Children's interstitial and diffuse lung disease (chILD) comprise a heterogeneous group of rare disorders associated with substantial morbidity and mortality. Population-based epidemiological data remain scarce in low- and middle-income countries, limiting health system planning and policy development. We aimed to estimate the prevalence and temporal trends of chILD in Colombia using nationwide administrative healthcare data.

We conducted a retrospective, population-based study using Colombia's Registro Individual de Prestación de Servicios de Salud (RIPS) from 2016 to 2024. chILD cases were identified using ICD-10 codes for chILD in individuals aged 0-18 years. Prevalence was estimated overall, by year, sex, age group, and diagnosis. Crude and WHO age-standardized prevalence rates were calculated per 100,000 population. Temporal trends were assessed using Poisson regression and LOESS smoothing.

A total of 4608 chILD -related healthcare encounters were identified. The average annual crude prevalence was 3.32 per 100,000 children (age-standardized: 3.39 per 100,000). Prevalence was highest in infants younger than 1 year and showed a secondary increase during adolescence. No relevant sex differences were observed. A significant annual increase in reported cases was detected (IRR 1.022; 95% CI 1.011-1.034), with a marked decline during the COVID-19 pandemic. Alveolar and fibrotic interstitial lung disease categories accounted for most cases.

This first nationwide study provides robust real-world evidence on the epidemiology of chILD in Colombia, revealing substantial healthcare utilization and distinct age-related patterns. Administrative data represents a valuable complementary tool for surveillance of rare pediatric lung diseases.

This study aimed to explore the risk factors for preoperative deep vein thrombosis (DVT) in patients with traumatic lower-extremity fracture (TLEF), analyze the correlation and predictive efficacy of the systemic immune-inflammation index (SII) in DVT development, and establish a corresponding nomogram prediction model.

This study retrospectively analyzed the clinical data of 950 patients who underwent surgery for TLEF at our hospital between May 2022 and April 2024. The enrolled patients were randomly divided into the training group (665 cases) and the validation group (285 cases) at a 7:3 ratio. We performed univariate and multivariate logistic regression analyses in the training dataset to screen independent risk factors for preoperative DVT in TLEF patients. R Studio was used to construct the nomogram model. The goodness-of-fit test and ROC curve were adopted to evaluate the efficacy of the model.

Age, fracture site, SII, D-dimer and APTT were identified as independent predictive factors for preoperative DVT. The nomogram exhibited good agreement with the ideal model in both the training and validation datasets.

The nomogram prediction model for preoperative DVT risk in TLEF patients was developed by incorporating SII and other risk factors. It can assist clinical practitioners in early assessment of DVT development.

Dysglycemia is frequently observed in patients with non-traumatic intracranial hemorrhage (ICH) and has been linked to adverse clinical outcomes. However, the prognostic impact of longitudinal blood glucose trajectories in critically ill non-traumatic intracranial hemorrhage remains incompletely understood.

We conducted a retrospective cohort study using the MIMIC-IV database (United States, 2008-2019), including 2,260 critically ill non-traumatic ICH patients. Latent class mixed modeling (LCMM) was employed to identify distinct longitudinal blood glucose trajectory subtypes, utilizing blood glucose data collected during the initial 72 h of ICU admission. Associations between trajectory groups and mortality were assessed using multivariable Cox proportional hazards regression.

Four glucose trajectories were identified: Trajectory 1 (persistent low), Trajectory 2 (moderate stable), Trajectory 3 (progressive decline), and Trajectory 4 (progressive increase). Significant differences in baseline characteristics were observed across trajectories. Even after adjusting for baseline blood glucose and other potential confounders, the 28-day mortality risk remained significantly elevated in Trajectories 2-4 compared to Trajectory 1, with hazard ratios of 1.71 (95% CI: 1.33-2.20), 1.87 (95% CI: 1.25-2.80), and 2.41 (95% CI: 1.64-3.54), respectively. Consistent findings were observed for 180-day and 1-year mortality.

