Comparison of sialylation of maltase-glucoamylase in brush-border and soluble fractions of the small intestine of immature rats.

Two fractions of high-molar-mass soluble neutral maltase-glucoamylase (G1 and G2) of distal small intestine of 18-day-old rats separated on Sepharose 4B differ in sialylation which is reflected in their pI values obtained by chromatofocusing. The major soluble G1 fraction shows eight sialylated peaks converted by neuraminidase into a single fraction eluted at pH 4.21. Fraction G2 is less sialylated and neuraminidase causes its pI shift to 4.36. The chromatofocusing pattern suggests that G1 contains more acidic and G2 more basic glycoforms than their membrane-bound counterpart. Presence of less acidic pI values in the soluble G1 fraction of 18-day-old rats than in that of 13-day-old rats indicates that developmental decrease of sialylation concerns not only membrane-bound but also the soluble membrane-type of maltase-glucoamylase.     

Effect of hydrocortisone on sialyltransferase activity in the rat small intestine during maturation. Changes along the villus-crypt axis and in fetal organ culture

Sialyltransferase activity was assayed in rat intestinal cells isolated as fractions reflecting the villus-crypt axis of differentiation. In 13-day-old rats both endo- and exogenous sialyltransferase activity reached their maximum in undifferentiated crypt cells and their peaks overlapped. In contrast, sialyltransferase of the adult intestine was 4-fold lower than that of sucklings in the crypts, with slight tendency to be transferred to the villus cells. Hydrocortisone applied to 10-day-old rats caused three days later a precocious drop of sialyltransferase activity in the crypt cells. Unlike in vivo, glucocorticoid responsiveness was accompanied by increased sialyltransferase activity in fetal small intestine cultivated for 17 days.     

Performic acid toxicity studies on stabilized HEp-2 cells

Since performic acid is used as a potent disinfectant, chemical sterilant and/or skin antiseptics, information related to its toxicity for living tissues was needed to evaluate the degree of its biotolerance and compare it to that of peracetic acid. In tests on cultured HEp-2 cells distinct cytotoxic effects occurred after treatments with 0.05% and higher concentrations. The 0.005% to 0.000,05% concentrations had only minor effects on the morphology of cells, if passaged they were capable of further growth, but were clearly inhibited in their growth ability. The lowest concentration tested (0.000005%) had no appreciable effect on HEp-2 cells. At the same concentration levels, the cells were affected to a greater degree with performic acid than with peracetic acid treatment. The use of cell cultures as a tool to study in vitro toxicity of various materials is discussed.     

Transport,localization and physiological effect of 6-benzyladenme-8-14C in apple shoots

The transport of radioactivity of 6-benzyladenine-8-¹⁴C applied to one-year old apple shoots was studied. Simultaneously, labelled metabolites of this cytokinin were studied separately in the xylem and phloem above and below the place of application. According to the results obtained, it can be assumed that 6-B and its metabolites are transported in one-year old apple shoots acropetally through the xylem and basipetally through the phloem, while penetrating from the xylem to the phloem. Besides 6-B-8-¹⁴C, a complex of cytokinin with sugar, also adenosine and adenine were found in the phloem.     

The cytokine midkine and its receptor RPTPζ regulate B cell survival in a pathway induced by CD74

Lasting B cell persistence depends on survival signals that are transduced by cell surface receptors. In this study, we describe a novel biological mechanism essential for survival and homeostasis of normal peripheral mature B cells and chronic lymphocytic leukemia cells, regulated by the heparin-binding cytokine, midkine (MK), and its proteoglycan receptor, the receptor-type tyrosine phosphatase ζ (RPTPζ). We demonstrate that MK initiates a signaling cascade leading to B cell survival by binding to RPTPζ. In mice lacking PTPRZ, the proportion and number of the mature B cell population are reduced. Our results emphasize a unique and critical function for MK signaling in the previously described MIF/CD74-induced survival pathway. Stimulation of CD74 with MIF leads to c-Met activation, resulting in elevation of MK expression in both normal mouse splenic B and chronic lymphocytic leukemia cells. Our results indicate that MK and RPTPζ are important regulators of the B cell repertoire. These findings could pave the way toward understanding the mechanisms shaping B cell survival and suggest novel therapeutic strategies based on the blockade of the MK/RPTPζ-dependent survival pathway.