[Research progress in physiological function of the rare sugar D-allose].

D-allose, a rare sugar with anti-oxidant, anti-inflammatory, anti-cancer, immunosuppressing and other physiological functions, has become a research hotspot in recent years. This paper describes the physical and chemical properties, synthesis methods, metabolism, physiological functions, and applications of D-allose, aiming to promote the functional development of D-allose and facilitate the application of D-allose in the food field and clinical treatment.

Extracellular vesicle encapsulated Homer1a as novel nanotherapeutics against intracerebral hemorrhage in a mouse model.

Homer1a and A2 astrocytes are involved in the regulation of inflammation induced by intracerebral hemorrhage (ICH). However, there is no anticipated treatment strategy based on the anti-inflammatory effect of Homer1a and A2 astrocytes. Here, we successfully induced A2 astrocytes in vitro, and then we report an efficient method to prepare Homer1a EVs derived from A2 astrocytes which making it more stable, safe, and targetable to injured neurons.

D-allose Inhibits TLR4/PI3K/AKT Signaling to Attenuate Neuroinflammation and Neuronal Apoptosis by Inhibiting Gal-3 Following Ischemic Stroke.

Background: Ischemic stroke (IS) occurs when a blood vessel supplying the brain becomes obstructed, resulting in cerebral ischemia. This type of stroke accounts for approximately 87% of all strokes. Globally, IS leads to high mortality and poor prognosis and is associated with neuroinflammation and neuronal apoptosis.

d-allose protects brain microvascular endothelial cells from hypoxic/reoxygenated injury by inhibiting endoplasmic reticulum stress.

Ischemic stroke is an acute brain disease with a high mortality rate. Currently, the only effective method is to restore the blood supply. But the inflammation and oxidative stress induced by this approach can damage the integrity of the endothelial system, which hampers the patient's outcome.

Extended endoscopic endonasal approach for resecting anterior intrinsic third ventricular craniopharyngioma.

Background: The surgical treatment of the extended endoscopic endonasal approach (EEEA) is a safe and effective treatment for suprasellar craniopharyngiomas. However, due to damage to the hypothalamus and third ventricle floor (TVF), EEEA is generally regarded as unsuitable in treating intrinsic third ventricle craniopharyngioma (ITVC) that is entirely within the third ventricle. Until now, there have been only a small number of reports using EEEA to treat TVC a supra-infrachiasmatic approach.

Pseudocapsule-Based Resection for Pituitary Adenomas the Endoscopic Endonasal Approach.

Introduction: The endoscopic endonasal approach (EEA) is a safe and effective treatment for pituitary adenomas (PAs). Since extracapsular resection (ER) of PAs improves tumor resection and endocrine remission rates, the interface between the pseudocapsule and gland draws increasing attention. However, it is difficult to precisely dissect the tumor along the exact boundary, and complete removal of the tumor increases the risks of normal tissue damage and cerebrospinal fluid (CSF) leakage.

Effect of PITX2 genetic variants on the susceptibility to stroke in the Chinese Han population.

Purpose: Stroke is a multifactorial and complex disease caused by the obstruction or rupture of cerebrovascular. To explore the influence of genetic factors on stroke susceptibility, we investigated the association between four single nucleotide polymorphisms (SNPs) in the paired-like homeodomain transcription factor 2 (PITX2) gene and stroke risk.

Methods: A total of 977 volunteers including 476 stroke patients and 501 control individuals were recruited.

Clinical Efficacy of the Multilayered Skull Base Reconstruction Using In Situ Bone Flap in Endoscopic Endonasal Approach for Craniopharyngioma.

 The aim of the study is to summarize and analyze the efficacy of the multilayered skull base reconstruction using in situ bone flap in endoscopic endonasal approach (EEA) for craniopharyngiomas.  A retrospective review of 65 patients who underwent resection of their histopathology confirmed craniopharyngiomas performed at a single institution. Based on the team's understanding and mastery of skull base reconstruction techniques, patients were divided into two groups according to the methods of reconstruction in two periods.

Metastatic large cell neuroendocrine lung cancer to the foramen magnum: A case report.

Rationable: Large cell neuroendocrine carcinoma of the lung is rare, especially in the area of the foramen magnum. No previous studies have reported metastatic large cell neuroendocrine lung cancer to the foramen magnum. This paper will be the first time to report this special case.

High-Mobility Group Box 1 Neutralization Prevents Chronic Cerebral Hypoperfusion-Induced Optic Tract Injuries in the White Matter Associated with Down-regulation of Inflammatory Responses.

