This study aimed to compare the clinical outcomes of endoscopic combined intrarenal surgery (ECIRS) in the prone hip-flexed split-leg position with conventional percutaneous nephrolithotomy (PCNL) for the treatment of complex renal calculi.

We retrospectively analysed 168 patients with complex renal calculi, including 82 who underwent ECIRS and 86 who underwent conventional PCNL. Baseline demographic and stone characteristics, perioperative outcomes, initial stone-free rate (SFR) within 1-3 days after surgery, final SFR after completion of all planned treatments, auxiliary procedures, double-J stent indwelling duration, length of hospital stay, and postoperative complications were compared between groups. Logistic regression analyses were performed to evaluate factors associated with residual stones after the initial procedure, with additional clinically informed sensitivity analysis using prespecified covariates.

Baseline demographic characteristics, stone features, and postoperative outcomes, including intraoperative ureteral catheterization time, complication rates, Clavien-Dindo classification, and final SFR after completion of all planned treatments, were comparable between the two groups (all P>0.05). In this retrospective cohort, ECIRS in the prone hip-flexed split-leg position was associated with earlier stone clearance after the index procedure, reflected by a higher initial SFR (74.39% versus [vs] 50.00%, P=0.001) and a lower requirement for auxiliary procedures (29.27% vs 46.51%, P=0.021). These findings were accompanied by a shorter hospital stay (6.44 vs 8.61 days, P<0.001), shorter double-J stent indwelling duration (2.81 vs 4.79 weeks, P=0.002), and shorter operative time (P=0.012). Multivariable and sensitivity analyses further demonstrated that ECIRS was independently associated with lower odds of residual stones after the initial procedure (odds ratio 0.40, 95% confidence interval 0.20-0.80, P=0.009).

Single-position ECIRS in the prone hipflexed split-leg configuration was feasible for selected patients with complex renal calculi and was associated with earlier stone clearance and shorter perioperative recovery metrics. However, the final SFR after completion of all planned treatments was comparable between groups, and whether this positional configuration confers benefit beyond ECIRS in alternative positions could not be determined from this comparison. Further prospective studies are required to validate these findings.

Optimizing the treatment of ischemic stroke is an urgent task in modern medicine. One of its causes is acute thrombosis of internal carotid artery due to atherosclerotic lesion. Conventional thrombolysis is effective only for carotid artery stenosis < 50%, and carotid endarterectomy in acute phase of stroke is associated with high morbidity and mortality. Endovascular technologies are preferable for carotid artery thrombosis. Direct vacuum thrombectomy and thrombectomy using stent-retrievers are ineffective in 10-25% of patients. The authors present treatment of ischemic stroke caused by internal carotid artery thrombosis using the FilterWire system for protection against distal embolism. Technology of thrombectomy is described in detail, and its advantages over other methods are highlighted. The feasibility of simultaneous stenting of symptomatic stenosis of internal carotid artery is justified.

Searching for optimal anesthesia type in patients undergoing carotid endarterectomy (CEA) has been ongoing since the origin of carotid surgery. Nevertheless, there is still no consensus on this issue. This review of randomized clinical trials (RCTs) defines the impact of anesthesia type - general anesthesia (GA) vs. regional anesthesia (RA) - on results of CEA. We found no significant difference in perioperative rate of major adverse cardiovascular events between CEA under GA and CEA under RA. Cumulative frequency of carotid intravascular shunting was much more high in patients who underwent CEA under GA (897/2044, 43.9% vs. 279/2068, 13.5%). However, clinical significance of the aforementioned difference is debatable due to variable indications and often unfounded criteria for intravascular shunting following CEA under GA. The article also highlights the features of perioperative hemodynamic status depending on anesthesia type. However, actual impact of hemodynamic status on perioperative outcomes was not assessed in the RCTs reviewed. Despite the progress in searching for optimal method of anesthesia for CEA, debate continues in community of carotid surgery experts between proponents of GA and RA. Indeed, available RCTs are characterized by some limitations not allowing them to fully disclose appropriate problems. This highlights the need for further research and systematization of available knowledge to determine the most effective and safe method of anesthesia for CEA.

Internal carotid artery ostium is the most common localization of stenotic lesions of extracranial arteries. Stroke in carotid basin usually follows acute occlusion of internal carotid artery as a result of atherosclerotic plaque rupture and vascular thrombosis, ineffective anticoagulation in patients with cardiac arrhythmias. The main purpose of invasive interventions for internal carotid artery stenosis is prevention of postoperative stroke. Currently, two surgical interventions are common: carotid endarterectomy (CEA) and "protected" internal carotid artery stenting (CAS). According to recommendations for the treatment of asymptomatic internal carotid artery stenosis, CEA combined with optimal drug therapy is preferable. However, several large meta-analyses demonstrated comparable long-term mortality and stroke rate for CEA and CAS. The purpose of this report was to highlight the results of large-scale studies comparing efficacy and safety of various surgical treatments with optimal drug therapy in patients with asymptomatic internal carotid artery stenosis receiving modern optimal drug therapy. When choosing any treatment strategy for asymptomatic carotid stenosis, one should pay attention to correction of modifiable risk factors for adverse cardiovascular events, including through optimal drug therapy. Additional studies are needed to stratify specific risk factors of stroke in patients with internal carotid artery stenosis in addition to asymptomatic status.

