聚氨酯/液晶复合膜的抗凝血性能研究

以聚醚型聚氨酯为基质材料 ,分别与向列型、胆甾型液晶化合物在适当溶剂中溶解共混后 ,利用溶剂蒸发法在聚四氟乙烯板上浇铸成膜。详细研究了液晶含量对复合膜动态凝血性能 ,血小板粘附性能以及溶血性能的影响。研究结果表明 :只有当复合膜中的液晶重量份数超过 30 %时 ,复合膜才表现出良好的抗凝血性能 ,且随液晶含量的增加 ,复合膜的抗凝血性能有明显的改善 ,尤其是复合膜表面吸附的血小板数量随液晶含量的增加而明显减少     

不同液晶类型的聚氨酯/液晶复合膜的血液相容性

本研究合成了三种亲水性胆甾醇液晶化合物 ,用元素分析法、红外光谱、差热分析以及偏显镜观察对其结构和性能进行了表征。利用聚氨酯与上述液晶化合物制备复合膜 ,研究了不同液晶类型对聚合物 /液晶复合膜的影响。研究表明 ,胆甾醇液晶化合物有利于改善聚合物材料的血液相容性     

纳米碳改性聚氨酯复合材料的表面抗凝血性能

研究纳米碳改性聚氨酯聚合材料表面的血液相容性。将经过表面处理的纳米碳分散到聚氨酯体系中，制成聚氨酯／纳米碳复合薄膜。通过血小板荧光标记人全血灌注实验和羊全血体外循环等实验，观察和测定血小板在材料表面的粘附作用以及血液中血红蛋白浓度、纤维蛋白原浓度的变化，探讨纳米碳对聚氨酯抗凝血性能的影响。实验结果显示聚氨酯／纳米碳表面血小板的粘附明显低于单纯聚氨酯对照组：体外循环4h后，血液中血红蛋白浓度、纤维蛋白原浓度的变化程度减小。表明纳米碳与聚氨酯的复合可以提高材料的血液相容性。     

介入诊疗聚氨酯(PU)导管的抗凝血研究进展

扼要概述了介入诊疗聚氨酯(PU)导管的凝血过程、影响因素、改善PU导管材料抗凝血性的途径以及导管用材料抗凝血性能的表征.     

聚二甲基硅氧烷／聚氨酯共混体系的表面结构和抗凝血性能

本文用光电子能谱（ＸＰＳ）、衰减全反射红外光谱（ＡＴＲ）及扫描电子显微镜（ＳＥＭ），研究了一系列不同结构聚二甲基硅氧烷／聚氨酯（ＰＤＭＳ／ＰＵ）共混体系的表面化学组成和表面形态结构．研究结果表明：共混物具有织态状微相分离结构；在垂直表面方向上化学组成具有不均匀性，软段和聚二甲基硅氧烷在表面富集，氧原子优先在表面层中分布．对吸附血小板形态观察及再钙化时间的测定表明，聚二甲基硅氧烷／聚氨酯共混物的抗凝血性能优于聚氨酸，和共混物的表面形态结构和化学组成相关。     

碳纳米管/聚氨酯复合材料的制备及生物相容性评价

目的 制备和评价碳纳米管/聚氨酯复合材料的生物相容性。方法 通过溶胶-凝胶方法制备碳纳米管/聚氨酯复合材料,对其力学性能进行测试;根据ISO10993指南,选取溶血实验、动态凝血实验、血小板黏附实验、血小板活化实验、细胞毒性实验和材料局部植入方法对复合材料的生物相容性进行评价。结果 复合材料无明显细胞毒性,并表现出比聚氨酯材料更好的抗溶血性能、动态凝血性能、抑制血小板黏附性能以及组织相容性。结论 碳纳米管－聚氨酯复合材料具有优良的生物相容性,可以作为制备组织工程细胞生长支架、人工血管、药物载体的基础材料。     

不同聚氨酯Dacron材料抗血栓性能的比较

运用不同编织Dacron和不同氨基甲酸酯涂层的Dacron血管修补物进行试验.整个材料置于富血小板血浆中,与血小板接触,随后分析三种血小板的释放物质,即β—血栓球蛋白,血小板4因子和血栓烷B_2,还有血小板停滞数.这些常用来确定材料本身形成血栓的程度.在某些实验中Dacron—氨基甲酸酯复合物显示具有比其它任何常用的血管外科材料更好的抗血栓性.虽然在血管外科和病人的处理中有不断改进,但是在临床上移植物的血栓形成仍是一个重要问题,在有利于这种现象(即血液流动、血液的特性、周围阻力)的条件下,移植材料仍起着重要的作用.     

