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Objective@#To discuss the etiology, pathogenesis, clinical manifestation, diagnosis and therapy of sphenoid wing dysplasia(SWD) associated with neurofibromatosis type Ⅰ(NF-Ⅰ).@*Methods@#We retrospectively reviewed its clinical manifestations, imaging, surgical treatment, complications and postoperative outcome of one NF-Ⅰ patient with SWD.@*Results@#A 14 years-old girl presented with pulsating exophthalmos, loss of vision and café au lait spots. Radiological studies showed right-side orbital enlargement and complete absence of the greater wing of the sphenoid. Titanium mesh was tailored intraoperatively to close the defect as a barrier between the orbital cavity and the cranium and then covered by periosteum.The patient developed postoperative infectious which was controlled by after antibiotic treatment and proper drainage. Proptosis improved significantly after surgery within a month. Ocular pulsation subsided and clinical symptoms improved at 28-month follow-up.@*Conclusions@#Sphenoid greater wing dysplasia associated with neurofibromatosis type Ⅰ is a rare inherited autosomal dominant disorders. The treatment should be customized to each patient. Titanium mesh reconstruction is patients with symptomatic sphenoid dysplasia. It can correct the proptosis and pulsating exophthalmos without the risk of bone resorption and recurrence.However, high risk of infection is associated with the procedure.
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OBJECTIVE:To study the preventive effect of Qingnao tablet on cerebral ischemia-reperfusion injury in rats. METHODS:Rats were randomly divided into sham operation group,model group,Naoluotong capsule group (positive control, 0.05 g/kg),Qingnao tablet high-dose,medium-dose,low-dose groups(1.52,0.76,0.38 g/kg),10 in each group. Rats in all ad-ministration groups were intragastrically given relevant medicines,rats in sham operation group and model group were intragastrical-ly given equal volume of sodium carboxymethylcellulose solution,once a day,for 5 d. After 1 h of last administration,all rats were induced for cerebral ischemia-reperfusion injury model by suture-occluded method except for sham operation group. After 22 h of ischemia-reperfusion,neurological function deficit scoring was conducted;the pathological changes of the hippocampus were ob-served;superoxide dismutase (SOD),adenosine triphosphate (ATP),lactate dehydrogenase (LDH),tumor necrosis factor α(TNF-α)levels in brain tissue were measured. RESULTS:Compared with sham operation group,rats in model group appeared dif-ferent degrees of neurological deficits(score declined),sparse neurons,irregularly arranged in hippocampus as well as other patho-logical changes;ATP,SOD levels in brain tissue were decreased(P<0.01),LDH,TNF-α levels were increased(P<0.01). Com-pared with model group,neurological function deficit scores in Qingnao tablet doses groups were increased(P<0.05),neurologi-cal deficits were improved. Except for sham operation group,brain tissue indexes in other administration groups were significantly improved(P<0.05 or P<0.01). CONCLUSIONS:Qingnao tablet can increase ATP and SOD levels in brain tissue homogenate of model rats with cerebral ischemia-reperfusion,decrease LDH and TNF-α levels,and obviously improve rats'cerebral ischemia-re-perfusion injury.
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Objective To study the dynamic expression and distribution of high mobility group box 1 (HMGB-1)in diffuse axonal injury (DAI)in rats and to clarify its involvement in the inflammatory reaction after DAI in rats,in order to provide new targets for the clinical treatment of DAI.Methods A DAI model was established using a coronal rotation device and evaluated by HE,Glees-Marsland silver staining,and Mallory phosphotungstic acid hematoxylin staining.Immunohistochemistry,Western blot and RT-PCR were used to detect the expression and distribution of HMGB-1 in the cortex of DAI rats at 6 h,1 d,3 d and 7 d.And TUNEL was used to examine the apoptosis of neurons in DAI rats.Results Immunohistochemical results showed that at 6 h and 1 d after DAI,the number of HMGB-1-positive cells decreased,but at 3 and 7 d it began to increase.Western blot also showed that during the early stage after DAI (6 h and 1 d),the level of HMGB-1 protein in the cortex was significantly lower than that in the control group,but at the late stage (3 and 7 d)after DAI it significantly increased compared with that in the control group until 7 d.RT-PCR showed that at 6 h after DAI there was no significant increase in the level of HMGB-1mRNA,but at 1 d there was a slight increase compared with the control group;at 3 and 7 d,it showed an obvious significance.TUNEL staining indicated that the significant neuronal apoptosis appeared as early as 6 h after DAI,and reached the peak at 3 d;it started to decrease at 7 d but still remained at a relatively high level.Conclusion The dynamic expression and distribution of HMGB-1 showed significant changes with the time course after DAI in rats.They decreased at the early stage but increased at the late stage.At the early stage, HMGB-1 is mainly passively released by the necrotic neurons,and at the late stage it may be actively secreted by the active inflammatory cells.HMGB-1 may mediate the post-DAI neural cell apoptosis by inducing the inflammatory reaction.