Adolescent ; Cranial Nerve Neoplasms ; Facial Nerve ; Humans ; Male ; Neurilemmoma ; Parotid Region ; pathology

Bronchogenic Cyst ; Child ; Humans ; Male ; Neck ; pathology ; Young Adult

Objective To investigate the spatial distribution and clustering areas of Budd-Chiari syndrome in Heze City,Shandong Province,and to provide epidemiological information for further exploring the etiology and related risk factors of the disease.Methods Detailed residential addresses of 342 cases of patients (residents of Heze City) with diaphragm type Budd-Chiari syndrome diagnosed between 1995 and 2004 in Heze Municipal Hospital,Heze Shan County Central Hospital,Affiliated Hospital of Xuzhou Medical College,Shandong Provincial Hospital and Beijing Xuanwu Hospital were collected.Geographic information system (GIS) was used as a platform for data management and display.The nearest neighbor index,Ripley's K(d) function,Ripley's L(d) function and the nearest neighbor clustering method were applied to detect the spatial characters of Budd-Chiari syndrome in Heze City,Shandong Province.Crimestat 3.0 was used for spatial analysis.Results The nearest neighbor distance analysis showed that the nearest neighbor index was 0.6767 (Z =-11.4387,P ＜ 0.01).That was an aggregation at the first-order spatial scale.Within the study area,the first clustering radius of Budd-Chiari syndrome was 6.66 km,and the first clustering strength was 5.40; the average radius of the strongest clustering area was 126.61 km,and the clustering strength was 12.52,while the biggest clustering radius was larger than 222 km.After corrected by population,the gathering strength was slightly higher than that before the correction.Ten first-order hot spots were formed,and 95％ confidence interval aggregation number was 7,which meant the results were statistically significant(P ＜ 0.05),main clustering areas are in Mudan District,Shan County and Juancheng.One secondorder hot spot was gathered based on the first-order hot spot.Conclusions Spatial distribution of Budd-Chiari syndrome in Heze City,Shandong Province has showed spatial aggregation and heterogeneity.This study has a great epidemiological significance for further exploring the cause of Budd-Chiari syndrome.

Objective To compare 99Tcm-MIBI MPI with delayed enhancement MRI (DE-MRI) in patients with idiopathic dilated cardiomyopathy (IDCM). Methods Forty patients with IDCM were included. They underwent both rest 99Tcm-MIBI myocardial perfusion imaging and DE-MRI within 7 days. 99Tcm-MIBI MPI was performed to identify diffuse or segmental abnormal perfusion patterns including reduced or defect perfusion segments. DE-MRI images were divided into 4 categories: no delayed enhancement, septal, subendocardial and transmural delayed enhancement, x2 test was used for data analysis. Results Diffuse and segmental perfusion abnormality on 99Tcm-MIBI MPI were found in 19 (47.5%) and 21 (52.5%)patients respectively, while DE-MRI enhancement was simultaneously found in 5 patients of the former (5/19, 26.3%) and 18 (18/21, 85.7%) of the latter (x2 =14.401, P＜0. 001). For those (n=18) with both segmental perfusion abnormality and DE-MRI enhancement, the number of segments of the 4 DE-MRI respectively. A significant difference was found in the DE-MRI enhancement categories between normal and defect perfusion segments (x2 = 29. 183, P ＜0.001 ) and between reduced and defect perfusion segments as well (x2 =25. 110, P＜0. 001). Conclusions Both diffuse and segmental perfusion abnormalities on 99Tcm-MIBI MPI can be found in patients with IDCM. DE-MRI enhancement is more frequently found in patients with segmental perfusion abnormality.

