Morphology of composite film prepared by polymerizing styrene in poly(vinyl chloride) film

Styrene and the styrene-additive mixtures (kerosene, dioxane, ethylene dichloride, or dioctylphthalate) were soaked into a poly(vinylchloride) film and then styrene was polymerized. Subsequently, poly(styrene) was extracted with CCl₄ and the microporous membrane was obtained, of which the morphology was studied. It is elucidated that the additives affect the morphology of the resultant composite films.     

Polymeric ultraviolet absorber

Polymeric fine powder, prepared by polymerization of glycidylmethacrylate–divinylbenzene, was reacted with 2,4-dihydroxylbenzophenone. The resultant polymer was effective as a polymeric ultraviolet absorber, and no migration was observed in polypropylene.     

High-field conduction and carrier traps in polyethylene copolymerized with various monomers

The electrical breakdown and electrical conduction of ethylene copolymers have been studied. The electric strength of ethylene copolymers containing an optimum content of halogen moieties such as bromophenyl and fluoroethylene groups was found to be higher than that of LDPE over the wide temperature range from ?196°C to 90°C. Also, conduction currents in the copolymers were suppressed at high electric fields. X-ray-induced thermally stimulated currents (TSC) revealed that halogen comonomers act as carrier traps with a depth of about 0.4 eV. Consequently, the introduction of comonomer-containing halogen groups into polyethylene suppresses electron acceleration as a result of an increase in trapping and scattering of conduction electrons. This leads to an increase in electric strength which is determined by the electron avalanche breakdown.     

Copolymerization of styrene–m-divinylbenzene in the presence of poly(vinyl chloride)

The crosslinking copolymerization of styrene (St)-m-divinylbenzene (m-DVB) in the presence of poly(vinyl chloride) (PVC) was studied. The rate of the copolymerization decreased with the addition of PVC powder, because of the depressing of the diffusion of the monomers to the polymerizing center and the difficulty in the transfer of the polymer radicals in the swelled PVC powder. The exponential value of the benzoyl peroxide concentration and the activation energy of the copolymerization were obtained as 0.67 and 17.4 kcal/mol, respectively. The monomer reactivity ratios of St and m-DVB were determined as r₁ = 0.25 and r₂ = 1.42 (M₁: St, M₂: m-DVB). From the extraction of the resultant polymer composite with THF, both the grafting of the St-m-DVB copolymer onto PVC and the entanglement of PVC with St-m-DVB copolymer seems to occur in the St-m-DVB-PVC system.     

Defective control of apoptosis, radiosensitivity, and spindle checkpoint in ataxia telangiectasia

We examined the regulation of apoptosis, radiosensitivity, and spindle checkpoint in response to DNA-damaging agents in ataxia telangiectasia (AT)-derived lymphoblastoid cell lines (AT-LCLs), which lack AT mutated (ATM) protein expression. In addition to the previous findings that AT-LCLs are defective in regulation of cell cycle at the G1, S, and G2-M checkpoints in response to X-ray irradiation (X-IR) and are highly sensitive to X-IR (J. Biol. Chem., 271: 20486-20493, 1996), we showed for the first time that AT-LCLs were defective in X-IR-associated spindle checkpoint control. The cells were also resistant to early apoptosis as much as LCLs derived from patients with Li-Fraumeni syndrome (LFS-LCLs). Terminal deoxynucleotidyl transferase-mediated nick end labeling assay of LCLs, however, demonstrated a significant increase in apoptotic cells among AT-LCLs cultured over a longer period after X-IR. These findings were in contrast to those of LFS-LCL, which showed very little increase in terminal deoxynucleotidyl transferase-mediated nick end labeling-positive population, even in cells with hyperploidy. Thus, although early apoptosis and cell cycle controls in response to DNA damage are disrupted in both ATM and p53 mutations, cells from AT patients are much more susceptible to late-onset apoptosis than those of LFS. These differences may depend on the level of accumulation of DNA damage and/or threshold that triggers late-onset cell death in ATM or p53 mutations. Our findings allow a better understanding of the role of ATM in p53-dependent and independent signal transduction pathways in response to DNA damaging agents.