To investigate the structural and functional alterations of intestinal goblet cells and the mucus barrier in rats with hypertriglyceridemia acute pancreatitis (HTG-AP), and to evaluate the potential mechanism involved in the progression to severe HTG-AP. Twenty-four specific pathogen-free male Sprague-Dawley rats were divided into control group, biliary acute pancreatitis (BAP) group, hypertriglyceridemia (HTG) group, and HTG-AP group using a random number table method, with six rats in each group. In the BAP group, the BAP model was established by retrograde injection of 3.5% sodium taurocholate (0.3 mL/min) at 2 mL/kg through the pancreaticobiliary duct. In the HTG group, a polyethylene glycol-polypropylene glycol block copolymer was administered intraperitoneally at 0.50 g/kg once daily for 7 days to establish the HTG model. In the HTG-AP group, after the HTG model had been established, caerulein was administered intraperitoneally at 50 μg/kg once every one hour on day eight, and injections were continued for 7 days to induce HTG-AP. The control group received an equal volume of normal saline (2 mL/kg). All rats were sacrificed at 24 hours after modeling. Hematoxylin-eosin (HE) staining was performed to assess histopathological changes in the pancreas, ileum, and colon, and pathological scores were calculated. Western blotting was performed to determine the expressions of CD4, CD8, ZO-1, and Occludin. Enzyme linked immunosorbent assay (ELISA) was performed to measure secretory immunoglobulin A (sIgA) level in intestinal mucosa. Alcian blue/periodic acid-Schiff (AB/PAS) staining was performed to evaluate mucus layer structure and to measure mucus layer thickness and goblet cell number. Double immunofluorescence staining was performed to detect NOD-like receptor protein 6 (NLRP6) and mucin 2 (MUC2) expression and their colocalization. 1) Compared with the control group, the BAP, HTG, and HTG-AP groups showed intestinal inflammatory changes of varying degrees. The HTG-AP group exhibited the most severe intestinal inflammation, accompanied by extensive acinar necrosis, hemorrhage, and marked edema; the pancreatic histopathological score was higher in the HTG-AP group than that in the BAP group (12.95±1.31 vs. 7.30±1.59, P<0.05). In addition, inflammatory cell infiltration in the ileum and colon extended through the full thickness of the intestinal wall, with massive loss of crypt goblet cells. 2) Intestinal immune function and barrier function were impaired in the BAP, HTG, and HTG-AP groups, and the impairment was most pronounced in the HTG-AP group. Compared with the BAP group, the HTG-AP group showed higher CD4 and CD8 expressions in the ileum (CD4/β-actin: 6.664±0.034 vs. 3.524±0.042, CD8/β-actin: 3.135±0.034 vs. 1.118±0.028, both P<0.05), a lower sIgA level in ileal mucosal supernatant (ng/L: 150.00±44.72 vs. 410.00±54.89, P<0.05), and decreased ZO-1 and Occludin expressions in the colon (ZO-1/β-actin: 0.46±0.13 vs. 0.59±0.20, Occludin/β-actin: 0.33±0.12 vs. 0.60±0.07, both P<0.05). 3) AB/PAS staining showed that the mucus layer of the colonic mucosal epithelium was altered in the BAP, HTG, and HTG-AP groups; the HTG-AP group exhibited severe mucus layer injury with more evident mucus depletion in goblet cells. Compared with the BAP group, the HTG-AP group had a thinner colonic mucus layer (μm: 10.20±4.69 vs. 16.80±4.38, P<0.05) and fewer mucus-containing goblet cells (cells/crypt: 4.30±1.34 vs. 7.52±1.93, P<0.05). 4) Double immunofluorescence staining showed that, compared with the control group, colonic NLRP6 and MUC2 expression and their colocalization signals were decreased in the BAP, HTG, and HTG-AP groups, and the decrease was most evident in the HTG-AP group. Disruption of the intestinal mucus barrier may be an important mechanism contributing to the progression to severe HTG-AP, and the NLRP6/MUC2 axis may serve as a potential therapeutic target.
Cardiac arrest is a prevalent clinical emergency characterized by its high incidence, sudden onset, challenges in resuscitation, and low success rates. Timely and effective cardiopulmonary resuscitation (CPR) is the key to improving the success rate of patient rescue. Currently, manual CPR serves as the primary clinical approach. Due to the high intensity of physical exertion, the depth and frequency of external chest compression decrease with the extension of CPR time, resulting in a lower success rate of CPR. Although existing mechanical resuscitation devices address issues such as compression frequency, amplitude, and reduce the physical burden on medical staff, they are associated with complications for patients (e.g., sternum and rib fractures). Additionally, these devices are often expensive, bulky, and reliant on external power sources, limiting their clinical utility. To address these issues, the medical staff of the department of critical care medicine of the Second Affiliated Hospital of Zunyi Medical University designed a cardiac resuscitation device specifically for critical care and obtained a National Utility Model Patent of China (patent number: ZL 2019 2 2003762.8). The device is 25 cm long, 20 cm wide, 25 cm high, and weighs approximately 2.5 kg. On one side of the main body, there are longitudinally arranged adjustment knobs, a power switch, a power jack, and a heat dissipation window. The left side of the device features a touchscreen display, which shows parameters including screen contrast, alarm volume, defibrillation energy, time, battery level, heart rate, and electrocardiogram waveforms. Below the touchscreen, a physical control interface-comprising up/down keys, left/right keys, and function buttons-allows adjustment of all parameters displayed on the screen. To the right of the control interface, there is a shock current device that can be directly removed and placed closely to the patient for defibrillation treatment. There is a 48 V lithium battery inside the device, and a solar panel on the other side wall of the main body, which can automatically charge via sunlight. There is a strap on the other side wall of the main body, which contains a flexible sponge layer for comfortable wearing. The upper wall of the main body is equipped with a handle for easy carrying. The heartbeat restorer for critical care medicine has a simple structure, small size, light weight, low cost, easy operation, and strong mobility. It can meet the needs of cardiac arrest patients in different places, especially those in disaster areas who cannot be sent to the hospital for rescue in a timely manner. It is worthy of clinical promotion and application.
To analyze the clinical features, treatment mode selection, factors influencing prognosis and current clinical application of continuous blood purification (CBP) in critically ill children in a tertiary hospital in the Ningbo region, and provide evidence for optimizing critical care strategies for pediatric patients. A retrospective cohort study was conducted, enrolling 395 critically ill children who underwent CBP treatment at the Women and Children's Hospital of Ningbo University from January 2017 to December 2024. Clinical data of the children were collected and analyzed, including general demographic characteristics, distribution of primary diseases, CBP treatment-related parameters (including vascular access, anticoagulation method, and treatment mode), and prognosis. The children were divided into the survival group and the non-survival group according to their prognosis, and further stratified into the 2017-2020 group and the 2021-2024 group based on the treatment period. Clinical characteristics, intervention measures, and prognosis-related indicators were compared among different groups to explore the temporal trends in CBP application and the influencing factors of prognosis. A total of 395 children were enrolled, including 219 males and 176 females. The median age was 78 (24, 157) months, and the median body weight was 18 (12, 40) kg. Among them, 305 cases survived and 90 cases died, with a mortality of 22.8%. According to the treatment period, 134 cases were assigned to the 2017-2020 group and 261 cases to the 2021-2024 group. The main primary diseases were sepsis [27.1% (107/395)], renal failure [25.3% (100/395)], and acute poisoning [24.1% (95/395)] in order of frequency. The predominant CBP treatment mode was continuous veno-venous hemodiafiltration [CVVHDF; 60.8% (240/395), followed by hemoperfusion [HP; 15.7% (62/395)], therapeutic plasma exchange [TPE; 9.1% (36/395)], and hybrid blood purification treatment [HBPT; 14.4% (57/395)]. The right internal jugular vein was the main vascular access [51.1% (202/395)], and systemic heparin anticoagulation was the primary anticoagulation method [93.7% (370/395)]. The overall incidence of complications was 15.2% (60/395), mainly including thrombocytopenia and catheter-related infection. Compared with the survival group, the non-survival group had significantly younger age [months: 38.0 (6.0, 72.5) vs. 100.0 (30.0, 159.0)], lower body weight [kg: 12.3 (7.0, 20.0) vs. 22.5 (13.0, 43.0)], higher proportions of combined multiple organ dysfunction syndrome [MODS; 95.6% (86/90) vs. 22.0% (67/305)], use of vasoactive drugs [92.2% (83/90) vs. 20.3% (62/305)], mechanical ventilation [100% (90/90) vs. 40.7% (124/305)], and extracorporeal membrane oxygenation (ECMO) support [5.6% (5/90) vs. 0.7% (2/305)], as well as shorter hospital stay [days: 9.0 (3.8, 16.3) vs. 15.0 (9.0, 26.0)], all P<0.05. Additionally, the non-survival group had higher proportions of primary diseases including necrotizing encephalopathy, hypernatremia, hemophagocytic syndrome, and post-congenital heart disease surgery (all P<0.05). Compared with the 2017-2020 group, the 2021-2024 group showed significantly increased age [months: 102.0 (28.0, 160.5) vs. 42.0 (17.0, 102.0)] and body weight [kg: 18.5 (13.0, 45.0) vs. 15.0 (11.0, 29.0)], decreased overall mortality rate [18.8% (49/261) vs. 30.6% (41/134)], higher proportion of right internal jugular vein as vascular access, increased ratio of regional citrate anticoagulation [5.7% (15/261) vs. 0.7% (1/134)], reduced proportion of combined MODS [33.0% (86/261) vs. 50.0% (67/134)], elevated rate of ECMO support [2.7% (7/261) vs. 0% (0/134)], and shortened hospital stay [days: 11.0 (6.0, 21.0) vs. 17.0 (12.0, 34.0)], all P<0.05. Moreover, the 2021-2024 group had a lower proportion of sepsis and a higher proportion of renal failure among primary diseases (both P<0.05). CBP represents a valuable therapeutic modality for critically ill children. Its efficacy is closely linked to patient age, the underlying disease, and the extent of organ support required. Optimizing anticoagulation strategies, improving vascular access selection, and implementing early intervention hold promise for further reducing mortality and improving prognosis.
