Search Results (6,311)

Urban forests support wildlife populations across North America and the world. Yet, challenges remain for research and practice to integrate wildlife habitat as a core component of the myriad objectives that urban foresters manage. Ecosystem services have been adopted as a dominant paradigm in urban forestry for both advocacy and management, yet accounting for contributions to wildlife habitat does not fit squarely within typical ecosystem service frameworks. The i-Tree program, a suite of urban forest ecosystem service models and tools developed by the US Forest Service, presented an opportunity to link widely used urban forest assessment field protocols with indicators of suitable habitat. In this reflection piece, we demonstrate how the i-Tree Wildlife project assessed whether urban forest structural assessment methods could be applied to assess wildlife habitat provision, operationalizing the fundamental question “How do urban forests support wildlife?” We describe the development process for integrating bird habitat suitability models for 12 species present in the northeastern US, ten native and two non-native birds, into the flagship i-Tree Eco tool. We offer reflections, challenges, and opportunities from this process. Ultimately, the improvement of ecosystem assessment tools like i-Tree can assist practitioners who aim to manage healthy and productive urban forests that benefit people and wildlife. Full article

The Collatz conjecture concerns the iteration of the map $f\left(n\right)=3n+1$ for odd n and $f\left(n\right)=n/2$ for even n. In this paper, we study the level sets $l_x=\{n\in \mathbb{N}\mid L\left(n\right)=x\}$, where $L\left(n\right)$ denotes the Collatz length. Using the parity representation of Collatz trajectories, we partition each $l_x$ according to the number of odd steps and analyze the corresponding means ${\mu }_{x,k}$. Under a natural scaling assumption, these means satisfy an approximate geometric progression, so that $log{\mu }_{x,k}$ is approximately linear in k. Computations for $n\le 100,000$ and $10\le x\le 50$ show highly stable regression parameters and near-perfect linear fits. Full article

Natural killer T (NKT) cells bridge innate and adaptive immune responses and play a critical role in anti-tumor immunity. The goal of the study was to assess NKT cell and T cell function in lymphoma patients and to investigate whether specific cytokines correlate with outcomes and/or immune cell function. Patient diagnoses were confirmed by histology. NKT and T cell number and function were assessed by flow cytometry and stimulation with artificial antigen-presenting cells (aAPCs) followed by ELISA and quantitative RT-PCR (qPCR). Cytokine expression levels were compared using online databases, and protein levels in the plasma were assessed by ELISA. NKT cell activation, indicated by at least 1.5-fold IFN-γ induction over baseline following stimulation, was detected in 82% of healthy donors, compared to 44% of lymphoma patients. Lymphoma patients have significantly higher levels of circulating pro- and anti-inflammatory cytokines IL-10, IL-6, and Sema4D as compared to healthy donors. In addition, NKT cell function in the blood correlated with NKT cell function in the bone marrow in lymphoma patients. We found that aAPC-qPCR can be used to quickly assess immune cell function in cancer patients. Circulating NKT cell function positively correlated with bone marrow NKT cell function, suggesting that circulating NKT responses reflect systemic immune competence. Outcome-associated transcriptomic analyses showed that lower expression of TGF-β, IL-6, IL-10, and IFN-γ mRNA correlated with poorer clinical outcomes, whereas higher Sema4D expression was associated with worse prognosis, identifying Sema4D as a potential immunologic biomarker linked to disease progression and immune dysfunction in B cell lymphoma. Full article

Purpose: To compare hypopyon detection using anterior segment optical coherence tomography (ASOCT) versus slit lamp examination (SLE) in microbial keratitis, and to evaluate intra- and inter-grader agreement for ASOCT hypopyon measurement. Methods: Two masked graders independently evaluated ASOCT images for hypopyon presence or absence in eyes with microbial keratitis, with disagreements resolved by consensus. A subset of hypopyon eyes underwent triplicate height measurement using two methods (endothelial length and vertical height). The proportion of eyes with hypopyon, Cohen’s kappa, and intraclass correlation coefficients (ICCs) were calculated comparing diagnostic performance of ASOCT versus SLE. Results: Inter-grader agreement for hypopyon detection on ASOCT was excellent (κ = 0.94; 95% CI 0.84–1.00) and intra-grader agreement was excellent (κ = 0.89–1.00). ASOCT detected hypopyon in 67.1% of eyes versus 57.0% by SLE. Using ASOCT consensus grading as the reference standard, SLE demonstrated a detection proportion of 83.0% (95% CI, 71.4–92.1%). Intra-grader reproducibility was excellent for both endothelial length and vertical height measurements (ICC 0.977–0.996). Inter-grader agreement was good for endothelial length (ICC 0.831) and vertical height (ICC 0.827), though a statistically significant inter-grader bias was identified for vertical height only (Wilcoxon exact p = 0.006). Conclusions: Among eyes with gradable ASOCT images, ASOCT detected a greater proportion of hypopyon than SLE and demonstrated excellent intra-grader and good inter-grader measurement reproducibility. Endothelial length showed slightly superior inter-grader concordance to vertical height measurement. Full article

