Objective: To investigate the relationship between academic achievements of high school students and the results of California Psychological Inventory (CPI) of them. Method: Seventy-one higher school students were tested by CPI-RC (revised Chinese version). Their academic achievements were recorded. Results: Nine of the 23 CPI traits, such as Re (responsibility), So (socialize), Wb (comfortable), Ac (achievement), Py (psychologized), Cm (communality), To (tolerance), Sc (self-control), V3 (self accomplishment) had significant correlation with academic achievements (r=0.24～0.33, p＜0.05). Students with different prefer (literal arts or science) showed different CPI traits. Students with better academic achievements had higher scores on So, Sc, Wb, To and V3. Conclusion: CPI traits have some relationship to academic achievements of high school students and to their academic preference.

Objective To investigate the effects of ginkgolide B on neuronal cell apoptosis,superoxide dismutase activity,malondialdehyde,interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum of rats with intracerebral hemorrhage in order to explore the role of ginkgolide B in suppressing the neuronal cell apoptosis.Methods A total of 175 male Wistar rats were randomly (random number)divided into sham operation group,intracerebral hemorrhage group,as well as low,medium and high dose treatment groups.The rat model of intracerebral hemorrhage was made with infusion of autologous whole blood to caudate nucleus in the right basal ganglia region.Ginkgolide B in dose of 5 mg/kg,10 mg/kg and 20 mg/kg was given to rats in the low,middle and high dose treatment groups by intraperitoneal injection once a day for 5 days after intracerebral hemorrhage.The rats with intracerebral hemorrhage in the sham operation groups received intraperitoneal administration of 1 mL saline.Animals were sacrificed by decapitation 2,6,12,24,48,72 h and 5 days after intracerebral hemorrhage.Brains were taken and blood samples were collected.Neuronal cell apoptosis was measured by using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL),and superoxide dismutase activity in serum was determined by using xanthine oxidase method,and serum malondialdehyde level was detected by using thiobarbituric acid reactive substance assay,and interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum were assayed with enzyme linked immunosorbent assay(ELISA).Statistical analysis was carried out by using one-way analysis of variance and least-significant difference test.Results As 2 h,6 h,12 h,24 h,48 h,72 h,and 5 days after intracerebral hemorrhage,the differences in the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels between the low dose treatment group and intracerebral hemorrhage group were not significant statistically(P ＞0.05).As 12 h,24 h,72 h,and 5 days after intracerebral hemorrhage,the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels in the medium dose and high dose treatment groups were significantly statistically lower than those in the intracerebral hemorrhage group(P ＜ 0.05),but these differences in above biomarkers were not significant statistically among these three groups 2 and 6 hours after intracerebral hemorrhage(P ＞ 0.05).Conclusions Ginkgolide B may lessen neuronal cell apoptosis by means of inhibition of free radical production and inflammatory reactions after intracerebral hemorrhage.

Objective To investigate the potential mechanism of inhibition of ursolic acid(UA) on growth of human gastric cancer cell lines SGC7901 in vitro.Methods SGC7901 cells were cultured in vitro,MTT assay was used to observe the effect of UA on growth of SGC7901 cells in various concentrations for different times.After SGC7901 cells were treated by 0—40 ?mol/L UA for 24 h,morphological changes were observed by inverted microscope.Apoptotic changes were detected by fluorescence microscopy and flow cytometry (FCM).Protein expressions of Bcl-2 and Bax were determined by Western blotting.Results UA(20—40 ?mol/L) could significantly inhibit the growth of SGC7901 cells in a(dose-and) time-dependent manner,the IC_(50) value of UA for SGC7901 cells for 12,24,36,and 48 h were((57.50?)1.18),(34.28?2.05),(27.54?1.11),and(24.83?1.02) ?mol/L,respectively.After UA((20—)40 ?mol/L) treatment for 24 h,SGC7901 cells turned round and floated at different levels;SGC7901 cells were arrested at G_0/G_1 phase and apoptosis was induced,and the apoptotic rate was increased along with the increase of UA concentration.Meanwhile Bcl-2 protein expression decreased,whereas Bax protein expression unchanged.Conclusion UA has a stronger antitumor effect on SGC7901 cells.Cytotoxic effect,proliferation inhibition,and apoptosis may be involoved in the mechanism of UA,and the apoptosis caused by UA may be enhanced by decrease of Bcl-2 protein expression.