Chronic cerebral hypoperfusion (CCH)-induced white matter lesions (WMLs) are region-specific with the optic tract (OT) displaying the most severe damages and leading to visual-based behavioral impairment. Previously we have demonstrated that anti-high-mobility group box 1 (HMGB1) neutralizing antibody (Ab) prevents CCH-induced hippocampal damages via inhibition of neuroinflammation. Here we tested the protective role of the Ab on CCH-induced OT injuries.

HMGB1 Neutralization Attenuates Hippocampal Neuronal Death and Cognitive Impairment in Rats with Chronic Cerebral Hypoperfusion via Suppressing Inflammatory Responses and Oxidative Stress.

High-mobility group box-1 (HMGB1) acts as a proinflammatory molecule once released into the extracellular space and inhibition of HMGB1 signaling has been reported be neuroprotective in neurodegenerative diseases. Besides, chronic cerebral hypoperfusion (CCH) causes cognitive impairment in neurodegenerative diseases. Here we tested the protective role of HMGB1 inhibition using anti-HMGB1 neutralizing antibody (Ab) against CCH in rats after bilateral common carotid artery occlusion (2VO).

PRL-3 is a potential glioblastoma prognostic marker and promotes glioblastoma progression by enhancing MMP7 through the ERK and JNK pathways.

Glioblastoma is the most common and aggressive type of primary brain malignancy and is associated with a poor prognosis. Previously, we found that phosphatase of regenerating liver-3 (PRL-3) was significantly up-regulated in glioblastoma as determined by a microarray analysis. However, the function of PRL-3 in glioblastoma remains unknown.

D-allose protects the blood brain barrier through PPARγ-mediated anti-inflammatory pathway in the mice model of ischemia reperfusion injury.

Our early experiments confirmed that D-allose was closely involved in the blood brain barrier (BBB) protection from ischemia reperfusion (IR) injury, but the regulatory mechanism is not fully defined. In this study, we aimed to investigate the role of D-allose in the protection of BBB integrity and the relevant mechanisms involved in the mice model of middle cerebral artery occlusion and reperfusion (MCAO/Rep). D-allose was intravenously injected via a tail vein (0.

Induction of antigen-specific cytotoxic T-cell response by dendritic cells generated from ecto-mesenchymal stem cells infected with an adenovirus containing the MAGE-D4a gene.

The present study aimed to investigate the feasibility of using ecto-mesenchymal stem cell (EMSC)-derived dendritic cells (DCs) for glioma immunotherapy following infection by a recombinant adenovirus containing the melanoma-associated antigen D4a (MAGE-D4a) gene. The cultured EMSCs were infected by the adenoviral plasmid containing MAGE-D4a (pAd/MAGE-D4a). Efficiency of transfection was evaluated through the detection of green fluorescent protein-marked MAGE-D4a.

[Alarming effect of intraoperative neuroelectrophysiological monitoring in microvascular decompression for primary trigeminal neuralgia].

Objective: To explore the alarming effect of intraoperative neuroelectrophysiological monitoring in microvascular decompression (MVD) for primary trigeminal neuralgia.

Methods: In 2014, a total of 44 patients with an initial diagnosis of primary trigeminal neuralgia were consecutively recruited for surgery. And 41 of them with an intraoperative confirmation of primary trigeminal neuralgia underwent MVD.

Resveratrol inhibits oxygen-glucose deprivation-induced MMP-3 expression and cell apoptosis in primary cortical cells via the NF-κB pathway.

Resveratrol (Res) or trans-3,4',5-trihydroxystilbene, has been proven to exert neuroprotective effects in cerebral ischemia. The aim of the present study was to investigate whether Res has neuroprotective effects in primary cortical neurons subjected to transient oxygen-glucose deprivation (OGD) via inhibiting the expression of the gene encoding stromelysin-1, also known as matrix metalloproteinase-3 (MMP-3), and via inhibiting cell apoptosis. Primary cortical cells were exposed to OGD, followed by reoxygenation to induce transient ischemia.

Resveratrol protects primary cortical neuron cultures from transient oxygen-glucose deprivation by inhibiting MMP-9.

It was recently shown that resveratrol exerts neuroprotective effects against cerebral ischemia in mice. The aim of the present study was to further confirm these effects in in vitro primary cortical neuron cultures with transient oxygen-glucose deprivation (OGD), and to investigate whether these effects are due to the inhibition of matrix metalloproteinase-9 (MMP-9) and of cell apoptosis. Neuronal primary cultures of cerebral cortex were prepared from BALB/c mice embryos (13-15 days).