Background/Objectives: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder for which MRI-based AI systems are increasingly used for diagnosis and prognosis. However, many published approaches remain misaligned with the requirements of trustworthy clinical use. Predicted risks are often poorly calibrated, explanations are frequently limited or non-actionable, guideline-aligned reporting is uncommon, and longitudinal prediction is inconsistently evaluated. In this paper, we conduct a PRISMA-guided structured review with scoping-style breadth of MRI-centric AI methods for AD diagnosis. This design supports a theme-based synthesis across heterogeneous study designs and is intended to summarize the current evidence base and derive practical design requirements for next-generation, clinically oriented pipelines that integrate calibrated staging, explainable outputs, and longitudinal risk modeling. Methods: Searches were conducted across Scopus, PubMed/PMC, and arXiv/bioRxiv (2014–2026; English; human AD/MCI imaging) and were supplemented by backward and forward snowballing. These searches yielded 2460 records. After deduplication, screening, and full-text eligibility assessment, 90 papers were included in the final synthesis. The included literature was organized into thematic streams spanning counterfactual reasoning and explainable AI (XAI), vision–language approaches for report and caption generation, longitudinal and survival-style modeling, and multimodal fusion and transformer-based methods combining MRI with clinical variables and other biomarkers. Vision–language methods were considered together with retrieval-augmented paradigms. Results: Key findings are that the field has shifted toward transformer architectures and multimodal fusion and shows increased interest in richer explanation mechanisms. Nevertheless, calibration metrics and robustness checks are inconsistently reported, external site-held-out validation and subgroup analyses remain relatively uncommon, and guideline-aligned structured reporting with explicit numeric provenance is rare. Vision–language and retrieval-augmented reporting methods are far more mature in general radiology than in AD MRI, highlighting a translational opportunity. Conclusions: Based on these findings, we recommend standardized reporting of classification calibration and longitudinal risk calibration, stronger site-held-out validation with subgroup robustness evaluation, clinically meaningful counterfactuals, and guideline-aligned reporting with reproducible numeric provenance embedded within reproducible pipelines. Full article

Interbody fusion cages are widely used to restore spinal stability, yet conventional designs often exhibit mechanical mismatch and limited biological integration. Functionally graded spinal cages incorporate spatial variations in composition and structure to better align mechanical properties with the surrounding bone environment. Although these designs have been extensively studied from an engineering perspective, their biological implications remain less clearly defined. This review examines how graded material composition, surface characteristics, porosity, and lattice architecture are associated with cellular and molecular responses relevant to bone regeneration. Reported biological responses include protein adsorption, immune modulation, angiogenesis, and osteogenic differentiation. Evidence from orthopaedic implants and tissue engineering systems suggests that such design features may influence mechanobiological pathways; however, direct experimental validation in spinal applications remains limited. Previous reviews primarily focus on material properties or mechanical performance of functionally graded spinal cages. This review presents a structured design-to-biology perspective linking graded implant features with biological responses relevant to spinal fusion. By integrating findings across biomaterials, mechanobiology, and implant design, this review presents a structured design-to-biology perspective and highlights current evidence, translational limitations, and key knowledge gaps in the field. Functionally graded spinal cages represent a promising but still evolving strategy, and further spine-specific mechanobiological and clinical studies are required to establish their impact on fusion outcomes. Full article