To investigate the association between acute kidney injury (AKI) and the gut microbiota by integrating 16S sequencing analysis with mendelian randomization (MR). 1) MR analysis: The genome-wide association study (GWAS) dataset for AKI from the FinnGen consortium and the GWAS dataset for gut microbiota composition from the Dutch Microbiome Project were selected to screen single nucleotide polymorphism (SNP) associated with AKI as instrumental variable (IV) for genetic variation, using AKI as the exposure factor. Potential causal associations between AKI and gut microbiota were analyzed using a two-sample, one-way MR analysis with the primary analysis method of inverse variance weighted (IVW). Heterogeneity analysis was performed using the Cochran Q test. Potential pleiotropy was assessed using the MR-Egger intercept test. Sensitivity analysis was performed using the leave-one-out test. 2) Clinical cohort study: Consecutive patients admitted to the intensive care unit (ICU) of Qingdao Municipal Hospital between December 2024 and March 2025 were prospectively enrolled. Patients were classified into the AKI group or the non-AKI group based on the occurrence of AKI during their ICU stay, according to the diagnostic criteria from Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guidelines (2012). Baseline clinical data were collected within 48 hours of ICU admission, including gender, age, height, weight, body mass index (BMI), major comorbidities, vital signs, serum creatinine (SCr), blood routine, C-reactive protein (CRP), interleukin-6 (IL-6), etc. Anal swabs were collected from patients within 48 hours of ICU admission for 16S rDNA high-throughput sequencing. Significant difference analysis and linear discriminant analysis effect size (LEfSe) were performed to characterize the gut microbiota profile in AKI patients and to further validate the findings from the MR analysis. 1) MR analysis results: Using the GWAS summary statistics for gut microbiota and AKI, the MR analysis revealed that the genetic liability to AKI was associated with decreased abundance in six gut microbial taxa and increased abundance in one taxon. IVW analysis showed that at the genus level, genetic susceptibility to AKI was associated with lower abundance of Collinsella (β=-0.144, P=0.029), Lachnospiraceaenoname (β=-0.131, P=0.040), Roseburia (β=-0.126, P=0.047), and Parasutterella (β=-0.198, P=0.023). At the species level, AKI genetic susceptibility was linked to reduced abundance of Parasutterellaexcrementihominis (β=-0.197, P=0.024) and Roseburia unclassified (β=-0.280, P=0.012), while being associated with increased abundance of Bacteroidesintestinalis (β=0.358, P=0.013). Cochran Q test showed no heterogeneity, MR-Egger intercept test revealed no pleiotropy, and leave-one-out analysis verified the robustness of the results. 2) Clinical cohort study results: A total of 129 patients were initially enrolled. After excluding 25 patients with incomplete clinical data and 10 whose samples failed to generate sufficient 16S rDNA gene amplification for sequencing, 94 patients were included in the final analysis comprising 72 cases in the AKI group and 22 cases in the non-AKI group. Apart from higher SCr levels in the AKI group than those in the non-AKI group, no statistically significant differences were observed in other baseline clinical characteristics between the two groups. 16S rDNA high-throughput sequencing yielded 6 868 647 high-quality reads, which were clustered into 13 025 amplicon sequence variant (ASV). Significant difference analysis at the species level showed that, compared with the non-AKI group, patients in the AKI group had a relative enrichment of Streptococcus anginosus and Novosphingobium sp. B0.09-8. Conversely, the relative abundances of uncultured Prevotellasp., Alistipesshahii, uncultured Coprococcussp., Collinsellatanakaei, Streptococcus equinus, Alistipesindistinctus, Klebsiellasp. GRB36, and uncultured Oscillospirasp. were significantly lower in the AKI group. LEfSe analysis identified Veillonella unclassified, Ligilactobacillus unclassified, Collinsellatanakaei, Atopobium unclassified, and Streptococcus anginosus as potential biomarkers for the AKI group, whereas Alistipesshahii, uncultured Prevotella sp., and Agathobacter unclassified were more characteristic of the patients in the non-AKI group. The MR analysis suggests that the occurrence of AKI exerts an influence on the gut microbiota profile, characterized by a reduction in the abundance of the genus Collinsella. Findings from the real-world study further indicate significant differences in gut microbiota composition between patients with and without AKI. Overall, the gut microbiota of AKI patients is characterized by an enrichment of pro-inflammatory bacteria and a depletion of commensal symbionts. The genus Collinsellamay may serve as a potential biomarker for AKI.
To investigate the role and underlying mechanism of the protein kinase B (Akt)/sirtuin 3 (SIRT3) signaling pathway in hyperoxia-induced acute lung injury (HALI). 1) In vivo experiments: C57BL/6J mice were randomly assigned to a control group (normoxia) or a HALI group (≥95% oxygen), with six mice in each group. After 24 hours of exposure, lung histopathological changes were evaluated by hematoxylin-eosin (HE) staining, and the lung wet/dry weight (W/D) ratio was calculated. Apoptosis-related proteins in total lung lysates (cleaved caspase-3, Bax, and Bcl-2) and mitophagy-related proteins in mitochondrial fractions [p62, Beclin-1, and microtubule-associated protein light chain 3-II/I (LC3-II/I)] were measured by Western blotting. 2) In vitro experiments: Mouse type II alveolar epithelial cells (AEC II) MLE-12 in the logarithmic growth phase were used. Cells were divided into control group, H2O2 group (500 μmol/L H2O2 to mimic the HALI), and H2O2+3-methyladenine (3-MA) group. After 24 hours, cell viability was assessed by cell counting kit-8 (CCK-8), apoptosis was quantified by flow cytometry, and related proteins were detected by Western blotting. To explore the role of mitophagy in H2O2-induced apoptosis, cells were pretreated 2 hours before modeling with 10 μmol/L 3-MA, a mitophagy inhibitor. In additional experiments, cells were divided into control, H2O2, H2O2+Ly294002, and H2O2+SC-79 groups; 10 μmol/L Ly294002 (Akt inhibitor) or SC-79 (Akt activator) was added 2 hours before modeling to investigate the involvement of Akt signaling in mitophagy-mediated protection against H2O2-induced apoptosis. SIRT3 was further knocked down to determine whether it functions downstream of Akt in this protective pathway. 1) In vivo results: Under light microscopy, the control group exhibited clear and regularly arranged alveolar structures, whereas the HALI group showed marked inflammatory cell infiltration, edema, and thickened alveolar walls. The lung W/D ratio was higher in the HALI group than that in the control group (11.5±1.1 vs. 5.4±0.8, P < 0.05). Compared with the control group, the HALI group showed increased expression of pro-apoptotic proteins Bax, cleaved caspase-3 [Bax (Bax/GAPDH): 0.49±0.06 vs. 0.18±0.05, cleaved caspase-3 (cleaved caspase-3/GAPDH): 1.71±0.07 vs. 0.63±0.06, both P<0.05], and decreased expression of anti-apoptotic protein Bcl-2 (Bcl-2/GAPDH: 0.39±0.05 vs. 1.03±0.08, P<0.05). Mitophagy-related markers were also altered, with increased LC3-II/I ratio and Beclin-1 [LC3-II/I ratio: 2.16±0.06 vs. 1.10±0.10, Beclin-1 (Beclin-1/GAPDH): 1.04±0.08 vs. 0.42±0.04, both P<0.05], and decreased p62 (p62/GAPDH: 0.41±0.04 vs. 0.99±0.08, P<0.05), suggesting that apoptosis and mitophagy may be involved in HALI progression. 2) In vitro results: Compared with the control group, H2O2 treatment reduced cell viability, Bcl-2, and p62 [cell viability: (48.45±6.48)% vs. (96.80±2.27)%, Bcl-2 (Bcl-2/GAPDH): 0.57±0.07 vs. 0.82±0.05, p62 (p62/GAPDH): 0.39±0.06 vs. 1.03±0.07, all P<0.05], while increasing apoptosis rate, LC3-II/I ratio, Beclin-1, Bax, and cleaved caspase-3 [apoptosis rate: (16.12±1.76)% vs. (6.54±0.75)%, LC3-II/I ratio: 2.05±0.12 vs. 0.97±0.07, Beclin-1 (Beclin-1/GAPDH): 0.69±0.05 vs. 0.18±0.03, Bax (Bax/GAPDH): 0.53±0.07 vs. 0.29±0.04, cleaved caspase-3 (cleaved caspase-3/GAPDH): 0.63±0.04 vs. 0.19±0.04, all P<0.05]. Compared with the H2O2 group, 3-MA pretreatment further aggravated apoptosis [cell viability: (34.00±5.05)% vs. (48.45±6.48)%, apoptosis rate: (22.21±3.05)% vs. (16.12±1.76)%, cleaved caspase-3 (cleaved caspase-3/GAPDH): 1.03±0.09 vs. 0.63±0.04, Bax (Bax/GAPDH): 0.69±0.07 vs. 0.53±0.07, Bcl-2 (Bcl-2/GAPDH): 0.30±0.04 vs. 0.57±0.07, p62 (p62/GAPDH): 0.64±0.05 vs. 0.39±0.06, Beclin-1 (Beclin-1/GAPDH): 0.34±0.04 vs. 0.69±0.05, LC3-II/I ratio: 1.64±0.05 vs. 2.05±0.12, all P<0.05], indicating that inhibition of mitophagy promotes MLE-12 apoptosis. Similar changes were observed after adding the Akt inhibitor Ly294002, whereas the Akt activator SC-79 produced effects opposite to those of 3-MA, suggesting that Akt activation promotes mitophagy and thereby suppresses apoptosis. Compared with the H2O2+SC-79 group, SIRT3 knockdown (H2O2+SC-79+siSIRT3) increased apoptosis rate, cleaved caspase-3, Bax, and p62 [apoptosis rate: (10.30±0.96)% vs. (8.82±0.95)%, cleaved caspase-3 (cleaved caspase-3/GAPDH): 0.69±0.05 vs. 0.44±0.05, Bax (Bax/GAPDH): 0.99±0.06 vs. 0.49±0.04, p62 (p62/GAPDH): 0.59±0.06 vs. 0.38±0.04, all P<0.05], and decreased SIRT3, Bcl-2, and Beclin-1 [SIRT3 (SIRT3/GAPDH): 0.48±0.05 vs. 0.68±0.04, Bcl-2 (Bcl-2/GAPDH): 0.64±0.05 vs. 0.78±0.05, Beclin-1 (Beclin-1/GAPDH): 0.68±0.04 vs. 0.79±0.04, all P<0.05]. These findings indicate that SIRT3 knockdown attenuates SC-79-induced mitophagy and enhances apoptosis, supporting SIRT3 as an important downstream effector of the Akt pathway. Activation of the Akt/SIRT3 signaling pathway promotes mitophagy to inhibit alveolar epithelial cell apoptosis, thereby attenuating HALI.
