Search Results (35,695)

Laparoscopic cholecystectomy is now established as the worldwide gold standard for the treatment of benign gallbladder disease. Despite technical advancements, bile duct injury (BDI) remains a major concern, especially in patients with obesity. It is well known that in patients with a Body Mass Index (BMI) ≥ 30 kg/m², identification of Calot’s triangle and the achievement of the Critical View of Safety (CVS) during laparoscopic cholecystectomy (LC) are made more challenging due to excessive visceral adiposity and concomitant hepatic steatosis reducing the workspace. Near-Infrared Fluorescence Cholangiography (NIRF-C) with Indocyanine Green (ICG) has emerged as an innovative, safe and effective technique to visualize the biliary anatomy and minimize the risk of iatrogenic BDI. However, its specific benefit in patients with obesity remains under-discussed compared to the general population. The main aim of this narrative review is to evaluate whether the intraoperative use of ICG in patients with obesity may reduce operative times and the risk of BDI. A focused review of the literature is performed on articles from 2010 to 2025 published on PubMed, Scopus and Web of Science. The application of ICG fluorescence in LC for patients with obesity represents a tangible clinical advantage, not only for anatomical identification and significant improvement of procedural efficiency, but also for the reduction in operative time. Full article

Background: Left ventricular (LV) thrombosis after blunt trauma is uncommon and is most often attributed to traumatic coronary artery injury; however, it can also arise from severe myocardial contusions. Here, we report a case of LV thrombosis due to severe myocardial contusion without coronary artery injury. Case Presentation: A 36-year-old man struck by industrial fan fragments presented with hemorrhagic shock. Focused Assessment with Sonography for Trauma revealed cardiac tamponade. An emergent sternotomy was performed under cardiopulmonary bypass via the femoral vessels, which exposed severe contusion-associated hemorrhage with epicardial–myocardial dissection at the LV apex. On postoperative day (POD) 5, transthoracic echocardiography showed apical akinesia with mural thrombi; prophylactic anticoagulation was escalated and later transitioned to warfarin. Coronary computed tomography on POD 21 and invasive angiography at 6 months revealed negative findings. The thrombi resolved within 3 months; however, apical akinesia persisted. After discontinuing anticoagulation, a transient ischemic event occurring at 9 months prompted direct oral anticoagulant therapy. Apical akinesia persisted for over 7 years without recurrent thrombosis. Conclusion: This case underscores the importance of vigilance for intracardiac thrombosis in severe contusions, as well as the value of stepwise imaging (contrast echocardiography) and cautious, individualized discontinuation of anticoagulation when regional dysfunction persists. Full article

Background: Cemented and cementless fixation techniques in total hip arthroplasty (THA) each present distinct biomechanical properties and perioperative risk profiles. While cementless fixation has gained increasing popularity, large-scale nationally representative comparisons of perioperative outcomes between cemented and cementless elective THA remain limited. This study aimed to compare complication rates, healthcare utilization, and temporal trends between cemented and cementless elective THA using the National Inpatient Sample. Methods: A retrospective cohort study was conducted using the National Inpatient Sample database from 2016 to 2021. Adult patients undergoing elective primary total hip arthroplasty were identified using ICD-10-PCS codes and categorized into cemented and cementless fixation groups. Patient demographics, comorbidities, indications, postoperative complications, length of stay, hospital charges, and in-hospital mortality were compared. Multivariate logistic regression analysis was performed to evaluate the independent association between fixation type and postoperative complications while adjusting for demographic, clinical, and hospital-level variables. Results: A total of 81,668 elective THAs were identified, including 40,290 cemented (49.33%) and 41,378 cementless (50.67%) procedures. Cemented THA was associated with a shorter length of stay (2.09 ± 1.88 vs. 2.26 ± 2.47 days, p < 0.001) and lower total hospital charges ($65,584.53 ± 48,797.21 vs. $72,186.84 ± 49,860.20, p < 0.001). Unadjusted analyses demonstrated higher rates of acute kidney injury and sepsis in the cementless group. After multivariate adjustment, cemented fixation was associated with lower odds of acute kidney injury (OR 0.87, 95% CI 0.79–0.96, p = 0.004). However, cemented THA was associated with higher odds of postoperative delirium (OR 1.20, 95% CI 1.02–1.42, p = 0.030), blood transfusion (OR 1.27, 95% CI 1.17–1.37, p < 0.001), and periprosthetic fracture (OR 1.32, 95% CI 1.02–1.71, p = 0.035). Rates of myocardial infarction, pneumonia, venous thromboembolism, urinary tract infection, and in-hospital mortality were similar between groups. Temporal analysis demonstrated comparable utilization trends, with a decline in elective procedures during 2020–2021. Conclusions: In this nationwide analysis, cemented total hip arthroplasty was associated with lower risk of acute kidney injury, shorter length of stay, and lower hospital charges, but higher odds of postoperative delirium, blood transfusion, and periprosthetic fracture compared with cementless fixation. These findings highlight distinct perioperative risk profiles between fixation strategies and may assist surgeons in individualized decision-making for elective total hip arthroplasty. Full article

