Aim To investigate the effects of 4-aminopyridine (4-AP),K+ channel blocker, on the gastrointestinal function of murine. Methods Charcoal suspension was used to detect the effects of 4-AP on gastrointestinal motility of mice in vivo, contraction of isolated fundus longitudinal strips and duodenum of rats were studied in vitro,gastric acid secretion was measured by Gastric Secretion Test. Results 4-AP(5 mg?kg -1,ig)inhibited the gastrointestinal motility of mice. 4-AP(5 mmol?L -1) increased the maximum contractive force and minimum relaxation force, decreased the amplitude and frequency of the isolated duodenum peristaltic contraction. 4-AP(2.5 mg?kg -1,ip) significantly enhanced gastric acid secretion of rats. Conclusion 4-AP inhibited gastrointestinal motility and enhanced gastric acid secretion in murine.

OBJECTIVE:To investigate the infusion solutions which are compatible with Compound kushen injection. METHODS:The insoluble particles of kushen injection in four kinds of infusion solutions were detected respectively by light blockage method.RESULTS:Insoluble particles of different size and number were noted for Compound kushen injection when mixed respectively with four kinds of infusion solutions,but the insoluble particles in all kinds of infusion solutions except 10% glucose injection were all within the range specified in China Pharmacopeia(2005 edition).CONCLUSION: 0.9% sodium ch-loride injection is the optimal compatible infusion solution for Compound kushen injection.

Objective To explore the clinical effect of Tuina therapy for knee osteoarthritis (KOA) patients and their musculus quadriceps fexoris strength. Methods The 114 patients with KOA who met the inclusion criteria were randomly divided into the observation group and the control group (57 in each group). The patients in observation group were treated with Tuina therapy, and the control group were treated with Meloxicam. All the patients were treated for 30 days. The Isokinetic muscle strength test was used to evaluate the strength of the four biceps femoris muscle, and HSS score and pain score were observed before and after treatment. Results The total effective rate of the observation group was 91.2% (52/57), and the control group was 71.9% (41/57). The difference between 2 groups was statistically significant (χ2=3.971, P=0.018). After treatment, the HSS scores (79.0 ± 2.0 vs. 66.3 ± 1.4; t=3.121, P<0.01) in observation group were significantly higher than that in control group, and the pain scores (1.7 ± 1.1 vs. 3.2 ± 1.1; t=2.953, P<0.01) in observation group were significantly lower than that in control group. The PT (59.91 ± 25.90 Kgm vs. 55.17 ± 25.88 Kgm, t=2.652), AP (30.04 ± 12.59 W vs. 28.02 ± 17.03 W, t=3.618), TW (496.47 ± 257.26 Nm vs. 466.19 ± 225.70 Nm, t=3.227) of 60/s isokinetic muscle strength test and PT (37.22 ± 18.73 Kgm vs. 32.54 ± 15.22 Kgm, t=2.511), AP (39.43 ± 18.02 W vs. 36.14 ± 23.88 W, t=2.183), TW (326.03 ± 159.38 Nm vs. 267.66 ± 156.93 Nm, t=2.073) of 180/s isokinetic muscle strength test in observation group were significantly higher than those in control group (P<0.05). Conclusions Tuina therapy could improve KOA patients' musculus quadriceps fexoris strength, which curative effect were better than oral treatment of Meloxicam.

Objective To investingate the expression method of bcl-2 and it's significance in osteogenic tumor and tumor-like diseases.Method The protein of PCNA, p53, Fas and bcl-2 were examined immunohistologically in osteosarcoma, ossifying fibroma, fibeous dysplasia of bone and normal bone callus. The results were analysed combing with the information of metastasis and hisomorphology.Results PCNA and p53 were highly expressed in low-differentiated osteosarcoma, bcl-2 were highly expressed at high-differentiated osteocoma and ossifying fibroma. When PCNA, p53 and bcl-2 were all expressed at high level, the metastasis rate was high, when only bcl-2 was expressed at high level, the progmosis was better. Conclusion The mechanism for benign and malignant tumor are different, the benign and low-degree malignant tumor may be caused by over accumulated mutation cells sipported by high level of bcl-2, while malignant tumor may be the result of multi-gene cooperation abnormally.

Aneurysmal bone cyst of mastoid bone is seldom, here one case was reported. The mastoid bone of the patient presented with a baloon-like swelling full of non-coagulated blood and serous-hemorrhagic fluid. CT scan demonstrated a large expansile destructive mass located in left mastoid bone region with the thin or absent cortical bone. The MRI demonstrated T2-weighted images and clear boudary from surrounding tissue. Pathologic reported that the mastoid bone was repalcement with lacunar divided by fibro-tissue, containing numerous hemosiderin, giant cells and inflammatory cells. A surgery was performed and the patient was cured.
Bone Cysts, Aneurysmal ; diagnosis ; pathology ; surgery ; Humans ; Magnetic Resonance Imaging ; Mastoid ; pathology ; Tomography, X-Ray Computed

Objective To determine the toxicity, maximal dose and clinical practicality of VM26 (teniposide) plus radiotherapy for postoperative brain neurospongioma. Methods Twenty patients were alloted in phase Ⅰ trial. The total dose was 60 Gy for the field radiotherapy (30 fractions of 2 Gy over six weeks). Teniposide at three dose levels (50 mg/m2, 75 mg/m2 and 100 mg/m2) was given intravenously once a week, totally five weeks. Dose escalation was based on each level, with a minimum of five patients in cohort if severe toxicity was not observed until the maximum tolerance dose(MTD). Results The predominant form of toxicity was hematologic toxicity. Four patients developed grade 3, 4 leucopenia when a second level of MTD (75 mg/m2) was given. Conclusion Combined radiotherapy and teniposide for postoperative brain neurospongioma is well tolerated. The dose of 50 mg/m2 for phase Ⅱ clinical trial was recommended.

