Objective To determine the value of detection of H ras oncogene mutation in urine exfoliated cells as clinical indicator of tumor presence, recurrence and stage.Methods Point mutation at codon 12 of H ras gene was assayed by polymerase chain reaction followed by analysis of single strand conformation polymorphism in urine exfoliated cells from 48 patients with transitional cell carcinoma before operation and 28 patients with non urothelial cancer or normal individuals. The mutation was further confirmed by dideoxy mediated chain termination method of DNA sequencing. Cytology analysis was carried out simultaneously. Bladder tumor specimens were obtained from 48 patients during operation, and histologically elevated for tumor content and grading.Results 48%(23 of 48) of the patients were detected by their aberrant band in SSCP. All aberrant bands displayed a mutant H ras sequence, where 15% (7 of 48) of the patients displayed, apositive cytological analysis. Analysis of abnormalities with tumor stage revealed that the greater detection of high pathological stage (Ⅲ Ⅳ) compared with low stage (Ⅰ Ⅱ) was related to the recurrence of transitional cell carcinoma.Conclusion Our results suggest that the detection of H ras mutations may be of clinical value in the detection of TCC.

Objective To determine the toxicity of therapeutical Serratia marcescans vaccine when repeated intracerebral administration into rat brain.Methods SD rats are prepared by intracranial embedding location catheter and were randomly divided into 8 groups:namely normal control,lunar control group(give NS in same dose),low dosage group,middle dosage group and high dosage group of acute stage or restore stage.Three dosage of vaccine S311 were administrated(low 320 million/kg,middle 1600 million/kg,high 8000 million/kg).The embedding catheter rats were fixed point injecting vaccine,once per day for 15 days with microsyringe of microdialysis device.While continuously record the common status,appetite,body weight of animals.25 days later,Animals were killed to observe the morphology of brain.Results The main pathologic changes of high dosage group were inflammatory cell infiltration into the tissues around injecting location,subarachnoid space,and ependyma.The inflammatory cell is mainly gial cell,monocytes,lymphocytes.No degeneration and necrosis of brain tissue were observed.The inflammatory reaction of brain tissues around injecting location was correlated with the dosages.Except the inflammation around injecting location,the other brain tissues were normal and absent of organic pathological changes.After 25 days restoration,the inflammation around injecting location was absorbed.Conclusions The method of intracranial embedding catheter and fixed point injecting is successful.Intracranial administration of therapeutical Serratia marcescans vaccine is mainly effect on location around injecting to elicit localized,reversible,and non-specific inflammatory reaction.

AIM:To investigate the protective effect of lycopene on primary mouse cerebrocortical neurons ex -posed to tert-butyl hydroperoxide ( t-BHP) and its mechanisms of in vitro.METHODS:Primary cerebrocortical neurons of newborn C57 mice were extracted and divided into normal group , t-BHP group, lycopene +t-BHP group and lycopene group.The neuronal damage was induced by t-BHP exposure for 24 h, and the cell viability was examined by MTT assay . ROS content was measured by flow cytometry , and the protein levels of Bax , Bcl-2, caspase-3, cleaved caspase-3 and cyto-chrome C were examined by Western blot .RESULTS:The primary mouse cortical neurons expressed MAP-2 protein.Ly-copene at concentration of 4μmol/L reversed the decrease in cell viability .Flow cytometry revealed that lycopene treatment attenuated ROS content under the condition of t-BHP exposure.In addition, the protein level of Bcl-2 was increased, and the expression of Bax , cleaved caspase-3 and cytochrome-C was suppressed in lycopene +t-BHP group.CONCLUSION:The protective effect of lycopene on cortical neurons with t-BHP-induced injury may be involved in the mechanism of neuro-nal antioxidative response by down-regulating caspase-3 and Bax/Bcl-2 through the mitochondrial apoptotic pathway .

AIM:To establish a mouse model of immuno-inflammation in central nervous system (CNS) associated with cognitive dysfunction.METHODS:C57BL/6J male mice were divided into 3 groups.Lipopolysaccharide (LPS) was intraperitoneally injected into the mice to induce cognitive impairment.Morris water maze test, passive avoidance test and pole test were used to observe the behavioral changes of mice.The histomorphology was analyzed by the method of immunofluorescence.The detailed molecular mechanism was determined by Western blot.RESULTS:Compared with saline group, LPS induced mouse sickness behavior and memory loss.Microglia activation and neuronal loss in the hippocampus were observed.The expression of neuroinflammatory proteins COX-2 and iNOS in the brain of LPS-induced mice was increased.CONCLUSION:Intraperitoneal injection of LPS induces cognitive dysfunction in mice.