Objective To study morphological changes of rabbit artery endothelial cell injury and atherosclerosis caused by high fluoride and the role of selenium. Methods Twenty healthy male New Zealand white rabbits, body weight (2.0 ± 0.5)kg, were randomly divided into control group(drinking deionized water, fed basic diet), fluoride group(drinking fluoride 100 mg/L deionized water, fed basic diet), selenium group(drinking selenium 1 mg/L deionized water, fed basic diet), fluoride plus selenium group(drinking fluoride 100 mg/L deionized water, selenium 1 mg/L of deionized water, fed basic diet). The experimental period was 6 months. At 0, 3, 6 months of the experiment, serum fluorine and selenium levels were determined. At the end of the experiment,thoracic aorta was collected to observe its pathology and ultrastructural changes. Results Serum fluoride was significantly higher at the 3rd and the 6th month of experiment(all P ＜ 0.01 ) in fluoride group[ (0.589 ± 0.146),(0.772 ± 0.175)mg/L] and fluoride plus selenium group[ (0.502 ± 0.094), (0.693 ± 0.158)mg/L] than in control group[ (0.174 ± 0.002), (0.208 ± 0.031 )mg/L] and serum fluoride was significantly higher at 6 months than at 3 months(P ＜ 0.05 ) in fluoride group. Serum selenium was significantly higher at the 3rd and the 6th month of experiment (all P ＜ 0.01 ) in selenium group[ (0.252 ± 0.022), (0.319 ± 0.052)mg/L] and fluoride plus selenium group[ (0.239 ±0.016), (0.294 ± 0.018)mg/L] than in control group[(0.135 ± 0.014), (0.167 ± 0.019)mg/L], and serum selenium was significantly higher at the 6th month than at 3rd month of experiment in selenium group(P ＜ 0.05). Endothelial cell apoptosis indices were (4.92 ± 1.32)%, (30.30 ± 6.80)%, (6.57 ± 2.14)% and (14.29 ± 2.99)%, respectively in control group, fluoride group, selenium group and fluoride plus selenium group. Their main effect of fluorine and selenium was statistically significant (F = 106.833,20.082, all P ＜ 0.01 ). There were antagonistic effect between fluoride and selenium(F = 30.402, P ＜ 0.01 ). Pathological changes of rabbit aortic endothelial cells in fluoride group included endothelial with attached fibrin and red blood cells, and structural of the cells changed, with serious vascular injury; in fluoride plus selenium group apoptosis of endothelial cells decreased, with reduced number of attached red blood cells and fibrin, endothelial cell structure normal, the extent and scope of vascular damage significantly reduced. Conclusions Appropriate amount of selenium inhibits the apoptosis of endothelial cells induced by high fluoride, reduces aortic structural damage caused by high fluoride, and maintains the integrity of endothelial cells, thereby antagonizes the vascular damage and atherosclerosis induced by high fluoride.

Multi-target drugs attract increasing attentions for the therapy of complicated neurodegenerative diseases. In this study, a computer-assisted strategy was applied to search for multi-target compounds by the pharmacophore matching. This strategy has been successfully used to design dual-target inhibitor models against both the acetylcholinesterase (AChE) and poly (ADP-ribose) polymerase-1 (PARP-1). Based on two pharmacophore models matching and physicochemical properties filtering, one hit was identified which could inhibit AChE with IC50 value of (0.337 +/- 0.052) micromol x L(-1) and PARP-1 by 24.6% at 1 micromol x L(-1).
Acetylcholinesterase ; metabolism ; Cholinesterase Inhibitors ; pharmacology ; Computer-Aided Design ; Drug Discovery ; methods ; Poly(ADP-ribose) Polymerase Inhibitors

The antitussive activity assay for the root extraction of Disporum cantoniense was carried out with coughing mice induced by ammonia liquor. The results showed that the ethanol and water extractions of D. cantoniense possess strong antitussive activity, and the high dose of the former was better than positive control, and then the constituents of the ethanol extraction were separated and purified by various modern chromatographic techniques. Their structures were identified by physico-chemical properties and spectroscopic data. As a result, eight compounds were isolated and identified as stigmast-4-en-3-one(1), (22E, 24R)-ergosta-5, 7, 22-trien-3beta-ol(2), obtucarbamate A(3), obtucarbamate B(4), neotigogenin(5), azo-2, 2'-bis[Z-(2,3-dihydroxy-4-methyl-5-methoxy) phenyl ethylene] (6),dimethyl {[carbonylbis (azanediyl)] bis( 2-methyl-5, 1-phenylene) j dicarbamate (7) , and quercetin-3-O-pB-D-glucopyranoside(8). All compounds were isolated from this plant for the first time, and the result of bioactivity-directed isolation showed that compounds 3, 4, and 6 had obvious effect on antitussive activity, and compound 6 had the same level as positive control.
Animals ; Antitussive Agents ; chemistry ; isolation & purification ; pharmacology ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; pharmacology ; Ethanol ; chemistry ; Female ; Liliaceae ; chemistry ; Male ; Mice