Background/Objectives: Posterior C1–C2 fusion is commonly used for unstable traumatic odontoid injuries, but it is less commonly used for patients who initially undergo nonoperative management and later require salvage fusion. This study compared hospital length of stay, short-term complications, and postoperative radiographic alignment between salvage posterior C1–C2 fusion after failed nonoperative management and primary posterior C1–C2 fusion. Materials and Methods: A retrospective cohort study was performed of 106 adult patients who underwent posterior C1–C2 instrumented fusion for traumatic cervical spine injuries from 2011 to 2023. Patients were stratified into the salvage fusion group after radiographic nonunion following attempted nonoperative management with external immobilization or the primary fusion group, who underwent initial surgical management. The primary outcome was hospital length of stay. Secondary outcomes included postoperative radiographic alignment, screw loosening, hardware failure, revision surgery, and 30-day emergency department visits. Propensity score matching and full-cohort augmented inverse probability weighting were used to account for baseline differences between groups. Results: Twenty-seven patients underwent salvage fusion and 79 underwent primary fusion. Propensity score matching produced 25 matched pairs. In the matched cohort, salvage fusion was associated with significantly shorter length of stay than primary fusion, with a median of 2 versus 5 days, respectively (p < 0.001). This remained significant in the full-cohort augmented inverse probability weighting analysis, where salvage fusion was associated with a 2.41-day reduction in length of stay (95% CI, −3.63 to −1.19; p < 0.001). Short-term complications were uncommon in both groups, and no clear sign of increased screw loosening, hardware failure, revision surgery, or 30-day emergency department visits was observed in the salvage cohort. Salvage fusion was also associated with lower postoperative C2–C7 lordosis and a greater C1 lamina–occiput distance. Conclusions: Salvage posterior C1–C2 fusion for radiographic nonunion after attempted nonoperative management was not associated with higher short-term complication rates compared with primary fusion. While surgical-admission length of stay was shorter in the salvage cohort, this difference should be interpreted cautiously because salvage and primary fusion occur in different admission contexts and do not reflect the total episode-of-care burden. Early postoperative alignment differences were observed, but these were not correlated with clinical outcomes or longitudinal imaging, and their long-term significance remains unclear. Future multicenter studies should evaluate total healthcare utilization, fusion status, longitudinal alignment, and patient-reported outcomes after salvage C1–C2 fusion. Full article

Background: Failure of liberation from mechanical ventilation remains common despite successful spontaneous breathing trials (SBTs) and is associated with increased morbidity, prolonged ICU stay, and mortality. We aimed to evaluate the role of diaphragm and lung ultrasound for predicting composite liberation failure, including SBT failure and post-extubation failure, in adults. Methods: We conducted a systematic review with descriptive synthesis in accordance with PRISMA-DTA guidelines. The review protocol was developed a priori but was not prospectively registered. MEDLINE, EMBASE, and Cochrane CENTRAL were searched from inception to 20 January 2026. Adult studies evaluating diaphragm ultrasound (diaphragm thickening fraction [DTF], diaphragmatic excursion [DE]) and/or lung ultrasound in patients undergoing SBTs were included. Risk of bias was assessed using Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2). Results: Six studies (n = 430) were included. DTF demonstrated the most consistent association with liberation failure (AUC range 0.64–0.99; sensitivity 78–100%). DE showed a similar but less consistent association (AUC range 0.77–0.86). Elevated lung ultrasound scores—reflecting aeration loss from cardiogenic edema, acute respiratory distress syndrome (ARDS), atelectasis, or pneumonia—were associated with extubation failure. Conclusions: DTF shows potential clinical utility as an adjunct for predicting liberation outcomes. LUS offers complementary insight into aeration loss regardless of etiology. Standardization of measurement protocols and larger prospective studies are needed. Full article

There are ongoing discussions about predictive policing systems being unfair, for example, by exhibiting racial bias. Law enforcement in some cities, such as Los Angeles, California, and Baltimore, Maryland, have initiated the integration of these systems into their decision-making processes, and some of these systems were advertised as being unbiased. However, later studies discovered that these methods could also be unfair due to feedback loops and being trained on historically biased recorded data. Comparative studies on predictive policing systems are few and insufficiently comprehensive. Crucially, the relative fairness of predictive policing methods with regard to traditional hot spot-based policing has not been established. Moreover, the relationship between fairness and accuracy is complex and requires further study. Furthermore, the case of Baltimore City, Maryland, USA, has not yet been systematically analyzed despite its relevance as an early adopter of predictive policing technologies with a fraught history of social justice concerns around policing. An improved understanding of these questions could better inform policy decisions around predictive policing technologies both in Baltimore and beyond. Therefore, in this work we perform a comprehensive comparative simulation study on the fairness and accuracy of predictive policing technologies in Baltimore. Our results suggest that the situation around bias in predictive policing is more complex than previously assumed. While we find that predictive policing exhibits bias due to feedback loops, as previously reported, we also find traditional hot spot-based policing to have similar issues. Although predictive policing is found to be more fair and accurate than hot spot policing in the short term, it also amplifies bias more quickly, suggesting the potential for worse long-run behavior. In Baltimore, the bias in these systems tended toward over-policing White neighborhoods in some cases, unlike in previous studies. However, when the analysis was restricted to some specific crime types, this tendency differed. Overall, this work demonstrates a methodology for city-specific evaluation and compares behavioral tendencies of predictive policing systems, showing how such simulations can reveal inequities and long-term tendencies. We recommend that authorities and community stakeholders use simulation methodologies to assist in collaboratively navigating the complexities around fairness in predictive policing. Full article

