To evaluate arterio-venous gas parameters-P(ca-v)CO2 or ΔPCO2, Ca-vO2, and P(v-a) CO2/Ca-vO2 ratio, and to develop a novel Heart-Lung Coupling (HLC) index defined as (ΔPCO2/Ca-vO2)/Cardiac Index to quantify the interaction between ventilatory efficiency and circulatory performance in pulmonary arterial hypertension (PAH). In this single-center retrospective study, patients with PAH who underwent right heart catheterization between September 2019 and May 2024 were evaluated. After exclusions, 115 patients were included (35 idiopathic PAH [IPAH] and 80 congenital heart disease-associated PAH [CHD-PAH]). Hemodynamics, arteriovenous gas parameters, and functional indices, including 6-min walk distance (6MWD) and NT-proBNP, were analyzed. The HLC was calculated and compared between groups. Association with functional parameters was assessed using Spearman correlation and multivariate linear regression after LASSO selection. Receiver operating characteristic analysis evaluated the ability of HLC to identify impaired exercise capacity (6MWD < 350 m). ΔPCO2, Ca-vO2 and P(v-a) CO2/Ca-vO2 ratio were significantly higher in IPAH than CHD-PAH (8.3 vs. 3.5 mmHg, p < 0.001; 4.8 vs. 3.4 mL/dL, p = 0.005; 1.84 vs. 1.11, p < 0.001, respectively). The HLC index was also higher in IPAH (median 0.82 vs. 0.40, p = 0.001). HLC showed modest correlation with 6MWD (r = 0.27, p = 0.04) and NT-proBNP (r = 0.24, p = 0.021). In multivariate regression, HLC remained independently associated with 6MWD (β = 32.86, 95% CI: 5.15-60.57, p = 0.021). Discrimination of impaired exercise capacity was limited (AUC of 0.55). The HLC index integrates gas exchange and cardiac output to characterize heart-lung interaction in PAH. This novel physiological metric may provide complementary insights into cardiopulmonary coupling and functional limitation.

In chronic diseases, accelerated muscle mass loss is associated with poor clinical outcomes. Computed tomography (CT) is considered a reference standard for assessing muscle mass, but it is limited for longitudinal assessment. Ultrasound (US) is more suitable for longitudinal measurements, but limited reliability data or reference values exist to inform clinical adoption. This pilot study evaluated the reliability of rectus femoris (RF) muscle US measurements [cross-sectional area (CSA) and shear-wave elastography (SWE) stiffness] and investigated their relationship with CT-derived truncal muscle mass. Forty healthy living liver donors undergoing abdominal CT were included. CT-derived skeletal muscle area and skeletal muscle index at T12 and L3 were quantified using deep learning. US B-mode and SWE RF images obtained with manual and automated measurements. Reliability was assessed using intraclass correlation (ICC). Agreement between manual and automated methods was evaluated using the Dice coefficient. US and CT measurements associations were evaluated using Pearson correlation and multiple linear regression. Inter-reader agreement for manual US CSA was excellent (ICC=0.95, 95% CI: 0.88-0.97). Test-retest reliability of SWE was good (ICC=0.78, 95% CI: 0.67-0.87). Automated and manual methods showed strong agreement (Dice coefficient 0.94) and good reliability (ICC=0.85, 95% CI: 0.75-0.91). RF CSA demonstrated weak but significant correlations with CT-derived skeletal muscle area at both T12 and L3 levels (r=0.37 to 0.40, P<0.05). US parameters showed moderate predictive value for CT-derived skeletal muscle index at L3 (adjusted R²=0.70). In conclusion, RF US measurements are reliable, and automated measurements are feasible but show a modest correlation with CT-derived muscle mass measurements.

