Introduction/Objective: Heart Failure with Preserved Ejection Fraction (HFpEF) is increasingly recognized as a metabolic disorder. This review investigates the role of ceramidemediated lipotoxicity in its pathogenesis, focusing on how aberrant ceramide accumulation drives myocardial dysfunction. Methods: We synthesized and critically evaluated current preclinical and clinical literature from major electronic databases (PubMed/MEDLINE, Embase, Web of Science) up to March 2026. Using a hierarchical evidence classification framework (Level 1: human HFpEF myocardium; Level 2: HFpEF-specific animal models; Level 3: related disease models; Level 4: in vitro studies), we analyzed evidence across calcium handling, apoptosis, autophagy, inflammation, and fibrosis pathways. Results: Ceramide lipotoxicity represents an important pathological nexus. It directly impairs cardiomyocyte function by disrupting calcium homeostasis and ion channels (SERCA2a, RyR2, Kv4.3). Concurrently, it triggers mitochondrial and death receptor-mediated apoptosis, inhibits autophagic flux via AMPK/mTORC1 dysregulation, and activates pro-inflammatory (NF-κB, IL-6, TNF-α) and pro-fibrotic (TGF-β/Smad3) signaling pathways. These mechanisms collectively lead to diastolic dysfunction and disease progression. Interventions targeting ceramide synthesis (SPT inhibitors) or downstream effects show therapeutic promise in experimental models. Discussion: The available evidence is derived predominantly from Level 3 models (diabetic cardiomyopathy, obesity-induced dysfunction) and Level 4 in vitro studies. Direct validation in human HFpEF myocardium (Level 1) and HFpEF-specific animal models (Level 2) remains a critical unmet need. The ceramide-centered hypothesis is most directly applicable to the metabolic/obesity-related phenotype of HFpEF, given the phenotypic heterogeneity of the syndrome. Therapeutic translation faces hurdles, including a lack of tissue selectivity, ceramide species complexity, and unknown long-term safety of inhibiting essential sphingolipid functions Conclusion: Ceramide-mediated lipotoxicity constitutes a significant pathogenic mechanism in the metabolic phenotype of HFpEF. However, this conclusion is largely inferred from preclinical models recapitulating metabolic stress. Direct validation in human HFpEF myocardium is urgently needed. Future research must prioritize human tissue lipidomics, development of multifactorial animal models, and targeted clinical trials to translate these findings into effective therapies.

Background Uterine incision dehiscence (UID) can mimic intestinal obstruction features following cesarean delivery (CD), posing a diagnostic challenge due to overlapping symptoms with common postoperative ileus. This study aims to highlight the clinical and radiological distinctions between these conditions. Methods This case series study was conducted at two Chinese Hospital between April 2020 and June 2022. Three patients with UID mimicking intestinal obstruction (study group) and three with postoperative ileus (comparison group) were included. Data on clinical symptoms, laboratory results, CT findings, and surgical outcomes were analyzed. Results In the study group, the mean interval from cesarean delivery to symptom onset was approximately 9 days, whereas in the comparison group it was about 1.3 days. Lower abdominal pain was the predominant initial symptom in UID cases. Platelet counts in the study group averaged 496.7 × 10⁹/L, and CRP levels averaged 287 mg/L, both appearing higher than the corresponding values in the comparison group (182.7 × 10⁹/L and 144.9 mg/L, respectively). CT imaging in UID cases demonstrated characteristic findings, including discontinuity of the uterine muscle layer, pelvic free air, and diffuse peritonitis. All patients with UID underwent laparotomy, during which surgical site infections and abscesses were identified, while patients in the comparison group with postoperative ileus were managed successfully with conservative treatment. Conclusion UID mimicking intestinal obstruction presents distinct features, including delayed onset, severe inflammation markers, and specific CT signs. Clinicians should maintain high suspicion for UID in patients with prolonged or atypical postoperative symptoms.

