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Postoperative nausea and vomiting (PONV) remain among the most common and distressing complications following general anaesthesia, significantly affecting patient satisfaction, recovery times, and healthcare costs. Although ondansetron at a dose of 4 mg IV has long been considered the gold standard for PONV prophylaxis, emerging literature suggests that higher doses may improve efficacy in select high-risk populations. However, the relationship between ondansetron dose, anaesthetic regimen, and PONV incidence remains poorly defined, particularly when using a combination of propofol induction and sevoflurane maintenance. This prospective observational study aimed to evaluate the incidence of early PONV (within the first two postoperative hours) following pre-induction administration of ondansetron 4 mg in patients receiving propofol-sevoflurane anaesthesia and to assess the influence of demographic and perioperative factors on emesis incidence. One hundred fifty high-risk adult patients aged 18-60 years undergoing elective surgery under general anaesthesia were enrolled. All received ondansetron 4 mg IV during premedication, propofol for induction, and sevoflurane for maintenance. Episodes of nausea and vomiting were recorded at 30, 60, 90, and 120 min postoperatively. Statistical analyses included Mann-Whitney U tests for continuous variables and Fisher's exact tests for categorical data, with significance set at p < 0.05. A total of 150 patients were included in the analysis. The mean age of the cohort was 39.9 ± 13.1 years, with a predominance of female patients (63.3%). The overall incidence of early postoperative nausea and vomiting (within 120 min) was 9.3% (14/150). Most episodes were mild in severity, with only a small proportion of patients experiencing repeated vomiting. No statistically significant associations were identified between PONV and demographic variables such as age, sex, body mass index, smoking status, or prior history of PONV (p > 0.05). However, a higher proportion of PONV was observed among patients undergoing otorhinolaryngological procedures, although this did not reach statistical significance when analysed across all surgical departments. Ondansetron 4 mg IV administered pre-medication, combined with propofol induction and sevoflurane maintenance, effectively reduced early PONV incidence to 9.3% among high-risk adults. A higher incidence of PONV was observed in patients undergoing ENT procedures. These findings support the continued use of 4 mg as a sufficient and safe prophylactic dose for early postoperative periods, while underscoring the need for larger comparative studies evaluating dose-response relationships and late PONV outcomes.
To evaluate the effects of cardiopulmonary bypass (CPB) on peripheral white blood cell counts, neutrophil surface marker expression, and neutrophil function by comparing patients undergoing on-pump CABG (ONCAB) versus off-pump CABG (OPCAB), and to identify CPB-related immunological and inflammatory alterations. Patients undergoing on-pump CABG (ONCAB) or off-pump CABG (OPCAB) were recruited. Blood samples were collected preoperatively and at 24 h postoperatively. The primary outcome was the neutrophil-to-lymphocyte ratio (NLR) measured at 24 h after surgery. Secondary outcomes included monocyte Human leukocyte antigen-DR (HLA-DR) expression, lymphocyte programmed cell death protein-1 (PD-1) expression, and neutrophil surface markers (CD11b, CD18, CXCR2, CD35, CD63, CD66b, CD88, and programmed cell death-ligand 1). Neutrophil apoptosis, reactive oxygen species (ROS) production, and plasma inflammatory mediators (interleukin-6, tumor necrosis factor-alpha, interleukin-10) were also measured. Postoperative clinical outcomes and laboratory parameters were recorded. Data from 36 ONCAB patients and 18 OPCAB patients were analyzed. Postoperative NLR was significantly higher in the ONCAB group than in the OPCAB group (16.6 ± 6.1 vs. 13.1 ± 3.9; p = 0.015). This difference was attributable to lower lymphocyte counts in the ONCAB group (0.7 ± 0.2 vs. 0.8 ± 0.2 × 109/L; p = 0.002), whereas neutrophil counts did not differ significantly between groups. In both groups, monocyte HLA‑DR expression decreased and lymphocyte PD-1 expression increased after surgery. CPB did not result in significant alterations in neutrophil adhesion, chemotaxis, degranulation markers, ROS production, or apoptosis. ONCAB patients had higher postoperative levels of aspartate aminotransferase (AST), cardiac troponin I (cTnI), and procalcitonin (PCT), as well as longer durations of mechanical ventilation and intensive care unit stay. CPB elevates the NLR after CABG primarily, accompanied by reduced level of lymphocyte count, but not neutrophil count or molecular markers of neutrophil functional. These results might reflect a higher risk of short-term complications after on-pump CABG.
