Significant contribution of small icebergs to the freshwater budget in Greenland fjords.

Icebergs represent nearly half of the mass loss from the Greenland Ice Sheet and provide a distributed source of freshwater along fjords which can alter fjord circulation, nutrient levels, and ultimately the Meridional Overturning Circulation. Here we present analyses of high resolution optical satellite imagery using convolutional neural networks to accurately delineate iceberg edges in two East Greenland fjords. We find that a significant portion of icebergs in fjords are comprised of small icebergs that were not detected in previously-available coarser resolution satellite images. We show that the preponderance of small icebergs results in high freshwater delivery, as well as a short life span of icebergs in fjords. We conclude that an inability to identify small icebergs leads to inaccurate frequency-size distribution of icebergs in Greenland fjords, an underestimation of iceberg area (specifically for small icebergs), and an overestimation of iceberg life span.

Friction at the bed does not control fast glacier flow.

The largest uncertainty in the ice sheet models used to predict future sea level rise originates from our limited understanding of processes at the ice/bed interface. Near glacier termini, where basal sliding controls ice flow, most predictive ice sheet models use a parameterization of sliding that has been theoretically derived for glacier flow over a hard bed. We find that this sliding relation does not apply to the 140 Greenland glaciers that we analyzed. There is no relationship between basal sliding and frictional stress at the glacier bed, contrary to theoretical predictions. There is a strong relationship between sliding speed and net pressure at the glacier bed. This latter finding is in agreement with earlier observations of mountain glaciers that have been largely overlooked by the glaciological community.

Characterization and classification of lymphoid cells after pokeweed mitogen stimulation.

Human peripheral blood mononuclear cells (PBMC) were stimulated with pokeweed mitogen (PWM) for 3 days and subsequently cultured in medium for another 3 days. It was shown that mononuclear phagocytes (MNP), although present initially in the PBMC cultures, disappeared shortly after the addition of PWM. It was concluded that MNP, although obligatory for stimulation, were no longer required for further transformation of cells after stimulation. At the ultrastructural level stimulation of PBMC with PWM resulted in the generation of 2 types of blast cells. The first type were characterized by the presence of polyribosomes throughout the cytoplasm, large and swollen mitochondria and a few short strands of rough endoplasmic reticulum. The second type of blast cell showed a dispersed pattern of ribosomes, a number of smaller mitochondria and some long strands of rough endoplasmic reticulum. In parallel with a decrease in the number of type I blast cells, plasma cells were found in the stimulated cell cultures. Labeling for surface-membrane immunoglobulins was positive only in type I blast cells and after a longer period in plasma cells. These observations suggest the transformation of type I blast cells into plasma cells, both being derived from the B-cell line. Type II blast cells probably represent transformed cells of the T-cell line.

The use of a peroxidase-anti-peroxidase complex for the visualization of monoclonal antibodies on the ultrastructural level.

Human peripheral blood mononuclear cell (PBMC) were treated with a panel of monoclonal antibodies (MoAbs) for the demonstration of membrane antigens at the ultrastructural level. The bound MoAbs were linked by rabbit anti-mouse IgG to a peroxidase-anti-peroxidase (PAP) complex composed of monoclonal mouse anti-peroxidase antibodies and horse radish peroxidase. This labelling method with a three step incubation procedure resulted in clear demonstration of the membrane antigens. Moreover, the use of the PAP complex as marker permitted the recognition of monocytes not only by morphology but also by their endogenous peroxidase pattern. In addition, it was observed that the MoAbs used, supposedly specific for T lymphocytes, reacted to a certain degree with monocytes.

Electronmicroscopical observations on monocyte-lymphocyte interactions upon stimulation with pokeweed mitogen latex conjugate.

In this study we report on the preparation and application of pokeweed mitogen (PWM) conjugated to latex particles. This conjugate (PWM-latex) was prepared by incubation of PWM with latex particles in the presence of glutaraldehyde. The effect of the addition of PWM-latex to human peripheral blood mononuclear cells (PBMC) was fully comparable to the addition of PWM alone i.e. differentiation of lymphocytes into blast cells followed by proliferation of these blast cells as measured by DNA synthesis and total cell number. Electronmicroscopically PWM-latex was found to be taken up by monocytes within the first 24 h after addition. Although no direct interaction could be observed between PWM-latex and lymphocytes, the latter were found to differentiate into blast cells. Due to interactions of these blast cells with latex-containing monocytes, latex particles were obviously released from the phagocytes and close contacts between latex particles and blast cells were regularly seen. In addition, it was found that blast cells of T cell origin, as judged by their positive reaction with anti-T cell monoclonal antibodies, had taken up latex particles. Based on enzyme-cytochemical, functional and light microscopical studies, monocytes could not be detected in the PWM-latex-driven PBMC stimulation after 6 days. At the electronmicroscopical level evidence was found that the inability to demonstrate macrophages could be due to the release of the lysosomal enzyme content and of parts of the cytoplasm.

Anti-pokeweed mitogen antiserum inhibits and enhances blastogenesis of mononuclear cells induced by pokeweed mitogen.

The interaction between pokeweed mitogen (PWM) and peripheral blood mononuclear cells (PBMC) was investigated using rabbit anti-PWM antiserum (anti-PWM) and 125I-PWM. Incubation of PBMC with PWM in the presence of anti-PWM resulted in an inhibition of the mitogenic effect of PWM. Anti-PWM predominantly blocked the interaction of PWM with monocytes, which is essential for optimal stimulation of lymphoid cells with PWM. Addition of anti-PWM to PBMC at several time-points after incubation with PWM showed inhibition of mitogenic activity when anti-PWM was added within 8 hours. However, enhancement of PWM-induced blast cell formation was found when anti-PWM was added after 48 hours. Further analysis revealed that the inhibition of PWM stimulation was mediated by the F(ab')2 part of anti-PWM IgG. On the other hand F(ab')2-anti-PWM was not able to enhance the effect of PWM. Incubation of PBMC with 125I-PWM and anti-PWM simultaneously, decreased the binding of PWM to both lymphocytes and monocytes. In contrast, addition of anti-PWM 48 hours after the incubation of PBMC with PWM resulted in an increased binding of PWM to monocytes. These results show that anti-PWM can modulate the lymphocyte reaction to PWM and suggest two possible mechanisms by which PWM can stimulate PBMC, both of which are dependent on the interaction of PWM with monocytes.

In vitro effect of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonic acid (APD) on the function of mononuclear phagocytes in lymphocyte proliferation.

The effect of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonic acid (APD) on pokeweed mitogen-stimulated and non-stimulated cultures of peripheral blood mononuclear cells was studied in vitro. It is shown that APD can inhibit partially lymphocyte proliferation when added to a suspension of mononuclear cells before stimulation, but that lymphocyte proliferation can continue when the drug is withdrawn. In contrast; when APD is added to the cell suspension together with the mitogen, lymphocyte proliferation remains low even when the drug is withdrawn. Addition of different concentration of mononuclear phagocytes (MNP) to non-adherent cells, followed by stimulation in the presence of APD, indicates that APD acts on MNP function preferentially and does not affect lymphocyte proliferation.