The Oncotype DX 21-gene recurrence score (RS) is widely used to guide adjuvant chemotherapy decisions in early-stage estrogen receptor-positive, HER2-negative breast cancer. However, its high cost and frequent discordance with conventional clinicopathologic risk assessment raise questions regarding whether RS can be substituted by other indicators or selectively omitted in specific clinical settings. In this narrative review, we examined whether RS can be reliably predicted or replaced by clinicopathologic or pathology-derived factors, and whether there are patient groups in whom RS testing has limited impact on treatment decision-making. A comprehensive literature search and structured screening process identified 54 studies that treated RS as an outcome variable, together with additional reports addressing selective testing strategies. Across diverse analytical approaches, RS could not be consistently substituted by existing indicators. Although modest correlations were observed, substantial case-level discordance persisted, particularly within the intermediate RS range, where predictive performance deteriorated near clinically relevant decision thresholds. In contrast, RS testing appeared less influential in treatment decisions for patients with clearly defined low- or high-risk clinicopathologic profiles or favorable special histologic subtypes. Overall, current evidence indicates that RS cannot be reliably replaced by other indicators, while its clinical value varies by context, suggesting that a selective rather than uniform application of RS testing may be reasonable in some settings.

The objective of this study was to provide clinical and pathological characterization, and evaluation of the diagnostic and prognostic implications of levodopa response in Parkinson's disease (PD), multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Long-duration levodopa response in patients with pathology-confirmed PD, MSA, and PSP was collated from medical records. Associations between definite levodopa response (>50% motor improvement sustained >2 years) with clinical and pathological features were reported. Risk of disease milestones using multivariate Cox regression and diagnostic accuracy parameters were estimated for several measures of levodopa response. Fourteen percent of 132 patients with PD (57.1% men, age at onset 60.0 ± 11.8 years) did not have a definite levodopa response associated with older age and postural-instability and gait-difficulty subtype without global or nigral pathological differences. Definite levodopa responders had 55% lower falls, 69% lower dementia risk, and 69% increased survival. Eight percent of 115 patients with MSA (55.7% men, age at onset 57.9 ± 10.4 years) showed a definite levodopa response without distinctive clinical or pathological features, and no impact on disease milestones. Two percent of 191 patients with PSP (64.4% men, age of onset 67.6 ± 7.6 years) showed a definite levodopa response associated with a PSP-parkinsonism subtype, and more frequent and severe Lewy copathology. Definite levodopa response showed excellent diagnostic accuracy (sensitivity 86.4% and specificity 95.8%) to distinguish PD from MSA and PSP. Short-duration (acute dopaminergic drug challenge) response had suboptimal diagnostic value and modest correlation with long-duration response. Levodopa response in PD, MSA, and PSP has important clinical, pathological, diagnostic, and prognostic implications. ANN NEUROL 2026.

Colon cancer remains one of the leading causes of cancer-related deaths worldwide and is associated with high rates of recurrence and metastasis despite advances in therapy. The tumor microenvironment (TME), characterized by complex immune and stromal interactions, plays a pivotal role in tumor progression and treatment resistance. Neutrophil extracellular traps (NETs), an emerging component of the TME, have been implicated in promoting tumor invasion, metastasis, and immune evasion. However, their specific role in colon cancer remains unclear. Comprehensive transcriptomic analyses were conducted using datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to identify NETs-associated genes involved in colon cancer. Single-cell RNA sequencing (scRNA-seq) was utilized to assess cellular heterogeneity, and spatial transcriptomics mapped NETs activity and cell-cell interactions within the TME. A prognostic model was constructed using multivariate Cox and LASSO regression analyses based on key NETs-related genes. Model performance was validated using internal and external cohorts. Additionally, colocalization analysis between TUBB2A eQTL signals and colorectal cancer overall survival GWAS effects was performed to investigate potential genetic correlations. Two distinct NETs-related molecular subtypes of colon cancer were identified, differing in immune composition, metabolic activity, and gene expression profiles. NETs-high malignant cells demonstrated metabolic reprogramming involving oxidative phosphorylation and cellular respiration, contributing to immune escape and therapeutic resistance. A four-gene prognostic signature (ARRDC1, TUBB2A, DUSP5, and SLC2A3) was developed and showed moderate prognostic discrimination across internal and external cohorts, indicating potential value for risk stratification but limited predictive accuracy at the current stage. Colocalization analysis revealed a modest negative correlation between TUBB2A expression and overall survival and cancer-specific survival, suggesting that increased TUBB2A expression may be associated with adverse clinical outcomes. This study reveals that NETs-associated genes play crucial roles in colon cancer progression, immune modulation, and metabolic reprogramming. The identified four-gene signature may serve as a candidate biomarker for risk stratification in colon cancer, although further validation is needed.

