Xuan Wu Hospital of the Capital Medical University

The authors declare no conflicts of interest. Supplementary Figure 1: Histopathological and immunohistochemical features of intracranial lesion tissue. (A) Foamy histiocytes are seen (haematoxylin and eosin, original magnification×200). (B) Foamy histiocytes are positive for CD68 (×200). (C) Histiocytes are negative for CD1a (×200). (D) Histiocytes are negative for Langerin (×200). Suplementary Figure 2: 18F-FDG-PET/CT images at initial diagnosis. (A-C) PET/CT scan shows multiple metabolically active lesions in the bilateral cerebellar hemispheres, sellar region, and pineal region (green circles). (D-F) PET/CT scan demonstrates metabolically active abnormal bone lesions involving the bilateral pelvic bones, femurs, and multiple bones of the feet (green and blue circles). Supplementary Figure 3: 18F-FDG-PET/CT images after dabrafenib treatment. (A-C) PET/CT scan shows complete normalization of metabolic activity in the CNS lesions after 15 months of dabrafenib treatment. (D-F) PET/CT scan demonstrates metabolic normalization in the bone lesions after 15 months of dabrafenib treatment. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Bloodstream infection (BSI) is associated with a high mortality, ranging from 17 to 32%. Once pathogens enter the bloodstream, they can activate platelets and trigger systemic inflammation. Antiplatelet agents suppress platelet activation and modulate inflammatory responses; however, it remains unclear whether their use reduces mortality in patients with BSI. This study aimed to evaluate the impact of antiplatelet therapy on clinical outcomes in patients with BSI. We retrospectively analyzed patients diagnosed with BSI at Xuanwu Hospital, Capital Medical University, between 2013 and 2023. Patients were categorized into antiplatelet and non-antiplatelet groups. Propensity score matching was performed to minimize potential confounders, including age, sex, body mass index, year of onset, Charlson Comorbidity Index, and anticoagulant therapy. For the primary outcome (30-day all-cause mortality), group differences were analyzed using the logistic regression models, with results reported as odds ratios and 95% confidence intervals. Secondary endpoints, including respiratory failure, septic shock, acute kidney injury, and bleeding events, were similarly compared using the logistic regression. Subgroup analyses were performed according to causative pathogens and types of antiplatelet agents, with covariates showing standardized mean differences >0.1 included in the models. After Propensity score matching, a total of 248 patients were included in the analysis, with 124 patients in each group). The 30-day all-cause mortality following BSI diagnosis was significantly lower in the antiplatelet group (OR 0.35; 95% CI 0.17-0.71, P = 0.004). Septic shock, respiratory failure, acute kidney injury, and bleeding events showed no significant differences between groups (OR 1.08; 95% CI 0.50-2.34; P = 0.843, OR 0.72; 95% CI 0.33-1.60; P = 0.424, OR 1.20; 95% CI 0.31-2.33; P = 0.608, OR 0.71; 95% CI 0.55-2.37; P = 0.712). Subgroup analyses revealed that antiplatelet therapy significantly reduced mortality in patients with Gram-negative BSI (OR 0.26; 95% CI 0.08-0.87; P = 0.029). In addition, clopidogrel monotherapy was associated with lower mortality (OR 0.17; 95% CI 0.03-0.90; P = 0.017). In patients with BSI, antiplatelet therapy significantly reduced 30-day all-cause mortality without an increasing risk of bleeding.

BackgroundDetermining the location of paraclinoid aneurysms (PAs) is crucial. We aimed to evaluate the utility of paraclinoid high-resolution MRI (HRMRI) in determining PA locations.MethodsWe enrolled patients with suspected PAs who underwent our HRMRI sequence in 6 months. PAs were categorized into five types based on their origin from the internal carotid artery (ICA): Superior ophthalmic segment (Type S), Ventral ophthalmic segment (Type V), Medial clinoidal segment (Type M), Lateral clinoidal segment Type L, and Posterior clinoidal segment) (Type P). The paraclinoid HRMRI protocol included five main sequences: TOF-MRA, coronal and saggital high-resolution T2-weighted images, coronal and saggital enhanced high-resolution T1-weighted images. We utilized cerebrospinal fluid (CSF) notch and cavernous sinus enhanced signals to determine the location of PAs.ResultsSixty-nine patients with 75 PAs were included. Based on our classification, there were 10 Type S, 2 Type V, 45 Type M, 11 Type L, and 7 Type P PAs. Among the Type S PAs, 9 were fully located within the subarachnoid space, and 1 was in the juncture area. Both Type V PAs were situated within the cavernous sinus. Among the Type M PAs, 34 were located in the cavernous sinus, and 1 was in the juncture. Of the Type L PAs, 5 were within the cavernous sinus, and 1 was in the juncture area. All 7 Type P PAs were located within the cavernous sinus.ConclusionsHRMRI sequences may assist in determining the location of PAs and could provide useful information for clinical decision-making, especially when radiation-free or iodine-free evaluation is preferred.Trial registrationThe clinical trial of China Internal Aneurysm Project (NCT03115905).

