We summarised active surveillance data to identify patterns and ecological factors correlated with AIV detection in wild birds, through a systematic review and meta-analysis. We screened 2851 articles from the PubMed and Scopus databases, out of which 197 met our eligibility criteria and were selected for further analysis. The dataset encompassed 367 wild bird species from 72 avian families. The pooled prevalence of sampled birds was 4.80% (95% CI: [3.91-5.77%]) across 900,469 samples collected during the period 1971-2023, with substantial heterogeneity ( ) across studies. Among continents, Central America displayed the highest prevalence at 9.89% (95% CI: [2.25-21.99%]), albeit based on relatively few samples (n=4205). In temperate regions, prevalence peaked in autumn, at 5.82% (95% CI: [3.84-8.15%]), while in tropical regions, prevalence was notably higher during the dry season (2.33%, 95% CI: [0.38-5.54%]) than during the wet season (0.22%, 95% CI: [0.00-0.90%]). Prevalence varied significantly across avian families, with Anatidae, the most extensively sampled family, exhibiting a prevalence of 6.19% (95% CI: [5.10-7.37%]). Migratory species and those associated with freshwater habitats also exhibited higher AIV detection. Moreover, meta-regression analyses revealed that seasonal patterns of AIV detection differed across regions. Despite this, high heterogeneity across studies remained, likely driven by differences in surveillance intensity, diagnostic methods, and unmeasured ecological factors. This meta-analysis highlights key spatial, taxonomic, and temporal patterns in AIV prevalence among sampled birds. The findings underscore the need for harmonised, representative surveillance to better anticipate emerging avian influenza risks.

Upper tract urothelial carcinoma (UTUC) presents distinct diagnostic and therapeutic challenges because of its rarity, anatomic constraints, frequent understaging at biopsy, and risk of systemic recurrence after radical nephroureterectomy. Current perioperative management is driven primarily by clinicopathologic risk factors, which may be insufficient to identify occult molecular residual disease (MRD) or to determine which patients are most likely to benefit from systemic therapy. This narrative review summarizes available evidence on circulating tumor DNA (ctDNA) in UTUC and related urothelial carcinoma settings, classifies the level of evidence supporting each application, and proposes a research framework for prospective evaluation. The strongest UTUC-specific evidence supports ctDNA as a prognostic biomarker associated with recurrence risk, whereas predictive validity for selecting chemotherapy, immune checkpoint inhibitors, antibody-drug conjugates, targeted therapy, or surveillance intensity remains unproven. Evidence from muscle-invasive bladder cancer, including ctDNA-correlative and ctDNA-guided perioperative trials, provides biologic rationale but should not be directly translated into routine UTUC care without disease-specific validation. We outline key implementation questions, including target population, assay selection, timing, false-positive and false-negative results, lead-time bias, and integration of plasma ctDNA with utDNA. Prospective UTUC-specific trials are needed to determine whether ctDNA-guided perioperative strategies improve survival, reduce unnecessary toxicity, and are cost-effective.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer death, and existing HCC risk stratification models in cirrhosis poorly identify patients at the highest risk. We evaluated whether baseline antinuclear antibody (ANA) status is independently associated with incident HCC and whether adding ANA improves risk prediction. We conducted a single-center, retrospective cohort of adults (age ≥18 years) with established cirrhosis and clinically obtained ANA testing within 12 months of cirrhosis diagnosis. Follow-up began at the cirrhosis index date; the primary outcome was incident HCC. Associations were assessed using cause-specific Cox models with prespecified clinical covariates. We compared discrimination for a clinical model with and without ANA and performed inverse-probability–weighted and immunologic (IgG/neutrophil-to-lymphocyte ratio) sensitivity analyses in complete cases. Among 1,023 participants [mean age 53.7 years (SD 10.9); 57% male], 102 developed incident HCC over a median 4.7 years of follow-up. HCC incidence was lower in ANA-positive versus ANA-negative patients (1.10 vs. 3.73 per 100 person-years; log-rank P < 0.001). ANA positivity was associated with lower HCC risk in multivariable models (HR, 0.32; 95% CI, 0.20–0.52). Adding ANA improved discrimination (C-index 0.727–0.750) and model fit (likelihood-ratio P < 0.001). Findings were consistent in weighted and laboratory-complete sensitivity analyses. In cirrhosis, baseline ANA positivity is independently associated with lower incident HCC risk and provides incremental prognostic information beyond routine clinical factors. Prospective validation and mechanistic studies are warranted.Significance:Natural autoantibodies (ANA) are routinely measured, inexpensive, and widely accessible, yet their prognostic value in cirrhosis is not used for HCC risk stratification. In this retrospective cohort, baseline ANA positivity was independently associated with lower incident HCC risk and improved model discrimination beyond clinical factors. These findings support repurposing a common clinical test to refine individualized surveillance intensity and motivate prospective validation and mechanistic studies.

