Rats were divided into 3 groups and inflicted with total body irradiation of 5 Gy of gamma rays from a 60Co source,15% TBSA full thickness burns,or both of them respectively.The changes of lipid peroxide,cytochrome oxidase,NADH-cytochrome C reductase,catalase and superoxide dismutase activities were observed.It was found that the MDA content of hepatic mitochondria was significantly elevated in all the 3 goups on the 2nd and 6th day postinjury,and there was a third peak of MDA elevation in the the burn group on the 10th day postinjury.The increase of MDA in hepatic mitochondria was probably due the combined action of 2 factors.(1) increased production of toxic active oxygen species such as O2-and H2O2 as a result of increased activity of NADH-cytochrome C reductase and cytochrome oxidase,and (2) alterations of the defence mechanism against this active oxygen species due to lowered activity of superoxide dismutase and catalase.

Objective High mobility group box-1 protein ( HMGB1) plays an essential role in regulating energy metabolism of tumor cells via affecting mitochondrial autophagy .The aim of this study was to explore the effect of HMGB 1 on mitochondrial biogene-sis and cell energy metabolism in anoxia environment . Methods HepG2 cells were divided into normoxia control group ( cells were cultured in a culture box containing 5%CO2) , hypoxia control group ( cells were cultured in a culture box containing 1%O2+5%CO2+94%N2 ) , hypoxia HMGB1 siRNA group ( cells were cultured in a culture box containing 1% O2+5% CO2+94% N2 after transfected with HMGB1 siRNA) and hypoxia NC siRNA group ( cells were cultured in a culture box containing 1%O2+5%CO2+94%N2 after trans-fected with negative control siRNA ) .MTS assay was carried out to measure cell proliferation rate .The alterations of mitochondrial bio-genesis associated proteins were detected by RT-PCR and western blot.Mitochondrial density and morphology were determined by transmission electron microscopy (TEM).The ATP content in whole cell extracts was determined with a colorimetric ATP detection kit . Results Compared with the hypoxia control and hypoxia NC siR-NA group, the proliferationof hypoxia HMGB1 siRNA group was significantly inhibited, especially in 48 h and 72 h(P<0.05).Com-pared with hypoxia control group and hypoxia NC siRNA group , the expression of PGC 1α, NRF1and TFAM in hypoxia HMGB1 siRNA group were decreased significantly ( P<0.05) .Western blot results showed that , compared with normoxia control group , the expressions of PGC1α(0.494±0.210 vs 0.090±0.020), NRF1(1.080±0.470 vs 0.581±0.190)and TFAM(1.585±0.340 vs 0.792±0.350) protein in hypoxia 24 h group were increased obviously ( P<0.05) .Compared with hypoxia control group and hypoxia NC siRNA group , the expres-sions of PGC 1α, NRF1 and TFAM protein in hypoxia HMGB1 siRNA group were significantly decreased (P<0.05).Compared with hypoxia control group , the content of ATP in the HMGB 1 siRNA hypoxia group was significantly decreased , and hypoxia 12 h and 24 h were the most obvious ( P<0.05) . Conclusion HMGB1 could maintain cell energy metabolism by regulating mitochondrial biogene-sis so that cells could continue to proliferate in adverse anoxia environment .

Objective To study the effect of indole- 2,3-dione on the content and release of monoamine neurotransmitters in rat brain.Methods The Wistar rats were given indole-2,3-dione (50,200mg?kg~(-1),ip), and the content of acetylcholine(Ach) and dopamine(DA) in corpus striatum were detected two hours later;the releases of DA,5-hydroxy-tryptamine(5-HT) and norepinephrine(NE) in cortex and corpus striatum slices were examined before and after perfusion with the artificial cerebrospinal fluid(ACSF)that contained indole-2,3-dione. Results The rats given indole-2,3-dione were observed higher concentration of Ach and DA in their corpus striatum compared with that in cortex. Moreover the results also showed indole- 2,3-dione promoted the release of DA in cortex and corpus striatum slices. Conclusion Indole-2,3-dione can regulate the balance between Ach and DA release in rat brain.

Limbic encephalitis is a new type of autoimmune encephalopathies.The clinical manifestation is primarily defined by the subacute onset of short-term memory loss,seizures,confusion and psychiatric symptoms.The diseases usually have a variety of clinical manifestations,and are very serious,occurring with or without tumor association.Routine detection of serum and cerebrospinal fluid (CSF) and imaging tests show no specificity,but associated antibodies can be detected in serum and (or) CSF.Early identification,tumor resection and immunotherapies are helpful in improving the prognosis of patients.This article aims to study the pathogenesis,classification,clinical features and treatment of antibody-associated limbic encephalitis and to improve the diagnosis and prognosis of the disease.