Tag: statistics

Eat Weight Disord. 2025 Nov 21;30(1):89. doi: 10.1007/s40519-025-01798-1.

ABSTRACT

PURPOSE: The Children’s Eating Behavior Questionnaire (CEBQ) is a reliable and widely used tool to assess eating behavior traits in children. However, currently no Danish version of the CEBQ exists. This study aimed to translate the CEBQ into Danish and investigate its psychometric properties and factor structure in children with overweight and obesity. Secondly, differences in eating behavior traits between children with overweight and obesity were explored.

METHODS: Children (7-14 years) were recruited from a 10-week multicomponent lifestyle camp. Parents completed the CEBQ with their child before camp, and anthropometry was measured. CEBQ is scored from 1 to 5, with higher scores indicating a higher tendency toward a specific behavior. A confirmatory factor analysis (CFA) was performed to test the original eight-factor structure. Internal reliability was assessed using McDonald’s Omega.

RESULTS: In total, 190 children (12.3 ± 1.36 years) participated. The CFA confirmed the eight-factor model, with all items loading significantly on their respective factors. Internal reliability was acceptable for the full CEBQ scale (ω = 0.85) and most subscales (ω ≥ 0.70) but only moderate for Satiety Responsiveness (ω = 0.59) and Emotional Undereating (ω = 0.65). No statistically significant difference was found between children with overweight and obesity according to the Bonferroni-adjusted alpha.

CONCLUSIONS: The Danish CEBQ is a valid tool to assess eating behavior traits in Danish children with overweight and obesity; although, generalizability may be limited due to a relatively small sample size. Future studies should further validate the Danish CEBQ by assessing test-retest reliability, construct validity, and factor structure in a generalizable sample across weight categories.

LEVEL OF EVIDENCE: Level V, Cross-sectional, Psychometric study.

PMID:41269440 | DOI:10.1007/s40519-025-01798-1

Breast Cancer Res Treat. 2025 Nov 21;215(1):12. doi: 10.1007/s10549-025-07862-9.

ABSTRACT

PURPOSE: To evaluate differences in clinical outcomes, treatments received, recurrence, and sociodemographic characteristics in patients with triple-negative breast cancer (TNBC) classified as invasive lobular carcinoma (TNBC-ILC) or invasive carcinoma of no special type (TNBC-NST).

METHODS: Using national registry data, we conducted a retrospective, population-based cohort study of 6449 women diagnosed with primary TNBC (stratified by histological subtype) in Sweden (2007-2021). Clinical and treatment data were analyzed using descriptive statistics, logistic regression, machine learning (Boruta/XGBoost), and Cox proportional hazards models adjusted for patient age, tumor size, grade, nodal status, comorbidities, and receipt of adjuvant chemotherapy (ACT).

RESULTS: TNBC-ILC accounted for 2.7% of all TNBC cases and affected older patients (median age 70 vs 62 years). Compared to TNBC-NST, TNBC-ILC had lower Ki-67, fewer high-grade tumors, higher T stage, and greater socioeconomic vulnerability. Machine learning identified age and post-operative tumor size as key predictive features of TNBC-ILC. ACT was administered to 40% of TNBC-ILC versus 59% of TNBC-NST cases (P < 0.001), with a survival benefit observed only in TNBC-NST. TNBC-ILC patients aged 50-64 years were less likely to receive ACT. Despite lower proliferative activity, TNBC-ILC was associated with worse overall (OS; adj-HR 1.39, 95% CI 1.04-1.86) and disease-specific survival (DSS; adj-HR 1.98, 95% CI 1.41-2.79), particularly in patients ≥ 50 years of age. TNBC-ILC patients ≥ 75 years had the poorest 5-year survival (DSS 55%; OS 42%).

CONCLUSIONS: TNBC-ILC is a distinct subgroup with older age, lower grade and Ki-67, undertreatment, and poorer survival, emphasizing the need for age- and subtype-specific treatment strategies.

PMID:41269430 | DOI:10.1007/s10549-025-07862-9

Mol Biomed. 2025 Nov 21;6(1):114. doi: 10.1186/s43556-025-00353-9.

