BACKGROUND: Therapeutic methods for of peripheral facial nerve injury include surgery, physical therapy and drug treatment, but the treatment effect is not ideal in some certain cases. OBJECTIVE: To study the effect of autologous platelet rich plasma on repair of facial nerve injury. METHODS: The bilateral destroyed buccal nerve branches of the 10 white rabbits were put in silica gel nerve regeneration chamber, one side injected with platelet rich plasma as experimental group, the other side injected with normal saline as control group. The general observation, neuroelectrophysiology detection, histological observation, image analysis and evaluation of facial nerve regeneration recovery were performed at 8 weeks after surgery. RESULTS AND CONCLUSION: The action potential latency of the orbicularis oris at the experimental side was significantly lower than that at the control side, and the action potential amplitude (M wave) of compound nerve muscle of the experimental side was significantly higher than that of the control side (P < 0.01). Compared with the control side, the regenerative nerves of the experimental side were more mature with more regenerative axons, and the differentiation of myelin sheath was more mature and the thickness of myelin sheath was wel -distributed. Meanwhile, the diameters of axons were closed to the normal diameter, and the nerve axons were more intensive and arranged more regularly, the outer membrane of nerve fiber was thicker and the col agen fiber and elastic fiber layer were increased when compared with the control group. The number of regenerative axons of the control side was less, and the axons were distributed irregularly and poorly developed, and a large number of fibrous connective tissues were observed. The vacuolar degeneration at the control side was more than the experimental side. The regenerated nerve in the experimental side was better than the control side in the diameter of myelinated axon, area, myelin sheath thickness and axon count, and there were significant differences between two groups (P < 0.01). It indicates that platelet rich plasma has a promoting effect in the repair and regeneration of facial nerve.

Objective To teach neurosurgical residents of standardized training by using teaching method with multi-modality visualization and to explore its application effects.Methods Total 122 students were randomly divided into two groups:multi-modality visualization teaching group (n=61) and traditional teaching group (n=61).The evaluation of teaching effect was conducted by questionnaire of students and the analysis of test scores after the course.Comparison between the two groups was made by using independent sample t test.Results Questionnaire showed that the satisfaction of teaching mode (88.5％),learning efficiency (93.4％),and training results (90.1％) with multi-modality visualization teaching group were statistically higher than traditional group (P＜0.05).Test score showed that results of theory test (88.5 ± 5.1),on-spot examination (91.6 ± 5.5),and overall score (89.3 ± 5.2) were also statistically higher in multi-modality visualization teaching group than that of control group (P＜0.05).There was no significant difference in clinical skills assessment between two groups.Conclusions Teaching with multi-modality visualization can significantly improve the efficiency of neurosurgical clinical teaching and promote the training effect of students,which provides a new strategy of neurosurgical clinical teaching.

Objective:To analyze risk factors for prognosis of adult patients with traumatic brain injury (TBI), construct the prognostic model of TBI and evaluate its predictive value.Methods:A case-control study was used to analyze the clinical data of 522 patients with TBI admitted to Xijing Hospital of Air Force Medical University from March 2011 to September 2019, including 438 males and 84 females; aged 18-75 years [(44.9±15.0)years]. According to the Glasgow outcome score (GOS) at discharge, the patients were divided into good prognosis group (GOS 4-5 points, n=165) and poor prognosis group (GOS 1-3 points, n=357). The two groups were compared with regards to qualitative data such as sex, underlying diseases, causes of injury, multiple injuries, open injuries, intracranial foreign bodies, cerebral herniation, consciousness status on admission and at discharge, surgery, lung infection on admission, tracheostomy, ventilator-assisted ventilation, hospital-acquired pneumonia/pathogenic bacteria and intracranial infection, and quantitative data such as Glasgow coma score (GCS) on admission and at discharge, age, measurements on admission [systolic blood pressure, diastolic blood pressure, mean arterial pressure, temperature, heart rate, creatinine, urea nitrogen, blood sodium, blood potassium, blood glucose, prothrombin time (PT), activated partial thromboplastin time (APTT), platelets, international normalized ratio (INR), pupil size of both eyes] and length of hospital stay. Univariate analysis and Lasso regression analysis were used to screen the risk factors affecting the prognosis of TBI patients, and the selected influencing factors were included in multivariate Logistic regression analysis to identify independent risk factors and construct regression equations. R was used to draw a visual nomogram based on regression equation for predicting the prognosis of TBI patients. The prognostic predictive value of the nomogram was evaluated by using the receiver operating characteristic (ROC) curve, and the area under the curve (AUC), Youden index, sensitivity, specificity and consistency index (C index) were calculated. Results:Univariate analysis showed that there were significant differences between the two groups in underlying diseases, open injuries, cerebral herniation, consciousness status on admission and at discharge, lung infection on admission, tracheostomy, ventilator-assisted ventilation, hospital-acquired pneumonia/pathogenic bacteria, GCS on admission and at discharge, age, and measurements on admission (systolic blood pressure, mean arterial pressure, body temperature, heart rate, creatinine, urea nitrogen, blood potassium, blood glucose, PT, INR, pupil size of right eye) (all P<0.05 or 0.01). There were no significant differences between the two groups in gender, causes of injury, multiple injuries, intracranial foreign bodies, surgery, intracranial infection, measurements on admission (diastolic blood pressure, blood sodium, APTT, platelets, pupil size of left eye) and length of hospital stay (all P>0.05). After screening by Lasso regression model, the results of multivariate Logistic regression analysis showed that GCS on admission ( OR=0.67, 95% CI 0.62, 0.73, P<0.01), age ( OR=1.03, 95% CI 1.01, 1.04, P<0.01), blood glucose on admission ( OR=1.17, 95% CI 1.06, 1.30, P<0.01) and INR on admission ( OR=17.08, 95% CI 2.12, 137.89, P<0.01) could be used as the main risk factors to construct the prediction model, and the regression equation was constructed: Logit [ P/(1- P)]=-0.398× "GCS on admission"+0.024× "age"+0.158×"blood glucose on admission"+2.838×"INR on admission"-1.693. The AUC for the prognosis prediction in adult patients with TBI using R based on a visual nomogram model was 0.87 (95% CI 0.83, 0.89, P<0.01). The Youden index for the predicted probability was 0.60 (sensitivity of 85.2% and specificity of 75.2%), with the C index of 0.87. Conclusion:Age, GCS on admission, blood glucose on admission and INR on admission are the main risk factors affecting the prognosis of TBI in adults, and the nomogram drawn by these parameters can better predict their clinical outcome.

