Objective To investigate the relationship between the type of gliding contusion and its mechanism with site of force.Methods The site undergoing contusion and ways of force are respectively determined by skull anatomy location and details of these cases.Then,the 132 specimens of brain,which have been fixed by formalin,are sliced in coronal section and sagittal section and stained with HE,observed under microscope.ResultsGliding brain contusion could appeared at the top and bottom region of brain respectively.Top-injury type,were observed in 65 cases(49.24%),base-injury type,were found in 38 cases(28.78%).There were 29 cases(21.96%) in which contusion could be found at both top and base of brain,we called mixed type.We found that the injury area depend on the ways of force-act:the top-injury type mostly caused by the force on cupular part of pars zygomatica in acceleration,the base-injury type mainly caused by the force on occipitalia in deceleration and the mixed type caused by the force on the boundry of the calvaria and occipital in deceleration.Conclusion The type of gliding contusion is relevant with mechanism and site of force.

Objective To investigate the effects of penehyclidine (PHCD) pretreatment on nuclear factor kappa B ( NF-kB ) activity during lipopolysaccharide ( LPS )-induced acute lung injury ( ALl ) in neonate rats.Methods Thirty 7-day old Wistar rats of both sexes weighing 18-21 g were randomly divided into 3 groups ( n =10 each): group Ⅰ control (group C); group Ⅱ LPS; group Ⅲ PHCD. Group Ⅱ and Ⅲ received intraperitoneal ( group IP) LPS 3 mg/kg. In group Ⅲ PHCD 5 mg/kg was administered IP at 30 min before LPS respectively. The animals were killed at 4 h after LPS administration. The lungs were immediately removed. The W/D lung weight ratio was measured. The TNF-α, IL-1 βand IL-10 content in the lung were detected by ELISA and expression of NF-kB p65 was detected by immuno-histochemical staining.Results LPS significantly increased W/D lung weight ratio, TNF-α, IL-1 β, IL-10 content and NF-kB p65 expression in the lung as compared with control group. PHCD administered before LPS significantly attenuated the LPS-induced changes. Electron microscopy showed that PHCD before LPS significandy ameliorated the LPS-induced histological damages. Conclusion Pretreatment with PHCD can attenuate LPS-induced acute lung injury though inhibition of NF-kB activation and inflammatory response of lung tissue in neonate rats.

Objective To explore the effects of 4-phenylbutyric acid(PBA) on cognitive dysfunction after chronic cerebral hypoperfusion and underlying mechanisms.Methods 62 male Sprague Dawley rats in clean degree were divided into sham group(n=14),chronic cerebral ischemia group(bilateral carotid arteries occlusion,2VO group,n=24),and chronic cerebral ischemia with PBA treatment(2VO+PBA group,n=24).The chronic cerebral ischemia models were produced by the occlusion of bilateral common caroid artery for 1 month.During the hypoperfusion,the rats were injected intraperitoneally with 11.25 mg · ml-1 PBA(90 mg · kg-1 · d-1) or equal volume of saline once a day for 3 days followed by every other day for 27 days.Learning and memory abilities were tested by Morris water maze and novel object recognition test.The expression and distribution of NR2A in hippocampus were examined by Western blot and immunohistochemistry.Results Morris water maze test showed that the 2VO group had significantly longer latent time than sham group in searching platform (P＜0.01) (from 2nd day to 7th day latency time),and the 2VO+PBA group had dramatically shorter latent time than 2VO group (2nd,5th,6th,7th (P＜0.01),3rd(P＜0.05)).Then the rats' memory test showed that 2VO group spent markedly longer time than sham group to reach the location of the former platform(P＜0.01),but the 2VO+PBA group spent dramatically shorter latent time than 2VO group (P＜0.01).The novel object recognition test showed the exploration ratio and discrimination index of novel object in 2VO group were noticeably smaller than that in sham group (P＜0.01),but the exploration ratio and discrimination index of novel object in 2VO+PBA group were noticeably higher than that in 2VO group (P＜0.01).The Western blot data showed that the level of NR2A in 2VO group was significantly lower than that in sham group (P＜0.01),but the level of NR2A in 2VO+PBA group was significantly higher than that in 2VO group (P＜0.05).The level of NR2B in hippocampus of 2VO group had no significant difference with sham group and 2VO+PBA group (P＞0.05).Immunohistochemistry data was consistent with the data of Western blot for NR2A level and distribution.The ratio of p-CREB/total CREB in 2VO group(0.62±0.04) was remarkably lower than that in sham group(1.00±0.07),but the ratio of p-CREB/total CREB in 2VO+PBA group(0.97±0.07) was remarkably higher than that in 2VO group(P＜0.01).Conclusion NR2A reduction is associated with chronic cerebral hypoperfusion-induced cognitive impairment,which is rescued by the PBA treatment.It suggests that PBA may have a therapeutic effect on preventing chronic cerebral hypoperfusion-induced cognitive impairment.