ABSTRACT

For over 70 years, methotrexate (MTX) has remained a first-line chemotherapeutic agent for acute lymphoblastic leukemia (ALL), playing a pivotal role in maintenance therapy. Understanding the genetic determinants of MTX efficacy is therefore essential for improving clinical outcomes. However, studies on MTX efficacy-related polymorphisms remain limited, particularly for non-coding variants, for which most evidence is based on statistical associations. Here, through integrative bioinformatics analysis and systematic meta-analysis, we identified rs1544105, a non-coding SNP in the folylpoly-γ-glutamate synthetase (FPGS) gene, as closely associated with MTX efficacy. Compared with the GG genotype, the AA genotype increased disease progression risk (OR: 2.23; 95% CI: 1.16-4.30; p = 0.017) and elevated plasma MTX concentration-to-dose ratios at 24 h (WMD: 2.27; 95% CI: 1.04-4.40; p = 0.002) and 40 h (WMC: 0.02; 95% CI: 0.00-0.04; p = 0.033). Using prime editing, we generated homozygous mutant (GG) 293T cells, demonstrating that rs1544105 A > G increased FPGS expression (~ 1.5-fold, p < 0.05) and intracellular MTX retention (p < 0.05). Moreover, both cell-based and animal experiments confirmed that rs1544105 A > G markedly improved MTX efficacy. Mechanistically, dual-luciferase reporter and electrophoretic mobility shift assays revealed that rs1544105 A > G enhanced the binding affinity of the SNP-containing sequence for the transcription factor CREB1, thereby increasing FPGS transcriptional activity and ultimately augmenting MTX efficacy. Our multidimensional study, integrating data analysis with cellular, molecular, and animal experiments, highlights the remarkable regulatory role of a single SNP, rs1544105, in modulating MTX therapeutic response and provides a basis for individualized MTX-based maintenance therapy in ALL patients.

PMID:41269429 | DOI:10.1186/s43556-025-00353-9

Discov Oncol. 2025 Nov 21;16(1):2138. doi: 10.1007/s12672-025-02403-8.

ABSTRACT

BACKGROUND: Factor Xa (FXa) plays a role in promoting cancer growth and metastasis via protease-activated receptors. The main aim of this study was to investigate the effect of FXa inhibition, which is known to play a crucial role in cancer metabolism in hypoxia, on the behaviour of colorectal cancer cell lines HCT116 and HT29 using FXa inhibitor-rivaroxaban.

METHODS: The studies were conducted under both normoxic and hypoxic conditions. The immunofluorescence method was used to assess the expression of key elements in tumor metabolism, including HIF1 alpha, LDHA, and GLUT1, following the administration of Rivaroxaban, which does not affect cell viability.

RESULTS: Hypoxia resulted in increased expression of HIF1 alpha and LDHA. However, it was observed that the expression levels decreased in the rivaroxaban-treated group. It is noteworthy that no statistically significant difference was observed in GLUT1 expression. Moreover, the analysis of E-cadherin and N-cadherin expression levels revealed that Rivaroxaban significantly impacted migration under hypoxic comparison to the control group. These findings were further corroborated by the statistical results of the wound patency in the wound healing experiment. The results reveal that the inhibition of FXa with Rivaroxaban may represent a novel target for the treatment of tumor hypoxia.

CONCLUSIONS: The findings of this study suggest that Rivaroxaban has the potential to be both an effective anticoagulant and an anticancer agent against CRC under both hypoxic and normoxic conditions. This paper puts forward an alternative utilization method for Rivaroxaban.

PMID:41269426 | DOI:10.1007/s12672-025-02403-8

Sleep Breath. 2025 Nov 21;29(6):361. doi: 10.1007/s11325-025-03537-3.

ABSTRACT

PURPOSE: The aim of this study was to evaluate the elasticity and stiffness of the sternocleidomastoid (SCM) muscle in patients with obstructive sleep apnea syndrome (OSAS) using ultrasound shear wave elastography (SWE), and to investigate the potential relationship between SCM muscle stiffness and the severity of OSAS.

METHODS: This study included 72 patients with OSAS diagnosed by polysomnography (PSG) and 35 age- and sex-matched healthy controls who were admitted to the chest diseases outpatient clinic. Following the diagnosis, all participants underwent ultrasound shear wave elastography (SWE) to evaluate the elasticity and stiffness of the sternocleidomastoid (SCM) muscle. SWE measurements were performed in a standardized supine position, with care taken to ensure minimal muscle contraction during imaging. The mean shear wave velocity (SWV) values were recorded for both the right and left SCM muscles. The severity of OSAS was categorized based on apnea-hypopnea index (AHI) scores into mild, moderate, and severe groups. The SWE values were then statistically compared between OSAS subgroups and healthy controls. Correlation analyses were also performed between SCM stiffness (SWV) and AHI values to assess the relationship between muscle stiffness and disease severity.

RESULTS: A total of 107 individuals were included in the study: 72 patients with OSAS and 35 healthy controls. The OSAS group showed significantly higher BMI, body fat ratio, neck circumference, and sternocleidomastoid (SCM) muscle stiffness values compared to controls (p < 0.01). Shear wave elastography revealed a significant increase in SCM stiffness with advancing OSAS severity. Spearman’s correlation analysis showed that right and left SCM stiffness values were also positively correlated with OSAS severity (r = 0.164 and r = 0.241, respectively; p < 0.001).