Background: Stroke–heart syndrome (SHS), particularly acute myocardial injury, is a critical complication following acute ischemic stroke (AIS). The C-reactive protein–triglyceride–glucose index (CTI) integrates inflammatory and metabolic parameters but remains unexplored in the context of post-stroke cardiac complications. This study investigated whether CTI predicts cardiac injury patterns and 90-day clinical outcomes in AIS patients. Methods: A two-center retrospective cohort study was conducted in AIS patients undergoing endovascular treatment (EVT). Cardiac troponin I (cTnI) trajectories were classified into: no injury, non-dynamic elevation, and dynamic elevation. The primary endpoint was poor functional status at 90 days (modified Rankin Scale [mRS] 3–6); the secondary endpoint was 90-day all-cause death. Results: Among 493 individuals (median age 69 years, 42% female), higher baseline CTI was associated with a greater likelihood of dynamic troponin elevation (adjusted odds ratio [aOR] per 1-unit increase = 1.56 (1.26–1.94); p < 0.001). Patients with dynamic elevation had significantly worse outcomes compared to those with no injury. Elevated CTI was an independent predictor of 90-day poor functional outcome (Q4: aOR = 3.04 (1.53–6.05); p < 0.001) and mortality (Q4: aOR = 2.82 (1.33–6.00); p = 0.007). Conclusions: In EVT-treated AIS patients, the CTI is a predictor of SHS and adverse 90-day outcomes. This easily calculable index may help identify individuals at higher risk of cardiac complications after AIS. Full article

Spinal cord injuries disrupt the motor, sensory, and autonomic functions routinely carried out by the spinal cord, with injury progressing from primary mechanical damage from the initial trauma to a secondary phase driven by inflammation and cellular cascades. This disruption significantly impacts the patient’s ability to perform basic physiological and voluntary functions seen in a normal spinal cord, which often results in long-term disability and dependence on supportive care. Stem cell therapies, including mesenchymal stem cells, neural stem cells, and induced pluripotent stem cells, have been investigated as potential regenerative approaches that may promote repair through neuroprotection, remyelination, and axonal regeneration. Preclinical studies have demonstrated encouraging results in motor and sensory recovery following injury; however, clinical evidence remains limited and variable. Some studies report improvements in motor and sensory function post-injury, with improvements in bladder and bowel management, tissue repair, and other functions. Overall, the outcomes vary based on cell type, delivery method, and the stage of spinal cord injury. The key challenges of stem cell therapy include safety concerns and the limited number of small-scale studies currently available. Additionally, understanding the variability in therapeutic outcomes and identifying optimal treatment conditions are critical steps toward advancing stem cell therapies in spinal cord injury repair. This review aims to characterize and summarize the stem cell approach to the treatment of spinal cord injuries, while also critically highlighting the limitations of current preclinical and clinical evidence, as well as the importance of continued investigation into the long-term and functional recovery processes and possibilities, as well as the patient’s quality of life following treatment with stem cells for spinal cord injury. Full article