聚六亚甲基碳酸酯聚氨酯脲的制备与性能评价

目的评价聚六亚甲基碳酸酯聚氨酯脲(PCU)的性能。方法通过拉伸试验、96℃±4℃热水水解试验、次氯酸钠溶液中氧化实验、全血凝血时间实验、测定动态凝血时间实验、血小板黏附实验等,分别测定了PCU的力学性能、耐水解性、耐氧化性和抗凝血性,并与国外产品Chronoflex(Chro)进行对比。结果PCU的强度与Chro相近,但其弹性和柔性逊色于Chro,PCU的耐水解性能和耐氧化性能略优于Chro,PCU和Chro都具有良好的抗凝血性能。结论PCU是一种性能与Chro相近的“生物稳定”聚氨酯。     

小口径微孔聚氨酯人造血管生物力学性能研究

目的分析小口径聚氨酯人造血管的微观形态,探讨聚氨酯人造血管管壁厚度对其渗透性能和拉伸强度的影响。方法通过在直径为4mm玻璃棒模具上复合均匀厚度的聚氨酯膜,并加入一定量的致孔剂,研制出具有微观多孔结构的小口径聚氨酯人造血管。采用扫描电镜表征其微观多孔结构,根据ISO7198国际标准设计了一套人造血管渗透性能的测试装置来测试其水渗透性能,并通过INSTRON万能强力仪(型号:5566)测试其拉伸强度。结果小口径的聚氨酯人造血管的内、外表面以及截面均呈微孔结构,微孔的大小在100μm以下,大小和分布比较均匀,并且随着人造血管壁厚度的增加,其渗透性能逐渐减小,拉伸强度先增大后减小,实验测试结果均与国外研究在同一范围。结论用聚氨酯材料研制的小口径人造血管在部分生物力学性能方面能满足人体血管置换要求。     

Heterotypic interference between influenza viruses A/Aichi/2/68 and B/Massachusetts/1/71.

Virus particles produced by MDCK cells mixedly infected with 3 PFU/cell each of A/Aichi/2/68 (H3N2) (Aichi) and B/Massachusetts/1/71 (Mass) influenza viruses exclusively possessed haemagglutinin (HA) of Mass, although approximately one-fifth of the mixed yield had coding potential for Aichi serotype. Synthesis of major viral proteins of Aichi was markedly suppressed by co-infecting Mass. By increasing the multiplicity of co-infecting Aichi to 30 PFU/cell, interference became reciprocal. Aichi interfered with replication of Mass more severely than Mass did with replication of Aichi. All the major viral proteins of both Aichi and Mass were expressed within the infected cells.     

Pathogenicity of PMV-3/parakeet/Netherlands/449/75 for chickens

Infection of 1-day-old chicks with PMV-3/parakeet/Netherlands/449/75 (449) by intramuscular, intranasal or contact routes resulted in severe impairment of growth in all groups compared to uninfected control birds. In the group infected intramuscularly with 449 virus 16/22 birds died within 14 days of infection. No clinical signs were seen in 6-week-old chickens infected with 449 by intramuscular, intranasal or contact routes. One-day-old chicks infected with a large dose of NDV-B(1) and one-day-old chicks placed in contact with these birds also showed significant impairment of growth compared to uninfected controls.     

Recent H1N1 viruses (A/USSR/90/77, A/Fiji/15899/83, A/Firenze/13/83) replicate poorly in ferret bronchial epithelium

Summary Three recent wild-type H1N1 influenza virus isolates (A/USSR/90/77, A/Fiji/15899/83 and A/Firenze/13/83) replicated poorly in organ cultures of ferret bronchial tissue compared with the replication of an H3N2 wild-type virus (A/England/939/69). All four viruses replicated well in nasal turbinate tissue. Examination of one H1N1 virus (A/USSR/90/77)in vivo showed heavy infection in the upper respiratory tract of ferrets but little in the lower respiratory tract. These results raise the possibility that the mildness of human influenza arising from the H1N1 strains may be due to lack of capacity to attack the lower respiratory tract as well as the presence of antibody in previously exposed persons.With 1 Figure     

O2 Delivery and the Venous PO2-O2 Uptake Relationship in Pump-Perfused Canine Muscle