CONCLUSION: Ultrasound shear wave elastography revealed increased SCM muscle stiffness in OSAS patients, correlating with disease severity. These findings suggest that SCM muscle biomechanical properties may serve as a supplementary marker in evaluating and monitoring OSAS progression.

PMID:41269419 | DOI:10.1007/s11325-025-03537-3

Mol Neurobiol. 2025 Nov 21;63(1):113. doi: 10.1007/s12035-025-05485-1.

ABSTRACT

Long COVID has been associated with persistent neurological symptoms that impair cognitive function and quality of life, raising questions about the role of genetic factors in symptom severity and persistence. Apolipoprotein E (APOE) polymorphisms, known for their relevance in neurodegenerative diseases, may significantly influence neurological outcomes in long COVID patients. This study aimed to investigate the relationship between APOE polymorphisms, specifically single nucleotide polymorphisms (SNPs) rs7412 and rs429358, and neurological and cognitive symptoms in long-term COVID patients. APOE genotypes were identified through the analysis of SNPs rs7412 and rs429358. Cognitive and behavioral assessments were conducted using the Mini-Mental State Examination (MMSE), the Pfeffer Functional Activities Questionnaire, the Beck Inventory for mood assessment and the Epworth Sleepiness Scale (ESS). Statistical analyses included Mann-Whitney U test, chi-square or Fisher’s exact test, and odds ratio calculation, using R Studio and GraphPad Prism. The results indicated that the ε2ε3 genotype was associated with lower scores on the BECK, suggesting fewer depressive symptoms, while the ε3ε3 genotype was linked to an increase in depressive symptoms. Furthermore, analyses of APOE alleles showed an opposite pattern concerning daytime sleepiness: carriers of the ε2 allele exhibited greater daytime sleepiness, whereas ε3 allele carriers reported less sleepiness, as measured by the ESS. The analysis of the rs7412 SNP revealed significant impacts on both BECK and ESS scores. These findings suggest that APOE polymorphisms, particularly the ε2 and ε3 alleles, play a crucial role in modulating neurological and cognitive symptoms associated with long COVID. The results highlight the potential of genetic screening to identify patients at higher risk of persistent cognitive and emotional alterations, emphasizing the importance of personalized management strategies and the need for further research in diverse populations.

PMID:41269415 | DOI:10.1007/s12035-025-05485-1

Acta Med Acad. 2025 Nov 20. doi: 10.5644/ama2006-124.488. Online ahead of print.

ABSTRACT

OBJECTIVE: This study analyzed PhD theses defended in Croatia between 1992 and 2023, with the aim of examining national trends, institutional contributions, disciplinary patterns, and data-related challenges.

METHODS: This retrospective time-trend study utilized the administrative data obtained from the Croatian Bureau of Statistics. Data on the number of defended PhD theses were collected by year, university, and school/department. Linear regression models were applied to assess temporal trends at both the national and institutional levels.

RESULTS: A total of 17,578 PhD theses were defended in Croatia between 1992 and 2023. The national output increased substantially, reaching a peak of 1,338 theses in 2012, followed by a subsequent decline and a gradual recovery. The University of Zagreb accounted for 74.8% of all defended theses, followed by the Universities of Osijek, Rijeka, and Split. Across institutions, the medical, economic, and engineering faculties were the most productive. Linear regression analyses demonstrated statistically significant upward trends at both the national level and across all major public universities. Collectively, medical schools produced 18% of all theses, with newer institutions, particularly those in Split and Osijek, exhibiting later but consistent growth. However, notable data inconsistencies were observed, including non-standardized institutional nomenclature, variable data granularity, and discrepancies among official reports.

CONCLUSION: Croatia’s PhD output expanded markedly after 2000, reflecting the maturation and expansion of its higher education system. Regional universities and medical schools substantially increased their contributions, indicating national academic growth. Sustained institutional support will be essential to sustain progress and foster disciplinary development.

PMID:41268749 | DOI:10.5644/ama2006-124.488

Per Med. 2025 Nov 21:1-9. doi: 10.1080/17410541.2025.2592528. Online ahead of print.

ABSTRACT

BACKGROUND: Urinary bladder cancer (UBC), the tenth most common globally with a male predominance, has its risk factors like smoking and single nucleotide polymorphisms (SNPs), yet the MYC gene’s role, especially the rs9642880 GT/TT polymorphism on chromosome 8q24.21, in cancer susceptibility is underexplored.

