Purpose:To compare with the efficacy in the immediate effects and toxicities on patients with advanced gastric cancer treated with 5-fluorouracil (5-FU) and leucovorin (LV) combined with oxaliplatin or paclitaxel. Methods:Forty patients with advanced gastric cancer, whose metastases to organs or sites included liver, lymphy node, abdominal cavity, abdominal wall, etc, were enrolled in this study, and was randomly divided into two groups (A and B groups). The A group of 20 patients (70% of them were retreated patients) were treated with a combination of oxaliplatin, leucovorin(LV) and 5-fluorouracil(5-FU) continuous infusion regimen. The B group of 20 patients (55% of them were retreated patients) were treated with a combination of paclitaxel, leucovorin (LV) and 5-fluorouracil(5-FU) continuous infusion regimen. Results:Of the 40 evaluable patients, there were two complete responses and seven partial responses (response rate 45%) in the A group, and nine partial responses (response rate 45%) in the B group. All patients were evaluable for toxicities. The most common toxicities were bone marrow depression,peripheral neuropathy,digestive tract toxicities and liver function damage in the A group. The most common toxicities were bone marrow depression and liver function damage in the B group. Conclusions:These two regimens (5-fluorouracil and lcucovorin combined with oxaliplatin or paclitaxel) showed good efficacy and acceptable toxicities in advanced gastric cancer patients, and the 5-fluorouracil and leucovorin combined with oxaliplatin regimen may have some virtues, such as economics, convenience of medication and less serious toxicities.[

Objective:To study the feasibility of microarc oxide treatment on the enhancement of titanium-ceramic bonding strength. Method:Titanium samples in the size of 25 mm?3 mm?0.5 mm were prepared with smooth surface(group 1),rough surface(group 2) and microacrc oxide treated surface(group 3). Nickel-chromium alloy samples in the same size were prepared (group 4). The surface of the samples was observed by scanning electron microscope(SEM) and dispersive spectrometry analysis. Then, the samples were bonded to porcelain. The bonding interface was observed by SEM. The bonding strength of the samples was measured by a three-point bending test according to ISO 9693.Results:Microarc oxide treated surface was rough and porous. The interface of microarc oxide treated surface bonded to porcelain was compact. The bonding strength(MPa) of the samples of group 1,2,3 and 4 to porcelain was 30.79?1.3,36.12?3.03,45.84?3.15 and 48.35?3.06 respectively(group 3 vs group 1 or 2 P0.05). Conclusion:The microarc oxide treatment on titanium can increase the titanium-ceramic bond strength.

Objective:To evaluate the effect of preoxidation on the bonding strength of titanium to porcelain.Method:12 titanium plates(25 mm?3 mm?0.5 mm) were pre-oxidated according to usual preoxidation procedure and 12 without preoxidation were used as the controls.The samples(6 in each group) were then bonded with bonding porcelain,opaque porcelain,dentin porcelain and glaze of Duceratin(Degussa) or Vita titankeramik(Vita) respectively.The bonding strength of Ti/porcelain was evaluated using three-point bending test according to ISO 9693 1990 standard. The interface of Ti/porcelain bonding was observed by SEM.Results:Bonding strength(MPa) of Ti/Duceratin preoxided group and the corresponding control was 41.910?2.778 and 33.097?5.297(P0.05),respectively.SEM observation showed inter-lock and tight bonding of Ti/porcelain in pre-oxidated interface,more cracks and gaps between Ti and porcelain in non-pre-oxidated interface.Conclusion:Pre-oxidation may improve bonding strength of Ti/Duceratin system, while has no significant effect on bonding strength of Ti/Vita titankeramik system.