Objective To investigate the kinetics of absorbing timosaponin by AB-8 resin.Methods Static absorption experiment,dynamic absorption experiment and series dynamic absorption experiment were carried out,and then the content of timosaponin was detected by spectrophotometry.Finally,the static absorption curve and the dynamic absorption curve were figured out.Results The result of static absorption experiment showed that the parameters of Lagergren equation are Kad=0.0186,r=0.9986,and the parameters of Dumwals-Wagner are K=0.0081,r=0.9958.In dynamic absorption experiment,the leaking of timosaponin is found and the penetrating point is at 600mL(0.1g/mL).Conclusion The mechanism of AB-8 resin absorbing timosaponin is characterized as liquid membrane diffusion at the early phase and intragranular diffusion at the later phase.Leaking phenomena in dynamic absorption experiment can be solved by three tubes in series.Therefore,this method can be used for the research of Chinese herbal medicine.

BACKGROUND: It has been found that vascular endothelial growth factor can induce the differentiation of bone marrow mesenchymal stem cells into endothelial cells, but can the vascular endothelial growth factor gene promote the differentiation of bone marrow mesenchymal stem cells into vascular endothelial cells in the damaged organ under the hypoxic environment? OBJECTIVE: To observe whether human bone marrow mesenchymal stem cells induced by vascular endothelial growth factor could differentiate into vascular endothelial cells under hypoxia. METHODS: The third passage of human bone marrow mesenchymal stem cells were cultured in vitro. Cells in the control group were cultured with conventional culture medium, while those in experimental group were cultured with adenovirus vector containing vascular endothelial growth factor in 5% O2. After 2 weeks of culture, morphological observation and surface-related molecular detection were performed. The levels of vascular endothelial growth factor and endothelial nitric oxide synthase were detected by ELISA. The expression of endothelin and prostacyclin was detected by RT-PCR and western blot assay. RESULTS AND CONCLUSION: (1) The number of cells in the control group was more than that in the experimental group. The cells in the control group were crowded and arranged irregularly, showing a fiber-like growth, while those in the experimental group were mostly triangular or polygonal, exhibiting a colony-like growth. (2) CD31 was negative in the control group, while CD105 was positive and the positive rate was 99.7%, indicating that the cells still showed the phenotype of bone marrow mesenchymal stem cells. The positive rate ofCD31 was significantly increased to 30.33% in the experimental group and the positive rate of CD105 expression was decreased to 58.11%, indicating a typical phenotype of endothelial cells. (3) Compared with the control group, the expression of endothelin, vascular endothelial growth factor and endothelial nitric oxide synthase increased significantly in the experimental group (P < 0.05), and the expression of prostacyclin decreased significantly (P < 0.05). All these findings indicate that vascular endothelial growth factor can promote the differentiation of human bone marrow mesenchymal stem cells into vascular endothelial cells under hypoxia.

BACKGROUND:Kalikrein 1 is an important component of the kalikrein-kinin system. Studies have shown that kalikrein can protect the cardiovascular system by promoting angiogenesis and inhibiting myocardial inflammation, but there is no report on its effect on inducing differentiation of stem cels. OBJECTIVE: To determine the transfection efficiency of kalikrein 1 adenoviral vector in rat bone mesenchymal stem cels. METHODS:Using adenovirus as a vector, the target gene kalikrein 1 was transfected into rat bone marrow mesenchymal stem cels. Fluorescence microscopy, MTT method and flow cytometry were used to investigate the effect of transfection and determine the optimal multiplicity of infection. RESULTS AND CONCLUSION:Adenovirus carrying kalikrein 1 was successfuly transfected into rat bone marrow mesenchymal stem cels. Results from flow cytometry showed that the transfection efficiency was associated with the multiplicity of infection. When the multiplicity of infection was 150, the transfection efficiency was 80.8%. MTT results showed that when the multiplicity of infection was 200, the cel growth was inhibited remarkably. These findings indicate that adenovirus-mediated kalikrein 1 can be successfuly transfected into rat bone marrow mesenchymal stem cels with the optimal multiplicity of infection=150.