BackgroundBaker's cysts can cause significant vascular complications including popliteal vein compression and deep vein thrombosis (DVT), yet no validated tool exists to predict which patients are at highest risk. We aimed to develop and internally validate a clinical nomogram for predicting vascular complications in patients with Baker's cysts.MethodsWe conducted a retrospective cohort study of 1,364 consecutive patients diagnosed with Baker's cysts between January 2015 and December 2024 at a single tertiary center. The primary outcome was a composite of vascular complications (symptomatic popliteal vein compression >50%, DVT involving the popliteal vein, pseudothrombophlebitis, or popliteal artery compression). Multivariate logistic regression identified independent predictors, which were incorporated into a nomogram. Internal validation was performed using 1,000 bootstrap resamples and 10-fold cross-validation.ResultsVascular complications occurred in 137 patients (10.0%). Of the total cohort, 923 (67.7%) presented with symptomatic cysts, while 441 (32.3%) were incidental findings. Five independent predictors were identified: cyst size >40mm (adjusted OR 2.78, 95% CI 1.86-4.15), rheumatoid arthritis (aOR 2.24, 1.46-3.43), venous insufficiency (aOR 2.42, 1.52-3.86), anticoagulant therapy (aOR 1.86, 1.19-2.91), and age >65 years (aOR 1.72, 1.16-2.56). The nomogram demonstrated good discrimination (AUC 0.83, 95% CI 0.79-0.87) and calibration (Hosmer-Lemeshow p = .66). Risk stratification identified low-risk (2.6%), intermediate-risk (12.5%), and high-risk (35.7%) groups. The median time to complication was 14.2 months overall, with significantly earlier occurrence in high-risk patients (8.3 months).ConclusionsWe developed and internally validated a clinical nomogram based on five readily available variables that can stratify patients with Baker's cysts into risk groups for vascular complications. This tool may help tailor surveillance intensity and timing of intervention. External validation in independent cohorts is required before broad clinical implementation.

Background Risk stratification for prostate cancer (PCa) progression or aggressiveness is often based on clinicopathologic features, some of which may be influenced by genetic factors. We developed a novel, germline polygenic risk score (PRSagg) to predict likelihood of developing aggressive PCa. Methods PRSagg was developed using data from 38,688 patients with PCa (case-only analysis) from the Million Veteran Program (MVP) through a genome-wide search for variants associated with PCa grade group at diagnosis. We tested associations of PRSagg with grade group using the entire MVP dataset using the .632 bootstrap method. In an MVP cohort with localized PCa that was initially monitored without treatment, we tested PRSagg for association with unfavorable outcomes (subsequent development of grade group 4-5, metastasis, and/or biochemical recurrence after definitive treatment). We performed external validation in data from patients in the PRACTICAL Consortium (n=45,214) and from participants in the ProtecT randomized trial who underwent active monitoring (n=316). Odds ratios (ORs) were calculated per standard deviation (SD) increase with 95% confidence intervals, while adjusting for age, genetic ancestry, a previously developed polygenic score for risk of PCa (PHS601), and a polygenic score for benign elevated prostate-specific antigen (PRSPSA). For the outcome of metastasis, we additionally adjusted for PSA at diagnosis. Results In the MVP training dataset, PRSagg (172 variants) was associated with higher grade group at diagnosis (OR = 1.53 [1.51-1.56]) and with increased risk of unfavorable outcomes during monitoring (OR = 1.13 [1.09-1.18]). These findings were confirmed in the external datasets. PRSagg was associated with greater odds of higher grade group at diagnosis (OR = 1.09 [1.06-1.11]). Among ProtecT participants undergoing active monitoring, PRSagg was associated with higher risk of metastasis (OR = 2.15 [1.02-3.88]). Among MVP participants with high polygenic risk of developing any PCa, the risk of aggressive disease was highest in men with high PRSagg and low genetic risk of PSA elevation. Conclusions Among men who develop PCa, a weighted sum of common germline variants (PRSagg) is independently associated with PCa aggressiveness. These findings may inform future study of germline influence on tumor evolution and risk-stratified intensity of active surveillance.