Four distinct blood glucose trajectories observed during the first 72 h of ICU admission among critically ill patients with non-traumatic ICH were independently associated with 28-day and longer-term mortality. These findings may support early risk stratification and inform future prospective studies.

After recanalization in acute ischemic stroke, cerebral ischemia/reperfusion injury (CI/RI) drives a cascade of pathophysiological events that worsen clinical outcomes, yet effective therapeutic options remain limited. Given the neuroprotective potential of Huperzine A (HupA), the efficacy of HupA injection (HAI, a major clinical formulation of HupA) against CI/RI and its underlying molecular basis warrant investigation.

In a mouse model of CI/RI, neurological performance, locomotor ability, cerebral infarction, histopathological alterations, and apoptotic neurons were jointly used to assess the anti-CI/RI effect of HAI at two different doses. An integrated transcriptomic and proteomic strategy was adopted to decipher the key anti-CI/RI mechanisms of HAI and then validated experimentally.

Compared with vehicle‑treated CI/RI mice, HAI intervention significantly alleviated neurobehavioral deficits, decreased infarct size, mitigated histopathological damage, and suppressed neuronal apoptosis (P < 0.01). Both separate and combined transcriptomic and proteomic analyses highlighted that the complement and coagulation cascades, together with inflammation, were strongly correlated with HAI's beneficial action in preventing CI/RI. Indeed, HAI treatment effectively normalized the dysregulated mRNA and protein levels of pivotal targets within the complement and coagulation cascades, including C3, C5, C9, CFB, MASP2, F7, F10, F12, and SERPINE1, in the damaged cortical tissues of CI/RI mice (P < 0.05). Moreover, this intervention markedly attenuated the abnormally elevated expression of multiple inflammatory mediators, including TLR2, TLR4, TNF-α, IL-1β, IL-6, CCL2, CCL5, CXCL1, ICAM1, S100A9, LCN2, MMP8, and MMP9, at both the mRNA and protein levels (P < 0.01).

Collectively, our data suggest that HAI may confer efficacy against CI/RI by modulating the complement and coagulation cascades and orchestrating the inflammatory response. Although further investigation is warranted, these preliminary findings provide a foundation for accelerating the clinical translation of HAI as a novel neuroprotectant against CI/RI in ischemic stroke.

The cardiovascular, kidney, and metabolic effects of hormone replacement therapy (HRT) in postmenopausal women, particularly those who initiate treatment after age 65, remain incompletely characterized. The objective of this systematic review was to evaluate evidence on these outcomes, with a focus on women aged 65 years and older.

PubMed, Embase, Scopus, and the Cochrane Library were searched for studies published between January 1, 2021, and February 28, 2026. Eligible studies included randomized controlled trials and secondary or post-trial analyses evaluating HRT in postmenopausal women, particularly women aged 65 years and older. Outcomes included cardiovascular, renal, and metabolic endpoints. Risk of bias was assessed using RoB 2 where applicable, and evidence was synthesized narratively. The review protocol was registered in PROSPERO (CRD420261338310).

Of 1701 records identified, 6 reports met the inclusion criteria, all derived from three parent trials: the Women's Health Initiative Hormone Therapy Trials (WHI-HT), Early versus Late Intervention Trial with Estradiol (ELITE), and Kronos Early Estrogen Prevention Study (KEEPS). HRT effects varied by regimen and timing. In WHI-HT analyses, conjugated equine estrogens (CEE), alone or with medroxyprogesterone acetate (MPA), lowered low-density lipoprotein cholesterol (LDL-C) but increased triglycerides and systolic blood pressure; CEE plus MPA had a less favorable coronary profile than CEE alone. ELITE supported less favorable vascular effects with later initiation, while KEEPS showed neutral long-term findings. No trial was designed specifically for women aged ≥65 years, and evidence in this age group was limited to subgroup analyses of broader postmenopausal women. Additionally, no studies included renal outcomes.

Future prospective studies should evaluate cardiovascular, kidney, and metabolic outcomes across HRT regimens and timing in older postmenopausal women to guide individualized treatment decisions.

