聚醚型聚氨酯材料表面纤维蛋白原的吸附性研究

本文采用放射性同位素标记的方法研究了嵌段聚醚型聚氨酯在纯纤维蛋白原溶液中和稀释血浆中的表面纤维蛋白原吸附性规律，考察了聚醚型聚氨酯的特性粘数及溶液体系中的ＮａＣｌ浓度对材料表面纤维蛋白原吸附性的影响，结果表明，随着聚合物特性粘数的增大，材料表面的纤维蛋白原吸附量呈降低的趋势；溶液体系中盐浓度的降低导致纤维蛋白原凝固性增强，在纯纤维蛋白原溶液中，材料表面纤维蛋白原的吸附量相应增多，而在稀释血浆中，纤维蛋白原的吸附量相应减少，在达到最低值后又有上升的趋向，表明纤维蛋白原在材料表面的吸附还受血浆中其它大分子的影响。     

Effect of biologically active coating on biocompatibility of Nitinol devices designed for the closure of intra-atrial communications

Anti-thrombogenicity and rapid endothelialisation are prerequisites for the use of closure devices of intra-atrial communications in order to reduce the risk of cerebral embolism. The purpose of this study was therefore to assess the effect of bioactive coatings on biocompatibility of Nitinol coils designed for the closure of intra-atrial communications. Nitinol coils (n = 10, each) and flat Nitinol bands (n = 3, each) were treated by basic coating with poly(amino-p-xylylene-co-p-xylylene) and then coated with either heparin, r-hirudin or fibronectin. Anti-thrombogenicity was studied in vitro in a dynamic model with whole blood by partial thromboplastin time (PTT), platelet binding and thrombin generation, respectively, and cytotoxicity by hemolysis. Endothelialisation was studied on Nitinol bands with human umbilical venous endothelial cells (HUVEC) by 3-(4,5-dimethylthiazole-2yl)-2,5-triphenyl tetrazolium (MTT) assay and immnuofluorescence analysis of Ki67, vinculin, fibronectin and von Willebrand Factor. Uncoated or coated devices did not influence hemolysis and PTT. r-Hirudin (but not heparin) and fibronectin coating showed lower platelet binding than uncoated Nitinol (p < 0.005, respectively). Heparin and r-hirudin coating reduced thrombin formation (p < 0.05 versus Nitinol, respectively). HUVEC adhesion, proliferation, and matrix formation decreased in the order: fibronectin coating > uncoated Nitinol > r-hirudin coating > heparin coating > basic coating. MTT assay corroborated these findings. In conclusion, r-hirudin and fibronectin coating, by causing no acute cytotoxicity, decreasing thrombogenicity and increasing endothelialisation improve in vitro biocompatibility of Nitinol devices designed for the closure of intra-atrial communications.     

Stereoselective determination of cetirizine and studies on pharmacokinetics in rat plasma

Enantiomers may confer benefits over racemates in therapeutic uses and we developed a chiral separation method of cetirizine enantiomers, a second generation H1 histamine receptor antagonist, in rat plasma. alpha1-Acidglycoprotein based chiral stationary phase(AGP-CSP), monitored with UV at 230 nm was used to separate the enantiomers. Observed enantioselectivity (alpha) was 2.0. The AGP-CSP was also used at a preparative scale to isolate the enantiomers with an optical purity of greater than ee 99%. In addition, an analysis was carried out for the cetirizine enantiomers in rat plasma to study the differences of enantiomers in pharmacokinetics. Both (+)- and (-)-cetirizine were separated using a reversed-phase column of AGP, and were detected at the range of 2.5-200 microg ml(-1) in plasma. Although there was no recognizable differences in pharmacokinetics between the enantiomers in rat, the method appears to be useful for their pharmacokinetic studies.     

多发性骨髓瘤患者血清IL-6活性与急性相蛋白浓度的相关性研究

运用敏感的B_9细胞增殖试验检测了81例多发性骨髓瘤(MM)患者血清IL-6活性,同时分析了标本的几种急性相蛋白含量,结果表明,68％MM患者血清中IL-6活性大于5μ/ml(正常对照为5μ/ml以下),几种急性相蛋白中C-反应性蛋白(CRP)在MM时升高(P<0.01),平均达正常对照组的17倍以上,MM患者补体C_4与正常对照组无差异(p>0.05),C_3、白蛋白及转铁蛋白在MM时分别比正常下降24.42％、38.83％和32.80％,且与疾病分期有关,在血清IL-6大于5μ/ml的55例中,IL-6活性与CRP、C_3、白蛋白的相关系数分别为0.46,-0.34和-0.29,IL-6与转铁蛋白浓度相关不明显。本文结果提示:CRP、C_3及白蛋白等含量的变化可作为反映MM病情的简易而敏感的指标。     

氧分压在体监测仪的研制

作者报道一种稳定性较高的氧分压在体监测，为医学研究、临床诊断提供一种新的可靠的测试方法及设备，具有较大的应用价值。     

大白鼠前脑、脑干和小脑向孤束核的纤维投射——HRP法和ARG法研究

本实验用HRP法、WGA—HRP法和ARG法进一步研究了大白鼠前脑、脑干和小脑向孤束核的纤维投射及其局部定位关系。作者发现皮质32及8区、三叉神经脊束核尾侧亚核投射到孤束核头段;皮质24及8a区、三叉神经脊束核尾侧亚核投射到孤束核中段;皮质23及13区,中脑导水管周围灰质和三叉神经脊束核尾侧亚核投射到孤束核尾段。此外,结果还证明室旁核、下丘脑外侧区、兰斑核、K—F氏核、小脑顶核、中缝大核、网状大细胞核、外侧网状核、及延髓网状结构向孤束核的纤维投射,均存在着一定的局部定位关系。本文结合前脑、脑干向孤束核的纤维投射讨论了内脏活动调节及针刺镇痛效应的中枢机理并对大白鼠孤束核的分段(头、中及尾段)标准提出了新建议。     

