Citations

Abstract Background: This study investigated the experience of intimate partner violence (IPV) and its association with quality of life (QoL) in cancer patients. Methods: A descriptive quantitative cross-sectional survey design was used. Study participants comprising 144 patients with cancer were recruited from the Radiation Oncology Clinic, University College Hospital (UCH), Ibadan. The Quality of Life in Adult Cancer Survivors (QLACS), Intimate Partner Conflict Experience (IPCE), and a demographic form were used for data collection. Data were analyzed using frequency, percentages, Mann-Whitney U test, Kruskal-Wallis, and Fisher exact tests. Results: The results showed that 25 (17.4%) of the 144 patients with cancer in the study reported experiencing IPV in the past 12 months. Psychological IPV was most commonly reported by 21 (84.0%) of those who experienced IPV. The results showed significant differences in IPV severity by gender (U = 28.50, Z = −2.176, P = 0.030) and marital status (U = 10.50, Z = −2.651, P = 0.008). Female patients with cancer and those who formerly lived with a spouse/partner reported more IPV severity. Fisher exact test ( P = 0.042) and χ 2 [(df = 1, n = 25) = 4.738, P = 0.030] confirm a significant association between IPV and QoL. Patients with cancer experiencing high IPV were more likely to have poorer QoL than those experiencing low IPV. Conclusion: These findings suggest that some patients with cancer experience the double jeopardy of IPV and cancer with significant consequences on their QoL. This underscores the need for targeted psychosocial interventions to identify and mitigate the adverse effects of IPV to improve QoL outcomes for affected patients with cancer.

Abstract Eosinophils play an important role in mediating itch and inflammation in dermatitis. The role of the eosinophil granule protein eosinophil peroxidase (EPX) in mediating inflammation and itch was tested in a dermatitis mouse model. Mice were sensitized to trimellitic anhydride (TMA) and subsequently challenged chronically on the ear to establish dermatitis. Loss of EPX (in EPX−/− mice) or blocking EPX with the drug resorcinol significantly reduced dermatitis in mice exposed to TMA. Resorcinol also reduced levels of thymic stromal lymphopoietin protein (TSLP) in skin. Further studies showed that EPX increased different cytokines in keratinocytes in cell culture via 2 distinct mechanisms. EPX-induced TSLP expression requires lysophosphatidic acid signaling while EPX-induced expression of TNF-α, CSF2, CSF3, and IL1a required IL-1 signaling. We also showed that blocking IL-1 reduced inflammation in skin following TMA exposure in mice. Thus, EPX is an important mediator of inflammation and itch, that are mediated via at least 2 pathways. This suggests that both EPX and its signaling pathways may provide novel therapeutic strategies in dermatitis.

Abstract Repetitive head impacts are common in contact and collision sports and are linked to structural brain changes and an elevated risk of neurodegenerative diseases such as Chronic Traumatic Encephalopathy. Identifying early in vivo structural markers remains challenging. Although diagnosis currently requires post-mortem confirmation, clinical symptoms, including cognitive impairment and behavioural changes, are reflected in the diagnosis of Traumatic Encephalopathy Syndrome. These symptoms align with dysfunction in key brain regions—amygdala, hippocampus and thalamus—which support memory, emotion and behaviour and commonly show tau pathology in Chronic Traumatic Encephalopathy. This study uses shape analysis to examine structural differences in these regions between former American football players and unexposed asymptomatic controls and evaluates the influence of age, head impact exposure and clinical diagnosis on brain structure. We analyzed brain morphology in former American football players (n = 163) and unexposed, asymptomatic controls (n = 53). Structural segmentation was performed with FreeSurfer 7.1, and the shape analysis pipeline was used to generate subregional reconstructions. Vertex-level morphometry, based on the logarithm of the Jacobian determinant and radial distance, quantified local surface area dilation and thickness. Group differences were examined with covariate-adjusted linear regression models contrasting football players and controls, as well as participants with and without a Traumatic Encephalopathy Syndrome diagnosis. Partial correlations examined the influence of age, age of first football exposure and cumulative head impact index metrics, including frequency, linear acceleration and rotational force. Models were adjusted accordingly for age, body mass index, education, race, imaging site, apolipoprotein ϵ4 status and total intracranial volume. Former football players exhibited bilateral surface area contractions in the hippocampus and amygdala, along with reduced amygdala thickness, compared to controls. Older age was associated with widespread surface contractions and thinning across all regions, except for preserved thickness in the left hippocampus. An earlier age of first exposure to football correlated with surface contractions in the thalamus and left hippocampus. Greater cumulative linear acceleration was linked to bilateral hippocampal surface contractions and reduced thickness in the left thalamus, while greater rotational force exposure was associated with hippocampal thinning. No significant structural differences were found between players with and without a diagnosis of Traumatic Encephalopathy Syndrome. These findings extend volume-based research by revealing localized alterations in surface area dilation and thickness and emphasize the roles of age and repetitive head impact exposure in long-term brain changes.

ABSTRACT Objective Fetal surgery (FS) for spina bifida (SB) repair improves infant outcomes; however, spontaneous preterm birth (sPTB) is common. We aimed to evaluate maternal and fetal immune responses following FS for SB repair. Method Pregnant participants undergoing fetoscopic SB repair at 24–26 weeks of gestational age (GA) were prospectively recruited and compared to GA matched low‐risk controls. Blood samples were collected at baseline, 2‐week post‐surgery (POD14), and delivery. Cytokine analysis, flow cytometry, and T cell receptor (TCR) sequencing were performed. Results sPTB occurred in 5/6 of the FS group (0/6 of controls). Maternal blood in the FS group demonstrated increased alpha‐fetoprotein (AFP) and anti‐inflammatory IL‐1RA at baseline and POD14, increased pro‐inflammatory IL‐8 only post‐operatively, and elevated growth factors throughout. T cell phenotypes following FS revealed reduced TH17 frequency but increased activation receptors on cytotoxic T cells. At delivery, the FS cohort had reduced Th2 and Th17 helper T cells and CD4+ memory T cells, but CD8 T cells still showed increased activation. No TCR expansion was detected post‐surgery, suggesting antigen‐independent activation. Cord blood in FS repaired neonates had increased AFP, IL‐8, IL‐1RA. Conclusion Systemic immune changes following FS, particularly T cell maturation and activation, were observed. Further characterization of these mechanisms may help predict and prevent surgery‐induced PTB, improving outcomes.

