Search Results (1,368)

Metal anodes promise improvements in energy density and cost; however, their performance is determined within the first several nanometers at the interface. This review reports on how polymer-based artificial solid electrolyte interphases (SEIs) are engineered to stabilize Li and aqueous-Zn anodes, and how these designs are now evaluated against operando readouts rather than post-mortem snapshots. We group the related molecular strategies into three classes: (i) side-chain/ionomer chemistry (salt-philic, fluorinated, zwitterionic) to increase cation selectivity and manage local solvation; (ii) dynamic or covalently cross-linked networks to absorb microcracks and maintain coverage during plating/stripping; and (iii) polymer–ceramic hybrids that balance modulus, wetting, and ionic transport characteristics. We then benchmark these choices against metal-specific constraints—high reductive potential and inactive Li accumulation for Li, and pH, water activity, corrosion, and hydrogen evolution reaction (HER) for Zn—showing why a universal preparation method is unlikely. A central element is a system of design parameters and operando metrics that links material parameters to readouts collected under bias, including the nucleation overpotential (η_nuc), interfacial impedance (charge transfer resistance (R_ct)/SEI resistance (R_SEI)), morphology/roughness statistics from liquid-cell or cryogenic electron microscopy (Cryo-EM), stack swelling, and (for Li) inactive-Li inventory. By contrast, planar plating/stripping and HER suppression are primary success metrics for Zn. Finally, we outline parameters affecting these systems, including the use of lean electrolytes, the N/P ratio, high areal capacity/current density, and pouch-cell pressure uniformity, and discuss closed-loop workflows that couple molecular design with multimodal operando diagnostics. In this view, polymer artificial SEIs evolve from curated “recipes” into predictive, transferable interfaces, paving a path from coin-cell to prototype-level Li- and Zn-metal batteries. Full article

Background: Current low milk supply (LMS) definitions use subjective maternal perceptions or arbitrary thresholds for 24 h milk production (MP), potentially misclassifying cases. This study aimed to re-evaluate the definition of LMS using data-driven approaches and investigate associated maternal risk factors. Methods: Lactating mothers 4–26 weeks postpartum (n = 460) provided demographic, obstetric, and infant data and measured 24 h MP and infant milk intake using the test-weighing method. Infant growth was calculated as their weight-for-age z-score. Latent profile analysis, receiver operating characteristic curve analysis, and multinomial logistic regression were used for classification, diagnostic evaluation, and risk factor assessment for LMS. Results: Four milk supply classes emerged: Class 1 with adequate MP, infant intake and infant growth (n = 254); Class 2 with high MP exceeding infant demand and adequate growth (n = 30); Class 3 with slow infant growth despite moderate MP (n = 120); and Class 4 with extremely low MP and high formula intake (n = 56). Classes 1 and 2 were grouped as the normal milk supply group (61.7%), while Classes 3 and 4 formed the LMS group (38.3%). New thresholds were identified for 24 h MP (708 mL/24 h, area under the curve (AUC) = 0.92) and infant breast milk intake (694 mL/24 h, AUC = 0.94) with high diagnostic accuracy. Moreover, practical alternative thresholds for infant average daily weight gain (26 g, AUC = 0.89), formula intake (122 mL/24 h, AUC = 0.89) and formula-to-growth ratio (4 mL/g, AUC = 0.94) were established for the identification of LMS. Minimal breast growth during pregnancy (Odds ratio (OR) = 4.6, 95% confidence interval (CI): 2.3–9.6), advanced maternal age (OR = 2.1, 95% CI: 1.0–4.5), and gestational diabetes mellitus (OR = 2.1, 95% CI: 1.1–4.0) were significant risk factors related to the LMS subgroups. Co-existence of maternal advanced age and overweight showed greatly amplified risk of LMS (OR = 3.7, 95% CI: 1.3–10.5), and a more pronounced risk was observed for the combination of minimal breast growth and advanced maternal age (OR = 9.2, 95% CI: 3.0–28.3). Conclusions: This data-driven classification of LMS and identified risk factors may enhance the precision of LMS diagnosis and guide targeted interventions for lactating mothers. Full article

