Transport of benzenesulfonic acid derivatives through the rat erythrocyte membrane

Summary Transport of benzenesulfonic acid derivatives through the rat erythrocyte membrane was studied. The transport properties, such as pH-dependence and effects of reagents reacting with amino-groups, were similar to those of anions like Cl^– through the human erythrocyte membrane. The rate of transport of anions through rat erythrocyte membranes is higher than through those of other mammals, such as guinea pig and bovine erythrocyte membranes. This relatively high rate of transport makes the rat erythrocyte membrane suitable for use in comparative studies on the transports of slowly penetrating substances, such as organic anions. The transport velocities of benzenesulfonic acid derivatives were compared with their physico-chemical properties. It was shown that the hydrophobicity has no effect on the transport, but the electronic property has a significant effect: the transport rate is mainly dependent on thee ^– donor capacities. This feature is the inverse to the well-known inhibitory effect of these derivatives on other anion transport: the inhibition is mainly dependent on thee ^– acceptor capacities. It is suggested that the transport is regulated by the binding capacity of anions to the transport site.     

Inhibiton of platelet aggregation by 1-alkylimidazole derivatives,thromboxane a synthethase inhibitors

1-Alkylimidazole derivatives of various sidechain lengths with various functional groups at the terminal end of the alkychain inhibited the synthesis of thromboxane A₂ from arachidonic acid by rabbit platelets and the conversion of prostaglandin H₂ to thromboxane A₂ by the microsomes of rabbit platelets. These enzyme inhinitors were anti-aggregatory as examine with rabbit and human platelet-rich plasma under various experimental conditions.     

Immunocytochemical detection of enhanced expression of c-myc protein in the heart of cardiomyopathic hamster

An immunocytochemical study was performed to examine the expression of cellular c-myc protein in the heart of 30-, 120- and 180-day-old cardiomyopathic Syrian UM-X7.1 hamsters. The heart of age- and sex-matched BIO-RB hamster was used as normal control. In paraffin sections, an immunostaining for c-myc was markedly increased in cytoplasm of cells from the UM-X7.1 heart as compared with that of the BIO-RB heart which showed a weak staining. However, c-myc was localized in nuclei of cells in frozen sections of the heart. Specific cell types of the heart were differentiated with anti-vimentin, and we found that the increased expression of c-myc was present in nuclei of muscle cells of the UM-X7.1 myocardium. A quantitative study of c-myc-positive nuclei of muscle and nonmuscle cells was carried out by a video micrometer. The mean number of c-myc-positive nuclei of muscle cells was significantly higher in the cardiomyopathic heart than in the control heart from hamsters of all ages studied. These results suggest that the increase of c-myc protein may relate to the pathological state or pathogenesis of the hereditary cardiomyopathy.     

A macrolide antibiotic,roxithromycin, inhibits the growth of human myeloid leukemia HL60 cells by producing multinucleate cells

The antiproliferative effect of roxithromycin (RXM) was studied using human myeloid leukemia HL60 cells. RXM inhibited the growth of HL60 cells in a concentration-dependent manner, and significantly inhibited growth at concentrations above 75 M. This growth inhibition was not associated with specific cell cycle arrest and DNA synthesis was not impaired. In addition, the number of viable cells remained almost unchanged in the presence of 100 M RXM. RXM induced growth inhibition at least partly by the formation of multinucleate cells. Both flowcytometric and morphological examination revealed that more than 40% of the RXM-treated cells were binucleate. These findings demonstrate that RXM is a potent new modulator of cell cycle progression in HL60 cells and suggest that the inhibition of cytokinesis by this drug may provide a new model for studying mitosis.     

Cloning and sequence analysis of Vibrio parahaemolyticus ompK gene encoding a 26-kDa outer membrane protein, OmpK, that serves as receptor for a broad-host-range vibriophage, KVP40

Abstract The ompK gene of Vibrio parahaemolyticus 1010 (RIMD 2210001) encoding an outer membrane protein (OMP), OmpK, which serves as the receptor for a broad-host-range vibriophage, KVP40, was cloned and sequenced. The gene consisted of 789 nucleotides encoding 263 amino acids. Since the first 20 amino acids most likely constitute the signal peptide, mature OmpK would consist of 243 amino acids with a calculated molecular mass of 27458 Da. Sequence comparisons indicate that OmpK is unique among Vibrio OMPs so far sequenced, but may be distantly related to Tsx of enteric bacteria and is homologous to an Aeromonas hydrophila OMP, protein IV.     

Bound acetylcholine in the nerve ending particles

Abstract—

• 1 The bound ACh of rabbit brain tissue homogenate was studied with the French press technique by means of which nerve endings can be ruptured under isotonic condition.
• 2 Two fractions of B-ACh, stable and labile were obtained which were roughly equal in amount. The yield of B-ACh after disruption of nerve ending particles was about 28 per cent of the initial total ACh and higher than that formed after the hypotonic disruption.
• 3 The results support the view that the stable fraction of B-ACh is enclosed inside the vesicle membrane, while the labile fraction is present in the cytoplasm of the cell.
• 4 ACh released from such intact vesicle fractions was roughly parallel to the ionic strength of the solution at 0°, without relation to the nature of the ion itself.
• 5 Electronmicroscopic examination with PTA showed that the vesicles released by the French press technique were largely intact, although the nerve ending particles were completely disrupted by the same treatment.