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Objective To review the clinical data and visual outcomes after treatment of patients with dysthyroid op-tic neuropathy ( DON) .Methods We retrospectively examined the clinic data of the 38 patients (67 eyes) suffer-ing from DON and analysed the effect of glucocorticoids , radiation and orbital decompression .Results The study included 14 men and 24 women.32 patients ( 84.2%) received multiple treatment modalities .LogMAR vision acuity changed from (0.60 ±0.59) before treatment to (0.18 ±0.09) after treatment(P<0.01) .There were 59 eyes (88.1%) in the treatment effective group , 8 eyes (11.9%) in the ineffective group .38 eyes underwent ini-tial treatment with intravenous steroid pulse therapy and 35 eyes ( 92.1%) were effective .29 eyes were treated with other modalities and 24 eyes(82.8%) were effective(P<0.01).There were 3 eyes (5.1%) suffering from fixed eyeball movement in the effective group , while 4 eyes ( 50%) in the ineffective group ( P <0.05 ) .The thickness of the supraocular muscle group in the effective group was (7.63 ±1.19 ) mm, (8.81 ±0.83 ) mm in the ineffective group (P<0.05).Mean defect of the visual field was (2.41 ±2.82) in the effective group and (11.98 ± 7.07 ) in the ineffective group ( P<0.05 ) .Conclusions Treatment with multiple modalities effectively improved visual outcomes in cases of DON .Intravenous pulse steroid therapy was recommended as the initial modality .
RESUMEN
Objective To observe the time-course expression of calcium-calmodulin dependent protein ki-naseⅡδ (CaMKⅡδ) in cerebral cortex after traumatic brain injury (TBI). Methods The TBI rat model was established. The expression of CaMKⅡδ in cerebral cortex around injured area was tested by Western blotting and immunohistochemical staining . Results Western blotting revealed expression of CaMKⅡδ in normal rat brain cortex. It gradually increased after TBI, peaked after 3 days, and then returned to normal level. The result of immunohistochemical staining was consistent with that of West-ern blotting. Conclusion The expression of CaMKⅡδ around injured area after TBI increased initially and then decreased. It could be used as a new indicator for wound age determination following TBI.