The article presents the history of translations of Plato's dialogues as made by A. Bronikowski (1817-1884), their assessment formulated by the contemporary for the translator recipients and today's opinions on them. Bronikowski began his translation work on the legacy of Plato in the '50s of the 19th century and carried them out systematically, despite the many adversities, until his death. The article presents the most important criticisms of the reviewers of Bronikowski's translations, which focused on the flaws of his style. The critics pointed out numerous shortcomings, archaisms, which hindered and prevented smooth reading of the text by readers unfamiliar with the language of the original. Most of the criticisms came from the Warsaw environment, especially from K. Kozłowski, the son of the first Polish translator of Plato, FA. Kozłowski. Among the defenders of Bronikowski there were K. Libelt and J.I. Kraszewski. They raised the subject of difficulty which the translator had to deal with and the lack of literary taste of the audience. It seems that both parties were partially right. Bronikowski's text was indeed not suitable for smooth reading in many places, however, it could serve as a useful tool for students who acquainted themselves with the Greek originals of the dialogues.
Bassingthwaighte, James B.
A four-region (capillary plasma, endothelium, interstitial fluid, cell) multipath model was configured to describe the kinetics of blood-tissue exchange for small solutes in the lung, accounting for regional flow heterogeneity, permeation of cell membranes and through interendothelial clefts, and intracellular reactions. Serotonin uptake data from the Multiple indicator dilution “bolus sweep” experiments of Rickaby and coworkers (Rickaby DA, Linehan JH, Bronikowski TA, Dawson CA. J Appl Physiol 51: 405–414, 1981; Rickaby DA, Dawson CA, and Linehan JH. J Appl Physiol 56: 1170–1177, 1984) and Malcorps et al. (Malcorps CM, Dawson CA, Linehan JH, Bronikowski TA, Rickaby DA, Herman AG, Will JA. J Appl Physiol 57: 720–730, 1984) were analyzed to distinguish facilitated transport into the endothelial cells (EC) and the inhibition of tracer transport by nontracer serotonin in the bolus of injectate from the free uninhibited permeation through the clefts into the interstitial fluid space. The permeability-surface area products (PS) for serotonin via the inter-EC clefts were ∼0.3 ml·g−1·min−1, low compared with the transporter-mediated maximum PS of 13 ml·g−1·min−1 (with Km = ∼0.3 μM and Vmax = ∼4 nmol·g−1·min−1). The estimates of serotonin PS values for EC transporters from their multiple data sets were similar and were influenced only modestly by accounting for the cleft permeability in parallel. The cleft PS estimates in these Ringer-perfused lungs are less than half of those for anesthetized dogs (Yipintsoi T. Circ Res 39: 523–531, 1976) with normal hematocrits, but are compatible with passive noncarrier-mediated transport observed later in the same laboratory (Dawson CA, Linehan JH, Rickaby DA, Bronikowski TA. Ann Biomed Eng 15: 217–227, 1987; Peeters FAM, Bronikowski TA, Dawson CA, Linehan JH, Bult H, Herman AG. J Appl Physiol 66: 2328–2337, 1989) The identification and quantitation of the cleft pathway conductance from these