 (sFRP2) may promote muscle regeneration and reduce fibrosis, but its ability to reverse the established external anal sphincter (EAS) fibrosis and restore function is not known. This study examined whether sFRP2 promotes functional and structural recovery in a rabbit model of established EAS muscle fibrosis. Adult female rabbits underwent EAS myotomy and, six weeks later, received local injections of sFRP2 or saline. Anal canal pressure was recorded before injury, immediately after myotomy, six weeks post-injury, and every two weeks for six weeks following treatment. Myotomy significantly reduced anal canal pressure and induced fibrosis in the EAS muscle at 6 weeks. sFRP2 treatment restored anal canal pressure to near pre-injury levels within two weeks after sFRP2 injection, which remained elevated six weeks post-treatment, while saline-treated rabbits maintained low pressure. In the sFRP2 compared to saline treated animals, 1) histological analysis demonstrated significant increase in EAS muscle percent, 2) hydroxyproline assay showed reduced collagen content, 3) western blot analysis revealed increased expression of eMyHC, Myogenin, and active JNK, along with reduced Vimentin, TGF-β1, and nuclear active β-catenin, while Col1A1 and pSmad2/3 showed a downward trend, 4) proteomic analysis showed reduced fibrogenesis and TGF-β signaling, with activation of PCP-JNK, and striated muscle contraction pathways. These findings suggest that sFRP2 restores EAS muscle function and promotes muscle regeneration thus representing a potential novel therapy for the injury-induced anal sphincter dysfunction.

High‑risk (HR) human papillomaviruses (HPVs) rely on the continuous expression of the E6 and E7 oncoproteins to reshape epithelial biology, drive and sustain malignant transformation. The high‑risk E7 oncoprotein is multifunctional, and its phosphorylation by Casein Kinase II (CKII) is a key post translational modification that amplifies its oncogenic potential. Therefore, it is important to extensively delineate the consequences of E7 phosphorylation on HPV-driven transformation and malignant progression. Here, we identify Vangl1, a core planar cell polarity (PCP) scaffold protein, as a novel, phosphorylation‑dependent interactor of HPV‑16 E7. Through proteomics, biochemical and cell-based assays, this study established that CKII‑mediated phosphorylation is required for Vangl1 recruitment, and that this interaction is more pronounced with HPV‑16 E7, revealing a new mechanism by which HR HPVs might disrupt epithelial organization. In CaSki cells and ectopic expression models, E7 expression profoundly disrupts Vangl1 homeostasis, creating a biphasic proteostatic imbalance in which phosphorylated Vangl1 is aberrantly stabilised. This retention parallels E7 stability, revealing a reciprocal oncogenic stabilization. Furthermore, we found that Vangl1 is depleted in cytoskeletal cell fractions in the presence of E7, and that E7 translocates to membrane compartments where it colocalizes with Vangl1. In line with this, we identified that this abnormal Vangl1 stabilization occurs from its mislocalization and impaired trafficking arising from E7's interference with the Adaptor-Related Protein Complex 1 Subunit Mu 1 (AP1M1). Functionally, Vangl1 siRNA-mediated ablation in CaSki spheroids mirrors E6/E7 loss, leading to disrupted spheroidal architecture, reduced invasion, and increased sensitivity to chemotherapeutic stress. These phenotypes position Vangl1 as a key downstream effector through which E7 reshaped epithelial behaviour. Taken together, our findings reveal a CKII-dependent mechanism by which HPV-16 E7 hijacks a core planar polarity component to destabilize epithelial structure and promote malignant traits; thus, positioning Vangl1 as a potential druggable target in HPV-associated cervical cancer.

The clustering states of cell surface C-X-C chemokine receptor 4 (CXCR4) play a critical role in cancer metastasis. We previously reported a "Pro-Clustering Polymers (PCP)" system, P-BS-CM1 → P-CM2, for the treatment of metastatic triple-negative breast cancer (TNBC). Subsequent studies demonstrated that PCP enhanced CXCR4 blockade and metastasis suppression by disrupting CXCR4 association-disassociation dynamic equilibrium and shifting the receptor toward a hyper-clustered state. As an alternative strategy to disrupt this equilibrium, shifting CXCR4 toward a less clustered, more dispersed state, i.e., inhibiting CXCR4 clustering, remains largely underexplored. Herein, we developed a "De-Clustering Polymer (DCP)" system, P-BS-pHLIP, which introduces steric hindrance to block receptor-receptor interactions and thereby inhibits CXCR4 clustering. Side-by-side comparisons of DCP with our previously developed PCP system revealed that different modes of CXCR4 manipulation dictate divergent downstream biological outcomes. PCP preferentially impaired tumor cell motility by inducing mitochondrial dysfunction and energy depletion, whereas DCP preferentially reduced tumor cell adhesiveness by downregulating multiple adhesion molecules. Both PCP and DCP exert potent anti-metastatic efficacy in multiple TNBC metastatic models. Collectively, this study demonstrates that engineered polymeric systems that biophysically manipulate receptor clustering states, via either pro-clustering or de-clustering, represent promising therapeutic strategies for suppressing cancer metastasis.