Background: Waist circumference (WC) has become an essential diagnostic marker of metabolic syndrome; however, its accuracy in reflecting insulin resistance remains uncertain, particularly among Asian people who develop metabolic complications at lower levels of adiposity. Methods: We analyzed 20,202 adults (8886 men and 11,316 women) from the Korean National Health and Nutrition Examination Survey (KNHANES) 2015 and 2019–2021. All analyses accounted for the survey sampling weights and the complex survey design. WC, insulin resistance, and β-cell function were assessed using fasting insulin level, HOMA-IR, and HOMA-β. Associations between WC and insulin indices were evaluated using correlation analyses, stratification by WC deciles, and multivariable regression models adjusted for demographic and metabolic covariates. Results: WC was positively associated with HOMA-IR in both sexes (all p < 0.001). In the fully adjusted model, HOMA-IR remained significantly associated with WC [men, β = 0.014 (95% CI, 0.011–0.016); women, β = 0.009 (95% CI, 0.008–0.011)]. Subgroup analyses stratified by age revealed significant associations across all age groups. The association was stronger in older adults, particularly among men, whereas women exhibited significant associations across all ages with a larger age-related increase. Conclusions: WC is independently associated with insulin resistance in Korean adults, with stronger associations in older adults and consistent associations in women. These findings support WC as a simple yet pathophysiologically meaningful marker of metabolic risk and highlight the necessity of refining WC cutoff values for clinical screening of Asian populations and an age-specific approach for diagnosing metabolic syndrome. Full article

Purpose: This study evaluates a novel, non-invasive method using a virtual reality (VR) headset with integrated eye trackers to assess retinal function by measuring the recovery of the pupillary response after light adaptation in patients with age-related macular degeneration (AMD). Methods: In this pilot study, fourteen patients with clinically confirmed AMD and 14 age-matched healthy controls were exposed to alternating bright and dark stimuli using a VR headset. The dark stimulus duration increased incrementally by 100 milliseconds per trial, repeated over 50 cycles. The pupillary response to the re-onset of brightness was recorded. Data were analyzed using a linear mixed-effects model to compare recovery patterns between groups and a convolutional neural network to evaluate diagnostic accuracy. Results: The pupillary response amplitude increased with longer dark stimuli, i.e., the longer the eye was exposed to darkness the bigger was the subsequent pupillary amplitude. This pupillary recovery was significantly slowed by age and by the presence of macular degeneration. Test diagnostic accuracy for AMD was approximately 92%, with a sensitivity of 90% and a specificity of 70%. Conclusions: This proof-of-concept study demonstrates that consumer-grade VR headsets with integrated eye tracking can detect retinal dysfunction associated with AMD. The method offers a fast, accessible, and potentially scalable approach for retinal disease screening and monitoring. Further optimization and validation in larger cohorts are needed to confirm its clinical utility. Full article

Hepatocellular carcinoma (HCC), the most common primary liver malignancy, usually develops in patients with cirrhosis, yet the metabolic mechanisms that distinguish the two conditions remain poorly understood. This study aimed to explore metabolic dysregulations in HCC compared with cirrhosis and to identify potential biomarkers, especially lipids, with diagnostic and prognostic value. We prospectively studied 81 patients—41 with HCC and 40 with cirrhosis—using high-resolution UHPLC-QTOF-ESI⁺-MS to characterize their serum lipidome. Across both groups, 322 metabolites were identified, but their distribution was strikingly different. Patients with HCC showed higher levels of sphingolipids, glycerophospholipids, diglycerides, sterols, and certain fatty acids, reflecting tumor-related metabolic rewiring. In contrast, cirrhotic patients had increased D-glucose, 5-hydroxymethyluracil, lysophospholipids, acylcarnitines, and specific fatty acid derivatives. Several lipids, such as CerPE(d16:2/24:1(2OH)), SM(d18:0/14:0), PA(36:6), and GlcCer(d18:1/12:0), displayed excellent discriminative accuracy, highlighting their role as putative biomarkers. These findings underscore the importance of lipid metabolic reprogramming in HCC, characterized by membrane remodeling, energy adaptation, and oxidative stress resistance. Integrating lipidomic profiling into clinical practice could improve early detection and risk stratification in cirrhotic patients. Larger, multicenter studies are needed to validate these biomarkers and assess their therapeutic implications. Full article