Allicin protects rat cortical neurons against mechanical trauma injury by regulating nitric oxide synthase pathways.

Allicin, a small molecule that is responsible for the typical smell and most of the functions of garlic, possesses a broad spectrum of pharmacological activities and is considered to have therapeutic potential in many pathologic conditions. In the present study, we investigated the potential protective effect of allicin in an in vitro model of traumatic brain injury (TBI) using primary cultured rat cortical neurons. We found that allicin treatment significantly reduced mechanical trauma-induced lactate dehydrogenase (LDH) release and inhibited apoptotic neuronal death in a dose-dependent manner.

Osthole attenuates spinal cord ischemia-reperfusion injury through mitochondrial biogenesis-independent inhibition of mitochondrial dysfunction in rats.

Background: Osthole, the main bioactive compounds isolated from the traditional Chinese medical herb broad Cnidium monnieri (L.) cusson, has been shown to exert spectrum of pharmacologic activities. The aim of this study was to investigate the potential neuroprotective effects of osthole against spinal cord ischemia-reperfusion injury in rats.

Anti-inflammatory effect of D-allose in cerebral ischemia/reperfusion injury in rats.

D-allose, a type of rare sugar, can produce inhibitory effects on activated leukocytes in various organs, including immunosuppressive effects and anti-inflammatory effects, as well as anti-oxyradical effects. The present experiment was performed to investigate the potential anti-inflammatory effects of D-allose in acute cerebral ischemia/reperfusion (I/R) injury. Transient middle cerebral artery occlusion model was applied in rats.

Protective effects of hydrogen sulfide in a rat model of traumatic brain injury via activation of mitochondrial adenosine triphosphate-sensitive potassium channels and reduction of oxidative stress.

Background: Hydrogen sulfide (H2S) is considered an important neuromodulator in the central nervous system. We designed the present study to investigate the effects of exogenous H2S in a rat model of traumatic brain injury (TBI) and the mechanism(s) that underlie this effect.

Methods: We induced a TBI model by controlled cortical impact injury.

A randomized controlled study comparing omeprazole and cimetidine for the prophylaxis of stress-related upper gastrointestinal bleeding in patients with intracerebral hemorrhage.

Object: Patients with intracerebral hemorrhage (ICH) are at high risk for severe stress-related upper gastrointestinal (UGI) bleeding, which is predictive of higher mortality. The aim of this study was to evaluate the effectiveness of omeprazole and cimetidine compared with a placebo in the prevention and management of stress-related UGI bleeding in patients with ICH.

Methods: In a single-center, randomized, placebo-controlled study, 184 surgically treated patients with CT-proven ICH within 72 hours of ictus and negative results for gastric occult blood testing were included.

ABCG2 protects kidney side population cells from hypoxia/reoxygenation injury through activation of the MEK/ERK pathway.

Breast cancer resistance protein 1 (BCRP1/ABCG2) is used to identify the side population (SP) within a population of cells, which is enriched for stem and progenitor cells in different tissues. Here, we investigated the role of extracellular signal-regulated kinase (ERK) 1/2 in the signaling mechanisms underlying ischemic/hypoxic conditions in kidney SP cells. Kidney SP cells were isolated using Hoechst 33342 dye-mediated fluorescein-activated cell sorting and then incubated under hypoxia/reoxygenation (H/R) with or without verapamil, a selective BCRP1/ABCG2 inhibitor.

The microsurgical treatment of cranio-orbital tumors assisted by intraoperative electrophysiologic monitoring and neuronavigation.

Objective: Total resection of cranio-orbital tumors without any major complications is still a challenge for neurosurgeons. Intraoperative electrophysiologic monitoring and neuronavigational system have been widely used in microneurosurgery, but their effects during microsurgical treatment of cranio-orbital tumors warrant further investigation.

Methods: Thirty-eight patients with cranio-orbital tumors admitted to our hospital underwent microsurgery assisted by intraoperative electrophysiologic monitoring.

The anti-inflammatory effects of D-allose contribute to attenuation of cerebral ischemia-reperfusion injury.

It has been proved that multiple independently lethal mechanisms are involved in cerebral ischemia-reperfusion injury. Inflammatory processes, mediated by activated leukocytes, have been implicated in the mechanisms of cerebral ischemia-reperfusion injury. In addition, the leukocytes accumulated in the perivascular areas during the inflammatory responses after reperfusion will transform oxygen to reactive free radicals, release cytotoxic products and vasoactive substances, which further promotes brain injury.