Acute kidney injury (AKI) results from renal damage that triggers oxidative stress, inducing apoptosis, structural abnormalities in cells and their organelles, and even mitochondrial DNA instability. Tocilizumab is a monoclonal antibody inhibitor of interleukin-6, initially used to treat rheumatoid arthritis and later tested for COVID-19 treatment, which may have a protective effect on AKI.

To evaluate the effect of tocilizumab on renal function and oxidative profile in rats with ischemic AKI.

This is an experimental study using a quantitative approach with animals. The animals were randomized into four groups: SHAM (control); TCZ (tocilizumab); I/R (ischemia/renal reperfusion, clamping of both renal pedicles for 30 minutes); and TCZ + I/R. Tests were performed to assess renal function (inulin clearance and plasma creatinine), renal oxidation (urinary peroxides, malondialdehyde-derived oxidative substances), and endogenous antioxidant agents (thiols).

Regarding renal function, the treated group showed improvement in inulin clearance (IR 0.24 ± 0.3 vs TCZ + IR 0.65 ± 0.05; p < 0.05) and plasma creatinine levels (IR 2.3 ± 0.6 vs TCZ + IR 0.8 ± 0.3; p < 0.05). Analysis of the oxidative profile revealed a reduction in peroxides, confirming an attenuation of the redox mechanism (IR 15.8 ± 2.8 vs. TCZ + IR 3.7 ± 1.3; p < 0.05).

Tocilizumab demonstrated renoprotective effects, improving renal function and reducing oxidative stress.

Background Whether endovascular recanalization (ER) plus medical treatment reduces the risk of stroke or death compared with medical treatment alone in patients with symptomatic nonacute intracranial artery occlusion (sNAIAO) is uncertain. Purpose To compare clinical outcomes following ER plus medical treatment versus medical treatment alone in patients with sNAIAO. Materials and Methods This multicenter, prospective cohort study enrolled consecutive participants with sNAIAO at six comprehensive stroke centers in China from January 2020 to October 2023. The primary outcome was any stroke or death within 30 days after enrollment or ischemic stroke in the same region as the qualifying artery between 30 days and 1 year after enrollment. The difference in the primary outcome between groups was assessed by using Kaplan-Meier analysis with log-rank testing. Results Of the 436 participants included in the final analysis (median age, 57 years; IQR, 50-65 years; 322 male and 114 female participants), 288 underwent medical treatment alone, and 148 underwent ER plus medical treatment (hereafter, the ER group). Compared with medical treatment alone, ER plus medical treatment increased the incidence of the primary outcome (adjusted hazard ratio [aHR], 2.80; 95% CI: 1.55, 5.08; P < .001). Within 30 days of enrollment, the risk of stroke or death was greater in the ER group than in the medical group (aHR, 21.74; 95% CI: 5.00, 95; P < .001). Between 30 days and 1 year after enrollment, there was no evidence of a difference between groups in the incidence of ischemic stroke in the territory of the qualifying artery (aHR, 0.62; 95% CI: 0.24, 1.62; P = .33). Conclusion In patients with sNAIAO, medical treatment alone was associated with better clinical outcomes compared with ER plus medical treatment. The observed higher event rate in the ER group suggested potential procedure-related risks. © RSNA, 2026 Supplemental material is available for this article. See also the editorial by Chaudhary and Wilseck in this issue.

Warfarin, the anticoagulant of choice for durable left ventricular assist devices (LVADs), has a narrow therapeutic index and extensive pharmacologic interactions that make dose optimization challenging. Inadequate time in the therapeutic range increases the risk of thrombotic and hemorrhagic complications. We sought to evaluate the safety and efficacy of apixaban as an alternative anticoagulant for HeartMate (HM) 3 LVADs.

We analyzed data for patients with HM3 LVADs treated at our center between 2018 and 2024, comparing thromboembolic and hemorrhagic events between patients receiving warfarin and those who transitioned to apixaban due to adverse events or labile therapeutic responses on warfarin.