ABSTRACT INTRODUCTION Neighborhood deprivation increases dementia risk, although mechanisms remain unclear. We tested a framework in which modifiable risk factors and cerebral small vessel disease (SVD) mediate the link between neighborhood deprivation and cognition. METHODS In 585 cognitively healthy midlife adults (ages 40–59), neighborhood deprivation was derived from postcodes, cognition was assessed using the COGNITO, lifestyle risk factors were measured using clinical assessments, and SVD (white matter hyperintensities, lacunes, microbleeds, perivascular spaces) was assessed on 3T magnetic resonance imaging. Multivariate analyses examined association pathways among these variables. RESULTS Neighborhood deprivation was associated with poorer cognition ( r = 0.36, p < 0.001), greater prevalence of modifiable risk factors ( r = 0.36, p < 0.001), and greater SVD burden ( β = 0.18, p = 0.008). Serial mediation showed that the effects of deprivation on cognition were indirect, possibly operating via lifestyle risk and SVD, explaining 20% of the total effect, whereas SVD alone explained 28%. DISCUSSION Neighborhood disadvantage relates to poorer cognition, possibly mediated through vascular risk factors and cerebrovascular disease. Highlights Neighborhood deprivation linked to poorer cognition in healthy midlife adults Deprivation linked to small vessel disease (SVD) and modifiable risk factors (chiefly cardiovascular risk) Association between deprivation and cognition mediated by modifiable risk and SVD Mediation was exclusive to hypertensive SVD, but not cerebral amyloid angiopathy (CAA)‐related SVD

Background: Post-treatment prognosis and monitoring are critical for determining the timing of salvage treatment in glioblastoma patients but has been challenging due to difficulties differentiating progression from treatment effects in conventional images. This exploratory study aimed to establish the correlation of radiomics image features from time series of amino acid tracer 18F-DOPA PET images, with outcomes, using machine learning and dimension reduction analysis. Methods: 18F-DOPA PET images were collected for a patient cohort with wild-type IDH and unmethylated MGMT who underwent dose-escalated radiation therapy. Quantitative features were derived from the high uptake region (T/N > 2.0) in pre- and post-radiation therapy follow-up 18F-DOPA PET images. A customized workflow was utilized for pre-selecting predictive features, followed by manifold learning. Machine learning algorithms were employed to establish associations between imaging features and remaining survival (RS), defined as the time between a follow-up scan and date of death. Results: The ML models exhibited 81–83% ROC_AUC in predicting RS evaluated on an independent test dataset. A RS map is proposed for monitoring tumor alterations through serial 18F-DOPA PET scans, demonstrating superior sensitivity and better correlation with survival compared to the RANO criteria. Conclusions: Our study demonstrates that ML models utilizing FU 18F-DOPA PET images have the potential to effectively predict future survival outcomes in patients with glioblastoma treated with dose-escalated radiation therapy. The capability to assess changes in tumor over time through imaging can potentially assist in patient stratification and the selection of salvage treatments, while also aiding in distinguishing treatment effects from genuine tumor progression.

Background Admixture mapping can be leveraged to identify genomic loci associated with disease traits in admixed individuals such as Hispanic Americans. Methods and Results We characterized fine‐scale population structure of participants (n=105 108) in the multiethnic eMERGE‐III (electronic Medical Records and Genomics) cohort, using reference panels from the 1000 Genomes Project and a Native American cohort. We defined “genetically admixed Hispanic Americans” as those having ≥10% Native American genetic ancestry (n=5025), in addition to European (specifically, Iberian) and African genetic ancestry. This population descriptor was subsequently applied to 3 other cohorts: the MESA (Multi‐Ethnic Study of Atherosclerosis; n=1176), WHI (Women’s Health Initiative; n=2873), and the HCHS/SOL (Hispanic Community Health Study/Study of Latinos; n=7804). We inferred local ancestry along the genome in genetically admixed Hispanic Americans in each cohort using RFMix2 with phased haplotypes from SHAPEIT2. Local ancestry proportions were used for admixture mapping of lipid traits (low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, total cholesterol, and triglycerides) using extended linear mixed models that incorporated multiple or single ancestries. After accounting for fixed‐effect covariates and random effects, ancestry proportions at the following loci were associated with lipid traits in the HCHS/SOL cohort: 11q12.2 ( P =6.8×10 −7 ) with low‐density lipoprotein cholesterol, 2p23.3 ( P =5.2×10 −7 ) with total cholesterol, and 11q23.3 ( P =7.3×10 −12 ) with triglycerides. The LDL cholesterol and triglyceride loci replicated in at least one independent cohort, whereas the total cholesterol locus showed suggestive evidence for replication in the eMERGE cohort ( P =0.073). Native American (NAMR) ancestry appeared to drive the LDL‐C association, whereas both NAMR and Iberian population in Spain (IBS) ancestries contributed to the triglyceride signal. Conclusions Admixture mapping in genetically admixed Hispanic Americans identified genomic loci influencing lipid traits and the different ancestral origins driving these associations.