Impaired microglial glycolysis promotes inflammatory responses after intracerebral haemorrhage via HK2-dependent mitochondrial dysfunction.

Introduction: Intracerebral haemorrhage (ICH) is a devastating disease that leads to severe neurological deficits. Microglia are the first line of defence in the brain and play a crucial role in neurological recovery after ICH, whose activities are primarily driven by glucose metabolism. However, little is known regarding the status of glucose metabolism in microglia and its interactions with inflammatory responses after ICH.

Subchronic exposure to di-(2-ethylhexyl) phthalate (DEHP) elicits blood-brain barrier dysfunction and neuroinflammation in male C57BL/6J mice.

Exposure to di-(2-ethylhexyl) phthalate (DEHP) can cause neurotoxicity but the mechanism is not clear. Blood brain barrier (BBB) is one of the most important tissues to protect the brain. However, whether DEHP can disrupt the BBB or not remains unclear.

Role of complement C1q/C3-CR3 signaling in brain injury after experimental intracerebral hemorrhage and the effect of minocycline treatment.

Aim: The complement cascade is activated and may play an important pathophysiologic role in brain injury after experimental intracerebral hemorrhage (ICH). However, the exact mechanism of specific complement components has not been well studied. This study determined the role of complement C1q/C3-CR3 signaling in brain injury after ICH in mice.

Neutrophil to lymphocyte ratio predicting poor outcome after aneurysmal subarachnoid hemorrhage: A retrospective study and updated meta-analysis.

Background: The relationship between neutrophil to lymphocyte ratio (NLR) and poor outcome of aneurysmal subarachnoid hemorrhage (aSAH) is controversial. We aim to evaluate the relationship between NLR on admission and the poor outcome after aSAH.

Method: Part I: Retrospective analysis of aSAH patients in our center.

Influence of Nurse-Led Health Education on Self-Management Ability, Satisfaction, and Compliance of Elderly Patients with Chronic Obstructive Pulmonary Disease Based on Knowledge, Belief, and Practice Model.

Objective: Knowledge, belief, and behavior model (knowledge-attitude-practice (KAP)) is known as a cognitive model. Health education is important to the prognosis of patients, including chronic obstructive pulmonary disease (COPD) patients. However, the investigation regarding health education based on the KAP model is few.

Inhibition of Mer exacerbates early brain injury by regulating microglia/macrophage phenotype after subarachnoid hemorrhage in mice.

Background: Polarization of microglia/macrophages toward the pro-inflammatory phenotype is a crucial contributor to neuroinflammation after subarachnoid hemorrhage (SAH). Mer belongs to the TAM receptor tyrosine kinases family, which is known to play a significant role in the resolution of inflammation. However, the effect and mechanism of Mer after SAH remain unclear.

Sex-Associated Differences in Neurovascular Dysfunction During Ischemic Stroke.

Neurovascular units (NVUs) are basic functional units in the central nervous system and include neurons, astrocytes and vascular compartments. Ischemic stroke triggers not only neuronal damage, but also dissonance of intercellular crosstalk within the NVU. Stroke is sexually dimorphic, but the sex-associated differences involved in stroke-induced neurovascular dysfunction are studied in a limited extend.

Probenecid-Blocked Pannexin-1 Channel Protects Against Early Brain Injury Inhibiting Neuronal AIM2 Inflammasome Activation After Subarachnoid Hemorrhage.

Aim: Previous studies have proved that inhibiting inflammasome activation provides neuroprotection against early brain injury (EBI) after subarachnoid hemorrhage (SAH), which is mainly focused on the microglial inflammatory response, but the potential role of neuronal inflammasome activation in EBI has not been clearly identified. This study examined whether the pannexin-1 channel inhibitor probenecid could reduce EBI after SAH by inhibiting neuronal AIM2 inflammasome activation.

Methods: There are and parts in this study.

Changes of FSTL1 and MMP-9 levels in patients with acute cerebral infarction and its relationship with hemorrhagic transformation.

Background: hemorrhagic transformation is a serious complication of acute ischemic stroke, which may lead to poor prognosis and delayed use of anticoagulant therapy.

Methods: 125 patients with cerebral infarction from December 2019 to December 2020 in the Second Affiliated Hospital of Zhejiang University were selected. All patients did not receive intravascular therapy, intravenous thrombolysis and other reperfusion treatment; and the relevant laboratory data were collected within 24 h after admission.

Metformin Alleviates Neuroinflammation Following Intracerebral Hemorrhage in Mice by Regulating Microglia/Macrophage Phenotype in a Gut Microbiota-Dependent Manner.

The gut microbiota plays a key role in regulating intracerebral hemorrhage (ICH)-induced neuroinflammation. The anti-neuroinflammatory effects of metformin (Met) have been reported in many central nervous system (CNS) diseases. However, whether Met regulates neuroinflammation through the gut microbiota in ICH-induced brain injury remains unknown.

The Critical Role of Erythrolysis and Microglia/Macrophages in Clot Resolution After Intracerebral Hemorrhage: A Review of the Mechanisms and Potential Therapeutic Targets.

Intracerebral hemorrhage (ICH) is a common cerebrovascular disorder with high morbidity and mortality. Secondary brain injury after ICH, which is initiated by multiple hemolytic products during erythrolysis, has been identified as a critical factor accounting for the poor prognosis of ICH patients. Clot resolution and hematoma clearance occur immediately after ICH via erythrolysis and erythrophagocytosis.