Background: Dental caries in children has been explored not only as a local oral condition but also in relation to potential systemic inflammatory changes. This study evaluated systemic inflammatory biomarkers and hematologic indices in children with dental caries and examined their association with caries severity, as assessed by the DMFT index. Methods: In this exploratory cross-sectional sibling-controlled study, 114 participants were included: 75 children with dental caries and 39 unaffected siblings serving as controls. All participants underwent blood testing, including inflammatory biomarkers (TNF-α, NGAL) and hematologic indices (NLR, LMR, PLR, IIC, MCVL, SII, SIRI, AISI). Group comparisons were performed using parametric or nonparametric tests, depending on data distribution. Correlation analyses were conducted within the caries group. Age- and sex-adjusted univariate and multivariable linear regression models were used to identify predictors of DMFT, and logistic regression was applied to evaluate associations with high caries burden (DMFT ≥ 6). Results: Children with caries showed higher NGAL, PLR, and MCVL, and lower LMR than controls, while IIC showed a non-significant upward trend. Correlation analysis revealed strong associations among several inflammatory indices, largely reflecting shared computational components. DMFT showed a modest positive correlation with LMR, whereas associations with classical inflammatory biomarkers such as TNF-α and NGAL were weak or absent. In age- and sex-adjusted models, several markers showed borderline associations with DMFT, but none remained independently significant in multivariable analyses. Age was the strongest predictor of DMFT, while sex showed no significant effect. Logistic regression for high DMFT confirmed age as the only significant determinant. Conclusions: In this exploratory pediatric cohort, children with dental caries showed differences in selected systemic inflammatory and hematologic biomarkers compared with unaffected siblings. However, most biomarkers showed only limited independent associations with caries severity after adjustment, with age emerging as the primary determinant of DMFT. These findings suggest that systemic inflammatory markers have limited independent explanatory value for caries severity and should be interpreted as exploratory rather than clinically definitive.

Contrast-induced acute kidney injury (CI-AKI) remains a concern in patients with ST-elevation myocardial infarction (STEMI) undergoing emergent percutaneous coronary intervention (PCI), but creatinine-based CI-AKI definitions incompletely capture longer-term renal trajectories. Early tubular stress biomarkers such as tissue inhibitor of metalloproteinases-2 (TIMP-2) may provide incremental risk information beyond conventional functional markers. In this prospective single-centre cohort, we enrolled 88 consecutive STEMI patients undergoing urgent coronary angiography with or without PCI. Routine laboratory parameters were obtained at admission and 48h. Serum TIMP-2 was measured 2h after the procedure using a standardized sandwich ELISA. Early CI-AKI was defined by conventional creatinine-based criteria within 48h, whereas 90-day chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m² or persistent creatinine elevation at 90 days. We evaluated paired changes, between-group differences by 90-day CKD status, correlations, multivariable linear and logistic regression, and receiver operating characteristic (ROC) discrimination. Early CI-AKI occurred in 6/88 patients (6.8%), whereas 90-day CKD was diagnosed in 15/88 (17%), indicating substantial delayed renal dysfunction beyond the 48-h window. The median 2-h serum TIMP-2 concentration was 1.20 ± 0.38 ng/mL. TIMP-2 showed modest correlations with creatinine and urea and remained independently associated with higher 90-day creatinine in multivariable linear regression (B = + 12.0 µmol/L per 1-ng/mL increase; p = 0.016) after adjustment for baseline creatinine and clinical covariates. In parsimonious logistic models, TIMP-2 demonstrated a borderline association with 90-day CKD (odds ratio ≈ 6.38; p = 0.056), while older age was a significant predictor. Standalone ROC discrimination for 90-day CKD was limited (AUC 0.528; 95% confidence interval 0.39-0.65; p = 0.668). In STEMI patients undergoing emergent angiography/PCI, 90-day CKD was considerably more frequent than early creatinine-defined CI-AKI, underscoring the need for extended renal follow-up. A single 2-hour serum TIMP-2 measurement reflects early tubular stress and independently associates with 90-day creatinine, but offers only modest standalone discrimination for 90-day CKD. TIMP-2 is therefore more likely to have a role within multivariable or biomarker panel-based risk stratification pathways rather than as an isolated classifier.