Objective To investigate the antitumor effects and the possible mechanisms of dendrit-ic cells co-cultured with cytokine-induced killer cells(DC-CIK)in combination with sorafenib on two lung adenocarcinoma cell lines,A549 cells(harboring KRAS gene mutation)and PC-9 cells(harboring EGFR gene mutation). Methods DC and CIK cells were routinely generated in vitro by stimulating PBMCs isola-ted from lung cancer patients with different cytokines and then co-cultured after a week of culturing. Flow cy-tometry analysis(FCM)was used to analyze the phenotype of DC-CIK cells after 7 days of co-culturing. The 50% inhibitory concentration(IC50 )of sorafenib against tumor cells was detected by MTT assay. The tumor cells were treated with DC-CIK cells alone or in combination with sorafenib. The proliferation of tumor cells was tested by CCK-8 kit and dynamically monitored by real-time cellular analysis(RTCA). Annexin-V/ PI staining was used to examine the apoptosis rates in each group. Real-time fluorescent quantitative PCR and FCM were respectively performed to detect the expression of natural killer group 2 member D ligands (NKG2DLs)at mRNA and protein levels after the treatment with sorafenib for 24 h. Results There was no significant difference between the IC50 of sorafenib against A549 and PC-9 cells after a 24-hour exposure(P﹥0. 05). Compared with the DC-CIK biotherapy,treating the tumor cells with DC-CIK cells in combination with sorafenib significantly inhibited the cell proliferation and increased the total apoptosis rates of tumor cells(P﹤0. 05). Moreover,the inhibition rates to tumor cell proliferation were enhanced along with the in-crease of effect-to-target ratio(E/ T). Compared with the single-factor treatment groups,the normalized cell index(NCI)in the combined treatment group was significantly decreased. Blocking NKG2D could abate the inhibitory effect of DC-CIK cells on tumor cell proliferation(P﹤0. 05). The expression of NKG2DLs(inclu-ding ULBP1,UBLP2 and ULBP3)on tumor cells at mRNA and protein levels were increased to different ex-tent after treating with 5 μmol/ L of sorafenib for 24 h. Conclusion There was no significant different be-tween the inhibitory effects of sorafenib on the proliferation of lung adenocarcinoma cancer cells harboring KRAS or EGFR gene mutation. The antitumor effects of DC-CIK cells combined with sorafenib on lung ade-nocarcinoma cells might be induced by regulating the NKG2D-NKG2DLs pathway and enhancing apoptosis. Moreover,the antitumor effects of the combined treatment were better than those of single-factor treatments.