Objective To investigate the influence on the behavior of withdrawal and relapse after deep brain stimulation of bilateral nucleus accumbens in morphine-dependent rats. Methods The rats with a strong unconditioned preference were discarded in preconditioning test, the selected rats were distributed into five groups randomly. After operation,morphine hydrochloride was injected subcutaneously into SD rats for 12 days (once every day,initial 5 mg/kg,increasing by 5 mg/kg per time,stable in 20 mg/kg ). A modified electrical circuit was used to procedure the DBS,the parameter was 130 Hz,150 A,60 s,l h/d,14 d. CPP test was used to exam the effect of DBS. A minor morphine dose (3 mg/kg) was injected to induce the behavior of relapse, and CPP was tested again after 24 h. Two-way ANOVA was performed on the data with Bonferroni posttest. Result ①After CPP training,CPP score of group morphine, morphine + sham and morphine + DBS was ( 155. 87 ± 20. 45 ) s, (107.33 ± 18.10)s,(135.45 ±22.09)s,and had significant difference with group of control( ( -70.34 ± 15.40) s)(t = 9.45,P＜0.01; t = 6.94,P＜0.01;t = 8.04,P＜0.01).②After 7 days' DBS,the CPP score in group of morphine + DBS reduced significantly compared to group of morphine( t = 4.21, P＜0.01) and morphine + sham( t=1.10, P＜0.05).0n the 14th day,there was more pronounced reduction ( t = 5. 15, P＜0.01; t = 3.92, P＜ 0.01). ③ 24 hours after the minor morphine dose was injected,the CPP score in morphine + DBS didn't increase significantly, and had significant difference with group of morphine ( t = 4.04, P＜0.01) and morphine + sham ( t= 4. 13, P＜0.01). Conclusion DBS bilateral nucleus accumbens in morphine-dependent rats can interfere the behavior of morphine-induced CPP and relapse.

Aim To establish cerebrocardiac syndrome model in rats. Methods Right middle cerebral artery of rat was occluded (MCAO) with nylon thread and Ⅱ lead ECG was monitored continuously within 2 h to record the emerging of arrhythmias. 30 min, 2 h, 24 h after middle cerebral artery occlusion or 6 h reperfusion after 2 h occlusion, left ventricular myocardiums were observed with transmission electron microscope to find the morphological damage and brains were marked with TTC to locate infarction area. Results (14.9?11.4) minutes after MCAO, 71%(60/85)model rats had abnormal ECG changes including 38 %(32/85)premature ventricular contraction, 27 %(23/85)atrial premature beats, 5%(4/85)ventricular tachycardia, 1.2%(1/85)sinus tachycardia. Arrhythmias sustained (29.0?23.2 )minutes. Ventricular myocardial cell injury was obvious: chaotic and broken mitochondria ridges, aggregated chromatin under the nucleus membrane, deposited glycogen granules in the cytoplasma. 30 min, 2h, 24h after MCAO the infarction rates were 8.7%?1.1%,11.4%?2.3% and 13.7%?3.1% respectively. Conclusion A stable cerebrocardiac syndrome model in rat might be induced by means of occluding right middle cerebral artery and the morphological bases of cerebrogenic cardiac arrhythmias are myocardial cell injury caused by cerebral infarction.

Objective To investigate the effects of triptolide on proliferation,apoptosis and the changes of Ski,Smad3,Smad7 and collagen type I(ColI) in cultured rat mesangial cells induced by transforming growth factor (TGF)-β1.Methods Cultured HBZY-1 rat mesangial cells were divided into 5 groups:(1)normal control group; (2)TGF-β1 group (10 μg/L); (3)-(5)triptolide (0.4,2,10 μg/L)+TGF-β1 (10 μg/L) groups.The cell proliferation was detected by MTT.Apoptosis of mesangial cells was detected by TUNEL assay.The expressions of Ski,Smad3,Smad7 mRNA were examined by real-time quantitative PCR.The expressions of Ski,Smad3,Smad7 and ColI protein were detected by Western blotting.The localizations of Ski and Smad3 protein were detected by laser confocal fluorescence microscope.Results Compared with the normal control,TGF-β1 (10 μg/L) significantly stimulated mesangial cells proliferation,while decreased apoptosis.The mRNA and protein expressions of Ski,Smad7,Smad3 and ColI protein expression in TGF-β1 group were increased (P ＞0.05).In comparison with TGF-β1 group,triptolide could significantly inhibit TGF-β1-induced mesangial cells proliferation in dose-dependent manner,and promote the apoptosis of mesangial cells.In TGF-β1 group,mRNA and protein expresscons of Ski and Smad7 were increased (P＜0.05),Smad3 mRNA and protein were decreased (P ＞0.05),and ColI protein was decreased (P＜0.01).In comparison with TGF-β1 group,fluorescence intensity of Ski,Smad3 proteins was significantly increased in cytoplasm,while decreased in nucleus.Conclusions Triptolide can inhibit TGF-β1-induced mesangial cells proliferation through regulating the expressions of Ski,Smad7 mRNA and protein,inhibiting Ski.Smad7 translocation to the nucleus,and down-regulating Smad3 mRNA and protein expression.Triptolide can promote apoptosis of mesangial cells.

Delicacy management is an important issue to the hospital logistics mode innovation,which is the only way to realize a scientific hospital logistics management.This article proposes the practical ways to push on the hospital logistics delicacy management from many respects,such as working regulation,consumption measurement,contract supervision,cost accounting,structure control and convergence supporting.