ObjectiveTo study the optimum method to evaluate the motor function of cerebral palsy neonatal rats caused by intrauterine infection. Methods48 Wistar 17 d pregnant rats were consecutively injected with lipopolysacchide (LPS) (450 μg/kg) for 2 d (LPS group), and other 10 Wistar 17 d pregnant rats (control group) were injected with the same dose of saline. The neonatal rats were selected randomly in control group (A) (n=60) and LPS group (n=120), the latter was divided into intervention group (B1, n=60) and nonintervention group (B2, n=60). The CP rats were identified with neurobehavior detection on the 25th day. Then the CP rats in the B1 group (B1CP) continued their intervention, the CP rats in the B2 group (B2CP) and 10 rats random from group A (A′) were raised routinely. They were assessed with neurobehavior detection and improved BBB assessment on the 25th and 42nd day. ResultsThere were 7 CP rats in B1 group, and 13 in B2 group. There was significant difference in the scores of hanging test, slopes test, open-field experiment, resist captured reaction between the 25th and 42nd day in B1CP group (P<0.01), as well as in improved BBB assessment (P<0.01), but not in neurobehavior detection; while there was not significant difference in B2CP group and in A′ group in all the assessment above. ConclusionNot neurobehavior detection, but hanging test and BBB assessment, can be used to evaluate the motor function of cerebral palsy rats caused by intrauterine infection.

BACKGROUND: It has been demonstrated that insulin-like growth factor-1 (IGF-1) is a kind of neurotrophic factor and protects from cerebral ischemia/reperfusion injury, the expression of IGF-1 is associated with the attack of ischemic stroke. The effects of IGF-1 and its receptor (IGF-1R) on neurobehavioral function are to be further studied.OBJECTIVE: To observe the effects of IGF-1 and IGF-1R on neurobehavioral function in rat models of cerebral ischemia/reperfusion injury.DESIGN: A randomized controlled observation.SETTING: Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College.MATERIALS: The experiments were carried out in Shandong Key Laboratory for Prevention and Treatment of Brain diseases. Twenty-eight healthy adult Wistar rats of clean degree, weighing 220-260 g, were provided by the experimental animal center of Shandong University.METHODS: The rats were randomly divided into experimental group (n =24) and sham-operated group (n =4). The middle cerebral artery occlusion/reperfusion (MCAO/R) models were established by inserting a thread through left external-internal carotid arteries. The sham-operated rats were given the same treatments except inserting thread. ①Neurologic deficit test: The rats in the experimental group were assessed according to Bederson standard after 1-hour ischemia and 6, 12-hour, 1, 3, 7 and 14-day reperfusion respectively. The sham-operated rats were assessed at corresponding time points; Without neurologic deficit was marked as 0 point; flexion of anterior claws as 1 point; unable to act against the pushing from the contralateral side as 2 points; circling while walking as 3 points; shaking as 4 points;unconscious mind as 5 points. ② Sample collection and treatment: The samples in the experimental group were collected after 1-hour ischemia and 6, 12-hour, 1, 3, 7 and 14-day reperfusion, and those in the sham-operated group ere collected at 24 hours postoperatively. The rats were anesthetized, brain samples were got at about 5 mm posterior to optic chiasma after brains were removed completely, then serial coronal sections (5 μm) were prepared, and 1 from 10 sections was stuck to the cover glasses treated with poly-L-lysine. ③ Morphological observation of neurons: The neurons in brain were observed by toluidine blue staining. ④ Detection of IGF-1 and IGF-1R: The expressions of IGF-1 and IGF-1R in cortex and striatum were detected with immunohistochemical technique, 4 fields were randomly selected to count the positive cells under high-power microscope (×400).MAIN OUTCOME MEASURES: ① The neurologic deficit; ② Morphological changes of neurons in brain; ③ Expressions of IGF-1 and IGF-1R in cortex and striatum.RESULTS: All the 28 rats were involved in the analysis of results. ① The neurologic deficit: The scores of neurologic deficit were (1.50±058) and (1.50±0.78) in rats after 7 and 14-day reperfusion, which were lower than that in rats after 6-hour reperfusion [(3.00±0.00), P ＜ 0.05]. ② Morphological changes of neurons in brain: The neurons in ischemic area appeared as paryopyknosis and became irregular in shape, there were obvious gaps around the cells, also deeply stained as purplish blue, nucleolus disappeared, and there were many scattered cellular fragments. ③ Expressions of IGF-1 and IGF-1R in cortex and striatum: The numbers of IGF-1 positive cells in cortex were (8.75±2.06), (11.13±1.14),(19.75±3.18), (17.38±3.11 ) and (11.23±2.28) respectively in rats after 6, 12-hours and 1, 3, 7-day reperfusion, which all were higher than that in sham-operated rats [(3.88±1.46), P ＜ 0.05], the numbers of IGF-1 positive cells in striatum were(8.25±2.21), (11.34±2.21), (18.23±2.64), (18.56±2.34) and (11.31±2.14) respectively in rats after 6, 12 hours and 1, 3, 7days reperfusion , which were also higher than that in sham-operated rats [(4.12±2.24), P ＜ 0.05]. The numbers of IGF-1R positive cells in cortex were (7.63±1.50), (10.50±2.34), (15.55±3.12), (15.37±3.01), (8.86±2.75) respectively in rats after 6, 12-hours and 1,3,7-day reperfusion, which all were higher than that in sham-operated rats [(4.13±1.81), P ＜0.05]. Those in striatum were (8.33±2.31), (10.24±2.09), (14.72±2.17), (14.24±2.77), (8.38±2.05), which were also higher than that in sham-operated rats [(3.76±2.35), P ＜ 0.05].CONCLUSION: The neurological function is damaged after cerebral ischemia/reperfusion, but it has a trend of self-recovery. The expressions of IGF-1 and IGF-1R are mainly distributed in cortex and striatum. Higher expressions of IGF-1 and IGF-1R maintain during 12 hours to 7 days after reperfusion and have a peak value at 1-3 days, which suggests that early expression of IGF-1 and IGF-1R are certain related to the recovery of neurological function.

