Myocardial dysfunction is a major determinant of mortality after cardiac arrest, yet the molecular events driving post-resuscitation injury remain incompletely understood. Nitric oxide (NO) has been proposed as a cardioprotective adjunct during extracorporeal life support (ECLS), but its mechanistic impact on myocardial recovery is unclear. We investigated whether NO supplementation during ECLS modulates oxidative stress, metabolic pathways, and apoptotic signaling in the post-cardiac arrest heart.

Male Sprague Dawley rats underwent hypothermic cardiac arrest followed by ECLS resuscitation with or without NO supplementation (20 ppm). Myocardial tissue was analyzed using bulk RNA sequencing, quantitative RT-PCR, oxidative stress assays (MDA, 3-nitrotyrosine, total oxidant/antioxidant status), and TUNEL staining to characterize pathway-level alterations.

NO supplementation markedly increased cardiomyocyte apoptosis (46%±3 vs. 27%±2; p < 0.0001). Transcriptomic profiling revealed > 550 differentially expressed genes, highlighting upregulation of inflammatory and apoptotic cascades (MAPK, TNF, NF-κB, proteasome/TLR pathways) and profound suppression of metabolic programs essential for myocardial recovery, including fatty acid oxidation, branched-chain amino acid metabolism, and oxidative phosphorylation. NO induced a striking oxidative-nitrosative imbalance, with elevated MDA, 3-nitrotyrosine, and total oxidant status and reduced total antioxidant capacity, resulting in a threefold increase in the oxidative stress index.

NO administration during ECLS drives a coordinated oxidative-inflammatory-apoptotic response and disrupts metabolic pathways necessary for myocardial recovery, suggesting a mechanistic basis for worsened post-arrest myocardial injury. These findings have direct implications for optimizing resuscitation strategies in human ECLS and may inform future therapeutic modulation of NO signaling.

Chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVDs) have shared risk factors and mechanisms. CVDs are highly prevalent in COPD patients. Additionally, the risk of suffering a cardiovascular (CV) event is increased following an exacerbation and remains elevated for months afterwards. This link between exacerbations and increased CV risk further highlights the importance of preventing exacerbations. Clinical management during and after exacerbations regarding the prevention of CV events remains to be optimised. CV events occur in patients with COPD who have not previously been diagnosed with CVD. Conventional CV risk tools have historically underestimated the risk of CV events in patients with COPD. All patients with COPD should be investigated for CVDs and markers of CV risk should be assessed at the time of COPD exacerbations. Improving survival in COPD depends on reducing the risk of exacerbations, particularly severe exacerbations, addressing identified CV risk factors and managing CVDs when identified according to guidelines.

Extradural anterior clinoidectomy is increasingly used to improve exposure and proximal vascular control in aneurysm surgery, but its isolated effect on an otherwise uncompromised optic nerve remains unclear. To evaluate the functional, structural, and electrophysiological impact of EAC with optic canal unroofing in patients without preoperative optic nerve compression or optic canal pathology. We conducted this single-center study included 16 adults who underwent no-drill extradural anterior clinoidectomy (EAC) during microsurgical clipping of ruptured aneurysms (January 2023-December 2024). Patients with visual or optic pathway pathology were excluded. Postoperative assessment (6-12 months) included visual acuity, automated perimetry (visual field index, VFI), OCT-derived retinal nerve fiber layer (RNFL) thickness, and visual evoked potentials (P100 latency). Eyes were compared using paired tests, with repeated-measures ANOVA for quadrant-based ΔRNFL. Visual acuity was preserved in all patients. Global RNFL thickness was similar in ipsilateral and contralateral eyes (95.8 ± 12.7 vs. 99.2 ± 18.6 μm; p = 0.230). Quadrant ΔRNFL varied by quadrant, but no pairwise differences remained after correction, with a trend toward greater thinning in the superior quadrant. VFI was similar (p = 0.7); one patient had inferior nasal quadrantanopia and two had mild blind-spot enlargement. P100 latency was comparable (114.8 ± 9.7 ms vs. 113.8 ± 8.9 ms; p = 0.223). No major EAC-related neurovascular complications were observed. Extradural anterior clinoidectomy was not associated with statistically significant optic nerve impairment, although visual field changes occurred in 3/16 patients (18.75%) with a trend toward superior RNFL thinning.