Pathological cardiac hypertrophy is a major contributor to heart failure and is characterized by complex molecular mechanisms involving transcriptional and epigenetic regulation, signal transduction, metabolic remodeling, inflammatory responses, and extracellular matrix remodeling. Although conventional pharmaceutical treatments may alleviate the progression of cardiac hypertrophy, their clinical effectiveness is limited by poor cardiac selectivity, systemic side effects, and limited efficacy in reverseing pathological remodeling. Recently, nanoparticle-based strategies have emerged as a promising therapeutic approach for cardiac hypertrophy owing to their ability to enhance cardiac-targeted drug delivery, enable controlled or stimuli-responsive drug release, and reduce off-target toxicity through improved biodistribution. This review systematically summarizes the design strategies of nanoparticle-based therapies for pathological cardiac hypertrophy, including material platforms such as inorganic, organic, and biomimetic nanoparticles, key delivery strategies such as passive targeting, active targeting, biomimetic targeting, and stimulus-responsive release, and administration routes including intravenous, intraperitoneal, intradermal, inhalation, and oral administration. In addition, this review provides a comprehensive summary of the preclinical applications of the above strategies in the fields of gene and epigenetic regulation, antioxidant, anti-inflammatory, and anti-fibrotic treatments. Finally, this review analyzes the challenges in clinical translation on the basis of critical issues, including long-term biosafety, insufficient targeting efficacy, large-scale production, and appropriate administration routes.

Cervical transforaminal and interlaminar epidural steroid injections (CTFESI and CILESI) are commonly used to treat cervical radicular symptoms. There is limited literature comparing the two procedures with some concerns of increased risk of complications after CTFESI.

Compare the rates of cervical spine surgery, post-procedure opioid use, and complications after CTFESI and CILESI.

Retrospective propensity matched cohort comparison utilizing a large global database was performed of adult patients with diagnostic codes for cervical radiculopathy undergoing CTFESI or CILESI. Each cohort was matched for age, sex, race/ethnicity, BMI and obesity codes, nicotine use, mental health diagnoses, chronic cardiovascular, pulmonary and renal diseases, pre-procedural opioid use, and prior spine surgery. The primary outcome was the rate of eventual anterior cervical decompression and fusion, total disc replacement, and/or neuroforaminotomy. Secondary outcomes included post-procedure opioid use and major (stroke, myocardial infarction, paralysis, and seizure) and minor (headache, pallor, syncope, flushing) complications.

The rate of cervical spine surgery was higher for CTFESI compared to CILESI. Post-procedure opioid use was also higher for the CTFESI. Compared to CILESI, CTFESI was associated with greater risk of stroke, seizures, myocardial infarction and minor complications. There was no difference in risk of paralysis.

This study demonstrates that patients undergoing CILESI were less likely to use opioid medications post-procedurally, have less major and minor complications and lower likelihood of having surgery as compared to CTFESI. These differences may be due to sampling biases between the two groups that were part of the clinical decision process in selecting the approach.

Daytime napping is a culturally embedded practice in Mediterranean populations, yet its health impacts remain unclear. When assessed in an international context, the impact of napping shows mixed results. This systematic review evaluated the associations between daytime napping, health outcomes, quality of life, and lifespan in Mediterranean populations, where napping is culturally embedded. Following PRISMA guidelines, electronic searches of Embase, PsycINFO, PubMed, and SCOPUS were conducted. Eligible studies were empirical, peer-reviewed, and only included samples from the Mediterranean region. Findings were inconsistent across all health outcomes. However, there was a trend for short naps (≤30 min/day) to be associated with beneficial cardiovascular outcomes and metabolic health. In contrast, longer naps (>30 min/day) were more often associated with increased risk of cardiometabolic diseases in older adults. Interpretation was limited by methodological heterogeneity, including varied nap definitions, over-reliance on self-reports, and poor evaluation and/or adjustment for sleep disorders or excessive daytime sleepiness. These findings imply that naps should be seen as part of the broader Mediterranean lifestyle and future research should use validated, standardised assessments of napping while simultaneously accounting for sleep disorders, daytime sleepiness, and nocturnal sleep. This will lead to better insights into the role of culturally embedded napping in health.