The aim of this study was to evaluate the long-term efficacy and safety of Gamma Knife surgery (GKS) for sporadic vestibular schwannoma (VS), focusing on the durability of tumor control and the necessity of extended posttreatment imaging surveillance. This retrospective study included patients with sporadic VS treated with single-session GKS between May 1991 and January 2020 at a single center. Tumors were classified into the following anatomical types using a modified Koos-based system: type A (intracanalicular), type B (cerebellopontine angle), type C (mild brainstem compression), and type D (severe brainstem compression with fourth ventricle deviation). A subgroup analysis in patients without salvage treatment within the first 5 years after GKS and with ≥ 5 years of follow-up was performed to assess long-term stability. Salvage treatment rates, functional outcomes, and adverse events were evaluated. Overall, 878 patients (488 female, median age 57 years) with sporadic VS treated with single-session GKS were included in the analysis. A subgroup of 793 patients (438 female, median age 58 years) remained free of salvage treatment during the first 5 years after GKS and had ≥ 5 years of follow-up. The median clinical follow-up duration was 154.5 months. Salvage treatment was required in 7.5% of the patients, with a significantly higher incidence in patients with type D tumors (24.7% at 5 years) compared with type A-C tumors (3.6%) (subdistribution hazard ratio 2.319, p = 0.036). In the subgroup of patients with stable disease, the cumulative incidence of salvage treatment at 15 years was 2.1%, and true tumor progression was identified in only 2 patients (0.3%). Notably, tumor type at the time of GKS did not significantly influence the risk of salvage treatment beyond 5 years in the subgroup. Serviceable hearing preservation improved in more recent treatment periods: patients with pre-GKS Gardner-Robertson class 1 hearing had a 10-year preservation rate of 63% in the late treatment period (2005-2023) compared with 48% in the early period (1991-2004). Among late adverse events, cyst-related complications were the most common (3.1%), whereas trigeminal neuralgia (1.6%), persistent facial palsy (0.1%), and malignant transformation (0.2%) were infrequent. GKS provided durable long-term tumor control and functional preservation in patients with small- to medium-sized VS. True tumor progression beyond 10 years was not observed in this cohort, suggesting that the intensity or frequency of routine imaging surveillance can be reduced or individualized after 10 years in patients with stable disease during the first 5 years after GKS. However, because delayed adverse events (e.g., cyst formation, trigeminal neuralgia, and malignant transformation) can still occur, follow-up strategies should be tailored according to initial tumor characteristics and the posttreatment clinical course.

Background: Uveal melanoma (UM) metastasis follows variable temporal trajectories, with recurrences ranging from rapid onset to decades post primary therapy. Outcomes after metastasis also vary significantly. Predicting high-risk “early” progressors from “late” recurring phenotypes would facilitate tailored approaches to management. Methods: A literature review was conducted to synthesise clinicopathologic and molecular predictors of metastatic latency and their impact on survival outcomes in patients with UM. Results: Early dissemination is associated with older age, male sex, larger basal dimensions, and ciliary body involvement. Genetically, monosomy 3, 8q gain and BAP1 loss drives a rapid-progression phenotype and poor survival. Conversely, SF3B1 mutations define a distinct late-onset cohort (median &gt;6 years) with persistent lifetime risk. PRAME expression significantly accelerates metastatic kinetics, even in Gene Expression Profiling Class 1 tumours. While early recurrence correlates with dismal outcomes, late-onset disease is associated with extended post-metastasis survival and greater eligibility for interventions like liver-directed therapy. Key Message: Metastatic timing is related to biologic rather than stochastic determinants. Integrating molecular profiling with clinical staging and patient factors allows for more precise temporal risk stratification. These insights are essential for tailoring surveillance intensity and selecting candidates for emerging adjuvant therapies, such as tebentafusp and protein kinase C inhibitors.