The relationship between stress and Parkinson’s disease is regarded as complex and multifaceted, although a direct causal link has not yet been conclusively proven. One prevailing hypothesis is based on the activation of the hypothalamic–pituitary–adrenal (HPA) axis and the consequent elevation of glucocorticoid levels. Prolonged exposure to these hormones may exacerbate oxidative stress, thereby rendering the dopaminergic neurons within the brain’s subcortical structures more susceptible to degeneration. Furthermore, stress may intensify neuroinflammation through the activation of microglia—a mechanism that could constitute a significant factor in the pathogenesis of Parkinson’s disease. Another important concept concerns the direct interaction of stressors with the dopaminergic system. Physiological and psychological stress can alter dopaminergic transmission by affecting both the synthesis and release of dopamine, as well as the sensitivity of dopamine receptors. Severe or chronic stress may contribute to the disruption of dopaminergic mechanisms and accelerate the onset of clinical symptoms in predisposed individuals. Furthermore, many researchers draw attention to the role of stress-induced aggregation of α-synuclein—a key protein implicated in the pathogenesis of Parkinson’s disease. Clinical data suggest a highly probable link between post-traumatic stress disorder and an increased risk of developing Parkinson’s disease, although these findings remain inconclusive. It is possible that stress acts not as a primary cause, but rather as a modifying factor that interacts with genetic predisposition, accelerating or triggering neurodegenerative processes. The aim of our narrative review was to examine these concepts and discuss possible directions for future research into the interaction between stress and Parkinson’s disease. Full article

Background: Dysplasia or absence of anterior communicating artery (ACoA) is a common variation in the circle of Willis (COW) anomaly, and it may elevate the risks of cerebrovascular diseases. We aimed at investigating the association of ACoA dysplasia/absence with plaque imaging features of middle cerebral artery (MCA) atherosclerosis. Methods: We analyzed the prospective data from a vessel wall imaging cohort of adult patients suffering from acute ischemic stroke or transient ischemic attack due to intracranial atherosclerosis (2014 to 2020). Patients demonstrating MCA atherosclerotic plaques were included. The ACoA dysplasia/absence and other incomplete COW configurations were identified on magnetic resonance angiography. The MCA plaques were evaluated through high-resolution vessel wall imaging. Results: Of the 107 patients with MCA atherosclerosis, 29.9% showed ACoA dysplasia/absence. The patients with ACoA dysplasia/absence were more likely to have concomitant dysplasia/absence of anterior cerebral artery (71.9% vs. 18.7%, p < 0.001). For the 158 MCA plaques identified, those with ACoA dysplasia/absence exhibited a significantly higher prevalence of symptomatic status (58.7% vs. 31.3%, p = 0.001) and non-positive remodeling (58.7% vs. 26.8%, p < 0.001) than those without this variant. Regression analyses further demonstrated the robust association of ACoA dysplasia/absence with symptomatic status (odds ratio, 5.158; 95% confidence interval, 1.744–15.254; p = 0.003) and non-positive remodeling (odds ratio, 6.92; 95% confidence interval, 2.396–19.982; p < 0.001) of MCA atherosclerosis. Conclusions: As a common variation among patients with MCA atherosclerosis, ACoA dysplasia/absence may elevate the possibility to develop symptomatic MCA atherosclerosis, which showed non-positive remodeling. Stroke risk stratification based on the ACoA morphology needs further validation. Full article

