Construction and validation of a perioperative concomitant lower extremity deep vein thrombosis line graph model in patients with aneurysmal subarachnoid hemorrhage.

Background: To develop and validate a nomogram for predicting the probability of deep venous thrombosis (DVT) in patients with aneurysmal subarachnoid hemorrhage (aSAH) during the perioperative period, using clinical features and readily available biochemical parameters. Methods: The least absolute shrinkage and selection operator (LASSO) regression technique was employed for data dimensionality reduction and selection of predictive factors. A multivariable logistic regression analysis was conducted to establish a predictive model and nomogram for post-aSAH DVT. The discriminative ability of the model was determined by calculating the area under the curve (AUC). Results: A total of 358 aSAH patients were included in the study, with an overall incidence of DVT of 20.9%. LASSO regression identified four variables, including age, modified Fisher grade, total length of hospital stay, and anticoagulation therapy, as highly predictive factors for post-aSAH DVT. The patients were randomly divided into a modeling group and a validation group in a 6:4 ratio to construct the nomogram. The AUCs of the modeling and validation groups were 0.8511 (95% CI, 0.7922-0.9099) and 0.8633 (95% CI, 0.7968-0.9298), respectively. Conclusions: The developed nomogram exhibits good accuracy, discriminative ability, and clinical utility in predicting DVT, aiding clinicians in identifying high-risk individuals and implementing appropriate preventive and treatment measures.

Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.

AIMS: Rasd1 has been reported to be correlated with neurotoxicity, metabolism, and rhythm, but its effect in case of subarachnoid hemorrhage (SAH) remained unclear. White matter injury (WMI) and ferroptosis participate in the early brain injury (EBI) after SAH. In this work, we have investigated whether Rasd1 can cause ferroptosis and contribute to SAH-induced WMI. METHODS: Lentivirus for Rasd1 knockdown/overexpression was administrated by intracerebroventricular (i.c.v) injection at 7 days before SAH induction. SAH grade, brain water content, short- and long-term neurobehavior, Western blot, real-time PCR, ELISA, biochemical estimation, immunofluorescence, diffusion tensor imaging (DTI), and transmission electron microscopy (TEM) were systematically performed. Additionally, genipin, a selective uncoupling protein 2(UCP2) inhibitor, was used in primary neuron and oligodendrocyte co-cultures for further in vitro mechanistic studies. RESULTS: Rasd1 knockdown has improved the neurobehavior, glia polarization, oxidative stress, neuroinflammation, ferroptosis, and demyelination. Conversely, Rasd1 overexpression aggravated these changes by elevating the levels of reactive oxygen species (ROS), inflammatory cytokines, MDA, free iron, and NCOA4, as well as contributing to the decrease of the levels of UCP2, GPX4, ferritin, and GSH mechanistically. According to the in vitro study, Rasd1 can induce oligodendrocyte ferroptosis through inhibiting UCP2, increasing reactive oxygen species (ROS), and activating NCOA4-mediated ferritinophagy. CONCLUSIONS: It can be concluded that Rasd1 exerts a modulated role in oligodendrocytes ferroptosis in WMI following SAH.