BACKGROUND: Synaptic density, a key index of structure and function of brain tissues, is related to cognitive function. Synaptic loss occurs during human brain aging and in Alzheimer disease (AD), inducing the changes of synaptic density.OBJECTIVE: To observe quantitative synaptic alterations in human brain and changes of synaptic density in different parts during normal aging so as to compare them with those of AD patients.DESIGN: Sampling survey.SETTING: Senile Neurological Department of General Hospital of Chinese PLA.PARTICIPANTS: Pathological data were selected from General Hospital of Chinese PLA from June 1996 to December 2002. Inclusion criteria: had no major nervous system diseases and neuropathological changes. Brain tissues of 28 corpses in normal aging group, 23 males and 5 females aged 23-100 years with an average of (65±22.8) years, were obtained at autopsy.All corpses were divided into three groups according to their age, namely,adult group (23-55 years old, n=9), senile group (64-72 years old, n=7),and ＞75 group (76-100 years old, n=12). Cerebral hippocampal samples of other six corpses diagnosed with AD were selected from clinic. The corpses included 5 men and 1 woman aged 76-94 years with an average of (83±7.7) years.METHODS: Response intensity of synaptophysin immunochemistry remained stable after 4-8 hours of death, so brains were obtained at autopsy after 8-72 hours of death and fixed with 4% formalin for at least 6 weeks.In normal aging group, tissues were taken from left superior frontal gyrus,striatal area of left occipital lobe, left putamen (striatum section, including head of caudate nucleus), and left hippocampus (from lateral geniculate body section to medial occipitotemporal gyrus). In AD cases, tissues were taken from left hippocampus of 4 corpses and right hippocampus of other 2. All sections were stained with hematoxylin eosin (HE), toluidine blue and synaptophysin immunostaining (rabbit anti-human synaptophysin polyclonal antibody from Beijing Zhongshan Biotechnology Co., Ltd.). Morphology and distribution of positive objects in synapse immunologic reaction were observed under the light microscope. Relation between absorbance in each region and age was determined with Pearson's coefficient. Differences among groups were analyzed with nonparametric test, and the differences in hippocampal CA3 area between ＞ 75 group and AD group were analyzed with the same test.MAIN OUTCOME MEASURES:① Absorbency of synaptophysin at various sites of normal aging group and correlation with age; ② absorbance value in CA3 area between AD patients and advanced aged normal subjects (＞75 years) was compared.RESULTS:All the 34 cerebral samples entered the final analysis.①Synaptophysin-positive granules of various size were scattered through neocortex, putamen and hippocampus, neuronal somata, neuroglia, vessels and white matter. Density was particularly strong over layers Ⅱ and Ⅲ in frontal lobe, and layer ⅣV in occipital lobe. ② Synaptophysin density was negatively correlated with age, which was -0.688 in frontal lobe, -0.592 in occipital lobe, -0.458 in putamen and -0.619 in hippocampal CA2 area,respectively (P = 0.000, 0.001, 0.014, and 0.000). ③ Significant difference in synaptic density in CA3 area was found between AD patients (0.031 3±0.003 0)and normal subjects over the age of 75 (0.040 7±0.005 3) (Z=-2.997, P=0.001)in nonparametric test.CONCLUSION:① Synaptic density was found to decrease in frontal lobe, occipital lobe, CA3 area of hippocampus and putamen with age; the changes had significant correlation with age.② Synaptic density of AD patients was lower than that of normal subjects, and their cognitive hypofunction was related to synaptic loss. ③ All tissues were obtained after 8-72 hours of death and fixed over 6 weeks, which to the greatest extent reduced the effects of tissue autolysis and formalin fixation on the results.

Objective:To observe the influences of functions of chemokine receptor 9(CCR9) on leukemia patients,we analyzed 38 typical T cell lymphocytic leukemia cases.Methods:The functions of T ALL and T CLL CD4+T cells towards TECK/CCL25 were determined by chemotaxis assay and adhesion assay.Results:Almost in all of the T ALL patients,TECK/CCL25(a ligand for CCR9)could induce a high chemotactic migration of T ALL CD4+ cells as well as a high adhesion.Conclusion:It indicates that CCR9 and its ligands may promote survival or proliferation of T ALL cells. [

Object To establish the method for quality control of Fushengkang Capsule. Methods Semen Livistonae Chinensis, Fructus Camptothecae Acuminatae and Rhizoma Curcumae in this capsule were identified by TLC. The content of camptothecine was determined by HPLC. Condition of HPLC was: Dikma Diamonsil C 18 column (250 mm? 4 6 mm, 5 ?m) the mobile phase was a mixture of methanol water (55∶45), the flow rate was 0 8 mL/min, and detection wavelength at 254 nm. Results The spots of TLC were clear and concentrative. There was a good linear relationship for camptothecine within the range of 0 050 6 - 0 253 0 ?g. The average recovery was 96 90%, RSD=1 74% (n=6). Conclusion This method is sensitive, accurate, reproducible and exclusive. It can be used for quality control of Fushengkang Capsule