Machine learning-based new classification for immune infiltration of gliomas.

Background: Glioma is a highly heterogeneous and poorly immunogenic malignant tumor, with limited efficacy of immunotherapy. The characteristics of the immunosuppressive tumor microenvironment (TME) are one of the important factors hindering the effectiveness of immunotherapy. Therefore, this study aims to reveal the immune microenvironment (IME) characteristics of glioma and predict different immune subtypes using machine learning methods, providing guidance for immune therapy in glioma.

Classification and treatment strategy for Moyamoya disease-related aneurysms.

Background: Moyamoya disease (MMD) is a cerebrovascular disorder characterized by progressive unilateral or bilateral stenosis of the distal internal carotid artery. As hemodynamic features in MMD patients alter, the comorbidity of intracranial aneurysm (IA) is sometimes observed clinically. We aim to investigate clinical characteristics and therapeutic strategies for the comorbidity of Moyamoya disease with intracranial aneurysms (MMD-IA).

Endovascular treatment of intracranial vertebral artery dissecting aneurysm, a case series study with two years follow up on complications.

Background: This study is aimed to analyze the clinical outcomes of endovascular treatments for patients with intracranial vertebral artery dissecting aneurysms.

Methods: Clinical data of 32 patients with vertebral artery dissecting aneurysms who underwent endovascular procedures in the Department of Neurosurgery of our University from January 2016 to December 2019 were retrospectively analyzed. Nine cases were treated with endovascular occlusion; 23 cases received reconstructive treatment, including 20 cases of stent combined with coil embolization, and 3 cases of stent implantation.

Analysis of the common complications and recurrence-related factors of superior parasagittal sinus meningioma.

Objectives: Parasagittal meningioma resection is prone to postoperative complications and tumor recurrence because the tumor invades the superior sagittal sinus. This study aimed to clarify the incidence of perioperative complications and the recurrence of superior sagittal paranasal meningiomas and explored potential predictors in this context.

Methods: The study retrospectively reviewed the clinical, imaging, and follow-up data of parasagittal meningiomas among patients who underwent microsurgical resection in the authors' institution from January 2008 to December 2017.

Analysis of the key prognostic genes and potential traditional Chinese medicine therapeutic targets in glioblastoma based on bioinformatics and network pharmacology methods.

Background: To analyze the key prognostic genes and potential traditional Chinese medicine targets in glioblastoma (GBM) by bioinformatics and network pharmacology.

Methods: GBM datasets were obtained from the Gene Expression Omnibus (GEO) database to clarify the differentially-expressed genes (DEGs) in the carcinoma and paracancerous tissues. The molecular functions (MF) and signaling pathways of enriched DEGs were analyzed by the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses.

CircRFX3 Up-regulates Its Host Gene RFX3 to Facilitate Tumorigenesis and Progression of Glioma.

Background: Glioma is classified as one of the most common types of primary brain tumors. The high expression of CircRFX3 has been found in glioma. However, its functional roles in glioma and underlying mechanism remain unknown.

, Driving the Microglial Polarization, Has a Sensitivity Profile After Subarachnoid Hemorrhage.

Increasing evidence suggests that triggering receptor expressed on myeloid cells 2 () is implicated in the pathophysiology of neuroinflammation. The aim here was to investigate the neuroprotective role of and its regulatory mechanism after subarachnoid hemorrhage (SAH). siRNA was administered to measure the detrimental role of in mediating microglial polarization and after experimental SAH.

LncRNA ANRIL Facilitates Vascular Smooth Muscle Cell Proliferation and Suppresses Apoptosis via Modulation of miR-7/FGF2 Pathway in Intracranial Aneurysms.

Background: Proliferation and apoptosis of vascular smooth muscle cells (VSMCs) are linked to intracranial aneurysm (IA) formation and progression. Long antisense noncoding RNA in the INK4 locus (ANRIL) has been reported to regulate VSMC functions in several cardiovascular diseases. However, little is known about how ANRIL influences VSMC proliferation and apoptosis during IA pathogenesis.

Single-Cell Sequencing of Glioblastoma Reveals Central Nervous System Susceptibility to SARS-CoV-2.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the recent global COVID-19 outbreak, which led to a public health emergency. Entry of SARS-CoV-2 into human cells is dependent on the SARS-CoV receptor, angiotensin converting enzyme 2 (ACE2) receptor, and cathepsin. Cathepsin degrades the spike protein (S protein), which results in the entry of viral nucleic acid into the human host cell.

Methylation associated miR-1246 contributes to poor prognosis in gliomas treated with temozolomide.

Objective: Glioblastoma (GBM) is the most aggressive type of glioma. In this study, we aimed to investigate the biological functions and the possible mechanisms of miR-1246 in glioma.

Methods: A miRNA-seq array was conducted in both the tumor tissues and the glioma cell lines treated with 5-Aza to determine the methylation statues of miRNAs.

Clinical Efficacy and Quality of Life Follow-Up of Reconstructive Endovascular Therapy for Acute Intracranial Vertebral Artery Dissection Aneurysms.

Intracranial vertebral artery dissection aneurysms (VADAs) may cause acute ischemia or hemorrhage, in which case urgent endovascular treatment will be needed. Although the majority of patients obtain a good functional outcome after surgery, a surprising finding has been a poor quality of life (QOL) in follow-up. The purpose of this study was to evaluate clinical efficacy in reconstructive endovascular therapy for acute intracranial VADAs and to analyze the factors contributing to subsequent QOL.