Gastric cancer is one of the leading causes of cancer-related deaths worldwide, and due to its late-stage diagnosis, the prognosis is poor. Therefore, researching biomarkers that can be used in early diagnosis and prognostic processes is crucial. Insulin-like growth factor (IGF) signaling pathways play critical roles in cellular proliferation, apoptosis, differentiation, and tumor progression. This study investigated the biomarker potential of IGF-1, IGFBP-4, IGFBP-5, and PAPP-A in gastric cancer. Forty gastric cancer patients and forty healthy individuals were included, and protein levels in serum samples were measured using the ELISA method. The findings showed that IGF-1 levels were significantly decreased in the gastric cancer group, while IGFBP-4 levels were significantly increased. IGFBP-5 levels were also lower in gastric cancer patients. In contrast, PAPP-A levels did not differ significantly between the two groups. ROC analyses revealed that IGF-1, IGFBP-4, and IGFBP-5 have good discriminatory properties in the diagnosis of gastric cancer, while PAPP-A offers low diagnostic value. In conclusion, this study suggests that IGF pathway components, particularly IGF-1, IGFBP-4, and IGFBP-5, might be promising biomarker candidates for gastric cancer. Full article

Background: Gastric cancer (GC) remains a significant health burden in the U.S, particularly among ethnic minorities. We identified patient-level risk factors contributing to advanced-stage (AS) diagnosis and poor survival to guide strategies to address GC-related health disparities. Methods: We conducted a retrospective cohort analysis of 18,396 histologically confirmed GC cases (4102 early-stage (ES) and 14,294 AS) diagnosed between 2000 and 2019, using data from the California Cancer Registry linked to the California Office of Statewide Health Planning and Development. Eligible cases were adults age ≥ 18 with complete diagnostic and follow-up data. Multivariable logistic and Cox regression models were used to identify predictors of AS-GC and five-year disease-specific (DSS) and overall-survival (OS) outcomes. Analyses were further stratified by Asian and Hispanic subgroups. Results: Korean heritage was the strongest predictor of ES-GC [OR 0.58 (95% CI, 0.47–0.71), p < 0.001] and was independently associated with the lowest GC-specific mortality risk [HR 0.73 (95% CI: 0.67–0.80), p < 0.0001]. The youngest age group (18–44 years) had the highest AS-GC rate (91.4%). Asian ethnicity, receipt of care at NCI-designated cancer centers, and prior upper endoscopy were associated with improved OS and DSS. In contrast, comorbidities such as GERD, diabetes, liver disease, smoking and alcohol abuse, and older age ≥ 75, U.S.-birth, and rural residence were linked to worse outcomes. Conclusions: Distinct demographic, clinical, and healthcare access factors contribute to disparities in GC outcomes. These findings support the development of culturally tailored early-detection programs, and risk-based screening for GC care, particularly in vulnerable populations. Full article

Background: Intellectual disability (ID) is a heterogeneous condition caused by diverse genetic factors, including single-nucleotide variants (SNVs) and copy number variants (CNVs). Whole-exome sequencing (WES) and clinical exome sequencing (CES) have become essential tools for identifying pathogenic variants; however, their relative diagnostic performance in ID has not been fully characterized. Methods: Children diagnosed with ID or related neurodevelopmental disorders underwent WES or CES. Identified variants were classified according to ACMG/AMP and ClinGen guidelines, with segregation analysis performed when parental samples were available. Diagnostic yields were compared across demographic, prenatal, and phenotypic subgroups. A multidimensional semi-quantitative scoring system encompassing 15 clinical domains (e.g., age at onset, neuro-motor function, seizures, MRI findings, vision, and dysmorphic features) was developed. Z-scores were calculated for each parameter, followed by hierarchical cluster analysis (HCA) and correlation modeling to define genotype–phenotype associations and pathway-level clustering. Results: A broad spectrum of pathogenic and likely pathogenic variants across multiple genes and biological pathways was identified in our study. CNV-associated cases frequently exhibited prenatal anomalies or multisystem phenotypes associated with large chromosomal rearrangements. Monogenic variants and their corresponding phenotypic profiles were identified through clinical exome sequencing (CES) and whole-exome sequencing (WES). Phenotypic HCA based on Z-scores revealed three major biological groups of patients with coherent genotype–phenotype relationships: Group 1, severe multisystem neurodevelopmental disorders dominated by transcriptional and RNA-processing genes (POLR1C, TCF4, HNRNPU, NIPBL, ACTG1); Group 2, intermediate epileptic and metabolic forms associated with ion-channel and excitability-related genes (SCN2A, PAH, IQSEC2, GNPAT); and Group 3, milder or focal neurodevelopmental phenotypes involving myelination and signaling-related genes (NKX6-2, PLP1, PGAP3, SMAD6, ATP1A3). Gene distribution significantly differed among these biological categories (χ² = 54.566, df = 34, p = 0.0141), confirming non-random, biologically consistent grouping. Higher Z-scores correlated with earlier onset and greater neurological severity, underscoring the clinical relevance of the multidimensional analytical framework. Conclusions: This study highlights the genetic complexity and clinical heterogeneity of intellectual disability and demonstrates the superior diagnostic resolution of WES and CES. Integrating multidimensional phenotypic profiling with genomic analysis enhances genotype–phenotype integration and enables data-driven phenotype stratification and pathway-based re-analysis. This combined diagnostic and analytical framework offers a more comprehensive approach to diagnosing monogenic ID and provides a foundation for future predictive and functional studies. Full article

