Background: The incidence of hyperlipidemic acute pancreatitis (HLAP) has been increasing annually. However, population-based morbidity assessments need to be updated. Early, rapid, and effective lipid-lowering may minimize pancreatic injury and improve clinical prognosis. It is essential to choose the proper treatment. However, treatment options for HLAP are controversial, and there is no uniform treatment protocol. Methods: In this retrospective study, 127 patients with hyperlipidemic severe acute pancreatitis (HL-SAP) were registered from January 2018 to December 2022 at the General Hospital of Ningxia Medical University. Medical and radiological records of hospitalized patients were collected to determine clinical features, severity, complications, mortality, recurrence rate, and treatment. Risk factors for HL-SAP were analyzed using multifactorial logistic regression. A propensity score matching method was used to compare the clinical outcomes of standard and plasma exchange therapies. Results: In this research, the prevalence of HLAP increased about 1.6 times, and the prevalence of HL-SAP was 50.60%. HL-SAP occurs most often in people between the ages of 30 and 39. Amylase exceeded 110 U/L in 84.3% of patients and 330 U/L in only 47.2%. 83.5% of HL-SAP patients had fatty livers and high body mass index (BMI). A total of 48.0% of patients experienced organ failure, ICU treatment (55.1%), recurrence (33.1%), and death (21.3%). Between the hyperlipidemic group and the biliary group in terms of age, gender, BMI, fatty liver, pleural effusion, abdominal constriction syndrome (ACS), multiple organ dysfunction syndrome (MODS), length of hospital, medical costs, morbidity and mortality, triglyceride, cholesterol, creatinine, blood glucose, D-dimer, amylase, albumin, lactate dehydrogenase, serum phosphorus, serum calcium, oxygenation index, and recurrence rate were statistically significant (P < 0.05). High BMI (P = 0.0038, odds ratio (OR) = 1.336, 95%CI: 0.99–1.804), high C-reactive protein (CRP) (P = 0.022, OR = 1.011, 95%CI: 1.003–1.019), low calcium (P = 0.003, OR = 0.016, 95%CI. 0.001–0.239), low albumin (P = 0.012, OR = 0.045, 95%CI: -0.062-0.192), and high D-dimer (P = 0.041, OR = 0.619, 95%CI: 0.053–2.510) were risk factors for HL-SAP, according to multifactorial logistic regression analysis. Adjusted for propensity score matching (PSM), Serum triglyceride (TG) was significantly lower in both the standard treatment (P < 0.001) and plasma exchange (P < 0.001) groups at 48 h compared with the initial test after the attack. Clearance (83.20% ± 0.0% vs. 84.4% ± 0.0%, P = 0.531), length of hospital stay (19.9 ± 4.9 vs. 19.8 ± 11.1, P = 0.092), and death (26.3% vs. 23.6%, P = 0.791) showed no difference between the two groups. However, the difference in medical costs(P = 0.039)between the two groups was statistically significant. Conclusion: The incidence of HLAP exhibited a significant increase, remarkable severity, recurrent trend, and mortality. High BMI, high CRP, low calcium, low albumin, and high D-dimer are risk factors for HL-SAP. Compared with standardized treatment, plasma exchange does not improve the prognosis of HL-SAP patients, and standardized treatment is equally effective, safe, and low-cost in early treatment.

A multifunctional polysaccharide-based hydrogel was developed for liver regeneration by integrating sodium alginate (SA), sodium lignosulfonate (SL), and 3D bioprinting technology. The hydrogel incorporated FH1@SA microspheres and CaO₂@ZIF-8@SL nanoparticles to reconstruct the hepatic microenvironment through coordinated oxygen generation, antioxidant activity, and anti-inflammatory modulation. The FH1@SA microspheres enabled sustained release of FH1, facilitating hepatocyte adaptation to hypoxia and promoting functional recovery. Meanwhile, the CaO₂@ZIF-8@SL nanoparticles achieved controlled oxygen release and pH-responsive degradation, while the lignosulfonate component scavenged reactive oxygen species and mitigated inflammatory stress. The 3D-printed hydrogel exhibited favorable mechanical strength, injectability, and cytocompatibility, effectively supporting hepatocyte proliferation and tissue regeneration. By simultaneously relieving hypoxia and oxidative stress, this polysaccharide hydrogel provides a synergistic strategy for enhancing hepatic repair, offering a promising platform for bioartificial liver construction and treatment of liver injury.

