to analyze appreciation and coping strategies of children hospitalized for COVID-19 and their primary caregivers during the illness and hospitalization process.

a qualitative and exploratory study, based on the McCubbin & McCubbin model (1993), with 25 participants: ten children hospitalized for COVID-19 and 15 primary caregivers. A semi-structured interview was used, and data were subjected to reflective thematic analysis.

children reported a predominantly negative appreciation of hospitalization, marked by fear, homesickness, pain, and discomfort with hospital routine. Their coping strategies included play, electronic devices, hygiene, and adherence to treatment. Caregivers also expressed negative assessments related to fear of death, isolation, and distress. Their strategies involved spirituality, religiosity, love for their children, and support from professionals and family members.

coping strategies differed between children and caregivers, highlighting the importance of care sensitive to the dyad's needs.

To evaluate the completeness and timeliness of records of severe acute respiratory syndrome (SARS) due to COVID-19 in the SIVEP-Gripe system in Brazil, from 2020 to 2023.

This was a descriptive study based on secondary, public, and anonymized data from SIVEP-Gripe, comprising 2,200,796 SARS due to Covid-19 records. Sixty-six sociodemographic, clinical, hospitalization, outcome, and treatment variables were analyzed. Completeness was classified according to Romero and Cunha (2006). Timeliness was assessed through the intervals between symptom onset and notification, notification and data entry, and notification and case closure, considering historical surveillance parameters (7, 30, and 60 days, respectively).

There was a predominance of variables classified as having very poor completeness throughout the analyzed period, despite a slight improvement in the good and excellent completeness classifications between 2020 and 2023. Regional heterogeneity was observed; Amapá, Mato Grosso do Sul, Santa Catarina, and Paraná achieved higher proportions of satisfactory completion, whereas Tocantins, Pernambuco, Mato Grosso, Rondônia, and Alagoas had the worst performance. Between 2020 and 2023, the average notification time decreased from 13 to 7 days. Data entry was performed on time in over 90% of records in most states, while case closure remained around 86%. Nevertheless, the 90% target for timely notification was not achieved.

Despite improvements in the timeliness of records, completeness remained unsatisfactory and uneven across states. These findings highlight the need to strengthen data entry practices and invest in continuous training and systematic monitoring to ensure more consistent data for surveillance and public health planning.

Early detection of obstructive sleep apnea (OSA) in adults with metabolic dysfunction associated steatotic liver disease (MASLD) remains a clinical challenge. Plasma proteomics provides a non-invasive tool for identifying individuals at elevated risk prior to symptom onset. We quantified 2911 plasma proteins in 17 375 OSA-free MASLD subjects from the UK Biobank (UKB). Participants were split into training and validation sets. Cox regression and Light Gradient Boosting Machine (LightGBM) with forward feature selection were used to identify and rank predictive proteins. Model performance was assessed by area under the receiver operating characteristic curve (AUC) in the validation set, and shapley additive explanations (SHAP) values were used to interpret feature contributions. Among 17 375 MASLD participants, 541 (3.1%) developed subsequent clinical diagnosis of OSA. Seven core proteins (FABP4, PON3, RTN4R, KIAA0319, CFC1, TFRC, CST3) were identified and combined into a protein risk score (ProRS). The ProRS stratified high- and low-risk individuals with C-index 0.727 and 10-year AUC 0.727, outperforming the clinical risk score (C-index 0.548). Integration with clinical factors further improved discrimination (C-index 0.765, 10-year AUC 0.765) and net benefit. The plasma protein-based ProRS predicts future OSA in MASLD and enhances risk stratification beyond clinical variables, supporting its potential for early, non-invasive screening and targeted intervention.

