Upregulation of liprin-α1 protein in the temporal neocortex of intractable epileptic patients and experimental rats.

Intractable epilepsy (IE) patients have synaptic dysfunction. However, the exact mechanism of synaptic function needs further elucidation. The aim of this study was to use immunohistochemistry, immunofluorescence, and Western blotting to investigate the expression of the Liprin-α1 protein, one of the synapse-associated proteins, in human IE brain tissues and experimental rats and to discuss the possible role of Liprin-α1 in IE. We selected 30 temporal neocortical tissue samples from patients with intractable temporal lobe epilepsy (TLE) and 10 histologically normal temporal lobes from controls. Fifty-six Sprague-Dawley rats were divided randomly into seven groups; one control group and six groups with epilepsy induced by lithium-pilocarpine administration. Temporal lobe tissues were taken from controls and from rats at 1, 3, 7, 14, 30, and 60 days postseizure. Liprin-α1 was mainly expressed in neurons of human controls and TLE patients and was significantly higher in TLE patients than in controls. Liprin-α1 was also expressed in neurons of control and experimental rats and it was significantly higher in experimental rats than in the control group. The expression of Liprin-α1 in animals in the experimental group gradually increased from Days 1 to 30 postseizure induction and reached a stable level when spontaneous recurrent seizures (SRS) appeared. These results suggest that an increased expression of Liprin-α1 in the brain may be associated with human IE.

Identification of recombinant intermediates of hepatitis B virus between genotype B and C in vitro.

OBJECTIVE: To detect the recombinant intermediates of hepatitis B virus (HBV) between genotype B and C in vitro. METHODS: Vector Plenti6/V5-D-topo-X was genetically modified by genotype B and C to transfect HepG2 cells. Then the HepG2 cells were amplified and sequence of the nucleic acid after the transinfection was tested and compared with RDP3Beta40 software package and bootscanning procedure in SimPlot program package. RESULTS: Three recombinant intermediates of HBV between genotype B and C were identified in vitro. Genotype C in the precore region plus the core gene spanning nucleotide positions from 1740-1838 to 2443-2485 contributed to the recombination with genotype B. Isolate R1 recombinant intermediate had 2 break points at nt2170-2172 and nt2188-2189. Nucleic acid changed from CAC to TGT and from GA to AC, respectively. Isolate R2 recombinant intermediate had a break point at nt1740-1 838, and 3 bases changed in different nucleic acid sites: from A to T at nt1740, from C to T at nt1753, and from G to A at nt1838, respectively. Isolate R3 recombinant intermediate had a break point at nt2443-2483, and 4 bases changed in different nucleic acid sites: from C to T at nt2443, from A to G at nt2452, from T to C at nt2480, and from C to T at nt2483, respectively. CONCLUSION: The recombinant intermediates of HBV between genotype B and C have been detected in vitro and the changes have been identified in the precore region plus the core gene in genotype B and C.

[On the auto-reference, auto-correlation and adaptive interference cancellation theories and techniques for single extracting flash visual evoked potential].

On the basis of analyzing the defects in traditional averaging theory for extracting evoked potential (EP), and by realizing the characteristic of spontaneous electroencephalo-signal (S-EES) as well as the special environment for extracting EP, we propose an auto-reference, auto-correlation, adaptive interference cancellation (AAA-ICT) for use in the single trial of flash visual evoked potential (FVEP). Firstly, the segment of reference signal, which has the best correlation with evoked electroencephalo-signal (E-EES), was obtained using the method for calculating the sliding correlation point by point between E-EES and reference signal; then, the cancellation factor between E-EES and the most correlative reference signal segment was derived by the least square method; at last, the single trial of FVEP was acquired by interference cancellation. By this method, FVEP can be extracted perfectly and the FVEP variability of individual inter-stimulation can be obtained.

Effects of intravenous mannitol on EEG recordings in stroke patients.

OBJECTIVES: To evaluate the usefulness of continuous EEG monitoring of stroke patients during and after intravenously infused mannitol. METHODS: Patients were rapidly administered 50 g of intravenous mannitol solution with continuous EEG monitoring for 3h pre- and post-drug infusion in the neurological intensive care unit. Visual and spectral analyses of EEG recording pre- and post-mannitol infusion were carried out. RESULTS: The study consisted of 47 patients. Of 38 patients with intracranial hemorrhage, 33 had abnormal EEG findings pre-mannitol administration. After mannitol therapy, visual analysis of the drug-induced EEG changes showed that the EEG findings were unchanged in 13 patients, demonstratively improved in 22 patients, and worse in 3 patients. The spectral analysis demonstrated that mannitol-induced EEG changes increased in alpha power and decreased in delta power in the lesion hemispheres, especially in the central and middle temporal areas. Maximal effects occurred 30 min post-mannitol infusion, and remained significant for 2h post-infusion. Of the 9 patients with cerebral infarction, only one with diffuse background slowing of one-side dominance pre-mannitol improved after the infusion of mannitol. CONCLUSIONS: The results of our investigation indicated that continuous EEG monitoring of mannitol treatment can reflect the brain edema, raised ICP in stroke patients, and provide assessment the drugs effects of antiedema and intracranial pressure lowering in vivo.

Effects of intravenous human albumin and furosemide on EEG recordings in patients with intracerebral hemorrhage.

OBJECTIVES: To characterize alterations in continuous EEG monitoring that occurs during and after intravenous infusion of human albumin or furosemide in patients with intracerebral hemorrhage. METHODS: Patients were rapidly administered 20% human albumin 50 ml or furosemide 40 mg intravenously with continuous EEG monitoring for 3h before and after drug infusion in the neurological intensive care unit. Visual and spectral analyses of EEG recordings before and after mannitol administration were carried out. RESULTS: The study consisted of 20 patients. Of 14 patients with human albumin treatment, a decrease in the slowing activity was visually noted in 9 cases after the drug infusion. The spectral analysis demonstrated that albumin-induced EEG changes increased in alpha power and decreased in delta power in the lesion hemispheres, especially in the central and middle temporal areas. The effects occurred after 30 min and were maximal 1h after the end of the infusion, then remained significant for 2h post-infusion. Of 6 patients with furosemide treatment, the EEG recordings before, during, and after the furosemide infusion were not statistically significantly different by visual and quantitative analyses. CONCLUSIONS: The results support the opinion that the available EEG monitoring techniques offer an inexpensive, non-invasive, and consistently reproducible technique for reflecting the therapeutic effects of therapeutics in lowering ICP and antiedema in stroke patients.

Down-regulation synaptic vesicle protein 2A in the anterior temporal neocortex of patients with intractable epilepsy.

Synaptic vesicle protein 2A (SV2A) involvement has been reported in the animal models of epilepsy. The aim of this study was to investigate the expression of SV2A in human intractable epilepsy (IE) brain tissue. Using immunohistochemistry, immunofluorescence, and Western blot, we detected SV2A expression in tissue samples from the anterior temporal neocortex of 33 patients who had been surgically treated for IE. We compared these tissues with nine histologically normal anterior temporal lobe samples from controls. SV2A immunoreactive staining was 0.1651+/-0.0564 in patient group and 0.2347+/-0.0187 in the control group (p<0.05) using immunohistochemistry, and this finding was consistently observed with Western blot analysis (0.1727 +/- 0.0471 versus 0.3976+/-0.0983, p<0.05). Immunofluorescence staining showed that SV2A was mainly accumulated in neurons. Our findings demonstrate that down-regulation of SV2A is present in patients with temporal lobe epilepsy.