Myocardial infarction (MI), a lethal coronary artery disease primarily triggered by atherothrombosis or an imbalance in myocardial oxygen supply and demand, stands as a leading cause of mortality worldwide. Promoting angiogenesis is recognized as an effective therapeutic strategy for MI, a process highly dependent on the functional status of endothelial cells (ECs). Small extracellular vesicles (sEVs), which are membrane-bound vesicles secreted by cells and enriched with bioactive molecules including proteins, lipids, and RNAs, are ubiquitously present in the secretome of diverse cell types such as stem cells, immune cells, and cardiac cells. Studies have confirmed that sEVs can deliver specific “cargo” such as miRNAs and cytokines via paracrine or endocrine pathways, activating key downstream signaling cascades. This effectively promotes EC proliferation, migration, and tube formation, thereby enhancing angiogenic capacity and ultimately mitigating pathological cardiac remodeling while improving prognosis post-MI. This review focuses on sEVs derived from various cellular sources, systematically summarizing their roles in promoting angiogenesis and the latest research advances in regulating EC function, aiming to provide novel insights for the effective treatment of MI.

Background Acute myocardial ischemia/reper fusion (MI/R) increases risk for cognitive decline, yet the underlying mechanisms mediating heart-brain communication remain poorly understood. Small extracellular vesicles (sEVs) have emerged as novel long-range signaling mediators and may play a critical role. MethodsMI/R was induced by transient ligation of the left anterior descending artery. Cognitive performance was assessed using multiple behavioral tests. sEVs derived from cardiomyocytes were labeled to track their distribution and cellular uptake in the brain. Heart and brain tissues were analyzed for microRNAs (miRNAs) expression using bioinformatics, qPCR, and RNAScope. The role of specific miRNAs was investigated through genetic inhibition of cardiomyocyte-derived sEVs release using Rab27a(f/f)Myh6-Cre(+) mice, pharmacological blockade of exosome, and AAV-mediated overexpression or knockdown. Results MI/R mice exhibited significant cognition deficits along with hypothalamic paraventricular nucleus (PVN) synaptic ultrastructural injury and dysfunction. sEVs released from injured cardiomyocytes were significantly elevated and preferentially accumulated in oxytocin neurons from the PVN. Inhibiting cardiomyocyte-derived sEVs ameliorated cognitive impairments and synaptic pathology. Conversely, injection of cardiomyocyte-derived sEVs into the PVN recapitulated MI/R-induced cognitive deficits. Among candidate miRNAs, miR-574-5p was identified as a key mediator. Its inhibition via miRNA sponge restored cognitive function. Bioinformatic analyses revealed that miR-574-5p targets genes involved in synaptic structure and GABA(B) receptor signaling. Conclusions Cardiomyocyte-derived sEVs contribute to MI/R-induced cognitive impairment through miR-574-5p. Upon delivery to the PVN and uptake by oxytocin neurons, miR-574-5p suppresses synaptic and GABA(B) receptor-related proteins, leading to synaptic disruption and cognitive decline. Targeting this pathway may represent a promising therapeutic approach for cognitive dysfunction associated with heart disease.

The continuous spread of mpox disease caused by mpox virus (MPXV) has posed great threat to global public health. The postattachment membrane fusion process of MPXV is mediated by a multimeric protein machinery, termed as entry-fusion complex (EFC). Among EFC components, A30 and H2 are the earliest identified interaction pair and play important roles in virus entry. Here, we determine the crystal structure of MPXV A30/H2 subcomplex via the tandem-fusion strategy, and show that A30 undergoes large conformational rearrangements upon H2 binding. Structural analysis reveals extended intersubunit interface and highly conserved intermolecular interactions. In vitro binding data further clarify key residues and elements involved in the A30/ H2 subcomplex formation. Finally, we show that the H2-A30 fusion protein, superior to A30 ectodomain alone or the ectodomain-mixture of H2+A30, can induce more potent neutralizing-antibody responses which could inhibit viral infection. These data provide valuable information for the understanding of poxvirus EFC assembly and the H2-A30-based immunogen design and optimization.