Pseudomonas aeruginosa bacteremic pneumonia carries exceptionally high mortality, yet there is a paucity of genomic characterization of the strains causing this infection. We performed hybrid sequencing (Illumina and Oxford Nanopore) of 12 non-redundant P. aeruginosa isolates from patients with severe bacteremic pneumonia admitted to the intensive care unit of a tertiary hospital between 2015 and 2023. The 12 isolates were assigned to nine distinct sequence types, suggesting that severe bacteremic pneumonia can arise from diverse P. aeruginosa lineages rather than being dominated by a single specialized or high-risk clone. In the combined dataset of our isolates and publicly available Korean P. aeruginosa genomes, type III secretion system exotoxin genotypes exoU and exoS showed a mutually exclusive and phylogenetically segregated distribution, as previously reported, with both genotypes represented among bacteremic pneumonia isolates. Carbapenemase genes were detected in only one isolate, PA22 (ST773), which harboured bla _NDM-1 together with bla _OXA-796 and was the only isolate displaying phenotypic carbapenem resistance and multidrug resistance. To assess the clonal relationship between bla _NDM-1-positive PA22 and the carbapenemase-negative ST773 isolate PA20 and to track the evolution of PA22 resistome within a broader epidemiological context, we investigated the population structure of a global ST773 dataset. Core genome MLST-based minimum spanning trees revealed a deep bifurcation within ST773, separating bla _NDM-1-positive and carbapenemase-negative lineages. Korean ST773 isolates formed two distinct clusters within the NDM-1-positive lineage, with the PA22-containing cluster phylogenetically proximal to isolates from the United States. Within the NDM-1-positive Korean cluster, bla _OXA-796 was located in conserved class 1 integron gene cassette arrays that exhibit ongoing structural diversification among closely related isolates, evidenced by variable integration of IS110 elements. Our findings demonstrate that severe bacteremic pneumonia arises from phylogenetically diverse P. aeruginosa lineages and provide genomic context for the NDM-1-producing ST773 clone that is rapidly emerging in Korea.

Endovascular aneurysm repair (EVAR) is used to treat patients with abdominal aortic aneurysm (AAA) who have suitable anatomy, while complex AAAs often require fenestrated and branched stent grafts, necessitating further refinement of the technique.

To evaluate the safety and efficacy of fenestrated/branched EVAR (F/B-EVAR) assisted by three-dimensional (3D) printing for treating complex AAA.

Retrospective cohort study.

This multicenter retrospective cohort study collected baseline data and clinical outcomes from patients treated with F/B-EVAR between January 2012 and June 2025. The population was divided into the 3D simulation group and the conventional measurement group. The 3D simulation group underwent a simulation to assess fenestration and branch positioning strategies. Study endpoints included procedural success rate, incidence of periprocedural complications and major adverse events, as well as procedural duration and radiation dose.

The mean age of patients was 70.2 ± 8.8 years, with 68.9% being male. Compared to the conventional measurement group, the 3D simulation group had a significantly higher procedural success rate (98.8% vs 91.6%, p < 0.001), shorter procedural duration ((115.2 ± 35.0) min vs (138.7 ± 43.7) min, p < 0.001), and lower radiation dose ((107.2 ± 43.9) mGy vs (144.5 ± 56.3) mGy, p < 0.001). Furthermore, although no significant differences were observed in the incidence of all-cause mortality and major cardiovascular adverse events during the 30-day follow-up between the two groups, the incidence of life-threatening major bleeding, major vascular complications, and acute kidney injury stage ⩾3 was significantly lower in the 3D simulation group.

F/B-EVAR guided by 3D simulation may allow for accurate planning of fenestration and branch positioning, potentially improving procedural success rate and suggesting a potential to enhance the quality of outcomes.

The randomised, double-blind, placebo-controlled, phase 3 Program fOr Evaluation of TYK2 inhibitor Psoriatic Arthritis-1 (POETYK PsA-1) trial evaluated the efficacy, safety, and tolerability of deucravacitinib, an oral, selective tyrosine kinase 2 inhibitor, in patients with PsA naïve to biologic disease-modifying antirheumatic drugs.

