ABSTRACT
Objective To assess the craniotomy in traumatic frontal sinus fracture cerebrospinal fluid( CSF) leaks.Methods Clinical data of 12 traumatic frontal sinus fracture CSF leaks from January 2010 to December 2014, who treated by craniotomy and conservation treatment was invalid were reviewed.Combined typical clinical presenta-tion and basicranial thin-layer computed tomography(CT),made qualitative diagnosis and localization.Craniotomy by bilateral coronary incision and epidural approach was performed.Repairation was mainly for the endocranium and the basicranium.Bone cement was used to reconstruct the osseous defect of the frontal sinus,and then with pedicle periosteal flap coverage.Dural defects was fixed with autogenous fascia.After operation,staying in bed and using anti-biotic for 7-14 days were required,while mannital or lumbar-drainage as needed.Results All 12 cases got posi-tive preoperative CT results.Craniotomy was performed,succeeded without reoperation.None of intracranial infection happened,while 1 case suffered from anosphrasia.Followed up for 3 -12 months, none CSF leaks relapsed. Conclusion Craniotomy by coronary incision,dispose the endocranium and the basicranium for the patients who suf-fered from frontal sinus fracture CSF leaks while conservation treatment is invalid,can obtain satisfied result.
ABSTRACT
AIM: To study signal transduction pathway of nitric oxide-induced PC12 cell death. METHODS: After PC12 cells were incubated with sodium nitroprusside(SNP), caspase-3 inhibitor Ⅱ plus SNP or p38 inhibitor-SB203580 plus SNP, cell survival rate was quantified by MTT assay and caspase-3 activity was measured with caspase-3 assay kits. RESULTS: SNP induced PC12 cell death in a dose- and time-dependent manner, and increased caspase-3 activity gradually. Both caspase-3 inhibitorⅡand SB203580 reduced cell death significantly, but SB203580 reduced caspase-3 activity significantly. CONCLUSION: NO might induce PC12 cell death through the activation of p38 and caspase-3.