BackgroundGamma transcranial alternating current stimulation (tACS) has shown promise in enhancing cognitive function in patients with Alzheimer's disease (AD). However, the impact of gamma tACS on regional glymphatic flow remain unclear.MethodA total of 46 patients with mild AD were randomly assigned in a 1:1 ratio to receive either 30 one‐hour sessions of 40Hz (gamma) tACS or sham stimulation over 15 consecutive days (Clinical Trial: NCT03920826). Global blood oxygen level‐dependent (BOLD) signals and cerebrospinal fluid (CSF) inflow coupling were measured using resting‐state functional MRI to evaluate glymphatic flow, which was acquired at baseline and right after the intervention, along with cognitive assessments.ResultsCompared to baseline, patients in the tACS group exhibited increased BOLD‐CSF coupling in the left frontal lobe, left posterior lobe, right posterior lobe, and bilateral rostral hippocampus at the end of the intervention. Additionally, changes in regional glymphatic flow in the right temporal lobe, right parietal lobe, and bilateral rostral hippocampus showed a positive correlation with changes in cognitive assessments.ConclusionThe findings demonstrated the beneficial effects of gamma tACS on regional brain glymphatic flow, which might represent a potential therapeutic mechanism of tACS.

The aim of this study is to investigate the role of hydroxycarboxylic acid receptor 1 (HCAR1) in glutamate-induced excitotoxic neuronal injury. The effective and safe concentrations of an endogenous HCAR1 agonist (L-lactic acid) and an exogenous HCAR1 agonist (3,5-dihydroxybenzoic acid, 3,5-DHBA) were determined using a CCK-8 assay. An excitotoxic injury model was established by stimulating mouse hippocampal neuronal cells (HT22 cells) with 20 mM glutamate, followed by intervention with safe concentrations of L-lactic acid and 3,5-DHBA. Neuronal survival and apoptosis were assessed by NeuN immunofluorescence staining and a TUNEL assay. The effects of HCAR1 agonists on glutamate transport were evaluated using vesicular glutamate transporter 1 (VGLUT1) immunofluorescence staining and qRT‒PCR. Additionally, qRT‒PCR was performed to quantify the expression of a neuronal excitability marker gene ( c-fos ), inflammatory factors and hcar1 . The results showed that HCAR1 agonists (L-lactic acid and 3,5-DHBA) significantly improved neuronal survival, reduced glutamate-induced apoptosis and decreased neuronal excitability ( p < 0.05). The activation of HCAR1 inhibited the transport of the excitatory neurotransmitter glutamate ( p < 0.05). The upregulation of HCAR1 expression led to the significant downregulation of the expression of inflammatory factors ( il-1β , il-6 and tnf-α ) ( p < 0.05). In conclusion, HCAR1 activation effectively suppresses glutamate-induced neuronal apoptosis, reduces the uptake of excitatory neurotransmitters, and downregulates proinflammatory factor expression, thereby exerting neuroprotective effects.

Abstract Background Current clinical management for orthostatic hypotension (OH) in α-synucleinopathies is passive and lacks specificity, and objective tools for accurately assessing the true risk level in OH patients are lacking. Therefore, this study aimed to develop an objective tool to quantify OH severity, enabling individualized and precision-based clinical management of OH. Methods From January 2021 to March 2025, patients with OH at Beijing Xuanwu Hospital were assigned an OH Symptom-Based Risk Score (0–2 points) based on symptom severity. Active standing tests were performed to continuously collect data including blood pressure (BP) and cerebral blood flow velocity (CBFv). Two predictive models were developed: one to identify patients with versus without OH symptoms, and another to predict high-risk patients prone to critical events among symptomatic patients (scoring 1–2 points). Results Among 172 patients with OH (86 asymptomatic, 50%), symptomatic patients showed greater orthostatic reductions in BP and CBFv (both maximum and mean decreases, all P < 0.05) than asymptomatic patients. OH Symptom-Based Risk Scores were significantly correlated with all orthostatic BP and CBFv decline parameters (all P < 0.001). Binary logistic regression models successfully identified symptomatic patients and predicted patients at high risk for critical events among symptomatic patients, with bootstrap-validated accuracy exceeding 70% in multiple models. Orthostatic BP and CBFv decline parameters were independent predictors of OH. Conclusion The established models provide an objective tool for quantifying OH risk severity, showing significant potential for early clinical warning and optimization of OH management strategies.

Aims This study examined the characteristics and high-risk phases of medication errors (MEs) involving low-molecular-weight heparin (LMWH) by analyzing medical malpractice litigation cases in China. Methods Cases were retrieved from China Judgements O

The data that support the findings of this study are available from the corresponding author upon reasonable request. Appendix S1: all70015-sup-0001-Supinfo1.docx. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.