Adults with active PsA, high-sensitivity C-reactive protein concentration ≥ 3 mg/L, and ≥ 1 PsA-related hand and/or foot erosion detectable via radiograph were randomised 1:1 to oral deucravacitinib 6 mg once daily or placebo through week (W) 16. At W16, patients continued receiving deucravacitinib or switched from placebo to deucravacitinib through W52. The primary endpoint was American College of Rheumatology 20% improvement in response (ACR20) at W16. Nonresponder imputation was used for missing data. Efficacy and safety were evaluated through W52. Post hoc rank analysis of covariance was used to evaluate structural damage with no missing data imputation.

In 670 patients, a significantly greater proportion of those receiving deucravacitinib vs placebo achieved ACR20 at W16 (54.2% vs 34.1%, P < .001). Responses with deucravacitinib were increased at W52. Patients who switched from placebo to deucravacitinib achieved improvements similar to those in patients who received continuous deucravacitinib. Inhibition of structural damage was observed at W16 and W52. At W16, incidences of serious adverse events (AEs) (deucravacitinib, 1.8%; placebo, 2.4%) and discontinuations due to AEs (2.4%; 1.8%) were low and remained low through W52, without imbalances in cardiovascular events, malignancies, or opportunistic infections. No new safety signals were detected; no deaths occurred.

Deucravacitinib demonstrated superiority vs placebo for clinical responses, patient-reported outcomes, and structural damage inhibition in patients with PsA, with favourable tolerability and safety.

Dyslipidemia substantially increases the risk of cardiovascular disease (CVD), particularly among those with a strong family history.

To evaluate the longitudinal impact of the PROgramme of Lifestyle Intervention in Families for Cardiovascular risk reduction (PROLIFIC) on lipid profile parameters over a 2-year period.

We conducted an open-label, cluster-randomized trial (NCT02771873) using families as the unit of allocation. Families were randomized 1:1 by computer-generated numbers to intervention or enhanced usual care. The intervention, delivered by nonphysician health workers, included annual cardiovascular risk assessments, dietary counseling to lower carbohydrate and saturated fat intake while increasing fiber intake, and promotion of physical activity. Fasting lipid profiles (total cholesterol, low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides) were measured at baseline, 12, and 24 months. Changes in lipid levels were analyzed between groups with generalized estimating equations, accounting for family clustering.

The study included 1671 participants (1111 women; mean age 40.8 years) from 750 families (368 in the intervention and 382 in the usual care group), with a 3% dropout over 2 years. At 24 months, the intervention group had significantly better lipid profiles than usual care. Mean differences were -24.23 mg/dL (95% CI -28.25 to -20.22, P < 0.001) for total cholesterol, -14.41 mg/dL (95% CI -18.36 to -10.45, P < 0.001) for LDL-C, +7.04 mg/dL (95% CI 5.76-8.31, P < 0.001) for HDL-C, and -9.04 mg/dL (95% CI -15.5 to -2.56, P = 0.006) for triglycerides.

A family-centered strategy combining lifestyle counseling, dietary changes, and healthcare support can significantly improve lipid profiles in high-risk individuals. Scaled to the population level, such interventions could lower dyslipidemia rates and help prevent CVD in low- and middle-income countries.

The menopause transition marks a period of accelerated cardiovascular risk in women, highlighting the importance of opportunistic screening and intervention in midlife primary care.

This article summarises current evidence linking menopause with cardiovascular disease (CVD) and appropriate interventions, including lifestyle optimisation and menopausal hormone therapy (MHT).

The midlife acceleration of CVD risk is driven by distinct cardiometabolic and vascular changes, with ovarian ageing independently associated with adverse lipid profiles, fat redistribution, vascular dysfunction and metabolic syndrome. Early, premature, surgical and symptomatic menopause further amplifies risk. Lifestyle optimisation and lipid-lowering therapy remain powerful strategies to mitigate these changes. MHT, although not recommended solely for primary or secondary CVD prevention, may be offered for symptom management and bone protection in appropriately selected women, and in cases of premature, early or surgical menopause. Midlife consultations provide a unique window for general practitioners to opportunistically risk stratify, initiate preventive measures and support informed MHT decision making, thereby shaping long-term cardiovascular trajectories.