Canine atopic dermatitis (AD) is a chronic allergic skin disease in which various immunological markers have been investigated. While peripheral eosinophil counts, serum allergen-specific immunoglobulin E (IgE), and cytokines have each been evaluated in allergic disorders, their simultaneous assessment in dogs with AD has rarely been reported in Korea. This study aimed to evaluate the diagnostic and clinical utility of these parameters in affected dogs. A total of 93 dogs were included between August 2019 and February 2020, comprising 65 dogs diagnosed with AD and 28 healthy controls. Clinical information, peripheral blood eosinophil counts and ratios, serum allergen-specific IgE using a multiple allergen panel (60 allergens), and cytokines related to T helper 2 (Th2) and T regulatory (Treg) cells (IL-4, IL-13, IL-31, TGF-β1) were analyzed. The mean age of AD dogs was 6.34 ± 3.99 years, with a predominance of small breeds and males. Eosinophil counts and ratios showed no significant difference between groups. In contrast, allergen-specific IgE levels were significantly elevated for several allergens, including Dermatophagoides pteronyssinus, Acarus siro, Tyrophagus putrescentiae, alder/birch, hazel, oak, cladosporium, and selected dietary antigens (pea, soybean, pumpkin, apple) (p < 0.05). Sensitization rates were also higher for Acarus siro, Tyrophagus putrescentiae, oak, and sheep sorrel (p < 0.05). Th2-related cytokines tended to increase and TGF-β1 tended to decrease in AD dogs, though without statistical significance. These findings indicate that peripheral eosinophil counts have limited diagnostic value, whereas allergen-specific IgE testing provides clinically useful information for the diagnosis and management of canine AD. Further research stratifying disease stages and assessing local tissue cytokine expression is warranted. Full article

In an aging society, solving problems associated with the diagnosis and treatment of dementia-related diseases represents a serious challenge. The aim of the study was to evaluate the possibility of applying molecular biology methods to test polymorphisms recognized in the global literature as potentially useful in assessing the risk of developing dementia in a group of patients with hyperlipidemia. A sample of 203 patients: 109 diagnosed with both dementia and hyperlipidemia, 94 with hyperlipidemia, and 101 individuals as an allele frequency control group—were genotyped. Additional data about cognitive decline and neuropsychological assessment were collected. Among all the studied polymorphisms, the frequency of the ABCA1 rs2230806 polymorphism differed between the analyzed groups. The GG genotype (p = 0.0002, RR = 3.22, CI = 1.63 ÷ 6.37) and the G allele (p = 0.0007, RR = 1.53, CI = 1.19 ÷ 1.97) were more frequent in patients diagnosed with dementia, specifically in those with Alzheimer’s disease. Furthermore, the GG genotype was more common in individuals with a shorter disease duration and lower scores on the Montreal Cognitive Assessment (MoCA) scale, and consequently, with greater cognitive function deficits during early stages of the diagnostic process. ABCA1 rs2230806 genotyping is a potential marker for the early identification of dementia risk in patients with hyperlipidemia, which supports the validity of exploring options for incorporating diagnostics based on molecular biology methods. Full article

