Purpose To explore the clinical characteristics of small intestinal tumors and its diagnosis. MethodsRetrospective analysis of cases. ResultsLdomyoma was most common among the benign small intestinal tumors(12/17),adenocarcinomawas most common among the malignant small intestinal tumors(45/ 76). The feature of the small intestinal tumors could be hemorrhage, abdominal pain, abdominal mass, fever and jaundice. Upper gastrointestinal tract barium oontrast study was performed in 28 cases,and the results of 21 cases were positive. Mesenteric arteriography was performed in 9 cases. It was confirmed by surgery that the results matched with the lesions. ConclusionsMesenteric arteriography is of great value in diagnosis of the small intestinal tumors endoscope retrograde cholangiopancreatography(ERCP), CT are also helpful.

Objective To explore the effects of aspirin on formation and dispersion of Pseudomonas aeruginosa (P.aeruginosa) biofilm.Methods The broth microdilution method was used to detect the minimal inhibitory concentration(MIC) of aspirin for P.aeruginosa.The anti-biofilm effects of aspirin on P.aeruginosa were determined on the microtiter plates combined with crystal violet staining.The serial dilution method for counting colony number on microtiter plate was used to explore the effects of aspirin on initial adherence of P.aeruginosa.Results The MIC values of aspirin against PAO1,PA18,PA53 and PA67 strains of Pseudomonas aeruginosa were 5,2.5,5 and 5 mg/mL respectively.Aspirin significantly inhibited the formation and dispersion of the biofilm of PAO1 and PA18 strains (t =5.65,P ＜ 0.05 and t =5.06,P ＜ 0.05 for inhibition;t =6.45,P ＜ 0.05 and t =6.26,P ＜ 0.05 for dispersion) at the concentration of 2.5 mg/mL.Similar effects were also found in the determination for PA67 and PA53 strains(t =6.45,P ＜0.05 and t =6.26,P ＜ 0.05 for inhibition;t =7.82,P ＜ 0.05;t =9.18,P ＜ 0.05 for dispersion) at aspirin concentration of 1.25 and 0.313 mg/mL respectively.Aspirin inhibited the initial adherence of P.aeruginosa at the concentration of 2.5 mg/mL(P ＜0.05).Conclusion Aspirin could significantly inhibit the initial adherence and biofilm formation of P.aeruginosa and disperse the 24 hour-formed mature bioiflm.

OBJECTlVE To establish a real-time cell analysis system ( RTCA) for early drug car-diotoxicity evaluation. METHODS An in vitro drug cardiotoxicity evaluation method was established using RTCA Cardio system and primary cultured cardiomyocytes of neonatal rats. The beating rate, am-plitude and beating rhythm irregularity ( BRl ) of cardiomyocytes were observered after antiarrhythmic drugs, such as quinidine and lidocaine were added, to assess the effect of the above method on cardio-toxicity evaluation. RESULTS RTCA Cardo E-Plate 96 was inoculated with primary cultured cardiomyo-cytes that began to beat after 24 h and beat regularly after 48 h. The stable beating was maintained for a minimum of three days. The beating of cardiomyocytes decreased rapidly from 155±5 to 0 after incuba-tion with quinidine. The beating recovered gradually after 6 h. Quinidine at 3.1μmol·L-1 caused the beat-ing rate to return to 124±16. Quinidine allowed the beating rate to return to normal when the concentra-tion was less than 100.0μmol·L-1 . The beating rate, amplitude and BRl of cardiomyocytes changed in a concentration-dependent manner when incubating with lidocaine. The higher the concentration, the more significant the inhibition of lidocaine on cardiomyocytes. CONCLUSlON The cardiotoxicity of quinidine and lidocaine can be detected accurately using RTCA Cardio system, suggesting that this system can be used in early evaluation of drug cardiotoxicity.

BACKGROUND: At present, studies concerning human umbilical cord blood mesenchymal stem cells (UCB-MSCs) transplantation for repair of rat spinal cord injury, brain tumor, and myocardial infarction have been reported, and studies that human UCB-MSCs were induced differentiation into osteogenic cells under certain conditions have also been reported at home and abroad. But application of UCB-MSCs transplantation in the treatment of osteonecrosis of animals has not yet been reported. OBJECTIVE: To observe the repair results of recombinant lentivirus vector tracing enhanced green fluorescent protein (EGFP)-transfected UCB-MSCs transplantation in treatment of ischemic necrosis of the femoral head in rabbits. METHODS: Bone morphogenetic protein-2 gene plasmid, recombinant lentivirus vector carrying EGFP and UCB-MSCs were co-cultured. Rabbit models of femoral head defects were made and randomly divided into 3 groups. There was no treatment in the normal group, control group with bone defects and experimental bone defects filled with UCB-MSCs tracing transfected by recombinant lentivirus vector carrying EGFP. At 4 and 8 weeks after treatment, the imaging and histological of the femoral head were observed.RESULTS AND CONCLUSION: Imaging and histology results showed that there were osteogenic response and new bone formation in the experimental group at 4 weeks, and the bone defects were basically repaired at 8 weeks after treatment. In the control group, the bone defects filled with fibrous connective tissue fiber connective tissues at 4 weeks, and the osteosclerosis could be found surrounding femoral head, bone defects filled with fibrous connective tissue fibers and bone trabecula distributed disorderly. The recombinant lentivirus vector tracing EGFP-transfected into UCB-MSCs has strong effects bone conduction and can repair ischemic necrosis of the femoral head.

