The translation of Blood Smears Reinterpreted was begun when the French original was still undergoing revisions. I was accorded the oppor tunity to question any statement or turn of phrase that was unclear to me or appeared liable to misinterpretation. It is my hope that as a result, ambiguities-particularly those inherent in differences between American and Eu ropean usage-have been removed and that I have at least ap proached the ultimate goal of any translation: to reflect the author's intention accurately while remaining as readable as the original. Beyond the role of translator, I was encouraged to assume the role of critic. As a result, some pages or even single sentences were hotly debated, sometimes for hours, as Marcel Bessis insisted that any inter pretations on which we could not agree should be so indicated. In fact our discussion invariably ended in agreement, though they led to changes of a sentence here or a word there and, on occasion, to the addition of a footnote or a brief paragraph.

Hemolysis during filtration through micropores studied by Chien et al. [I] showed a dependence on pressure gradient and pore diameter that, at the time of publication, did not permit an easy interpretation of the hemolytic mechanism. Acting on the assumption that thresholds of hemolysis are easier to correlate with physical forces than extents of hemolysis, we performed a series of experi ments repeating some of the conditions reported in [I] and then focusing on low L1P in order to define better the thresholds of hemolysis for several pore sizes. Employing a model of a deformed red cell shape at the pore entrance (based on micropipette observations) we related the force field in the fluid to a biaxial tension in the membrane. The threshold for lysis correlated with a membrane tension of 30 dynes/cm. This quantity is in agreement with lysis data from a number of other investigators employing a variety of mechanisms for introduc ing membrane tension. The sequence of events represented here is: a. Fluid forces and pressure gradients deform the cell into a new, elongated shape. b. Extent of deformation becomes limited by the resistance of the cell mem brane to undergo an increase in area. c. Fluid forces and pressure gradients acting on the deformed cell membrane cause an increase in biaxial tension in the membrane. d. When the strain caused by this tension causes pores to open in the membrane, the threshold for hemolysis has been reached [2].

Jean BERNARD * I should like to begin with an assumption and a paradox. The assumption is that leukemia is a disease of a stem cell characterized by pathologie alterations of that cell and its progeny. All present research and discussions are centered around the leukemic cell. So is this symposium, which would not take place except for our primary interest in the leukemic cell. This does not preclude, of course, consideration of other definitions and other approaches to the prOblem. By definition, then, the leukemic cells are abnormal cells and their metabolism and functions are presumed to be abnormal. Yet, the classification of the different types of leukemias is based upon the characteristics of normal cells. We talk of "lymphoblasts" and "myeloblasts" as predominant cell types in leukemia. This leads to a double paradox. In the first pi ace it is clearly illogical to classify abnormal cells by their resemblance to normal cells, since their very abnormality consists in not being normal. Yet, as a second paradox, the classifica ti on has had the happy consequence of ai ding us in the treatment and prognosis of leukemia for the past 25 years. A more detailed analysis shows that the consequence of this paradox are complex: while there exists a useful correlation between cellular types, treatment and prognosis, numerous problems and difficulties persist. The most serious of them concems the "unclassified leukemias" which are the reason for this reunion.