Background/Objectives: Methicillin-resistant Staphylococcus aureus (MRSA) is a multidrug-resistant pathogen that poses a major public health concern. It predominantly infects immunocompromised individuals and is frequently associated with severe pulmonary complications, including acute lung injury. Diosmetin, a natural flavonoid, known for its anti-inflammatory, antioxidant, and anti-infective properties. Nevertheless, its therapeutic mechanism in the treatment of acute pneumonia induced by MRSA remains unclear. Methods: In this study, we employed network pharmacology and molecular docking to elucidate the mechanisms underlying the therapeutic effect of diosmetin against MRSA-induced pneumonia. An MRSA pneumonia model was established in Balb/c mice. The impacts of diosmetin on murine pneumonia were evaluated by detecting biochemical indicators via HE staining, ELISA, RT-qPCR, and WB. In vitro experiments utilized RAW264.7 macrophages to establish an MRSA infection model for further validation of the therapeutic mechanisms of diosmetin. Results: In vivo results demonstrated that diosmetin alleviated MRSA-induced lung injury and reduced mortality by inhibiting the release of pro-inflammatory cytokines. Furthermore, compared with model mice, diosmetin-treated mice showed reduced phosphorylation levels of NLRP3, pro-caspase-1, ASC, and NF-κB p65, along with an increased level of IκBα in lung tissue. In vitro experiments indicated that diosmetin effectively reduced the levels of pro-inflammatory cytokines in MRSA-infected RAW264.7 macrophages and exerted anti-inflammatory effects by modulating the expression of NLRP3, pro-caspase-1, ASC, IκBα, and NF-κB p65. Conclusions: Our results demonstrate that diosmetin alleviates MRSA-induced pneumonia in mice, and this protective effect is achieved through dual inhibition of the NF-κB/NLRP3 inflammasome axis. Full article

Background: Magnesium regulates neuronal excitability, NMDA receptor activity, and cerebrovascular tone. Dysmagnesemia is common in patients with acute brain injury (>65%), yet large randomized trials of magnesium neuroprotection have been neutral despite strong physiological rationale and consistent observational associations with outcomes. A key limitation may be diagnostic misclassification: the total serum magnesium poorly reflects the biologically active ionized fraction and may misclassify magnesium status in 20–85% of ICU patients during critical illness. Purpose: This narrative review synthesizes current evidence on magnesium physiology, measurement limitations, and clinical implications in neurocritical care. Overview: We discuss the mechanisms of magnesium depletion, outline the conceptual “two-hit” model (chronic deficiency plus acute ICU losses), and highlight the potential value of ionized magnesium for improved patient evaluation. Emerging syndrome-specific data suggest that magnesium disturbances are associated with prognostic signals. Improved phenotyping may help explain prior trial neutrality and support stratified approaches to magnesium monitoring and repletion. Future studies should evaluate magnesium-guided strategies and phenotype-driven trials to clarify the therapeutic role of magnesium in neurocritical care. Full article

Acute coronary syndromes (ACS) remain time-critical clinical emergencies in which early diagnosis and accurate risk stratification determine management and outcomes. Although symptoms, electrocardiography, and high-sensitivity cardiac troponin (hs-cTn) provide a reliable framework for detecting myocardial injury, they offer limited insight into plaque instability, thromboinflammatory activity, vascular repair, and post-infarction remodeling. In this narrative review, we examine the biological rationale and current clinical evidence supporting brain-derived neurotrophic factor (BDNF) as a candidate biomarker in ACS, with particular attention to pre-analytical, analytical, and phenotypic sources of heterogeneity. Available studies show that circulating BDNF concentrations vary substantially according to biological matrix, timing of sampling, ACS subtype, and assay methodology, which likely contributes to inconsistent findings across cohorts. Overall, current evidence does not support BDNF as a diagnostic alternative to hs-cTn in rule-in or rule-out pathways. However, BDNF may have value in biological phenotyping and risk stratification by reflecting platelet activation, endothelial dysfunction, inflammatory signaling, and remodeling processes after ACS. Further progress will require standardized pre-analytical procedures, separate assessment of mature BDNF and proBDNF, serial sampling, and validation in large multicenter studies. Full article

