Background Neurosurgery represents one of the most challenging and delicate of any surgical procedure. Skull base tumors in particular oftentimes present as a very technically difficult procedures in the setting of neurosurgical teaching. Virtual reality technology is one of the most promising surgical planning tools. It can perform fast three-dimensional (3D) reconstruction of computed tomography (CT), magnetic resonance imaging (MRI) and other imaging data sets under conditions of virtual reality (VR). Surgical simulation can more intuitively understand the anatomical relationship of the surgical area in significantly greater detail. Methods Thirty clinical undergraduates from the class of 2016 were randomly divided into two groups: the traditional teaching group and the virtual reality teaching group. After the study concluded, the teaching effectiveness was evaluated by combining basic theoretical knowledge, case analysis and questionnaire survey methods. Results Comparative analysis between both groups showed the response effect of the virtual reality teaching group was better than that of the traditional teaching group (P < 0.05). There was also no difference between both groups in terms of the design of the surgical approach and the listing of surgical matters that required attention (P > 0.05).The results of theoretical knowledge assessment between both groups showed that the scores of basic theory, location, adjacent structure, clinical manifestation, diagnosis and analysis, surgical methods and total scores in the VR group exceeded those in the traditional teaching group (P < 0.05). Conclusions This study showed that VR technology might improve neurosurgical skull base teaching quality, which should be promoted in the teaching of clinical subjects.

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Noxious stimuli applied at doses close to but below the threshold of cell injury induce adaptive responses that provide a defense against additional stress. Epileptic preconditioning protects neurons against status epilepticus and ischemia; however, it is not known if the converse is true. During hypoxia/ischemia (H/I), lactate released from astrocytes is taken up by neurons and is stored for energy, a process mediated by monocarboxylate transporter 4 (MCT4) in astroglia. The present study investigated whether H/I preconditioning can provide protection to neurons against epilepsy through upregulation of MCT4 expression in astrocytes in vitro and in vivo. An oxygen/glucose deprivation protocol was used in primary astrocyte cultures, while rats were subjected to an intermittent hypoxia preconditioning (IHP) paradigm followed by lithium-pilocarpine-induced epilepsy as well as lactate transportation inhibitor injection, with a subsequent evaluation of protein expression as well as behavior. H/I induced an upregulation of MCT4 expression, while an IHP time course of 5 days provided the greatest protection against epileptic seizures, which was most apparent by 3 days after IHP. However, lactate transport function disturbances can block the protective effect induced by IHP. These findings provide a potential basis for the clinical treatment of epilepsy.

Hypoxic stressors contribute to neuronal death in many brain diseases. Astrocyte processes surround most neurons and are therefore anatomically well-positioned to shield them from hypoxic injury. Excitatory amino acid transporters (EAATs), represent the sole mechanism of active reuptake of glutamate into the astrocytes and neurons and are essential to dampen neuronal excitation following glutamate release at synapses. Glutamate clearance impairment from any factors is bound to result in an increase in hypoxic neuronal injury. The brain energy metabolism under hypoxic conditions depends on monocarboxylate transporters (MCTs) that are expressed by neurons and glia. Previous co-immunoprecipitation experiments revealed that MCT4 directly modulate EAAT1 in astrocytes. The reduction in both surface proteins may act synergistically to induce neuronal hyperexcitability and excitotoxicity. Therefore we hypothesized that astrocytes would respond to hypoxic conditions by enhancing their expression of MCT4 and EAAT1, which, in turn, would enable them to better support neurons to survive lethal hypoxia injury. An oxygen deprivation (OD) protocol was used in primary cultures of neurons, astrocytes, and astrocytes-neurons derived from rat hippocampus, with or without MCT4-targeted short hairpin RNA (shRNA) transfection. Cell survival, expression of MCT4, EAAT1, glial fibrillary acidic protein and neuronal nuclear antigen were evaluated. OD resulted in significant cell death in neuronal cultures and up-regulation of MCT4, EAAT1 expression respectively in primary cell cultures, but no injury in neuron-astrocyte co-cultures and astrocyte cultures. However, neuronal cell death in co-cultures was increased exposure to shRNA-MCT4 prior to OD. These findings demonstrate that the MCT4-mediated expression of EAAT1 is involved in the resistance to hypoxia injury in astrocyte-neuron co-cultures.

HBV has a relatively high mutation rate in its genome and most of these mutations are associated with the curative effect of nucleoside analogs. In this study, 1,424 patients with HBV-related liver diseases not treated with antiviral drugs, including 197 asymptomatic HBV carriers, 769 chronic hepatitis B patients, 145 acute-on-chronic liver failure (ACLF) patients, 187 HBV-related liver cirrhosis patients, and 126 HBV-related HCC patients, were selected to investigate the distribution and clinical significance of spontaneous YMDD mutations in liver diseases at different stages. Spontaneous YMDD mutations were detected in all stages of liver diseases and the YIDD variant was the dominant mutation type. The mutation rate was higher in genotype C strains than in genotype B strains. The χ(2) subdivision method showed that the spontaneous YMDD mutation rate in HCC was higher than that in other liver diseases. The difference in spontaneous YMDD mutation rates in patients with liver diseases infected with genotype C strains at different stages was statistically significant. Spontaneous YMDD mutation rates in patients with liver diseases infected with genotype C strains at different stages were then compared one to one using the χ(2) subdivision method. The results showed that the spontaneous YMDD mutation rate in HCC was higher than that in other liver diseases. Taken together, these results indicated that spontaneous YMDD mutations are more likely to occur in patients infected with genotype C strains, and genotype C strains with spontaneous YMDD mutations may be a risk factor for HCC.

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Rationale:An intracranial arachnoid cyst is a relatively common congenital benign lesion. A small number of patients present with neurological symptoms. Endoscopic fenestration has become a common treatment for arachnoid cysts in recent years, but intracerebral hematoma after surgery is rarely reported.Patient concerns:A 60-year-old woman with an arachnoid cyst in the left parietal and occipital lobes showed obvious progressive neurological deficits. She had weakness in her right limbs for 2 years and a sudden convulsion in her left limbs.Diagnosis:An arachnoid cyst in the left parietal and occipital lobes was detected on magnetic resonance imaging.Intervention:Endoscopic fenestration was performed for the cyst. However, she developed an intracerebral hematoma after surgery, which was detected by computed tomography. Due to the exacerbation of the patient's condition in the early stage after surgery, reoperation was performed to remove the hematoma.Outcomes:The patient was finally cured with no serious neurological deficits.Lessons:The rare complication of intracerebral hematoma after surgery for an arachnoid cyst can lead to a rapid deterioration in the patient's condition. More-adequate preoperative examination and neuronavigation should be conducted during surgery. Appropriate enlargement of the bone hole may help protect against this complication. Moreover, prompt reoperation for the intracerebral hematoma may improve the prognosis.