The risk factors for neurocognitive impairment outcomes vary among different types of surgeries. The risk factors for delayed neurocognitive recovery (DNR) in elderly patients following orthopedic surgery are unclear. The objective of this study was to identify the risk factors for early postoperative delayed neurocognitive recovery in elderly patients who underwent elective orthopedic surgery. The medical data of 166 elderly patients underwent elective orthopedic procedures were analyzed retrospectively. The cognitive scores on the day before the surgery and on the 7th postoperative day were assessed using the MoCA scale, and Z-scores were utilized to account for learning effects. The study population was divided into two groups according to whether DNR occurred by the 7th postoperative day or prior to discharge. Risk factors associated with postoperative DNR in elderly orthopedic patients were determined using logistic regression analysis. There were 166 elderly surgical patients, with an incidence rate of 28.9% DNR. Multivariate logistic regression analysis revealed that a history of drinking (OR = 6.853 [1.825-25.734], P = 0.004), cerebrovascular stenosis (mild: OR = 7.646 [1.432-40.833], P = 0.017; moderate or severe: OR = 5.593 [1.222-25.607], P = 0.027), a preoperative PaO2/FiO2 ratio of < 350 (OR = 2.549 [1.045-6.219], P = 0.040), and postoperative albumin levels of < 35 g/L (OR = 4.214 [1.489-11.923], P = 0.007) were independently associated with DNR on postoperative day 7. Furthermore, plasma albumin levels on postoperative day 1 showed a negative correlation with plasma interleukin 6 levels on postoperative day 3 (r = - 0.251, P = 0.006). Early DNR in elderly orthopedic patients appears to be associated with multiple factors, including a history of drinking, cerebrovascular stenosis, a preoperative PaO₂/FiO₂ ratio < 350, and postoperative albumin < 35 g/L.
Nasopharyngeal carcinoma (NPC) remains a therapeutically challenging malignancy due to its late diagnosis and limited treatment efficacy. Although metabolic reprogramming is a hallmark of cancer, the ubiquitin-mediated mechanisms underlying NPC progression are incompletely understood. Here, we demonstrate that tripartite motif-containing protein 47 (TRIM47) is significantly upregulated in NPC tissues and drives tumor aggressiveness. Through integrated in vitro and in vivo approaches, we found that TRIM47 promotes proliferation, migration, epithelial-mesenchymal transition (EMT), and tumor growth. Mechanistically, TRIM47 directly interacts with succinate dehydrogenase subunit B (SDHB)-a key component of mitochondrial complex II-via its B30.2/SPRY domain and catalyzes K48-linked polyubiquitination, leading to SDHB proteasomal degradation. This degradation induces metabolic reprogramming characterized by enhanced aerobic glycolysis, as evidenced by increased glucose consumption and lactate production. Critically, the oncogenic effects of TRIM47 were reversed by SDHB reconstitution. Moreover, supplementation with succinate, the enzymatic product of SDH, counteracted the tumor-suppressive effects of TRIM47 knockdown. Furthermore, exploiting the metabolic vulnerability induced by TRIM47, ascorbate treatment effectively suppressed TRIM47-driven tumor growth. Our results identify TRIM47 as a novel E3 ligase responsible for SDHB ubiquitination and degradation, thereby promoting Warburg-like metabolism and NPC progression. These findings unveil the TRIM47-SDHB axis as a promising therapeutic target and support metabolic intervention with ascorbate as a potential precision strategy for NPC treatment.