This study examines the impact of Strategic Planning (SP) on Crisis Management (CM) in public commercial banks operating in the western region of Libya. Using a descriptive–analytical approach, data were collected from 297 bank employees through a structured questionnaire with high reliability (Cronbach’s α &gt; 0.87). Descriptive statistics, Pearson correlation, and one-way ANOVA were employed for data analysis using SPSS. The findings indicate that both strategic planning practices and crisis management effectiveness are present at moderate levels. A positive but modest correlation was found between SP and CM (r ≈ 0.35), suggesting that higher levels of strategic planning are generally associated with improved crisis management, though the relationship remains limited in strength. Further analysis revealed that strategic planning dimensions—particularly strategic vision and alternative planning—have a statistically significant effect on crisis management effectiveness. No substantial differences were observed across gender, academic qualification, or years of experience, reflecting a high degree of organizational homogeneity. The study concludes that effective crisis management in the Libyan banking sector depends on an integrated and dynamic strategic planning framework supported by experienced personnel and adaptive leadership.

TDP-43 dysfunction is a defining feature of amyotrophic lateral sclerosis (ALS), yet no biofluid biomarker directly measures its functional activity. We developed a serum-based homogeneous time-resolved FRET (hTR-FRET) assay that quantifies TDP-43 RNA-binding activity using synthetic UU rich RNA probes. We analyzed 1,080 serum samples from controls, sporadic ALS, and genetic subgroups (C9orf72, SOD1) across multiple biorepositories. Cross-sectionally, TDP-43 ligation activity was elevated in ALS (mean 390 a.u.) versus controls (304 a.u.), yielding AUC = 0.79. Genotype means were 392 a.u. (sporadic), 382 a.u. (C9orf72), and 323 a.u. (SOD1); with a 366 a.u threshold achieved 95% specificity against controls. Longitudinally, Target ALS showed a modest but significant inverse correlation between TDP-43 activity and ALSFRS-R, while other cohorts exhibited similar non-significant trends. Elevated signal likely reflects increased extracellular, probe-competent TDP-43 species. This assay provides direct functional measurement of disease-relevant TDP-43 biology, supporting applications in diagnostic discrimination, genotype stratification, and progression monitoring in prospective studies.