ABSTRACT Background Endovascular aneurysm repair (EVAR) and open surgical repair (OSR) are both used for elective unruptured infrarenal abdominal aortic aneurysm (AAA), but their relative cost-effectiveness in the UK NHS remains uncertain. Research design and methods A lifetime Markov cohort model compared EVAR and OSR, incorporatingwaiting-list and perioperative mortality, postoperative survival, reinterventions, and imaging surveillance. Time-varying mortality effects were derived from reconstructed individual-patient-data meta-analysis, with equal long-term mortality assumed in the base case. Costs and QALYs were discounted at 3.5%. Uncertainty was explored through deterministic, probabilistic (10,000 iterations), and scenario analyses using alternative survival models. Results EVAR had higher lifetime costs (£17,710 vs £16,191) but greater QALYs (6.373 vs 6.219), yielding an ICER of £9,865/QALY. Probabilistic analysis produced a mean ICER of £9,793/QALY, with EVAR cost-effective in 56.1% and 62.2% of simulations at £20,000 and £30,000/QALY thresholds, respectively. Results were sensitive to survival modeling assumptions, EVAR device costs, perioperative mortality, and surveillance intensity. Conclusions Under contemporary time-varying mortality assumptions, EVAR is likely cost-effective versus OSR at standard UK thresholds, though conclusions depend on long-term survival assumptions and surveillance intensity.

Background: Minimal residual disease (MRD) assessment is an emerging tool for refining the risk of relapse following definitive therapy in non-small-cell lung cancer (NSCLC). However, data regarding its clinical impact on the decision-making process remain limited. We evaluated MRD feasibility and its impact in the real-world setting. Methods: A pooled retrospective analysis of longitudinal MRD data in NSCLC patients (n = 34: Signatera™ (Exome), n = 25, Guardant Reveal™, n = 9) was implemented. Co-primary endpoints: MRD feasibility and clinical impact on management (changes in surveillance intensity or therapy escalation/de-escalation). Secondary endpoints: sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), accuracy for recurrence detection, and MRD lead time. Results: MRD was feasible in 32/34 patients (94.1%); longitudinal testing included two samples in 15 patients (44.1%) and three samples in 2 patients (5.9%). Signatera™ (Exome) failed in 2/25 (8.0%) due to insufficient tissue. MRD influenced management in 20/34 (58.8%) patients, most commonly supporting therapy de-escalation (15/34, 44.1%), followed by imaging surveillance modification (3/34, 8.8%) and therapy escalation (2/34, 5.9%). In univariable analysis, tumor grade and STAS were associated with MRD-driven management impact, but neither remained significant in multivariable analysis. With a median follow-up of 18.9 months (IQR 8.5-30.7), MRD was positive in 6/32 (18.8%), while recurrence/progression occurred in 10/32 (31.3%) patients. MRD yielded 21 true negatives, five true positives, five false negatives (including two isolated brain recurrences), and one false positive, corresponding to a sensitivity of 50.0%, specificity of 95.5%, PPV of 83.3%, NPV of 80.8%, and an accuracy of 81.3%. The median MRD lead time (n = 5) was 1.31 months (range, 0.46-5.52). Conclusions: In this real-world cohort, MRD testing was feasible and frequently guided clinical decisions, mainly supporting treatment de-escalation. MRD was highly specific but less sensitive. Prospective studies are needed to define optimal testing intervals and validate MRD-guided strategies.

Prader-Willi syndrome (PWS) is a neuroendocrine disorder characterized by hypothalamic dysfunction, congenital hypotonia, abnormal growth trajectories, and impaired pubertal development, all of which contribute to a markedly increased risk of scoliosis, with a cumulative prevalence reaching up to 70-80% by skeletal maturity, significantly exceeding that of idiopathic scoliosis. Unlike idiopathic scoliosis, spinal deformity in PWS follows a distinct bimodal pattern, with critical vulnerability during infancy and a second acceleration during pubertal transition. Growth hormone (GH) therapy, a cornerstone of PWS management, substantially improves linear growth, body composition, and muscle strength, yet its relationship with scoliosis onset and progression remains a clinical challenge due to the potential for accelerated growth during critical developmental windows, which may unmask or exacerbate underlying spinal instability. Current scoliosis surveillance strategies in PWS are largely extrapolated from idiopathic scoliosis and fail to account for the unique neuroendocrine and biomechanical context of this syndrome. In particular, endocrine modifiers such as GH treatment status, growth velocity, hypogonadism, pubertal stage, body composition, and genotype-specific phenotypes are rarely integrated into structured monitoring protocols. In this narrative review, we synthesize epidemiological, mechanistic, and clinical evidence to elucidate the neuroendocrine and biomechanical pathways underlying scoliosis development in PWS, including the roles of hypotonia-related instability, altered vertebral growth modulation, and delayed epiphyseal maturation. We critically examine the dualistic effects of GH therapy, the impact of pubertal maturation, and genotype-phenotype associations as key determinants of scoliosis risk and progression. Building on this evidence, we propose an endocrine-informed, risk-stratified scoliosis monitoring framework that integrates growth dynamics, hormonal status, body composition, and spinal parameters to guide surveillance intensity, imaging strategies, and multidisciplinary referral. By shifting the focus from isolated curve detection to longitudinal, endocrine-guided surveillance, this review provides a clinically actionable model to optimize early identification and management of scoliosis in children and adolescents with PWS. This framework aims to support coordinated endocrine-orthopedic care and inform future prospective studies designed to refine outcome measures and ultimately improve long-term musculoskeletal and quality-of-life outcomes in this vulnerable population.