Background The red blood cell distribution width-to-albumin ratio (RAR) has emerged as a novel prognostic biomarker in critically ill patients. However, its association with mortality in sepsis patients, particularly in the context of sepsis-induced coagulopathy (SIC), remains unclear. Methods This retrospective cohort study analyzed adult sepsis patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) version 3.1 database. RAR was calculated from the first laboratory measurements within 24 hours of intensive care unit (ICU) admission. The primary outcome was 90-day all-cause mortality. Cox proportional hazards regression, subgroup analyses, and restricted cubic spline (RCS) regression were performed. Discriminative ability was assessed using receiver operating characteristic (ROC) curves. Results Of 26,854 patients meeting sepsis criteria, 17,499 were excluded due to missing RDW or albumin data. A total of 9,206 sepsis patients were included, with 5,649 (61.4%) meeting SIC criteria. The overall 90-day mortality was 38.1% (absolute rates: 23.9% in the lowest RAR quartile to 55.5% in the highest). In the fully adjusted model (age, sex, SOFA, Charlson Comorbidity Index, infection source, vasopressor use, mechanical ventilation, renal replacement therapy, and lactate), each unit increase in RAR was associated with a 9% increase in mortality risk (hazard ratio [HR]=1.09, 95% confidence interval [CI]: 1.08-1.10, P<0.001). Compared with the lowest quartile, patients in the highest RAR quartile had a significantly higher mortality risk (HR=2.07, 95% CI: 1.91-2.25). The association remained consistent across subgroups. RCS analysis revealed a significant non-linear exposure-response relationship (P for non-linearity <0.001). DeLong testing confirmed that RAR (AUC=0.648) had statistically significantly higher discriminative ability than SOFA score (AUC=0.613, P<0.001) and SIC score (AUC=0.593, P<0.001) for 90-day mortality, though all AUC values indicated moderate discrimination. Conclusions Elevated RAR was independently associated with increased 90-day mortality after comprehensive covariate adjustment (highest vs. lowest quartile: HR=2.07, 95% CI: 1.91-2.25), with modest but statistically significant incremental discriminative ability over SOFA and SIC scores. As a biomarker derived from routine blood tests, RAR may complement existing tools for early risk stratification in sepsis. These findings are hypothesis-generating and warrant prospective validation.

BACKGROUND:No clinically useful non-invasive biomarkers have been developed for diagnosis of chronic pancreatitis (CP), and molecular features of CP have not been characterised. Extracellular vesicles (EVs) consisted of abundant RNA species with specialised functions and clinical applications. OBJECTIVE:Our study aimed to construct a diagnostic model for CP and depict molecular landscape of CP based on EV long RNA (ExLR). DESIGN:Candidate ExLRs were defined using prespecified expression-quality criteria and complementary discovery-stage screens, and a resampling-based consensus feature selection in the training cohort yielded a five-ExLRs panel for model construction. The ExLRs-based CP diagnostic model (ExLRCPdscore) was further confirmed in another two independent validation cohorts with different controls. To elucidate the biological architecture of CP through ExLR profiling, we integrated ExLR-seq, single-cell data and clinical information. RESULTS:ExLRCPdscore constructed by random forest demonstrated excellent performance for detecting CP. Importantly, ExLRCPdscore could effectively detect early-stage CP, CP without alarm symptoms, CP without significant imaging findings and CP without risk factors. Using ExLR profiling and phenotypic data, we pinpointed MUC5B+ ductal cells exhibiting the strongest correlation with CP and derived an ExLR-based acinar-to-ductal metaplasia (ADM) score as a blood-based transcriptomic proxy of ADM-related programme. Integration of ExLR-seq and clinical information revealed significant associations between ADMscore and clinical characteristics, imaging findings and metabolic sequelae. CONCLUSION:Our study is the first to report an ExLRs-based diagnostic model that demonstrates exceptional robustness in differentiating CP from healthy controls and non-pancreatic disease controls. ExLRs offer a promising tool for CP molecular characterisation and pathophysiological quantification.