To investigate the factors influencing the apnea test (AT) and its clinical effects in brain death determination under updated criteria, and to provide evidence for optimizing and reducing the risk of false-negative results and complications. Based on the data from the Anhui Provincial Brain Injury Evaluation Quality Control Center, the data of brain-dead patients who completed AT with an off ventilator duration of 5-11 minutes were analyzed retrospectively. Data from January 2018 to March 2025 were used as the model development cohort, and the data from June to December 2025 were used as the external validation cohort. Demographic characteristics, clinical data, evaluation and examination indicators, AT operation details, etc. were extracted using standardized case report form. Temporal trends of AT positive rate and the incidences of severe hypercapnia, acidosis, hypoxemia and other complications when offline for 5-11 minutes were evaluated using the Cochran-Armitage trend test, and the key factors affecting the change of arterial partial pressure of carbon dioxide (PaCO2) and pH were analyzed by multiple linear regression model. The model development cohort included 384 patients with brain death, and the external validation cohort included 47 patients with brain death. There was no significant difference in baseline characteristics between the two cohorts (all P>0.05). With the extension of offline time, the positive rate of AT was gradually increased (Cochran-Armitage trend test: Z=3.52, P<0.001), rising from 76.5% (13/17) at 5 minutes to 91.7% (11/12) at 7 minutes, and plateaued after 7 minutes. The trend analysis of complications in the same period showed that the incidence of severe hypercapnia (PaCO2>80 mmHg, 1 mmHg=0.133 kPa) showed a significant increasing trend (Z=4.09, P<0.001), and was higher at 10 minutes than at 9 minutes [44.7% (59/132) vs. 21.6% (8/37), P<0.05]. Severe acidosis (pH<7.20) became more frequent over time (Z=-4.69, P<0.001), and was higher at 10 minutes than at 7 minutes [73.5% (97/132) vs. 58.3% (7/12), P<0.05]. The incidence of hypoxemia [arterial partial pressure of oxygen (PaO2) <60 mmHg] showed a decreasing trend (Z=-5.21, P<0.001), with no statistically significant difference in incidence between 7-11 minutes (F=0.859, P=0.525). The prediction model was established by multiple regression, indicated that offline time, pre-AT PaCO2, pre-AT pH, heart rate, and body weight collectively influenced post-AT PaCO2 (R2=0.284, P<0.001). Offline time, pre-AT pH, heart rate, and hemoglobin were associated with post-AT pH (R2=0.455, P<0.001). External validation indicated good performance for the pH model (mean absolute error was 0.038, R2=0.69) and acceptable performance for the PaCO2 model (mean absolute error was 6.21 mmHg, R2=0.62). When implementing the dual-criteria standard (PaCO2 and pH), an offline time window of 7 to 9 minutes can balance diagnostic efficacy for brain death with patient safety. Pre-intervention strategies, such as lowering pH or raising PaCO2 before disconnection, may shorten the time needed to reach AT targets. However, should be guided by a comprehensive assessment of individualized patient factors, including baseline pH, PaCO2, heart rate, hemoglobin, and body weight.
To explore the interventional effects of a targeted diaphragmatic function exercise bundle strategy, guided by ultrasound assessment, on nutritional status, diaphragmatic function, muscle strength, and hospital stay of mechanically ventilated patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) complicated by type II respiratory failure. A randomized controlled study was conducted. Patients with AECOPD complicated by type II respiratory failure who received mechanical ventilation in the Department of Critical Care Medicine, the Second Hospital of Tianjin Medical University from January to December 2024 were enrolled. Using a random number table, patients were divided into an experimental group and a control group. The control group received routine intensive care unit (ICU) treatment and nursing care. On the basis of routine care, the experimental group received a targeted diaphragmatic function exercise bundle strategy based on ultrasound assessment, including limb function exercises and respiratory function training. The duration and intensity of the exercises were adjusted according to the patient's vital signs, clinical condition, tolerance, and daily improvement in diaphragmatic function. The following indicators were compared between the two groups before the intervention and on the 7th day of intervention: nutritional indicators [albumin, total protein, hemoglobin, body mass index (BMI), Nutritional Risk Screening 2002 (NRS2002) score]; diaphragmatic function (diaphragmatic excursion, diaphragmatic thickness); blood gas analysis indicators (pH value, arterial partial pressure of oxygen, arterial partial pressure of carbon dioxide, base excess, lactate, alveolar-arterial oxygen gradient); and muscle strength. The duration of mechanical ventilation, length of ICU stay, and total hospital stay were also compared between the two groups. A total of 134 patients were finally enrolled, including 66 in the experimental group and 68 in the control group. There were no statistically significant differences in baseline data including gender, age, Acute Physiology and Chronic Health Evaluation II, nutritional indicators, blood gas analysis parameters, diaphragmatic excursion, diaphragmatic thickness, and muscle strength between the two groups (all P>0.05). Compared with before intervention, both groups showed varying degrees of improvement in diaphragmatic function indicators, blood gas analysis indicators, and muscle strength on the 7th day of intervention, but nutritional indicators decreased. On the 7th day of intervention, the experimental group had better nutritional indicators (albumin, total protein, hemoglobin, and BMI) than the control group [albumin (g/L): 27.49±3.78 vs. 26.03±3.76, total protein (g/L): 55.84±6.17 vs. 53.42±6.22, hemoglobin (g/L): 105.10±24.74 vs. 96.80±21.17, BMI (kg/m2): 24.84±2.55 vs. 24.12±1.13, all P<0.05]. The improvements in diaphragmatic excursion and diaphragmatic thickness were greater in the experimental group than in the control group [difference in diaphragmatic excursion before and after intervention (cm): 0.182±0.030 vs. 0.104±0.020; difference in diaphragmatic thickness before intervention and after intervention (cm): 0.023±0.004 vs. 0.014±0.002, both P<0.05], and muscle strength was enhanced in the experimental group compared with the control group (χ 2=21.860, P=0.001), whereas there were still no statistically significant differences in blood gas analysis indicators between the two groups (all P>0.05). Compared with the control group, the experimental group had a significantly shorter duration of mechanical ventilation [hours: 137.5 (90.8, 202.2) vs. 162.5 (92.5, 263.8)], shorter length of ICU stay [days: 9.0 (5.8, 14.5) vs. 11.0 (7.0, 18.0)], shorter total hospital stay [days: 12.0 (7.0, 20.0) vs. 17.0 (10.0, 23.5)], and a higher weaning success rate (89% vs. 76%), with all differences being statistically significant (all P<0.05). Implementation of the targeted diaphragmatic function exercise bundle strategy based on ultrasound assessment can effectively improve nutritional status and diaphragmatic function, enhance muscle strength, and shorten the duration of mechanical ventilation and hospital stay in mechanically ventilated patients with AECOPD complicated by type II respiratory failure. It can serve as an effective adjunctive treatment for these patients.