Prehabilitation is an emerging preoperative strategy designed to optimise patients' functional capacity before surgery to improve postoperative outcomes. Previous studies have demonstrated its clinical benefit, including enhanced recovery and reduced postoperative complications. However, the mechanisms underlying these benefits remain poorly understood. This exploratory study investigates the potential effects of prehabilitation on pre- and postoperative immune function. This prospective study utilized data and material from a subgroup of patients participating in the F4S PREHAB trial, which is a stepped-wedge trial investigating the effects of multimodal prehabilitation prior to major surgery. In this substudy, patients undergoing elective bladder, oesophageal, or rectal cancer surgery between June 2022 and November 2023, were included. Immune function was assessed at baseline, following the prehabilitation or usual care period, and on postoperative day 1 (POD1) by examining ex vivo cytokine production capacity, plasma cytokine concentrations, and mHLA-DR expression. This substudy included 130 patients: 102 in the prehabilitation group and 28 in the control group. Following prehabilitation, ex vivo production of pro-inflammatory cytokines was reduced, while ex vivo production of the anti-inflammatory cytokine IL-10 was increased. Plasma concentrations of IL-6 and IL-10 were decreased following prehabilitation. On POD1, no significant differences in postoperative immune function were observed between the prehabilitation and control groups. This study suggests that multimodal prehabilitation influences basal immune function, leading to a less inflammatory state. However, as no significant differences in immune function were observed between prehabilitation and control groups on POD1, the impact of prehabilitation on postoperative immune function may be limited.
Neuroimmune dysregulation, characterized by microglial overactivation and imbalances in mitochondrial dynamics within the central nervous system represents a core pathological mechanism in postoperative cognitive dysfunction (POCD). This study investigated the neuroinflammation-mitochondrial interaction through the establishment of in vivo and in vitro models using lipopolysaccharide (LPS). Findings indicated that LPS-induced microglial overactivation was associated with marked upregulation of mitochondrial fission proteins, including phosphorylated Drp1 at Ser616, mitochondrial Drp1, and Fis1, along with downregulation of mitofusin-2. These alterations promoted mitochondrial fragmentation in hippocampal neurons, which subsequently led to mitochondrial membrane potential depolarization, adenosine triphosphate depletion, and excessive production of reactive oxygen species. This cascade further activated the intrinsic apoptotic pathway via Bax/Bcl-2 imbalance and caspase-9/3 activation. Conversely, administration of the Drp1 inhibitor Mdivi-1 reduced microglial activation, attenuated inflammatory cytokine levels, restored mitochondrial network integrity and function, inhibited neuronal apoptosis, and ameliorated LPS-induced spatial memory impairment in behavioral assays. These findings indicate that microglial activation-induced mitochondrial fission plays a pivotal role in inflammation-related cognitive impairment. Moreover, they highlight mitochondrial fission as a promising therapeutic target for intervention in POCD.
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Urinary oxygen tension (PuO2) is a promising continuous biomarker of renal medullary oxygenation, but distal catheter measurements are distorted by transit delay and wall diffusion, especially during oliguria. We developed and validated a physics-based algorithm that reconstructs bladder PuO2 from the distal signal. We formulated complementary steady-state and transient diffusion-transport models that couple wall diffusion to a lumen mass balance and solve an inverse problem to estimate bladder PuO2. Performance was assessed on a bench-top catheter system with controlled flows and in eight swine undergoing hemorrhagic shock and resuscitation (68,788 paired samples). On the bench top, adjustment reduced mean bias relative to bladder PuO2 from - 10.9 to -0.64 mmHg, narrowed 95% limits of agreement from 39.1 to 15.8 mmHg, and improved correlation with ground truth (R2 0.53→0.94). In vivo, pooled bias decreased from + 20.9 ± 11.5 to -4.1 ± 13.5 mmHg and mean absolute error from 21.1 to 9.5 mmHg, with the largest gains at low urinary flow. Modeling transport delay and wall diffusion enables reconstruction of bladder PuO2 from distal catheter measurements, supporting reliable, real-time urinary hypoxia monitoring and broader application to other conduit-based analyte measurements.