Autophagy protein NRBF2 attenuates endoplasmic reticulum stress-associated neuroinflammation and oxidative stress via promoting autophagosome maturation by interacting with Rab7 after SAH.

Background: Neuroinflammation and oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study is the first to show that activation of autophagy protein nuclear receptor binding factor 2 (NRBF2) could reduce endoplasmic reticulum stress (ERS)-associated inflammation and oxidative stress after SAH.

Methods: Male C57BL/6J mice were subjected to endovascular perforation to establish a model of SAH.

Two Co(II) coordination polymers: magnetic properties and application values against chronic subdural hematoma.

In this current experiment, by applying the mixed-ligand synthesis method, two coordination polymers (CPs) containing Co(II) were created triumphantly with reaction between 1,3-bis(1-imidazoly)benzene (mbib) and Co(II) salts with the aid of diverse carboxylic ligands, and their chemical formulae are [Co(opda)(mbib)(HO)]·2HO (, Hopda is 1,2-phenylenediacetic acid) and [Co(mpda)(mbib)]·HO (, Hmpda is 1,3-phenylenediacetic acid). The two compounds' magnetic performances suggest that between the adjacent metal ions, there present the antiferromagnetic coupling. The evaluation of their treatment activity against chronic subdural hematoma was carried out and the relevant mechanism was studied simultaneously.

AXL kinase-mediated astrocytic phagocytosis modulates outcomes of traumatic brain injury.

Background: Complex changes in the brain microenvironment following traumatic brain injury (TBI) can cause neurological impairments for which there are few efficacious therapeutic interventions. The reactivity of astrocytes is one of the keys to microenvironmental changes, such as neuroinflammation, but its role and the molecular mechanisms that underpin it remain unclear.

Methods: Male C57BL/6J mice were subjected to the controlled cortical impact (CCI) to develop a TBI model.

Neutrophil extracellular traps, released from neutrophil, promote microglia inflammation and contribute to poor outcome in subarachnoid hemorrhage.

Evidence indicates that neutrophil has promoted inflammation in several central nervous system diseases. However, whether the peripheral blood levels of neutrophils are associated with the functional outcome after subarachnoid hemorrhage and its potential mechanism remain unclear. In this study, we showed that neutrophil levels in peripheral blood were higher in patients with subarachnoid hemorrhage ( < 0.

Neutrophil Extracellular Traps may be a Potential Target for Treating Early Brain Injury in Subarachnoid Hemorrhage.

Neuroinflammation is closely associated with poor prognosis in patients with subarachnoid hemorrhage (SAH). The purpose of this study was to investigate the role of neutrophil extracellular traps (NETs), which are important regulators of sterile inflammation, in SAH. In this study, markers of NET formation, quantified by the level of citrullinated histone H3 (CitH3), were significantly increased after SAH and correlated with SAH severity.

Wogonin Accelerates Hematoma Clearance and Improves Neurological Outcome via the PPAR-γ Pathway After Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity for which effective treatments are currently lacking. Wogonin is a major flavonoid compound isolated from Scutellaria radix. Accumulating evidence suggests that wogonin plays a crucial role in anti-inflammatory and anti-oxidative stress.

Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage.

Background: Neuroinflammation is closely associated with the poor prognosis in subarachnoid hemorrhage (SAH) patients. This study was aimed to determine the role of stimulator of IFN genes (STING), an essential regulator to innate immunity, in the context of SAH.

Methods: A total of 344 male C57BL/6 J mice were subjected to endovascular perforation to develop a model of SAH.

Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling.

Leucine-rich glioma inactivated 1 (Lgi1), a putative tumor suppressor, is tightly associated with autosomal dominant lateral temporal lobe epilepsy (ADLTE). It has been shown that Lgi1 regulates the myelination of Schwann cells in the peripheral nervous system (PNS). However, the function and underlying mechanisms for Lgi1 regulation of oligodendrocyte differentiation and myelination in the central nervous system (CNS) remain elusive.

Accuracy of magnetic resonance venography in diagnosing cerebral venous sinus thrombosis.

Objectives: The non-specific clinical manifestations and lack of effective diagnostic techniques have made cerebral venous sinus thrombosis (CVST) difficult to recognize and easy to misdiagnose. Several studies have suggested that different types of magnetic resonance venography (MRV) have advantages in diagnosing CVST. We conducted this meta-analysis to assess the accuracy of MRV in identifying CVST.

Phosphodiesterase-4 inhibition confers a neuroprotective efficacy against early brain injury following experimental subarachnoid hemorrhage in rats by attenuating neuronal apoptosis through the SIRT1/Akt pathway.

Phosphodiesterase-4 (PDE4) plays a fundamental role in a range of central nervous system (CNS) insults, however, the role of PDE4 in early brain injury (EBI) after subarachnoid hemorrhage (SAH) remains unclear. The current study was designed to investigate the role of PDE4 in EBI after SAH and explore the potential mechanism. The SAH model in Sprague-Dawley rat was established by endovascular perforation process.

Minocycline Effects on Intracerebral Hemorrhage-Induced Iron Overload in Aged Rats: Brain Iron Quantification With Magnetic Resonance Imaging.

Background And Purpose: Brain iron overload is a key factor causing brain injury after intracerebral hemorrhage (ICH). This study quantified brain iron levels after ICH with magnetic resonance imaging R2* mapping. The effect of minocycline on iron overload and ICH-induced brain injury in aged rats was also determined.