Protein phosphorylation, a key post-translational modification, plays a crucial role in regulating cellular activities in eukaryotes. Dysregulation of phosphorylation is closely linked to the pathogenesis of various diseases Recent advancements in phosphoproteomics have driven substantial improvements in mass spectrometry technologies, enrichment strategies, and data analysis methodologies, thereby offering a powerful and precise tool for elucidating the spatiotemporal dynamics of phosphorylation events. Nevertheless, several challenges remain, such as the limited sensitivity for detecting low-abundance signals, throughput constraints of single-cell technologies, and the absence of standardized workflows, all of which impede clinical translation. Moving forward, AI-driven experimental design, spatial omics coupling, and interdisciplinary technological integration will drive the transition of phosphoproteomics from basic research to precision medicine, providing novel insights for disease diagnosis and treatment. This review aims to comprehensively summarize recent technological developments and future trends in phosphoproteomics, focusing on its clinical translation potential and associated challenges.

ObjectivesThe purpose of this study is to discover how occupational burnout influences the health status of emergency nurses and to investigate the mediation effect of work–family behavior role conflict.DesignA multi-center cross-sectional study.Setting and participantsA questionnaire survey of 1,540 emergency nurses from 30 tertiary hospitals in China was conducted between December 26, 2023, and January 18, 2024.MethodsUsing an online questionnaire, we performed a cross-sectional survey to collect demographic data and information about occupational burnout, work environment, work–family behavior, role conflict, and emergency nurses’ health status. The PROCESS macro for SPSS 26.0 was used to analyze the moderated mediation model, and the bootstrap approach was used to investigate the mediating effects.ResultsThe findings revealed that 57.3% of the nurses had experienced occupational burnout. A substantial positive association was identified between professional burnout, work–family behavior role conflict, and somatic symptoms (r = 0.493, 0.534; p < 0.001). Occupational burnout was found to be a significant predictor of somatic symptoms, with work–family conflict serving as a mediator (β = 0.616, t = 13.295, R2 = 0.488, p < 0.01). Our research found that nurses’ work environment mediated the association between burnout and work–family behavior role conflict (β = 0.007, t = 3.647, p < 0.01), indicating that a positive work environment may reduce the impact of burnout on family role conflict.ConclusionWork–family behavioral role conflict and the nursing work environment were found to partially mediate the association between occupational burnout and the health outcomes of emergency nurses. These findings suggest that, while interventions aimed at mitigating work–family role conflict and improving the work environment are essential, they may not be sufficient on their own to safeguard nurses’ health. Additional strategies are needed to comprehensively address the health risks associated with occupational burnout. Moreover, the interplay among burnout, work–family conflict, and environmental factors underscores the necessity of integrated and multifaceted intervention approaches to alleviate the health burden experienced by emergency nurses effectively.

Background Early diagnosis of pancreatic cancer (PC) remains challenging, particularly in patients with chronic pancreatitis (CP). Currently, imaging is often inaccurate and biopsy is inherently invasive. This is the first network meta-analysis (NMA) comparing blood-based biomarkers for differentiating PC from CP. Methods PubMed and EMBASE were searched for studies evaluating blood-based biomarkers for distinguishing PC from CP. Risk of bias was assessed with QUADAS-2. We conducted individual biomarker meta-analysis with generalized bivariate models. For the NMA, we applied a Bayesian inference approach via a Markov-chain Monte Carlo random effects model. The surface under the cumulative ranking curve was used to rank the diagnostic performance of the biomarkers. Results Across 139 enrolled studies, 49 biomarkers or panels were analyzed. For differentiating PC from CP, tumor polypeptide antigen (TPA) had the highest area under the summary receiver operating characteristic curve (AUSROC) (0.92). The NMA revealed that microRNA-196b (miR-196b) ranked highest in sensitivity (OR 3.74e+27), while the combination of carbohydrate antigen 19–9 (CA199) and a panel of eight extracellular vesicle long RNAs (exLRs) exhibited the highest specificity (OR 3.78). For early-stage (stage I and II) PC, the eight exLRs showed the highest relative sensitivity (OR 7.00), and carcinoembryonic antigen (CEA) demonstrated the highest specificity (OR 4.70). Conclusion CA199 demonstrated only moderate diagnostic discrimination between PC and CP, with reduced efficacy in early-stage PC. Combining CA199 and eight exLRs exhibited promising differential diagnostic efficacy with both high sensitivity and specificity.