Anaphylaxis during pregnancy is a rare but potentially life-threatening condition for both mother and fetus, requiring rapid recognition and immediate treatment. Although the fundamental mechanisms of anaphylaxis in pregnancy are similar to those in nonpregnant women, physiological adaptations of pregnancy, peripartum exposures, and fetal considerations substantially complicate diagnosis, management, and prevention, contributing to variability in care and avoidable adverse outcomes. In this multidisciplinary review, experts in allergy-immunology, obstetrics, anesthesiology, and epidemiology synthesize current evidence on the epidemiology, triggers, pathophysiology, diagnostic challenges, management, outcomes, and prevention of anaphylaxis throughout pregnancy, labor, and delivery. We highlight how gestational cardiovascular and respiratory changes may obscure classic diagnostic features, emphasize the safety and critical importance of prompt intramuscular epinephrine use as first-line therapy, and review maternal and fetal outcomes associated with timely versus delayed intervention. Strategies for risk stratification, allergology workup, prevention of recurrence, and implementation of coordinated care pathways are discussed. This review underscores the need for increased awareness, structured interdisciplinary collaboration, and integration of prevention-focused strategies across obstetric and allergy care. By providing a practical, evidence-based framework, it aims to support health professionals in optimizing diagnosis, management, and maternal-fetal safety when anaphylaxis occurs during pregnancy.
Previous studies have established a strong link between central nervous system inflammation and depression development. However, the role and function of circulating cytokines in depression remain a topic of debate. Bidirectional MR analyses used GWAS data from the GWAS Catalog, UK Biobank, and IEU database, including two depression cohorts and 41 circulating cytokines. Animal experiments explored the association between IL-17 A, IL-1β, and depression by assessing cytokine expression in control and CUMS rats, with or without IL-17 A/IL-1β inhibitors. A potential directional association was found between depression and increased circulating IL-17 A (OR: 7.896, 95%CI: 1.962-31.782, P = 0.004, FDR = 0.019), with consistent findings in an independent cohort (OR: 1.732, 95%CI: 1.012-2.963, P = 0.045, FDR = 0.049). Circulating IL-1β was suggested as a risk factor for depression in both cohorts (OR: 1.036, 95%CI: 1.0002-1.0727, P = 0.049, FDR = 0.049; OR = 1.015, 95%CI: 1.002-1.029, P = 0.028, FDR = 0.046). Another MR study suggested IL-17 A exacerbated IL-1β dysregulation in depression (OR: 1.142, 95%CI: 1.034-1.261, P = 0.009, FDR = 0.031; OR: 1.224, 95%CI: 1.093-1.371, P < 0.001, FDR < 0.001). Animal experiments showed dynamic elevations of IL-17 A and IL-1β under CUMS. IL-1β inhibition alleviated depressive-like symptoms, whereas IL-17 A inhibition had little effect. Our findings suggest that circulating IL-17 A may serve as a potential downstream inflammatory indicator, but not a causative factor for depression. A mutually reinforcing relationship may exist between elevated IL-1β and IL-17 A and depression.