To analyze the influence of local and systemic factors on reparative processes of laparotomy wound for optimized choice of abdominal closure strategy.

A retrospective analysis enrolled 62 patients with penetrating abdominal wounds. Local (intra-abdominal complications, risk of abdominal compartment syndrome, number of relaparotomies) and systemic (total blood protein and urea) factors were assessed.

Statistical analysis revealed predictors of suture failure. Independent risk factors of aponeurotic suture failure were serum urea (odds ratio 0.754; p=0.020) and total protein (odds ratio 1.195; p=0.028) upon abdominal closure. Local factors (surgical site infection, peritonitis, abdominal compartment syndrome) were absolutely associated with failure (p<0.001).

A formalized algorithm consistently evaluates local factors and serum protein/urea with high predictive value of positive result (91.11%). Original algorithm objectifies the choice of abdominal closure strategy (primary suturing, controlled negative pressure or programmable hernia) and minimizes the risk of suture failure.

To define the impact of anaesthesia (general [GA] vs. regional [RA]) on results of carotid endarterectomy (CEA).

There were 1732 CEAs in 2012-2025. CEA under RA was performed in 1153 cases, CEA under GA - in 579 cases. The primary perioperative endpoints were ipsilateral ischemic stroke, any ischemic stroke, hyperperfusion-induced intracerebral haemorrhage, myocardial infarction, death and major adverse cardiovascular events (MACE). The secondary endpoints were clinically significant bleeding, carotid intravascular shunting, cranial nerve injury, postoperative pneumonia and conversion of RA to GA.

There were no significant between-group differences in the incidence of postoperative ipsilateral ischemic stroke+any other ischemic stroke (GA 2.8% [n=16] vs RA 2% [n=23]; p=0.309). Myocardial infarction was significantly more common in the GA group (GA 1% [n=6] vs RA 0.1% [n=1]; p=0.007). Postoperative in-hospital mortality was also significantly higher in the GA group (GA 1.9% [n=11] vs RA 0.6% [n=7]; p=0.012). Both groups did not differ in the incidence of hyperperfusion-induced intracerebral hematomas (GA 0% [n=0] vs. RA 0.3% [n=3]; p=0.555) or major adverse cardiovascular events (GA 4.1% [n=24] vs. RA 2.5% [n=29]; p=0.063). Carotid intravascular shunting was significantly more common in the GA group (GA 17.1% [n=99] vs. RA 7.8% [n=90]; p< 0.001). No significant differences were found for other outcomes. Conversion from regional to general anaesthesia occurred in 1.6% of cases.

RA for CEA is safe and followed by low rate of conversion to general anaesthesia. When compared with GA, regional anaesthesia demonstrated significant advantages in key outcomes, including lower rates of myocardial infarction and in-hospital postoperative mortality. Carotid intravascular shunting was significantly less common in the RA group.

This study aimed to validate the knowledge-attitude-practice (KAP) model in coronary heart disease (CHD) patients and their family caregivers, and examine the moderating role of dyadic care types. Data were collected from 281 patient-caregiver dyads, and moderated mediation models were constructed. In both patients and caregivers, knowledge and attitudes had significant direct effects on disease management practices, with attitudes partially mediating the knowledge-practice relationship. Among the four dyadic care types (patient-oriented, caregiver-oriented, collaborative, and incongruent), incongruent dyads showed a significantly stronger direct effect of patients' knowledge on their self-management practices (β = 0.94, 95% CI: 0.4, 1.49) than congruent configurations. Conversely, incongruent dyads significantly weakened the association between caregivers' knowledge and their health attitudes (β = -0.32, 95% CI: -0.60, -0.03), and reduced the impact of caregivers' knowledge on caregiving practices (β = -0.99, 95% CI: -1.53, -0.44). These findings emphasize the need for tailored health education and interventions based on specific dyadic interaction types.

