SYNOPSISMagnetic latex particles were prepared by the emulsion polymerization of styrene at 70°C in the presence of a commercial ferrofluid containing surfactant-stabilized magnetite particles in the aqueous phase or its modification by ultrafiltration, using potassium persulfate as an initiator. The effects of diversified variables such as the amounts of initiator, monomer, and additive (calcium chloride and fluorescent dyes) on the polymerization reaction and particle characteristics were investigated. The general polymerization features were analogous to those of ordinary emulsion polymerizations. Transmission electron microscopy revealed that when the commercial ferrofluid was used the magnetite particles localized in the latex particles and the magnetite content varied from particle to particle and that when the ferrofluid was used after ultrafiltration the magnetite particles were dispersed well in the latex particles.
SYNOPSISEmulsion polymerization of styrene and methyl methacrylate in the presence of a ferrofluid was briefly studied. Thermal properties of the resulted latex particles were investigated by TG-DTA analysis. Determination of the residue weight after the thermal analysis that indicated complete decomposition of the organic components was found to be a facile and practical method to determine the magnetite content in the latex particles. The method was applied to magnetic polystyrene latex particles prepared in the presence of various amounts of the ferrofluid. Analysis of the results suggested that the magnetite content in the latex particles is primarily determined by the weight ratio of the ferrofluid to monomer.
Summary To elucidate the mechanism of E-roscilc formation between T cells and sheep red blood cx-lls{SRBC). the effect of variousagentsaifectingihLM'unctionorcytoplasmicstruclures(microtLibules and microtilaments) and organdies (mitocliondria and rough endoplasniic reliculum) was invcstieatcd. E-rosciie formation was greath inhibited by agents that block cither the energy producmg systcnr(KCN and NaNilur the integration ot tiiicrofilaments (cytochalasin B. dihydrocytochalasin B_ ;nui cytochalasin D). On ihe other hand, theic was little or no suppression by either inhihitors ot proici'n synthesis (cytlolieximide and puromycin). agenls that block Ihe polymeti^aiion ol microtubules (coldiicine. podophyllotoxin and vinblastinc). or chemicals disconnecting surface membrane proteins from the iniracellular strLietural proloiiis (chlnrpromazine. ^dibucaine. liydroccrtlsonc. and propranolol). The calcium ionophorc A23187. which transports Cn-' into ihe cyiosol. inhibited the F-rosette formation iiUhe presence of Ca-\ but nol in its absence. I-rum these results, we concluded thai new synthesis of ATE' and the struciural inlegration o\' niicrofilaments arc indispensable for the E-rosette formation, whieh is triggered by an interaetion between the Iigand (Tl ITS) and ils corresponding receptor (CD2). A certain levdorintraeelluIarCa-^ is also involved m the E-rosctte formalion.lMRODUCTION Thymus-derived (T) lymphocytes spontaneously form E-rosctte aggregates with sheep red blood cells (SRBC). and serve as a surface marker for the earliest stage of the expression of hLiman T-Iincage cells (1-3). E-roscttes are widely used in clinical immunology lo identify or to separate T eells (4-6). although their precise intracellular mechanism is unknown.Receni studies on E-rosette formation have shown that it is dependent upon a specilic interaction between the CD2 moleeule on T eells (7-9) and the complementary structure on SRBC termed the Tl I target structure (Tl ITS: iO.ll). The TllTS has been bioehemieally characterized and shown to be a 42 kDa glycoprotcin (10.11). CD2 binds LFA-3. a 55-70 kDa moleeule expressed on human endothelial. epithelial and connective tissue cells in most tissues, as well as human T and B lymphocytes, granuloeytes. and erythrocytes (12).On the other hand, little is known about the participation of eytopiasmie structures and organelles during E-rosette formation, although several reports suggest they probably play an important role. A study of the mechanism of capping of the surface immunoglobulins(slg) on B cells by corresponding anlibodies revealed that this phenomenon was suppressed by corticosteroids maintaining fluidity of membranes. the calcium ionophore A23187 causing Ca-**" tlux. and reagents aetingon microtilaments such as eytochalasin B (13). Another stud\ of lymphocyte adhesion to eultured Feycr's patch high endothelial venule reported that the adhesion oflymphoeytes was suppressed by NaN? and cytoehalasin L) (14). Moreover, the inhibitory effe-n of eytochalasin B and NaNi on Erosette tbrmation h...
A population of human erythrocytes (free A(3) cells) which was entirely unagglutinable with anti-A hemagglutinins was successfully separated from human blood group A(3) erythrocytes by affinity chromatography on a column of lima bean anti-A hemagglutinin (LBH)-Sepharose. The hemagglutinating and the binding properties of free A(3) cells with purified LBH and purified eel serum anti-H hemagglutinin (ESH) were investigated. It has been revealed that there exists a bulk of H antigens on free A3 cells, whereas the number of A antigens on a free A(3) cell is only 9 % of that on an A(1) cell. However, no appreciable difference was observed in the binding constants of A(1) and free A(3) cells to LBH and ESH. From these results it is assumed that the structure of the A antigens on free A(3) cells is identical with, or at least similar to, that on A(1) cells, but the density of the antigens on the surface of free A(3) cells is too low to induce the agglutination of the cells with LBH or anti-A serum.
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