Objective:To investigate the clinical efficacy of intramedullary nailing combined with bone cement in repair of segmental bone defects after tumor resection.Methods:A retrospective analysis was conducted of the 5 patients with malignant bone tumor who had been treated at Department of Orthopaedics, Qiannan People's Hospital from April 2018 to September 2019 for remaining segmental bone defects following limb salvage surgery. They were 4 males and one female, aged from 11 to 55 years (average, 35.4 years). Their defects ranged from 6 to 21 cm (average, 12.3 cm) after tumor resection. By the Karnofsky performance score (KPS) for long-term quality of life, all of them scored less than 50 points. Of them, 3 were treated by interlocking intramedullary nails and bone cement filling, and 2 by elastic intramedullary nails and bone cement filling. In the 2 cases with defects of 21 cm and 13 cm, the fixation was assisted by a plate and an external fixator. Defect length after resection, operation time and intraoperative bleeding were recorded; the efficacy was evaluated by the Enneking functional evaluation of reconstructive procedures after surgical treatment of tumors of the musculoskeletal system, visual analogue scale (VAS), and KPS.Results:All the 5 patients had uneventful surgery, with operation time ranging from 112 to 225 min (average, 154.2 min), intraoperative bleeding from 300 to 500 mL (average, 382 mL), and defect length after resection from 6 to 21 cm. The 5 patients were followed up for 6 to 28 months. Of them, 2 died of disease progression 6 and 7 months after surgery, respectively. According to the Enneking's evaluation, one patient scored 28 points, 2 patients 23 points and 2 patients 21 points, giving a high degree of satisfaction. Their VAS scores 6 months after surgery ranged from 1 to 6, averaging 3.6; their postoperative KPS scores ranged from 60 to 80, averaging 72.Conclusion:In repair of segmental bone defects after tumor resection, intramedullary nailing combined with bone cement filling can relieve pain of patients and lead to satisfactory short-term curative efficacy.

Objective To develop a simple and effective method for monitoring cortical ischemia after temporary occlusion of the parent arteries during anterior circulation intracranial aneurysm surgery. Methods Fifty-two patients with anterior circulation aneurysm (58 aneurysms) received craniotomy from April to November 2008, and at the same time,cortical electroencephalograpby (EEG) and scalp EEG were monitored during the surgery.According to the international 10/20 electrode placement system, scalp electrodes were placed on O1, O2, P3, P4, T5, and T6 for monitoring the changes in the depth of anesthesia. A cortical strip electrode was placed on the cortical surface supplied by the artery that was possibly blocked during the operation, which was used to monitor the possible cortical ischemia. For patients who had cortical EEG suppression after the temporary occlusion of the parent arteries Were compared with the changes of scalp EEG. Whether there were ischemic events in the corresponding supply territory after vascular occlusion were observed after surgery. Results Of the 58 aneurysms, 40 aneurysms and 41 major arteries were occluded temporarily. After being occluded temporarily in 19 arteries of 18 patients, cortical EEG changed significantly,while scalp EEG did not change significantly. Only 9 patients had ischemic events in the corresponding supply territories after the occlusion in the cortical EEG significant change group. The changes in the depth of anesthesia had the consistent impact on cortical and scalp EEG. Conelusions Simultaneous monitoring of cortical and scalp EEG is a simple and effective method for monitoring cortical ischemia during anterior circulation intracranial aneurysm surgery, and may effectively identify the effect of anesthesia on EEG.

ObjectiveTo investigate the effects of Linggui Zhugantang （LGZGT）-containing serum on primary astrocytes （AS） induced by β amyloid 1-42 （Aβ_1-42） in a rat model of Alzheimer's disease （AD） and explore the phagocytic and degradative effects of LGZGT on Aβ. MethodAn AD model was established by inducing AS with Aβ_1-42. The cells were divided into normal group， model group， LGZGT low-， medium-， and high-dose （LGZGT-L， LGZGT-M， and LGZGT-H） groups， and donepezil hydrochloride group. The model group was treated with Aβ_1-42 at a final concentration of 10 μmol∙L^-1. The LGZGT-L， LGZGT-M， and LGZGT-H groups were treated with 10% serum containing LGZGT on the basis of the model group. Cell viability was assessed using a cell counting kit-8 （CCK-8）， lactate dehydrogenase （LDH） activity was measured using an LDH assay kit， and cell morphology was observed using an inverted microscope. The expression of Aβ-related degradation enzymes insulin-degrading enzyme （IDE） and cathepsin D （CTSD） was detected using Western blot， and the fluorescence intensity of cathepsin B （CTSB） was measured using immunofluorescence. The content of Aβ_1-42 in cells was determined using an enzyme-linked immunosorbent assay （ELISA）. ResultCompared with the normal group， the viability of AS in all groups decreased， and Aβ_1-42 at different concentrations had inhibitory effects on AS proliferation. After administration， compared with the normal group， the cell survival rate of the model group decreased significantly （P<0.05）. Compared with the model group， the cell survival rates of the LGZGT-H group and donepezil hydrochloride group increased significantly （P<0.05）. The LDH activity of cells in the model group was significantly increased compared with that in the normal group （P<0.05）， and cell bodies were swollen and enlarged with increased protrusions and elongation， suggesting more obvious cell damage. Compared with the model group， the LDH activity of cells in the donepezil hydrochloride， LGZGT-L， LGZGT-M， and LGZGT-H groups decreased significantly （P<0.05）. After administration， the cell swelling in the LGZGT-M， LGZGT-H， and donepezil hydrochloride groups improved， cell protrusions shortened， and cell clustering decreased. Compared with the normal group， the expression of IDE and CTSD in the model group decreased significantly （P<0.05）. Compared with the model group， the expression of IDE increased significantly in the LGZGT-M and LGZGT-H groups （P<0.05）. Compared with the model group， the expression of CTSD increased significantly in the LGZGT-L， LGZGT-M， LGZGT-H， and donepezil hydrochloride groups （P<0.05）. The average fluorescence intensity of CTSB in the model group was significantly lower than that in the normal group （P<0.05）. Compared with the model group， the average fluorescence intensity of CTSD in the LGZGT-L， LGZGT-M， LGZGT-H， and donepezil hydrochloride groups increased significantly （P<0.05）. The intracellular content of Aβ_1-42 in cells in the model group was significantly higher than that in the normal group （P<0.05）. After administration， compared with the model group， the intracellular content of Aβ_1-42 in cells in the LGZGT-L， LGZGT-M， LGZGT-H， and donepezil hydrochloride groups decreased significantly （P<0.05）， and LGZGT-containing serum reduced Aβ_1-42 in a dose-dependent manner （P<0.05）. ConclusionLGZGT has a protective effect on Aβ_1-42-induced AS and can promote the degradation of Aβ. Its mechanism may be related to reducing Aβ toxicity， enhancing cell viability， promoting the expression of IDE， CTSD， and CTSB， and restoring lysosomal function.