The configuration of interventional radiology (IR) suites often limits simultaneous access to the patient's airway and anesthesia equipment. This constraint may lead to suboptimal sedation in patients at increased risk of airway obstruction due to patient safety concerns. We conducted a randomized pilot trial to evaluate whether high-flow nasal oxygen (HFNO; F&P Optiflow™) reduces hypoxic events compared with a standard non-rebreather mask in this high-risk population undergoing deep sedation. Patients at increased risk of airway obstruction or hypoxia during deep sedation were randomized to receive 100% oxygen via HFNO at 70 L/min (HFNO group) or via non-rebreather mask at 8 L/min (standard-of-care [SoC] group). All patients received continuous intravenous propofol to achieve unconsciousness while maintaining spontaneous ventilation. The primary endpoint was total length of desaturation episodes [ToLDE], in minutes, defined as oxygen saturation [SpO2] ≤92%. Secondary outcomes included the number of desaturation episodes, bispectral index (BIS) excursions (defined as episodes of BIS value ≥ 61), postanesthesia care unit (PACU) length of stay, and patient-reported symptoms. A total of 101 patients were analyzed (HFNO group: n = 50; SoC group: n = 51). Mean ToLDE time was 0.34 min (median, 0; range 0-6.5 min) in the HFNO group and 0.97 min (median, 0; range 0-19.8 min) in the SoC group (P = 0.158). Desaturation occurred in 14% of HFNO patients vs. 26% of SoC patients (P = 0.212). The median number of BIS excursions was significantly higher in the SoC group (4; range, 0-19) than the HFNO group (2; range, 0-15; P = 0.005). Median PACU stay was shorter in the HFNO group (20 min; range, 0-60) vs. in the SOC group (26 min; range, 5-60) (P = 0.076). Patient-reported symptoms were less frequent and less severe in the HFNO group (12% vs. 16%). HFNO did not significantly reduce hypoxic events compared with a standard non-rebreather oxygen delivery device in patients at increased risk of airway obstruction during deep intravenous sedation. However, HFNO was associated with improved sedation stability and patient experience, supporting further investigation in larger studies. ClinicalTrials.gov ID: NCT04171037; Date of original registration: November 19, 2019; This study was retrospectively registered. Study principal investigator: Gang Zheng; This manuscript adheres to the applicable Consolidated Standards of Reporting Trials (CONSORT) guidelines.
Currently, palliative care provision for patients with heart failure (HF) is limited and usually not tailored to the specific needs they might have. In this study, we sought to gain a better understanding of the needs and expectations expressed by patients with HF regarding palliative care. We conducted semi-structured interviews with inpatients and outpatients across the entire HF trajectory. The interview guide was developed in a multidisciplinary team with input from patient representatives and covered all eight domains of palliative care according to the National Consensus Project Guidelines on Quality Palliative Care. Interviews were digitally recorded, transcribed, coded and analyzed based on the thematic analysis approach by Braun and Clarke. A total of 18 interviews were conducted with patients spanning NYHA classes I-IV and INTERMACS profiles 2-7. Six patients were currently on durable and three on temporary mechanical circulatory support. Participants expressed needs and expectations across all eight domains of palliative care. Some needs were specific to HF, e.g. for more HF expertise among all healthcare providers. Other needs were more generally associated with serious illnesses, e.g. long term access to psychological counselling for patients and caregivers, help with coming to terms with limited life expectancy, or provision of information in accessible language. Patients with HF express a host of unmet needs, many of which could be addressed by palliative care. Our study offers a nuanced description of patient needs that can inform the development of services and interventions in the future. German Clinical Trials Registry DRKS000334836.
Depression is a major global health burden with limited treatment efficacy. Ferroptosis, an iron-dependent form of regulated cell death, is implicated in its pathogenesis, but causal genetic links and cell-type-specific mechanisms remain unclear. We employed a multi-omics framework integrating two-sample Mendelian randomization (MR) using blood cis-eQTLs (eQTLGen/GTEx) and depression (FinnGen), single-cell eQTL (sceQTL) mapping in peripheral immune cells (OneK1K cohort), bioinformatic analyses, and in silico molecular docking. MR identified 42 ferroptosis genes associated with depression. Replication across cohorts pinpointed ribosomal protein RPL8 as a key protective factor (β = -0.02 to -0.06, PFDR < 0.05). RPL8 expression was enriched in blood/immune cells. sceQTL analysis revealed its protective effect was mediated through 11 immune cell subtypes (e.g., CD4+/CD8+ T, B, NK cells; β range: -0.016 to -0.040, PFDR < 0.05). Molecular docking predicted high-affinity binding between RPL8 and the ferroptosis execution ligand Ncoa4-9A (ΔG = -9.3 kcal/mol). PheWAS indicated a favorable safety profile for RPL8 modulation. This study presents genetic evidence suggesting a potential causal link between ferroptosis and depression, and identifies RPL8 as a potential immune cell-mediated protective factor. Based on these findings, we propose the "immune-ribosome-ferroptosis" axis as a promising direction for future therapeutic exploration.