Diagnostic attribution of neuropsychiatric symptoms in SLE (NPSLE) remains challenging. This study evaluated whether cerebrospinal fluid (CSF) antisuprabasin (SBSN) antibody can serve as a diagnostic biomarker for NPSLE.

In this single-centre, prospective cohort study, patients with SLE presenting with new-onset neuropsychiatric or neurological symptoms were screened between January 2022 and October 2025. Final diagnoses were adjudicated by an independent committee blinded to CSF anti-SBSN antibody results. Patients were classified as NPSLE, SLE with central nervous system infection (SLE-CNSI) or SLE without NPSLE or CNS infection (SLE-Other). CSF anti-SBSN antibody levels were measured by ELISA. Diagnostic performance was assessed for identifying NPSLE against a combined non-NPSLE comparator group comprising SLE-CNSI and SLE-Other.

Among 190 screened patients, 148 were included in the final analysis, including 48 with NPSLE, 59 with SLE-CNSI and 41 with SLE-Other. CSF anti-SBSN antibody levels showed a stepwise increase across groups, with median concentrations of 47.60 ng/mL in SLE-Other, 72.82 ng/mL in SLE-CNSI and 88.94 ng/mL in NPSLE; all pairwise comparisons were significant (all p<0.001). For identifying NPSLE versus non-NPSLE comparators, CSF anti-SBSN antibody achieved an area under the receiver operating characteristic curve (AUROC) of 0.830, with a sensitivity of 0.812 and specificity of 0.740 at the optimal cut-off of 76.36 ng/mL. CSF anti-SBSN antibody had a higher AUROC than CSF white blood cell count (0.830 vs 0.743; p=0.041) and serum antiribosomal P antibody (0.830 vs 0.665; p=0.003). The three-marker model further increased the AUROC to 0.892 and significantly outperformed CSF anti-SBSN antibody alone (p=0.009).

CSF anti-SBSN antibody was significantly elevated in NPSLE and demonstrated good diagnostic performance for identifying NPSLE among patients with SLE presenting with neuropsychiatric symptoms. These findings support CSF anti-SBSN as a promising candidate diagnostic biomarker for NPSLE, particularly when combined with conventional CSF inflammatory and serological markers.

To estimate the risk of venous thromboembolism (VTE) in a nationwide cohort of newly diagnosed patients with SLE and in a cohort of established patients with SLE at Karolinska University Hospital compared with the general population.

Individuals with SLE were identified from the National Patient Register and matched to general population comparators on age, sex and residence. Follow-up was from diagnosis/matching until incident VTE, death, emigration or study end. The Karolinska cohort was followed from enrolment and additionally stratified by lupus nephritis (LN) and antiphospholipid antibody (aPL) positivity. Incidence rates (IR) of VTE were estimated and adjusted HRs with 95% CIs were estimated using Cox models. Time-dependent adjusted HRs were estimated using flexible parametric survival models.

In the nationwide cohort (N=4335), the mean age at inclusion was 49 years, 83% were female and mean follow-up was 7.4 years. The VTE IR was 8.8 per 1000 person-years compared with 2.8 in comparators, corresponding to an HR of 3.3 (95% CI 2.9 to 3.8). In the Karolinska cohort (N=784), the HR was 4.9 (95% CI 3.7 to 6.5). VTE risk was highest in the first few years after SLE diagnosis. LN was not significantly associated with VTE, and aPL positivity was associated with a 60% higher hazard, which was non-significant and attenuated after excluding individuals with prior VTE.

SLE is associated with an over threefold increased risk of VTE, in particular soon after SLE diagnosis, underscoring the need for individualised VTE risk assessment.