Objective To determine whether chronic stress could potentiate learning and memory impairment in old mice, and, if so, what the underlying mechanism is. Methods Sixty male mice were divided randomly into control group and chronic stress group. Mice in stress group were stressed everyday by one of the stressors including cold exposure, restraint, level shake and so on. The ability of learning and memory was determined by Morris water maze test, and the histopathologic changes in CA3 field of the hippocampus were examined under a light micro-scope. Serum corticosterone level was determined by enzyme-linked immunosorbent assay. Western blot was per-formed to determine the expression of β-site amyloid precursor protein-cleaving enzyme 1 and Aβ1-42 in hippocam-pus of the brain. Results Compared with the control group, the results showed that chronic stress could increase the escape latency and swimming distance of old mice during training session in the Morris water maze test. The neuropathological changes were characterized by the decreased neuron number,soma shrinkage and condensation,or nuclear pyknosis in the CA3 field of hippocampus in the stress group. On the other hand, the expression of Aβ1-42 and BACE1 protein in hippocampus were increased, as well as the serum corticosterone concentration in the stress group. Conclusion Chronic stress can potentiate learning and memory impairment and pathological damage in CA3 field of the hippocampus in old mice, which may be related to chronic stress up-regulated the levels of BACE1 and Aβ1-42 mediated by corticosterone.

Objective:To investigate the effect on proliferation and apoptosis of T-cell leukemia cells by silencing NRP-1 ( Jurkat cells).Methods:The lentivirus plasmid which expresses NRP1 gene specific shRNA was constructed in our preliminary ex-perimental.We transfected the lentivirus plasmid to human T-cell Lymphoma cells.The proliferation of Jurkat cells different groups and effect on cell proliferation after chemotherapy drug EPI-treated were found by CCK-8 kit.The proliferation level and apoptosis rate of the cells were detected by flow cytometry and Annexin-V-FITC/PI method.Results:The proliferation level of NRP-1 /shRNA interference group was decreased significantly in 48 h,72 h,96 h,which was compared with the control groups.The apoptosis rate of the NRP-1/shRNA interference group was increased compared with control groups.The chemotherapy drug sensitivity of epirubicin ( EPI ) test results showed that EPI concentration was 0.025,0.05,0.1,0.2,0.4 μg/ml,the NRP-1/shRNA interference group of cell growth inhibition rate was increased,the corresponding control group difference had statistical significance(P<0.05).We choose the drug con-centration of the EPI IC50 for next experiments.NRP-1/shRNA interference group cell apoptosis rate increased significantly after induction,compared with the control groups difference was statistically significant ( P<0.05 ).Compared with control group, the expression level of Bcl-2 protein was decreased and the expression level of bax protein was increased significantly after EPI induction.The percentage of cells at G0/G1 phase increased significantly,while those at S phase decreased significantly.Conclusion:Plasmid shRNA-NRP1 inhibited the expression of NRP1 in Jurkat cells and decreased the proliferation level of Jurkat cells and promote their apoptosis and enhance their drug sensitivity;the molecular mechanism may relate to down-regulation of Bcl-2 and up-regulation of Bax.and arrested the cell cycle at G0/G1 phase.