Macrophage polarization is involved in the pathogenesis of acute respiratory distress syndrome (ARDS). However, the upstream regulators that shape macrophage inflammatory phenotypes under pathological conditions remain poorly understood. Pro-brain-derived neurotrophic factor (proBDNF) has recently been implicated in immune regulation, but its role in macrophage polarization and the underlying mechanisms are still unclear. Lipopolysaccharide (LPS) stimulation of NR8383 alveolar macrophages was used to model inflammation in vitro. ProBDNF expression was manipulated via adenoviral overexpression or knockdown. Polarization-related gene expression was measured by RT-qPCR, cytokine secretion was assessed by ELISA, and protein levels were examined by Western blotting and immunofluorescence. Neurotrophin receptor expression, including Ngfr/p75NTR and Ntrk2/TrkB, was also evaluated by RT-qPCR. Notch1 pathway activation was assessed by examining NICD levels and the expression of its downstream targets, Hes1 and Hes5. To further assess pathway involvement, NICD knockdown experiments were performed. LPS stimulation significantly increased proBDNF expression in NR8383 cells. Overexpression of proBDNF promoted a shift toward a pro-inflammatory (M1) phenotype, as indicated by increased expression of Cxcl9 and Nos2 and reduced expression of M2 markers (Arg1 and Mrc1). In contrast, proBDNF knockdown produced the opposite effect. Consistently, proBDNF overexpression increased TNF-α secretion and reduced IL-10 production, whereas proBDNF knockdown produced the opposite trend. NR8383 cells expressed Ngfr/p75NTR and Ntrk2/TrkB, with Ngfr showing a more inflammation-responsive pattern. These changes were accompanied by corresponding alterations in Notch1 signaling activity, reflected by changes in NICD, Hes1, and Hes5 expression. Importantly, silencing NICD markedly attenuated the pro-inflammatory polarization induced by proBDNF overexpression. In contrast, inhibition of Notch1 signaling did not affect proBDNF expression, supporting the interpretation that Notch1 functions downstream of proBDNF in this model. ProBDNF promotes macrophage polarization toward pro-inflammatory phenotypes under LPS stimulation, at least in part via Notch1 pathway activation. These findings identify a proBDNF-Notch1 regulatory axis in macrophage-driven inflammation and offer new insight into neuroimmune mechanisms underlying inflammatory lung injury.
Acute coronary syndrome (ACS) remains a leading cause of morbidity and mortality worldwide, where timely diagnosis is critical. Prehospital assessment is challenging due to limited diagnostic resources and high clinical uncertainty. Artificial intelligence (AI) has emerged as a potential tool to support early diagnosis, risk stratification, and triage. This scoping review aimed to map the current evidence on AI applications in the prehospital assessment of suspected ACS and to identify existing knowledge gaps. A scoping review was conducted in accordance with PRISMA-ScR guidelines. A comprehensive search of PubMed, Scopus, Web of Science, and Embase was performed up to May 2026. Studies evaluating AI-based models using prehospital data for ACS diagnosis, prediction, or triage were included. 19 studies involving 319,709 patients were included. AI-based models, particularly ECG-based deep learning and multimodal approaches, demonstrated promising diagnostic performance, with AUC values generally ranging from approximately 0.81 to 0.99, sensitivity from 73% to 94%, and specificity from 56% to 99%. These models improved sensitivity, reduced diagnostic variability, and enhanced triage efficiency in some settings. Risk prediction models showed moderate to good performance (AUC ~ 0.71-0.95) but were more variable. Emerging applications extended beyond diagnosis to risk stratification and decision support, including prediction of cardiogenic shock and need for revascularization. AI shows considerable potential to improve prehospital assessment of suspected ACS, particularly through enhanced ECG interpretation and multimodal data integration. However, current evidence remains limited by methodological constraints. Future prospective, multicenter studies with standardized approaches are essential to support clinical implementation.