We included 47 patients, 16 of whom remained on warfarin, while 31 transitioned to apixaban. Both cohorts had identical baseline characteristics. Rates of all-cause bleeding per 100 patient-years were similar for warfarin (33) and apixaban (29), p = 0.24. The relative risk (RR) of major bleeding within the first 3 months of anticoagulation was significantly lower with apixaban-RR 0.08 (95% CI, 0.01-0.65, p = 0.01), with an incidence rate of 6.4% on apixaban versus 43.8% on warfarin. All-cause bleeding occurred less frequently with apixaban at 32% compared to 68.8%-RR 0.14 (95% CI 0.03-0.62, p = 0.009). Hemocompatibility improved in the apixaban group, evidenced by an increase in hemoglobin (11 ± 2 to 12 ± 2 g/dL, p < 0.001) and a decrease in lactate dehydrogenase (427 ± 129 to 221 ± 83 U/L, p < 0.001). Thrombotic events were identical.

In patients with HM3 LVADs, apixaban may be a safe and clinically effective alternative to warfarin.

VACTERL association (VA) is a well-known group of congenital defects affecting multiple organs. Although esophageal atresia (EA) has been reported in 50%-80% of patients with VA, only a few studies have compared EA with and without VA.

This retrospective study reviewed the data of patients diagnosed with EA in Seirei Hamamatsu General Hospital between January 2000 and March 2025. The data analyzed included sex, age, anatomic EA type, and VA diagnosis. Data were compared between the patients of EA with VA and those of EA without VA.

During the study period, 37 patients, including 17 male and 20 female patients, were diagnosed with EA; of these, 11 (29.7%) were also diagnosed with VA. The incidence of a long gap was significantly higher in patients of EA with VA (54.5%) than in those of EA without VA (19.2%). The mean age at esophageal reconstruction was significantly higher in patients of EA with VA (208.5 days) than in those of EA without VA (47.2 days).

To the best of our knowledge, this is the first study to report a significantly higher incidence of a long gap in patients of EA with VA compared to those of EA without VA; this result might be associated with a significant difference in the mean age of esophageal reconstruction between the two patient groups. These findings raise the possibility that the incidence of a long gap might be higher in patients of EA with VA than in those of EA without VA.

In addition to dyspnea and edema, gastrointestinal discomfort is common among patients with heart failure (HF). Reduced cardiac output can lead to inadequate perfusion of the intestinal mucosa and subsequent impairment of the intestinal barrier. Levosimendan, a novel inotropic agent, binds to cardiac troponin C to enhance calcium sensitivity, activates ATP-dependent potassium channels in cardiomyocytes and vascular smooth muscle cells, exerts positive inotropic and vasodilatory effects, and reduces free radical generation, thereby improving systemic hemodynamics including intestinal circulation. However, clinical evidence regarding its protective effects on the intestinal barrier in HF patients remains limited, and the underlying mechanisms require further clarification. This study aims to investigate whether levosimendan confers protective effects on the intestinal barrier in HF patients and to explore its potential mechanisms.

Network pharmacology was first used to analyze potential mechanisms of levosimendan in treating intestinal barrier dysfunction among HF patients. A total of 62 hospitalized patients with acute exacerbation of HF with reduced ejection fraction (HFrEF) were enrolled based on echocardiographic left ventricular ejection fraction. According to clinical medication regimens, patients were assigned to a conventional treatment group (n=31) or a levosimendan treatment group (n=31). The conventional treatment group received standard anti-HF therapy, while the levosimendan treatment group received levosimendan in addition to standard therapy. Enzyme-linked immunosorbent assays were used to measure plasma levels and changes in the intestinal-barrier proteins zonulin, intestinal fatty acid binding protein (I-FABP), proinflammatory cytokines [interleukin (IL)-17, IL-6, and tumor necrosis factor (TNF)-α], anti-inflammatory cytokine IL-10, and N-terminal pro-brain natriuretic peptide (NT-proBNP). Improvements in cardiac function and gastrointestinal symptoms were evaluated using the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the Gastrointestinal Symptom Rating Scale (GSRS).

