פרסומים

Human blood leukocytes and platelets and mouse peritoneal macrophages emit very rapid and very intense Luminol-dependent chemiluminescence (CL) signals when treated with streptococci, staphylococci, or with zymosan, which have been preopsonized with arginine-rich histone, dextran sulfate or polyanetholesulfonate (liquoid). Liquoid alone at 10-30 micrograms/2 X 10(5) leukocytes also triggers intense CL responses in the absence of a carrier. Strong CL can also be triggered, and at the same levels, when the various polyelectrolytes are simply mixed with the bacteria or zymosan and added to the leukocyte suspensions. The CL responses induced by the polyelectrolyte-bacteria complexes greatly exceed those triggered in leukocytes by antibody-complement-coated particles. Liquoid also shows a unique property of markedly augmenting CL signals which have already been induced by other ligand-coated bacteria or zymosan particles. Streptococci and staphylococci were found to be much superior to zymosan, Gram-positive bacilli, or E. coli as carriers for the various polyelectrolytes in the CL reaction. Neither protamine sulfate, lysozyme, myeloperoxidase, crystalline ribonuclease (all cationic in nature), chondroitin sulfate, heparin, nor alginate sulfate acted as ligands for triggering CL, when used to opsonize bacteria or zymosan. The induction of CL in blood leukocytes by the various ligand-coated bacteria is markedly inhibited by azide, KCN catalase, aminotriazole, and EDTA, agents known to inhibit the production of oxygen radicals following stimulation of leukocytes by opsonized bacteria. Two children diagnosed for chronic granulomatous diseases (CGD) of childhood and an apparently healthy sister of one of the male patients completely failed to respond with CL either to the polyelectrolyte-bacteria complexes, liquoid or antibody-coated bacteria and zymosan. It is proposed that liquoid be employed for the rapid screening of defects in certain oxygen-dependent metabolic processes in both PMNs and macrophages. It is also suggested that polyelectrolytes like the ones described in this study may markedly enhance the bactericidal properties of leukocytes and macrophages towards both extracellular and intracellular microorganisms and may perhaps also augment the tumoricidal effects of activated macrophages.

Brominated surfactants are prepd. by the complete bromination of the double bonds in the hydrophobic chains of the oleic acid [112-80-1], linoleic acid [60-33-3], Span 80 [1338-43-8], Span 85 [26266-58-0], Tween 80 [9005-65-6], and Tween 85 [9005-70-3]. The addn. of Br increases the sp. gr. of the surfactant mol. to values above that of water, allowing the formation of oil-in-water emulsions with denser droplets, i.e., the surfactants are emulsifiers and weighting agents. The surfactant properties of the brominated surfactants are discussed. [on SciFinder(R)]

Both antibodies and complement components are essential for successful phagocytosis of many virulent microorganisms (1,2). Although the mechanisms by which opsonins promote particle uptake are not fully understood, it has been suggested that both electrostatic and hydrophobic forces act in concert with specific receptors for Fc and C3b to facilitate interiorization of particles (2,3). In the case of group A streptococci, opsonization by immunoglobulins abolishes the anti-phagocytic properties of the M-antigen (4,5). Since one mechanism by which opsonins may act is to decrease repulsion forces between negative charges present on the surface of the particle and phagocyte, cationic ligands may function as effective opsonins (6–11). In addition, cationic substances may participate in bacteriolysis. We recently suggested (11) that the breakdown of bacterial cells following phagocytosis is mediated indirectly by leukocyte cationic proteins and phospholipases which activate autolytic enzymes and not by lysosomal enzymes directly.

Various polyelectrolytes were investigated regarding their capacity to inhibit the binding of human IgG to Fc-receptors on group A streptococci, type M1. Of cationic substances, protamine and arginine-rich histone inhibited significantly, while lysine-rich histone, concanavalin A, lysozyme, polymyxin B, ribonuclease and tuftsin did not. Of anionic materials, liquoid was inhibitory, in contrast to chondroitin sulphate, dextran sulphate, DNA and heparin. Washing experiments showed that the inhibition was caused by binding of the polyelectrolytes to the streptococci. The finding that heated IgG inhibited the binding of histone to the streptococci also indicated a close relation between the binding sites for these compounds. Diffusion-in-gel experiments with alkaline extract of M1 demonstrated that the substances blocking the IgG Fc-receptor were bound to polyglycerophosphate, suggesting that the inhibition of the IgG uptake was due to interaction with lipoteichoic acid. Leukocyte and platelet extracts could modify the binding of IgG, probably by an enzymatic digestion of the receptors. The arginine-rich histone was also capable of inhibiting the binding of IgG to type M15 group A streptococci and to one group G strain. However, the polyelectrolytes had no effect on the binding of IgG to Staphylococcus aureus or of IgA to type 4 group A streptococci.