Extracorporeal membrane oxygenation (ECMO) is a vital cardiopulmonary life support technology and one of the key therapeutic measures for extracorporeal life support in critically ill patients. To secure the cannula and prevent catheter-related bloodstream infections, the current clinical practice involves covering the catheter puncture site locally with a sterile transparent dressing. However, due to the large diameter of ECMO cannulas, inadequate shaping during dressing application can compromise the seal of the dressing, increasing the risk of infection. Simultaneously, direct contact of the cannula with the patient's skin can easily lead to local device-related pressure injuries. Furthermore, the large surface area of ECMO dressings and varying levels of skill among healthcare professionals in shaping the dressings further compromise the effectiveness of fixation. To address the aforementioned issues, the department of critical care medicine at Zhongda Hospital affiliated with Southeast University has invented a moldable applicator for securing ECMO cannulas, which has been granted a National Utility Model Patent of China (patent number: ZL 2022 2 1954859.2). The device is shaped like scissors and primarily consists of two symmetrically crossing clamping bodies, a connecting part, and a handle. The cross-section of each clamping body is semi-circular. Its hard outer shell is adhesively bonded to an internal soft cushion, ensuring airtight adaptation to catheters of different sizes, thus forming an "Ω"-shaped lifting platform to effectively prevent potential infection and pressure injury risks. The connecting part is equipped with a recoil component-when catheter shaping is complete, releasing the handle causes the clamps to automatically open, facilitating the next step in the procedure for nurses. The handle is designed with anti-slip finger rings, enhancing grip stability and ensuring effective anti-slip performance. With its practical design and user-friendly operation, the product helps prevent infection risks, reduce pressure injuries, and improve nursing efficiency, demonstrating significant value for clinical promotion.
To investigate the relationship between changes in serum thyroid hormone levels and postoperative acute kidney injury (AKI) as well as the severity of AKI in patients with acute type A aortic dissection (ATAAD), and to evaluate their predictive value for in-hospital mortality. A retrospective study was conducted. Patients who underwent surgery for ATAAD and received treatment in the Department of Intensive Care Medicine of Nanjing Hospital Affiliated to Nanjing Medical University from January 2021 to December 2023 were enrolled. General information, thyroid function, biochemical indicators, blood routine, procalcitonin, coagulation function and other data were collected. Patients were divided into AKI group and non-AKI group based on whether AKI occurred after surgery. In addition, patients were divided into NTIS group and non-NTIS group based on whether they developed non-thyroidal illness syndrome (NTIS). The factors associated with AKI and the impact of thyroid hormone levels on the stage of AKI were analyzed. The predictive value of thyroid hormone and serum creatinine (SCr) for in-hospital mortality was analyzed using the receiver operator characteristic curve (ROC curve). A total of 176 postoperative ATAAD patients were enrolled. AKI occurred in 105 patients (59.7%), including 46 cases (26.1%) of stage 1 AKI, 32 cases (18.2%) of stage 2 AKI, and 27 cases (15.3%) of stage 3 AKI. NTIS occurred in 113 patients (64.2%), the incidence of NTIS in the non-AKI group and in patients with stage 1, stage 2, and stage 3 AKI was 54.9% (39/71), 56.5% (26/46), 84.4% (27/32), and 77.8% (21/27), respectively. Compared with the non-AKI group, the AKI group had higher body mass index, proportion of vasopressors and cardiac stimulants used, incidence of pulmonary infection and NTIS, blood transfusion, reoperation, and continuous renal replacement therapy (CRRT), higher predicted mortality and actual mortality, as well as longer total hospital stay and the length of intensive care unit stay, and lower levels of free tri-iodothyronine (FT3), total tri-iodothyronine (TT3), and free thyroxine (FT4), and there were statistically significant differences in SCr, uric acid, blood sodium, alanine transaminase, aspartate transaminase, creatine kinase, MB isoenzyme of creatine kinase, white blood cell count, procalcitonin, platelet count, prothrombin time, activated partial thromboplastin time, and fibrinogen between the two groups (all P<0.05). The NTIS group had higher postoperative day 1, 3, and 5 SCr levels, overall AKI incidence, and incidences of stage 2 and stage 3 AKI than the non-NTIS group (all P<0.05). FT3, TT3, FT4, and total thyroxine (TT4) decreased with increasing severity of AKI stage (all P<0.05), while TSH slightly increased with increasing severity of AKI stage (P>0.05). ROC curve analysis showed that the area under the curve (AUC) and 95% confidence interval (95%CI) of FT3, TT3, and postoperative day 1 SCr for predicting in-hospital mortality were 0.770 (0.636-0.904), 0.812 (0.708-0.916), and 0.719 (0.597-0.840), respectively. The combination of the three had the highest AUC, which was 0.838 (0.732-0.944). The incidence of AKI is relatively high in patients following ATAAD surgery. The decline in FT3 and FT4 levels may contribute to the occurrence and progression of AKI. The lower the thyroid hormone levels, the more severe AKI and the worse the prognosis. FT3 and TT3 combined with postoperative day 1 SCr may serve as auxiliary predictors of in-hospital mortality in ATAAD patients.