Allogeneic blood is a limited and globally scarce resource. Protocols based on the Patient Blood Management (PBM) program, incorporating therapeutic alternatives to reduce the use of red blood cells (RBCs), fresh frozen plasma (FFP), and platelet concentrates (PCs), have become urgently needed. The aims of this study were: as a primary objective, to evaluate whether the implementation of a Patient Blood Management (PBM) protocol reduces allogeneic transfusion in patients undergoing coronary artery bypass grafting (CABG); and as a secondary objective, to assess the impact of transfusion on clinical outcomes and mortality following CABG surgery. The study analyzed patients ≥ 18 years undergoing isolated and elective on-pump coronary artery bypass grafting (CABG), including both arterial and venous grafts. Data were retrospectively collected for two distinct periods, forming two groups: Pre-PBM (2010) and Post-PBM (2012), based on the implementation of a multidisciplinary PBM protocol aimed at optimizing erythropoiesis, hemostasis, and physiological tolerance to anemia. Statistical analyses included between-group comparisons, correlation analyses, and multiple regression to identify independent predictors of increased mortality. Statistical significance was defined as a p-value < 0.05. A total of 3,564 patients undergoing CABG were stratified into the Pre-PBM (n = 2,150) and Post-PBM (n = 1,414) groups. Implementation of a PBM protocol was associated with a significantly reduced allogeneic transfusions-RBC (62.7% to 48.4%), FFP (13.1% to 6.7%), and PC (5.4% to 3.0%) (p < 0.001). Mortality decreased from 4.5% to 3.1% (p = 0.042), with lower deep sternal wound infection rates (p < 0.001). Transfusion was an independent risk factor for increased mortality, with RBC (OR 3.63, 95% CI 2.20-5.99, p < 0.001), FFP (OR 5.69, 95% CI 3.91-8.27, p < 0.001), and PC (OR 6.45, 95% CI 4.07-10.24, p < 0.001) therapy demonstrating a dose-dependent association. Even in low-risk patients (EuroSCORE ≤ 2), allogeneic transfusion was associated with a significantly higher mortality (p < 0.001). Implementing a PBM protocol was associated with significant reductions in blood transfusions, infection rates, and mortality following CABG. Allogeneic transfusion was a strong predictor of adverse outcomes, including higher mortality, supporting the routine use of PBM strategies in CABG.
Heart failure (HF) affects over 64 million people worldwide, with prevalence projected to reach 3% by 2030. In advanced stages, when medical therapy fails and transplantation is limited by organ shortages, left ventricular assist devices (LVADs) represent a viable alternative. This retrospective, single-center study reports 10-year outcomes from the first Chilean LVAD program using the HeartWare (HVAD) device. Between 2013 and 2015, nine patients with advanced HF received HVAD implants. The mean age was 42.2 ± 15.8 years, with a left ventricular ejection fraction of 22% ± 4.1%. One-year survival was 77.8%, and 10-year survival for those using LVAD as destination therapy was 62.2%. All patients experienced at least one infection, with driveline infections being most common (55.5%). Bleeding events affected 77.7%, including gastrointestinal bleeding and severe epistaxis (both 22.2%). Neurological complications occurred in 33.3% of patients. Despite these events, four patients remained on LVAD support after 10 years, with no mechanical device failures requiring replacement. This case series highlights the feasibility, durability, and clinical relevance of long-term LVAD support in low-donation settings. Findings support LVADs as a destination therapy in selected patients and emphasize the importance of multidisciplinary care and structured follow-up.
The purpose of this study is to clarify the role of LINC01094 in acute cerebral infarction (ACI) and to explore its potential molecular mechanisms. A total of 121 patients with ACI and 133 healthy controls were enrolled in this study. The expression levels of LINC01094, miR-499a-5p, and inflammatory markers (CRP, IL-6) were measured using RT-qPCR. The levels of MDA, SOD, and ROS were measured using commercial assay kits. The diagnostic value of LINC01094 for ACI was evaluated using ROC curve analysis. CCK-8 assay and flow cytometry were utilized to measure cell viability and apoptosis. The subcellular localization of LINC01094 in SH-SY5Y cells was determined. The predicted targeting relationship between LINC01094 and miR-499a-5p was validated using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Serum LINC01094 expression was significantly elevated in ACI patients and demonstrated diagnostic value for ACI. miR-499a-5p expression was markedly reduced in both ACI patients and in vitro/in vivo models, showing a significant negative correlation with LINC01094 expression in patients. Downregulation LINC01094 mitigated OGD/R-induced damage in SH-SY5Y cells and cerebral injury in MCAO rats, while inhibition miR-499a-5p reversed this protective effect. Furthermore, CACNB2 was confirmed as a direct target of miR-499a-5p. LINC01094 participates in the pathological process of ACI injury by competitively binding to and inhibiting the activity of miR-499a-5p. These findings suggest that LINC01094 may serve as a potential therapeutic target for ACI treatment.