Colorectal cancer remains a leading cause of cancer-related morbidity and mortality with stage III disease carrying a substantial risk of recurrence despite curative resection. Accurate risk stratification is essential to optimize surveillance and guide adjuvant therapy. Traditional risk models rely heavily on pathologic features, but recent studies suggest that body composition metrics, particularly imaging-based assessments of skeletal muscle mass, may offer additional prognostic value. The skeletal muscle index (SMI), derived from routine CT imaging, has emerged as a promising surrogate marker of frailty. However, the relationship between temporal changes in SMI and cancer recurrence remains poorly understood. A retrospective cohort study was performed using single-institution data from over 500 patients who underwent resection for stage III colorectal malignancy. SMI at diagnosis (SMIdx) was measured using staging CT imaging and follow-up measurements (SMIfu) were obtained at the most recent scan prior to recurrence to capture changes preceding radiologic evidence of disease. Patients were paired using propensity score matching and temporal changes in SMI were evaluated using conditional logistic regressions. Receiver operating characteristics and decision curve analysis were performed to determine whether change in SMI can stratify patients into meaningful risk groups to guide surveillance. A decrease in SMI was independently associated with increased risk of disease recurrence with an odds ratio of 2.23 per 10% decline (95% CI: 1.15-4.35, p = 0.018). Baseline muscle status was not associated with recurrence (OR 1.01 per cm2/m2, 95% CI: 0.97-1.05, p = 0.585). The optimal risk stratification threshold was θ = 2.11%, (θ = SMIfu / SMIdx - 1) with a sensitivity of 90% and specificity of 60%. Decision curve analysis showed net clinical benefit over a wide range of thresholds, θ = ±11%. These results were reproduced in an internally validated cohort. Postoperative decline in skeletal muscle index is a significant, independent predictor of colorectal cancer recurrence. Clinically relevant risk stratification thresholds have been proposed and support the conclusion that longitudinal monitoring of SMI may have value to escalate surveillance intensity rather than being a passive prognostic marker. Future studies should focus on validating these thresholds in large, multi-center cohorts.

BPI26-023: Interval Relative Survival After Resection of Pulmonary Carcinoid: Implications for Surveillance Duration and Intensity.

Background: The prognosis of chronic kidney disease (CKD) typically requires longitudinal estimated glomerular filtration rate (eGFR) data, making risk stratification difficult at initial consultation. Furthermore, eGFR-based clinical decisions often overlook the critical factor of patient age. This study aimed to establish a simplified predictive model for progressive CKD and quantify the impact of clinical interventions. Methods: Utilizing a historical dataset (1988-2003) from the pre-renin-angiotensin system inhibitor (RASi) and pre-sodium-glucose cotransporter 2 inhibitor (SGLT2i) era, we developed heatmaps to predict the probability of reaching eGFR < 30 mL/min/1.73 m2 by age 80 years. The model also estimated the risk reduction from smoking cessation and pharmacological therapies. The predictive performance for age + eGFR was assessed using standard calibration and discrimination metrics, and clinical utility was evaluated using decision curve analysis across a range of threshold probabilities. Risk reclassification analyses compared age +eGFR-based categories with conventional eGFR-based stratification. Results: Regarding the risk of eGFR < 30 mL/min/1.73 m2 by age 80 years, simulations confirmed a correlation between age and eGFR. At age 40 years, an eGFR of ~57 mL/min/1.73 m2 indicated a 50% probability of progressing to CKD stage 4 by age 80 years. This threshold decreases to 53 and 48 mL/min/1.73 m2 at 50 and 60 years of age, respectively. Calibration and discrimination analyses demonstrated acceptable agreement between predicted and observed risks. Decision curve analysis showed that an age + eGFR threshold of approximately 115 primarily provided a net benefit at lower threshold probabilities, supporting intensified surveillance strategies, whereas an age +eGFR of 100 showed a positive net benefit across a broader range of thresholds, comparable to the conventional eGFR < 45 mL/min/1.73 m2 criterion. While proteinuria markedly increased risk, smoking cessation provided a 9.4-11.2% risk reduction. Combined RASi and SGLT2i treatment showed the greatest impact, reducing progression probability by 31.2-40.0% (e.g., reducing a 50.0% baseline risk to 32.1% in 40-year-old men). Conclusions: The age + eGFR rule represents a simple, clinically interpretable heuristic for age-adjusted risk stratification based on a single eGFR measurement and may offer potential clinical utility for guiding surveillance intensity and consideration of earlier intervention strategies. However, external validation is required before clinical application.

