Identification of a Signature for Predicting Prognosis and Immunotherapy Response in Patients with Glioma.

Glioma is a deadly tumor that accounts for the vast majority of brain tumors. Thus, it is important to elucidate the molecular pathogenesis and potential diagnostic and prognostic biomarkers of glioma. In the present study, gene expression profiles of GSE2223 were obtained from the Gene Expression Omnibus (GEO) database.

Acute Treatment with Nicotinamide Riboside Chloride Reduces Hippocampal Damage and Preserves the Cognitive Function of Mice with Ischemic Injury.

Nicotinamide adenine dinucleotide (NAD) is a critical cosubstrate for enzymes involved in supplying energy to the brain. Nicotinamide riboside (NR), an NAD precursor, emerges as a neuroprotective factor after chronic brain insults. However, researchers have not determined whether it improves cognition after acute ischemia.

Galectin-1 Contributes to Vascular Remodeling and Blood Flow Recovery After Cerebral Ischemia in Mice.

Galectin-1 is found in the vasculature and has been confirmed to promote angiogenesis in several cancer models. Furthermore, galectin-1 has been demonstrated to improve the recovery of cerebral ischemia. However, whether vascular remodeling contributes to this improvement is still unknown.

Systematic evaluation during early-phase ischemia predicts outcomes in middle cerebral artery occlusion mice.

Identifying outcome predictors for ischemic stroke is beneficial for choosing correct intervention protocols. Thus, it is necessary to systemically evaluate histological outcome-associated changes such as hemodynamics, behavior, and body weight during the early phase of ischemia. Here, 50 mice were subjected to 45-min middle cerebral artery occlusion (MCAO) using Longa's method.

Non-invasively triggered spreading depolarizations induce a rapid pro-inflammatory response in cerebral cortex.

Cortical spreading depolarization (CSD) induces pro-inflammatory gene expression in brain tissue. However, previous studies assessing the relationship between CSD and inflammation have used invasive methods that directly trigger inflammation. To eliminate the injury confounder, we induced CSDs non-invasively through intact skull using optogenetics in Thy1-channelrhodopsin-2 transgenic mice.

Endovascular thrombectomy versus medical treatment for large vessel occlusion stroke with mild symptoms: A meta-analysis.

It remains controversial as to whether mechanical thrombectomy (MT) is safer and more beneficial in patients with large vessel occlusion stroke (LVOS) presenting with a National Institutes of Health Stroke Scale score ≤ 8. We therefore conducted a meta-analysis of the published data.We searched PubMed and Embase and pooled relevant data in the meta-analyses using fixed effects models.

A Case of Subacute Combined Degeneration of the Spinal Cord with Infective Endocarditis.

Background. Subacute combined degeneration (SCD) is a rare cause of demyelination of the dorsal and lateral columns of spinal cord and is a neurogenic complication due to cobalamin deficiency. Anemia of chronic disease (ACD) occurs in patients with acute or chronic immune activation, including infective endocarditis.

A simple method for the formalin fixation of lungs in toxicological pathology studies.

Optimized lung preparation for detailed structural evaluation is required to improve consistency in preclinical safety evaluation, differences of opinion exist among regulatory agency personnel regarding the optimal methods for routine formalin fixation of lungs from rodent toxicology studies. The simple tracheal ligation fixation method emphasizes tracheal ligation before opening the thorax instead of attempting to re-inflate after lung collapse when opening the thorax. Photomicrographs of this method demonstrated an unprecedented ability to maintain the natural lung architecture, in contrast to the unavoidable changes in the alveolar environment by the intratracheal instillation and vascular perfusion methods.

Rapidly activated epidermal growth factor receptor mediates lipopolysaccharide-triggered migration of microglia.

Previous reports have suggested that epidermal growth factor receptor (EGFR) is involved in microglia activation characterized by cell morphology changes, cytokine production and cell migration; and the biochemical regulation of the microglia migration is a potential therapeutic target following CNS inflammatory damages. However, the role of EGFR in microglia motility after inflammatory stimulation remains unknown. In the present study, lipopolysaccharide (LPS) was found to trigger rapid EGFR phosphorylation within 10 min, which was sustained during long-term stimulation in both primary microglial cells and the cultured BV2 microglial cells, furthermore, blocking EGFR phosphorylation by AG1478 significantly attenuated the LPS-induced chemotactic and chemokinetic migration of microglia.

Inhibition of mTOR pathway restrains astrocyte proliferation, migration and production of inflammatory mediators after oxygen-glucose deprivation and reoxygenation.

Glial scar is a major impediment to axonal regeneration in central nervous system (CNS) disorders. Overcoming this physical and biochemical barrier might be crucial for axonal regeneration and functional compensation during the progression of CNS disorders. The mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase, involved in process of cell proliferation, migration, autophagy and protein synthesis.

Subchronic toxicological study of two artemisinin derivatives in dogs.

