An assessment of token value and effectiveness: A replication.

The purpose of the current study was to conduct a systematic replication of Fiske et al. (2015) to extend the behavior-analytic literature on token reinforcement. Specifically, the researchers addressed several of the limitations of Fiske et al. by including specific conditioning procedures, creating a controlled history of reinforcement with the token system, including participants with and without disabilities to extend the generality of the findings, and equating the magnitude of reinforcement across the primary and paired-token conditions. The current study evaluated the reinforcing value of tokens by using progressive-ratio schedules to compare the efficacy of primary reinforcement, paired tokens, and unpaired tokens. The results suggest that paired tokens may function as reinforcers, but they were not as consistently effective as primary reinforcers.

"Other" behavior and the DRO: The roles of extinction and reinforcement.

Jessel et al. (2015) provided some evidence to suggest that "other" behavior is strengthened in the differential reinforcement of other behavior (DRO). The present study is a systematic replication of the Jessel et al. procedures. The effects of DRO and extinction on target responding, target-other responding (a response with an established history of reinforcement), and nontarget-other responding emitted by children with intellectual and developmental disabilities and children with no known diagnoses were compared. Other behavior increased in at least one DRO condition for each participant, suggesting that other behavior increases when using DRO, at least initially. Under extinction, target responding and target-other responding decreased to low rates for three of the five participants; however, rates of nontarget-other responding were elevated compared to the DRO condition. These results suggest that increased rates of target-other responding and nontarget-other responding during the DRO condition may be a result of extinction-induced variability.

Effects of targeted phosphorylation site mutations in the DNA-PKcs phosphorylation domain on low and high LET radiation sensitivity.

The present study investigated the effect of targeted mutations in the DNA-dependent protein kinase catalytic subunit and phosphorylation domains on the survival of cells in response to different qualities of ionizing radiation. Mutated Chinese hamster ovary V3 cells were exposed to 500 MeV/nucleon initial energy and 200 keV/µm monoenergetic Fe ions; 290 MeV/nucleon initial energy and average 50 keV/µm spread-out Bragg peak C ions; 70 MeV/nucleon initial energy and 1 keV/µm monoenergetic protons; and 0.663 MeV initial energy and 0.3 keV/µm Cs137 γ radiation. The results demonstrated that sensitivity to high linear energy transfer radiation is increased when both S2056 and T2609 clusters each contain a point mutation or multiple mutations are present in either cluster, whereas the phosphoinositide 3 kinase cluster only requires a single mutation to induce the sensitized phenotype of V3 cells. Additionally, the present study demonstrated that sensitivity to DNA cross-linking damage by cisplatin only requires a single mutation in one of the three clusters and that additional point mutations do not increase cell sensitivity.

Comparison of cellular lethality in DNA repair-proficient or -deficient cell lines resulting from exposure to 70 MeV/n protons or 290 MeV/n carbon ions.

Charged particle therapy utilizing protons or carbon ions has been rapidly intensifying over recent years. The present study was designed to jointly investigate these two charged particle treatment modalities with respect to modeled anatomical depth-dependent dose and linear energy transfer (LET) deliveries to cells with either normal or compromised DNA repair phenotypes. We compared cellular lethality in response to dose, LET and Bragg peak location for accelerated protons and carbon ions at 70 and 290 MeV/n, respectively. A novel experimental live cell irradiation OptiCell™ in vitro culture system using three different Chinese hamster ovary (CHO) cells as a mammalian model was conducted. A wild-type DNA repair-competent CHO cell line (CHO 10B2) was compared to two other CHO cell lines (51D1 and xrs5), each genetically deficient with respect to one of the two major DNA repair pathways (homologous recombination and non-homologous end joining pathways, respectively) following genotoxic insults. We found that wild-type and homologous recombination-deficient (Rad51D) cellular lethality was dependent on both the dose and LET of the carbon ions, whereas it was only dependent on dose for protons. The non-homologous end joining deficient cell line (Ku80 mutant) showed nearly identical dose-response profiles for both carbon ions and protons. Our results show that the increasingly used modality of carbon ions as charged particle therapy is advantageous to protons in a radiotherapeutic context, primarily for tumor cells proficient in non-homologous end joining DNA repair where cellular lethality is dependent not only on the dose as in the case of more common photon therapeutic modalities, but more importantly on the carbon ion LETs. Genetic characterization of patient tumors would be key to individualize and optimize the selection of radiation modality, clinical outcome and treatment cost.