Background/Objectives: Strength training is a widely recommended form of physical activity due to its extensive health benefits and positive effects on musculoskeletal function, although improper technique and balance deficits may increase injury risk. While sex differences in spinal curvature and postural control have been identified in the general population, it remains unclear whether these differences persist among recreationally strength-trained individuals. This cross-sectional study investigated sex-specific differences in sagittal spinal alignment and static balance and examined potential associations between spinal curvature and postural control in trained young adults. The authors hypothesized that sex-related differences would persist despite regular training and that relationships between spinal alignment and balance would demonstrate sex-specific patterns. Methods: This cross-sectional study included 124 young adults (59.7% men and 40.3% women). Anthropometric measurements included height, weight, waist circumference, and hip circumference. Sagittal spinal curvature was assessed using an electronic inclinometer, and balance parameters were evaluated using a stabilometric platform under eyes-open and eyes-closed conditions. Results: Statistically significant sex-related differences were observed in sacral angle (p < 0.001) and lumbar lordosis (p = 0.02). Balance assessment revealed significant differences between sexes in several parameters under eyes-open conditions (p < 0.05), as well as in mean COP velocity in the anteroposterior direction under eyes-closed conditions (p = 0.003). In women, sacral inclination was positively but weakly correlated with selected balance parameters (r = 0.299–0.306, all p < 0.05), indicating an association between spinal alignment and postural control. Conclusions: The findings indicate sex-specific differences in sagittal spinal curvature and balance, with sacral alignment associated with balance performance in women. Differences in selected balance parameters were also observed independently of spinal curvature. These results highlight the importance of considering sex and spinal biomechanics when assessing postural control in strength-trained individuals and support further research in larger, more diverse populations with varying training experience and age ranges. Full article

Background/Objectives: The objective was to evaluate whether surgical timing (daytime vs. nighttime) influences intraoperative and postoperative outcomes in pediatric supracondylar humerus fractures. Methods: A retrospective observational cohort study was conducted at a tertiary center. Pediatric patients aged ≤14 years who underwent surgery for supracondylar humerus fractures between January 2010 and December 2022 were included. Fractures were classified according to the Gartland system. Patients with open fractures, associated neurovascular injury, compartment syndrome, or incomplete follow-up were excluded. Primary outcomes included need for open reduction, reoperation, neuropathy, and loss of joint mobility. Patients were grouped according to the time of surgery: daytime (08:00–22:00) or nighttime (22:00–08:00). Stratified analyses were performed based on fracture severity. Results: Eighty-six patients were included: 56 underwent daytime surgery and 30 underwent nighttime surgery. Groups were comparable in age, sex, and fracture severity. Nighttime surgery was associated with a significantly higher rate of open reduction (33.3% vs. 10.7%, p = 0.023; RR = 3.11). Reoperation (16.6% vs. 5.4%, p = 0.121) and postoperative neuropathy (23.3% vs. 8.9%, p = 0.131) were more frequent in the nighttime group, although these differences were not statistically significant. In complex fractures (Gartland III–IV), nighttime surgery was associated with a significantly higher reoperation rate (20.8% vs. 2.6%, p = 0.026). Conclusions: Nighttime surgery was associated with higher rates of open reduction and reoperation, particularly in complex supracondylar humerus fractures. However, given the retrospective design and limited sample size, these findings may be influenced by residual confounding and should be interpreted as exploratory. Full article

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by persistent mucosal inflammation and dysregulated immune–metabolic responses. Koumiss, a traditional fermented mare’s milk, has long been used in ethnomedicine for gastrointestinal disorders; however, its molecular mechanisms in UC remain unclear. In this study, an integrated multi-omics approach combining network pharmacology, quantitative proteomics, and molecular docking was employed to elucidate the therapeutic mechanism of koumiss powder (KP) in a dextran sulfate sodium (DSS)-induced murine colitis model. Network pharmacology identified twelve bioactive compounds targeting fourteen UC-associated proteins, predominantly enriched in the peroxisome proliferator-activated receptor (PPAR) signaling pathway. In vivo experiments demonstrated that high-dose KP significantly alleviated disease activity, improved colon shortening and histopathological injury, reduced serum TNF-α and IL-6 levels, and restored anti-inflammatory cytokines IL-4 and IL-10. Proteomic analysis further revealed activation of the PPAR signaling pathway, with significant upregulation of Plin4 and Sorbs1. Immunofluorescence staining further confirmed that KP restored the expression of PPARA and increased the levels of Plin4 and Sorbs1 in colonic tissues. Molecular docking confirmed strong binding affinities between key koumiss-derived lipid metabolites, including 13(S)-HOTrE and stearoyl ethanolamide, and PPAR-related target proteins. Collectively, these findings demonstrate that koumiss exerts protective effects against experimental UC primarily through activation of PPAR-mediated lipid metabolic and anti-inflammatory pathways. This study provides mechanistic insight into the biological activity of koumiss and highlights the value of multi-omics integration in natural product research. Full article