Proton therapy for head-and-neck (HN) cancer offers superior organ-at-risk sparing compared to photon therapy, but is challenged by frequent anatomical changes during treatment. These changes need to be monitored with routine verification CTs (vCTs), which are used to trigger adaptive replans when deemed necessary by the clinical team. To investigate whether nominal plan robustness evaluation (RE) data-specifically the magnitude and spatial characteristics of high-dose regions (hotspots)-can predict the development of clinically significant hotspots on verification CTs (vCTs) and guide planning strategies that minimize the need for adaptive replanning. This retrospective study analyzed 46 patients with p16-positive oropharyngeal cancer treated with proton therapy. Clinical treatment plans were robustly evaluated using 12 uncertainty scenarios combining 3mm setup and±3.5% range errors. Each plan was recalculated on periodic vCTs throughout the treatment course to assess plan degradation. The maximum RE hotspot magnitude and location were compared with vCT hotspot characteristics. A subset of five cases underwent proof-of-concept replanning to reduce RE hotspots and assess downstream vCT dose effects. Patients requiring adaptive replanning due to vCT hotspots had significantly higher RE hotspot magnitudes of the nominal plan compared to those who did not (p=0.008). For replanned cases, higher RE hotspots were moderately correlated with closer proximity of RE and vCT hotspots (r=-0.59, p=0.009). Across all patients, a modest correlation (r=0.58, p<0.001) was observed between RE and vCT hotspot magnitudes. Further, the rate of plan degradation over the course of treatment via hotspot formation was found to increase with increasing RE hotspot magnitude. Replanning to reduce RE hotspots led to an average 5.6% reduction in vCT hotspot dose for the five patients studied, suggesting that reducing RE hotspots may reduce the frequency of replans. Nominal plan robustness evaluation is predictive of both the magnitude and location of hotspots observed on vCTs, and plans with higher RE hotspots tend to degrade faster over the treatment course. Minimizing RE hotspots during treatment planning may reduce the need for adaptive replanning and enhance clinical workflow efficiency.

Blood speckle imaging for the assessment of aortic valve velocity in healthy children: Reproducibility and comparison with Doppler echocardiography.

Prevalence, risk factors, and outcomes of QT prolongation in primary and RASopathy-associated hypertrophic cardiomyopathy.

Reduced serum FGF17 levels are associated with deficits in motivation, pleasure, and expression in antidepressant-free patients with major depressive disorder.

Prominent sex differences exist in severe mental illness (SMI), with increasing evidence pointing towards a pivotal role for sex hormones. Elucidation of these hormonal influences is crucial to tailor sex-specific prevention and treatment. To investigate potential shared genetics and bi-directional causal effects between sex hormone traits and SMI (depressive disorder, bipolar disorder and schizophrenia-spectrum disorder), we computed genetic correlations using linkage disequilibrium score regression and bi-directional summary-level Mendelian Randomization (MR). A range of sensitivity methods was applied and potential mediators were investigated using multivariable MR. Sex-stratified data from genome-wide association studies were used, if available further stratified on menopausal status. We also incorporated other sex hormone traits (progesterone, sex hormone-binding globulin, prolactin, age of menarche, age of menopause) in exploratory analyses. We found a widespread pattern of statistically significant, modest genetic correlations between oestrogen/testosterone levels and depressive disorder/schizophrenia-spectrum disorder, in both positive and negative directions and in both sexes (ranging between -0.22 and 0.13). With MR, evidence for causal effects was largely lacking; apart from weak evidence for a causal, increasing effect of testosterone levels on schizophrenia-spectrum disorder risk in males, which was mediated by CRP. Conversely, there was very weak evidence for a causal, increasing effect of liability to schizophrenia-spectrum disorder on testosterone levels in both sexes. This study offers new insights into the complex aetiology of SMI by comprehensively mapping genetic associations with sex hormone traits, emphasizing the need to further investigate sex hormones' impact on SMI using larger and more precisely phenotyped samples to identify individuals particularly vulnerable to hormonal disturbances.