Metastatic vascular calcification and calcinosis universalis, as severe complications of parathyroid hyperfunction and hyperparathyroidism, have attracted more attention in patients with renal secondary hyperparathyroidism and primary hyperparathyroidism. But, they are of little concern in patients with long-term negative calcium balance related parathyroid hyperfunction or hyperparathyroidism caused by calcium and/or vitamin D insufficiency (CVI). CVI is common in the population. Relatively low level of serum calcium and negative calcium balance caused by long-term CVI result in parathyroid hyperfunction or hyperparathyroidism, which may cause secretion of PTH beyond the physiological level, leading to bone absorption and release of a large amount of bone calcium into the blood. It may not only cause bone loss and osteoporosis, but also form metastatic vascular calcification or calcinosis universalis presented by cardiovascular diseases and other multi-organ lesions. Early calcium deposition can gradually fade after reasonable treatment, but middle arterial calcification is not easy to fade once it occurs. Therefore, vascular calcification and calcium deposition should be actively prevented and early screened and diagnosed. The early prevention, diagnosis and treatment of parathyroid hyperfunction or hyperparathyroidism can prevent, delay, or even reverse the occurrence and development of metastatic vascular calcification and calcinosis universalis, which is significant for disease prevention and protecting the patients' health influenced by these diseases.

Primary hyperparathyroidism is a disease with a large potential population. Some cases of primary hyperparathyroidism are non-primary, preventable and curable at early stage, requiring long-term follow-up after surgery. Therefore, all-round and full-cycle management are necessary for primary hyperparathyroidism, which involves an enhancing focus on etiological prevention, early detection, prompt diagnosis, timely intervention, multi-disciplinary standardized diagnosis and treatment, and postoperative scientific management. Meanwhile, implementing a "12+5+1" multidisciplinary joint diagnosis and treatment model, along with a two-way referral model, to achieve the transition from a disease-oriented diagnostic and treatment model to a patient-oriented, all-round and full-cycle interdisciplinary management model. This management can reduce the incidence and recurrence rate of primary hyperparathyroidism, and related osteoporosis or osteopenia, fractures, nephrolithiasis, metastatic vascular calcification, and systemic abnormal migratory calcium deposits, improve the overall quality of life and prognosis of patients.

Objective To investigate the effect of lycium barbarum polysaccharides (LBP) on apoptosis and autophagic death in primary cultured hippocampal neurons after oxygen glucose deprivation and reoxygenation (OGD/R) injury.Methods Primary cultured hippocampal neurons were exposed to OGD/R.The cells were randomly divided into 5 groups:control group,OGD/R group,and OGD/R+LBP groups (15,30 and 60 μg/mL LBP).The cell viability was assessed by MTT assay.The cell damage was evaluated through detecting the lactate dehydrogenase (LDH) release rate.Apoptosis rate was detected by TUNEL,and cleaved Caspase-3 was identified by immunofluorescence staining.Protein expression was detected by Western blotting.Results As compared with the control group,OGD/R group had significantly decreased cell viability (P＜0.05);and significantly increased cell viability and decreased LDH release rate were noted in the LBP (15,30 and 60 μg/mL) treatment groups as compared with those in the OGD/R group (P＜0.05).The 60 μg/mL LBP treatment group had significantly smaller number of TUNEL-positive cells than the OGD/R group(P＜0.05).Immunofluorescence staining and Western blotting both revealed that 60 μg/mL LBP treatment group had significantly decreased Beclinl level and ratio of cleaved Caspase-3/Caspase-3 and ratio of microtubule-associated protein light chain (LC)3 Ⅱ/LC3Ⅰ,and statistically increased p62 level and ratio of Bcl-2/Bax as compared with OGD/R group (P＜0.05).Conclusion LBP treatment protects primary hippocampal neurons from OGD/R injury via inhibiting apoptosis and autophagic cell death.

Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
Mice ; Animals ; Hypoxia ; Oxidative Stress ; Autophagy ; Cognition ; Sirolimus/therapeutic use*