AIM To study the effects of A? 25～35 and Apo E4 on neuronal intracellular free Ca 2+ ([Ca 2+ ] i). METHODS Hippocampal and cortical neurons suspension of newborn(0～3 days) SD rats was produced. After incubated with fura 2/AM,the neurons suspension was divided into four groups: control, A? 25～35 , Apo E4, A? 25～35 +Apo E4. Each groups [Ca 2+ ] i was measured using a RF 5000 dual wavelength spectrofluorometer after incubated with double distilled water, A? 25～35 , Apo E4, A? 25～35 +Apo E4 for 3 min, respectively. The neurons outocorrelation function(ACF) of the scattering light intersity was analyzed by the microscope quasi elastic light scattering(MQLS) technique The frequency shift line width by ACF. The ? can sympolize the cell menbrane flilidity. RESULTS Both A? 25～35 and Apo E4 could significantly enhance hippocampal and cortical neurons rest [Ca 2+ ] i, furthermore, the effect of 5 ?mol?L -1 A? 25～35 was higher than the effect of 1 ?mol?L -1 A? 25～35 ( P

AIM　To study the effects of Aβ25～35 and Apo E4 on neuronal intracellular free Ca2+(［Ca2+］i). METHODS　Hippocampal and cortical neurons suspension of newborn(0～3 days) SD rats was produced. After incubated with fura-2/AM,the neurons suspension was divided into four groups: control, Aβ25～35, Apo E4, Aβ25～35+Apo E4. Each groups ［Ca2+］i was measured using a RF-5000 dual wavelength spectrofluorometer after incubated with double distilled water, Aβ25～35, Apo E4, Aβ25～35+Apo E4 for 3 min, respectively. The neurons outocorrelation function(ACF) of the scattering light intersity was analyzed by the microscope quasi-elastic light scattering(MQLS) technique The frequency shift line width by ACF. The Γ can sympolize the cell menbrane flilidity. RESULTS　Both Aβ25～35 and Apo E4 could significantly enhance hippocampal and cortical neurons rest ［Ca2+］i, furthermore, the effect of 5 μmol*L-1 Aβ25～35 was higher than the effect of 1 μmol*L-1 Aβ25～35 (P<0.05), and they also amplified KCl-induced rise in ［Ca2+］i in hippocampal and cortical neurons(P<0.05). The interaction of Aβ25～35 and Apo E4 could also significantly enhance hippocampal and cortical neurons rest ［Ca2+］i andamplified KCl-induced rise in ［Ca2+］i in hippocampal and cortical neurons(P<0.05), but they had no synergic or additive effect.The frequency shift line widith Γ of both hippocampal and cortical neurons were decreased by both Aβ25-35 and ApoE4. CONCLUSION　Aβ25～35 and Apo E4 could enhance neuronal intracellular free Ca2+, amd decrease meirpma; ,e,brame f;iodotu. But their interaction had no synergic or additive effect. It suggested that the amplified effect of Aβ25～35 and Apo E4 on neuronal ［Ca2+］i and membane fluidity may be relative to their neurotoxity.

Objective To explore the relationship between the MRI enhancement ratios of liver parenchyma in hepatobiliary phase with gadobenate dimeglumine (Gd-BOPTA)and liver function.Methods Fifty-nine patients who underwent Gd-BOPTA-enhanced MRI were retrospectively enrolled in the study.The enhancement ratio of signal to noise ratio and enhancement ratio of the contrast ratio were calculated.The relationships between the enhancement ratio and CTP grading and MELD score were analyzed.Results The signal enhancement ratios in hepatobiliary phase in patients with CTP A classification were higher than those with CTP B classi-fication (P <0.01).Meanwhile,the ratios in patients with MELD scores less than 10 points were higher than those with MELD scores more than 10 points (P <0.01).Conclusion The MR enhancement degree of liver parenchyma in the hepatobiliary phase with Gd-BOPTA may reflect the liver function.