Cellular senescence drives aging and age-related disease through the accumulation of senescent cells and their senescence-associated secretory phenotype (SASP). Emerging evidence suggests intermittent (“hit-and-run”) senolytic interventions may improve healthspan by reducing senescent cell accumulation and the SASP. Healthy adults aged 45–79 were recruited for a decentralized, single-arm pilot study (NCT06953518) evaluating 2 days of nutraceutical supplementation (Qualia Senolytic). Fingerstick blood samples and validated quality of life (QoL) questionnaire data were collected on days 0 and 7. Primary outcomes were SASP biomarkers measured by the Olink^® Target 48 Cytokine panel, including tumor necrosis factor (TNF), interleukin-1 beta (IL-1β), interleukin-8 (CXCL8), and vascular endothelial growth factor A (VEGFA). Protein data were analyzed using linear mixed models and Wilcoxon signed-rank tests. Seventy-one adults enrolled and 53 (74.6%) provided paired protein samples. No significant changes occurred in primary outcomes. Exploratory unadjusted analyses revealed significant reductions in the established senescence chemokines CXCL9 and CXCL10, as well as CCL8 and CXCL11, and increases in interleukin-17F and oncostatin M. QoL significantly improved without safety concerns, though results are expectation-sensitive. Preliminary findings support the feasibility of this decentralized approach and identify candidate SASP biomarker signals in healthy adults warranting validation in randomized, placebo-controlled trials. Full article

Itraconazole is an antifungal drug used to treat chytridiomycosis, one of the leading causes of global amphibian decline in species such as the critically endangered Panamanian golden frog (Atelopus zeteki). Despite its widespread use for prophylaxis and treatment in both assurance colonies and free-ranging amphibians, there is minimal pharmacologic information to guide dosing. In experiment A, frogs were exposed to 0.01% itraconazole for 10 min and tissue samples were analyzed at various time points from 1 to 84 h. In experiment B, frogs were divided into six groups and exposed to itraconazole in different combinations of concentration (0.01% or 0.001%) and time (5, 10, or 15 min) over 10 days of treatment. Tissue concentrations were quantified via high-performance liquid chromatography. In experiment A, following a one-time dose, itraconazole concentrations remained high until the end of the experiment at 84 h. In experiment B, at 0.01% itraconazole daily for 10 days, skin and liver concentrations were high and increased substantially over the 10-day treatment course. Frogs exposed at the lower concentration (0.001%) had tissue concentrations that appeared to remain steady. At the reported doses over 10 days, there was no histologic evidence of hepatic toxicity, although one frog was found dead in the low-dose bath at 84 h and could not be further analyzed. This experiment is an excellent example of assurance colonies providing evidence-based information for the improved care and welfare of amphibians in order to prepare for future free-ranging populations. Full article

Parkinson’s disease (PD) is a prevalent neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of Lewy bodies. Over recent decades, various cellular mechanisms underlying PD have been elucidated, including autophagy, mitochondrial dysfunction, neuroinflammation, and axonal transport. Among them, axonal transport plays a critical role in maintaining the dynamic homeostasis of proteins, membrane-bound organelles, and cellular metabolism within neurons. Unfortunately, a comprehensive overview of axonal transport in PD remains absent. In this review, we synthesized the current literature on axonal transport in PD, leveraging neurotoxic and genetic models to explore the causes and consequences of axonal transport alterations in PD. Through this summary, we aim to deepen our understanding of PD pathogenesis and provide potential therapeutic targets for intervention. Full article

Breast cancer is one of the most devastating malignancies in women worldwide. A growing body of evidence has linked neoplastic growth, invasion, metastasis, immune escape, and therapeutic resistance to infiltrating tumor-associated macrophages. In a breast cancer mass, macrophages are largely polarized to two main subtypes, M1 and M2, albeit with continuum intermediates, based on their immunological behaviors, gene signatures, and functional roles. While the former portrays proinflammatory and anti-cancer effects, the latter elicits the opposite impacts. M2 macrophages have gained rising attention as they are largely involved in fostering an immune-suppressive, cancer-promoting landscape and are imperative for malignant features across breast cancer subtypes. Through a positive feedback paracrine loop, M2 macrophages can be enriched by a plethora of dysregulated oncogenic signaling mediators, exemplified by CSF1/CSF1R, STAT3, IL-6, YAP, PI3K, PDK1, and AKT. These modulators could be released from or activated by surrounding malignant cells, fibroblasts, secreted extracellular vesicles, cell fragments generated after chemotherapies, hypoxia, dysregulated immune checkpoint pathways or oncometabolites. This review aims to discern the molecular cues fortifying M2 subpopulations. Moreover, recent advances in single-cell sequencing, spatial, and computational approaches have refined the understanding of TAM heterogeneity, while clinical translation remains limited by low therapeutic specificity, compensatory signaling, and differences between murine and human macrophage biology. Future therapeutic regimens should include strategies aimed at correcting aberrations that favor M2 polarization and are justified with divergences between humans and mice. Full article