Mitochondrial autophagy, also referred to as mitophagy, clears damaged mitochondria and has dual functions in disease development and liver homeostasis in response to liver pathologies. Mesenchymal stem/stromal cells (MSCs) are most commonly used to treat liver failure because they are easy to obtain and present no ethical problems. However, the molecular mechanisms by which MSCs promote liver failure progression are not fully understood. This study explored the distinct mitophagy states in hepatocytes and macrophages during MSCs therapy. To investigate tissue-specific mitophagy in acute liver failure (ALF), we generated a single-cell transcriptome (scRNA-seq) atlas of liver tissue from healthy mice, ALF mice and human umbilical cord mesenchymal stem/stromal cell (hUC-MSC)-transplanted mice. The data revealed the complex cellular landscape of liver tissue during ALF progression, revealing alterations in metabolic fluxes and mitophagy activation. Through the intersection of single-cell sequencing data with mitophagy-related genes (MRGs), a total of 24 differentially expressed MRGs were identified. Gene Ontology (GO) analysis further revealed that the ubiquitinating enzyme Arih1 was significantly upregulated after MSC transplantation, whereas the mitophagy genes Bnip3L/NIX and Beciln1 were significantly downregulated in mononuclear phagocytes(MPs). Our research demonstrated that during the development of ALF, mitophagy within hepatocytes is suppressed, whereas in MPs, mitophagy is excessively activated. MSCs are capable of alleviating disease progression by modulating the distinct mitophagy states of cells, providing an important resource for investigating mitophagy regulation in hepatic homeostasis and disease development.

BACKGROUND: Bloodstream infections (BSIs) caused by gram-positive cocci (GPC) and gram-negative bacilli (GNB) are major causes of sepsis. However, their distinct effects on host responses remain poorly characterized at the single-cell level. This study used single-cell transcriptomics to define pathogen-specific monocyte heterogeneity in BSIs to identify the mechanisms underlying clinical differences.

Background: The pathogenesis of sepsis-induced cardiomyopathy (SIC) remains unclear, and the lack of effective treatment options results in high mortality rates. There may be interactions between gut microbiota dysbiosis, serum metabolic changes, and SIC; however, research in this area is limited. This study aims to provide a theoretical basis for targeted interventions to improve the gut microbiome, thereby enhancing cardiac function and prognosis in patients with SIC. Methods: This prospective cohort study enrolled 48 septic patients admitted to the intensive care unit (ICU) of a tertiary general hospital in Ningxia, China, between March 2024 and March 2025. Patients were stratified into SIC (n=28) and SEPSIS (n=20) groups. Age- and sex-matched healthy controls (HC, n=10) were also recruited. Fecal samples from all three groups were analyzed via 16S rRNA gene amplicon sequencing, and serum samples from the SIC and SEPSIS groups were analyzed via LC–MS-based untargeted metabolomics. Spearman’s correlations linked microbial and metabolic alterations to echocardiographic parameters and myocardial injury markers. Results: Compared with the SEPSIS and HC groups, the SIC group presented significant differences in both the α and β diversity of the gut microbiota (all P<0.05). Compared with that in the SEPSIS group, the Bacillota/Bacteroidota ratio was significantly lower in the SIC group (P<0.05); compared with the SEPSIS and HC groups, the SIC group presented significantly increased abundances of genera such as Parabacteroides and Clostridium innocuum group and significantly decreased abundances of genera such as Oscillospiraceae_UCG-003 and Lachnospiraceae_UCG-004 (all P<0.05). Forty-nine differential metabolites were identified (VIP≥1, P<0.05): hippuric acid, estrone glucuronide, and TMAO were elevated, while 15-deoxy-Δ12,14-prostaglandin J2 was reduced in the SIC group (all P<0.05). Differential genera/metabolites correlated strongly with SIC diagnostic indicators: e.g., Parabacteroides positively correlated with estrone glucuronide, hippuric acid, and GLS, and negatively with LVEF. Conclusion: Gut microbiota dysbiosis differs between patients with Sepsis-induced cardiomyopathy and healthy individuals or patients with sepsis. Additionally, the serum metabolic profile changes in SIC patients differ from those in patients with sepsis, and these characteristic changes are significantly associated with clinical indicators related to the diagnosis of SIC.