METHODS: We searched in Medline, Scopus and Web of Science databases for relevant studies. Odds ratios (OR) with 95% confidence intervals (CIs) were computed using DerSimonian and Laird random-effect models. Heterogeneity was assessed using I² statistics. Statistical analyses were performed using R, version 4.4.2.

RESULTS: Data from 53,957 subjects was analyzed, including 8,002 UBC patients and 45,955 controls, with median age ranging from 44.5 to 68.7 years. We found significant association between the rs9642880 GT/TT polymorphism and increased UBC risk (OR 1.249, 95% CI 1.188-1.297, p < 0.001). This association was consistent across American (OR 1.43 95% CI 1.20-1.70), Asian (OR 1.25 95% CI 1.17-1.34), and Caucasian (OR 1.21 95% CI 1.13-1.29) ethnic groups, with low heterogeneity (I² = 0%). Subgroup analyses by genotyping method and source of control further supported these results.

CONCLUSION: This meta-analysis provides robust evidence that the T allele of the rs9642880 polymorphism in the MYC gene significantly increases susceptibility to UBC across Asian, American, and Caucasian populations.

PMID:41268746 | DOI:10.1080/17410541.2025.2592528

J Med Virol. 2025 Nov;97(11):e70719. doi: 10.1002/jmv.70719.

ABSTRACT

Genome-wide association studies (GWAS) have identified numerous genetic loci associated with COVID-19 susceptibility and severity. However, it remains unclear which variants specifically contribute to the progression from hospitalization to critical illness. To address this, we identified 394 symptom-differentiating SNPs (sdSNPs) by directly comparing GWAS summary statistics between critical and hospitalized COVID-19 cases. Among these, 13 were missense variants that may trigger phenotype conversion. To investigate their functional consequences, we performed structural modeling to evaluate the impact of these variants on protein stability. Eight proteins were predicted to be affected, including FUT2, ICAM5, IFNA10, PLSCR1, IZUMO1, ICAM1, RASIP1, and MICB, suggesting potential disruptions in immune signaling and host response pathways. Furthermore, Mendelian randomization analyses provided direct causal evidence: SMR analysis based on lung eQTL data demonstrated that higher FUT2 expression was significantly associated with increased risk of critical COVID-19 (β = 0.227, p = 2.69 × 10^-3), compared to a weaker effect in hospitalized COVID-19 (β = 0.096, p = 3.97 × 10^-2). In contrast, MR analysis using cis-pQTLs revealed that higher plasma levels of soluble ICAM5 (sICAM5) exerted protective effects, with stronger estimates in critical COVID-19 (β = -0.186, p = 5.54 × 10^-7) than in hospitalized COVID-19 (β = -0.095, p = 1.69 × 10^-4). These findings identify a distinct set of severity-specific genetic variants and offer mechanistic insights into how missense mutations may influence disease progression through structural and regulatory pathways.

PMID:41268733 | DOI:10.1002/jmv.70719

Psychol Med. 2025 Nov 21;55:e355. doi: 10.1017/S0033291725102286.

ABSTRACT

BACKGROUND: Individuals with first-episode psychosis (FEP) face markedly increased excess mortality, yet the long-term trends and key contributing factors remain insufficiently characterized. This study aimed to examine long-term mortality patterns, standardized mortality ratios (SMRs), and associated factors in a FEP cohort.

METHODS: This population-based cohort study included 1,389 individuals diagnosed with FEP, followed for up to 25 years. Mortality outcomes were obtained from Hong Kong’s centralized hospital database (CMS) and coroner’s court reports, with SMRs calculated. Baseline sociodemographic and clinical, as well as long-term treatment-related factors of all-cause, natural, and unnatural mortality were analyzed.

RESULTS: Among 1,389 participants, 137 deaths (9.86%) occurred during the follow-up period with the overall SMR of 6.56 (95% CI, 5.50-7.71). The cumulative incidence rate of unnatural mortality increased sharply over the first 10 years and that of the natural cause of death started to increase after the first decade of the illness. Male gender and poorer social functioning were associated with increased all-cause mortality risk, while male gender, lower education, and baseline hospitalization raised unnatural mortality risk. Greater monthly antipsychotic variability during the first 10 years increased all-cause mortality risk in the period after the initial 10 years.

CONCLUSIONS: This 25-year follow-up study of FEP highlighted the changes in the long-term mortality pattern of FEP and thus the phase-specific needs of individuals with FEP. Therefore, it is important to integrate physical care into mental health services, as well as stage-specific and individualized care for patients with psychotic disorders to reduce long-term excess mortality.

PMID:41268721 | DOI:10.1017/S0033291725102286