Essential role of MALAT1 in reducing traumatic brain injury.

As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration.

Atorvastatin combined with dexamethasone in chronic subdural haematoma (ATOCH II): study protocol for a randomized controlled trial.

Background: Chronic subdural haematoma (CSDH) is a common condition in the elderly that often requires neurosurgical management. For small CSDH, evidence has emerged that statins may reduce haematoma volume and improve outcomes, presumably by reducing local inflammation and promoting vascular repair. We wish to extend this evidence in a study that aims to determine the efficacy and safety of atorvastatin combined with low-dose dexamethasone in patients with CSDH.

Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury.

MicroRNA-491-5p (miR-491-5p) plays an important role in regulating cell proliferation and migration; however, the effect of miR-491-5p on neovascularization after traumatic brain injury remains poorly understood. In this study, a controlled cortical injury model in C57BL/6 mice and an oxygen-glucose deprivation model in microvascular endothelial cells derived from mouse brain were established to simulate traumatic brain injury in vivo and in vitro, respectively. In the in vivo model, quantitative real-time-polymerase chain reaction results showed that the expression of miR-491-5p increased or decreased following the intracerebroventricular injection of an miR-491-5p agomir or antagomir, respectively, and the expression of miR-491-5p decreased slightly after traumatic brain injury.

Neat1 decreases neuronal apoptosis after oxygen and glucose deprivation.

Studies have shown that downregulation of nuclear-enriched autosomal transcript 1 (Neat1) may adversely affect the recovery of nerve function and the increased loss of hippocampal neurons in mice. Whether Neat1 has protective or inhibitory effects on neuronal cell apoptosis after secondary brain injury remains unclear. Therefore, the effects of Neat1 on neuronal apoptosis were observed.

Hypoperfusion assessed by pressure reactivity index is associated with delayed cerebral ischemia after subarachnoid hemorrhage: an observational study.

Background: Dysfunction of cerebral autoregulation is one of the pathophysiological mechanisms that causes delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). Pressure reactivity index (PRx) have been confirmed to reflect the level of cerebral autoregulation and used to derive optimal cerebral perfusion pressure (CPPopt). The goal of this study is to explore the associations between autoregulation, CPPopt, PRx, and DCI.

Pentraxin 3 contributes to neurogenesis after traumatic brain injury in mice.

Emerging evidence indicates that pentraxin 3 is an acute-phase protein that is linked with the immune response to inflammation. It is also a newly discovered marker of anti-inflammatory A2 reactive astrocytes, and potentially has multiple protective effects in stroke; however, its role in the adult brain after traumatic brain injury is unknown. In the present study, a moderate model of traumatic brain injury in mice was established using controlled cortical impact.

Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice.

Recent evidence suggests that CC chemokine ligand 20 (CCL20) is upregulated after subarachnoid hemorrhage (SAH). Here, we investigated the functions of CCL20 in SAH injury and its underlying mechanisms of action. We found that CCL20 is upregulated in an SAH mouse model and in cultured primary microglia and neurons.

Intraventricular Hemorrhage Growth: Definition, Prevalence and Association with Hematoma Expansion and Prognosis.

Background/objectives: The objective of this study is to propose a definition of intraventricular hemorrhage (IVH) growth and to investigate whether IVH growth is associated with ICH expansion and functional outcome.

Methods: We performed a prospective observational study of ICH patients between July 2011 and March 2017 in a tertiary hospital. Patients were included if they had a baseline CT scan within 6 h after onset of symptoms and a follow-up CT within 36 h.

Apolipoprotein E promotes white matter remodeling via the Dab1-dependent pathway after traumatic brain injury.

Introduction: Axonal injury results in long-term neurological deficits in traumatic brain injury (TBI) patients. Apolipoprotein E (ApoE) has been reported to activate intracellular adaptor protein Disabled-1 (Dab1) phosphorylation via its interaction with ApoE receptors. The Dab1 pathway acts as a regulator of axonal outgrowth and growth cone formation in the brain.

Failure of tocilizumab in treating two patients with refractory SAPHO syndrome: a case report.

Synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is a rare autoinflammatory disease with no standard treatment. Interleukin (IL)-6 inhibitors represent a novel therapeutic option for rheumatoid arthritis and some autoinflammatory diseases. However, the clinical utility of IL-6 inhibitors in treating SAPHO syndrome has been poorly investigated.

Apolipoprotein E Affects In Vitro Axonal Growth and Regeneration via the MAPK Signaling Pathway.

Following central nervous system injury in mammals, failed axonal regeneration is closely related to dysneuria. Previous studies have shown that the obvious effects of apolipoprotein E (ApoE) on traumatic brain injury (TBI) were associated with an axonal mechanism. However, little information on the actions of ApoE and its isoforms on axonal regeneration following TBI was provided.

Efficacy and Safety of Microvascular Decompression and Gamma Knife Surgery Treatments for Patients with Primary Trigeminal Neuralgia: A Prospective Study.

Purpose: To compare efficacy and safety of microvascular decompression (MVD) and Gamma Knife surgery (GKS) treatments for trigeminal neuralgia.

