Tumorigenicity of the optical enantiomers of the diastereomeric benzo[a]pyrene 7,8-diol-9,10-epoxides in newborn mice: exceptional activity of (+)-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene.

The tumorigenicities of benzo[a]pyrene and each optical enantiomer of the diastereomeric benzo[a]pyrene 7,8-diol-9,10-epoxides derived from trans-7,8-dihydroxy-7,8-dihydrobenzol[a]pyrene were tested by sequential intraperitoneal injection of mice with 1,2, and 4 nmol, or with 2, 4, and 8 nmol of each compound on the 1st, 8th, and 15th day of life, respectively. The experiment was terminated when the animals were 34--37 weeks old. (+)-7beta, 8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzol[a]pyrene [(+)-BP-7beta,8alpha-diol-9alpha,10alpha-epoxide 2] had exceptional tumorigenicity, whereas benzo[a]-pyrene and the other three optically pure isomers of the benzo[a]pyrene 7,8-diol,9,10-epoxides had little or no activity. These results demonstrate differences in the carcinogenic activities of optically active isomers of a polycyclic hydrocarbon diol epoxide. Eleven percent of control mice had pulmonary tumors, whereas 71% and 100% of the mice treated with a total dose of 7 or 14 nmol of (+)-BP-7beta,8alpha-diol-9alpha,10alpha-epoxide 2, respectively, had pulmonary tumors. Control mice had an average of 0.12 pulmonary tumors per mouse, whereas mice treated with a total dose of 7 or 14 nmol of (+)-BP-7beta,8alpha-diol-9alpha,10alpha-epoxide 2 had 1.72 and 7.67 pulmonary tumors per mouse, respectively. Mice treated with 14 nmol of (-)-BP-7alpha,8beta-diol-9beta,10beta-epoxide 2, (-)-BP-7beta,8alpha-diol-9beta,10beta-epoxide 1, or (+)-BP-7alpha,8beta-diol-9alpha,10alpha-epoxide 1 had 0.13, 0.25, and 0.34 pulmonary tumors per animal, respectively.     

Opposite sorting of tissue factor in human umbilical vein endothelial cells and Madin-Darby canine kidney epithelial cells

Tissue factor (TF) is a 48-kD transmembrane glycoprotein that triggers the extrinsic pathway of blood coagulation by interacting with the plasma coagulation factor VII (FVII). TF is also a true receptor in that a cellular signal is generated when activated FVII (FVIIa) binds to TF. For both of these functions, the cellular surface distribution of TF is important, since FVII is primarily available on the apical side of vascular endothelial cells and on the basolateral side of epithelial cells lining the internal and external surfaces. We show that in endothelial cells, TF (both antigen and procoagulant activity) is sorted to the apical surface, whereas in wild-type and stably transfected Madin-Darby canine kidney epithelial cells (MDCK), which form tight junctions and express TF constitutively, TF antigen is on the basolateral surface. No significant clotting activity is detectable on this surface. Truncated TF (cytoplasmic tail residues 246 to 263 deleted) is sorted as wild-type in MDCK cells.     

Distribution of T cells and signs of T-cell activation in the rheumatoid joint: implications for semiquantitative comparative histology

A prerequisite for comparative histology of synovial tissue by means of biopsies is insight into the distribution of a marker under study. This investigation focuses on the variation in the presence of T cells and signs of T-cell activation within the rheumatoid joint. For this purpose, multiple slides from several pieces of synovial tissue from different parts of a joint were stained and scored for the expression of CD3, CD25, HLA-DR, Ki67 and interferon-gamma. The variation in scores for the presence of T cells and markers of activation was more pronounced in slides prepared from different pieces of tissue than in slides from one piece of tissue. Based on multiple analysis of variance, methods are suggested to establish a reliable overall score for the expression of a certain marker within a joint. Following validation, such methods may prove to be useful by allowing semiquantitative histology of synovial tissue for studies on arthritis.      

酒精性肝病的实验动物模型的研究文献综述

酒精性肝病包括酒精性脂肪肝、酒精性肝炎、酒精性肝纤维化及酒精性肝硬变. 四者是渐进性的过程,亦可不同类型同时存在,严重危害患者健康. 要探讨酒精性肝病的发病机制及病理过程,需良好的实验动物模型,经众多学者努力,现已创建了多种模型,并在不断改进. 笔者对此做一综述.     

Factor XI antigen and activity in human platelets

Washed platelets, contaminated with less than 0.20% plasma factor XI, were examined for the presence of factor XI antigen and activity. These platelets contained a factor-XI-like coagulant activity (0.67 +/- 0.11 U/10(11) platelets) that remained constant after successive washes. By means of indirect immunofluorescence, a monospecific antibody to factor XI showed specific staining of both normal platelets and platelets from patients deficient in plasma factor XI. Radiolabeled Triton extracts of washed platelets and labeled purified factor XI solutions were analyzed for factor XI antigen by Staph A immunoprecipitation analysis using antibody to purified plasma factor XI followed by SDS gel electrophoresis. On unreduced gels, the platelet material ran as a single band having an apparent molecular weight of 220,000 daltons, whereas purified plasma factor XI gave a single band at 160,000 daltons. On reduced gels, the platelet material analyzed as a single band at 52,000 daltons, whereas purified factor XI gave a single band of 80,000 daltons. Analysis of a partially purified factor XI preparation from platelets by immunoelectrophoresis revealed that the platelet preparation displayed a slightly lower cathodal electrophoretic mobility at pH 8.6 than did plasma factor XI and yet appeared to possess complete antigenic identity with plasma factor XI. These results indicate that platelets possess a form of factor XI that exists as a disulfide-linked 52,000-dalton tetramer in contrast to the plasma form that circulates as a 80,000-dalton disulfide-linked dimer.     