Lung transplantation is the definitive therapy for end-stage respiratory diseases. To expand the donor lung pool, ex vivo lung perfusion (EVLP) has been developed for the assessment of marginal donor lungs. However, current evaluation methods remain limited. This study aimed to develop non-invasive imaging and monitoring techniques for the quantitative and early assessment of pulmonary function during EVLP. Three novel approaches were established: (1) lung thermography during the initial reperfusion period to assess pulmonary function, (2) optical oxygen saturation (SaO₂) imaging to assess pulmonary oxygenation, and (3) real-time lung weight measurement as an early indicator of transplant suitability. Lung thermography revealed that lung surface temperature at 8 min after shunt closure was significantly lower in non-suitable cases than in suitable cases (25.1 ± 0.6 °C vs. 27.8 ± 1.2 °C, P < 0.01). Optical SaO₂ imaging demonstrated a strong correlation between lower lobe SaO₂ calculated from SaO₂ imaging and PaO₂/FiO₂ (P/F) ratio in the lower pulmonary vein (R = 0.855, P < 0.01), with SaO₂ being significantly lower in non-suitable cases. Real-time lung weight measurement showed that lung weight gain increased significantly after 40 min in non-suitable cases compared with suitable cases (51.6 ± 46.0 g vs. -8.8 ± 25.7 g, P < 0.01). These three approaches proved effective for the quantitative and early assessment of pulmonary function during EVLP. This review was created based on a translation of the Japanese review written in the Japanese Journal of Artificial Organs in 2024 (Vol. 53, No. 3, pp. 216-220).

Rare-variant association studies typically perform gene-level tests in which coding variants are filtered (or 'masked') and aggregated based on functional annotation and allele frequency. Through a systematic literature review, we cataloged 664 masks used across 234 studies and found that masking strategies (that is, sets of masks) rarely repeat across studies and are rarely justified. To quantify their impact on association results, we applied all previously employed strategies to 54 traits within 189,947 UK Biobank exomes. Here we find that the number of significant associations greatly depends on the masking strategy (ranging from 58 to 2,523 associations), which is a key reason for the modest overlap (<30%) of associations between separate published analyses of this dataset. We empirically determine masking strategies with high discovery power for low-frequency and rare variant gene-level associations across numerous datasets and traits, and we use these to explore the impact of other factors on burden test results. These findings offer a baseline strategy in burden tests to increase study power and replicability, addressing one source of inconsistency in previous studies.

Against the backdrop of escalating global plastic pollution, there is an urgent need to elucidate the systemic health risks posed by nanoplastics (NPs) as emerging environmental contaminants that enter higher organisms through the food chain. This study employed a three-level trophic transfer model, examining the pathway from polystyrene nanoparticles to Tenebrio molitor larvae and subsequently to mice, offering a comprehensive elucidation of the mechanisms behind the multiorgan toxicity associated with food chain-transferred nanoplastics (FCT-NPs). Our results demonstrated extensive accumulation of FCT-NPs across multiple organs via systemic circulation. Integrative multiorgan omics analysis revealed that FCT-NPs primarily induced two major categories of multiorgan comorbidities: cardiovascular diseases and metabolic disorders, with the liver identified as a central metabolic hub that potentially regulates other organs through bile acid-mediated metabolic crosstalk. Mechanistically, dysregulation of key genes, such as MTOR and FN1, activated Wnt and TGF-β signaling pathways, which in turn promoted organ fibrosis. Additionally, aberrant expression of critical regulators─including CAT, LPL, NQO1, and APOE─was found to drive oxidative stress and disrupt lipid metabolism. These findings provide crucial scientific evidence for FCT-NPs risk assessment and underscore the imperative for enhanced plastic pollution control and further investigation into long-term exposure effects.

A 45 year old patient presented with left upper visual field defect and decreased vision on the first postoperative day following "stent-assisted endovascular embolization for a ruptured left middle cerebral artery aneurysm with subarachnoid hemorrhage" performed in the neurology department. Lumbar puncture showed normal cerebrospinal fluid pressure initially, but repeated follow-up measurements during hospitalization indicated elevated intracranial pressure. The patient exhibited unequal pupil size, with a positive relative afferent pupillary defect (RAPD) in the left eye and slight pallor of the left optic disc. Half a month later, the patient developed decreased vision in the right eye. Fundus examination revealed optic disc hyperemia, edema with blurred margins, multiple peripapillary cotton-wool spots accompanied by small patchy hemorrhages, and scattered microaneurysms in the macular area. Based on the medical history, the diagnosis was confirmed as: left eye surgery-associated posterior ischemic optic neuropathy, and right eye Purtscher retinopathy. After treatment with mecobalamin tablets, citicoline sodium capsules, and compound vitamin B tablets, the ocular symptoms in the right eye showed some improvement.

We reported a middle-aged man who initially presented with anhidrosis for 20 years and subsequently developed severe orthostatic hypotension, gastrointestinal dysmotility, and urogenital dysfunction. Due to progressive symptom aggravation, he was hospitalized and underwent comprehensive clinical assessment, neurophysiological studies, autonomic function tests, and multidisciplinary team (MDT) evaluation. The final diagnosis was pure autonomic failure (PAF). This case describes in detail the patient's long diagnostic course, differential diagnostic reasoning, the pivotal role of MDT management, and individualized treatment strategies and outcomes. The report aims to enhance the understanding of primary autonomic disorders characterized by neurogenic orthostatic hypotension for physicians, emphasizing the importance of systematic etiological screening and multidisciplinary collaboration in rare disease diagnosis and management to reduce misdiagnosis and improve prognosis and quality of life.