The objective of our study was to profile and compare the systematic changes between orally administered artesunate and intramuscularly injected artemether at a low dose over a 3-month period (92 consecutive days) in dogs. Intramuscular administration of 6 mg kg-1 artemether induced a decreased red blood cell (RBC) count (anemia), concurrent extramedullary hematopoiesis in the spleen and inhibition of erythropoiesis in the bone marrow. We also observed a prolonged QT interval and neuropathic changes in the central nervous system, which demonstrated the cortex and motor neuron vulnerability, but no behavioral changes.

Continual naringin treatment benefits the recovery of traumatic brain injury in rats through reducing oxidative and inflammatory alterations.

Naringin is neuroprotective in ischemia and other disease models. However, the effects of naringin are unknown after traumatic brain injury (TBI). The present study explored the role of naringin for neuroprotection in TBI rats.

[Efficient method for analyzing absorbed ingredients of traditional Chinese medicine genitana macrophyllae radix].

In present study, a method for analyzing the absorbed ingredients of traditional Chinese medicine QinJiao has been developed. A rat everted gut sac (EGS) model has been established, and the transporting capacity of gut sacs was identified by histological examinations. The ingredients including loganic acid, sweroside, gentiopicroside, and swertiamarian in serosal solution absorbed by active transport of rat everted ileum and jejunum from Qinjiao extraction were determined using an HPLC method.

Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury.

Background: Emerging evidence indicates that reactive microglia-initiated inflammatory responses are responsible for secondary damage after primary traumatic spinal cord injury (SCI); epidermal growth factor receptor (EGFR) signaling may be involved in cell activation. In this report, we investigate the influence of EGFR signaling inhibition on microglia activation, proinflammatory cytokine production, and the neuronal microenvironment after SCI.

Methods: Lipopolysaccharide-treated primary microglia/BV2 line cells and SCI rats were used as model systems.

Blocking epidermal growth factor receptor attenuates reactive astrogliosis through inhibiting cell cycle progression and protects against ischemic brain injury in rats.

Excessive astrogliosis is a major impediment to axonal regeneration in CNS disorders. Overcoming this inhibitory barrier of reactive astrocytes might be crucial for CNS repair. Up-regulation and activation of epidermal growth factor receptor (EGFR) has been shown to trigger quiescent astrocytes into reactive astrocytes in response to several neural injuries.

Inhibiting epidermal growth factor receptor attenuates reactive astrogliosis and improves functional outcome after spinal cord injury in rats.

As a physical barrier to regenerating axons, reactive astrogliosis is also a biochemical barrier which can secrete inhibitory molecules, including chondroitin sulfate proteoglycans (CSPGs) in the pathological mechanism of spinal cord injury (SCI). Thus, inhibition of astroglial proliferation and CSPG production might facilitate axonal regeneration after SCI. Recent studies have demonstrated that epidermal growth factor receptor (EGFR) activation triggers quiescent astrocytes into becoming reactive astrocytes and forming glial scar after CNS injury.

Galectin-1 attenuates astrogliosis-associated injuries and improves recovery of rats following focal cerebral ischemia.

Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regulated in activated astrocytes around ischemic infarct.

Galectin-1 enhances astrocytic BDNF production and improves functional outcome in rats following ischemia.

Galectin-1, an endogenous mammalian lectin, has been implicated in a variety of CNS disorders. However, its role in cerebral ischemia is still elusive. In the present study, we investigated the effect of recombinant galectin-1 on production of astrocytic brain-derived neurotrophic factor (BDNF) and functional recovery following ischemia.

Tamoxifen alleviates irradiation-induced brain injury by attenuating microglial inflammatory response in vitro and in vivo.

Irradiation-induced brain injury, leading to cognitive impairment several months to years after whole brain irradiation (WBI) therapy, is a common health problem in patients with primary or metastatic brain tumor and greatly impairs quality of life for tumor survivors. Recently, it has been demonstrated that a rapid and sustained increase in activated microglia following WBI led to a chronic inflammatory response and a corresponding decrease in hippocampal neurogenesis. Tamoxifen, serving as a radiosensitizer and a useful agent in combination therapy of glioma, has been found to exert anti-inflammatory response both in cultured microglial cells and in a spinal cord injury model.

Tamoxifen attenuates inflammatory-mediated damage and improves functional outcome after spinal cord injury in rats.

Tamoxifen has been found to be neuroprotective in both transient and permanent experimental ischemic stroke. However, it remains unknown whether this agent shows a similar beneficial effect after spinal cord injury (SCI), and what are its underlying mechanisms. In this study, we investigated the efficacy of tamoxifen treatment in attenuating SCI-induced pathology.

C16, a novel advanced glycation endproduct breaker, restores cardiovascular dysfunction in experimental diabetic rats.

Aim: Advanced glycation endproducts (AGE) have been implicated in the pathogenesis of diabetic complications, including diabetic cardiovascular dysfunction. 3-[2-(4-Bromo-phenyl)-1-methyl-2-oxo-ethyl]-4,5,6,7-tetrahydro-benzothiazol-3-ium bromide (C16), a novel AGE breaker, was investigated for its effects on the development of cardiovascular disease in diabetic rats.

Methods: Rats that had streptozotocin-induced diabetes for 12 weeks were divided into groups receiving C16 or vehicle by gavage.