Cerebral small vessel disease (CSVD) is genetically heterogeneous, and translating regional association signals into biologically plausible effector-gene hypotheses remains challenging. We performed a cross-phenotype and cross-species integrative genomic analysis of the FOXF2-centered proximal chromosome 6 region using publicly available genome-wide association study summary statistics for lacunar stroke, small-vessel disease ischemic stroke subtype and white matter hyperintensity volume. The chr6:0-2.5 Mb interval was treated as the primary regional analysis, whereas FOXF2 ± 1 Mb and FOXF2 ± 500 kb were examined as nested sensitivity windows. Linkage disequilibrium, regional gene annotation, quantitative trait locus evidence, colocalization, fine-mapping, GWAS Catalog records and human and mouse brain vascular transcriptomic data were integrated within a predefined candidate-prioritization framework. Lacunar stroke showed the strongest regional evidence, with rs7766042 meeting the predefined broad-window local correction threshold, although no signal reached conventional genome-wide significance. The SVD ischemic stroke subtype and WMH signals did not meet their corresponding local correction thresholds. Phenotype-specific lead variants showed low pairwise linkage disequilibrium, a pattern consistent with regional signal heterogeneity but not sufficient to establish distinct causal signals. FOXF2 and FOXC1 were prioritized as leading neurovascular candidates, whereas EXOC2 and GMDS were retained as secondary positional candidates. Several regional variants overlapped FOXF2 eQTL annotations; however, formal colocalization showed little evidence for a shared causal variant (PP.H4 = 0.0604), and fine-mapping did not resolve a single causal variant. Human and mouse brain vascular transcriptomic analyses provided cross-species expression-based cellular context for FOXF2 and FOXC1. These findings support regional candidate-gene prioritization at the proximal chromosome 6 locus while emphasizing that the available evidence does not establish a definitive multi-signal or multi-gene causal architecture.

Ferroptosis, a critical pathological mechanism in ischemic stroke (IS), is activated during the early phase of cerebral ischemia-reperfusion injury (CI/RI). Dendrobium officinale polysaccharide (DOP), the primary bioactive component of Dendrobium officinale, exhibits diverse pharmacological activities, including antioxidant, anti-inflammatory, and immunomodulatory effects. DOP has been suggested to exert neuroprotective effects by inhibiting ferroptosis; however, its specific role and underlying mechanisms in IS-related ferroptosis remain unclear. In this study, in vivo and in vitro CI/RI models were established using middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R), respectively. DOP was administered under a paradigm combining long-term pretreatment and short-term post-ischemic intervention, and its neuroprotective effects were evaluated. In MCAO/R mice, DOP significantly alleviated neurological deficits, reduced the cerebral infarct volume, and mitigated neuronal damage. These effects were associated with decreased Fe²⁺ accumulation and lipid peroxidation, ameliorated mitochondrial impairment, and upregulated the expression of key ferroptosis-related proteins, including nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4). Consistent with in vivo findings, DOP enhanced the viability of HT-22 cells subjected to OGD/R, decreased reactive oxygen species, and restored the mitochondrial membrane potential, accompanied by increased Nrf2 and GPX4 expression. Notably, knockdown of Nrf2 attenuated GPX4 expression and diminished the protective effects of DOP. Collectively, these findings suggest that DOP exerts neuroprotective effects against CI/RI, at least in part, by inhibiting ferroptosis through the Nrf2/GPX4 signaling pathway, supporting its potential role in preventive and early-stage intervention strategies for ischemic stroke.

Vascular endothelial growth factors (VEGFs) and their endothelial tyrosine kinase receptors are crucial mediators of vasculogenesis and angiogenesis, with FLT1 (VEGFR1) acting as a decoy receptor for VEGFs. Alternative polyadenylation (APA) of Flt1 transcripts produces a truncated mRNA transcript encoding soluble (s) FLT1, which contains only the extracellular ligand-binding domain. The relative roles of full-length (fl) FLT1 and sFLT1 in angiogenesis are incompletely understood. Alternative polyadenylation is an important post-transcriptional mechanism of gene regulation that is increasingly recognized to affect the expression of many genes related to cardiovascular diseases. However, there are no in vivo models available to target APA and to examine the physiological roles of gene isoforms.

We here generated mice by introducing silent mutations into the Flt1 exon 13/intron 13 5' splice site through homology-directed repair with CRISPR/Cas9 gene editing. Embryonic development, postnatal retinal vascular development, and reparative angiogenesis were evaluated in models of hindlimb ischaemia and myocardial infarction, complemented by assessments of cardiac functional recovery and cell phenotypes through snRNAseq, as well as in vitro assays examining endothelial cell phenotype and function. The introduction of specific splice site mutations within Flt1 to activate APA led to a complete loss of flFLT1 and an increase in sFLT1 expression. Using this mouse model, we demonstrate that sFLT1 alone is sufficient for developmental vasculogenesis, whereas the specific loss of flFLT1 enhances reparative revascularization and angiogenesis and improves cardiac recovery after myocardial infarction.

Our findings show that APA can be effectively targeted to modulate FLT1 isoform expression in vivo. Our mouse model may help to understand diseases driven by an imbalance in FLT1 isoform expression. Given the widespread presence of APA signals, our approach could furthermore serve as a model for studying the function of other truncated gene isoforms.