In recent years, venovenous extracorporeal membrane oxygenation (VV-ECMO) has emerged as a critical intervention in the management of adult respiratory failure, with its clinical application expanding at a rapid pace annually. For critically ill patients receiving VV-ECMO support, achieving and maintaining a balance between oxygen supply and oxygen consumption is of paramount importance. Oxygen supply primarily relies on cardiac output and arterial oxygen content; notably, in patients under VV-ECMO support, arterial oxygen content is closely linked to the parameter configurations of both VV-ECMO and mechanical ventilators. Therefore, based on national and industrial needs, this document has been formulated by integrating the latest advancements and practical experience in this field from both domestic and international sources. Its core objectives are to standardize the adjustment of oxygen supply during the combined use of mechanical ventilators and VV-ECMO, provide unambiguous guidance for healthcare professionals, and ultimately enhance the success rate in the treatment of severe respiratory conditions.

Pesticides have been associated with mitochondrial toxicity in humans through various mechanisms,including oxidative stress,reduced adenosine triphosphate(ATP)production,and alterations in mitochondrial DNA copy number,with potential links to chronic diseases and mitochondrial dysfunction.[1]These effects,often mediated by respiratory chain inhibition or increased reactive oxygen species,may trigger metabolic decompensation or unmask latent mitochondrial disorders in susceptible individuals.[1]

BACKGROUND:Despite statin medication, a substantial number of patients with coronary heart disease (CHD) do not meet guideline-recommended lipid goals, increasing dependence on combination lipid-lowering methods. However, evidence comparing the lipid-modifying effectiveness of ezetimibe added to statins of varying intensities is lacking, creating confusion about the best treatment options in clinical practice. This research sought to assess and compare the effectiveness of statins of varying intensities in conjunction with ezetimibe for enhancing lipid profiles in individuals with CHD. SOURCES OF MATERIAL:PubMed, Embase, Cochrane Library, and Web of Science were searched to January 1, 2026 for randomized controlled trials (RCTs) comparing statin monotherapy with statin-ezetimibe therapy in CHD. Network meta-analysis was performed using Stata 17.0, with surface under the cumulative ranking curve-based ranking. Outcomes were low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), total cholesterol (TC), non-HDL-C, and apolipoprotein B (ApoB). ABSTRACT OF FINDINGS:A total of 38 RCTs involving 7340 patients with CHD were included. Network meta-analyses demonstrated that moderate-intensity statin (MIS) therapy coupled with ezetimibe regularly resulted in significant enhancements in LDL-C, HDL-C, TC, non-HDL-C, and ApoB levels. For LDL-C reduction, MIS plus ezetimibe was comparable in efficacy to a high-intensity statin (HIS) plus ezetimibe. For TG, HIS combined with ezetimibe was rated highest, while no significant change was noted in comparison to MIS combined with ezetimibe. Rosuvastatin plus ezetimibe may demonstrate the greatest efficacy among MIS-based combination regimens. CONCLUSION:Adding ezetimibe to MIS medication in patients with CHD provides a more balanced cholesterol-lowering strategy than statin dosage increase alone, with effectiveness equivalent to HIS-based treatment across several lipid measures.

Clinically, cardiac arrest, cardiopulmonary resuscitation, and ischemic stroke, as major contributors to cerebral ischemia/reperfusion injury (CIRI), leads to cognitive decline, brain dysfunction, and neurological disability. Increasing evidence has highlighted the significant role of neurovascular unit (NVU) damage in the development of CIRI, leading to disruptions in the blood-brain barrier (BBB), alterations in cerebral blood flow regulation, and enhanced neuroinflammation. Over time, the concept of NVU has gained prominence, with research emphasizing the intricate interactions between cells and their microenvironment, which are essential for tissue repair and functional recovery. Among the various cell types in the NVU, pericytes have attracted renewed attention. These cells are crucial for the formation and upkeep of the NVU, with their dysfunction linked to various central nervous system (CNS) diseases. Cerebral pericytes are vital for regulating BBB integrity, permeability, and blood flow, while also contributing to a wide range of functions, including contractility, immune responses, migration, angiogenesis, and stem cell potential. They are pivotal in the pathological progression of cerebral ischemia/reperfusion. However, the study of pericytes has been hindered due to the lack of specific biomarkers. A deeper understanding of pericytes is expected to enhance recognition of their role in the NVU. Studies from databases such as PubMed and Web of Science, up to 2025, have been reviewed to provide a comprehensive overview of pericyte interactions within the NVU and CIRI, offering valuable insights for future research and clinical applications.

