Association of hydration status and in-hospital mortality in critically ill patients with ischemic stroke: Data from the MIMIC-IV database.

BACKGROUND: Hydration plays a critical role in the pathophysiological progression of ischemic stroke. However, the impact of extreme hydration on the mortality of critically ill patients with ischemic stroke remains unclear. Therefore, our objective was to evaluate the association between hydration, as indicated by the blood urea nitrogen to creatinine ratio (UCR), and in-hospital mortality in critically ill patients with ischemic stroke. METHODS: Data from the Medical Information Mart for Intensive Care (MIMIC-IV) database were utilized. Patients with ischemic stroke admitted to the Intensive Care Unit (ICU) for the first time were identified. The exposure variable was the hydration state represented by the UCR. The study outcome measure was in-hospital mortality. The primary analytical approach involved multivariate Cox regression analysis. Kaplan-Meier curves were constructed, and subgroup analyses with interaction were performed. RESULTS: A total of 1539 patients, with a mean age of 69.9 years, were included in the study. Kaplan-Meier curves illustrated that patients in higher UCR tertiles exhibited increased in-hospital mortality. Accordingly, the risk of in-hospital mortality significantly rose by 29 % with every 10 units increase in UCR. Subgroup analysis indicated a robust association between UCR and in-hospital mortality in each subgroup, with no statistically significant interactions observed. CONCLUSION: Hydration status is significantly associated with in-hospital all-cause mortality in critically ill patients with ischemic stroke. This finding underscores the importance of closely monitoring critically ill patients for adequate hydration and implementing appropriate rehydration strategies.

Long-term L-3-n-butylphthalide pretreatment attenuates ischemic brain injury in mice with permanent distal middle cerebral artery occlusion through the Nrf2 pathway.

L-3-n-butylphthalide (NBP), which is used for treatment of mild and moderate acute ischemic stroke, exerts its effects by modulating the Nrf2 pathway. However, it has not been established whether NBP exerts its preventive effects in high-risk ischemic stroke patients through the Nrf2 pathway. We investigated whether NBP exerts its preventive effects through the Nrf2 pathway in long-term NBP pretreated dMCAO mice models. Nrf2+/+ wild-type and Nrf2-/- knockout mice were randomized into the vehicle group (equal volume vegetable oil), NBP-low-dose group (20 mg/kg) and NBP-high-dose group (60 mg/kg). The drug was administered once daily by gavage for a month. Then, a permanent distal middle cerebral artery occlusion model (dMCAO) was established after pretreatment with NBP. Neurological deficits, cerebral infarct volumes, brain water contents, activities of SOD, GSH-Px and MDA levels were determined. Further, axonal injury and demyelination, expression levels of Nrf2, HO-1 and NQO1 in ischemic brains were determined. Long-term NBP pretreatment significantly improved neurological functions, reduced cerebral infarction volumes, reduced brain water contents, increased SOD, GSH-Px activities, decreased MDA contents, reduced neurological injuries, axonal damage as well as demyelination, while increasing Nrf2, HO-1 and NQO1 mRNA as well as protein expressions in dMCAO mice models.

Corrigendum to "Long-term L-3-n-butylphthalide pretreatment attenuates ischemic brain injury in mice with permanent distal middle cerebral artery occlusion through the Nrf2 pathway" [Heliyon 8 (7), (July 2022), Article e09909].

[This corrects the article DOI: 10.1016/j.heliyon.2022.e09909.].

Conditioned Media of Choroid Plexus Epithelium Cells Attenuates High Pi-Induced Calcification of MOVAS Cells by Inhibiting ROS-Mediated Signal Pathways.

Vascular calcification was an independent risk of cardiovascular and cerebrovascular diseases (CCDs). Studies reported that conditioned media of choroid plexus epithelium cells (CPECs-CM) showed potential neuroprotective effects. However, the protective effect of CPECs-CM against vascular calcification (VC) has not been reported yet. Herein, high phosphate (HPi)-induced calcification model in mouse aortic vascular smooth muscle cells (MOVAS) was established, and the protective effects and underlying mechanism of CPECs-CM against HPi-induced calcification were explored. The results indicated that CPEC cells were successfully isolated and cultured, and CPECs-CM co-treatment significantly inhibited HPi-induced calcification of MOVAS cells through blocking alkaline phosphatase activity and expression. CPECs-CM co-treatment also suppressed reactive oxide species-mediated DNA damage in HPi-treated MOVAS cells. Moreover, dysfunction of MAPKs and PI3K/AKT pathways both contributed to HPi-induced calcification of MOVAS cells, and CPECs-CM co-treatment attenuated HPi-induced calcification by normalizing MAPKs and PI3K/AKT expression. Taken together, our findings provide evidence that CPECs-CM had the potential to inhibit vascular calcification with potent application in chemoprevention and chemotherapy of human CCD.