Public transport systems increasingly adopt algorithmic management through GPS surveillance, rating systems, and automated sanctions, yet the psychological mechanisms linking these technologies to workers' mental health remain poorly understood and theoretically fragmented.To develop an integrated multilevel theoretical framework synthesizing pathways from algorithmic control mechanisms to psychological risk in public transport drivers.PRISMA-guided systematic integrative review of 48 peer-reviewed studies (2016-2025) from 4,812 initial records sourced from Scopus, Web of Science, and PubMed.Structured data extraction captured control mechanisms, psychological outcomes, and mediating pathways.Thematic synthesis integrated Job Demand-Control Model, Conservation of Resources Theory, and Algorithmic Management Theory.Four control mechanisms emerged: GPS tracking (panoptic surveillance), rating systems (emotional labour demands), dynamic pricing (income volatility), and automated sanctions (deactivation fear).Platform workers experience 59.6% higher digital speed determination and 36.3% more third-party ratings than traditional workers.The trilevel framework (technological organizational psychological) yielded six propositions: surveillance intensity hyper-vigilance ( = -4.213),algorithmic opacity procedural anxiety, income volatility depressive symptoms (23 -41% prevalence), rating pressure emotional exhaustion (41-67% high burnout), task defragmentation reduced accomplishment, and deactivation fear chronic precarity (78% report chronic fear).Algorithmic management operates as psychological governance eroding worker mental health through surveillance, opacity, and precarity.Human-in-command regulation requires: algorithmic transparency mandates, mandatory mental health risk audits, participatory co-design, human review of deactivations, and minimum wage protections aligned with ILO principles.

The rapid development of smart technologies and digital infrastructure has transformed the way governments and organizations monitor and manage urban environments. Smart societies rely on advanced technologies such as artificial intelligence, Internet of Things devices, biometric identification systems, and large-scale data analytics to improve public services, enhance security, and optimize urban management. Digital surveillance systems have become a central component of smart city governance by enabling real time monitoring of public spaces, transportation systems, communication networks, and citizen activities. While these technologies provide numerous benefits in terms of public safety, crime prevention, and efficient resource management, they also raise significant concerns regarding privacy protection and civil liberties. Digital surveillance technologies collect and analyze vast amounts of personal and behavioral data, which may create risks related to unauthorized monitoring, data misuse, and excessive governmental control. Civil liberty advocates argue that widespread surveillance may undermine fundamental democratic principles such as freedom of expression, freedom of association, and the right to privacy. As smart societies continue to expand the use of surveillance technologies, it becomes increasingly important to understand how these systems influence public perceptions of privacy, governance transparency, and civil rights protection. This study analyzes the effect of digital surveillance systems on civil liberties within smart societies. The research develops a conceptual model that examines the relationships between digital surveillance intensity, perceived privacy risk, governance transparency, and protection of civil liberties. Data were collected from citizens, technology professionals, and policy analysts involved in smart city initiatives. Structural Equation Modeling using Smart Partial Least Squares was employed to test the relationships between constructs. The results indicate that increased digital surveillance intensity significantly raises perceived privacy risks among citizens. However, governance transparency and regulatory oversight mechanisms play a critical role in mitigating negative perceptions and protecting civil liberties. The study contributes to digital governance and technology policy research by providing empirical insights into the complex relationship between surveillance technologies and civil liberty protection in smart societies. The findings highlight the need for balanced governance frameworks that ensure security benefits while safeguarding individual rights and democratic values.