Network pharmacology indicated that the effects of levosimendan on intestinal barrier dysfunction in HF patients may involve inflammation-related pathways such as IL-17 and TNF. Clinically, after treatment, zonulin decreased by 32.94 ng/mL in the levosimendan treatment group versus 15.05 ng/mL in the conventional treatment group (P<0.05). I-FABP decreased by 6.97 pg/mL in the levosimendan treatment group but increased by 35.16 pg/mL in the conventional treatment group (P<0.05). IL-6, IL-17, and TNF-α decreased by 1.11 pg/mL, 1.21 pg/mL, and 2.83 pg/mL, respectively, in the levosimendan treatment group, whereas they increased by 7.68 pg/mL, 0.67 pg/mL, and 2.38 pg/mL in the conventional treatment group (all P<0.05). IL-10 decreased by 24.48 pg/mL in the conventional treatment group but increased by 24.98 pg/mL in the levosimendan treatment group (P<0.05). NT-proBNP increased by 7.35 pg/mL in the conventional treatment group but decreased by 4.73 pg/mL in the levosimendan treatment group (P<0.05). KCCQ scores increased by 0.36 in the conventional treatment group and 1.86 in the levosimendan treatment group, GSRS scores decreased by 1.00 in the conventional treatment group and 2.40 in the levosimendan treatment group, respectively, but the differences were not statistically significant (both P>0.05).

Levosimendan not only improves HF and gastrointestinal symptoms in hospitalized patients with acute exacerbation of HFrEF but also reduces plasma intestinal barrier factor levels. These effects may be associated with decreased plasma proinflammatory cytokines and increased anti-inflammatory cytokines after treatment, potentially involving IL-17 and TNF signaling pathways.

Carotid atherosclerosis (CAS) plaques are independent risk factors for stroke, and chronic vascular inflammation is involved in their pathogenesis. This study aims to explore the association between the systemic immune-inflammation index (SII) and CAS, analyze sex-specific differences in this association, and provide evidence for the early prevention and control of atherosclerosis.

This single-center cross-sectional study included adults who underwent health examinations and completed carotid ultrasound assessments at Xiangya Hospital of Central South University between January and December 2023, among whom those with CAS were classified as a CAS group, and those without CAS were classified as a normal control group. Demographic characteristics, anthropometric measurements, and laboratory data were collected. Participants were categorized into Quartile 1 to 4 based on SII . Four binary logistic regression models were constructed to progressively adjust for confounders and evaluate the association between SII and CAS, with further stratification by sex. Mediation analyses stratified by sex. Mediation analyses stratified by sex were performed using the Bootstrap method (5 000 resamplings), with white blood cell and monocyte counts as mediators. Sensitivity analyses were conducted to verify robustness.

A total of 19 788 participants were included, of whom 7 567 (38.24%) had CAS. Compared with controls, individuals with CAS had significantly higher proportions of males, age, waist circumference, systolic and diastolic blood pressure, fasting glucose, and white blood cell count (all P<0.001), and significantly lower high-density lipoprotein cholesterol levels (P<0.001). Logistic regression revealed notable sex heterogeneity. After adjusting for age and sex (Model 2), higher SII (Quartile 4) was significantly associated with increased CAS risk [odds ratio (OR)=1.26, 95% confidence interval (CI) 1.14 to 1.39, P<0.01]. This association persisted after further adjustment for metabolic risk factors (Model 3; OR=1.18, 95% CI 1.07 to 1.31, P<0.01). However, after additional adjustment for inflammatory markers such as C-reactive protein, white blood cell, and monocyte counts (Model 4), the association was substantially attenuated and became non-significant in the overall population and in men (P>0.05). Notably, among women, SII remained significantly associated with CAS across all models in both Quartile 2 (OR=1.19, 95% CI 1.02 to 1.39) and Quartile 4 (OR=1.20, 95% CI 1.01 to 1.43) groups (all P<0.05). Mediation analysis showed that in the overall population, white blood cell count exerted a complete mediating effect (indirect effect β=0.03, 95% CI 0.01 to 0.05, P<0.01; accounting for 46.3% of the total effect), while monocyte count partially mediated the association (indirect effect β=0.01, 95% CI 0 to 0.02, P<0.01; accounting for 18.9% of the total effect). Among men, the mediating role of inflammatory cells was amplified, with white blood cell count serving as a complete mediator (indirect effect β=0.04, 95% CI 0.02 to 0.06, P<0.01; accounting for 74.3% of the total effect) and monocyte count as a significant partial mediator (indirect effect β=0.01, 95% CI 0 to 0.02, P<0.05; accounting for 24.2% of the total effect). Among women, the mediating effect of monocyte count (β=0, 95% CI 0 to 0, P>0.05), and white blood cell count (β=0.01, 95% CI 0 to 0.02, P>0.05) were not statistically significant. After adjusting for all confounding factors, the direct effect of SII on CAS remained statistically significant in all cases (all P<0.05). Sensitivity analyses confirmed the robustness of the findings.

