Objective To study the imaging characteristics of intracranial dysembryoplastic neuroepithelial tumors(DNT),and to evaluate the role of CT and MRI in their diagnosis.Methods We presented 8 DNTs cases confirmed histopathologically after operation.CT and MRI features were retrospectively analyzed(3 cases received MR scan only and 5 had both studies),compared with the surgical findings and pathological appearance.Results Eight patients had totally 11 tumors with multifoci in 2 cases.Six DNTs were located in the temporal lobe,1 lesion involved the parietal lobe,1 in the frontal lobe,1 in the brain stem,1 in the cerebellum,and 1 in the frontal and temporal lobe simultaneously.All lesions were observed intracortically,and partial of them extended into the subcortical location.On 5 non-contrast CT scans,3 DNTs were homogeneously hypodense;1 case contained isodense nodules within the hypodense focus.Peripheral spotty calcification was found in 1 case.On pre-contrast MR images,all lesions showed hypointense on T_1-weighted images,moreover,multicystic change with more markedly decreased signal intensity was observed.The DNT had a well-demarcated,multinodular gyriform configuration,or a soap bubble appearance at the cortical margin.On T_2-weighted images,high signal intensity of the tumors was seen except for hypointense calcification.The bone remodeling of the adjacent calvaria was noticed in(1 case.) The tumors had slightly increased signal intensity on FLAIR(fluid attenuated inversion recovery) in 2 cases,and homogeneously mild hyperintense on PDW(proton density weighted imaging),while the isointense focus was observed in one case on DWI(diffusion weighted imaging).No obvious enhancement was identified except 1 lesion with mild enhancement following intravenous administration of contrast material.3 tumors had ill-defined contours,whereas the others showed well-demarcated margins.No surrounding vasogenic edema was present except 2 foci with slight edema.Conclusion DNT usually shows characteristic radiologic findings,in combination with the clinical presentation and history,the diagnostic accuracy should be improved,and,as such,unnecessary radiation and/or chemotherapy may be avoided.

Objective To determine the median effective target plasma concentration (EC50) of remifentanil inhibiting responses to skull-pin placement when combined with propofol in the female patients undergoing neurosurgery.Methods Sixteen female patients,aged 20-60 yr,with body mass index of 18-30 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective neurosurgery under general anesthesia,were enrolled in this study.Anesthesia was induced with propofol and remifentanil given by target-controlled infusion and iv rocuronium 0.6 mg/kg.The target plasma concentration (Cp) of remifentanil and propofol was set at 5 ng/ml and 3 μg/ml,respectively.At 3 min after tracheal intubation,the target Cp of remifentanil was adjusted and set at 5 ng/ml in the first patient.The skull-pin was placed after the target effect-site and plasma concentrations were balanced.The Cp increased/decreased by 20％ each time in the next patient depending on whether or not the response to skull-pin placement was positive.The ratio between the two successive concentrations was 1.2.The response to skull-pin placement was defined as positive when heart rate and/or mean arterial pressure increased by 20％ of the baseline value within 1 min after placement.The EC50 and 95％ confidence interval of remifentanil required to inhibit responses to skull-pin placement were calculated when combined with propofol.Results The EC50 (95％ confidence interval) of remifentanil required to inhibit responses to skull-pin placement was 3.74 (3.43-4.09) ng/ml when combined with propofol.Conclusion When combined with propofol,the EC50 of remifentanil inhibiting responses to skull-pin placement is 3.74 ng/ml in the female patients undergoing neurosurgery.

Objective To compare the effects of different anesthetics on the recovery of neurologi-cal function after intracranial aneurysm embolization. Methods One hundred patients of both sexes with aneurysmal subarachnoid hemorrhage, aged more than 18 yr, with body mass index of 18. 5-24. 0 kg∕m2 , of American Society of Anesthesiologists physical status Ⅱ or Ⅲ and WFNS grade Ⅰ-Ⅳ, with the thick-ness of subarachnoid hemorrhage more than 4 cm, were divided into 2 groups (n= 50 each) using a random number table: propofol group (group P) and sevoflurane group (group S). After anesthesia induction, group P received intravenous infusion of propofol 100-300 μg·kg-1 ·min-1 , while the end-tidal sevoflu-rane concentration was maintained at 1. 4％-3. 5％ in group S. Immediately before induction (T0 ), imme-diately after the end of induction (T1 ), immediately after successful embolization of aneurysm (T2 ) and at 1, 2, 3 and 5 days after surgery (T3-6 ), central venous blood samples were collected for determination of plasma neuron-specific enolase and S100β protein concentrations by enzyme-linked immunosorbent assay. The development of postoperative cerebral vasospasm and delayed ischemic neurological deficit was recorded. The patients were followed up, and the Glasgow outcome score and occurrence of newly developed cerebral infarction were recorded within 6 months after surgery. Results There was no significant difference in the concentrations of plasma neuron-specific enolase and S100β protein at each time point, incidence of postop-erative cerebral vasospasm and delayed ischemic neurological deficit, or Glasgow outcome score and inci-dence of newly developed cerebral infarction within 6 months after surgery between two groups (P>0. 05). Conclusion Propofol and sevoflurane exert no effect on the recovery of neurological function after intracra-nial aneurysm embolization.

Establishing an effective three-dimensional (3D) culture system to better model human neurological diseases is desirable, since the human brain is a 3D structure. Here, we demonstrated the development of a polydimethylsiloxane (PDMS) pillar-based 3D scaffold that mimicked the 3D microenvironment of the brain. We utilized this scaffold for the growth of human cortical glutamatergic neurons that were differentiated from human pluripotent stem cells. In comparison with the 2D culture, we demonstrated that the developed 3D culture promoted the maturation of human cortical glutamatergic neurons by showing significantly more MAP2 and less Ki67 expression. Based on this 3D culture system, we further developed an disease-like model of traumatic brain injury (TBI), which showed a robust increase of glutamate-release from the neurons, in response to mechanical impacts, recapitulating the critical pathology of TBI. The increased glutamate-release from our 3D culture model was attenuated by the treatment of neural protective drugs, memantine or nimodipine. The established 3D human neural culture system and TBI-like model may be used to facilitate mechanistic studies and drug screening for neurotrauma or other neurological diseases.