Dysphagia is commonly assessed with qualitative and image-based diagnostic tools, which are often costly, technically demanding, and limited in their ability to support individualized rehabilitation. Electroencephalography (EEG) has recently emerged as a quantitative, cost-effective, and accessible alternative to characterize sensorimotor activity during swallowing, though its potential in dysphagic populations has not been systematically explored. This study investigated neural dynamics in 50 post-stroke dysphagic patients, 32 post-stroke non-dysphagic controls, and 21 healthy adults performing a swallowing task. EEG recordings from primary motor regions (C3, Cz, C4) were analyzed using event-related spectral perturbation (ERSP) to quantify alpha (8–13 Hz) and beta (15–30 Hz) event-related desynchronization, alongside hemispheric lateralization indices. Group comparisons revealed significantly reduced beta desynchronization in both post-stroke groups compared to healthy participants, with additional alpha and beta deficits at C3 and Cz distinguishing dysphagic patients from non-dysphagic controls. Dysphagic patients further exhibited abnormal lateralization not observed in other groups. These findings identify distinct alterations in motor cortical dynamics and hemispheric balance in dysphagia, supporting EEG-derived biomarkers as promising tools for diagnosis and clinical follow-up. The accessibility of EEG reinforces its potential integration into routine workflows to enable objective and personalized management of post-stroke dysphagia. Full article

Background: The clinical heterogeneity of autism spectrum disorders (ASDs) results from dynamic interactions between genetic susceptibility and environmental exposures. Autism is increasingly recognized as involving neuroimmune dysregulation, which may contribute to ASD severity. Several studies indicate that ASD patients exhibit increased levels of VCAM-1, suggesting endothelial dysfunction and enhanced leukocyte infiltration into the brain, which may have adverse bearing on synaptic plasticity, axon growth, and repulsion. Similarly, elevated PGE2 drives microglial activation and excitotoxicity. The present study examines possible links between VCAM-1 and PGE2 levels and ASD severity. Methods: VCAM-1 and PGE₂ concentrations were measured in children with ASD aged 2–6 years and analyzed for age effects and correlations with behavioral severity. Participants were grouped as mild, moderate, or severe based on Autism Diagnostic Observation Schedule-2 (ADOS-2) scores. Results: VCAM-1 levels were subnormal in 39.3% (n = 24), and PGE₂ levels were above normal in 32.8% (n = 20). Mean VCAM-1 levels decreased significantly with age (F(4, 56) =2.98, p = 0.026) and also, were higher in moderate (U = 36.00, Z = −3.96, p < 0.001) and severe (U = 155.50, Z =−2.70, p = 0.007) ASD groups, with mean ranks rising from 14.46 (mild) to 41.13 (severe). PGE₂ did not differ between severity and age groups (p > 0.05). VCAM-1 correlated moderately with ADOS-2 scores (rho = 0.577, p < 0.001), whereas PGE2 did not (rho = 0.108, p = 0.406), suggesting higher VCAM-1 is linked to increased behavioral severity in ASD. Conclusions: Inflammation-related biomarkers could be reflecting a heterogeneous set of neuroimmune mechanisms underlying ASD, which may drive behavioral outcomes. Full article

Background: ADAR1 (ADAR), ADAR2 (ADARB1), and ADAR3 (ADARB2) are deaminase adenosine RNA-specific enzymes that play a significant role in RNA metabolism. ADAR1 (ADAR) and ADAR2 (ADARB1) catalyze A-to-I editing and ADAR3 (ADARB2) plays a regulatory role. The role of these three genes still remains unknown in head and neck cancers (HNSCC). The aim of this study is to reveal the role of deaminase adenosine RNA-specific enzymes in pathomechanisms of HNSCC and to investigate their potential utility as diagnostic and/or prognostic biomarkers. Methods: The quantitative PCR analysis was conducted using RNA isolated from 22 pairs of matched tumor and adjacent normal tissues, 76 formalin-fixed paraffin-embedded (FFPE) tumor samples, and a panel of HNSCC cell lines (DOK, SCC-25, SCC-40, FaDu, and CAL-27). In parallel, transcriptomic and clinical data from the Cancer Genome Atlas HNSCC cohort were analyzed. Patients were stratified into high- and low-expression groups, and statistical assessments included overall survival and progression-free interval analyses, evaluation of gene expression in relation to clinicopathological parameters, correlation with other genes, and functional pathway exploration using gene set enrichment analysis. Results: ADARB2 was significantly downregulated in HNSCC tumor tissues compared to adjacent normal mucosa (p = 0.044), with discriminatory potential to distinguish malignant from non-malignant tissues (AUC = 0.692, p = 0.029). TCGA data confirmed ADAR (p < 0.0001) and ADARB1 (p < 0.0001) upregulation in tumors, while ADARB2 was markedly reduced (p = 0.04). Patients with high ADARB2 expression showed significantly longer overall survival (pa = 0.0121; pb = 0.0098), with a trend toward improved progression-free survival (pb = 0.0681). Subsite analysis revealed high ADAR expression correlated with poor OS in pharyngeal tumors (p < 0.05), whereas high ADARB2 expression was linked to improved DFS (pa = 0.0023, pb = 0.0047). GSEA indicated that low ADARB2 expression was enriched in oncogenic pathways, including Wnt/β-catenin (p = 0.006), MYC targets (p = 0.009), and TGF-β1 (p = 0.009). Conclusions: ADARB2 expression was significantly reduced in HNSCC tumor tissues compared to normal mucosa and demonstrated strong discriminatory power for distinguishing malignant from non-malignant samples. High ADARB2 expression was associated with markedly improved overall survival, whereas low expression correlated with enrichment of oncogenic pathways, including Wnt/β-catenin, Notch, and Hedgehog, consistent with a poorer clinical prognosis. These findings highlight ADARB2 as a promising diagnostic biomarker and independent prognostic factor in HNSCC. Full article