A significant sex-specific heterogeneity exists in the association between SII and CAS. High SII is an independent correlate of CAS in women, driven primarily by direct effects and not mediated by white blood cell or monocyte counts. In men, SII influences CAS predominantly through complete mediation by white blood cells and partial mediation by monocytes. These findings suggest the differentiated value of SII in CAS risk assessment across sexes and provide evidence to support sex-targeted screening and intervention strategies.

To determine the long-term risk factors for rehemorrhage (primary outcome) in patients with ruptured brain arteriovenous malformations (BAVMs) after different treatment strategies and to evaluate the impact of different treatment strategies on lesion obliteration (secondary outcome) over a 10-year follow-up.

This single-center retrospective cohort included 645 patients with ruptured brain arteriovenous malformations (BAVMs) treated between 2010 and 2019, with a median follow-up of 96 months. Patients were randomly divided into training (70%) and validation (30%) cohorts to identify and validate predictors of rehemorrhage-free survival (RFS). Cox regression analyses were performed to assess risk factors for RFS, while logistic regression and propensity score matching (PSM) were used to evaluate the impact of treatment strategies on obliteration and rehemorrhage.

Obliteration was observed in 66.0% (384/582) of the patients, and 109 patients (16.9%) experienced rehemorrhage. In the training set, the multivariate Cox regression analysis revealed that, deep location ((hazard ratio (HR) = 2.033, 95% confidence interval (CI) = 1.166-3.545; p = 0.012)/posterior location (HR=2.215, 95% CI=1.213-4.043; p = 0.010), lesion diameter >6 cm (HR = 4.901, 95% CI = 2.046-11.737; p < 0.001), and multiple drain veins (HR = 2.287, 95% CI = 1.207-4.335; p = 0.011), were significant independent risk factors for rehemorrhage-free survival. In the validation set, lesion diameters of 3-6 cm (HR = 4.910, 95% CI = 1.677-14.377; p = 0.004) and >6 cm (HR = 19.416, 95% CI = 5.152-73.173; p < 0.001) remained significant in the multivariate Cox regression analysis. After PSM, univariate logistic analysis revealed that, compared with radiosurgery, preradiosurgery embolization + radiosurgery resulted in a lower non-obliteration rate ((odd ratio) OR = 0.352, 95% CI = 0.134-0.926; p = 0.034).

Lesion size, lesion location, and multiple draining veins were independently associated with long-term RFS. Preradiosurgical embolization improved the obliteration rate but did not significantly alter the risk of rehemorrhage. These findings directly inform treatment selection for ruptured BAVMs.

To observe the effect of bilateral cerebellar high-frequency rTMS on swallowing function and swallowing phase in patients with PSD.

42 patients with PSD were randomly divided into bilateral cerebellar stimulation group and sham group (stimulating coil and scalp at a 90° angle). The rTMS stimulation parameters are 10 Hz,120% rMT, with 9 s intervals and 1 s stimulus, totaling 500 pulses. Before and after 3-week treatment, the MEPs amplitude of the suprahyoid muscles of the bilateral cerebral cortex was recorded as an index to quantify the excitability of the cerebral swallowing cortex. The VFSS was carried out for all patients before and after 3-week treatment, assessing the severity of dysphagia with FDS, assessing the risk of leakage and aspiration with PAS, and recording the swallowing phase.