To analyze the occurrence and clinical characteristics of poor inguinal incision healing after weaning in patients undergoing peripheral veno-arterial extracorporeal membrane oxygenation (VA-ECMO), and to explore its risk factors and clinical management strategies. A retrospective case-control study was conducted to select VA-ECMO patients admitted to the intensive care unit (ICU) of the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital) from February 2022 to February 2025 as the study objects. All patients were weaned from ECMO under open surgery and were divided into normal incision healing group and poor incision healing group according to the healing of the inguinal incision on the side of ECMO catheterization after weaning. The basic data, clinical parameters and laboratory indicators between the two groups were compared, and the risk factors of poor inguinal incision healing after weaning in patients undergoing VA-ECMO were analyzed by univariate and multivariate Logistic regression analyses. Finally, 41 patients undergoing VA-ECMO were enrolled, including 23 males and 18 females. Among the 41 patients, 27 patients had normal inguinal incision healing, 14 patients had poor inguinal incision healing, and the incidence of poor incision healing was 34%. There were statistically significant differences between the two groups of patients in terms of ECMO catheterization location and ECMO catheterization protocol (both P<0.05). The patients in the poor incision healing group often completed ECMO intubation in the operating room, and most of them chose the unilateral semi-incision catheterization protocol. Compared with the normal incision healing group, the length of ICU stay, the duration of mechanical ventilation and the duration of continuous application of vasoactive drugs in the poor incision healing group were longer [length of ICU stay (days): 29.0 (21.0, 39.0) vs. 15.0 (10.0, 19.0), duration of mechanical ventilation (hours): 454.0 (170.0, 789.0) vs. 134.0 (45.0, 269.0), duration of continuous application of vasoactive drugs (days): 18.5 (6.5, 24.3) vs. 5.0 (2.0, 12.0), all P<0.05], 3-day accumulated fluid balance overload after ECMO weaning [mL: 616.5 (-249.3, 2 148.0) vs. -878.0 (-1 603.0, -387.0), P<0.05], suggesting that the poor healing of inguinal incision after VA-ECMO weaning was related to the above factors. The results of univariate Logistic regression analysis showed that unilateral semi-incision catheterization [odds ratio (OR)=21.000, 95% confidence interval (95%CI) was 2.868-153.754, P=0.003], length of ICU stay>10 days (OR=5.571, 95%CI was 1.042-29.790, P=0.045) and positive 3-day accumulated fluid balance after ECMO weaning (OR=16.133, 95%CI was 3.244-80.224, P=0.001) were the risk factors for poor inguinal incision healing after weaning in patients undergoing VA-ECMO. The variables with statistical significance in univariate Logistic regression analysis were incorporated into the binary multivariate Logistic regression model. The analysis results showed that unilateral semi-incision catheterization (OR=13.203, 95%CI was 1.295-134.632, P=0.029) and positive 3-day accumulated fluid balance after ECMO weaning (OR=14.178, 95%CI was 1.985-101.245, P=0.008) were independent risk factors for poor inguinal incision healing after weaning in patients undergoing VA-ECMO. Fourteen patients with poor healing of inguinal incisions presented with massive exudate from the incision (12 cases), delayed incision healing (7 cases), non-healing of the incision (7 cases), incision infection (4 cases), lymphatic leakage (4 cases), and incision dehiscence (3 cases). In addition to routine dressing change, 12 cases underwent negative pressure sealed drainage (VSD), 7 cases underwent reoperation for debridement, and 2 cases underwent flap repair. Four patients died in the ICU with unhealed incisions, 2 patients had unhealed incisions at the time of discharge referral, and the remaining patients' groin incisions eventually healed. The incidence of poor healing of inguinal incisions after weaning from VA-ECMO is relatively high, mainly manifested as excessive exudate from the incision, delayed incision healing, non-healing of the incision, incision infection, lymphatic leakage, and incision dehiscence. Unilateral semi-incision catheterization and positive 3-day accumulated fluid balance after ECMO weaning are independent risk factors for poor inguinal incision healing in patients undergoing VA-ECMO. Early application of VSD is an effective solution for treating poor incision healing accompanied by a large amount of exudate.
To establish a predictive model for acute kidney injury (AKI) in patients undergoing extracorporeal cardiopulmonary resuscitation (ECPR), and to evaluate and validate its predictive value. A multicenter retrospective cohort study was conducted. 1) The clinical data of the patients undergoing ECPR during cardiopulmonary resuscitation (CPR) admitted to the First Hospital of Jiaxing between January 2016 and August 2024 were collected as the modeling cohort. The clinical data included patient characteristic information, relevant treatment information during ECPR, post-extracorporeal membrane oxygenation (ECMO) operation parameters, and ECMO-related variable information. The patients were divided into an AKI group and a non-AKI group according to the occurrence of AKI during ECMO support. The differences in clinical characteristics between the two groups were compared. Multivariate Logistic regression analysis was used to screen independent risk factors for AKI during ECMO therapy, and a nomogram model was established. The predictive value of the model was evaluated by receiver operator characteristic curve (ROC curve). Internal validation of the model was performed using the Bootstrap method with 1 000 resamplings. The predictive performance of the nomogram model was verified using calibration curves and the Hosmer-Lemeshow test, and the clinical utility of the model was assessed by decision curve analysis (DCA). 2) The clinical data of the patients who received ECPR during CPR admitted to the First People's Hospital of Tongxiang and the First People's Hospital of Pinghu from May 2024 to June 2025 were selected for external validation. The predictive efficacy of the model was evaluated by ROC curve analysis. 1) A total of 108 ECPR patients were finally enrolled in the modeling cohort, among whom 78 developed AKI during ECMO treatment and 30 did not, with an AKI incidence of 72.2%. Compared with the non-AKI group, the patients in the AKI group had higher Sequential Organ Failure Assessment (SOFA) score, serum creatinine (SCr), blood lactic acid, lower procalcitonin (PCT), and longer hypoperfusion time (all P<0.05). There were no significant differences in other clinical data between the two groups. Multivariate Logistic regression analysis showed that increased SOFA score [odds ratio (OR)=1.288, 95% confidence interval (95%CI) was 1.055-1.571, P=0.013], SCr (OR=1.010, 95%CI was 1.002-1.018, P=0.015) and blood lactic acid (OR=1.151, 95%CI was 1.036-1.279, P=0.009), and prolonged hypoperfusion time (OR=1.059, 95%CI was 1.007-1.114, P=0.026) were independent risk factors for AKI during ECMO in ECPR patients. A nomogram prediction model was constructed based on the above independent risk factors. ROC curve analysis showed that the area under the ROC curve (AUC) of the nomogram model for predicting AKI in ECPR patients was 0.858 (95%CI was 0.782-0.934, P<0.001), with a sensitivity of 71.8% and a specificity of 83.3%. After 1 000 Bootstrap resamplings, the C-index was 0.822. The Hosmer-Lemeshow test and calibration curve showed good fitness between the predicted and ideal probabilities (χ2=6.402, P=0.602), indicating favorable model performance. DCA results suggested that using the nomogram model achieved higher net benefit for most patients. 2) A total of 31 patients who received ECPR were enrolled for external validation. There were no significant differences in baseline data such as gender, age, or underlying diseases as well as four core independent risk factors for constructing a nomogram predictive model between the external validation cohort and the primary cohort, meeting the requirements of external validation design. ROC curve analysis showed that the AUC of the nomogram model for predicting AKI in ECPR patients was 0.833 (95%CI was 0.654-1.000, P<0.001), with a sensitivity of 70.0% and a specificity of 85.7%. A nomogram model for predicting AKI in ECPR patients is established based on hypoperfusion time combined with SOFA score, SCr, and blood lactic acid. The model has been confirmed to possess good predictive value through both internal and external validation.
To investigate the predictive value of ultrasound evaluation of intercostal muscle combined with diaphragmatic function for weaning and extubation outcomes in neurocritically ill patients. A retrospective case-control study was performed. Clinical data of patients receiving invasive mechanical ventilation via tracheal intubation admitted to the neurology intensive care unit (ICU) of The First Affiliated Hospital of Wannan Medical University (Yijishan Hospital of Wannan Medical University) from April 2023 to April 2025 were collected. Patients were divided into a weaning failure group and a weaning success group according to weaning and extubation outcomes. General baseline data, eye opening and motor reaction scores before extubation, air leakage volume of tracheal intubation cuff leak test, cough ability before extubation, routine blood test and blood biochemical indicators within 48 hours before extubation, and basic vital signs, respiratory mechanics parameters, arterial blood gas analysis results as well as intercostal muscle function indicators [intercostal muscle thickness at the end of inspiration (ICMTei), intercostal muscle thickness at the end of expiration (ICMTee), thickening fraction of intercostal muscle (TFic)] and diaphragmatic function indicators [diaphragmatic excursion (DE), diaphragmatic thickness at the end of inspiration (DTei), diaphragmatic thickness at the end of expiration (DTee), diaphragmatic thickening fraction (DTF)] assessed by ultrasound at the end of spontaneous breathing trial (SBT) were compared between the two groups. Meanwhile, the inpatient outcome indicators of patients were collected. Binary multivariate Logistic regression analysis was used to screen the influencing factors of weaning and extubation outcomes in neurocritically ill patients undergoing invasive mechanical ventilation via tracheal intubation. Receiver operator characteristic curve (ROC curve) was plotted to analyze the predictive value of the combination of TFic, DE and DTF for weaning and extubation outcomes in neurocritically ill patients undergoing invasive mechanical ventilation via tracheal intubation. A total of 233 neurocritically ill patients undergoing invasive mechanical ventilation via tracheal intubation were initially enrolled. After excluding 40 patients aged<18 years or ≥80 years, 55 patients with treatment abandonment or voluntary discharge, 11 patients with unclear ultrasound images, 5 patients undergoing tracheotomy before extubation and 11 patients with incomplete clinical data, 111 patients were finally included in the analysis, including 32 cases in the weaning failure group and 79 cases in the weaning success group. Univariate analysis showed that there were statistically significant differences in Glasgow Coma Scale (GCS) score at admission, eye opening and motor action scores before extubation, air leakage volume of tracheal intubation cuff leak test, cough ability before extubation, rapid shallow breathing index (RSBI) at the end of SBT (all P<0.05). At the end of SBT, TFic in the weaning failure group was higher than that in the weaning success group [15.76% (13.12%, 21.24%) vs. 10.00% (8.33%, 13.33%), P<0.05], while DE and DTF were lower than those in the weaning success group [DE (cm): 1.10 (1.05, 1.20) vs. 1.36 (1.25, 1.45), DTF: 18.75% (16.85%, 24.75%) vs. 27.27% (22.73%, 31.58%), both P<0.05]. Multivariate Logistic regression analysis showed that elevated TFic [odds ratio (OR)=0.731, 95% confidence interval (95%CI) was 0.583-0.917, P=0.007], elevated DE (OR=4.494, 95%CI was 1.663-12.146, P=0.003) and elevated DTF (OR=1.381, 95%CI was 1.078-1.770, P=0.011) were independent influencing factors for successful weaning and extubation in neurocritically ill patients undergoing invasive mechanical ventilation via tracheal intubation. ROC curve analysis showed that TFic, DE and DTF alone had certain predictive value for successful weaning in neurocritically ill patients undergoing invasive mechanical ventilation via tracheal intubation, and the combined application of the three indicators achieved the highest predictive value, with an area under the ROC curve (AUC) of 0.972 (95%CI was 0.948-0.997, P<0.001), a sensitivity of 88.6% and a specificity of 96.9%. Analysis of hospital outcome indicators showed that length of ICU stay, total length of hospital stay and total mechanical ventilation duration in the weaning failure group were longer than those in the weaning success group [length of ICU stay (days): 31.00 (18.25, 49.25) vs. 20.00 (8.00, 32.00), total length of hospital stay (days): 34.50 (22.00, 50.00) vs. 25.00 (16.00, 37.00), total mechanical ventilation duration (days): 18.50 (12.00, 30.25) vs. 8.00 (3.00, 10.00), all P<0.05]. Ultrasound assessment of TFic combined with DE and DTF has high application value in predicting successful weaning and extubation in neurocritically ill patients.