Objective:To explore the protective effect and related mechanism of rebamipide on non-steroid anti-inflammatory drug (NSAID) related small intestinal mucosal injury.Methods:A total of 21 C57BL/6 mice were selected and by random number table method, they were divided into negative control group (0.9% NaCl gavage for four days), indomethacin modeling group (20 mg/kg indomethacin gavage for four days) and rebamipide intervention group (20 mg/kg indomethacin gavage for four hours and then 320 mg·kg -1·d -1 rebamipide gavage for four days), seven mice in each group. After modeling, the injury of mice intestinal mucosa of indomethacin modeling group and rebamipide intervention group was evaluated by gross observation as well as pathological analysis. The serum levels of interleukin (IL)-6, IL-10, trefoil factor 3 (TFF3), prostaglandin E2 (PGE2) and epidermal growth factor (EGF) in mice were detected by enzyme-linked immunosorbent assay (ELISA). The expression of IL-6, IL-10, TFF3, cyclooxygenase 2( COX2) and EGF at mRNA level of mice small intestinal tissues were examined by real-time quantitative polymerase chain reaction (qRT-PCR). And the relative expression of TFF3, COX2 and EGF at protein level of mice small intestinal tissues were determined by Western blotting. Levene test and independent sample t test were used for statistical analysis. Results:The scores of gross observation and histopathology of mice small intestinal mucosa injury of rebamipide intervention group were both lower than those of indomethacin modeling group (2.80±0.45 vs. 4.60±1.14, 1.67±0.52 vs. 3.00±0.71), and the differences were statistically significant ( t=2.667 and 3.618, P=0.029 and 0.006). The mouse serum level of IL-6 and the expression of IL-6 at mRNA level in intestinal tissues of indomethacin modeling group were both higher than those of the negative control group, however the serum level of IL-10 was lower than that of the negative control group ((48.83±5.40) ng/L vs. (40.96±5.92) ng/L, 5.23±2.36 vs. 1.12±0.56, (168.50±10.57) ng/L vs. (186.30±7.77) ng/L), and the differences were statistically significant ( t=2.307, 3.372 and 3.366; P=0.047, 0.007 and 0.012). The expression of IL-6 at mRNA level in mice small intestinal tissues of rebamipide intervention group was lower than that of indomethacin modeling group (1.74±0.82 vs. 5.23±2.36), however, the expression of IL-10 at mRNA level was higher than that of indomethacin modeling group (6.44±3.46 vs. 1.22±0.83), and the differences were statistically significant ( t=3.409 and 3.025, P=0.008 and 0.014). The serum levels of TFF3, PGE2 and EGF, the expression of TFF3 at mRNA level of small intestinal tissues, the relative expression of COX2 and EGF at protein level of small intestinal tissues of indomethacin modeling group were all lower than those of the negative control group ((131.20±16.37) ng/L vs. (150.30±9.66) ng/L, (32.68±6.88) ng/L vs. (41.51±3.20) ng/L, (112.70±17.17) ng/L vs. (138.20±10.10) ng/L, 0.43±0.22 vs. 1.20±0.50, 0.33±0.25 vs. 1.30±0.43, 0.28±0.19 vs. 1.15±0.10), and the differences were statistically significant ( t=2.290, 2.645, 2.867, 3.097, 3.405 and 7.106; P=0.048, 0.021, 0.025, 0.017, 0.027 and 0.002). The mice serum levels of PGE2 and EGF, expression of TFF3, COX2 and EGF at mRNA level of small intestinal tissues, as well as the expression of TFF3 and EGF at protein level of small intestinal tissues of rebamipide intervention group were all higher than those of indomethacin modeling group ((43.55±5.28) ng/L vs. (32.68±6.88) ng/L, (153.30±15.66) ng/L vs. (112.70±17.17) ng/L, 2.48±1.70 vs. 0.43±0.22, 2.95±1.56 vs. 0.88±0.45, 3.97±2.54 vs. 0.98±0.76, 1.47±0.26 vs. 0.72±0.35, 1.08±0.36 vs. 0.28±0.19), and the differences were statistically significant ( t= 2.711, 3.658, 2.656, 2.856, 2.524, 3.013 and 3.435; P=0.024, 0.008, 0.026, 0.019, 0.033, 0.039 and 0.026). Conclusions:Rebamipide alleviates small intestinal mucosal injury induced by indomethacin by inhibiting the expression of inflammatory factors and promoting the expression of intestinal mucosal protective factors suggesting that rebamipide plays a protective role in NSAID related small intestinal injury by maintaining the chemical barrier of the intestinal mucosal.

OBJECTlVE To investigate the action mechanism of antidepressant fluoxetine on hERG ( ether-a-go-go-related gene ) potassium channel, and the effect of protein kinase C ( PKC ) agonist phorbol-12-myristate-13-acetate ( PMA) on fluoxetine inhibition. METHODS The whole cell patch clamp technique was used to record the change in hERG potassium current ( IKr ) on HEK293 cells that stably expressed hERG potassium channel ( hERG-HEK293 steady-state cells) , which was treated with fluoxe-tine 0.01, 0.1, 1 and 10μmol·L-1 , to study the concentration-and voltage-dependence of the effects on IKr, and to observe the changes in activation, inactivation and recovery dynamics of hERG potassium channel treated with fluoxetine 1μmol·L-1 . On this basis, the effect of PMA of 1μmol·L-1 on inhibition of fluoxetine 1 μmol·L-1 was explored. RESULTS Fluoxetine 0.01, 0.1, 1 and 10 μmol·L-1 inhibited IKr on hERG-HEK293 steady-state cells in a concentration- and voltage-dependent manner. The half maximal inhibitory concentration ( lC50 ) was about 0. 8 mmol·L-1 , and the Hill coefficient was about 1. 1. Fluoxetine 1 μmol·L-1 could reduce the activation, deactivation and recovery currents of IKr and affect the activation and recovery of hERG potassium channel. After fluoxetine inhibition of IKr became stable, PMA 1 μmol·L-1 could inhibit the blocking effect of fluoxetine on hERG potassium channels. CONCLUSlON Fluoxetine has obvious inhibitory effect on IKr of hERG-HEK293 steady-state cells, but the effect could be inhibited by PKC agonist PMA.

