Clinical features of mild encephalitis/encephalopathy with a reversible splenial lesion in children / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the clinical features of mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) in children.</p><p><b>METHODS</b>The clinical data of 8 children with MERS were retrospectively analyzed.</p><p><b>RESULTS</b>The mean age of onset was 5 years and 2 months (range 10 months to 12 years). The major clinical features included a history of prodromal infection, and among these children, 5 had pyrexia and 4 had vomiting. Of all the children, 6 were manifested as convulsion and 3 each were manifested as disturbance of consciousness and paroxysmal paropsia. Cranial diffusion-weighted magnetic resonance imaging (MRI) showed high signals in the splenium of the corpus callosum. Among these children, one child had symmetric and multiple long T1 and long T2 signals in the bilateral centrum semiovale and part of the temporal white matter. MRI reexamination performed after 5-30 days showed the disappearance of abnormal signals in all the children. The children were followed up for 3 months to 2 years, and no child experienced abnormal neurodevelopment.</p><p><b>CONCLUSIONS</b>The development of MERS in children is closely associated with infection. MERS is characterized by high signals in the splenium of the corpus callosum on cranial diffusion-weighted MRI. Most children have good prognosis.</p>

Correlation factors of electrical status epilepticus during sleep in children / 中国当代儿科杂志

<p><b>OBJECTIVE</b>The pathogenesis of electrical status epilepticus during sleep (ESES) in children remains unknown. We undertook a retrospective study of epileptic children who presented with ESES to investigate the correlation factors of ESES.</p><p><b>METHODS</b>Thirty epileptic children with ESES (ESES group) and 30 age-and sex-matched epileptic children without ESES (control group) admitted to Maternal and Child Health Care Hospital of Tangshan between January 2000 and July 2006 were enrolled. The results of questionnaire and laboratory examinations were compared between the two groups.</p><p><b>RESULTS</b>Nine patients had a family history of epilepsy in the ESES group, but only 2 patients in the control group (<0.05). Language disorder was found in 11 patients in the ESES group, but only 2 patients in the control group (<0.05). Thirteen patients were confirmed with epileptic syndrome in the ESES group, but only 5 patients in the control group (<0.05). Twenty five patients in the ESES group showed mental retardation, but only 5 patients from the control group (<0.01).</p><p><b>CONCLUSIONS</b>ESES may be correlated with family history of epilepsy, epileptic syndrome, mental retardation and language disorder.</p>

Gamma-Schisandrin inhibits production of amyloid beta-protein 42 in M146L cells / 药学学报

<p><b>AIM</b>To investigate the inhibition of amyloid beta-protein 42 (Abeta42) production in M146L cells by gamma-schisandrin.</p><p><b>METHODS</b>M146L cells which can produce considerable Abeta42 in vitro were treated with gamma-schisandrin (1.67, 5.00 and 15.00 microg x mL(-1)), beta-secretase inhibitor (S4562, 100.00 microg x mL(-1)) and gamma-secretase inhibitor (S2188, 13.68 microg x mL(-1)), separately. Cell counting kit-8 (CCK-8) was used to assess cell viability. Enzyme-linked immunosorbent assay (ELISA) was carried out to determine the amount of Abeta42. Western blotting was used to examine C99, an intermediary product of APP cleaved by beta-secretase. beta-Secretase and gamma-secretase activities were assayed by commercial kits.</p><p><b>RESULTS</b>The CCK-8 assay indicated that different concentrations of gamma-schisandrin had no neurotoxicity on the cultured M146L. And the ELISA test showed that the amount of Abeta42 secreted by M146L cells treated with gamma-schisandrin (5.00 and 15.00 microg x mL(-1)) decreased obviously as compared with solvent control. The results of Western blotting test indicated that there was no change of C99 contents and beta-secretase activity in gamma-schisandrin treated cells, while gamma-secretase activity decreased obviously.</p><p><b>CONCLUSION</b>gamma-Schisandrin inhibited production of Abeta42 in M146L cells through inhibiting gamma-secretase.</p>