Rosuvastatin Alleviates Intestinal Injury by Down-Regulating the CD40 Pathway in the Intestines of Rats Following Traumatic Brain Injury.

Statins have been reported to suppress CD40 expression and nuclear factor (NF)-κB activation, which are both up-regulated in the intestines following traumatic brain injury (TBI)-induced intestinal injury. In this study, we aimed to investigate the effects of the statin rosuvastatin on post-TBI jejunal injury in rats, focusing on potential mechanisms involving the CD40/NF-κB signaling pathway. The jejunal CD40 expression was determined by western blotting.

Akt Specific Activator SC79 Protects against Early Brain Injury following Subarachnoid Hemorrhage.

A growing body of evidence demonstrates that Akt may serve as a therapeutic target for treatment of early brain injury following subarachnoid hemorrhage (SAH). The purpose of the current study was to evaluate the neuroprotective effect of Akt specific activator SC79 in an experimental rat model of SAH. SAH was induced by injecting 300 μL of blood into the prechiasmatic cistern.

Increased Expression of NLRP3 Inflammasome in Wall of Ruptured and Unruptured Human Cerebral Aneurysms: Preliminary Results.

Background: A growing body of evidence suggests that inflammation actively participates in cerebral aneurysm initiation, progression, and rupture. The primary objective of this study was to assess the expression of NLR family, Pyrin-domain containing 3 (NLRP3) inflammasome in human cerebral aneurysms.

Methods: Aneurysmal domes (19 ruptured and 17 unruptured) from patients undergoing surgical treatment for ruptured or unruptured cerebral aneurysms were analyzed.

Cortical network switching: possible role of the lateral septum and cholinergic arousal.

Background: Cortical networks undergo large-scale switching between states of increased or decreased activity in normal sleep and cognition as well as in pathological conditions such as epilepsy. We previously found that focal hippocampal seizures in rats induce increased neuronal firing and cerebral blood flow in subcortical structures including the lateral septal area, along with frontal cortical slow oscillations resembling slow wave sleep. In addition, stimulation of the lateral septum in the absence of a seizure resulted in cortical deactivation with slow oscillations.

Knockdown of nuclear factor erythroid 2-related factor 2 by lentivirus induces differentiation of glioma stem-like cells.

Glioma stem cells (GSCs) are key in the progression and recurrence of glioblastoma. Inducing the differentiation of GSCs is an important therapeutic target for glioblastoma. Nuclear factor erythroid 2-related factor 2 (Nrf2) has been reported to be important in maintaining the stem cell status of GSCs; however, its association with differentiation has not been studied.

Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro.

Background: Translocation of high-mobility group box 1 (HMGB1) from nucleus could trigger inflammation. Extracellular HMGB1 up-regulates inflammatory response in sepsis as a late mediator. However, little was known about its role in subarachnoid hemorrhage-inducible inflammation, especially in the early stage.

Nuclear receptor nur77 promotes cerebral cell apoptosis and induces early brain injury after experimental subarachnoid hemorrhage in rats.

Nur77 is a potent proapoptotic member of the nuclear receptor superfamily that is expressed predominantly in brain tissue. It has been demonstrated that Nur77 mediates apoptosis in multiple organs. Nur77-mediated early brain injury (EBI) involves a conformational change in BCL-2 and triggers cytochrome C (cytoC) release resulting in cellular apoptosis.

Cyclosporin A ameliorates early brain injury after subarachnoid hemorrhage through inhibition of a Nur77 dependent apoptosis pathway.

Nur77 is a potent pro-apoptotic member of the orphan nuclear receptor superfamily. It has been demonstrated that can mediate apoptosis in many system cells in response to extracellular stimuli. Our previous study revealed Nur77-mediated apoptotic also involved in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH).

Biphasic activation of nuclear factor kappa B and expression of p65 and c-Rel after traumatic brain injury in rats.

Background And Object: Nuclear factor kappa B (NF-κB) functions as a key regulator in the central nervous system and regulates the inflammatory pathway. There are two peaks of cerebral NF-κB activation after neonatal hypoxia-ischemia and subarachnoid hemorrhage. Our previous studies found that NF-κB activity was up-regulated at an early stage and remained elevated at day 7 after traumatic brain injury (TBI).

Glycyrrhizic acid confers neuroprotection after subarachnoid hemorrhage via inhibition of high mobility group box-1 protein: a hypothesis for novel therapy of subarachnoid hemorrhage.

Subarachnoid hemorrhage usually results in poor clinical outcome and devastating neurological deficits. The early brain injury and delayed vasospasm after subarachnoid hemorrhage (SAH) are involved in the poor prognosis to the patients, while the mechanisms have not been well elucidated. Previous studies found an up-regulation of Toll-like receptor 4 (TLR4), inflammatory factors and high-mobility group box 1 (HMGB1) in the cortex after SAH.

Expression of the NLRP3 inflammasome in cerebral cortex after traumatic brain injury in a rat model.

Inflammatory response plays an important role in the pathogenesis of secondary damage after traumatic brain injury (TBI). The inflammasome is a multiprotein complex involved in innate immunity and a number of studies have suggested that the inflammasome plays a critical role in a host inflammatory signaling. Nucleotide-binding domain, leucine-rich repeat, pyrin domain containing 3 (NLRP3) is a key component of the NLRP3-inflammasome, which also includes apoptotic speck-containing protein (ASC) with a cysteine protease (caspase)-activating recruitment domain and pro-caspase1.

Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: a pilot study.

Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH.

Expression of intestinal CD40 after experimental traumatic brain injury in rats.

Background: Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI.