Delay discounting (DD), a measure of impulsivity, describes the rate at which rewards lose value as the delay to their receipt increases. Greater discounting has been associated with cigarette smoking and various other types of drug abuse in recent research. The present study examined whether DD predicts treatment outcome among cigarette smokers. More specifically, the authors examined whether baseline discounting for hypothetical monetary rewards predicted smoking status at 24 weeks postpartum among women who discontinued smoking during pregnancy. Participants were 48 pregnant women (10.5 = 4.1 weeks gestational age at study entry) who participated in a clinical trial examining the use of incentives to prevent postpartum relapse. Several sociodemographic characteristics (being younger, being less educated, and reporting a history of depression) assessed at study entry were associated with increased baseline DD, but in multivariate analyses only DD predicted smoking status at 24 weeks postpartum. Greater baseline DD was a significant predictor of smoking status at 24 weeks postpartum. DD was reassessed periodically throughout the study and did not significantly change over time among those who eventually resumed smoking or those who sustained abstinence. The results extend the association of DD with risk for substance abuse to pregnant and recently postpartum cigarette smokers and demonstrate a significant relationship between DD and treatment outcome.

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We identified the Schizosaccharomyces pombe mex67 gene (spmex67) as a multicopy suppressor of rae1-167 nup184-1 synthetic lethality and the rae1-167 ts mutation. spMex67p, a 596-amino-acid-long protein, has considerable sequence similarity to the Saccharomyces cerevisiae Mex67p (scMex67p) and human Tap. In contrast to scMEX67, spmex67 is essential for neither growth nor nuclear export of mRNA. However, an spmex67 null mutation (⌬mex67) is synthetically lethal with the rae1-167 mutation and accumulates poly(A) ؉ RNA in the nucleus. We identified a central region (149 to 505 amino acids) within spMex67p that associates with a complex containing Rae1p that complements growth and mRNA export defects of the rae1-167 ⌬mex67 synthetic lethality. This region is devoid of RNA-binding, N-terminal nuclear localization, and the C-terminal nuclear pore complex-targeting regions. The (149-505)-green fluorescent protein (GFP) fusion is found diffused throughout the cell. Overexpression of spMex67p inhibits growth and mRNA export and results in the redistribution of the diffused localization of the (149-505)-GFP fusion to the nucleus and the nuclear periphery. These results suggest that spMex67p competes for essential mRNA export factor(s). Finally, we propose that the 149-505 region of spMex67p could act as an accessory factor in Rae1p-dependent transport and that spMex67p participates at various common steps with Rae1p export complexes in promoting the export of mRNA.

Delay discounting (DD) describes how the value of a reinforcer decreases as delay to its delivery increases. Relationships between DD and various aspects of drug abuse have been demonstrated reliably. A potential barrier to wider adoption of DD techniques is that results are often expressed in terms that may be too abstract or unfamiliar to a broader audience, particularly when describing or comparing hyperbolic DD functions or values of k. In an effort to potentially make DD results more accessible, the current report explores use of an ED50 value in characterizing DD functions, similar to that used in pharmacology research for characterizing dose-effect functions. The ED50 proposed with regard to DD is the delay that is effective in discounting the subjective value of the delayed reinforcer by 50%. Additionally, a convenient method for calculating ED50 values for DD is discussed.

These results offer a more efficient procedure for experimentally promoting smoking abstinence, while providing further evidence that an initial period of sustained abstinence produces a profile of changes consistent with an overall lowering of relapse risk.

The breast cancer tumor suppressor BRCA2-interacting protein, DSS1, and its homologs are critical for DNA recombination in eukaryotic cells. We found that Dss1p, along with Mlo3p and Uap56p, Schizosaccharomyces pombe homologs of two messenger RNA (mRNA) export factors of the NXF-NXT pathway, is required for mRNA export in S. pombe. Previously, we showed that the nuclear pore-associated Rae1p is an essential mRNA export factor in S. pombe. Here, we show that Dss1p and Uap56p function by linking mRNA adapter Mlo3p to Rae1p for targeting mRNA-protein complex (mRNP) to the proteins of the nuclear pore complex (NPC). Dss1p preferentially recruits to genes in vivo and interacts with -FG (phenylalanine glycine) nucleoporins in vivo and in vitro. Thus, Dss1p may function at multiple steps of mRNA export, from mRNP biogenesis to their targeting and translocation through the NPC.

Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. It has demonstrated neuroprotective properties against many forms of dementia. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of Aβ. While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit Aβ-related damages.

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