胶体硒免疫层析法检测抗-HIV(1+2)抗体的评价

目的 对检测抗-HIV抗体的胶体硒免疫层析法进行评价。方法 用胶体硒免疫层析试剂检测HIV国家参考品、已经确证的临床阴、阳性标本，评价此法的灵敏度、特异性。结果 快速胶体硒法试剂特异性较好，灵敏度尚可，可以满足快速筛查抗-HIV的要求。结论 此法可用于紧急情况下的抗-HIV的筛查，鉴于其灵敏度有待进一步提高，目前尚不能替代酶标法的检测。同时，该法不适用于献血者献血前的筛查。     

Segregation of presynaptic inputs on an identified target neuron in vitro: structural remodeling visualized over time.

Sensory cells of Aplysia form chemical synapses with the motor cell L7 in culture. Under certain conditions, sensory cells will also form electrical connections with each other. Sites of chemical synaptic interaction between the sensory cells and L7 are located at varicosities along sensory cell processes that overlie the main axons of L7, since these structures have been shown ultrastructurally to contain active zones. Previous studies have suggested that the distribution of sensory cell varicosities can be restricted to exclusive regions of the motor cell by the presence of other sensory cells. We wished to investigate (1) how this segregated pattern is generated over time and (2) whether electrical coupling between sensory cells has an effect on this segregated pattern. Using fluorescent dye injection and low-light video microscopy, we visualized the distribution of varicosities for each of two sensory cells growing on L7. In cases in which sensory cells are not electrically coupled, the varicosities from these two cells are spatially segregated on the target after 4 d in culture but not after 2 d in culture. Examination of the varicosity distribution of the same sensory cells on the second and third day of growth indicated both an increased rate in the elimination of varicosities from previously occupied areas and a restriction of varicosity formation in new areas of the target when a second sensory cell is present. For sensory cells that are electrically coupled, varicosities from these cells were not spatially segregated on the target even after 4 d in culture. These observations in vitro suggest that segregation of synaptic inputs by Aplysia sensory cells, which show little spontaneous activity of action potentials, can emerge over time via a process that includes both the elimination of existing sensory varicosities and the restriction of new varicosity formation. Our results also suggest that electrical connections between presynaptic cells can disrupt the segregation of their varicosities on a target, resulting in significant changes in the developing connectivity.     

Acquired and inherited thrombophilic factors and the risk for residual venous thrombosis

Acquired and inherited thrombophilic factors increase the risk for (recurrent) venous thrombotic disease. However, little is known about the pathophysiological mechanisms causing these recurrences, or the persistence of thrombosis despite adequate treatment. Because residual thrombosis has been associated with a worse prognostic outcome, we performed an explorative study in order to investigate the prevalence of residual thrombotic lesions after anticoagulant treatment in patients with deep venous thrombosis. Thrombotic parameters as assessed by ultrasonography after a 12-week course of anticoagulants were used. Both thrombophilia in general and acquired thrombophilia in particular were found to be associated with the extent of residual thrombosis. Of the individual thrombophilic factors, protein C deficiency, prothrombin 20210A mutation, active malignant disease and lupus anticoagulant were associated with an increased risk of residual thrombotic mass. Patients with inherited thrombophilia did not differ from patients without any thrombophilic abnormality with regard to residual thrombotic mass [relative risk (RR) 1.3, 95% confidence interval (CI) 0.9-1.8], while acquired thrombophilic disorders increased the risk for residual thrombotic mass as compared to patients without any defect (RR 1.7, 95% CI 1.2-2.2). Although these results should be confirmed in a larger study, they might help us form hypotheses concerning why patients with thrombophilia are more prone to recurrent venous thromboembolic disease.     

Lymphocytes expressing alpha1beta1 integrin (very late antigen-1) in peripheral blood of patients with arthritis are a subset of CD45RO(+) T-cells primed for rapid adhesion to collagen IV

We report that very late antigen-1 (VLA-1(+)) CD3(+)CD45RO(+) T-cells are selectively segregated from VLA-1(-) peripheral blood (PB) mononuclear cells (MC), in which CD3(+) T-cells are evenly CD45RO(+) and CD45RO(-), when PBMC are stained with a monoclonal antibody (mAb) to VLA-1 and passaged on immunomagnetic columns. In contrast, both VLA-1(+) and VLA-1(-) MC isolated from synovial fluid (SF) are mainly CD45RO(+)CD3(+) T-cells. VLA-1(+) MC formed 13 +/- 5.3% of MC eluting from columns loaded with PBMC of patients with seropositive rheumatoid arthritis (n = 6) and 2.3 +/- 1.6% of patients (n = 4) with other arthritides (P < 0.022). Importantly, only the VLA-1(+) MC from PB and SF adhered to collagen IV upon triggering with phorbol 12-myristate 13-acetate. Moreover, adhesion and migration on collagen IV were preferentially maintained in lines cultured from VLA-1(+) T-cells, and both were inhibited by mAb to the VLA-1 alpha1 I domain. These results suggest that VLA-1(+) CD45RO(+) T-cells in patients with arthritis could play a role in both systemic and local inflammation by rapidly adhering to collagen IV.     

Muscle energy metabolism in human phosphofructokinase deficiency as recorded by 31P nuclear magnetic resonance spectroscopy

31P nuclear magnetic resonance studies of a patient with phosphofructokinase deficiency in muscle provided the following new findings: First, ATP metabolism is disturbed at rest and during exercise. At rest, ATP levels are lower than normal and continue to decline during exercise. Second, exercise kinetics are normal, suggesting a normal mitochondrial fuel supply although glycolysis is blocked. Third, no "phosphate trapping" is observed during prolonged low-level exercise. Fourth, postexercise recovery is abnormally prolonged by the slow dephosphorylation of sugar phosphates, which has an in vivo half-life of about nine minutes. These findings demonstrate how muscle tissue adapts to a block in a major bioenergetic pathway.