ABSTRACT Background Parents of children with Autism Spectrum Disorder (ASD) often exhibit subclinical autistic traits, known as the Broad Autism Phenotype (BAP). While BAP is recognized as a familial characteristic associated with ASD, limited evidence exists regarding how specific parental traits relate to children’s behavioral, adaptive, and developmental outcomes in low- and middle-income clinical settings. Understanding these associations may be relevant for developmental and neurorehabilitation contexts in which parent – child interaction plays an important role in the child’s learning environment. Methods This descriptive cross-sectional study included 95 children (aged 2–12 years) newly diagnosed with ASD and both biological parents, recruited from a tertiary Child Development Center. Child autism severity was assessed using the Childhood Autism Rating Scale–2 (CARS-2); adaptive functioning using the Vineland Adaptive Behavior Scales – II (VABS-II); behavioral problems using the Child Behavior Checklist (CBCL); and developmental level using the Developmental Profile–3. Parental autistic traits were measured using the Autism-Spectrum Quotient (AQ). Correlation and regression analyses were used to examine associations between parental AQ traits and child outcomes. Results BAP (AQ ≥ 23) was present in 50% of mothers and 47% of fathers. Total parental AQ scores were not associated with child autism severity. However, higher parental communication-trait scores were associated with greater externalizing behavior in children (p < .05). Certain parental AQ subdomains, particularly communication and attention-to-detail traits, showed modest negative correlations with children’s motor functioning and developmental level. In multivariable analysis, paternal communication traits remained independently associated with poorer motor skills (β = −0.276, p = .034). Conclusions Parental BAP traits, particularly those related to communication and social reciprocity, may be associated with variability in behavioral, motor, and developmental outcomes in children with ASD. Although parental traits were not associated with autism severity, these findings suggest that considering family phenotype may be relevant when examining child developmental profiles within family-centered neurodevelopmental and rehabilitation frameworks. Further longitudinal research is needed to clarify the nature and direction of these relationships.

Patients with heart failure and reduced ejection fraction (HFrEF) commonly show signs of systemic inflammation. Interleukin-1 (IL-1) is a pro-inflammatory cytokine, known to modulate cardiac function. We aimed to determine the effects of treatment with anakinra, recombinant IL-1 receptor antagonist (IL-1Ra), on plasma IL-1Ra levels. We measured IL-1Ra levels at baseline and longest available follow-up to 24 weeks in 63 patients (44 males, 40 self-identified Black-Americans) with recent hospitalization for HFrEF, and systemic inflammation (C-reactive protein [CRP] levels >2 mg/L) who were assigned to anakinra (n=42 [66.7%]) or placebo (n=21 [33.3%]) as part of the REDHART2 clinical trial (NCT0014686). Cardiorespiratory fitness was measured as peak oxygen consumption (VO 2peak ). Baseline plasma IL-1Ra levels were 380 [290 to 1046] pg/mL. On-treatment IL-1Ra levels were significantly higher in the patients treated with anakinra vs. placebo (3,994 [3,372 to 5,000] pg/mL vs. 492 [304 to 1370] pg/mL, P <0.001). The longest available follow-up was 6 weeks in 10 patients (15.9%), 12 weeks in 12 patients (19%), and 24 weeks in 41 patients (65.1%). On-treatment IL-1Ra levels and interval change in IL-1Ra showed a modest inverse correlation with on-treatment CRP levels (R=-0.269, P =0.033 and R=-0.355, P =0.004, respectively) and no statistically significant correlations with VO 2peak values ( P >0.05). Patients with recently decompensated HFrEF and systemic inflammation treated with recombinant IL-1Ra, anakinra, have a significant several-fold increase in plasma IL-1Ra levels. On-treatment IL-1Ra levels however show only a modest correlation with CRP levels and not with (VO 2peak ).

Researchers have long speculated that sleep quality is tied to academic performance. This paper examines this relationship through a meta-analysis using the PRISMA 2020 guidelines. To clarify the relationship between sleep quality and academic performance, this study examined data from 72 independent effect sizes extracted from 59 articles involving 163,357 participants. The results indicate a modest positive correlation between sleep quality and academic performance (r = 0.17). Factors such as social jetlag significantly but negatively moderated the relationship between sleep quality and academic performance (r = −0.104), while sleep duration showed a significant positive correlation (r = 0.132). The school subject (Q = 14.986), age of participants (Q = 8.606), and culture (Q = 4.585) were significant moderators. Furthermore, while the research method did not significantly moderate the relationship between sleep quality and academic performance, the positive and significant association is robust across self-reported, objectively measured, and other-reported sleep quality, despite descriptive differences in effect-size magnitude. Given that sleep is an important physiological process associated with learning and development, students’ sleep quality warrants careful attention.

