RESUMO
Objective To investigate the diagnosis and treatment of intracranial venous sinus thrombosis caused by trauma. Methods The clinical data of 13 patients had definite diagnosis by clinic and imaging, were analyzed retrospectively. Three patients received removal of hematoma and bone flap operation; 2 received anticoagulant therapy in early phase and intravenous thrombolysis; 2 accepted intrasinus interventional catheter-directed thrombolysis; ventriculoperitoneal shunt operation was performed in 1 patient for enjoying sub-optimal effects of conservative treatment; and the other 5 patients with transverse sinus embolism accepted conventional treatment for their symptom-free or having mild symptom. Results Intracranial venous sinus thrombosis caused by trauma was likely to locate in the superior sagittal sinus and transverse sinus; these patients mostly manifested as severe diffuse brain swelling combined with a fractured skull, epidural hematoma or intracerebral hematoma. Ten patients got clinical cure, 2 focal symptom and 1 mild mental retardation. Three days to 6 months after treatment, good results were noted in 8 patients performed DSA and in 5 patients performed MRV. Conclusion Early treatment should be given once the definite diagnosis is made in patients with intracranial venous sinus thrombosis caused by trauma, and anticoagulant and thrombolytic therapy are the main methods.
RESUMO
The present study was designed to observe if puerarin decreases lens epithelium cell (LEC) apoptosis induced partly by peroxynitrite (ONOO(-)). One hundred and eight rats were randomly divided into control group (n=36), streptozotocin (STZ) group (n=36) and STZ + puerarin group (n=36). The rats in the control group intraperitoneally (i.p.) received 0.5 ml of saline. The rats in STZ group and STZ + puerarin group received intraperitoneal injection of STZ (45 mg/kg). Three days later, the rats in STZ + puerarin group were given puerarin (140 mg/kg per day, i.p.). On days 20, 40 and 60 of the experiment, morphologic changes of lenses were observed with slit lamp. Then the animals were sacrificed for further analysis. The amount and percentage of apoptotic LECs were determined by flow cytometry. Nitrotyrosine (NT, the foot print of ONOO(-)) was examined by immunohistochemistry. Apoptosis-related genes (iNOS, etc.) were analyzed by gene array. The results showed that in the control group, all the lenses were clear. In STZ group, gradually severe opacity of the lens was observed on days 20, 40 and 60. But in STZ + puerarin group, mild opacity of the lens was observed on day 20 and more severe on day 40, but markedly decreased on day 60. In the control group, mild apoptosis of LECs was observed. In STZ group, time-dependent increase in apoptosis of LECs was observed. In STZ + puerarin group, mild apoptosis of LECs was observed on day 20, significantly increased on day 40, but markedly decreased on day 60. There was no expression of NT in the lens in the control group, but an increased expression of NT in STZ group. In STZ + puerarin group, mild expression of NT was observed on day 20, significantly increased on day 40, but markedly decreased on day 60. There was no expression of iNOS in the lens in the control group, but continuous up-regulation of iNOS expression in STZ group. In STZ + puerarin group, mild expression of iNOS was observed on day 20, significantly increased on day 40, but markedly decreased on day 60. Except the changes of iNOS related to NO production, the other apoptosis-related genes, including BCL-2 and SOD were down-regulated, while NF-kappaB and TNFR1-FADD-caspase signal transduction way were up-regulated in STZ group. The results were opposite in STZ + puerarin group and the control group. These findings show that NT is expressed in diabetic rat lens, which proves that LEC apoptosis in diabetic lens is partly induced by ONOO(-) which may be a new oxidative damage way to form cataract. Puerarin partly decreases LEC apoptosis induced by ONOO(-) and is a potential medicine for therapy of diabetic cataract. The mechanism of puerarin dealing with diabetic cataract may be related to its direct inhibition of LEC apoptosis and antagonism of ONOO(-) in diabetic rats.