Effect of solvents and initiators on the cationic copolymerization of 1,3-dioxolane with 5-methyl-2,3-dihydro-2-furanone

The cationic copolymerization of 1,3-dioxolane ( 1 ) with 5-methyl-2,3-dihydro-2-furanone ( 2 ) which has two functional groups, a carbon-carbon double bond and a lactone ring, was carried out with three triethyloxonium salts (Et₃O⁺Y^?, Y^?: BF, FeCl and SbCl), with the boron trifluoride ethyl ether complex, and with tin tetrachloride in nitrobenzene, dichloromethane, and toluene at 0°C. On the basis of the NMR analysis of the microstructure of the copolymer, it was revealed that the growing species of 1 attacked exclusively the carbon-carbon double bond of 2 in the cross-propagation from 1 to 2 , regardless of the solvents and initiators used, except when triethyloxonium hexachloroantimonate was used as initiator. With the latter initiator, the ring opening reaction of 2 by the attack of the growing species of 1 occurred competitively with the usual vinyl addition, although the latter mode of reaction was predominant. The ring opening reaction of 2 with this initiator is probably caused by some specific interaction of monomer 2 with the counter anion.     

Specific effect of antimony(V) containing initiators on the cationic copolymerization of 1,3-dioxolane with 5-methyl-2,3-dihydro-2-furanone

The copolymerization of 1,3-dioxolane ( 1 ) with 5-methyl-2,3-dihydro-2-furanone ( 2 ) was carried out in dichloromethane and nitrobenzene by use of triethyloxonium hexachloroantimonate, triethyloxonium hexafluoroantimonate, antimony pentachloride, antimony trichloride, and tin tetrachloride as initiators. The microstructures of the copolymers were analysed by means of ¹H-NMR, showing that monomer 2 was incorporated into the copolymer chain by the ring-opening reaction as well as by the ?normal”? vinyl addition, when triethyloxonium hexachloroantimonate, triethyloxonium hexafluoroantimonate, and antimony pentachloride were used. On the basis of NMR and IR studies on the complexation of Lewis acids with γ-lactones, it was concluded that the prominent effect of the initiators observed in the copolymerization of 1 with 2 was mainly attributable to the coordination between the initiator and the γ-lactone ring of monomer 2 .     

Vinyl polymerization. 120. Mutual copolymerization of p-substituted styrenes through radical mechanism

The radical mutual copolymerization of p-substituted styrenes, such as p-methoxy-, p-chloro-, p-bromo-, p-cyanostyrene, and styrene was carried out with one another at 30°C. in the dark. As initiator, azobisisobutyronitrile was used. The plots of the copolymerization rates against HAMMETT 's σ values showed no linear relationships and the concave curves were obtained therefrom. The relative reactivities of p-substituted styrenes with a definite p-substituted polystyryl radical, which were shown by the reciprocal of monomer reactivity ratio r₁, were plotted against σ values and concave curves were also obtained. The relative reactivities of p-substituted polystyryl radicals with p-substituted styrene were calculated from the ratios r₂ and the propagation rate constants in homopolymerization. the plots of them against σ values gave straight lines with different ρ values, according to the polarity of substituents. These results suggest that polar structures in transition state affected markedly the copolymerization rates. The effect of substituents on resonance stabilization was also quantitatively estimated.     

Lysosome is a primary organelle in B cell receptor-mediated apoptosis: an indispensable role of Syk in lysosomal function

To investigate the mechanism of B cell receptor (BCR)-mediated apoptosis, we utilized immature B cell lines, DT40 and WEHI-231. In both cell lines, BCR-crosslinking caused the increase in lysosomal pH with early apoptotic changes characterized by chromatin condensation and phosphatidylserine exposure. This increase was detected in c-Abl-deficient DT40 cells but not in Syk-deficient cells, which corresponded to the fact that the former cells but not the latter revealed BCR-induced apoptosis. In contrast, BCR-crosslinking caused no apparent change in mitochondrial transmembrane potential. Therefore, the lysosomal change might be a primary event in BCR-induced apoptosis in DT40 cells. The increased activity of cathepsin B and apoptosis-preventing effect of a cathepsin inhibitor suggested a significant role of lysosomal enzymes in this apoptosis. By microscopic studies, lysosomes of wild-type DT40 cells fused to BCR-carrying endosomes became enlarged and accumulated one another. In contrast, these changes of lysosomal dynamics did not occur in Syk-deficient cells but transfer of wild-type Syk restored the lysosomal changes and apoptosis. These results demonstrated that the lysosomal change accompanied with the activation of lysosomal enzymes is a primary step in BCR-crosslinking-mediated apoptosis and Syk is responsible for this step through the fusion of BCR-carrying endosomes to lysosomes.     

Role of Bcl-2 family proteins in apoptosis: apoptosomes or mitochondria?