Spinal cord stimulation (SCS) has become increasingly widespread in recent years for the management of refractory chronic pain, primarily owing to the development of novel waveform technology allowing variable spinal cord modulation, and indication expansion. The existing literature suggests that despite having favorable initial responses, the efficacy of SCS sometimes is reduced over time. To restore analgesic efficacy, a strategy of altering stimulation waveforms known as salvage therapy has been used. Here, we consolidate the existing evidence and describe the efficacy of salvage therapy. A literature search using relevant keywords was conducted on PubMed, Web of Sciences, and Cochrane Library data bases, yielding a total of 809 articles. After a full text review and screening for consistency with eligibility criteria were conducted, 22 studies with a collective sample size of 1591 patients were included in the final analysis. Data extraction was performed by six reviewers, with a secondary reviewer verifying each entry. Of the 1591 patients included in our review, the most frequent indication for salvage therapy was loss of waveform efficacy and paresthesia coverage. In most studies, patients received salvage therapy after experiencing loss of efficacy with a single waveform. Most studies also did not strictly control the phase in which salvage therapy was implemented, with only eight of 22 studies reporting exclusively trial phase interventions. The efficacy of salvage therapy was found to be favorable, with 685 of 879 salvage therapy trials (77.9%) being reported as successful. New waveform technologies in SCS have expanded therapeutic options for patients with refractory chronic pain. Available evidence suggests that waveform switching may restore analgesic benefit in a subset of patients who experience loss of efficacy after an initial favorable response. However, many salvage strategies involve device revision or generator replacement, and the long-term durability of these interventions remains uncertain. Further prospective studies are needed to better define patient selection, timing of intervention, and long-term outcomes after waveform-based salvage strategies.
Anterior disc displacement with reduction (ADDwR) is a common temporomandibular joint disorder in adolescents. Conventional anterior repositioning splints (ARS) often lack anatomical adaptation, which may limit their therapeutic precision and patient comfort. This study aimed to compare the efficacy of a digitally designed anatomical repositioning splint (D-ARS) with that of a conventional ARS in adolescent ADDwR patients. In this randomized controlled trial, 82 adolescents (aged 12-16 years) with ADDwR were randomly allocated to receive either a D-ARS (n = 41) or an ARS (n = 41). At the 6‑month follow‑up, clinical outcomes were evaluated through three modalities: disc recapture was assessed by magnetic resonance imaging (MRI), condylar volume changes were measured using cone‑beam computed tomography (CBCT), and patient‑reported wearing comfort was quantified with the Oral Impacts on Daily Performance (OIDP) questionnaire. Statistical analyses included chi-square tests, t-tests, and non-parametric tests as appropriate. The D-ARS group achieved a significantly higher disc recapture rate than the ARS group (94.44% vs. 79.63%, p = 0.022). Both groups showed significant increases in condylar volume [D-ARS: +202.17 mm³ (95% CI: 177.72-226.63), ARS: +208.9 mm³ (95% CI: 178.8-241.25), both p < 0.001], with no intergroup difference (p = 0.5615). Patient-reported comfort was superior in the D-ARS group, with lower OIDP scores (14.43% vs. 35.63%, p < 0.001). At the 6-month follow-up, the D-ARS group exhibited significantly better disc recapture success and patient-reported wearing comfort than the ARS group, while no significant difference was observed between the two groups in terms of condylar growth promotion. Chinese Clinical Trial Registry (ChiCTR2400080947, registered on February 19, 2024). Available from: http://www.chictr.org.cn/.