Objective To observe the effects of low dose irradiation (LDI) on autoiogous CIK cell proliferation, phenotype and killing activity in tumor patients, and to provide the evidence for clinical application of adoptive immunotherapy with CIK cells. Methods Peripheral blood mononuclear cells (PBMC) were separated from 10 patients with malignant tumor, and CIK cells were cultured with different cytokines. (1) After 10 d culture, C1K cells were irradiated with different doses as 30, 50, 80, 100 and 200 Gy of X-rays was also detected. The CIK cell proliferation and killing activity were measured with 3H-TdR incorporation assay and 3H-TdR release assay, respectively and the percentage variation of CD3 +CD56 + were measured with flow cytometry after 24 h. ( 1 ) Autologous CIK cells were irradiated with 80 mGy X-rays. At different culture time ( 12, 24, 48, 72 h) after irradiation, the killing activity was measured with 3H-TdR release assay. (3) The effect of 3d low dose irradiation of 80 mGy X-rays on thekilling activity of CIK cells was also detected. Results After the CIK cells were irradiated with different doses as 50, 80, 100, 200 mGy of X-rays, the CPM values were 20 048.6 ± 2332. 2 ( t = 2.2, P ＜0.05), 21 832.2 ±2975.9 (t=3.5, P＜0.01), 21 000.3 ±2451.1 (t=3.3, P＜0.01), 19908.1 ±2051.0 ( t = 2.2, P ＜ 0.05 ), respectively and the proliferation of CIK cells were significantly higher than that of control group. The CD3 + CD56 + cell percentage of 50, 80, 100 mGy groups were ( 30.3 ±3.8)% (t=2.3, P＜0.05), (32.3±3.4)% (t=4.2, P＜0.01), (29.742.9)% (t = 2.4, P＜0.05 ), respectively. The killing activity of CIK cells of 80, 100 mGy groups were 55.2 ± 5.0 ( t = 3.3, P ＜ 0.01 ), 52.8 ± 4.1 ( t = 2.3, P ＜ 0.05 ), respectively. The killing activity of CIK cells up-regulated significantly at 24 h, dropped to normal levels at 48 h and 72 h. After 80 mGy X-ray irradiation for 3 consecutive days, the killing activity of CIK cells at different time points were 55.2 ± 5.3 (t = 2.6, P ＜0.05),61.9 ± 4.4 (t = 4.7, P ＜0.01), 67.2 ±5.7 (t = 5.7, P ＜0.01) for 24, 48, 72 h,respectively. Conclusions LDI might have the hormesis effect on CIK cells.

Objective:To produce the mcAb specifically reacting with lung cancer and to purificate its antigen.Methods:The mice were immunized with A549, the mcAb 2B9 was screened by indirect cell ELISA and immunohistochemistry, and its antigen was purificated by immunoaffinity chromatography.Results:A mcAb was obtained, which could react to lung cancer but very little or not to normal lung tissue and other caner tissues, and the antigen of the mcAb was purificated from the cell lysate.Conclusion:A mcAb which can react to lung cancer have been obtained and its antigen was purificated, they may be useful on clinic for diagnosis and prognosis of lung cancer.

AIM: To investigate the influence of Ginkgo biloba extract (EGb761) on c-jun expressions and motoneurons survival following root avulsion. METHODS: One hundred and eighty adult Sprague-Dawley female rats were randomly divided into control and EGb761 groups. Immediately after avulsion of C5-T1 nerve roots, the rats were injected ip with either 1 mL of EGb761 25 mg?kg~(-1)?d~(-1) or the same volume of normal saline, and the treatment repeated everyday. At 4 h to 6 weeks following avulsion, the C7 spinal segments of all rats were collected and prepared for c-jun immunocytochemistry and neutral red stain. The numbers of (c-jun) positive and survival motoneurons were counted and compared between two groups at each time point. RESULTS: In control rats following avulsion, c-jun positive motoneurons appeared at 4 h, reached its maximum at 1 d and declined to 2 weeks. Avulsion-induced motoneurons death started at 2 weeks, climbed to its maximum at 4 weeks-6 weeks. In EGb761 treated rats, both numbers of c-jun positive and survival motoneurons were more than that in control group at each time point. CONCLUSION: EGb761 attenuates avulsion-induced motoneurons death, and this effect may be related to up-regulation of c-jun gene in avulsed motoneurons. [

AIM and METHODS: The ratio of mitochondrial DNA (mtDNA) deletion was measured to find the relationship between mtDNA deletion and aged learning and memory deficit. The aged rats were divided into two groups, aged learning and memory deficit group and aged learning and memory normal group. The ratio of mtDNA deletion was measured by dilution polymerase chain reaction. RESULTS: There are deleted mtDNA (about 4834 bp) in the cerebral cortex, hippocampus and cerebellum of both young and aged rats. The ratios of deleted mtDNA were similar in the cerebral cortex,hippocampus and cerebellum of young rats (about 0.00018%). The ratio mtDNA of aged learning and memory normal rats had increased by five-fold in the cerebral cortex and hippocampus, or one-fold in the cerebellum over young rats. The ratio of aged learning and memory dificit rats had increased by one-fold in the cerebral cortex or 0.8-fold in the hippocampus or two-fold in the cerebellum over aged learning and memory normal rats.CONCLUSIONS: There was really the increase of mtDNA in aging rat brain. And this increase was double in amount in aged learning and memory deficit rats compared to the normal learning and memory aged rats. It is suggested that the mtDNA deletions in the brain regions associated with learning and memory may be contributed to the cellular and molecular mechanism of learning and memory deicit with aged rats.