Two maturation-associated mouse erythrocyte receptors of human B cells. II. Isolation and partial characterization of a B-cell lectin with specificity of R1.

Trypsin treatment of chronic lymphocytic leukaemia (CLL) cells which have the capacity to rosette with mouse erythrocytes (M), the BM+ subtype, inhibits their capacity to rosette and releases a substance into the supernatant which agglutinates mouse and rat erythrocytes but not erythrocytes of five other species tested. This substance has been named immature B-cell lectin (IBL). The specificity of IBL was further demonstrated by fluorescence labelling, absorption and latex rosetting. IBL does not bind to pronase-treated M (pro M), indicating that it has the specificity of R1 as distinct from R2 which binds to a pronase-resistant ligand on M. Other evidence that IBL is associated with B-cell membrane receptors for mouse erythrocytes is as follows: (1) The amount of IBL released into the supernatant correlated with the trypsin sensitivity of M rosetting with different clones of BM+ CLL cells. (2) Only small amounts of IBL were released from non-rosetting cells (T cells and mature B cells). (3) Binding properties of IBL were inhibited by extract of M but not extract from ox erythrocytes. (4) High-titre solutions of IBL conferred the capacity to form M rosettes on certain types of non-rosetting B cells. IBL has a dual binding specificity. Its binding to M is inhibited by fetuin and mannan, while its binding to B cells is not inhibited by these substances. The relationship of IBL to other membrane lectins including fibronectin is discussed. Preliminary characterization indicates a high-molecular-weight (at least 300,000 daltons) glycoprotein which has a pronounced tendency to aggregate in solution. The relationship of IBL to stages of human B-cell maturation is discussed.     

Extreme resistance to Potato leafroll virus in potato cv. Russet Burbank mediated by the viral replicase gene

High levels of field resistance to Potato leafroll virus (PLRV; Genus: Polerovirus; Family: Luteoviridae) were achieved by expression of the unmodified, full-length PLRV replicase gene in potato plants cv. Russet Burbank. A high degree of resistance was also achieved, but less frequently, by expression of a truncated construct of the replicase gene. In limited testing, neither miss-frame nor antisense constructs of the replicase gene conferred resistance. The degree of resistance expressed among different transformant lines ranged from near immunity to full susceptibility. Resistance to the Colorado potato beetle (Leptinotarsa decemlineata Say) was combined with resistance to PLRV by expression of the cry3A insect control protein gene from Bacillus thuringiensis var. tenebrionis in combination with the unmodified, full-length, viral replicase gene. Resistance was expressed as a reduced incidence of infection detectable by foliage symptoms or serological tests. Reduced incidence of infection was not associated with a decrease in virus antigen concentration in the few plants of resistant lines that became infected. Virus was not detected in the foliage of symptomless plants but was detected in progeny plants produced from the tubers of inoculated but symptomless test plants of some resistant lines. The resistance was effective under natural exposure and against plant-to-plant spread of PLRV by the aphid vector, Myzus persicae Sulzer. Three of the resistant lines selected in these studies were released and are now in commercial production.     

Basement membrane component changes in nerve allografts and isografts

This study describes immunocytochemical changes in laminin, which is an integral basement membrane (BM) component, during axonal regeneration through antigenic nerve allografts and nonantigenic nerve isografts. In normal rat nerve, laminin was localized in the BM of Schwann cells and the perineurium. During nerve allograft rejection, the perineurium and Schwann cells disappeared. However, the Schwann cell BMs persisted and became distorted and collapsed. In isografted nerves, the perineurium and Schwann cells were present, and only a few Schwann cell BMs appeared to be distorted; however, the staining for laminin was faint, indicating a possible BM breakdown. A new BM appeared as small rings around the Schwann cells after they had become associated with regenerated axons. Because only a limited axonal regeneration occurred in allografts as compared to isografts, it is concluded that the viable Schwann cells, and their BM architecture, are essential for regeneration through long nerve grafts.     

Reduced clot permeability and susceptibility to lysis in patients with acute coronary syndrome: effects of inflammation and oxidative stress

BackgroundStable angina is associated with unfavorable fibrin structure/function. It is not known how acute coronary syndromes (ACS) affect fibrin architecture.ObjectiveWe investigated fibrin clot properties and their determinants in ACS patients.Patients and methodsClot permeability, turbidity and fibrinolysis were assessed in 40 patients with ACS versus 40 controls with stable angina matched for age, sex, and risk factors.ResultsPatients with ACS had lower clot permeability (p = 0.001), faster fibrin polymerization (p = 0.008), and prolonged fibrinolysis time (p < 0.0001) than controls. C-reactive protein (CRP) and 8-epi-prostaglandin F_2α, a marker of oxidative stress, were the only independent predictors of clot permeability (R² = ?0.74; p < 0.0001 and R² = ?0.65; p < 0.0001, respectively) and fibrinolysis time in ACS patients (R² = 0.60; p < 0.0001 and R² = 0.59; p = 0.0002, respectively). In angina patients, fibrinogen and CRP predicted permeability (R² = ?0.71; p < 0.0001 and R² = ?0.62; p < 0.0001), and D-dimer predicted lysis time (R² = 0.54; p = 0.0005). In regression analysis models incorporating all patients, the only independent predictor of all clot variables was being an ACS patient (R² 0.51 to 0.85; p < 0.001).ConclusionsThis first study of clot properties in patients during an ACS demonstrated that compared with stable angina patients, their clots are composed of dense networks that are more resistant to lysis and these features are correlated with raised CRP and oxidative stress.