Under the conditions of both an increased red cell affinity for O(2) at a constant rate of O(2) delivery (arterial O(2) content x flow) and a decrease in the rate of O(2) delivery induced by hypoxic hypoxia at constant blood flow, we have obtained a linear relationship between the partial pressure of O(2) in the muscle venous effluent (P(v,)(O(2))) and O(2) uptake (.V(O(2))). The relationship is described by the equation .V(O(2)) = D(a) x P(v,)(O(2)) + .V(O(2)conv)) where D(a) is the apparent O(2) diffusion capacity and .V(O(2)conv)) is O(2) delivery-limited .V(O(2)), and D(a) x P(v,)(O(2)) represents the O(2) diffusion-limited .V(O(2)) .V(O(2)diff)). From these observations, we propose the hypothesis that .V(O(2)) consists of two additive values, .V(O(2)conv)) and .V(O(2)diff)). The mechanism underlying the reduction in .V(O(2)) that is induced by reducing O(2) delivery to markedly below the .V(O(2)conv)) value has only been investigated using a model based on the single compartment of diffusion-limited .V(O(2)), and has not been investigated in terms of this additive .V(O(2)) model. The single compartment analysis appears to overestimate the role of O(2) diffusion in limiting the reduction of .V(O(2)) that occurs in response to a decrease in O(2) diffusion capacity, as reflected by the .V(O(2))/P(v,)(O(2)) ratio. To gain better insight into the mechanism involved, we altered the rate of O(2) delivery by changing arterial P(O(2)) from normoxia (with inhalation of air) to hypoxia (by inhalation of 10-11 % O(2)) and blood flow (with high and low flow rates (n = 7 for both groups), and very low and ischaemic flow rates (n = 4 for both groups)) in pump-perfused dog gastrocnemius preparations during tetanic isometric contractions at 1 Hz. As rates of O(2) delivery were reduced from 23.2 to 10.9 ml min(-1) (100 g)(-1), significant decreases in P(v,)(O(2)) and .V(O(2)) were observed (P < 0.05). From the data of P(v,)(O(2)) and .V(O(2)) values within this range of O(2) delivery rates, we obtained the regression equation .V(O(2)) = 0.22 x P(v,)(O(2)) + 8.14 (r = 0.58). From the equation, the intercept of the .V(O(2))-axis was significantly different from zero (P < 0.05), in accordance with the observation that the .V(O(2)) /P(v,)(O(2)) ratio (ml min(-1) (100 g)(-1) Torr(-1)) increased from 0.54 to 1.35 (P < 0.05). However, at extremely low rates of O(2) delivery (5.6 and 7.3 ml min(-1) (100 g)(-1) the .V(O(2))/P(v,)(O(2)) ratio was 1.51 and 2.80 (P < 0.05), respectively. This indicates a break in the linear .V(O(2))-P(v,)(O(2)) relationship as the rate of O(2) delivery was reduced to below the .V(O(2)conv)) value of the .V(O(2))-axis intercept. These results suggest that the reduction in .V(O(2)) caused by extreme reductions in the rate of O(2) delivery is not attributable to a reduction in O(2) diffusion capacity, as expected from the .V(O(2))/P(v,)(O(2)) ratio, but to a reduction in the O(2) delivery-limited .V(O(2)) component, as evaluated by the .V(O(2))-axis intercept of the linear .V(O(2))-P(v,)(O(2)) relationship.     

Associations Between G/A1229, A/G3944, T/C30875, C/T48200 and C/T65013 Genotypes and Haplotypes in the Vitamin D Receptor Gene, Ultraviolet Radiation and Susceptibility to Prostate Cancer

Ultraviolet radiation (UVR) may protect against prostate cancer via a mechanism involving vitamin D. Thus, the vitamin D receptor (VDR) gene is a susceptibility candidate, though published data are discrepant. We studied the association of prostate cancer risk with five VDR single nucleotide polymorphisms (SNPs): G/A¹²²⁹ (SNP 1), A/G³⁹⁴⁴ (SNP 2), T/C³⁰⁸⁷⁵ (SNP 3), C/T⁴⁸²⁰⁰ (SNP 4) and C/T⁶⁵⁰¹³ (SNP 5), in 430 cancer and 310 benign prostatic hypertrophy (BPH) patients. The SNP 2 GG genotype frequency was lower in cancer than BPH patients (odds ratio = 0.63, 95% CI = 0.41–0.98, p = 0.039). SNPs 1 and 2, and SNPs 4 and 5, were in linkage disequilibrium. Two copies of haplotypes comprising SNPs 1‐2, G‐G (odds ratio = 0.63, p = 0.039), SNPs 2‐3 G‐C (odds ratio = 0.45, p = 0.008) and SNPs 1‐2‐3 G‐G‐C (odds ratio = 0.44, p = 0.006), but not SNPs 1‐3, G‐C (odds ratio = 0.81, p = 0.34), were associated with reduced risk (reference, no copies of the haplotypes) . These associations were observed after stratification of subjects by extent of UVR exposure. These data show that SNP 2 GG genotype mediates prostate cancer risk, complementing studies reporting this allele is protective in malignant melanoma pathogenesis. They further suggest that published associations of risk with SNP 1 may result from linkage disequilibrium with SNP 2.