To identify the risk factors of critical illness-related corticosteroid insufficiency (CIRCI) in patients with sepsis and to construct a nomogram model for predicting the occurrence of CIRCI in septic patients. A case-control study was conducted. A total of 50 patients with sepsis complicated by CIRCI who were admitted to Henan Provincial People's Hospital from January 2018 to December 2023 were enrolled as the CIRCI group. Meanwhile, 150 patients with sepsis but without CIRCI admitted during the same period were randomly selected as the control group. Baseline characteristics, etiologies of sepsis, vital signs, adrenal function indicators, serological parameters, intervention measures, disease severity scores, and prognosis-related outcomes were collected and compared between the two groups. Multivariate Logistic regression and inverse probability of treatment weighting (IPTW) regression analyses were performed to evaluate the correlation between various factors and the occurrence of CIRCI, screen out the influencing factors of CIRCI in septic patients, and construct a nomogram prediction model. The receiver operator characteristic curve (ROC curve) and calibration curve were used to assess the discrimination of the model. The Bootstrap method (with 1 000 repeated samplings) was adopted for internal validation, and the calibration curve was plotted to evaluate the calibration of the model. Decision curve analysis (DCA) was performed to assess the clinical validity of the model. After adjusting for confounding factors, univariate Logistic regression analysis showed that older age, history of type 2 diabetes mellitus, higher white blood cell count (WBC), higher procalcitonin (PCT) level, higher serum K+ level, higher Acute Physiology and Chronic Health Evaluation II (APACHE II), and higher Sequential Organ Failure Assessment (SOFA) were associated with an increased risk of CIRCI, whereas higher serum sodium (Na+) level was associated with a decreased risk of CIRCI (all P<0.05). In addition, CIRCI was associated with longer ICU length of stay, longer duration of mechanical ventilation, as well as higher rates of 28-day mortality and ICU mortality (all P<0.05). Multivariate Logistic regression and IPTW regression analyses revealed that history of type 2 diabetes mellitus [odds ratio (OR)=1.574, 95% confidence interval (95%CI) was 0.558-4.437, P=0.022], elevated PCT level (OR=4.271, 95%CI was 1.637-11.139, P=0.003), elevated serum K+ level (OR=2.115, 95%CI was 0.909-4.921, P=0.044), elevated APACHE II score (OR=1.258, 95%CI was 1.071-1.478, P=0.006), and elevated SOFA score (OR=1.236, 95%CI was 1.049-1.456, P=0.012) were independent risk factors for CIRCI. A nomogram prediction model was constructed based on the above 5 indicators. The ROC curve demonstrated that the model achieved an area under the curve (AUC) of 0.965 (95%CI was 0.942-0.989) for predicting the occurrence of CIRCI. The optimal cut-off value was 0.201, yielding a sensitivity of 92.0% and a specificity of 87.3%, indicating excellent discriminative performance. The calibration curve revealed a C-index of 0.966 and a Dxy statistic of 0.933 in the training cohort, reflecting very high predictive accuracy and strong discriminative ability. The standard error of the C-index was 0.028, supporting the reliability of this estimate. Furthermore, the calibration curve showed excellent agreement with the ideal reference line. DCA curve indicated that the model provided positive net benefit across a predefined threshold probability range of 0.05-0.50 (with the 95%CI based on 1 000 Bootstrap resamples not crossing zero). Notably, at threshold probabilities exceeding the event rate (approximately 0.25), the model outperformed both the treat-all and treat-none strategies. History of type 2 diabetes mellitus, elevated PCT, elevated K+, elevated APACHE II score and elevated SOFA score may be independent risk factors for CIRCI in septic patients. The constructed nomogram prediction model has high accuracy and effectiveness, which can be used for early identification and intervention of CIRCI, and is conducive to improving the prognosis of sepsis patients.
Reports of Hafnia infections in humans are infrequent, and the triad of Hafnia infection complicated by lung abscess and pneumothorax remains rarely documented. On January 25, 2025, a patient with a critical case of invasive Hafnia alvei pneumonia complicated by lung abscess and pneumothorax was admitted to Guangde Traditional Chinese Medicine Hospital. The patient had underlying comorbidities including diabetes mellitus and hepatitis B liver cirrhosis. The medical team identified severe pneumonia and its causative pathogen, Hafnia alvei through detailed examinations. An individualized treatment plan was formulated based on the results of drug susceptibility tests. However, the patient's condition progressed rapidly, and he experienced endotracheal intubation, mechanical ventilation, complicated by shock. Re-examination of imaging after treatment revealed progression of pulmonary cavities, along with the complication of lung abscess and tension pneumothorax. The neurological prognosis was poor after cardiopulmonary resuscitation (CPR), and the patient was discharged voluntarily. The triad of pneumonia, lung abscess, and pneumothorax caused by Hafnia alvei in this case has unique clinical manifestations, suggesting that clinicians should be alert to infections caused by rare pathogens such as Hafnia alvei when facing infected patients with multiple underlying diseases. Early identification of the invasive characteristics of the pathogen (rapidly progressive cavity plus secondary abscess/pneumothorax) is crucial. This case provides diagnostic and therapeutic insights for clinicians encountering similar infections, improving their understanding and management of Hafnia alvei infections.