Purpose:Early recognition of high-risk patients with hemorrhage remains challenging, as conventional indicators may lack sensitivity during the compensated phase of blood loss. The study evaluated whether visual scoring of photoplethysmography (PPG) morphology could support bedside risk stratification during acute hemorrhage. Methods:In this prospective observational study conducted in the emergency department of West China Hospital between August and October 2025, 500 adults with hemorrhage were enrolled, of whom 461 were included in the final analysis. Three trained physicians independently scored PPG morphology using an ordinal 0-100 visual scale in 10-point increments. The final score was determined through majority voting. The primary outcome was 28-day all-cause mortality, while the secondary outcome was intensive care unit (ICU) admission. Moreover, lactate-related risk stratification was explored separately. Results:Inter-rater agreement was good to excellent based on pairwise linear weighted kappa (0.74, 0.99, and 0.75), whereas overall agreement was moderate based on Fleiss' kappa (0.58). The visual PPG score demonstrated good discrimination for both 28-day mortality (area under the curve [AUC] 0.81) and ICU admission (AUC 0.88), with numerically superior performance to the shock index, mean arterial pressure, lactate, and base excess. Adding the visual PPG score to routine clinical indicators increased the AUC for ICU admission from 0.82 to 0.90. Conclusion:Visual PPG scoring may support early bedside risk stratification in hemorrhagic patients and warrants external validation.

BACKGROUND:Heart failure with preserved ejection fraction (HFpEF) is increasingly acknowledged as a major public health concern due to its complex pathophysiology, which involves neuroinflammation and sympathetic activation. The crosstalk between the heart and hypothalamic microglia in HFpEF, particularly the role of small extracellular vesicles (sEVs), remains insufficiently explored. METHODS:HFpEF was induced in mice by combining a long-term high-fat diet with the nitric oxide synthase inhibitor l-NAME (Nω-nitro-l-arginine methyl ester). Microglial depletion was achieved with PLX3397. GW4869 was administered via intraperitoneal injection. BV2 microglial cells were treated with sEVs derived from palmitate-treated HL-1 cardiomyocytes. Cardiomyocyte-specific miR-200c-3p sponge, mimic, and inhibitor were used for functional studies. The downstream target, DUSP1 (dual-specificity phosphatase 1), was validated through experimental approaches. RESULTS:The HFpEF mice exhibited activation of microglia and hypothalamic inflammation. Microglial depletion suppressed sympathetic activity and improved cardiac dysfunction. sEVs derived from the myocardium of HFpEF mice induced a proinflammatory M1 phenotype in microglia, leading to hypothalamic inflammation and sympathetic activation. Intraperitoneal injection of GW4869 reversed these changes in HFpEF mice. Similar pathological changes were observed in BV2 microglial cells treated with sEVs from palmitic acid-treated HL-1 cardiomyocytes. miR-200c-3p was markedly upregulated in sEVs derived from both HFpEF myocardial tissues and palmitic acid-treated HL-1 cells, as well as within microglia themselves. Cardiomyocyte-specific miR-200c-3p sponge inhibited microglial activation, hypothalamic inflammation, and sympathetic activation in HFpEF mice. Conversely, the miR-200c-3p mimic exacerbated proinflammatory responses in BV2 cells, while the miR-200c-3p inhibitor prevented the transition to a proinflammatory phenotype. DUSP1 was validated as a downstream target of miR-200c-3p in microglia. CONCLUSIONS:Our study reveals that HFpEF prompts cardiomyocytes to release sEVs enriched with miR-200c-3p, leading to hypothalamic inflammation and evoking sympathetic outflow, which in turn exacerbates cardiac dysfunction. Focusing on sEV-mediated communication between cardiomyocytes and microglia may offer a new therapeutic approach for HFpEF.

