ABSTRACT
Among ankle injuries, the injury to the distal tibiofibular syndesmosis is common and likely neglected. The stability of the distal tibiofibular syndesmosis is related to the depth of the fibular notch. In imaging diagnosis, X-ray examination cannot be used for a definite diagnosis of the injury to the distal tibiofibular syndesmosis. For diagnosis of the distal tibiofibular separation>3 mm, CT scan can be accurate but is not sensitive enough for a separation<1 mm while MRI is more sensitive in diagnosis of the injury. Arthroscopy has gradually been used as the "gold standard" in diagnosis of the injury to the distal tibiofibular syndesmosis due to its advantage of direct vision. The distal tibiofibular separation occurs in the injuries of pronation external rotation Ⅳ°, supination external rotation Ⅲ° and Ⅳ°, and pronation abduction Ⅱ° and Ⅲ° by the Lange-Hansen classification. Most patients with simple stable injury to the distal tibiofibular syndesmosis may have a good prognosis after nonoperative treatment. Surgical anatomic reduction and maintenance of stability of the distal tibiofibular syndesmosis are the basic management principles for unstable distal tibiofibular syndesmosis or the injury to the distal tibiofibular syndesmosis combined with ankle fracture. Screw fixation is the most commonly used in the surgical treatment of the injury. Elastic fixation has the advantages of maintaining the biological characteristics of the distal tibiofibular syndesmosis fretting joint, better reduction fault tolerance, and lower rates of complications and long-term reduction loss. The angle of nail placement is the key to maintaining good reduction of the distal tibiofibular syndesmosis, but there has been little description of the specific methods to ensure the theoretical angle of nail placement in practice. This article also reviews the prospects of the future treatment of the injury to the distal tibiofibular syndesmosis.
ABSTRACT
Objective:To investigate the effects of subanesthetic concentration of sevoflurane on the plasticity of dendritic spines in the prefrontal cortex neurons of juvenile rats.Methods:Thirty-six clean-grade male Sprague-Dawley rats, aged 24 days, weighing 50-60 g, were divided into control group (group C) and sevoflurane anesthesia group (group S) using a random number table method, with 18 rats in each group.Group S inhaled 1.2% sevoflurane and 50% oxygen (flow rate 1 L/min) for 3 h, while group C inhaled 50% oxygen (flow rate 1 L/min) for 3 h. Open-field test and Morris water maze test were performed at 3 days after anesthesia.Animals were sacrificed, and brain samples were then taken for determination of the number of apoptotic neurons in layer Ⅱ-Ⅲ of the prefrontal cortex, density of dendritic spines, and expression of postsynaptic density protein 95 and gephyrin by TUNEL staining, Golgi staining or Western blot.Results:Compared with group C, no significant change was found in total distance or time of staying at the central region in the open-field test or the average swimming velocity, escape latency or the number of apoptotic neurons in the Morris water maze test ( P>0.05), and the density of dendritic spines was significantly increased, and the expression of postsynaptic density protein 95 and gephyrin was up-regulated in group S ( P<0.05). Conclusion:Subanesthetic concentration of sevoflurane can enhance the plasticity of dendritic spines in the prefrontal cortex neurons of juvenile rats.
ABSTRACT
Objective To investigate the relationship between the plasticity of dendritic spines in entorhinal cortical neurons and mechanism of low-dose ketamine-induced reduction of cognitive dysfunction following sevoflurane anesthesia in aged rats.Methods Thirty-six pathogen-free healthy male SpragueDawley rats,aged 18 months,weighing 500-600 g,were divided into 3 groups (n=12 each) using a random number table:control group (group C),sevoflurane anesthesia group (group Sev) and ketamine group (group K).Group C received no treatment.Group Sev inhaled the mixture of air (flow rate 1 L/min) and 3.6％ sevoflurane for 3 h.In group K,ketamine 10 mg/kg was injected intraperitoneally,and 5 min later the mixture of air (flow rate 1 L/min) and 3.6％ sevoflurane was inhaled for 3 h.Open field test and Morris water maze test were performed 3 days after anesthesia.After the behavioral tests,the animals were sacrificed,and their brains were removed and cut into sections for determination of the density of neurons,density of dendritic spines,and expression of postsynaptic density protein-95 (PSD-95) and synaptophysin (SY38) in superficial laminaes (Ⅱ-Ⅲ) of entorhinal cortex using Nissl's staining,Golgi staining and immunohistochemistry,respectively.Results Compared with group C,the time of staying at the central region was significantly shortened,the escape latency was prolonged,the density of dendritic spines was decreased,and the expression of PSD-95 and SY38 was down-regulated in group Sev (P＜0.05).Compared with group Sev,the time of staying at the central region was significantly prolonged,the escape latency was shortened,the density of dendritic spines was increased,and the expression of PSD-95 and SY38 was upregulated in group K (P＜0.05).There were no significant differences in the density of neurons in entorhinal cortex between the three groups (P＞0.05).Conclusion The mechanism by which low-dose ketamine attenuates cognitive dysfunction induced by sevoflurane anesthesia may be related to the enhanced plasticity of dendritic spines in entorhinal cortical neurons of aged rats.