Objective To study the effect of local mild hypothermia on the expression of matrix metallopro- teinases-2/9 (MMP-2/9) and brain edema in experimental intracerebral hemorrhage (ICH) in rat. Methods One hundred and forty-five Wistar rats were randomly divided into a normothermia sham-operation (NSO) group ( n = 15 ), a normothermia intracerebral hemorrhage (NICH) group (n = 75 ) and a mild hypotbermia intracerebral hemor- rhage (MHICH) group (n = 75). Autologous arterial blood was stereotaxically injected into the right caudate nucleus of the rats of the NICH and MHICH groups to make intracerebral hemorrhage model. The rats in the MHICH group were then subjected to 4 hours of local mild hypothermia, while those in the NICH group were under the room temper- ature. The brain water content, permeability of brain-blood barrier (BBB) and expressions of MMP-2/9 were meas- ured by immunohistochemistry method at 6 h, 24 h, 72 h, 5 d and 7 d after operation. Results In NICH group, the brain water content, permeability of BBB and expression of MMP-9 all began to increase at 6 h and peaked at 3 d after injection of blood and still higher than the NSO group at 7 d. The expression of MMP-2 only began to increase little at 24 h and peaked at 5 d after operation and remained highly expressed at 7 d. In the MHICH group, the chan- ges of brain water content, permeability of BBB and expression of MMP-9 were similar to those of the NICH group, but the extent of changes was significantly lower at the every time point. In NICH group and MHICH group, MMP-9 expression was positively correlated with both the brain water content and the permeability of BBB, but MMP-2 ex- pression was not correlated with them. Conclusion Mild hypothermia might protect BBB against injury caused by ICH and relieve brain edema and inflammation reaction through inhibiting the expression of MMP-2/9.

Abstract: Objective　To screening new compounds that can inhibit the growth and biofilm formation of Staphylococcus aureus. Methods　Compounds that can inhibit the growth of Staphylococcus aureus were screened from the FDA approved drug library by 96 well plates. The absorbance value of 600 nm wavelength (OD600) was measured by Microplate Reader to detect the growth of Staphylococcus aureus planktonic cells in the culture supernatant. The minimum inhibitory concentration (MIC) of ozanimod against Staphylococcus aureus clinical isolates were detected by micro broth dilution method. The inhibitory effect of sub-inhibitory concentrations of ozanimod on the biofilm formation of Staphylococcus aureus was detected by crystal violet staining. Results　This study found that ozanimod could significantly inhibit the growth of Staphylococcus aureus SA113 (screening reference strain), and the MIC was 25.00 μmol/L. The MIC of ozanimod against 119 clinical isolates of Staphylococcus aureus [65 isolates of methicillin sensitive (MSSA) and 54 isolates of methicillin resistant (MRSA)] was 12.50 or 25.00 μmol/L. The MIC50 and MIC90 of ozanimod against the 119 Staphylococcus aureus isolates all were 25.00 μmol/L. This study found that 6.25, 12.50, 25.00 μmol/L of ozanimod could significantly inhibit the biofilm formation of 2 MSSA and 2 MRSA. The sub-MIC concentration of ozanimod (12.50 μmol/L) could significantly inhibit the biofilm formation of 14 MSSA and 11 MRSA, but had no inhibitory effect on the growth of planktonic cells of these Staphylococcus aureus isolates. Conclusion　Ozanimod can inhibit the growth of Staphylococcus aureus, including MRSA, and has good antibacterial activity. The sub-MIC concentration of ozanimod could significantly inhibit the biofilm formation of Staphylococcus aureus.

Objective To knowthe effect of selenium on expression ofnitric oxide synthase(eNOS) and inducible nitric oxide synthase(iNOS) induced by fluoride in ECV-304(human umbilical vein endothelial cells).Methods The cells,ECV-304,were divided into two groups and treated as follows,one group was treated with sodium fluoride at different doses(0,400,1 000 and 2 000 ?mol/L),the other was treated with sodium fluoride at different doses(0,400,1 000 and 2 000 ?mol/L)and added sodiumselenite(100 nmol/L) respectively.24 h of treatment,The activity ofeNOS and iNOS were measured by NO and NOS assay kits and the expression of eNOS mRNA and iNOS mRNA was analyzed by RT-PCR.Results The activity of eNOS and the expression of eNOS mRNA were down-regulated by fluoride with a dose dependent manner,while the activity of iNOS and the expression of iNOS mRNA were up-regulated.Selenium showed a significant antagonism to low level fluoride treated groups.Conclusion Seleniumcan antagonize the effect offluoride on the expression ofiNOSand eNOS in the vein endothelial cells when the fluoride exposure level is not toohigh.