BACKGROUND: Brain injury can induce the increased expression of basic fibroblast growth factor (bFGF) in brain,whereas FGFR is a very important player in the cell proliferation and differentiation, angiogenesis, skeletogeny, etc.OBJECTIVE: To observe the effect of bFGF and its receptor on neuronal apoptosis following cerebral ischemia/reperfusion injury in rats.DESIGN: A randomized grouping design and animal experiment.SETTING: Institute of Cerebrovascular Disease, Affiliated Hospital of Qingdao University Medical College.MATERIALS: Twenty-eight healthy adult Wistar rats of clean degree, weighing 220-260 g, were provided by the experimental animal center of Shandong University. Rabbit-anti-rat bFGF and fibroblast growth factor receptor-1(FGFR-1) monoclonal antibodies were provided by Wuhan Boster Biological Technology, Co.,Ltd.METHODS: The experiment was carried out in Shandong Key Laboratory for Prevention and Treatment of Brain diseases.① The rats were randomly divided into experimental group (n =24) and sham-operated group (n =4). Models of middle cerebral artery occlusion/reperfusion (MCAO/R) were established by thread occlusion via left external-internal carotid arteries, and 4 rats in the experimental group were sampled at 1-hour ischemia/6, 12-hour, 1, 3, 7 and 14-day reperfusion respectively. The rats in the sham-operated group were given the same treatment without inserting thread.After anesthesia, the brain was removed completely by cutting head, then the brain tissue at about 5 mm posterior to optic chiasma was cut down, then serial coronal sections (5 μm) were prepared. ② The brain tissues were stained with ematoxylin-eosin (HE), and the forms of neurons were observed under microscope. ③ TdT-mediated dUTP-biotin nick end labeling (TUNEL) method: there were buffy granules in nucleus which was positively stained (apoptosis). Four fields were randomly selected from cortex and striatum to count positive cells under high-power microscope (×400). ④ The sections were stained with rabbit-anti-rat bFGF and FGFR-1 monoclonal antibodies, 4 fields were randomly selected from cortex and striatum to count positive cells under high-power microscope (×400).MAIN OUTCOME MEASURES: Apoptosis and the expressions of bFGF and FGFR-1.RESULTS: All the 28 rats were involved in the analysis of results. ① In the experimental group, the neurons in the ischemic sites were obviously decreased, some neurons appeared as paryopyknosis and became irregular, also deeply stained as purplish blue, nucleolus disappeared, and there were many scattered cellular fragments. ② In the sham-operated group, there were a few apoptotic neurons in the brain tissue, and the apoptotic neurons were obviously increased after ischemia, which mainly observed in cortexes and striatums of frontal and paritetal lobes. In the experimental group, apoptotic cells in cortexes began to increase gradually at 6 hours, and there were more cells at 12hours and 3 days, which reached the peak value at 1 day, and began to decrease at 3 day, but there were still more apoptotic cells at 14 days than in the sham-operated group. The number of apoptotic neurons and the changing trend in striatums were generally the same as those in cortexes (P ＞ 0.05). ③ In the sham-operated group, there were weak bFGF expression in the neurons of brain tissue, but there were fewer lightly stained positive cells. After cerebral ischemia, the bFGF expressions were increased, mainly observed in cortexes and striatums. The bFGF expression appeared at 6 hours after cerebral ischemia/reperfusion, and the number was increased gradually and deeply stained as the time of reperfusion prolonged (Figure 3), it reached the peak value at 1-3 days, and then weakened gradually, but it was still higher than in the sham-operated group at 14 days [(5.01 ±1.71), (5.21 ± 1.62) cells/visual field; (2.03± 1.73),(2.46± 1.38) cells/visual field, P ＜ 0.05]. ④ In the sham-operated group, lightly stained FGFR-1 positive cells could be observed in brain tissue. At 6 hours after cerebral ischemia/reperfusion, the FGFR positive cells began to increased in cortexes and striatums, which were the most at 1-3 days, and gradually decreased after 3 days, and the number was still a little more than that in the sham-operated group at 14 days [(5.01± 1.41), (5.20± 1.33) cells/visual field; (2.25±1.67),(2.32± 1.61 ) cells/visual field].CONCLUSION: After cerebral ischemia/reperfusion, the expressions of endogenous bFGF and FGFR-1 may be activated in cortex and striatum, then inhibit the neuronal apoptosis, and play its neuroprotective role.