In contrast to former findings lysozyme was able to attack the cell walls of Staphylococcus aureus under acid conditions. However, experiments with 14C-labelled cell walls and ribonuclease indicated that, under these conditions, lysozyme acted less as an muralytic enzyme but more as an activator of pre-existing autolytic wall enzymes. Electron microscopic studies showed that under these acid conditions the cell walls were degraded by a new mechanism (i.e. "attack from the inside"). This attack on the cell wall started asymmetrically within the region of the cross wall and induced the formation of periodically arranged lytic sites between the cytoplasmic membrane and the cell wall proper. Subsequently, a gap between the cell wall and the cytoplasmic membrane resulted and large cell wall segments became detached and suspended in the medium. The sequence of lytic events corresponded to processes known to take place during wall regeneration and wall formation. In the final stage of lysozyme action at pH 5 no cell debris but "stabilized protoplasts" were to be seen without detectable alterations of the primary shape of the cells. At the same time long extended ribbon-like structures appeared outside the bacteria. The origin as well as the chemical nature of this material is discussed. Furthermore, immunological implications are considered.

DNA-mediated gene transfer was used to investigate the mode of inheritance of 5-methylcytosine in mouse L cells. Unmethylated phi X174 replicative form DNA remains unmethylated after its introduction and integration into these cells. On the other hand, phi X174 replicative form DNA that was methylated in vitro at its C-C-G-G residues retains these methylations as shown by restriction enzyme analysis with Hpa II and Msp I to detect methylation at this specific site. Although these unselected methylated vectors are prone to lose 30-40% of their methyl moieties upon transfection, this demethylation appears to be random. Once established, the resulting methylation pattern is stable for at least 100 cell generations. In order to examine the specificity of methylation inheritance, fully hemimethylated duplex phi X174 DNA was synthesized in vitro from primed single-strand phi X174 DNA by using 5-methyl deoxycytidine 5’-triphosphate. This molecule was inserted into mouse L cells by cotransformation and subsequently was analyzed by a series of restriction enzymes. Only methylations located at C-G residues were conserved after many generations of cell growth. The results suggest that the inheritance of the cellular DNA methylation pattern is based on a C-G-specific methylase that operates on newly replicated hemimethylated DNA.

In 1972, the World Health Organization’s "Meeting of Investigators on the Histological Definitions in Precancerous Lesions" defined a precancerous lesion as a "morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counter part" (Pindborg 1980). There are two generally accepted precancerous lesions in the oral cavity, leukoplakia and erythroplakia (Pindborg 1980). Leukoplakia is currently defined as "a white patch or plaque that cannot be characterized clinically or pathologically as any other disease" (WHO 1978). This definition has no histological connotation and is used in a strictly clinical sense (Pindborg 1980, Banoczy 1977). Erythroplakia is defined as a "bright red velvety plaque which cannot be characterized clinically or pathologically as being due to any other condition" (Pindborg 1980).

The less thermodynamically stable modification of tristearin [555-43-1], termed $\alpha$, is preserved when 1-10% of sorbitan monostearate [1338-41-6] emulsifier was added before allowing the molten fat to cool and crystallize. Several other emulsifiers were tested, and it was found that the combination of bulkiness of the hydrophilic groups and the appropriate length of the hydrophobic chains of a given emulsifier is necessary to preserve the $\alpha$-modification. Liq. emulsifiers and those having a pronounced hydrophilic character are not efficient as modifiers. The emulsifier was incorporated into the tristearin during crystn. from solvent without an immediate effect, but it affects subsequent behavior upon melting and resolidification. [on SciFinder(R)]

The author, one of the few surviving eyewitnesses from the Warsaw ghetto uprising, helped Yosef Kaplan create the Jewish Fighting Organization and led it in its early stages. He describes Kaplan’s contribution to the creation of the organization and his activities until his arrest and murder by the Nazis.