Peripheral nerve injuries involving critical-sized gaps remain a major clinical challenge. Although autologous nerve grafting is considered the gold standard for peripheral nerve repair, its clinical application is limited by the availability of donor nerve tissue and the risk of donor-site morbidity, including sensory deficits and functional impairment. Therefore, nerve guidance conduits (NGCs) have emerged as a promising alternative when combined with bioactive modulation strategies. In this study, we evaluated bisvinyl sulfonemethyl (BVSM)-crosslinked gelatin conduits integrated with electrical stimulation (ES) at different frequencies (0, 2, 20, and 200 Hz) in a rat sciatic nerve defect model over a 4-week recovery period (n = 10 per group). Structural regeneration was assessed by morphometric analysis, electrophysiology, macrophage infiltration, CGRP immunoreactivity, retrograde Fluorogold tracing, quantitative PCR of growth factors and inflammatory cytokines, and behavioral testing. Among all stimulation paradigms, low-frequency ES at 2 Hz produced the most pronounced regenerative effects. The 2 Hz group demonstrated significantly greater axon number, axonal density, and regenerated nerve area compared with control and high-frequency groups (p < 0.05). Electrophysiological assessments revealed improved nerve conduction velocity, higher MAP amplitudes, and shorter latencies. Enhanced macrophage recruitment and elevated CGRP expression were observed, suggesting coordinated neuroimmune and neurochemical activation. Gene expression analysis indicated upregulation of neurotrophic factors and balanced inflammatory cytokine responses under low-frequency stimulation. In contrast, high-frequency stimulation (200 Hz) failed to enhance overall regeneration and showed reduced axonal metrics, suggesting possible overstimulation-associated suppression. Collectively, these findings demonstrate that BVSM-crosslinked conduits provide a stable and biocompatible regenerative scaffold, and that appropriately tuned low-frequency electrical stimulation (2 Hz) optimally enhances structural, molecular, and functional recovery. The integration of material engineering with bioelectrical modulation represents a promising strategy for next-generation bioelectronic interfaces in peripheral nerve repair. Full article

Breathing-controlled electrical stimulation (BreEStim) is an innovative neuromodulation intervention that synchronizes deep voluntary breathing with peripheral electrical stimulation. Prior studies have shown its analgesic effects in healthy adults and spinal cord injury patients with neuropathic pain. The present study used EEG to examine BreEStim’s neural effects on sensory, affective, and cognitive components of pain. Fourteen healthy participants (7 M, 7 F) completed 30 min of BreEStim and conventional electrical stimulation (EStim) interventions in a randomized, crossover within-subject design. Electrical pain thresholds (EPT) and EEG were recorded pre- and post-intervention. Event-related potentials (ERPs) at pre-EPT-level stimuli before and immediately after each intervention were analyzed for early sensory (P30) and affective (P250) processing, while resting-state EEG assessed spectral power across delta, theta, alpha, and beta bands for cognitive processing. Both BreEStim and EStim increased EPT, indicating short-term habituation. There was no change in early ERP responses (P30) after each intervention, suggesting preserved sensory perception. BreEStim selectively reduced P250, reflective of the affective component of pain. BreEStim significantly increased delta and theta band power and reduced alpha band power on resting-state EEG analyses, whereas no significant changes after EStim were observed. Collectively, BreEStim preserves sensory encoding while selectively modulating affective and cognitive dimensions of pain, supporting its potential as a targeted, non-pharmacological neuromodulation strategy. Full article