Objective: To explore the diagnostic and therapeutic strategies for a rare critical case of extensive burns complicated by Stanford Type B aortic dissection and pulmonary artery embolism, analyzing the principles for resolving treatment conflicts and clinical outcomes. Methods: A retrospective analysis was conducted on the clinical data of a 55-year-old male patient admitted in September 2024 with extensive burns and vascular complications. The patient presented with 71% total body surface area (TBSA) burns, comprising 55% third-degree and 16% second-degree burns, mainly complicated by Stanford Type B aortic dissection (chronic), distal right pulmonary artery trunk and branch embolism, and near-complete thrombosis of the left upper limb. Clinical characteristics, laboratory test dynamics, surgical approach, and anticoagulation strategy were analyzed. Results: Enhanced CT angiography confirmed the diagnosis upon admission. Addressing the treatment conflict between aortic dissection and pulmonary embolism, a strategy of “staged surgery + close monitoring + cautious low-molecular-weight heparin anticoagulation” was adopted. Specific measures: (1) Wound management: Underwent 6 surgical procedures including debridement and eschar removal, heterograft skin grafting, Meek grafting, and autograft skin grafting to progressively close the wound. (2) Aortic dissection management: Control blood pressure (target systolic 100–130 mmHg; 1 mmHg = 0.133 kPa) and heart rate (target 60–80 bpm) to prevent dissection expansion. (3) Pulmonary embolism and thrombus management: Sodium low molecular weight heparin 4250 IU subcutaneously every 12 hours, with dynamic monitoring of D-dimer and coagulation function. During treatment, D-dimer decreased from 8.45 μg/L at admission to 2.93 μg/L, and C-reactive protein decreased from 246.96 mg/L to 133.62 mg/L. At 2.5 months postoperatively, wounds on the right upper limb and both lower limbs were largely closed, with good survival of chest and back skin grafts. The patient's condition was stable. Conclusion: Large-area burns complicated by Stanford Type B aortic dissection and pulmonary embolism present a critically ill condition with prominent treatment dilemmas. Under the premise of confirming the dissection as chronic with a relatively stable false lumen, cautious anticoagulation with low molecular weight heparin combined with dynamic monitoring and staged surgical strategies can control thrombus risk while avoiding aortic dissection rupture. This case provides preliminary experience for managing such complex cases, though further clinical research is needed for validation.

Sugar transporters (STs) are critical biological macromolecules that involved in the regulation of fungal development and responses to abiotic stresses. While monosaccharide- and sucrose-specific transporters have been extensively characterized in yeast and plants, knowledge of STs in filamentous fungi remains limited. Here, through genome mining, we identified 173 STs in the salt-tolerant fungus Aspergillus sydowii H-1 and classified them into nine subgroups. Notably, 37 of these STs showed active responses to high-salt stress, with the glycerol transporter AsSTL exhibiting particularly strong induction. Protein-protein interaction analysis revealed that AsSTL is regulated by multiple mitogen-activated protein kinases, including Hog1, Ssk22, Ste11, Pbs2 and Fus3. Functional validation via Hog1 knockout experiments demonstrated that Hog1 positively regulates AsSTL. Localization studies revealed that AsSTL localizes to the plasma membrane, where it mediates glycerol absorption. The deletion of AsSTL significantly impaired glycerol uptake, conidial production, growth, and stress tolerance to NaCl and H₂O₂ stress, and purple pigment synthesis. These findings establish AsSTL as a key Hog1-reglulated protein, essential for glycerol homeostasis, salt stress adaptation, and secondary metabolite production in A. sydowii H-1. This study highlights the critical roles of ST proteins in fungal stress responses and provides insights into potential mechanisms for improving stress tolerance in fungi.