To investigate the ameliorative effect of irisin on sepsis-associated acute kidney injury (SA-AKI) by inhibiting ferroptosis through the regulation of the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Sixty C57BL/6 mice were divided into four groups using a random number table method: control group, lipopolysaccharide (LPS) group, LPS+irisin group, and LPS+irisin+ML385 (Nrf2 inhibitor) group, with 15 mice in each group. The SA-AKI model was established by intraperitoneal injection of LPS at a dose of 10 mg/kg, while the control group received an equal volume of normal saline. In the LPS+irisin group, irisin (1 μg/kg) was intravenously injected 30 minutes prior to LPS administration. In the LPS+irisin+ML385 group, ML385 (30 mg/kg) was intraperitoneally injected 60 minutes before LPS injection, followed by irisin injection 30 minutes before LPS. All mice were anesthetized and sacrificed 24 hours after modeling. Blood samples were collected from the eyeballs for serum creatinine (SCr) and blood urea nitrogen (BUN) measurement using an automatic biochemical analyzer. Renal tissues were harvested for the following assessments: the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme linked immunosorbent assay (ELISA); histopathological changes were observed under light microscope after hematoxylin-eosin (HE) staining; mitochondrial morphology was observed under transmission electron microscope after uranium acetate staining; protein expressions of glutathione peroxidase 4 (GPX4), acyl-CoA synthetase long-chain family member 4 (ACSL4), Nrf2, and HO-1 were detected by Western blotting; the contents of Fe2+, malondialdehyde (MDA), reduced glutathione (GSH), and relative fluorescence intensity of reactive oxygen species (ROS) were also measured in renal tissues. 1) The levels of SCr, BUN, IL-6, and TNF-α in the LPS, LPS+irisin, and LPS+irisin+ML385 groups were higher than those in the control group (all P<0.05). Compared with the LPS group, the LPS+irisin group showed decreased levels of SCr, BUN, IL-6, and TNF-α [SCr (μmol/L): 31.70±3.94 vs. 65.75±7.02, BUN (mmol/L): 11.03±2.25 vs. 29.23±2.58, IL-6 (ng/L): 239.96±14.93 vs. 1 080.40±20.06, TNF-α (ng/L): 105.85±14.92 vs. 299.12±19.94, all P<0.05]. However, the levels of these indicators in the LPS+irisin+ML385 group were higher than those in the LPS+irisin group (all P<0.05). 2) Light microscopy revealed that compared with the control group, the LPS, LPS+irisin, and LPS+irisin+ML385 groups exhibited varying degrees of renal tubular dilation, tubular cell shedding, cellular vacuolization, and intratubular cast formation, with the most severe damage observed in the LPS group and the mildest damage in the LPS+irisin group. 3) Transmission electron microscopy showed that compared with the control group, the other three groups displayed varying degrees of mitochondrial enlargement, rounding and swelling, sparse and dissolved matrix, and reduced cristae, with the most pronounced changes in the LPS group, while mitochondrial morphology was only mildly altered in the LPS+irisin group. 4) Compared with the control group, the protein expression of GPX4 was decreased, while the protein expressions of Nrf2, HO-1, and ACSL4 were increased in the LPS, LPS+irisin, and LPS+irisin+ML385 groups (all P<0.05). Compared with the LPS group, the LPS+irisin group exhibited increased expression of GPX4, Nrf2, and HO-1, and decreased expression of ACSL4 (GPX4/GAPDH: 0.68±0.07 vs. 0.49±0.03, Nrf2/Lamin B: 1.03±0.04 vs. 0.82±0.06, HO-1/GAPDH: 0.93±0.02 vs. 0.66±0.04, ACSL4/GAPDH: 0.69±0.02 vs. 0.93±0.07, all P<0.05). Compared with the LPS+irisin group, the LPS+irisin+ML385 group showed decreased expressions of GPX4, Nrf2, and HO-1, and increased expression of ACSL4 (all P<0.05). 5) Compared with the control group, the levels of MDA, ROS, and Fe2+; were increased, while the level of GSH was decreased in the LPS, LPS+irisin, and LPS+irisin+ML385 groups (all P<0.05). Compared with the LPS group, the LPS+irisin group exhibited decreased levels of MDA, ROS, and Fe2+, and increased level of GSH [MDA (nmol/mg): 9.35±2.07 vs. 15.65±4.03, ROS (relative fluorescence intensity): 584.26±74.48 vs. 1 655.68±405.71, Fe2+ (nmol/mg): 9.24±3.82 vs. 26.99±7.95, GSH (nmol/mg): 91.50±7.99 vs. 43.13±11.85, all P<0.05]. Compared with the LPS+irisin group, the LPS+irisin+ML385 group showed increased levels of MDA, ROS, and Fe2+, and decreased level of GSH (all P<0.05). Irisin ameliorates LPS-induced SA-AKI in mice by inhibiting ferroptosis through the Nrf2/HO-1 signaling pathway, suggesting that irisin may serve as a potential therapeutic strategy for organ protection in sepsis.
To investigate the predictive value of neutrophil-to-lymphocyte ratio (NLR) combined with glycosylated hemoglobin A1c (HbA1c) for bloodstream infection in patients with pyogenic liver abscess (PLA). A retrospective cohort study was conducted. Patients with PLA admitted to Linyi Central Hospital from January 2020 to June 2024 were enrolled. Clinical data, comorbidities, clinical symptoms, signs, admission laboratory parameters, imaging data, and blood culture results were collected. Patients were divided into a bloodstream infection group (blood culture-positive) and a non-bloodstream infection group (blood culture-negative) according to their blood culture results, and differences in various indicators were compared between two groups. Multivariate Logistic regression analysis was used to identify independent risk factors for bloodstream infection. The receiver operator characteristic curve (ROC curve) was employed to evaluate the predictive value of NLR combined with HbA1c for bloodstream infection in patients with PLA. A total of 124 patients with PLA were enrolled, among whom 48 had positive blood cultures, yielding a positivity rate of 45.2%. The proportion of patients with diabetes, as well as levels of procalcitonin (PCT), HbA1c, and NLR, were higher in the bloodstream infection group than in the non-bloodstream infection group [diabetes proportion: 41.1% vs. 11.8%, PCT (ng/L): 18.98±12.16 vs. 14.19±11.85, HbA1c: 0.939±0.056 vs. 0.053±0.027, NLR: 28.08±13.64 vs. 21.69±11.37, all P<0.05]. Multivariate Logistic regression analysis revealed that elevated HbA1c at admission [odds ratio (OR)=1.289, 95% confidence interval (95%CI) was 1.097-1.513, P=0.002] and elevated NLR (OR=1.041, 95%CI was 1.007-1.075, P=0.016) were independent risk factors for bloodstream infection in patients with PLA. ROC curve analysis demonstrated that the combination of NLR and HbA1c predicted bloodstream infection with an area under the curve (AUC) of 0.824 (95%CI was 0.753-0.896, P<0.001); when the optimal cut-off value of 0.298, the sensitivity was 0.929 and the specificity was 0.603. The combination of NLR and admission HbA1c has predictive value for bloodstream infection in patients with PLA.
To investigate the protective effect of kynurenine 3-monooxygenase (KMO) inhibitor GSK180 against trauma-induced sepsis (TIS)-induced acute kidney injury (AKI) and to explore its underlying mechanism. Male SPF healthy Sprague-Dawley (SD) rats were randomly divided into groups using a random number table. (1) A normal control group, a sham-operated (Sham) group, and TIS groups at 12, 24, and 48 hours were established, and 6 surviving rats were finally retained in each group for statistical analysis. The normal control group received no treatment. The Sham group was subjected only to laparotomy exploration and gentle cecal palpation followed by abdominal closure, and 40 mL/kg normal saline was injected subcutaneously for fluid resuscitation after surgery until the rats recovered voluntary movement. TIS groups were treated with combined injury to establish the TIS-induced AKI model, and postoperative management was identical to that of the Sham group. Samples were collected at each time point to detect inflammatory indicators such as white blood cell count (WBC), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP), as well as serum creatinine (SCr) and blood urea nitrogen (BUN) to evaluate inflammatory response and renal injury. Based on the severity of renal injury, renal tissues of the corresponding groups were harvested for proteomic analysis to screen candidate target proteins for related mechanistic intervention experiments. (2) In the KMO inhibitor intervention experiment, rats were randomly divided into the Sham group, TIS group, and KMO inhibitor intervention group, with 6 surviving rats retained in each group for statistical analysis. Procedures in the Sham and TIS groups were the same as described above; the KMO inhibitor intervention group was intraperitoneally injected with the KMO inhibitor GSK180 (10 mg/kg) at 2 hours after model establishment, while the Sham and TIS groups were intraperitoneally injected with an equal volume of normal saline. The above inflammatory and renal function indicators were detected at 24 hours after surgery. Periodic acid-Schiff (PAS) staining was used to observe histopathological changes of renal tissues. Terminal-deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) staining was adopted to observe cell apoptosis in renal tissues. Mitochondrial ultrastructure changes were examined by transmission electron microscopy. Mitochondrial reactive oxygen species (ROS) and membrane potential were detected by flow cytometry. Western blotting was performed to determine the expression of KMO, mitochondrial dynamics-related proteins [dynamin-related protein 1 (DRP1) and its phosphorylated form at Ser616 (p-DRP1 Ser616), mitofusin 2 (MFN2), optic atrophy protein 1 (OPA1)], and the apoptosis-inducing protein Bcl-2-associated X protein (BAX). (1) Compared with the normal control group, significant inflammatory response and renal function injury were observed in TIS groups at all-time points, and peaked at the 24 hours, indicating the most severe renal injury at this time point. Proteomic analysis showed that KMO expression was upregulated in renal tissues of the TIS 24-hour group compared with the normal control group, which was thus selected as the target for subsequent intervention. (2) The KMO inhibitor intervention experiment showed that compared with the Sham group, the rats in the TIS group exhibited systemic inflammatory response and renal dysfunction. Pathological observations revealed aggravated renal damage, increased cell apoptosis, and ultrastructural damage. The level of intracellular ROS was elevated, mitochondrial membrane potential was decreased, and mitochondrial dynamics were imbalanced. Compared with the TIS group, KMO inhibition could improve both systemic inflammatory response and renal function, the levels of WBC, TNF-α, IL-6, CRP, SCr, and BUN were decreased [WBC (×109/L): 9.87±2.74 vs. 25.10±3.55, TNF-α (ng/L): 213.61±81.47 vs. 820.59±105.13, IL-6 (ng/L): 986.98±105.54 vs. 2 376.28±211.80, CRP (ng/L): 1 149.55±405.60 vs. 3 355.76±439.79, SCr (μmol/L): 57.67±12.36 vs. 129.67±10.52, BUN (mmol/L): 11.63±2.60 vs. 21.53±4.31, all P<0.05], alleviated histopathological changes in the kidney, ameliorated mitochondrial ultrastructural damage in renal cells, reduced mitochondrial ROS levels and stabilized membrane potential, and both cell apoptosis and mitochondrial dynamics balance had been improved, the phosphorylation level of DRP1 Ser616 and BAX expression were both decreased [p-DRP1 Ser616 protein (p-DRP1 Ser616/DRP1): 0.88±0.15 vs. 1.63±0.13, BAX protein (BAX/GAPDH): 1.24±0.13 vs. 2.40±0.26, both P<0.05], accompanied by upregulated expression of MFN2 and OPA1 [MFN2 protein (MFN2/GAPDH): 1.09±0.08 vs. 0.64±0.03, OPA1 protein (OPA1/GAPDH): 1.13±0.07 vs. 0.74±0.14, both P<0.05]. KMO is upregulated in TIS-induced AKI and serves as a key factor mediating renal injury. The KMO inhibitor GSK180 exerts renal protective effects by inhibiting DRP1-mediated mitochondrial fission, promoting MFN2/OPA1-dependent mitochondrial fusion, improving mitochondrial function, and alleviating inflammation, oxidative stress and cell apoptosis.