Adult ; Cholesterol, LDL ; blood ; Female ; Humans ; Insulin-Like Growth Factor Binding Protein 1 ; blood ; Male ; Reference Values

Objective To explore the effects of baicalin in the treatment of a preeclampsia (PE) rat model by detecting the expression of X-linked inhibitor of apoptosis protein (XIAP) and cysteine containing aspartate-9 (Caspase-9) and observing the ultrastructure of mitochondria in trophoblast cells.Methods Forty-eight pregnant Wistar rats were randomly divided into two groups:12 in the control group and 36 in the PE model group.The PE model was established with subcutaneous injection of l-nitro arginine methyl ester with 100 mg/kg per day from the 13th day of pregnancy.Beginning from the 16th day of pregnancy,the PE rats were injected with different doses of baicalin till cesarean section,and divided into three groups:non-intervention PE model group treated with saline (NIP group),low-dose baicalin intervention group (IDB group) at 50 mg/kg per day,and high-dose baicalin intervention group (HDB group) at 100 mg/kg per day.The rat tail artery blood pressure and 24-h urine protein level were measured at pregnant day 10,16 and 20.The levels of XIAP and Caspase-9 in placenta were measured by immunohistochemistry.The ultrastructure of mitochondria of trophoblast cells of the rat placenta was observed under electron microscope.T test,F test and LSD-t test were applied for statistical analysis.Results (1) On pregnant day 10,no significant differences were observed in rat tail artery systolic blood pressure,diastolic blood pressure and 24-h urine protein level between the control group and PE model group (all P＞0.05).On pregnant day 16 and 20,the systolic blood pressure,diastolic blood pressure and 24-h urine protein level of NIP,IDB and HDB groups were significantly higher than those of control group [pregnant day 16:systolic blood pressure:(137.74±5.21),(136.15±4.86),(138.28±4.79) and (110.57±3.79) mmHg (1 mmHg=0.133 kPa),diastolic blood pressure:(89.58 ± 5.50),(88.45 ± 8.59),(89.42 ± 6.29) and (80.28 ± 7.36) mmHg,24-h urine protein:(7.78 ± 0.45),(7.53 ± 0.54),(7.86± 0.57) and (6.45 ± 0.56) mg;pregnant day 20:systolic blood pressure:(145.26 ± 4.67),(131.28 ± 4.34),(130.93 ± 5.33) and (110.40 ± 6.92) mmHg,diastolic blood pressure:(89.87±6.55),(85.34±7.33),(84.64±7.36) and (80.19±7.34) mmHg,24-h urine protein:(11.18±0.42),(9.65±0.54),(9.06±0.56) and (6.31 ±0.45) mg] (all P＜0.01).On pregnant day 20,the systolic and diastolic blood pressure and 24-h urine protein level in IDB and HDB groups were significantly lower than in NIP group (all P＜0.05),but showed no significant differences between IDB and HDB groups (allP＞0.05).(2) Compared with NIP group,the expression of XIAP in control group,IDB and HDB groups were significantly increased(210.39±0.78,180.56±0.82,195.36±0.96 and 192.84± 1.06,all P＜0.01).There was no significant difference in the expression of XIAP between IDB and HDB groups (P=0.66).The expression of Caspase-9 in control group,IDB and HDB groups were significantly decreased compared with NIP group (210.36±0.55,195.53±0.96,198.42± 1.01 and 185.25±0.64,all P＜0.01).There was no significant difference in the expression of Caspase-9 between IDB and HDB groups (P=0.65).Ultrastructure of mitochondria in NIP group showed different degrees of damage,matrix swelling,and mitochondrial cristae bresk or disappearance.In IDB group,mitochondrial matrix swelling was not obvious,and mitochondrial cristae were visible.In HDB group,mitochondrial cristae were neat and clear.Conclusions Baicalin may play an important role in the treatment of preeclampsia by reversing the trophoblast apoptosis and improving the ultrastructure of mitochondria through its regulation of XIAP expression and downregulation of Caspase-9 expression.