Hypertrophic cardiomyopathy is the most common genetic cardiomyopathy and is characterized by unexplained myocardial hypertrophy. This condition exhibits marked clinical and prognostic heterogeneity. Advances in cardiovascular imaging techniques and genetic testing have significantly improved the diagnostic accuracy, phenotypic characterization, and prognostic assessment. Hypertrophic cardiomyopathy can present with a broad spectrum of genetic substrates and clinical presentations, ranging from asymptomatic individuals to those with heart failure, arrhythmias, and even sudden cardiac death. The first-line method for diagnosis, risk stratification, and follow-up of these patients is echocardiography, but additional techniques, such as cardiac magnetic resonance imaging, provide complementary information, such as quantification of fibrosis, and more accurate measurements. Genetic testing contributes to etiological diagnosis and family screening. Treatment options include both pharmacological therapy (such as beta-blockers, calcium channel blockers, and disopyramide), which is the first-line therapy, and septal reduction techniques (alcohol septal ablation, surgical myectomy), which should be reserved for selected patients. Recently, cardiac myosin inhibitors have emerged as a novel therapeutic option, demonstrating significant reductions in left ventricular outflow tract obstruction and improvement in symptoms.

Hypertrophic cardiomyopathy has evolved considerably with advances in imaging techniques, genetic evaluation, and targeted therapies. This review examines the primary diagnostic and management strategies, both established and emerging, for hypertrophic cardiomyopathy.

Neurovascular coupling (NVC) is essential for matching cerebral blood flow to neuronal activity. While NVC has been extensively studied in the cerebral cortex, far less is known about its regulation in deep brain regions such as the hypothalamus, particularly under pathological conditions. Heart failure (HF) is associated with impaired cortical NVC and cognitive dysfunction, but its impact on hypothalamic NVC remains unclear. Here, we investigated salt-evoked NVC in the hypothalamic supraoptic nucleus (SON) of rats with HF. In vivo two-photon imaging combined with real-time tissue oxygen measurements was used to assess parenchymal arteriole diameter and local P O 2 in the SON during a systemic hypertonic saline challenge in a rat model of HF. Pharmacological interventions and biosensor approaches were employed to dissect the contributions of key vasoactive signalling pathways. Under baseline conditions, HF rats exhibited reduced SON P O 2 compared with sham animals. Unexpectedly, salt loading in HF rats elicited a vasodilatory NVC response accompanied by a progressive increase in SON P O 2 , restoring oxygen levels toward those observed in sham rats. This polarity shift was mediated by adenosine signalling through A_2A receptors and depended on intact vasopressin (AVP) signalling. Notably, blockade of A_2A receptors unmasked an underlying AVP-dependent vasoconstriction, indicating the coexistence of competing vasoactive mechanisms during salt challenge. These findings demonstrate a state-dependent reorganization of hypothalamic NVC in HF, in which adenosine-dependent vasodilatation predominates over AVP-mediated vasoconstriction during salt loading. This adaptive shift highlights the dynamic regulation of neurovascular signalling in the hypothalamus and may have broader implications for neurohumoral control in cardiovascular disease. KEY POINTS: Neurovascular coupling (NVC) is well characterized in the cerebral cortex but remains poorly understood in the hypothalamic nuclei regulating homeostatic and neurohumoral functions. Heart failure (HF) is associated with a basal hypoperfused and hypoxic state of the hypothalamic supraoptic nucleus (SON), indicating impaired local neurovascular regulation at rest. During systemic salt loading, NVC in the SON of HF rats undergoes a polarity switch, with vasodilatation and improved tissue oxygenation replacing the vasoconstrictive response in sham animals. This state-dependent reorganization involves adenosine signalling via A_2A receptors and is functionally dependent on intact vasopressin/V_1A receptor signalling, indicating that opposing vasoactive pathways jointly shape the net vascular response to salt loading in HF. These findings highlight dynamic, region-specific regulation of hypothalamic neurovascular signalling in cardiovascular disease, with implications for neurohumoral control during homeostatic challenge.