The cerebral ischemia was produced by Pulsinellis method in Sparaque-Dawley rats. The brain edema and survival rate of rats with bilateral carotid and vertebral arteries occlusion for 60 min were observed in ip tetradrine at doses of 1 ~ 4 mg/kg groups and control rats.Superoxide dismutase and malondialdehyde in brain tissue were also measured by pyrogallol method and fluorescence spec-trometry. The results suggested that tetradrine have protective effect on cerebral ischemia, which was related to the inhibition of lipoxide and scavenging of oxygen free radical.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective: To investigate the effects of adenosine A 1 receptor agonist N 6 cyclohexyladenosine(CHA) on neurofunction after fluid percussion injury in rats. Methods: The effects of CHA intra cerebroventricular injection 10 min before brain trauma on rats neurofunction and neuropathological changes were evaluated. Results: Compared with the control group, CHA could ameliorate the behavior deficits and improve pathological change. Conclusion: Adenosine A 1 receptor plays an important neuroprotective role in rat secondary injuries following brain trauma.

Angiogenesis Inhibitors ; pharmacology ; therapeutic use ; Animals ; Antimetabolites, Antineoplastic ; therapeutic use ; Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Deoxycytidine ; analogs & derivatives ; pharmacology ; therapeutic use ; Drug Therapy, Combination ; Female ; Ginsenosides ; pharmacology ; therapeutic use ; Lung Neoplasms ; drug therapy ; pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation

Objective To explore the evolution and treatment of traumatic subdural effusion(TSE).Methods The clinicsl materials of 66 patients with TSE were analyzed retrospectively.Results 53 patients were cured with comervative therapy,and other patients were evolved into chronic subdural hematoma(CSDH).8 patients with CSDH were cured with surgery and others with conservative therapy.Conclusion Patients with TSE don't need surgery,and then patients with clinical characteristics will be operated when TSE evolves into CSDH.

Objective: : To observe whether cytokines rIL 2,TNF ?,I FN ? and anti CD3/anti glioma bispecific antibody(BsAb) can work coordinately, and to investigate how to further enhance cytotoxicity of T lymphocyte against human glioma cells by BsAb. Methods: There were 12 groups,contr ast method were used to analyze the effect of cytokines rIL 2,TNF ?,IFN ? to cytoxicity directed by BsAb by single and combined experiments. Cytotoxicity was assayed by standard 18 h 3H TdR incorporation release. Resul ts: rIL 2,TNF ?,IFN ? and BsAb could cooperatively enhance the cy totoxicity of effect cells( P

Objective To evaluate the influence of positive end-expiratory pressure (PEEP) on intracranial pressure and cerebral perfusion pressure in dogs with or without intracranial hypertension caused by frontal intracerebral hematoma. Methods Eighteen dogs were randomly divided into three groups. In Group B and Group C, the intracranial hypertension was respectively higher than 25 mmHg but less than 40 mmHg and higher than 40 mmHg induced by autoblood clotting injection into the right frontal lobe, while Group A as control was of normal intracranial pressure. PEEP was applied in increment of 3 cmH2O from 0 to 18 cmH2O, each level lasting 20 min. The intracranial pressure (ICP) was monitored by an optical fiber transducer implanted into left frontal lobe. Mean arterial pressure (MAP), heart rate (HR), and central venous pressure (CVP) were recorded simultaneously. Cerebral perfusion pressure (CPP) was calculated by the equation (CPP=MAP-ICP). Results With increasing PEEP level, ICP increased and CPP fell in Group A; ICP fell, MAP and CPP increased in Group B; ICP fell, MAP and CPP increased in Group C. CVP increased in all groups, and the increment was significantly higher in Group C than the other two groups (P

OBJECTIVE: To investigate the protective effects of mild hypothermia (33-35 degrees C) on the outcome of patients with severe traumatic brain injury (TBI) (GCS<8). METHODS: Patients in the mild hypothermia group were cooled to 33-35 degrees C by cooling blanket with muscular relaxant, and patients in the normothermia group were maintained at 37-38 degrees C. RESULTS: The result showed that the mortality was 26.1% (6/23) in the mild hypothermia group and 58.3% (14/24) in the normothermia group respectively (P<0.05). The mild hypothermia also markedly reduced intracranial pressure (P<0.01 and inhibited hyperglycermia (P<0.05). No significant side-effects were found during hypothermic treatment. CONCLUSIONS: Our clinical data have demonstrated that mild hypothermia is a useful method for management of patients with severe traumatic brain injury.