Integrins and adhesion molecules: Tumour necrosis factor-{alpha}-mediated dyscohesion of epithelial cells is associated with disordered expression of cadherin/{beta}-catenin and disassembly of actin filaments

Tumour necrosis factor (TNF)- induced, in a time- and dose-dependentfashion, dyscohesion (cell-cell dissociation) of the endometrialepithelial cells. TNF- impaired the ability of cells to aggregateand to attain compaction. The cell-cell adherent junction isa specialized region of the plasma membrane where cadherin moleculesact as adhesion molecules and actin filaments are densely associatedwith the plasma membrane through a well-developed plasmalemmalundercoat. Dyscohesion induced by TNF- was associated with thedisordered expression of cadherin\-catenin at the sites of cell-cellcontact. In addition, within the time-frame that dyscohesionwas induced, TNF- down-regulated the expression of actin mRNAonly at 100 ng/ml without modulating the overall amount of actinprotein, its -isoform or the amount of ribosylated actin. However,TNF--mediated dyscohesion of epithelial cells was associatedwith loss of plasmalemmal undercoat as well as intracytoplasmicaggregates of F-actin and a simultaneous increase in G-actin.The effect of cytochalasin-B, which disrupts actin filamentson cell-cell binding, was less pronounced than the effect ofTNF-, suggesting that the effect of this cytokine on dyscohesionis not solely dependent on the disassembly of actin filaments.These findings show that the induction of disordered expressionof adhesion molecules, as well as disassembly of actin filaments,are implicated in the dyscohesion induced by TNF-.     

IL-17 Eliminates the Therapeutic Effects of Myelin Basic Protein-Induced Nasal Tolerance in Experimental Autoimmune Encephalomyelitis by Activating IL-6

Interleukin (IL)-17 is a proinflammatory cytokine primarily secreted by Th17 cells, which are a CD4⁺ T-cell subset. Th17 cells and IL-17 are important in the pathogenesis of multiple sclerosis and in its established animal model, experimental autoimmune encephalomyelitis (EAE). However, it is unclear whether IL-17 contributes to EAE immune tolerance. We used the myelin basic protein (MBP) peptide MBP 68–86 to induce nasal tolerance to EAE, and simultaneously interfered with the tolerance by treatment with different doses of IL-17. We found that IL-17 dramatically interfered with MBP 68–86-induced immune tolerance. IL-17 administration increased IL-6 release, skewing T cell differentiation towards Th17 cells and decreasing the number of Treg cells. This led to an imbalance between Treg cells and Th17 cells and spurred the development of EAE.     

Nuclear and cytoplasmic bcl-2 expression in endometrial hyperplasia and adenocarcinoma

The bcl-2 proto-oncogene, which inhibits programmed cell death (apoptosis), has recently been found to be cyclically expressed in human endometrium. In order to investigate its role in endometrial hyperlasia and neoplasia, bcl-2 expression was studied in 25 cases of endometrial carcinoma and 20 cases of endometrial hyperplasia (eight simple, two complex, and ten atypical hyperplasias). Uniform intense cytoplasmic bcl-2 expression was found in all cases of non-atypical hyperplasia, and less strong positivity in eight out of ten cases of atypical hyperplasia. In well-differentiated carcinomas, nine out of ten showed weak to moderate bcl-2 expression, whereas six out of seven poorly differentiated carcinomas were bcl-2-negative. Moderately differentiated tumours were an intermediate group, with six out of eight being positive. Widespread localization of bcl-2 protein to the chromosomes of dividing cells was also demonstrated, regardless of cytoplasmic bcl-2 expression, with rare staining of interphase nuclei. Our findings suggest a role for bcl-2 in the natural history of endometrial neoplasia and studies are needed to determine its usefulness as a prognostic marker. The finding of bcl-2 localization to chromosomes has important implications for its mode and site of action.     

Two novel mutations in the EPM2A gene in a Korean patient with Lafora's progressive myoclonus epilepsy

The progressive myoclonus epilepsy of the Lafora type (LD; MIM 254780) is a rare autosomal recessive disorder characterized by epilepsy, myoclonus, progressive neurological deterioration, and the presence of periodic acid-Schiff-positive polyglucosan inclusions (Lafora bodies). Mutations in the EPM2A gene have recently been found to cause LD and about 30 or more mutations have been reported thus far. LD is relatively common in countries of the Mediterranean Basin, the Middle East, India, and Pakistan. Although a few sporadic cases with the typical LD phenotype have also been reported in the Far East including Korea and Japan, a recent effort to find mutations in Japanese LD families was not successful. In the present study, we report two novel mutations in a Korean girl with LD; a 1-bp insertion mutation (c.223insC; G75fsX107) in exon 1 and a missense mutation (c.559A>G; T187A) in exon 3 of the EPM2A gene. To our knowledge, this is the first report of a genetically confirmed case of LD in Koreans and also in the Far East.