Method: Patients with primary trigeminal neuralgia were randomly divided into 2 groups to undergo either MVD or GKS. All patients were followed for 2 years to evaluate efficacy, recurrence rates, and complications of treatment.

Neuroprotective effects of p53/microRNA‑22 regulate inflammation and apoptosis in subarachnoid hemorrhage.

The present study aimed to investigate whether the neuroprotective effects of p53/microRNA‑22 regulate inflammation and apoptosis in subarachnoid hemorrhage (SAH). In a mouse model of SAH, microRNA‑22 expression was upregulated. In addition, downregulation of microRNA‑22 in HEB cells increased the mRNA expression levels of interleukin (IL)‑6, induced cysteine rich angiogenic inducer 61 (Cyr61) expression, and suppressed the protein expression levels of B‑cell lymphoma 2‑associated X protein (Bax) and caspase‑3 activity.

Peli1 Contributions in Microglial Activation, Neuroinflammatory Responses and Neurological Deficits Following Experimental Subarachnoid Hemorrhage.

Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is closely associated with neuroinflammation. Microglial activation is an early event that leads to neuroinflammation after SAH. Peli1 is an E3 ubiquitin ligase that mediates the induction of pro-inflammatory cytokines in microglia.

Apolipoprotein E ε4: A Possible Risk Factor of Intracranial Pressure and White Matter Perfusion in Good-Grade Aneurysmal Subarachnoid Hemorrhage Patients at Early Stage.

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating and complicated disease with significant morbidity and mortality. Previous studies have shown that genetic susceptibility may play an important role in the outcome of a given individual with aSAH. This study evaluates the potential association in effects of the APOE allele on the early brain injury (EBI) in light of elevated intracranial pressure (ICP) and cerebral perfusion disorders in a consecutive series of non-comatose Chinese patients with aSAH.

DLK silencing attenuated neuron apoptosis through JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.

Objective: Dual leucine zipper kinase (DLK/MA3K12) has been reported involved in apoptosis and neuronal degeneration during neural development and traumatic brain injury. This study was designed to investigate the role of DLK with its adaptor protein JNK interacting protein-3 (JIP3), and its downstream MA2K7/JNK signaling pathway in early brain injury (EBI) after subarachnoid hemorrhage (SAH) in a rat model.

Design: Controlled in vivo laboratory study.

Tozasertib attenuates neuronal apoptosis via DLK/JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.

Background And Purpose: Since tozasertib is neuroprotective for injured optic nerve, this study is intended to test whether tozasertib reduces early brain injury after subarachnoid hemorrhage (SAH) in a rat model.

Methods: Two hundred sixteen (216) male Sprague-Dawley rats were randomly subjected to endovascular perforation model of SAH and sham group. SAH grade, neurological score, and brain water content were measured at 24 and 72 h after SAH.

Influence of apolipoprotein E and its receptors on cerebral amyloid precursor protein metabolism following traumatic brain injury.

Traumatic brain injury (TBI) is the leading cause of mortality and disability among young individuals in our society, and globally the incidence of TBI is rising sharply. Mounting evidence has indicated that apolipoprotein E (apoE: protein; APOE: gene) genotype influences the outcome after TBI. The proposed mechanism by which APOE affects the clinicopathological consequences of TBI is multifactorial and includes amyloid deposition, disruption of lipid distribution, dysfunction of mitochondrial energy production, oxidative stress and increases intracellular calcium in response to injury.

Value of noninvasive imaging in follow-up of intracranial aneurysm.

Follow-up is necessary for treated and untreated aneurysms. The purpose of this study is to assess the results of treated aneurysms, the development of untreated aneurysms and the incidence of new aneurysms through short-term follow-up with noninvasive imaging, including CTA and MRA. More-than-once follow-up imaging with either CTA or MRA was performed in 73 patients, 65 of them suffering SAH.

Delayed intracranial hemorrhage associated with antiplatelet therapy in stent-assisted coil embolized cerebral aneurysms.

Administration of oral clopidogrel plus aspirin is the most important regimen to reduce thromboembolic complications in stent-assisted coil embolization of cerebral aneurysm. However, such therapy may increase the risk of hemorrhage. The purpose of this study is to analyze the effect of two different antiplatelet regimens on hemorrhagic and thromboembolic complication rates around the stent-assisted coil embolization period.

Objective evaluation of the treatment methods of intracranial aneurysm surgery.

Objective: this study evaluated the clinical value of craniotomy and intravascular embotherapy in the treatment of intracranial aneurysms.

Methods: The clinical data of 126 cases of intracranial aneurysms from July 2008 to July 2009 was analyzed retrospectively, 86 cases of all were clipped and other 40 cases were coiled.

Results: in 86 cases with craniotomy (according to Hunt-Hess classification, 71 cases belong to grade I-III and 15 cases belong to grade IV-V), 1 case died, 3 cases recovered with serious nervous system symptoms, 9 cases recovered with Mild neurological symptoms, and the remaining 73 cases recovered with normal life and work.

The role of apolipoprotein e in the pathological events following subarachnoid hemorrhage: a review.

Subarachnoid hemorrhage (SAH) strikes individuals with devastating neurological results. Traditional viewpoints do not explain all the differences that are usually found in clinical practice. The role of genetic predisposition in SAH has recently been investigated.