Background and Objectives: NR5A1-related 46,XY differences of sex development (DSD) represent a heterogeneous group of conditions characterized by variable degrees of undervirilization, gonadal dysgenesis, and endocrine dysfunction. Mutations in the NR5A1 gene affect critical pathways of gonadal development and steroidogenesis, leading to complex diagnostic and management challenges. This narrative review aims to summarize the clinical spectrum, diagnostic algorithms, surgical management, and outcome data of pediatric NR5A1-related 46,XY DSD. Materials and Methods: A comprehensive search of PubMed, Scopus, and Web of Science databases was conducted, using terms related to NR5A1 mutations, ambiguous genitalia, gonadal dysgenesis, tumor risk, and surgical management. A total of 26 studies were initially identified, of which 16 met the inclusion criteria for pediatric patients (≤18 years) with confirmed 46,XY karyotype, NR5A1 mutation, and available clinical or surgical data. Results: NR5A1 mutations are associated with phenotypes ranging from complete female external genitalia to apparently normal males with later infertility. While Sertoli cell function during fetal life is often preserved, Leydig cell dysfunction leads to incomplete masculinization. Spontaneous virilization during puberty has been reported. Management of gonadal dysgenesis remains controversial: while streak-like intra-abdominal gonads carry high germ cell tumor risk, warranting early gonadectomy, well-formed testes may be preserved under strict surveillance. Conclusions: NR5A1-related 46,XY DSD requires individualized, multidisciplinary management integrating genetic, endocrine, surgical, and psychosocial expertise. Gonadectomy decisions should be risk-stratified and, when possible, delayed to allow patients to participate in decision-making. Early psychological support and lifelong follow-up are essential to optimize physical and psychosocial outcomes. Full article

Background: The morphology of the acromion has long been implicated in shoulder pathology, particularly in relation to subacromial impingement and rotator cuff disease. More recently, interest has shifted toward the posterior acromion, with studies examining its potential role in posterior instability, eccentric glenohumeral osteoarthritis, and massive rotator cuff tears. Methods: A critical literature review of nine studies assessing sagittal acromial tilt, posterior coverage, and acromial height was conducted, emphasizing reproducibility and clinical significance across different shoulder disorders. Results: In posterior instability and eccentric osteoarthritis, the acromion is generally described as more horizontally oriented, less covering posteriorly, and positioned higher. Conversely, in massive cuff tears, it tends to appear more posteriorly covering without consistent change in tilt. Although these trends suggest a possible biomechanical role for the acromion, reported values vary widely between studies, and significant overlap exists between pathological and control groups. Such variability is compounded by differences in imaging modality, definitions of anatomical landmarks, and the frequent reduction of three-dimensional structures into two-dimensional projections. These methodological inconsistencies undermine reproducibility and limit the clinical applicability of posterior acromial parameters. Conclusions: Posterior acromial morphology appears to influence shoulder biomechanics, but existing measurements should be considered population-level markers rather than diagnostic thresholds. Future research should adopt standardized, three-dimensional, pathology-independent reference models anchored to stable scapular landmarks and validated across imaging modalities to improve reproducibility and clinical utility. Full article