AIM:To investigate the effect of the N-terminal 24-amino acid (N24) overexpression in p55γre-gulatory subunit of phosphatidylinositiol 3-kinase ( PI3K) on the cell adhesion of human gastric carcinoma cell MGC 803. METHODS:MGC803 cells, which stably expressed GFP-N24 fusion protein and GFP alone , were generated by transfec-tion with pEGFPN-24 plasmid and control plasmid pEGFP-C1, respectively.The morphological change of the cells was ob-served under inverted microscope .The expression of GFP-N24 fusion protein was detected by Western blot .The adhesion of the cells was determined by cell adhesion assay .The effects of GFP-N24 fusion protein on the expression of E-cadherin andβ-catenin were analyzed by Western blot .The expression and secretion of matrix metalloproteinase 9 (MMP9) and u-rokinase-type plasminogen activator ( uPA ) in the MGC803 cells were detected by gelatin zymography .RESULTS:MGC803/GFP-N24 cell line steadily expressed GFP-N24 fusion protein and MGC803/GFP cell line steadily expressing GFP were successfully established , but the expression of fusion protein GFP-N24 was lower than that of the control protein GFP.The morphological changes of the transfected cells from paving stone to fibroblast cell form after gene transfection , and the cytoplasm secretory granules were increased significantly .The cell adhesion to fibronectin and collagen decreased after GFP-N24 transfection .GFP-N24 fusion protein increased the expression of cell adhesion molecule E-cadherin and de-creased the wnt signal pathway molecule β-catenin in the MGC803 cells.However, it did not affect the expression and se-cretion of tumor metastasis-related proteins MMP9 and uPA.CONCLUSION:Overexpression of N24p55γinhibits cell ad-hesion by influencing the expression of E-cadherin and β-catenin in the MGC803 cells.

