ABSTRACT Purpose: Stroke is an acute cerebrovascular disease. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with an established therapeutic effect on central nervous system diseases. This study examined the neuroprotective properties and possible mechanisms of AS-IV in stroke-triggered early brain injury (EBI) in a rat transient middle cerebral artery occlusion (MCAO) model. Methods: The neurological scores and brain water content were analyzed. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was utilized to determine the infarct volume, neuroinflammatory cytokine levels, and ferroptosis-related genes and proteins, and neuronal damage and molecular mechanisms were evaluated by terminal deoxynucleotidyl transferase dutp nick-end labeling (TUNEL) staining, western blotting, and real-time polymerase chain reaction. Results: AS-IV administration decreased the infarct volume, brain edema, neurological deficits, and inflammatory cytokines TNF-α, interleukin-1β (IL-1β), IL-6, and NF-κB, increased the levels of SLC7A11 and glutathione peroxidase 4 (GPX4), decreased lipid reactive oxygen species (ROS) levels, and prevented neuronal ferroptosis. Meanwhile, AS-IV triggered the Nrf2/HO-1 signaling pathway and alleviated ferroptosis due to the induction of stroke. Conclusions: Hence, the findings of this research illustrate that AS-IV administration can improve delayed ischemic neurological deficits and decrease neuronal death by modulating nuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway. Purpose disease ASIV AS (AS-IV diseases stroketriggered stroke EBI (EBI MCAO (MCAO model Methods analyzed 2,3,5triphenyl 235triphenyl triphenyl 2,3,5 2 3 5 TTC (TTC volume ferroptosisrelated related proteins nickend nick end TUNEL (TUNEL blotting realtime real time reaction Results edema TNFα, TNFα TNF α, α TNF-α interleukin1β interleukinβ interleukin 1β β IL1β, IL1β ILβ IL , (IL-1β) IL6, IL6 6, 6 IL-6 NFκB, NFκB NF κB, κB NF-κB SLCA SLC A SLC7A1 GPX4, GPX4 GPX (GPX4) ROS (ROS Meanwhile Nrf2/HO1 Nrf2HO1 NrfHO Nrf2/HO 1 Nrf2 HO Nrf Nrf2/HO- Conclusions Hence 5triphenyl 235 2,3, (IL-1β IL- SLC7A (GPX4 HO1 Nrf2HO 23 2,3 (GPX 2,

SUMMARY OBJECTIVE: This study aimed to develop and validate a practical nomogram to predict the occurrence of post-traumatic hydrocephalus in patients who have undergone decompressive craniectomy for traumatic brain injury. METHODS: A total of 516 cases were enrolled and divided into the training (n=364) and validation (n=152) cohorts. Optimal predictors were selected through least absolute shrinkage and selection operator regression analysis of the training cohort then used to develop a nomogram. Receiver operating characteristic, calibration plot, and decision curve analysis, respectively, were used to evaluate the discrimination, fitting performance, and clinical utility of the resulting nomogram in the validation cohort. RESULTS: Preoperative subarachnoid hemorrhage Fisher grade, type of decompressive craniectomy, transcalvarial herniation volume, subdural hygroma, and functional outcome were all identified as predictors and included in the predicting model. The nomogram exhibited good discrimination in the validation cohort and had an area under the receiver operating characteristic curve of 0.80 (95%CI 0.72–0.88). The calibration plot demonstrated goodness-of-fit between the nomogram’s prediction and actual observation in the validation cohort. Finally, decision curve analysis indicated significant clinical adaptability. CONCLUSION: The present study developed and validated a model to predict post-traumatic hydrocephalus. The nomogram that had good discrimination, calibration, and clinical practicality can be useful for screening patients at a high risk of post-traumatic hydrocephalus. The nomogram can also be used in clinical practice to develop better therapeutic strategies.

ABSTRACT Purpose: Spontaneous intracerebral hemorrhage (ICH) is still a major public health problem, with high mortality and disability. Ulinastatin (UTI) was purified from human urine and has been reported to be anti-inflammatory, organ protective, and antioxidative stress. However, the neuroprotection of UTI in ICH has not been confirmed, and the potential mechanism is unclear. In the present study, we aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in ICH-induced early brain injury in a C57BL/6 mouse model. Methods: The neurological score, brain water content, neuroinflammatory cytokine levels, oxidative stress levels, and neuronal damage were evaluated. Results: UTI treatment markedly increased the neurological score, alleviated brain edema, decreased the levels of the inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and NF-κB, decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and upregulated the levels of glutathione (GSH), superoxide dismutase (SOD), and Nrf2. This finding indicated that UTI-mediated inhibition of neuroinflammation and oxidative stress alleviated neuronal damage after ICH. The neuroprotective capacity of UTI is partly dependent on the ROS/MAPK/Nrf2 signaling pathway. Conclusions: UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation and oxidative stress.

Abstract In December 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) began to break out in the Hubei Province of China. At present, the epidemic situation in the world continues and the number of confirmed cases is increasing every day. A recent review showed that children under the age of ten years make up about 1% of the infected population, which cannot be ignored. Studies have shown that after SARS-CoV-2 infection children can show clinical symptoms of cardiovascular system damage in addition to typical respiratory symptoms. This article mainly discusses the possible damage of SARS-CoV-2 to children's cardiovascular system and related mechanisms. 2019 SARSCoV2 SARSCoV SARS CoV (SARS-CoV-2 China present day 1 population ignored SARS-CoV- childrens s mechanisms 201 (SARS-CoV- SARS-CoV 20 (SARS-CoV

ABSTRACT Purpose To evaluate the effects of controlled decompression and rapid decompression, explore the potential mechanism, provide the theoretical basis for the clinical application, and explore the new cell death method in intracranial hypertension. Methods Acute intracranial hypertension was triggered in rabbits by epidural balloon compression. New Zealand white rabbits were randomly put into the sham group, the controlled decompression group, and the rapid decompression group. Brain water content, etc., was used to evaluate early brain injury. Western blotting and double immunofluorescence staining were used to detect necroptosis and apoptosis. Results Brain edema, neurological dysfunction, and brain injury appeared after traumatic brain injury (TBI). Compared with rapid decompression, brain water content was significantly decreased, neurological scores were improved by controlled decompression treatment. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Nissl staining showed neuron death decreased in the controlled decompression group. Compared with rapid decompression, it was also found that apoptosis-related protein caspase-3/ tumor necrosis factor (TNF)-a was reduced markedly in the brain cortex and serum, and the expression levels of necroptosis-related protein, receptor-interacting protein 1 (RIP1)/receptor-interacting protein 1 (RIP3) reduced significantly in the controlled decompression group. Conclusions Controlled decompression can effectively reduce neuronal damage and cerebral edema after craniocerebral injury and, thus, protect the brain tissue by alleviating necroptosis and apoptosis.