West Nile virus (WNV) is a mosquito-borne flavivirus that remains an important public and veterinary health concern across Europe. Periodic outbreaks affecting humans, horses, and wildlife highlight the complex ecological interactions underlying viral circulation. This narrative review aims to synthesize current knowledge regarding WNV epidemiology, transmission dynamics, and surveillance strategies in Europe, with particular attention to the Romanian context. Available surveillance data indicate recurrent seasonal transmission in several European regions; however, reported case numbers may be influenced by differences in diagnostic capacity, reporting practices, and surveillance intensity among countries. Recent studies suggest that environmental variability, vector adaptation, and host community composition play important roles in shaping regional transmission risk, although the relative contribution of these factors remains incompletely quantified. Despite expanding surveillance networks and One Health initiatives, important knowledge gaps persist regarding the integration of environmental risk indicators, vector ecology, and operational preparedness into coherent risk-assessment frameworks. This review therefore examines current epidemiological patterns, evaluates surveillance approaches, and discusses emerging drivers of WNV transmission in Europe. As a narrative synthesis based on published literature and surveillance reports, this review is subject to limitations related to heterogeneity in available data and differences in national reporting systems. Nevertheless, a clearer understanding of these interacting factors may support improved surveillance strategies and more adaptive public health responses to future WNV transmission events. Reported surveillance data should be interpreted cautiously, as differences in national surveillance intensity, diagnostic capacity, and reporting frameworks across Europe may influence notified case numbers. Consequently, reported outbreaks do not necessarily reflect proportional differences in transmission intensity.

Surveillance practices after resection of extremity and truncal soft-tissue sarcoma (ETSTS) vary, with guidelines recommending physical exam and imaging every 3-6 months. Local and distant recurrence risks differ based on clinicopathological features including tumor grade and histopathologic subtype. The aim of this study was to evaluate surveillance patterns after ETSTS resection at our high-volume sarcoma referral center and determine if opportunities exist to de-escalate intensity of surveillance in appropriate patients. A retrospective review of patients with primary ETSTS who underwent resection and surveillance at our institution from 2016-2021 was performed. Patients with less than 2 years of follow-up after resection were excluded. Sarculator, a validated nomogram for soft-tissue sarcoma, was used to stratify patients into high- (<60%) and low-risk (≥60%) prognostic groups based on their predicted overall survival (OS) at 10 years. The cohort of 296 patients included 112 high- and 184 low-risk. 5-year OS was 70.5% in the high-risk group versus 90.9% in the low-risk group (P<0.001). Most patients did not recur during the study period (n=206). 26 patients recurred within 6 months from their initial surgery (18 high-risk, 8 low-risk) and all were offered immediate treatment after recurrence diagnosis. Of this cohort, 84.6% were offered immediate treatment after diagnosis of recurrence. Surveillance strategies after primary resection should be tailored to patient's individual risk. Patients with low-risk clinicopathologic features have a lower chance of recurrence in the first two years and frequent surveillance visits may not impact their oncologic outcomes.