CYP2D6-mediated drug-drug-gene interactions (DDGIs) are known to influence the pharmacokinetics of venlafaxine and its metabolism to O-desmethylvenlafaxine. Solanidine and 3,4-seco-solanidine-3,4-dioic acid (SSDA) have recently been investigated as candidate endogenous CYP2D6 biomarkers; however, they remain unexplored in East Asian populations, where dietary potato intake is relatively lower than that in Western populations. A prospective clinical study aimed to characterize venlafaxine DDGIs and explore the potential of solanidine as a candidate biomarker of CYP2D6 activity in healthy Korean adults. Twenty participants including 14 CYP2D6 normal metabolizers (NMs) and 6 intermediate metabolizers (IMs)-all confirmed as CYP2C19 NMs-were enrolled. Serial plasma samples for pharmacokinetic assessment were collected before and after coadministration of paroxetine, a potent CYP2D6 inhibitor. Solanidine and SSDA were also measured in plasma and urine. Compared to CYP2D6 NMs, IMs exhibited higher venlafaxine exposure but lower O-desmethylvenlafaxine exposure. Following CYP2D6 inhibition, phenotype-dependent differences in venlafaxine and O-desmethylvenlafaxine pharmacokinetics were attenuated. The metabolic ratio (MR) of plasma solanidine showed a modest positive correlation with both the MR of venlafaxine and CYP2D6 activity score. The MR of plasma solanidine decreased when CYP2D6 activity was reduced by paroxetine coadministration. These findings demonstrate phenotype-dependent DDGIs of venlafaxine and suggest the exploratory potential of solanidine as an endogenous biomarker of CYP2D6 activity in the Korean population, despite relatively lower dietary exposure to potato-derived precursors. This study provides preliminary evidence extending endogenous CYP2D6 biomarkers to an East Asian population with distinct dietary backgrounds.

Sagittal vertical axis, spinosacral angle, T1 pelvic angle, and spinopelvic angle: which parameters can predict improvement in quality of life after surgical correction of ankylosing spondylitis?

Aquaporin-4 (AQP4) is crucial for brain fluid regulation and glymphatic system function. Idiopathic normal pressure hydrocephalus (INPH) is characterized by impaired CSF flow and is treated with shunt surgery. This study investigated AQP4 levels in INPH patients to explore its role in pathophysiology and as a potential biomarker for shunt response. CSF samples from 233 INPH patients and 29 controls were analysed. AQP4 levels were compared between preoperative patients and controls, before and after shunt surgery (110 patients), and between shunt responders and non-responders (204 patients). A bead-based assay was used to measure AQP4, and outcomes were assessed by postoperative changes in maximum gait velocity. In unadjusted analyses, preoperative AQP4 levels were lower in INPH patients than in controls; however, this difference did not remain after adjustment for pre-analytical and demographic confounders (p = 0.87). Postoperative AQP4 levels were higher (median 1646 AU IQR 1347-1976) than preoperative levels (1166 AU IQR: 976-1345; p < 0.001) and the magnitude of increase showed a modest correlation with gait improvement (rₛ = 0.22, p = 0.022). Shunt responders had lower preoperative AQP4 levels median 1089 AU, IQR 971-1277) than non-responders (median 1213 AU, IQR 1074-1361; p = 0.008). Pre-analytical factors, including storage duration and sample processing, were strong determinants of measured AQP4 levels. CSF AQP4 levels in INPH did not differ from those in controls and were highly sensitive to pre-analytical sample handling. CSF AQP4 levels increased following shunt surgery. A potential prognostic value of CSF AQP4 is suggested but requires further investigation.