Apoptosis is an essential physiological process for the selective elimination of cells, which is involved in a variety of biological events. The Bcl-2 family is the best characterized protein family involved in the regulation of apoptotic cell death, consisting of anti-apoptotic and pro-apoptotic members. The anti-apoptotic members of this family, such as Bcl-2 and Bcl-x_L, prevent apoptosis either by sequestering proforms of death-driving cysteine proteases called caspases (a complex called the apoptosome) or by preventing the release of mitochondrial apoptogenic factors such as cytochrome c and AIF (apoptosis-inducing factor) into the cytoplasm. After entering the cytoplasm, cytochrome c and AIF directly activate caspases that cleave a set of cellular proteins to cause apoptotic changes. In contrast, pro-apoptotic members of this family, such as Bax and Bak, trigger the release of caspases from death antagonists via heterodimerization and also by inducing the release of mitochondrial apoptogenic factors into the cytoplasm via acting on mitochondrial permeability transition pore, thereby leading to caspase activation. Thus, the Bcl-2 family of proteins acts as a critical life–death decision point within the common pathway of apoptosis.     

Calmodulin and cyclic ADP-ribose interaction in Ca2+ signaling related to cardiac sarcoplasmic reticulum: superoxide anion radical-triggered Ca2+ release

Reactive oxygen species (ROS) are often shown to damage cellular functions. The targets of oxidative damage depend on the nature of ROS produced and the site of generation. In contrast, ROS can also regulate signal transduction. In this case, ROS may either induce or enhance events, which lead to forward directions of cellular signaling. The consequences of regulation of signal transduction can be observed in physiological processes such as muscle contraction. Here, we discuss the concentration-dependent effects of superoxide anion radical (*O2-) on Ca2+ release from the cardiac sarcoplasmic reticulum (SR). Recent studies suggest that the ADP-ribosyl cyclase pathway, through its production of cyclic adenosine 5'-diphosphoribose (cADPR), may control Ca2+ mobilization in cardiac muscle cells. *O2- has dual effects that are concentration dependent. At low concentrations (nearly nanomolar levels), *O2- induces Ca2+ release by stimulating synthesis of cADPR, which requires calmodulin for sensitization of ryanodine-sensitive Ca2+-release channels (RyRC). At these low concentrations, *O2- is responsible for regulation of cellular signal transduction. At higher concentrations (micromolar levels), *O2- produces a loss in the function of calmodulin that is to inhibit RyRC. This results in an increase in Ca2+ release, which is linked to cell injury. The difference in the functions of low and high concentrations of *O2- may result in two distinct physiological roles in cardiac muscle Ca2+ signaling.     

Chemical and biological properties of a peptidoglycan isolated from Treponema pallidum kazan.

A peptidoglycan layer of Treponema pallidum kazan was isolated by solubilization of whole cells with 1% warm sodium dodecyl sulfate and subsequent digestion of an insoluble residue with proteases. Electron microscopy revealed that the peptidoglycan was isolated as a single-layered sacculus of less than 5 nm in thickness, freed from axial filaments and an envelope sheath. An isolated peptidoglycan fraction was mainly composed of glucosamine, muramic acid, alanine, glutamic acid, ornithine, and glycine in molar ratios of 0.65:0.68:1.63:1.00:0.75:1.03. Amino (N)- and carboxyl (C)-terminal amino acid analyses suggested the involvement of at least a part of the glycine residue in cross-linking between the amino group of ornithine residue at one strand of the stem peptide subunit and the carboxyl group of alanine of the neighboring strand. The treponemal peptidoglycan lacked the immunoadjuvant activity both to stimulate antibody production and to induce delayed-type hypersensitivity against ovalbumin, as well as the properties necessary to stimulate guinea pig and mouse splenocytes and guinea pigs peritoneal macrophages, unlike the cell walls or peptidoglycans (group A type of Schleifer and Kandler's classification, Bacteriol. Rev. 36:407-477, 1972) isolated from many bacterial species parasitic to the mammal. However, the peptidoglycan activated the human complement system through the alternative pathway, as well as the classical one, and caused a liberation of 5-hydroxytryptamine in rabbit blood platelets in a similar manner to the cell wall peptidoglycans of both group A and B types.     

Detection and characterization of simian retroviruses homologous to human T-cell leukemia virus type I

Lymphoid cell lines were established from five different species of monkeys which were positive in antibodies cross-reactive with human T-cell leukemia virus type I (HTLV-I) and were shown to contain provirus sequences homologous to HTLV-I. Gene-specific probes of HTLV-I, gag, pol, env, pX, and LTR, hybridized efficiently with monkey DNAs from these cell lines under stringent conditions, indicating that the proviruses are very similar to HTLV-I along with whole viral genomes. However, the preliminary restriction mapping turned out the difference between simian retroviruses and HTLV-I and also among simian retroviruses. These findings suggest a common ancestor of simian and human retroviruses, but exclude the recent interspecies transmission between monkeys and humans.