Objective To investigate the neuroprotective effects and mechanism of phycocyanin in cerebral ischemia reperfusion injury in rats.Methods The model of middle cerebral artery occlusion reperfusion(MCAO/R) was established using the intraluminal filament occlusion with healthy adult male Wistar rats treated by phycocyanin.The apoptosis and the expression of bFGF and FGFR-1,IGF-1 and IGF-1R,iNOS and SOD were respectively determined by TUNEL and immunohistochemical staining to evaluate the effects of phycocyanin on above indexes.Results ① The rats showed neurobehavioral function disorders and the number of nerve cells reduced while apoptotic cells increased in ischemic area after ischemic reperfusion.In phycocyanin group,the number of apoptotic cells reduced siginificantly during reperfusion 12h~3d and the neurobehavioral function was better than that those in control group during reperfusion 7~14d.② In control group,the expressions of bFGF and FGFR-1 increased successfully from reperfusion 6h and reached a maximum at 1d,then subsided gradually in cortex and striatum.In phycocyanin group,the numbers of bFGF and FGFR-1 positive cells were higher than those in control group at the same time-points,which were significantly at reperfusion 1d and 12h~3d respectively.③ The expressions of IGF-1 and IGF-1R increased in cortex and striatum following cerebral ischemic and reperfusion.In phycocyanin group,the numbers of IGF-1 and IGF-1R positive cells in each time-point were higher than those in control group,which was significantly during reperfusion 6h~1d.④ In cotex and striatum,the iNOS and SOD expressed strongly and keep high level during 6h~7d with the maximum at reperfusion 1d.In phycocyanin group,iNOS expressed significantly higher during 12h~1d whlie SOD lower during 6h~1d than those in control group at the same time-point.Conclusion Phycocyanin might play a intrinsic antioxide effect by up-regulating SOD and down-regulating iNOS to inhibit neuronal apoptosis,and enhance the neuronal repairation by means of inducing the expressions of bFGF and IGF-1 following cerebral ischemic reperfusion in rats.

Objective To explore the change of serum high-sensitivity cardiac troponin T(hs-cTnT),myoglobin(MYO),creatine kinase isoenzyme(CK-MB)mass(CK-MB mass)and N-terminal pro-brain natriuretic peptide(NT-proBNP)levels in the patients with renal dysfunction.Methods The inpatients with renal dysfunction(excluding cardiac and skeletal muscle diseases)in our hos-pital were collected and divided into the compensation period group(30 cases),decompensation period group(24 cases)and uremia group(22 cases)according to serum urea and creatine concentration,and 36 healthy individuals were selected as the control group. Venous blood was collected on an empty stomach and separated for obtaining serum.Serum levels of hs-cTnT,MYO,CK-MB mass and NT-proBNP were measured by the electrochemiluminescent immunoassay.Results Serum hs-cTnT levels in the compensation period group,decompensation period group,uremia group and the control group were 16.4(10.9-24.2),17.0(13.0-25.5),25.9 (16.5-33.8),13.7(9.4 -19.7 )pg/mL respectively.Serum MYO levels were 52.4 (40.0 -96.5 ),87.9 (57.7 -118.3 ),115.7 (94.2-175.8),34.8(24.3-48.1)ng/mL,respectively.Serum CK-MB mass levels were 1.03(0.82 -1.75),1.31 (1.08 -1.69), 1.66(1.01-2.46),1.88(1.63-2.43)ng/mL,respectively.Serum NT-proBNP levels were 292.5(123.3-576.2),363.3(192.3-893.3),1 357.2(536.5 -4 662.9),110.3 (70.1 -196.3)ng/mL,respectively.The serum hs-cTnT,MYO and NT-proBNP levels were increased with renal function decrease.The nonparametric Kruskal-Wallis H test showed statistically significant difference a-mong groups(H =14.46,49.81 and 35.00,P <0.05 ).The CK-MB mass level had no statistically significant difference among groups(P >0.05).Conclusion The patients with renal dysfunction have the higher risk rate for complicating the cardiovascular e-vents.Early detection of cardiac markers conduces to the diagnosis of myocardial injury,the evaluation of the risk rate of myocardial infarction occurrence in future and the diagnosis of heart failure and evaluation of the risk rate of heart failure occurrence in future.

ObjectiveTo observe the effects of Balance Performance Monitor (BPM) on balance capacity of children with spastic cerebral palsy. Methods96 children (2～5 years old) with spastic cerebral palsy were randomly divided into the experimental group and the control group. BPM training combined with Bobath approach was used in the experimental group, and the Bobath approach was used in the control group. They were assessed with the BPM before and 2 months after training. Results2 months after training, the balance capacity in both groups improved than before（P<0.05）. Furthermore, the index of experimental group is better than those of the control group（P<0.05）. ConclusionBPM can improve the effects of Bobath approach on the balance capacity of the children with spastic cerebral palsy.