To evaluate the association and predictive value of mean arterial pressure (MAP) during cardiopulmonary resuscitation (CPR) regarding prognosis in patients with in-hospital cardiac arrest (IHCA). IHCA patients admitted to the emergency department of the Affiliated Hospital of Xuzhou Medical University from January 2020 to December 2022 were enrolled via the emergency medical record system. Based on the time-weighted average mean arterial pressure (TWA-MAP) levels during CPR, patients were divided into a low-level group (TWA-MAP<65 mmHg, 1 mmHg=0.133 kPa), a mid-level group (65 mmHg≤TWA-MAP<85 mmHg), and a high-level group (TWA-MAP≥85 mmHg). The rates of return of spontaneous circulation (ROSC), 3-day survival, and favorable neurological outcome were compared among the three groups. Multivariable binary Logistic regression analysis was used to explore factors influencing ROSC success rate, 3-day survival rate and favorable neurological outcome rate. Generalized additive model (GAM) was employed to analyze and construct exposure-response curves for TWA-MAP in relation to ROSC success rate, 3-day survival rate and favorable neurological outcome rate, respectively. Receiver operator characteristic curve (ROC curve) analysis was applied to evaluate the predictive value. A total of 486 patients were included, with 350 in the low-level group, 63 in the medium-level group, and 73 in the high-level group. There were no significant differences in indicators such as gender, age, medical history, and characteristics of cardiac arrest among the three groups. The ROSC success rate, 3-day survival rate, and favorable neurological outcome rate in the medium and high-level groups were higher than those in the low-level group (ROSC success rate: 82.5%, 75.3% vs. 17.1%; 3-day survival rate: 36.5%, 23.3% vs. 5.1%; favorable neurological outcome rate: 12.7%, 12.3% vs. 1.7%; all P<0.05). There were no significant differences observed between the medium and high-level groups (all P>0.05). Multivariable binary Logistic regression showed that 65 mmHg≤TWA-MAP<85 mmHg during CPR was a protective factor for 3-day survival [odds ratio (OR)=3.040, 95% confidence interval (95%CI) was 1.436-6.437, P=0.004], TWA-MAP≥85 mmHg was identified as a risk factor for mortality within 3 days (OR=0.390, 95%CI was 0.153-0.994, P=0.049). 65 mmHg≤TWA-MAP<85 mmHg served as a protective factor for achieving ROSC (OR=4.421, 95%CI was 1.013-19.280, P=0.048). Neither 65 mmHg≤TWA-MAP<85 mmHg nor TWA-MAP≥85 mmHg were independent predictors of favorable neurological outcome in patients (both P>0.05). Exposure-response curve indicated that ROSC success rate and 3-day survival rate increased with higher TWA-MAP. When TWA-MAP reached 60 mmHg, the ROSC success rate exceeded 60%; when at 80 mmHg, the ROSC success rate reached a plateau of approximately 80%. For 3-day survival, the rate reached 20.3% at a TWA-MAP of 60 mmHg, peaked at 37.2% at 76 mmHg, and declined thereafter. Although the favorable neurological outcome rate trended upward with increasing TWA-MAP, the correlation was not statistically significant. ROC curve analysis demonstrated that TWA-MAP had high predictive value for ROSC [area under the curve (AUC)=0.886, 95%CI was 0.852-0.919]; at a TWA-MAP cut-off of 60 mmHg, sensitivity was 90.7% and specificity was 66.2%. TWA-MAP also had predictive value for 3-day survival, with an AUC of 0.843 (95%CI was 0.777-0.909); at a TWA-MAP cut-off of 60 mmHg, sensitivity was 73.5% and specificity was 79.8%. Maintaining a higher level of MAP during CPR is associated with better survival rate in IHCA patients.
Sepsis is a state of uncontrolled systemic inflammation triggered by infection, characterized by multiple organ dysfunction resulting from dysregulated host immune responses. This pathological process involves not only the direct effects of pathogen invasion but also reflects a vicious cycle where infection triggers an inflammatory storm, leading to organ decompensation. During disease progression, acute respiratory distress syndrome (ARDS), as a typical complication in the terminal stage of sepsis, is closely associated with increased patient mortality and decreased long-term quality of life. Recent evidence indicates that, in addition to primary pulmonary injury, systemic pathological changes such as liver and kidney dysfunction, metabolic imbalance, and coagulation disorders may serve as important contributors to ARDS development through pathways including systemic inflammatory cascades and disruption of vascular endothelial integrity. Notably, the Sequential Organ Failure Assessment (SOFA) score, as a dynamic monitoring tool for sepsis, shows significant correlations between its parameter fluctuations and ARDS progression. However, comprehensive and in-depth research systems are currently lacking regarding the molecular interaction mechanisms, temporal association characteristics, and clinical predictive value between extrapulmonary organ injury and dynamic SOFA score evolution. Based on recent research advances, this article systematically elucidates the following key scientific questions: 1) The pathophysiological mechanisms underlying the transition from sepsis to ARDS; 2) The pathways through which systemic risk factors such as liver and kidney dysfunction act; 3) The strength of association between individual SOFA score components and ARDS development. By analyzing the temporal characteristics of multiple organ failure and the kinetic relationship with respiratory dysfunction, the research focuses on establishing a risk assessment system based on organ injury combination patterns, providing dual clinical guidance: 1) Individualized risk stratification based on organ injury characteristics; 2) Precision intervention strategies targeting specific pathological links. This theoretical framework will promote the transformation of ARDS prevention and treatment from pulmonary protection strategies to collaborative multi-organ management models, ultimately achieving individualized precision diagnosis and treatment for sepsis-associated ARDS.
The fiberoptic bronchoscope, when fully integrated with imaging systems, enables real-time observation of airway structures. It can assist in procedures such as clearing respiratory secretions, tracheal intubation assistance, and bronchoalveolar lavage. It is widely used in various settings, including intensive care unit (ICU), emergency department, anesthesiology, and critical care respiratory department. However, the fiberoptic bronchoscope currently used in clinical practice faces clinical issues such as susceptibility to accidental touch, low operational efficiency, and difficulty in adjusting height. To address these issues, medical staff from the department of critical care medicine of Zhongda Hospital Affiliated to Southeast University have designed a dedicated support stand for fiberoptic bronchoscopy and obtained a National Utility Model Patent of China (ZL 2020 2 3282155.9). The dedicated support stand for fiberoptic bronchoscopy comprises two core components: a telescoping vertical frame and a multifunctional articulating support structure. The apparatus incorporates a telescoping pole system to adapt its height to different operators and integrates multiple functional modules, including a display fixation unit (secured by limit grooves), a bronchoscope temporary storage component (Ω -shaped elastic clamps), and partitioned consumable management, thereby optimizing procedural workflows. A foot-pedal-operated non-contact waste bin ensures safe disposal of medical waste, mitigating cross-contamination risks. The modular design, combined with a 360degree angle rotatable bracket, enables flexible adjustment of operational angles to reduce operator musculoskeletal fatigue. This device was designed to fully consider the convenience of clinical use, aiming to simplify preoperative preparation procedures and enhance operational safety, which helps reduce the risk of scope slippage and contamination. Its structural features make it suitable for various clinical scenarios such as the ICU and emergency department, demonstrating strong potential for practicality.