递增负荷有氧运动14周影响不同衰老程度老年男性的生物学年龄

目的:观察有氧运动对不同衰老程度老年男性生物学年龄的影响。方法:于2002-09/12选择上海市杨浦区退休老年男性13名,年龄59～76岁,平均(64±5)岁,近期无系统健身运动经历。13名老年男性采用功率自行车进行14周递增负荷有氧运动。以最大心率的75%所对应的运动负荷为训练强度;在第4,8周末重新确定运动强度,第5～8周、9～14周以新负荷作为健身运动负荷。每周3次,起始2周每次持续20min,以后每隔2周每次增加5min。采用刘继武等推荐的生物学年龄成套测试方法测定生物学年龄。运动前和运动后测定生物学年龄以及身体形态、心血管、肺功能等生理指标。并根据生物学年龄与实际年龄的差距,分成提前衰老组(生物学年龄大于实际年龄)和延缓衰老组(生物学年龄小于实际年龄)进行对照分析。结果:①老年男性运动前生物学年龄大于实际年龄,差异无显著性意义(P=0.56),有氧运动后生物学年龄小于实际年龄,差异无显著性意义(P=0.066),有氧运动后生物学年龄小于运动前,差异有非常显著性意义[分别为(65.13±6.33),(67.15±7.13)岁,P<0.01]。②根据生物学年龄与实际年龄的差距,将老年男性分成提前衰老组7名和延缓衰老组6名。提前衰老组老年男性有氧运动前生物学年龄大于实际年龄,递增负荷有氧运动后生物学年龄接近实际年龄,低于运动前,差异有非常显著性意义[分别为(69.00±6.73),(71.90±7.55)岁,P<0.01]。延缓衰老组有氧运动前生物学年龄小于实际年龄,有氧运动后生物学年龄进一步减少,低于运动前,差异无显著性意义(P>0.05)。③提前衰老组老年男性有氧运动后腰围低于运动前,腰臀比高于运动前,差异有显著性意义[分别为(94.20±5.14),(99.58±6.48)cm;(0.95±0.03),(0.92±0.04)cm,P<0.05]。延缓衰老组老年男性上臂皮褶厚度低于运动前,差异有显著性意义[分别为(11.00±2.17),(14.42±2.33)mm,P<0.05]。其他身体形态指标变化差异无显著性意义。生理功能指标变化较明显,最大摄氧量、闭眼单脚站立时间均高于运动前,差异有显著性意义[分别为(36.08±5.40),(30.08±2.21)mL/(kg·min);(28.17±20.51),(12.4±14.78)s,P<0.05]。④两组老年男性有氧运动后心血管和肺功能指标中收缩压、舒张压均有下降,肺活量增加。其中延缓衰老组老年男性肺活量高于运动前,差异有显著性意义[分别为(3.98±0.69),(3.61±0.71)L,P<0.05]。结论:有氧运动对不同衰老程度老年男性生物学年龄、身体形态和生理功能均可产生良性影响,达到延缓衰老目的。     

A cost analysis comparing erythropoietin and red cell transfusions in the treatment of anemia of prematurity

BACKGROUND: Anemia of prematurity is invariably observed in very low birth weight infants and may become symptomatic enough to be treated with packed red cell transfusions. Recently, treatment of this condition with recombinant human erythropoietin has been advocated. STUDY DESIGN AND METHODS: To compare the costs of training symptomatic anemia in hospitalized premature infants with transfusions alone or with erythropoietin plus red cell transfusions as needed, cost estimates were derived from local hospital and published cost data. Decision analysis and sensitivity analysis were applied to a "base case." The base case was derived from results of a multicenter erythropoietin trial in the United States in which premature infants received 500 U of erythropoietin per kg of body weight each week. Because erythropoietin treatment began on average at 3 weeks of life, when infants were clinically stable, they had already received 3.5 red cell transfusions. During the 6-week treatment period, erythropoietin- treated infants received significantly fewer additional transfusions: a mean of 1.6 versus 1.1. RESULTS: The base-case cost in 1993 dollars for treating anemia in hospitalized premature infants with erythropoietin and transfusions was $1,326. This was nearly twice the cost of conventional treatment with transfusions alone ($721). If the 6-week treatment period alone is considered, erythropoietin is 3.6 times more costly: $840 versus $235. CONCLUSION: The largest available US study using erythropoietin to treat anemia in premature infants has demonstrated a small, but significant, reduction in transfusion needs. However, this study's cost data alone do not justify the widespread use of erythropoietin in premature infants. When this issue is probed in great depth, sensitivity analyses demonstrate that major reductions in erythropoietin's cost and/or improvements in its effectiveness quite possibly will make its use economically more attractive.