ABSTRACT
Ictal semiology is essential for the pre-operative evaluation of candidates for epilepsy surgery. We propose an ictal sign of temporal lobe epilepsy (TLE) termed tonic-automotor (TA), defi ned as contralateral tonic spasm of upper limb associated with ipsilateral hand automotor seizure and often accompanied ipsilateral head turning. We assessed the occurrence and lateralizing/localizing value of TA in TLE, we analyzed 129 seizures in 41 patients with TLE: 90 seizures in 30 patients with TLE of hippocampal sclerosis (TLE/HS) and 39 seizures in 11 patients with TLE of other lesions (TLE/ non-HS). When compared with unilateral automotor seizure and unilateral tonic spasm, TA occurred more frequently in TLE/HS patients (40% vs 10% and 16.7%). In addition, 24 seizures in 12 patients with TA were observed only in TLE/HS patients and contralateral to the seizure focus based on the side of tonic spasm. However, there was no signifi cant difference in the TLE/HS between dominant side and nondominant side. In addition, TA sign occurred relatively early in the ictal phase. Thus, TA may be a more reliable lateralizing sign of epileptogenic zone and a semiologic marker of TLE/ HS patients.
ABSTRACT
Objective To investigate the mechanism affecting on permeability of vascular endothelial cell by nitric oxide (NO). Methods Series concentration of sin-1（a donor of NO） were added to ECV 304, a cell line of human umbilical vein endothelium. Cell growth and expression of f-actin, a cytoskeleton protein were observed. Results Cell growth was inhibited with a dose from 6.25 to 100 μmol/L and was caused to death at the concentration of 50 to 100 μmol/L by sin-1. The expression of f-actin was suppressed obviously after cultured with 100 μmol/L sin-1 for 4 hours. Conclusion It suggests that anomaly increased NO can increase permeability of blood vessels by suppressing the expression of f-actin, inhibiting cell growth or even resulting in cell death.
ABSTRACT
Objective To investigate the mechanism affecting on permeability of vascular endothelial cell by nitric oxide (NO). Methods Series concentration of sin-1（a donor of NO） were added to ECV 304, a cell line of human umbilical vein endothelium. Cell growth and expression of f-actin, a cytoskeleton protein were observed. Results Cell growth was inhibited with a dose from 6.25 to 100 μmol/L and was caused to death at the concentration of 50 to 100 μmol/L by sin-1. The expression of f-actin was suppressed obviously after cultured with 100 μmol/L sin-1 for 4 hours. Conclusion It suggests that anomaly increased NO can increase permeability of blood vessels by suppressing the expression of f-actin, inhibiting cell growth or even resulting in cell death.