This study aimed to investigate the molecular mechanisms underlying dopaminergic injury induced by gestational and lactational atrazine (ATR) exposure in rat offspring, with a particular focus on non-coding RNA-mediated regulation. Pregnant rats were exposed to ATR during gestation and lactation. Offspring underwent behavioral testing at postnatal day 21 (PND21) and were sacrificed for midbrain tissue collection at PND28. Behavioral alterations, histopathological changes in the substantia nigra, and dopaminergic marker expression were assessed to evaluate ATR-induced neurotoxicity. Whole-transcriptome sequencing was then performed to identify differentially expressed mRNAs, miRNAs, and lncRNAs, followed by co-expression, protein–protein interaction, and competing endogenous RNA (ceRNA) network analyses. Key targets were validated by qRT-PCR. Candidate molecules identified from transcriptomic and ceRNA analyses were further examined in an ATR-induced neurotoxicity model established in RA-differentiated SK-N-SH cells. Dual-luciferase reporter, Ago2-RNA immunoprecipitation, and biotin-labeled RNA pull-down assays were used to examine putative binding relationships and molecular interactions. In addition, lentivirus-mediated Elavl4 overexpression was performed to further evaluate the role of this candidate regulator in ATR-induced Nurr1 downregulation. Gestational and lactational ATR exposure induced significant behavioral abnormalities in rat offspring. These changes were accompanied by histopathological alterations in the substantia nigra, including reduced TH immunoreactivity, as well as abnormal expression of dopaminergic markers, characterized by decreased TH and Nurr1 levels and increased α-syn expression. Together, these findings indicate the presence of dopaminergic injury. Whole-transcriptome analysis further revealed widespread dysregulation of mRNAs, miRNAs, and lncRNAs in ATR-exposed offspring. Subsequent integrative analysis suggested a potential ceRNA regulatory relationship among Elavl4, miR-301a-5p, and Nurr1, which was further supported by qRT-PCR. Dual-luciferase reporter, RIP, and RNA pull-down assays supported direct interactions between miR-301a-5p and both Elavl4 and Nurr1, as well as their association with the Ago2-containing silencing complex. Moreover, Elavl4 overexpression partially reversed ATR-induced Nurr1 downregulation in vitro. Gestational and lactational ATR exposure induced behavioral abnormalities and dopaminergic injury in rat offspring. Whole-transcriptome analysis combined with experimental validation suggests a potential association between the Elavl4/miR-301a-5p/Nurr1 ceRNA axis and ATR-induced dopaminergic injury, providing insight into the post-transcriptional mechanisms underlying developmental neurotoxicity. Full article

Erlotinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is widely used in cancer therapy; however, hepatotoxicity limits its clinical use. This study investigated the protective effects of Liv-52, a polyherbal hepatoprotective formulation, against erlotinib-induced hepatotoxicity in rats and compared its efficacy with melatonin. The animals (n = 24, Wistar albino rats) were randomly categorized into four groups: healthy (HG), erlotinib (ERG), Liv-52 + erlotinib (LEG), and melatonin + erlotinib (MEG). Liv-52 (50 mg/kg/day, orally) and melatonin (10 mg/kg/day, orally) were administered once daily for two weeks. Erlotinib (10 mg/kg, orally) was given every other day to ERG, LEG, and MEG groups for two weeks. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) were measured. Hepatic malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) levels were analyzed. Additionally, double immunofluorescence staining was performed to evaluate apoptotic (poly[ADP-ribose] polymerase-1 [PARP-1], apoptosis-inducing factor [AIF]), inflammatory (cyclooxygenase-2 [COX-2]), and anti-inflammatory (interleukin-10 [IL-10]) biomarkers in liver tissues. Histopathological examination was also conducted to assess structural alterations. Erlotinib significantly increased MDA, ALT, AST, and LDH while decreasing tGSH, SOD, and CAT (p < 0.001). Strong immunoreactivity for PARP-1, AIF, IL-10, and COX-2, as well as severe hydropic degeneration and necrosis, was observed in ERG (p < 0.05). Both Liv-52 and melatonin significantly ameliorated biochemical, histopathological, apoptotic, and inflammatory alterations (p < 0.05). Notably, Liv-52 demonstrated superior hepatoprotective efficacy compared to melatonin. These findings indicate that Liv-52 effectively attenuates erlotinib-induced hepatotoxicity by modulating oxidative stress, inflammatory responses, and apoptotic pathways, thereby preserving liver function and structural integrity. Full article