Immune checkpoint inhibitors (ICIs) have transformed cancer therapy but may cause immune-related adverse events (irAEs), including dry eye disease (DED). This study aimed to quantify the incidence of ICI-associated DED and to evaluate factors contributing to variability across studies. A systematic review and meta-analysis was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD420251091266). PubMed, the Cochrane Library, and Web of Science were searched from inception through September 13, 2025. Eligible studies included adults (≥18 years) treated with ICIs (anti-programmed cell death protein 1 (PD-1), anti-programmed death-ligand 1 (PD-L1), anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)) reporting DED outcomes with extractable ICI-exposed denominators. Two independent reviewers screened studies, extracted data, and assessed risk of bias using the Newcastle-Ottawa Scale (observational studies), ROBINS-I (non-randomized interventional studies), and Cochrane RoB 2 (randomized controlled trials). Pooled incidence and 95% confidence interval (CI) estimates were calculated using random-effects models on the logit-transformed scale and back-transformed to proportions. Subgroup analyses evaluated ICI class, combination therapy, and tumour type. Thirteen studies were included. The pooled incidence of DED among ICI-treated patients was 2% (95% CI: 1%-3%), with marked heterogeneity across studies (0.2%-65%), likely reflecting variation in surveillance intensity, diagnostic criteria, and ascertainment approaches. Combination ICI therapy (CTLA-4 plus PD-1) demonstrated a numerically higher pooled incidence (25%) than monotherapies (CTLA-4: 5%; PD-1: 13%; PD-L1: 15%), although subgroup differences were not statistically significant (p = 0.18); these regimen-stratified estimates were derived from a limited subset of studies with extractable regimen-specific denominators and heterogeneous surveillance intensity and therefore are not directly comparable to the overall pooled incidence. Lung cancer cohorts showed higher observed rates (41%) compared with melanoma (4%) and renal cancer cohorts (32%) (p = 0.05); however, these apparent subgroup differences may reflect not only tumour- or regimen-specific biology, but also systematic differences in surveillance intensity, access to ophthalmic assessment, and referral enrichment across cohorts, which may materially influence observed event rates. Mechanistic findings were consistent with immune-mediated lacrimal dysfunction, with abnormal Schirmer's test results reported in 62% of symptomatic cases. Most DED events were mild and managed with topical therapy, while a minority required escalation to systemic immunomodulation. DED occurs in approximately 1 in 50 ICI-treated patients in pooled estimates from heterogeneous study designs, although reported incidence varies substantially across study designs and ascertainment approaches. Combination therapy and ICI-treated lung cancer cohorts demonstrated numerically higher DED rates, but these subgroup estimates should be interpreted cautiously given potential differences in referral patterns and diagnostic intensity. Incidence variability highlights the need for standardized ocular assessment. High-risk patients should be proactively monitored to maintain quality of life and treatment adherence.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with chronic hepatitis B (CHB) accounting for more than half of the cases. Regular surveillance, including abdominal ultrasonography with alpha-fetoprotein testing every 6 months, enables early tumor detection and curative treatment; however, current guideline recommendations based mainly on age, sex, and race/ethnicity insufficiently capture individual risk variation, particularly among patients with CHB who do not have cirrhosis. In addition, real-world adherence to HCC surveillance is suboptimal-fewer than 40% of eligible patients receive surveillance at the recommended 6-month intervals. To improve both efficiency and impact, surveillance resources should be reallocated to patients whose estimated risk exceeds the cost-effective surveillance threshold. Recent studies support biomarker-based risk stratification as a more precise approach. For example, in untreated CHB, HBeAg-negative patients meeting inactive disease criteria with HBsAg <100IU/mL have an annual HCC incidence below the 0.2% cost-effectiveness threshold, suggesting that routine surveillance may be unnecessary. In antiviral-treated CHB, models such as PAGE-B and its derivatives can accurately identify low-risk patients who may safely forgo HCC surveillance. Conversely, for patients at extremely high risk, including those with cirrhosis, intensified strategies-such as abbreviated MRI or combined biomarker algorithms-may enhance early detection. Collectively, these findings support a transition from a categorical, one-size-fits-all approach toward a precision surveillance paradigm that tailors the need for and intensity of HCC surveillance to biomarker-defined risk, thereby optimizing resource use, improving adherence, and maximizing clinical benefit. Nevertheless, further large-scale, prospective studies across diverse populations are needed to validate biomarker thresholds and confirm the long-term safety of exempting very-low-risk patients with CHB from HCC surveillance.

Objectives: This study aimed to evaluate phenotypic associations between preoperative alkaline phosphatase (ALP) levels and clinical characteristics, and explore clinical factors associated for postoperative regrowth in craniofacial fibrous dysplasia. Methods: In this retrospective cohort (2003-2024), 71 surgically treated fibrous dysplasia patients were analyzed. Relationships between preoperative ALP (using age-stratified reference ranges) and key phenotypes (age at surgery, onset age, laterality, lesion type) were assessed via nonparametric tests. Associations with postoperative regrowth were assessed using Mann-Whitney U or Kruskal-Wallis tests for non-normally distributed continuous variables and χ2 or Fisher's exact tests for categorical variables. Results: Preoperative ALP levels significantly correlated with younger surgical age (16-19 vs. ≥19 years: 244.0 vs. 107.0 U/L, p < 0.001), earlier onset (0-16 vs. >16 years: 114.0 vs. 83.0 U/L, p = 0.030), bilateral lesions (176.0 vs. 106.2 U/L, p = 0.006), and polyostotic subtype (polyostotic fibrous dysplasia vs. monostotic fibrous dysplasia: 162.0 vs. 87.5 U/L, p < 0.001). However, neither ALP levels (p = 0.061) nor abnormal ALP rates (p = 0.090) predicted regrowth. Crucially, bilateral lesions were significantly associated with regrowth (83.3% (5/6) vs. 21.5% (14/65); p = 0.005). The overall regrowth rate was 8.5% (6/71). Conclusions: Bilateral lesions demonstrate significant association with postoperative regrowth risk, potentially guiding surveillance intensity. ALP correlates with phenotypic burden but shows limited prognostic utility. These findings, interpreted considering retrospective constraints, warrant validation in larger cohorts.