40 patients were finally included for statistical analysis. After three weeks treatment, PAS and FDS scores improved, and the oral transit time (OTT) and Swallowing Reaction Time (SRT) were shorter in both groups. These indexes changed more significantly in the cerebellar stimulation group than the sham group. The MEP amplitudes of the cerebral swallowing cortex increased bilaterally, and the MEP amplitude of the contralateral cerebral swallowing cortex increased more significantly in the cerebellar stimulation group than that in the sham group.

To patients with PSD, bilateral cerebellar high-frequency rTMS can improve the swallowing function, increased the excitability of the contralesional cerebral swallowing cortex and shorten OTT and SRT.

Cerebellar rTMS may improve swallowing performance by regulating motor control.

To investigate the association of different diurnal blood pressure patterns with heart rate variability (HRV) and hypertensive retinopathy (HR) risk in essential hypertension patients. A total of 181 patients (Jan 2023-Jun 2025) were grouped by nocturnal systolic blood pressure fall rate (SBPF): dipper (n = 57, 10%≤SBPF < 20%), non-dipper (n = 62, 0 ≤ SBPF < 10%), reverse-dipper (n = 62, SBPF < 0%). Ambulatory blood pressure (BP), HRV indices, and HR detection rate were compared. Reverse-dipper had higher nocturnal SBP (nSBP), 24-hour SBP (24hSBP) than the other two groups (all P < 0.05), and higher nocturnal DBP (nDBP) than dipper (P = 0.002). Dipper's HRV indices (SDNN, SDANN, RMSSD, PNN50, LF, HF) were better than non-dipper (P < 0.05); SDNN, SDANN, LF were better than reverse-dipper (all P < 0.001). Reverse-dipper's LF/HF was lower than others (P < 0.05). HR detection rates: 3.5% (dipper), 46.8% (non-dipper), 50.0% (reverse-dipper) (P < 0.001). Multivariable regression: BMI (OR = 1.131) was an independent risk factor; dipper (vs. reverse-dipper, OR = 0.031) was protective (P < 0.05). Reverse-dipper has the highest nocturnal BP load, dipper the most favorable (better autonomic regulation). Ambulatory BP monitoring and BMI control are crucial to reduce target organ damage.

The a body shape index (ABSI) and body roundness index (BRI) represent novel obesity biomarkers. This study aimed to determine their predictive capabilities for mortality risk in individuals with chronic kidney disease (CKD) and to compare their performance with traditional obesity markers of body mass index (BMI) and waist circumference (WC). We performed a cohort study by analyzing 6,577 adult CKD participants (mean age 60.372 years, 43.588% men) from the 1999-2018 National Health and Nutrition Examination Survey. We determined the prognostic value of ABSI and BRI for all-cause and cardiovascular disease (CVD) mortality using the Cox proportional hazard regression analysis. We also compared the predictive performance between ABSI, BRI and BMI and WC by time-dependent receiver-operating characteristic curves. The cohort experienced 2,532 (31.7%) deaths, including 921 CVD mortality, over a median of 90 months. Compared to the lowest quartile, the hazard ratios (95% confidence intervals) for the highest quartile of ABSI and BRI were 3.320 (2.803-3.934) and 1.157 (1.019-1.315), respectively, for all-cause mortality, and 3.796 (2.971-4.850) and 1.319 (1.041-1.671), respectively, for CVD mortality. Dose-response analysis revealed a positive and linear relationship between ABSI and mortality. A nonlinear relationship was identified between BRI with all-cause and CVD mortality. ABSI consistently outperformed BRI, BMI, and WC in predicting all-cause and CVD mortality across almost all follow-up periods. Thus, ABSI emerges as a promising obesity biomarker for predicting all-cause and CVD mortality risk in US adults with CKD, supporting its incorporation into routine CKD prognostication assessment.